For Vegans

I promise this page isn’t scary or mean!

Despite rumors to the contrary, I’m actually not on a rabid, foaming-at-the-mouth, steak-fueled mission to unveganize the world. My own diet is mostly plants, and I benefit in no way—financially or otherwise—if you decide to put an egg in your mouth instead of a lump of texturized vegetable protein. My sole goal with this blog is to squash out bad science and give folks access to accurate information about diet. What you decide to do with the stuff I say here is completely up to you.

As a former decade-long vegetarian (and vegan for the last few years of that), I understand and respect that food choices are sometimes based on more than our own health. Maybe you’re ethically opposed to killing animals for any reason, are concerned about the treatment of livestock on farms, or simply developed a crippling case of carnophobia after getting locked in a meat freezer when you were five (worst game of hide-and-seek ever). If this is you, I’m not here to talk you out of your choices or values—and even if we disagree on the specifics, I encourage you to live your life in whatever way you find most fulfilling.

Even though I don’t believe strict vegan diets are optimal from a health perspective, I do think there are ways to make the best out of a meatless, eggless, and dairyless situation. I’d like to offer some of those ideas on this page so that anybody personally committed to veganism can maximize their chance of staying healthy, and hopefully avoid the most common pitfalls us annoying ex-vegans blather on about. (Please note that this isn’t an endorsement for current omnivores to convert to veganism, and there’s no guarantee you’ll truly thrive even if you follow all the suggestions below—but I do think these guidelines will give vegans the best chance possible for warding off health problems.)

In no particular order of importance, here’s a summary of the list, followed by a more detailed version of each point:

  1. Eat real food—no fake meats, processed soy products, vegan junk food, etc.
  2. Avoid high omega-6 vegetable oils and take a vegan DHA supplement.
  3. Supplement with vitamin K2.
  4. Supplement with a vegan form of vitamin D3.
  5. Enhance your beta carotene absorption and conversion.
  6. Properly prepare any grains, legumes, or nuts you eat.
  7. Maximize iron absorption using vitamin-C-rich foods.
  8. Keep your thyroid in good shape.
  9. Take vitamin B12.
  10. Try going gluten-free.
  11. Eat some fermented foods.
  12. Supplement with taurine.
  13. Consider adding oysters or other non-sentient bivalves to your diet.

The long version:

1. Eat real foodI wholly believe the plant-based-diet doctors like Caldwell EsselstynJohn McDougall, and Joel Fuhrman are on the right track when they recommend eating things that actually still resemble food—leafy greens, fruit, tubers, squash, legumes, root vegetables, seaweeds, some nuts and seeds if they sit well with you, and so forth. Although I think many folks would do well with a higher fat intake than some of those doctors recommend (with some caveats we’ll talk about next), the concept of eating real food is a winner. This means ditching the fake soy meats, high-fructose corn syrup, artificial sweeteners, convenience snacks, TV dinners, and pretty much every single thing on this page. It may have been an exciting moment when you learned that Kellogg’s Unfrosted Pop-Tarts are vegan… but pop-tarts they remain. Occasionally indulging in something junkier won’t kill you, but don’t expect to stay healthy if everything on your plate was made by Morningstar Farms or Tofutti.

Just say no.

2. Avoid high-omega-6 vegetable oils like soybean oil, corn oil, cottonseed oil, sunflower oil, peanut oil, or margarines made from these oils. Instead, use heat-stable fats like coconut oil or red palm oil for cooking, and use macadamia nut oil or olive oil for cold dishes like salads. (Depending on where your city falls on the boondocks-to-urbia scale, the linked oils may be easier to order online than track down locally, but you can sometimes find them at specialty markets or request them through Whole Foods.)

Note: slashing your intake of omega-6 fats will reduce your omega-3 requirements, but I also recommend taking an algae-based vegan DHA supplement (like DEVA’s) and getting some ALA from ground chia seeds, hemp seeds, or flax seeds (always raw and not heat-treated, because their fats are extremely unstable). This is particularly important if you’re pregnant or breast-feeding.

"Soybean oil": writing it in Italian doesn't make the badness go away.

3. Secure a source of vitamin K2, pronto—especially if you want to stave off dental nightmares (like my own 14-cavity adventure). Woefully unknown to the public and mainstream health experts alike, vitamin K2 is critical for a healthy heart and skeletal system. Among other things, it helps shuttle calcium out of your arteries (where it contributes to plaque formation) and into your bones and teeth, where it rightfully belongs. There’s a new book out called “Vitamin K-2 and the Calcium Paradox” discussing this nutrient depth, but you can also find plenty of information on K2 online, like here and here.

Unlike vitamin K1, which is abundant in some vegan foods like dark leafy greens, vitamin K2 is only found in certain bacteria and animal products such as dairy, organ meats, and eggs. The chief vegan source is natto—a (not-so-appetizing) fermented soybean product that contains K2-producing bacteria. If you avoid soy, eat a raw food diet that disallows natto, or simply don’t want to shovel slimy ammonia-scented globs into your mouth, look for a vitamin K2 supplement containing menaquinone-4 or menaquinone-7 (usually abbreviated to MK-4 or MK-7). I personally use this brand for myself, both due to quality and cost, and can vouch for the incredible dental benefits it bestows.

4. Take enough vitamin D3 to get your blood level up to the 35 ng/ml markUnless you’re a Hawaiian lifeguard (or otherwise lucky enough to lounge outside all day in the sun), there’s a decent chance you’re deficient, especially if you live at a far northern latitude. Vitamin D is crucial for a wide variety of functions—everything from helping you absorb calcium to protecting against certain cancers—and it works in synergy with vitamins K and A to keep your teeth and bones strong. Unfortunately, since supplemental vitamin D3 is usually derived from wool, nearly all vegan versions contain vitamin D2, which is less potent and not always effective for preventing or fixing deficiency.

Source of Life Garden Vitamin D3 and Vitashine Vegan Vitamin D3 are currently the only vegan vitamin D3 supplements in existence. I highly recommend using either of those over the D2 versions more commonly available. I personally take about 5,000 IUs a day, but you may need to adjust your intake depending on your body size, how much sun you get, and whether you’re trying to aggressively treat a deficiency versus maintaining healthy vitamin D levels. (Also be aware that a small number of people react negatively to vitamin D supplementation, so be on the lookout for any adverse symptoms.)

5. Get the most out of your beta carotene. Vitamin A is crucial for healthy bone tissue, vision, proper hormone function, making fully-intact babies, and other things generally regarded as good. But plants don’t contain “true” vitamin A—only certain provitamins, particularly beta carotene, that your body converts into vitamin A. Unfortunately, the conversion process is wildly inefficient: most folks absorb only a tiny fraction of the beta carotene they consume, and only a fraction of that ever becomes vitamin A—leaving some vegans deficient even if they rival Bugs Bunny in carrot consumption. Although some people are just genetically doomed to be poor converters and will probably struggle as vegans no matter what they do, there are a few ways to maximize your absorption and conversion of vitamin A precursors:

  • Eat beta-carotene-rich foods along with some fat—such as oily dressing or avocado slices on a salad—to greatly increase the amount you absorb.
  • Identify and treat any food allergies, celiac disease, parasite infections, H. pylori infection, or low stomach acid, which can disturb your gut ecology and hinder absorption.
  • Make sure you’re getting sufficient iron and zinc from your diet, since these minerals are critical in converting beta carotene to vitamin A. If you’re deficient in them, your vitamin A status will probably be impaired.
  • Lightly cook some of your beta-carotene sources to break down fiber and improve absorption.

6. Properly prepare any grains, legumes, or nuts you eat. These foods contain phytates that block the absorption of minerals like calcium and iron, along with enzyme inhibitors and tannins that can cause digestive distress. If you choose to include grains, legumes, or nuts in your diet, you can neutralize some of the anti-nutrients and increase mineral availability by giving your food some tender lovin’ prep. For whole grains, do the following:

  1. Put the grains in a bowl filled with enough warm water to cover.
  2. Add apple cider vinegar or lemon juice at a ratio of 1 tablespoon for each cup of grain.
  3. Let it all soak for at least 7 hours at room temperature.
  4. Drain the soak water and cook the grains as you usually would.

For most legumes except dried lentils and split peas, follow the same steps as with grains—but soak larger beans for at least 24 hours (changing the soak water if they start to ferment) and double the amount of vinegar or lemon juice if you’re dealing with really small beans (2 tablespoons per cup of beans). Lentils and split peas should be soaked for 7 hours, but without any vinegar or lemon juice added. Raw nuts, too, should be soaked in warm water for 7 hours without an acidic medium, but you can sprinkle the soak water with sea salt (and then air-dry them once they’re done).

This may sound labor intensive, but it really doesn’t take all that much actual work—and your digestive system will thank you!

7. Eat high-vitamin-C foods along with iron-rich foods to enhance iron absorption, especially if you’re a pre-menopausal woman or otherwise struggle with anemia. Non-heme iron, the form found in plant foods, is less bioavailable than heme iron in animal products—but its absorption increases quite a bit in the presence of vitamin C. Try combining high-iron foods like chard, spinach, beet greens, lentils, beans, and quinoa with vitamin-C-rich foods like tomatoes, bell peppers, lemon juice, strawberries, oranges, papaya, kiwis, pineapple, grapefruit, or whatever else strikes your fancy. If you’re into green smoothies, those are prime opportunities to blend up something fruity and vitamin-C-packed with an iron-rich leafy green. Also avoid drinking tea or coffee with high-iron meals, since these beverages contain substances that reduce iron absorption.

8. Be kind to your thyroidHealth-conscious vegans may unintentionally wind up with two strikes against their thyroids: lack of iodine (either from cutting back on salt or switching from iodized salt to natural sea salt), and a menu packed with goitrogenic vegetables. Impaired thyroid function can result in fatigue, cold hands and feet, hair loss, poor concentration, trouble losing weight, and short-term memory rivaling your grandma’s—all of which you’ve probably heard a disgruntled soon-to-be-ex-vegan complain of at some time or another.

The best vegan source of iodine is seaweed, but some varieties contain much more than others. Here’s a table with the iodine content (among other nutrients) of several common sea vegetables.

Goitrogenic foods—which interfere with thyroid function—include cruciferous veggies like broccoli, cauliflower, Brussel sprouts, kale, kohlrabi, mustard, turnips, rutabaga, and cabbage, as well as soy products and millet. Strawberries, peaches, and spinach are also somewhat goitrogenic. You don’t have to give up these foods completely (crucifers in particular have some great anti-cancer compounds), but definitely scale back on them if they’re currently a large part of your diet, especially if you already have hypothyroid symptoms.

Not so innocent.

9. Take vitamin B12—about 10 mcgs a day, or 2000 mcgs once per weekI’d like to think this would be pretty obvious by now, but there are some lingering vegan authorities who seem to underplay the B-12 issue or even deny it altogether. Even “The China Study” makes B12 seem like small potatoes, when T. Colin Campbell writes: “If you do not eat any animal products for three years or more, or are pregnant or breastfeeding, you should consider taking a small B12 supplement on occasion.” This is sort of scary, since virtually every study conducted on the subject shows that vegans experience much higher rates of B12 deficiency than omnivores or vegetarians and have elevated homocysteine as a result (which increases blood clotting and raises your risk of heart disease). In fact, low B12 and high homocysteine probably contributed to the early demise of prominent vegans like H. Jay Dinshah and T. C. Fry (PDF).

Especially if you’re avoiding processed vegan foods (which are often fortified with vitamin B12), you’ll need to find a supplement and take it consistently, since there are really no reliable dietary sources of B12 for vegans. (Algae like spirulina, often rumored to contain B12, only has B12 analogues that won’t actually improve your B12 status.)

10. Try going gluten-free at least as a 30-day experiment, especially if you have possible “gluten sensitivity” symptoms like bloating, abdominal pain, joint pain, headaches, or migraines that aren’t improving from tweaking your diet in other ways.

11. Ferment some stuffRaw, unpasteurized fermented foods contain lovely bacteria that can help restore your gut flora, improve your digestion, and ultimately increase the nutrition you absorb from what you eat. It shouldn’t take more than 30 seconds on Google to find recipes for sauerkraut, kimchi, “real” pickles, fermented salsa, and other delectable vegan-friendly fermented fare, and most health food stores carry some of these things pre-made. “Wild Fermentation” by Sandor Katz is a great resource if you want to get your hands dirty in the lactobacillus-y goodness.

12. Consider supplementing with taurine, especially if you’re pregnant, nursing, or extremely active. Taurine is an amino acid found only in animal foods, and it plays an important role in brain development, maintaining healthy blood pressure, controlling blood glucose, reducing oxidative stress, and preventing damage to your retinas. Although your body can synthesize taurine from a combination of other amino acids, many folks—including children and pregnant or breast-feeding women—can’t produce enough of it to satisfy their needs without a direct dietary source, and at least one study has shown that vegan men have much lower levels of plasma taurine than nonvegetarians. NOW makes a vegan taurine powder, and there may be other brands out there if you do some sleuthing.

13. Look into “bivalveganism,” a combination of plant foods and non-sentient shellfish. It’s unfortunate this one ended up as unlucky #13, because I honestly think it could be a solution for a lot of struggling vegans. Bivalves—such as oysters and clams and mussels—are incredibly rich in nutrients that are absent or hard to get from plant foods. Oysters in particular are a great source of iron, B12, zinc, selenium, copper, and vitamin D, and have a small amount of true vitamin A as well. Bivalves don’t have a central nervous system and are generally not considered sentient by traditional criteria, so vegans who avoid other animal products may be more ethically comfortable consuming a few oysters per week. (If you want to hear about the potential role of bivalves in vegan diets from someone else’s mouth, here’s a very relevant article by Christopher Cox.)

That’s it for the Big Important Things. But for the sake of making this page insufferably long, here’s another pile of odds ‘n ends:

Keep in mind that it’s not what you eat—it’s what you absorb (or convert). Some diet-scrupulous vegans use programs like Cron-o-Meter to track their nutrient intake and ensure they’re hitting the RDA for vitamins, minerals, and amino acids. Unfortunately, these programs don’t distinguish between vitamin K1 or K2, don’t have RDAs set for nonessential amino acids like taurine, usually record beta carotene as “vitamin A” and don’t adjust for its abysmally low absorption rate (meaning that what looks like 100% of the RDA on paper might only be 1% of the RDA in your body), can’t tell you how much iron/zinc/magnesium/calcium you’re losing to phytates, can’t tell you how much non-heme iron you’re really absorbing—on and on. In other words, nutrient trackers can only show you what you’re putting in your mouth, not what your body can actually grab onto. (Worse yet, the USDA’s nutrient values may be wildly different than what’s on your own dinner plate, since the nutritional content of plant foods varies depending on growing conditions, soil quality, season, geography, and a host of other factors.)

Blood tests can’t tell you if you’re “deficient” in calcium. I don’t know if this belief is as common among regular vegans as it is among raw vegans, but some folks seem to think that a normal calcium value on their blood test is proof that they’re getting enough from their diet. This couldn’t be further from the truth. Calcium in your blood and calcium in your bones are two very different things, and in times of shortage, your body will happily yank calcium from your skeleton so you’ve got enough in your blood to stay alive. (Calcium is an electrolyte that helps keep your heart from spazzing out, and your body generally prioritizes “not dying” over losing bone density.)

When seeking health advice from pro-vegan resources, choose your sources wisely. This applies to pretty much any authority that dispenses advice about a diet they’re emotionally or financially invested in, and veganism is no exception. Steer clear of websites and forums that tend to “whitewash” bad experiences people have with veganism or that ban members who report health problems (not to name names). If someone says you can get all the B12 you need from licking your wrist, not washing your vegetables, or making sacrificial kale offerings to the Coenzyme Gods, run, far and fast. And as somebody who used to put full faith in everything I read on Vegsource.com, I’d also recommend doing your own research before trusting what you read on vegan sites about human digestive anatomy, meat studies in the news, and the miraculousness of seitan.

That said, my absolute favorite vegan expert is Jack Norris. Norris is a vegan RD who’s astoundingly honest about the shortcomings of a vegan diet, offers science-based solutions to health problems, and—unlike some others in his position—doesn’t sweep veganism’s potential pitfalls under the rug. Among all the plant-based health authorities out there, he is hands-down the most likely to give you the truth. Peruse his blog to get a balanced perspective of vegan issues without having bacon shoved in your face.

And if you’re sincerely interested in seeing the “other side” of vegan topics:

  • Tom Billings’ BeyondVeg is a fantastic resource for any truth-seekers in the health world, covering a range of topics relevant to vegans and raw vegans (including comparative anatomy of primates and humans, evolutionary history as it relates to the human diet, common raw vegan myths, and much more).
  • Meat: A Benign Extravagance” by Simon Fairlie is a must-read if your reasons for going vegan are at least partially environmental. There’s no doubt that our modern factory-farming practices suck, but this book shows—in meticulous, fantastically-researched detail—that reality is a lot more nuanced than we’re led to believe. Many vegan foods like strawberries, coffee, wine, chocolate, and asparagus are even more environmentally destructive than factory-farmed meat, and Fairlie shows that some of the damning statistics we hear about animal agriculture are grossly inflated. Based on Fairlie’s research, the most sustainable system is not a vegan one, but involves putting livestock on land unsuitable for plant crops, using animals like chickens and pigs to utilize food waste, and returning to decentralized agriculture.
  • If you’re interested in understanding why former vegans have un-veganized and questioned the ethical basis of veganism, check out the ex-vegan interviews on Rhys Southan’s blog, Let Them Eat Meat. Also worth reading is this detailed personal account of high-profile, former-vegan Tasha’s return to omnivorism. I’ve provided some of my own thoughts in an interview with the National Animal Interest Alliance.
And last but not least…

Don’t beat yourself up if you’re doing everything “right” and still not feeling awesome. Just like all those great-grandmas out there who lived to be 96 smoking a pack a day and choosing Guinness as their main food group, there are some folks who really do survive without animal products for a very long time. I have my doubts about how it’ll play out across generations, but on an individual basis, thriving vegans do exist (such as the phenomenal 60-year-old Lou Corona who’s been a raw vegan for 39 years (and who’s huge on fermented foods—hint hint)). But unlike the resilient great-grandmas who are viewed as lucky anomalies, the resilient vegans tend to get held up as universal examples of “Hey, if this person can do it, so can everybody.”

If you take nothing else away from this page, at least listen to this: humans are much, much more genetically diverse than most of us realize, and one person’s success as a vegan doesn’t guarantee your own. You may be truly physically incapable of absorbing or converting certain nutrients in their plant form. Your health history, your gut ecology, your medical conditions, and even what your mom ate while you were gestating all influence your current nutritional needs. Veganism is a modern experiment—a dietary situation humans have never before faced—and its full repercussions are still unknown. Trouble thriving is not a personal failure. As much as veganism roots itself in compassion, please consider that you, as a living breathing human, also deserve your own kindness.

495 responses

3 04 2012
Amanda Lynn Schulz

My brain is melting, as I type. I thought I knew where to start now Im even more confused and stressed out about doing this “right” then I was before I started this jouney. The more I learn the less I know.

3 04 2012
neisy

Sorry you feel that way, Amanda! I don’t usually believe in micromanaging our diets, but veganism is a situation where not everyone can automatically get what they need to stay healthy. There are no doubt many vegans who are doing okay without following all the tips on this page, but for long-term health and for people who are currently struggling on a vegan diet, I think the suggestions here are important.

If it seems overwhelming, think of it this way:
1) Eat a whole-foods diet with some fermented foods and seaweed, and consider including oysters or other bivalves
2) Favor monounsaturated and saturated fats over popular vegetable oils
3) Supplement with vitamin B12, vitamin D, vitamin K2, DHA, and possibly taurine

I think those are the most important.

21 09 2012
Richard

Today, 9.21.2012, the WHO tweeted:

“Choose unsaturated vegetable oils (olive, soy, sunflower, corn) rather than animal fats or oils high in saturated fats (coconut, palm)”

Minger does not agree with the unanimous biomedical community including Atkins Foundation’s paid lipid researcher Ronald Krauss assesment on the dangers of SFA and red meat particularly, instead she harbours scientifically dubious claims over the alleged, overstated at best, adverse effects of refined grains consumption.

Evaluation of the evidence between consumption of refined grains and health outcomes

“A total of 135 relevant articles were identified from database searches of studies published between 2000 and 2010. The great majority found no associations between the intake of refined-grain foods and cardiovascular disease, diabetes, weight gain, or overall mortality. A few studies found that very high intakes might be associated with some types of cancers, but at moderate levels of consumption the risks were not significant. The totality of evidence shows that consumption of up to 50% of all grain foods as refined-grain foods (without high levels of added fat, sugar, or sodium) is not associated with any increased disease risk. Nonetheless, eating more whole-grain foods remains an important health recommendation, and most consumers will need to reduce their current consumption of refined grains to no more than one-third to one-half of all grains in order to meet the targets for whole-grain foods”.

http://onlinelibrary.wiley.com/doi/10.1111/j.1753-4887.2011.00452.x/abstract;jsessionid=825E3490E9E84E6907F58729A666EDAC.d04t01?deniedAccessCustomisedMessage=&userIsAuthenticated=false

Meet your denialist, Denise Minger.

27 11 2012
melkoppelman

Interesting review, although it appears as though it was commissioned by the Australian grain industry itself – ‘Go Grains Health & Nutrition Ltd’ and it reads like it was.

This review seems to be looking at the ideal amount of refined grains as a percentage of total grains in the diet. In other words, it does not address the question of what percentage of the diet should be grains, only what percentage of included grains should be whole versus refined.

It also excluded a large body of relevant literature – the review only included refined grains if they were low in fat, sugar, and salt – this is valid for addressing the narrow question of the review but is not representative of reality.

So, first I’m confused as to why you have referenced this review when it has nothing to do with your preceding arguments about fat and oils. Second, if you are trying to find support for the high consumption of grains being healthy then I can suggest finding a review that was not commissioned by the grain industry, but rather one performed by an independent team of researchers.

20 03 2014
Natalie Prigoone

If you read well researched and documented books like “Brain Grain” and “Wheat Belly” all the science is there to back up Denise. Grains are bad news. Fat is fine.

28 08 2014
andrew easson

Mankind has made this situation of widespread sickness and obesity through the globalisation of refined processed food, hence the reason for a million so called food magicians who believe they can just wave their magic wand and we will all be restored to good health, dont you just love fairytales. When we wander from the path of nature we may very well take a dangerous and unknown journey. We have become sick in the western world since 1977 to present day when certain western governments decided to globalise refined sugar and introduce processed junk food on an unpresedented scale. We do not need food or diet Gurus or wise scientists promising us a one way ticket to the land of health and happiness. The animal kingdom do not have a health service, nor do they analyse or discuss food, they do not snack or eat processed food, wild animals never die of diabetese type 2 or suffer with obesity etc. All we need to do is this ( and i dont have a magic wand ). When we shop for our weekly / monthly groceries just simply buy very little or no processed foods, then buy a variety of what nature has provided such as, fruits, vegetables, nuts / seeds, and a little fish or poultry if desired ( optional ). Do not analsye or discuss food ever again, just simply eat clean and get on with life and enjoy your health. We do not need any special diets ever. peace…..Andrew.

24 09 2014
Kaitlyn Tillett

Make sure it’s all organic and not conventional or contaminated with GMOs!!!

1 03 2013
Wendy Myers

I agree wholeheartedly that few can get what they need nutritionally being vegan. I’m a health and nutrition coach. I was vegan for a mere 6 months and developed anemia, Vit D deficiency, B12 deficiency, adrenal fatigue, and thyroid insufficiency. No thanks! I did the diet after reading The China Study thinking it was the only way to be healthy. All evidence to the contrary! The proof is in the pudding. I choose my health! Now that I’m eating meat, my health is recovering.

27 04 2013
Ryan

Ms. Meyers,

I am currently seeking out a healthy diet, and to be quite honest, I am unsure of what a healthy diet consists of. I have listened to proponents of a whole foods, plant based diet, as well as those who advocate incorporating meat into one’s diet; the evidence is conflicting. Both sides argue the benefits of their particular diets, while at the same time; they refute diet/nutrition claims contrary to their own.

Ultimately, my goal is to draw my own conclusions, with regards to determining a truly healthy diet. At the current time, I have far too little information to go on, as my endeavor into finding what really works, pertaining to healthy diet, is limited by my knowledge on the subject matter.

After reading your post, it is evident you advocate incorporating meat into one’s diet. Additionally, you have provided information regarding the adverse health consequences of a vegan diet, leading me to believe proponents of a whole foods, plant based diet, have negated to discuss the health benefits of eating meat. You claimed while on the plant based diet, you developed anemia, Vitamin D deficiency, vitamin B12 deficiency, adrenal fatigue, and thyroid insufficiency. So there are serious health risks, as you pointed out, by completely eliminating meat and dairy from one’s diet. Likewise, proponents of the vegan diet, make claims coronary disease and various types of cancers, are attributed to a meat and dairy based diet. My question is whether or not one can obtain the vitamins you were deficient of, from whole foods, plant based diet, or, can one derive those vitamins solely from meat and dairy products? Furthermore, is there any truth to claims that coronary disease and certain types of cancers are linked to meat and dairy products? Lastly, if coronary disease and certain types of cancers are not linked to meat and dairy products, what then are they attributed to; what can we do to combat these diseases?

Thank you so much for your post.

Sincerely,
Ryan

29 04 2013
Jeff Puhek

Meat, fish, eggs are part of a “whole foods diet” these are “whole foods”, even if you are only purchasing part of the beast from the grocery or farmer’s market.

Humans are omnivores and there is plenty of science to back up that statement. As for your concern about coronary disease, I suggest the book “Track Your Plaque 2nd edition” by William Davis, MD (yes, it’s “that” Dr. Davis, of “Wheat belly” fame) where the actual cause of heart disease – atherosclerosis (plaque) – is exposed: the short answer is high-glycemic foods, mostly from processed grains and sugar, that increase small-pattern LDL particles (All LDL is not “bad” as in popular belief), and NOT from meat and dairy products.

Anyway, the healthiest diets eliminate all highly-processed foods. Start there.

17 07 2013
CT

I totally agree with you. As long as a person is eating a whole foods diet..whether it’s meat, eggs, dairy, plants, their health will be OK in the long-term. Health is not limited to strictly being on a plant-based diet but for those who decide to go vegan/raw vegan, they do it moreso for their beliefs in living a life more aligned with their values.

1 06 2013
lurkin'

Anyone who says, in English, that a diet needs to completely exclude meat in order to be based on plants has no idea what the word “based” means.

Check out the Mediterranean diet, the Okinawan diet, etc. – those are based on plants and include some meat and they have proponents too… :)

23 02 2014
georgemcnally

All these diets have their proponents and they all seem to find ‘science’ to support them. It seems that almost all experiments can be questioned as to their validity depending on all sorts of variables. In practice, it is difficult to complete eliminate confounding variables in the designs of studies. Given that, one has to go on one’s own experience. After having a heart attack I was persuaded by the lo-carb argument to go for that diet, including meat, fish and dairy. Within a short period of time I felt pretty terrible and by the end of the month I was experiencing chest pains and the like. At this stage I came across Dr. Esselstyn’s recommendations and was convinced by the effectiveness of his own work. Pretty soon I started to recover and my energy levels increased as my weight decreased. This is, of course, only personal testimony but in a world of confusing mis-information and interpretations one sometimes has to go with the choices that work pragmatically with oneself.

3 04 2014
LCC

True Mediterranean diet, based on those Cretians who had the best health benefits of the region (though many others did not) fasted about 1/2 of the year.

20 03 2014
Natalie Prigoone

Wheat is the cause of the problems. Wheat and sugars.

1 06 2014
Trent Black

OMG … I in 100% agreement with you. I have have 14 illnesses, all reversed, and I keep telling people, it is wheat and sugars.

https://sites.google.com/site/ketoenergy/illnesses-eliminated

2 06 2013
Stevil Chemsit

The body can actually store B12 in the liver, several years worth. So if you really did have B12 deficiency, it wasn’t from a vegan diet in just 6 months. Soy milk, Red bull, Cereals like cherios, cliff bars, fortified nutritional yeast, all have B12 at sufficient levels. If you had even a modicum of knowledge of nutrient distribution of foods, you’d be able to make sure you were getting these nutrients with hardly a thought.

It’s pretty obvious your nutritional background is severely lacking. You might want to pick up some science based nutritional books before you coach more people.

1 04 2014
Herban Revival

Why would anyone want to eat “Soy milk, Red bull, Cereals like cherios, cliff bars”. Those are not whole foods. They are processed.

3 04 2014
LCC

Oddly enough, most long-term (not short-term) veg*ans have very high rates of B12 deficiencies. Vegans have the highest, in some studies over 90%.

8 10 2014
Natnat

You’re telling people to learn something about nutrition and yet you’re recommending Red Bull and processed grains? LOL!

25 04 2013
Bernie

I only have one comment in reply to your first sentence – being a meat eater doesn’t mean you automatically get what you need to stay healthy either (ie, not just vegans) so wouldn’t your advice be applicable to everyone?

27 06 2013
unethical_vegan

“1. Eat real food.”
Please define “real” food. Are milled grains, processed by fermentation and high heat real food? How about spiced and macerated meat heated to high temperatures?

2. Avoid high-omega-6 vegetable oils
Good general advice.

3. Secure a source of vitamin K2
To my knowledge, there is no evidence that K1 is not sufficient.

4. Take enough vitamin D3 to get your blood level up to the 35 ng/ml mark.
To my knowledge, there is no evidence that D2 is not sufficient.

5. Get the most out of your beta carotene.
To my knowledge, there is no evidence that vegans are more likely to be deficient for retinoids.

6. Properly prepare any grains, legumes, or nuts you eat.
Can you provide peer-reviewed evidence that preparing grains, legumes, or nuts in the manner you propose is in any way beneficial.

7. Eat high-vitamin-C foods along with iron-rich foods to enhance iron absorption.
Good general advice.

8. Be kind to your thyroid.
Please provide a single study suggesting that consumption of broccoli, cauliflower, kale consumption *promote* hypothyroidism

9. Take vitamin B12
Good advice for vegans, vegetarians, the elderly and those with digestive problems.

10. Try going gluten-free at least as a 30-day experiment
Please provide a single study showing that “going gluten free” is beneficial for those who do not suffer from Celiacs or gluten allergies.

12. Consider supplementing with taurine.
Taurine is endogenously synthesized from cysteine in the pancreas. To my knowledge, there is no nutritional requirement for taurine.

13. Look into “bivalveganism,” a combination of plant foods and non-sentient shellfish.
Please explain why vegans should “look into” this.

On DHA:
DHA is endogenously synthesized from fats found in plants, grains and nuts. Billions of human beings live their entire lives without consumption of appreciable amounts of DHA. To my knowledge, there is no evidence that DHA “deficiency” is a medical phenomenon or that exogenous long-chain n-3 pufas are required for human health.

13 03 2014
Juan Perro

Plain wrong statement. Read your biochemistry before you write such fallacies about DHA being endogenously synthesized by humans. I quote Biochemistry, 5th edition

Jeremy M Berg, John L Tymoczko,

1 Johns Hopkins University School of Medicine
2 Carleton College
3 Stanford University
New York: W H Freeman; 2002.
ISBN-10: 0-7167-3051-0

Mammals lack the enzymes to introduce double bonds at carbon atoms beyond C-9 in the fatty acid chain. Hence, mammals cannot synthesize linoleate (18:2 cis-Δ9, Δ12) and linolenate (18:3 cis-Δ9, Δ12, Δ15). Linoleate and linolenate are the two essential fatty acids. The term essential means that they must be supplied in the diet because they are required by an organism and cannot be endogenously synthesized. Linoleate and linolenate furnished by the diet are the starting points for the synthesis of a variety of other unsaturated fatty acids.

13 03 2014
Juan Perro

Stupid keyboard :)… Continue…in case you mention that The ALA –> EPA –> DHA pathway, this is so inefficient in humans that the amount of EPA and DHA that is actually produced by elongation and desaturation is negligible to the point of both w3 been labelled as essential for humans.

15 11 2014
Julia

Thank you for your comment.

16 05 2012
Stevil Chemsit

It comes down to 3 basic guidelines.

1). Eat Whole foods (you can skip the oysters; non-vegans just like it when vegans eat questionably vegan foods. )

2) Take a B12 supplement, Vit D since we live in boxes all day, but this applies to everyone, not just vegans.

3) Exercise regularly. Exercise increases caloric requirements which will ultimately increase nutrient intake if you follow #1 & maintain your body weight. Exercise has a zillion other benefits from raising HDL, increasing bone density, regulating immune system function.

While D2 may be (1:1 to 1:10) as effective as D3 5000IU/day seems to work for most folks. If in doubt get tested. DHA is recommended, but the science is less clear as to whether it is truly detrimental. As of now, it’s a “just in case” I take it for that reason. I recommend this brand since it has EPA/DHA http://www.opti3omega.com/

Taurine, carnitine, creatine, carnosine is all speculative and has little to no scientific evidence vegans needs these. Yeah, creatine seems to enhance athletic performance, but being “fit” is different from being “healthy” Athletes, vegan or not, have specific needs that differ from normal folks. Caffeine is a better performance enhancing compound, but that doesn’t mean we need it.

I really would like to see the origins of the K2 recommendations , since K1 has been shown to increase bone mineralization, K2 is produced by gut microflora and shown to be absorbed by the body, human breast milk contains primarily K1, so there would’ve been some evolutionary pressure to weed it out if it wasn’t as effective as K2.

Most of the studies on poly-unsaturated fats & thrombosis are for people who fall into the “therapeutic group” BMI >30, non-vegan, sedentary life-style, etc… There’s a number of confounding variables with these types of studies.

I’m a vegan (10 awesome years), a professional chemist (food & pharma industry), & 40+ endurance athlete. Pick Up “Vegan for Life” – Jack Norris RD & Virginia Messina RD, and that’s pretty much give you the info you need.

I don’t just do “OK” I thrive on a vegan diet with those 3 rules.

22 10 2012
Dana Osuna

Clearly, you have an education backing that I lack in chemistry, but, from my own experimentation with Omega 3 (particularly high doses of EPA), it seems extremely pertinent to mental health. I was on purpose searching for a solution to bipolar disorder that allowed me to wean from my psych meds which were damaging my liver. After finding several Omega 3 studies on bipolar disorder, I began using what seemed to be the median therapeutic dose, 1000 mg per day (actually 1200, as my supplement, Futurebiotics New Havest Vegetarian EPA is 600 mg per capsule). I also take Ovega Omega 3 for DHA (it also has some EPA). Both products’ manufacturers say they are completely vegan. This along with 250 mg of magnesium, a good B Complex, and some extra niacin have my mental health better than it has ever been. I have been completely off my psych meds for months now. Before the addition of the high dosage of EPA, my results were definitely sub-optimum. This is merely my experience, but there are documented studies supporting similar findings.

My first Omega 3 supplementations were just in case too. I now wonder if it may have been the lack of it in my diet, ever, that caused a lifelong affliction.

Anyway, I know you weren’t arguing against it in any way. I don’t really know what makes all these things work. I just know the EPA helps me not feel out of control all the time. Magnesium helps me be less angry. Niacin makes the hallucinations stop. For me. It’s not a whole study, but just random info. (The B Complex is just just for good measure because there’s just no way I get enough of those in my diet.)

By the way, you’ve been doing this a little longer than I have, and I am only just now getting around to needing my vegan diet to be more healthy. So now, 7-8 years in, I’m just now ordering some books and things (I usually just search out what I want to know online). I’ve heard of Vegan for Life. I see you think it good. I just ordered Becoming Vegan by Brenda Davis and Vesanto Melina, both registered dieticians, and The Vegan Sourcebook by Joanne Stepaniak M.S.Ed. Do you know these books? Do you have an opinion?

6 12 2012
Pablo

How much fish one should eat every day to get “enough” DHA? because millions of quite normal people haven’t eaten fish every day (at most two days a week, maybe) int he context of a high fat diet with tons of o6 and few greens (so ver few short o3) and they are still alive and with mental lucidity.
Humans doesn’t need DHA, if one is a bit healthy. Pretty much statitic is done.

14 12 2012
Danielle

Dana, would you please Email me? I’m “bipolar II” and will not take psych meds (for the same reasons you wanted to go off of them). I would like to hear more about your method. dennychill@gmail.com. Thanks!

23 12 2012
Stevil Chemsit

I take a 400mg/200mg vegan DHA/EPA supplement “just in case”, because the literature is ambiguous. That said, the human body more easily converts ALA (C18:3), the Ω3 that flax seeds are well known for, into EPA than DHA Most literature I’ve come across puts the conversion ALA-EPA at ~8-10%. I eat ~3tbsp ground flax seeds/day in the form of bread, smoothies, and even my own plant based keifer.

There’s ~7000mg ALA, so @ a 10% conversion turns into ~700mg EPA. So in total that’s ~ 400mg/900mg EPA/DHA from plant sources.

The human body just has a problem with DHA, and in vegans, the predominant C22 Ω3 chain is DPA (missing a double bond compared to DHA), but again there’s no real evidence humans need more DHA than we can produce.

The nice thing about eating a good amount of ALA is that excess fats are stored unaltered. That is if you eat a lot of ALA it will end up in your adipose tissue.

The body constantly pulls fat out of storage, circulates it and puts most of it back. Only ~25% of the fat circulating in the blood is used for energy.

So eating flax seeds regularly will increase your Ω3 fatty acids in your blood all day long.

23 12 2012
Stevil Chemsit

Yes, I have those books. I find Vegan for Life, the most scientifically accurate and most general. I disagree with some points, like the lots of legumes bit, but I can see their point if they are trying to provide recommendations that fit most people’s eating habits.

I eat all whole food ftmp and eat ~4000Cal/day, so protein is never a concern for me. I take in 100g-150g/day without mock meats or supplements. I do love mock meats, so I limit them to the weekends only.

Jack Norris & Ginny Messina both have blogs and answer most questions on there. So if you have questions, post to their blogs.

Vitamins are all involved in aiding biochemical reactions and often their products are allosteric (indirect) regulators of even more reactions. There are several genetic disorders that can affect the equilibrium of one reaction or another that megadoses of vitamins might help.

One such disorder is homocystinuria and mega-doses of B6, B12, B9 (folate) along with methyl donors can help reduce the symptoms.

http://en.wikipedia.org/wiki/Homocystinuria

http://www.Theveganrd.com

http://www.jacknorrisrd.com

16 11 2012
Valerie Sims

Thank you for this lucid summary of how to eat.

29 09 2012
Richard

Two excellent and informative blog accounts on the fraud Minger has pulled up. Minger has been known for riduculing the plant-based doctors with a messianic self-confidence.

This 2-fold blog account reveals the fraud and takes a critical look whether the messianic self-confidence that has been constantly displayed by Dennis actually has any real substance. From mismanaging numbers in her alleged refutations to her cholesterol denialism/creationism.

1) Forks Over Knives and Healthy Longevity: A Missed Opportunity for the Cholesterol Skeptics

http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-healthy-longevity.html

2) Forks Over Knives and Healthy Longevity: Perhaps the Science is Legit After All

http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-healthy-longevity_17.html

25 12 2012
tequilatarian

If you could state your objections or corrections to this post without using hyperbolic insults, you might get more attention.

27 06 2013
unethical_vegan

Richard, Thanks for providing links to those posts. The fact that Minger has not responded to that thorough shellacking (not vegan) is telling.

23 12 2012
Dan Brown

I will be straight up honest. I do not respect much of what any woman says. They are Highly Opinionated Idiots. They read one damn article about something and all of sudden they become the go to person on that subject and just repeat and repeat and repeat whatever that article says. To me, Denise Minger is a very beautiful idiot. Nothing More! If you want to convince a man of what you say, use only the words that convey facts, everything else is bullshit.

25 12 2012
tequilatarian

Well, I don’t respect people who judge an entire gender negatively and ignore their posts outright.

12 02 2013
Leon Nel

Dear Dan. Seems your a perfect candidate to follow that guy from 30 Banana’s. All insults and prejudice , combined with distorted facts. Do a google search, you’d fit right in.

19 04 2013
Candice

I guess you don’t do so well with the ladies, maybe that’s why you’re a bitter sexist prick. By the way, I’m sure no one here has any respect for your ignorant opinions.

1 09 2013
Laurie

WOW— drag your wife by the hair much?

19 04 2013
Martin

If your confused after reading Denise Minger it’s because that’s what she,s trying to do. I would advise other sources. if you hope to clarify a little someday.

6 07 2013
Michael

Amanda, that last line of yours is exactly how I feel: the more I learn the less I know. I have for the past 6 months not really at any meat (beef, chicken, turkey,etc) and I’ve felt alright; but lately I’ve had some shrimp. I have a friend who for 30 years has been meat free and he said back before he was he had colon problems? This whole thing is truly complicated to a degree..everyone is different..UGGH! Somedays I cannot get my head around this whole thing! Even had a doctor who survived Cancer tell me that he eats very little if any meat? The longest living people I believe are closer to Vegetarians? Oh, help?!

4 04 2012
Amanda Lynn Schulz

Im not personaly struggling with diet, I feel fantastic, but Im not a full blown vegan either. I just feel bombarded with so much contradictory information and meat bashing, veg bashing and vegan bashing literature it sometimes can be over whelming, I think thats what I struggle with. Aside from the bivalves and this fermented foods business I currently follow those tips. Just trying to keep an open mind, strive to stay informed and sticking to the middle ground. Thanks for the break down Neisy. Much appreciated.

19 04 2013
Martin

ya the bashing is annoying and confusing, but as you certainly realise some people really are incompetent and/or ill-intentioned so pointing those out wouldn’t be bashing as you will certainly agree. About the sources, I was vague to say the least. After reading Minger I’d highly recommend the plantpositive channel and reading the China Study for yourself if you haven’t already. For a more complete “non-bashing” or debate type of information, you can’t pass up on the NutritionFacts.org channel. This one will certainly clear things up a little for you. I’m assume you are not familiar…

Hope I’ve been helpful in someway and please point me in the direction of interesting info.

Martin

4 04 2012
Richard

I would like also add a wonderful site for all health conscious vegans who thinks it’s a good idea to take advices in regards to veganism from Weston Price Protégés.

Total 98 videos. All about the paleo-mind set from which the author of this site derives her logic on vegan diets. A video serie exposing the problematism of people who collect their fame (and lecture remunerations) by serving low-carb, paleo and “real food” communities

Just a starter.

12 04 2012
Antznyopantz

The speaker’s ad hominem stance screams bias and lacks grace, though I don’t find his points relevant either.

Regardless of whatever “body of nutritional science” Ms. Minger may or may not be aware of – if a researcher ignores large correlations without referencing that accepted “body of science” to explain the irrelevance of the correlations, it is either sloppy work or intentional propaganda. If we understand the properties of these grains as well as the speaker implies, why aren’t they treated as a control rather than a variable? Why bother collecting the data on them at all?

Either way – Miss Minger wins the ethos slap fight: her writing/thoughts are much more qualified.

4 04 2012
Richard

“… choose your sources wisely. This applies to pretty much any authority that dispenses advice about a diet they’re emotionally or financially invested in”

I very much agree with the above.

Anyways, thanks for the tips Denise.

4 04 2012
Richard

“And as somebody who used to put full faith in everything I read on Vegsource.com, I’d also recommend doing your own research before trusting what you read on vegan sites about human digestive anatomy, meat studies in the news, and the miraculousness of seitan”

Denise this so cool. I actually did just that. First, I read vegsource’s stance on human anatomy then I proceeded and thought maybe the editor in chief of American Journal of Cardiology, William Clifford Roberts has also something to say about the issue. After all, he is an expert and published over 1300 scientific papers which all have been published in a scientific platform (I have an article called “the cause of atherosclerosis” particularly in my mind ). I still wasn’t convinced what Roberts was saying so I had to listen what the professor of evolutionary biology at the Dartmouth university, Nathaniel Dominy had to say about the issue of human anatomy and dead animal flesh. It turned out vegsource had it correct all the way.

Anwyways, my honest and sincere critique. This was a horrible article. First you make veganism look an endevour, a big mess, not worth the risks. Judged by you one ought to be lucky if surviving a month on this “experiment”. Next you go against the last bastion, the moral and ethical arguments by citing stupid links by ex-vegans. Atleast you could have provided some upside followed by vegan diet in regards to environment, health and animal welfare. No. You didn’t do that. Your income is dependent on not doing that. Your income is dependent spewing ridiculous BS about Lierre Keiths book and factory farms being more sustainable than strawberries. I feel pity for you.

Preparing the grains….LOL. Give me a break. Do I smell some pseudoscientific, appeal-to-tradition, paleo framework goin’ on here? I do.

4 08 2012
nyree

thanks for this video. awesome.

4 04 2012
Charlie

(The only difference between militant vegans and me is that they want to take my freedom to eat meat by any way possible, including preaching false dogma about health and science. But the true is that our very existence as a continuing species on this earth means we are utilizing resources that would otherwise be available for other creatures. That applies to every creature on earth as well.) Charlie
————————————————————————————————

http://letthemeatmeat.com/post/19779405568/dear-awesome-vegans-and-vegetarians-and-compassionate

That I see overwhelming evidence that vegans and I are entirely more similar than different. What is a vegan, then? What is veganism?
Vegans eat a lot of vegetables. I eat a lot of vegetables.
Vegans love animals. I love animals.
Vegans want to spare animals. Spare animals what, exactly? Death?
Vegans want to spare animals death. Impossible. Immortality is not an option for animals, not even the human animal. Suffering? Physical and mental suffering?
Vegans want to spare animals physical and mental suffering. I want to spare animals physical and mental suffering.
Vegans want to spare animals exposure to human brutality. I want to spare animals exposure to human brutality.
Vegans want to spare animals from ever experiencing anything painful, whether physical or mental. To never experience any pain or suffering, or less than perfect circumstances would defy the laws of the universe and subsequent reality which we are living beings in. Not even birth, the opposite of death, can occur without pain. To experience love, the most wonderful thing on Earth, we must experience some pain and suffering. Think of a person you love with all your heart, and now think of a time when that person caused you pain. That person lied to you, let you down, maybe hit you or just accidently ran over your foot with the car when they were backing out of the driveway. No matter, there was pain and suffering in there somewhere.
Vegans do not consume animal products of any kind. Impossible. Inside every vegetable is an animal and maybe another vegetable, and inside every animal is a vegetable, and maybe another animal. And on and on and on.

12 07 2012
Z

This is the most stupid argumentation I’ve seen ever.

29 08 2012
Weronika

agree :)

23 08 2014
leandro teixeira de jesus

Vegans=cancer.

17 06 2013
Rich Loammiser

Charlie, I appreciate your wanting to find common ground—instead of attempting to beat others into submission. You make a lot of good points. I worry that some people will not be willing to see your point of view because they are so deep in denial about how throughout human history we humans have depended upon consuming other animals and few of us would be here today if that were not the case. It may not be fair to the organism that ends up on someone’s plate, just like it won’t be fair if I get eaten by a mountain lion tomorrow. But that’s life on Earth.

5 04 2012
Richard

Denise, please. Do you seriously think vegans have something to gain from Tom Billings BeyondVeg when we already have PrimitiveNutrition :)

If primitivenutrion’s serie on paleo is the university, then BeyondVeg would not even qualify as a kindergarden. Do not underestimate your audience. It’s april 2012, you should be selling us the car of the season. Paleo is already debunked.

5 04 2012
neisy

Richard, these videos are a good example of a biased/unreliable source (selectively picked info that hinges largely on character attacks, uses abstracts instead of the full-text of many studies, often relies on secondary interpretations of research, and is made by someone with strong emotional investment in veganism). If he has any videos that specifically offer health advice for vegans, let me know and I’ll see if they’re solid enough to link to on this page.

22 05 2012
Doug Spoonwod

Neisy,

1. It’s not a character attack to point out that you don’t have background in nutrition or any relevant field here. Your education is not your character, nor is your character your education.

2. PrimitiveNutrition’s references allow one to find the full-text if one likes. You simply don’t know if he used the full-text of the studies he referenced or only the abstracts. Pretending that you do know such comes as misleading. Also on this point, the authors of the studies write the abstracts. So, using abstracts isn’t necessarily problematic in itself.

3. Plenty of PrimitiveNutrition’s references come from primary research. Oftentimes he relies on firsthand interpretation of research.

4. You have very little idea about the intensity of PrimitiveNutrition’s emotional investment in veganism and neither do I. You think you can mind read someone’s emotional state over the internet? Second, PrimitiveNutritiouses the term “whole food vegan” at one point in his videos. Someone who uses that term, I suspect, will usually *dislike* a vegan diet with a high amount of processed and refined foods *for most people* (he might make an exception for someone with gastroparesis, or someone with high caloric needs or strange food allergies). The class of diets which qualify as vegan include such highly processed food diets. So, there does exist an indication that PrimitiveNutrition might *strongly dislike* a part of veganism. If all that holds about him (which though speculative, seems highly likely), PrimitiveNutrition actually isn’t strongly emotionally invested in veganism, because if he were he would have to be strongly emotionally invested in highly processed vegan type diets. At best, he comes as strongly emotionally invested in a subclass of vegan diets.

5. It comes as unreasonable to request that PrimitiveNutrition supply specific health advice for vegans, even if he has the relevant background to do this, because he has too large and varied of a potential audience. It seems highly likely that registered dietitians who would normally recommend a whole food plant-based diet to most people, will NOT recommend such a diet to someone with gastroparesis. Or, in my particular case, though I believe that an RD would would usually recommend peanuts as a plant source of fat, I doubt that such an RD would recommend the same thing with me since I’m allergic. You have to know your audience before you can make intelligent recommendations, and the less homogenous your intended audience the more difficult it becomes to make intelligent recommendations.

I will add that PrimitiveNutrition does say this:

“You might think I am here to say animal foods are not good for you. I am not. If you are going hungry, any source of calories and nutrients is good for you. But if you have a choice they are probably not optimal for you over the long term. And if you care about our modern challenges, they are not right for us, as a community.”

http://plantpositive.squarespace.com/blog/2012/3/26/tpns-68-71-waking-to-realities.html

8 09 2012
Marie

Great response, Doug Spoonwood!

20 09 2012
Richard

LOL….priceless. “The lipid theory is bonked out” or how did you once put it? I love the comedy that follows when creationist/Sarah Palin crew try to pretend they a clue on the issues they impose their denialist beliefs upon.

A data of million genotypes shows the people with inherited mutation in one of the 9 SNPs studied, which all have crucial role in cholesterol metabolism, are exposed to life-long reduction in LDL-levels and have 54% decreased risk in dying due to CHD per every 1mmol/l (39mg/dl) drop in the LDL-fraction. None of the studied individuals had any other inherited differences in any other biomarker. Each of the inherited mutations in the nine different polymorphism lowers LDL with a different mechanism, neverthelss the end result is identical. This offers compelling evidence that the benefits that accrue with low LDL are independent of the mechanism used. In turn, this proves that dietary pattern that maintain very low LDL levels should be sought after. Animal fats fits in very poorly in this picture.

BTW one of the polymorphism studied was the HMG-CoA which is the one targeted by statins. Creationist/Cholesterol denialist/Masterjohn -crew maintain that the benefits of statins accrue due to pleitrophic effects instead of the lipid-lowering properties of statins. If so, one would have to explain why people with inherited mutation in HMG-CoA which causes life-long exposure to low LDL show 54% reduced risk in dying to cardiovascular causes per every 1mmol/l decrease in LDL-fraction.

Minger welcome to year 2012.

5 04 2012
Kamal Patel (@paindatabase)

Jack Norris is a favorite among Boston Vegan Association members! I was wondering when he would come up on a paleo blog.

With respect to vitamin D, I wonder if some vegans may not absorb all of it because of a relative lack of accompanying fat. According to a couple articles from last year…

“After supplementation with vitamin D3, the increment in plasma 25-hydroxyvitamin D was positively associated with monounsaturated fatty acids, and negatively associated with polyunsaturated fatty acids.”

http://www.nature.com/nrendo/journal/v7/n10/full/nrendo.2011.150.html

http://www.ncbi.nlm.nih.gov/pubmed/22190928?dopt=Abstract

This may be particularly applicable to vegans. In my brief vegetarian days, I would sometimes have some yogurt for breakfast. But I’d imagine that some vegans have a breakfast largely devoid of saturated+monounsaturated fat, unless they get some peanut or almond butter. A few times, I’ve seen vegan breakfasts consisting almost solely on fruit, along with a multivitamin and vitamin D.

6 04 2012
neisy

Anecdotally, I’ve seen quite a few McDougall-style vegans have trouble bringing up their vitamin D levels even with consistent supplementation, so you may be on to something! Thanks for the links!

6 12 2012
Pablo

the study doesn’t distinguish among different kind of fats. It is only about having fats along with the vitamin D pill.

5 04 2012
Fincharella

As always, you’ve provide a nice little escape hatch from diet dogma by bringing it back to a discussion of what we need to thrive and where we’re likely to find it :)

5 04 2012
rmv

Not a vegan in the least but love the recommendations. Going to pass this on to my vegan friends who aren’t doing that well on it but are determined to stick with it. I may not be able to convince them to eat meat, but hopefully they can find a better vegan diet than what they’re on now(everything they eat seems to come in a box or be cooked in canola oil).

5 04 2012
Amanda Schulz

I get a kick at how worked up people get over all this paleo, veg, vegan jive. Stress is about as good for your health as twinkies are! My husband is a professional athlete, we have been doing this meatless thing for a spell, and were going to keep doing it with little to no regard of the opinions of all those who seem obsessed with telling us its wrong, were going to keep doing it until we feel like shat, if that ever happens. Much like how I dont like lima beans, I dont like the taste of meat. I really find all this bashing so distasteful. At the end of the day we are all going to die of something if people believe its from eating meat. Let them believe it, if they believe little leperchans whisk them away to their demise, let them believe that too. Why does media seem to think the masses are so damned stupid we need to be told? Why are we so obsessed with whose right? Eat what ya like! it aint no skin off my ass. Im going to go make a green smoothie and smoke a Newport. Peace.

5 04 2012
julianne

Thanks Denise – this is a great article, I do sometimes have vegan clients, and this is a great go to article – you’ve outlined the issues and solutions really well.
A vegan here in NZ found that adding raw cottage cheese and raw egg yolks made all the difference – without having to eat bivalves.

When I did an analysis of Durianrider’s diet (on my blog) I found he got zero preformed vit A, and high beta carotene. In a blood test his vit A levels were excellent, he is one of the lucky good converters, yet doesn’t acknowledge others may not be.

5 04 2012
Kamal Patel (@paindatabase)

I read that article…very nice! It would be really cool if you did the same post, but for Lex Rooker’s all meat diet, and then compared the two. (like in clinical trials, how they compare extremes in order to generate hypotheses).

5 04 2012
julianne

Do you have a link to what he eats in a day?

6 04 2012
Kamal Patel (@paindatabase)

Yes, it is actually ridiculously simple:
“I eat once a day, about 2 lbs of mixed raw organ and muscle meat from grass fed beef” –Lex Rooker

http://www.rawpaleodiet.com/lex-rooker-usa/

8 04 2012
Craig Bates

You would have to guess at what the percetages of which organs are in the mix. Lex used to eat the Dog & Cat food from Slankers. Since many people started buying it for themselves they now offer a Primal mix for humans.

6 04 2012
neisy

I loved that blog post you wrote, Julianne (for anyone who hasn’t seen it: http://paleozonenutrition.com/2011/03/05/30-bananas-a-day-durianrider-an-analysis-of-his-paleo-vegan-diet/). I’m really glad he’s transparent with his blood work, because at the very least he’s a fascinating case study!

Someone recently sent me a video he did that shows both his 2009 blood test and his most recent one:

He didn’t mention this in his video, but his LDL went up significantly. Between 2009 and his last test, his numbers changed from the following (I converted it from mmol/l to mg/dl, but you can see the original numbers in the video if you pause it):

Triglycerides: from 53 to 62
Total cholesterol: From 135 to 186 (officially above Esselstyn’s “heart attack proof” line at 150)
HDL: from 50 to 58
LDL: from 73 to 116
Total cholesterol/HDL ratio: 2.7 to 3.2

8 04 2012
cobalamin

From wikipedia: “In humans, triglycerides are a mechanism for storing unused calories, and their high concentrations in blood correlates with the consumption of starchy and other high carbohydrate foods.”

It’s impossible for a person on a low-fat(5-10% fat) diet to develop heart disease because the body is working in primary metabolism, aka Glucose metabolism, unless someone’s body is already clogged up with fat, they will have trouble processing all those carbs. Secondary metabolism is a survival metabolism, low-carb diet, aka Fat metabolism.

HDL/LDL are transport proteins that transport fatty acids around plasma(blood), higher HDL/LDL just means a person is ingesting higher quantities of fat. In all reality, the flawed way of measuring blood cholesterol is limited to those that ingest oils, processed foods and cooked flesh. Skewing the truth to fit your view point doesn’t make you look intelligent.

13 06 2012
robroy777

You may be correct but if eating a ton of fruit and starches (such as sweet potatoes) generates consistently high glucose and fructose levels in the blood this may be problematic as both convert to AGEs (advanced glycated end-products) which gum up vessels and, because glucose is toxic to the bloodstream, may contribute to vascular inflammation, a likely driver of cardiovascular disease.

Anyway, I don’t honestly think man was meant to survive solely on fruits or meat alone as we are obviously omnivores and therefore most people likely need both animal products and plant products.

29 04 2013
Jeff Puhek

This is wrong on so many levels…..low-fat diets often are the cause of a person developing CVD! Look into trackyourplaque.com for real information with plenty of “success stories” from real people. So…”Skewing the truth to fit your view point doesn’t make you look intelligent” ….ahem….

31 05 2013
citizenphilp

Well, we still need to understand why, when the germans confiscated all animal fats between 1940-44 in Europe, CVD went down, despite all the stress to which these populations were submitted to. I wish some of you wouldn’t be powered by wishful thinking and cognitive dissonance. Where the….did you read or learn that low fat diets are the cause for most people to develop CVD, please!

3 06 2013
F. Jeff Puhek (@FJeffPuhek)

I probably should have qualified what I said a bit further. Not all low-fat diets cause CVD, However, the idea that dietary fat causes CVD is wrong. Blood sugar spikes from high-carb, usually grain-based foods – which are quite common in most “low-fat diet” foods, are the starting point in the formation of small-particle-sized LDL patterns, which are linked with the formation of arterial plaque. Where did I learn this? Started with my cardiologist, his book “Track Your Plaque” by William Davis, MD, and trackyourplaque.com. I then followed the references and did plenty of reading.

5 06 2013
Stevil Chemsit

That’s not entirely true. IF you over eat, whether it be from fats or carbs, you store the excess as fat. Guess what kind of fat glucose is converted to? It’s C16:0 Palimitic acid, a saturated fat and the one that increases LDL the most of all saturated fats. If you look at the Durian Rider, he has fairly high cholesterol. The video I saw had his total cholesterol at 185 and his LDL at 115, where the latter is above recommendations.

8 04 2012
julianne

Interesting, thanks, I hope he keeps posting his results.

9 04 2012
cobalamin

There is no such thing as “lucky good converters”.

Beta-carotene to Retinol(Vitamin A) conversion is strictly regulated by Thyroxine(T4). The conversion problem’s seem to happen to those with thyroid problems, probably because of the lack of Iodine and Vitamin D.

The Thyroid is also involved in the conversion of Beta Carotene to Vitamin A. (Hypothyroidism shows high levels of Beta Carotene in the Blood, meaning it is not being converted): http://outrageoushealth.weebly.com/the-thyroid.html

Vitamin D regulates the thyroid. http://www.goodhormonehealth.com/VitaminD.pdf

9 04 2012
cobalamin

There is no such thing as “lucky good converters”.

Beta-carotene to Retinol(Vitamin A) conversion is strictly regulated by Thyroxine(T4). The conversion problem’s seem to happen to those with thyroid problems, probably because of the lack of Iodine and Vitamin D.

The Thyroid is also involved in the conversion of Beta Carotene to Vitamin A. (Hypothyroidism shows high levels of Beta Carotene in the Blood, meaning it is not being converted): http://outrageoushealth.weebly.com/the-thyroid.html

Vitamin D regulates the thyroid. http://www.goodhormonehealth.com/VitaminD.pdf

22 10 2012
Dana Osuna

A vegan who eats cottage cheese and egg yolks is vegetarian, not vegan. As Amanda says, eat what ya like….but that’s not vegan. :)

6 04 2012
Richard

“Richard, these videos are a good example of a biased/unreliable source (selectively picked info that hinges largely on character attacks, uses abstracts instead of the full-text of many studies, often relies on secondary interpretations of research, and is made by someone with strong emotional investment in veganism”

Well what did you use as source when you told your readers Ancel Keys study is flawed and bogus? Are you referring to the segments in the primitivenutrition serie which analyzed the evolutionary interpretations of a shirtless supplement merchant, the one that is publishing your book. Or do you mean the clip where the paleo-accusations of “green-veggie” paradox is put under a critical scrutiny. I don’t see any personal attacks, you just might want to stop those childish accusations.

Do you think there’s even a hint of sweet irony with your comments above and the fact that you guide us vegans to Tom Bilings and Tasha’s site? Do you think there’s some irony in the fact you aknowledge the virtue of transparency with Jack Norris but dismiss the comprehensive analysis of paleo-diet made by paleo-diet expert, plantpositive? We don’t really see the transparancy in the “real food” community and you certainly are not being helpfull on this matter either. Don’t you think you are making childish accusations against primitivenutrition serie, after all you totally “borrowed” his work in the Ancel Keys blog post of yours. Isn’t imitation and plagiarisation the ultimate form of admiration. Why don’t you promote primitivenutrition site? You certainly found them usefull. I know this blog post is about vegans, not paleo, but I am trying give the reader a picture whether you should be considered as balanced information source or not. I think I am being helpfulll to your readers looking for good advices. Perhaps you are just a bit too emotionally invested in your own crusade. Just sayin’.

Now, speaking of Durianriders bloodwork. Compared to any paleo-eater with total serum cholesteol around 300, this digits looks fantastics. However, you don’t really have to look outside vegan sources to find out that Durianrider and Freelee are basically into an outdated concept. In fact what we see is Colin T Campbell, Esselstyn, McDougall speaking against the abuse of smoothies. I cannot why Durianrider has his cholesterol this high, I suspect it’s the 30 bananas smoothies and excess fructose that gets to reign freely when all the protective fiber is being destroyed. You certainly don’t see cholesterol figures like this among those consuming high starch diets. Do you think Durianriders dietary habits are a good proxy for vegans in general?

Here’s Dr William Castelli from Framingham study spewing vegan propaganda.

“You know, we know that if I can get your total cholesterol down around let’s say 100 to 130 or so, and I have maybe not quite a billion people on the earth like that, and those people cannot get atherosclerosis. You know in the China Study, for example, when Chou En-lai was dying of cancer he started a study in China just like the Framingham Study. The only difference was it was in 880,000,000 people so it was a little larger than the Framingham Study. But you know they found these villages in China where you couldn’t get a heart attack or you couldn’t get diabetes and the women couldn’t get breast cancer and you know their total cholesterol were 127, but the chances we could ever get Americans down that low with diet and exercise are not good”.

http://www.prescription2000.com/Interview-Transcripts/2011-02-18-william-castelli-heart-disease-lipids-transcript.html

22 10 2012
Dana Osuna

Wow. I’m a little lost in all the names and things here. Are there really vegans with cholesterol levels over 100-130? Mine hasn’t been that high in years.

6 04 2012
Richard

“officially above Esselstyn’s “heart attack proof” line at 150″

The heart-attack proof treshold was already popularized by Pritikin in the 1950′s. He borrowed it from other’s. Esselstyn is just borrowing from the older literature. The whole story is here:

http://www.pritikin.com/home-the-basics/about-pritikin/38-nathan-pritikin.html

And as said, Esselstyn 6 Campbell has made their stance against fruit-smoothies very clear.

6 04 2012
Richard

“I read that article…very nice! It would be really cool if you did the same post, but for Lex Rooker’s all meat diet, and then compared the two. (like in clinical trials, how they compare extremes in order to generate hypotheses)”.

There’s a tons of data of all meat diets. They get you in the very high risk group for sudden cardiadic death in weeks. This is why I think Denise would be more helpfull to society if paying more focus of the risk profiles of her blog readers. Kurt-Harris style diet makes total serum cholesterol skyrocket to 250-300 range for the 95% of the people in a matter of weeks. One Weston Price protégé was already killed by this most common cause in the west, sympton free heart-attack. He was 41 years of age.

I recommend the inuit-clips from primitivenutriton’s serie. Videos 27 and 28

Minger I wonder why you didn’t you include any seeds in your list. These foods are packed with minerals. Sesame seeds very rich in calcium. Also the recommended supplements you set forth are something I’ve never even heard before. There’s not a single vegan dieticians or doctors advocating K-2 and Taurin supplements. Jack Norris and Michael Greger f.ex recommends iodine supplementations in addition to vitamin D and b12 atleast for those who don’t do seaweeds. I think vegans would find MD Michael Gregers guidelines are more in synch with the science.

http://nutritionfacts.org/blog/2011/09/12/dr-greger%E2%80%99s-2011-optimum-nutrition-recommendations/

Also these 5000IU D-vitamin doses are not optimal for human health. There’s loads of studies in regards to this, it’s seems 2000IU is much better. I don’t you have really even done your homework properly. High doses of vitamin D is associated with all kinds of nasty things.

Vegeterians versus healthy omnivores (5.4.2012)

6 04 2012
I. G.

I´d caution against the vegan vitamin D3-product you mentioned: From what I know it is just impossible to extract vitamin D3 from plant sources. The company that produces the product is, when asked about production methods, very reluctant to provide answers or doesn´t answer at all (this is second-hand information). I would like to ask one question about legume-preparation: How long should legumes generally be cooked? Sally Fallon`s (Weston Price organisation) recipes ask for 4-6 hours cooking time which I simply cannot do. Do you know if the DHA from algae is as easily absorbed as from fish?

16 05 2012
TheVeganscientist

Extraction is not difficult, It’s just that plants do not produce D3, ftmp. The Vitashine D3 is the only vegan source extracted from Lichen, which have been shown to contain D3:

http://www.sciencedirect.com/science/article/pii/S1011134401002342

I got my 25OH Vit D tested in Feb and despite the Chicago winter, my level was a nice solid 47ng/mL on 5000IU Vitashine D3.

The other company basically feeds animal based D3 to bacteria and pretends it’s vegan. The bacteria is just packaging. I believe that’s probably the company you’re talking about.

6 04 2012
I. G.

@Richard: Seeds are usually high in Omega-6 so I do not know if they are to be recommended in high doses (as the vegan diet is already high in Omega-6 and low in Omega-3; forget about ALA, the conversation to DHA is extremely poor). The vitamin K2 is, from what I know, not only important for vegans as most individuals are deficient. Paul Jaminet has some good information on his website: http://www.perfecthealthdiet.com.

6 12 2012
Pablo

dha conversion is so poor…so why fish smells so awful? why all my family for generations are alive and live long lives most of them?
statitic on this issue is done yet.

search on pubmed for k1 conversion into k2 studies, at omnovorous diets.

Maybe it can be useful at a personal level for some, as b12, D, iodine

6 04 2012
leorossi

Great article, Denise! Thank you so much for helping vegans so much more than many vegan “experts”!

I’m a vegan myself, but I think it’s fundamental to have an open mind instead of just accepting as truth anything that would have positive implications on your chosen way of life. Research shows that a vegan diet has defficiencies, some of which can be quite serious, and as a vegan I think it’s my duty to not mislead people in a way that causes them to harm their bodies, while also being kind to animals.

Also, about taurine: fellow vegans, please understand that Red Bull is NOT a taurine supplement!!!

I would also like to add that if you are a vegan and you live in England (just London for the first link) you may want to take a look at these websites:

http://www.ahimsamilk.org/ (cow’s milk and ghee)
http://www.goodfoodnation.co.uk/ (eggs and cow’s milk, and soon other dairy and goat’s milk)

These companies are slaughter-free, meaning they don’t kill any of their animals in any stage of their lives. Personally, I think that’s kind of “ideologically vegan”, and I would definetely buy LOTS of eggs and dairy from them if I lived in England!

22 10 2012
Dana Osuna

:) I like the Red Bull comment. The problem I thought existed in egg and dairy production is what do they do with the males born? If they sell them, so goes the whole vicious cycle some more.

For the record, PETA already annoys me in that they forced this logic into my head and cost me cheese (I miss cheese), so I don’t need bashing comments.

6 04 2012
Richard

If this helps:

Nutrient Adequacy of a Very Low-FatVegan Diet

“This demonstrates that a very low-fatvegan diet with comprehensive nutrition education emphasizing nutrient-fortified plant foods is nutritionally adequate, with the exception of vitamin D. Vitamin D supplementation, especially for those with limited sun exposure, can help assure nutritional adequacy”.

http://www.sciencedirect.com/science/article/pii/S0002822305011545

6 04 2012
12: ‘The Fallacy Of Vegan/Vegetarian Diets’ | Denise Minger | Jimmy Moore Presents: Ask The Low-Carb Experts

[...] you haven’t seen Denise’s new “For Vegans” page on her blog where she outlines some simple ways for strict vegans to optimize their ability to be [...]

6 04 2012
Brian Greco

I love Denise Minger
I love Denise Minger
I love Denise Minger ;)

I would had just written EAT EGGS lol

6 04 2012
stabbyr

Heya Denise, nice page. When you say to supplement with taurine, I think you could also say to consider l-carnitine, carnosine, and especially creatine.

Three super rad blog posts but super rad people featuring why vegans might consider these nutrients:

Carnitine http://suppversity.blogspot.ca/2011/07/amino-acids-for-super-humans-part-iv_17.html

Creatine http://www.psychologytoday.com/blog/evolutionary-psychiatry/201202/your-brain-creatine

Carnosine http://thatpaleoguy.com/2011/02/21/carnosine-colons-and-cancer/ Beta alanine generates it.

Someone should make a supplement with all of these nutrients, B12 and the others. If they have, I haven’t found it.

There are probably going to be some people who can forgo this stuff more than others. We synthesize them all endogenously but our synthesis is by no means optimal, we have evolved to benefit from eating meat. This goes against the “meat has NO fiber and is nutritionally useless” meme but it’s the truth. I tried a vegan diet for a few months because I thought that factory-farmed meat and dairy was unhealthy (and it still might be, but I don’t know that) but soon discovered pastured bison. The first time eating meat in months was like a surge of energy, I was whole again within hours. I was supplementing with B12 already so I attribute this to the functional molecules contained in the muscles of animals.

The problem with this is that people write this off as superfluous, because after all in a population of people who suffer from disease en masse vegans have somewhat of a lower relative heart disease risk! Yeah okay I know you disagree with these arguments too :P. Well it’s not superfluous for me, that’s for sure. I like to feel my absolute best, within reason.

Cheers. Can’t wait for your book.

6 04 2012
Rachel Manning

Do you recommend a coenzyme B-compex and if so what brand? I cannot seem to find a decent brand with folate that’s not terribly pricey.

Thank you in advance, I enjoy reading your blog and find your critiques refreshing.

8 04 2012
6 04 2012
Ann

This is what we take for a CE B-complex – it is vegetarian and gluten-free, and has folic acid. I find orders from I-herb to be quickly shipped, and have been really pleased with their prices.

http://www.iherb.com/Country-Life-Gluten-Free-Coenzyme-B-Complex-Caps-120-Veggie-Caps/14591

8 04 2012
cobalamin

Avoid Vitamin B6 in the form of pyridoxine unless you want very lucid nightmares.

Much better option: http://www.wellnessresources.com/products/daily_energy.php

7 04 2012
Meredith

Denise this is a great post.

I bought that k2 book you recommended straight away and I am not disappointed. Very interesting indeed. If you created a “must reads” section for book recommendations I would buy them all I think. Thanks for the read!

7 04 2012
Heather

A great new site that discusses the dark side of extreme raw and vegan diets being pushed by misinformed zealots like the 30 Bananas a Day gurus is here:

http://30bananasadaysucks.com/

8 04 2012
Raw Food | Testing Five

[...] The chief vegan source is natto—a (not-so-appetizing) fermented soybean product that contains K2-producing bacteria. If you avoid soy, eat a raw food diet that …rawfoodsos.com/for-vegans/ [...]

8 04 2012
cobalamin

I recommend these supplements below because they are EU regulated and also because they ship worldwide at a very economical prices.

Vegan EPA/DHA: http://www.opti3omega.com/
Vegan Vitamin D3: http://www.vitashine-d3.com/

Vitamin B12 sublinguals should be taken once a day for a week to build up storage in the liver, twice a week for a month for security and then once a week after that.

Vitamin B12: http://www.devanutrition.com/vitamin_b12.html
Vitamin B12: http://www.jarrow.com/product/58/Methyl_B_12

Folic Acid(B9): Leafy greens contain the highest sources and this doesn’t only apply to Vegans. 3+ ripe juicy tomatos mixed with a salad is a delicious option.

Folic Acid supplement: http://www.jarrow.com/product/577/Methyl_Folate

Vitamin K2 should only be taken by those that popped antibiotics like candy. Like yourself Denise. Healthy gut bacteria in the colon convert K1 to K2.

I agree with you on the notion that gluten foods, oils and any other extremely processed food needs to be eliminated.

Oysters and mussels have organs, a heart; they are animals. They can never be considered “Vegan”.

9 04 2012
Craig Bates

Vitamin K2 is a fat soluble vitamin that needs bile to be absorbed. Bile gets reabsorbed before it reaches the colon. The colon doesn’t allow for easy absorbsion of anything besides salt and water anyway. It doesn’t make sense that you recommend a B-12 supplement but not K2.

9 04 2012
cobalamin

Wikipedia: “Bacteria can produce a range of vitamin K2 forms, including the conversion of K1 to K2 (MK-7) by bacteria in the small intestines.”

My mistake about where the conversion happens, I should of written gastrointestinal tract. Anyways, the problem is that most of the population doesn’t intake many if any leafy greens on a daily basis, hence less K1 intake, less K1 to K2 conversion, less K2 absorption. Add years of Vitamin K deficiency and a person needs to catch up.

For those healthy individuals that want to catch up with Vitamin K, very high sources of K1 are found in Dandelion greens, Chicory greens, radicchio, lettuce and any other somewhat dark leafy greens.

A lot of Vitamins, Minerals and short-chain fatty acids are produced and absorbed in the colon, how many of these nutrients get absorbed is based on the health of the person’s individual colon. For example, Biotin is produced and absorbed in the colon. Those that have been taking antibiotics like candy and slaughtering their colon’s with greasy foods will most likely also need to supplement Biotin and repair their gastrointestinal tracts with natural antioxidants from leafy greens or better yet, fresh carrot juice. Again, this is all based on the health of the individual.

Healthy individuals like myself that have only taken antibiotics as a child and never eaten beef in my life, don’t have trouble with gut flora. My flora converts K1 to K2 efficiently since my health is evident. My teeth are white and nails are very pink/smooth by simply ingesting leafy greens on a daily basis and getting enough Vitamin D through sunshine.

Have a read: http://www.veganhealth.org/articles/vitamink

I can’t recommend a Vitamin K2 supplement because I’ve never taken one since I’ve never needed one. I only recommend what I have taken. Try searching google with “vegan vitamin K2″, see what is available and be attentive at the ingredients. Especially for “titanium dioxide”, unless you want leukemia.

11 04 2012
Craig Bates

If you’re converting K1 to K2, you’re likely not converting enough. Dietary K1 isn’t associated with lower CHD risk. Dietary K2 is.

http://chriskresser.com/vitamin-k2-the-missing-nutrient

14 04 2012
el-bo

haha, richard…damned if you do, damned if you don’t :)

an interesting article…thank denise

14 04 2012
Christina Arasmo Beymer

Wonderful! I just found this because Jimmy Moore sent me a link in an email this morning. I just did an interview with Rhys: http://letthemeatmeat.com/post/20896431565/quasivegans-christina-arasmo-beymer-discusses-her#disqus_thread

15 04 2012
Tim Tobitsch

Great stuff as always, Denise. I have a lot of people who ask me questions about diet and I often feel unqualified to give solid answers. I’ve read Lierre Keith, but would never refer a vegetarian, vegan, or male person to her work without first feeling the need to apologize in advance because of her abrasive tone. It’s wonderful to have a resource I won’t be shy about directing other people toward!

16 04 2012
Lina

Hi Denise! I’m wondering how many animal products you eat in a a day.I’m fruitarian but my health is the most important thing in my life and I don’t want to end up with deficiencies or malnutrition although I feel great I’ve noticed that my hair starts to fallen out in a big quantities (I drink daily green juices,eat enough calories from organic fruits)

Thank you in advance,
Lina

17 04 2012
SLV-rapport om fisk - Ursprungsliv

[...] gäller tvåskaliga arter som musslor och ostron, så nämner Denise Minger i sin sida för veganer att de saknar centralt nervsystem, och kanske kan vara ett alternativ för en vegetarian eller [...]

17 04 2012
gsmullennix

I have three sister-in-laws who have been practicing vegetarians for decades. All share one commonality in particular…their teeth. Constant and severe dental work has cost them a fortune and caused great pain. I’ve sent them this post…but, those who want to improve the human design beyond what nature has wrought should always consider that they are just one member of a multi-million year specie development and changing it all in one lifetime is unlikely. Eat what we are. Thanks Ms Minger.

19 04 2012
Marty

Could you help me work out what I should be giving my 5 year old son. Although I have recently started eating animal products, my son doesn’t wish to – doesn’t like texture so would like to make sure he is supplemented with b12 and k2. I am not sure what type of b12 supplement he should have or k2. They don’t have to be vegan supplements either. Thanks for your help.

20 04 2012
Richard

@Marty

You may want to check out MD Micheal Klaper’s book “Pregnancy, children and the vegan diet”. Choose professionals instead of untrained broscientist’s online pushing anti-vegeterian agenda at the cost of their appeal-to-tradition fallacies.

20 04 2012
Marty

Thanks, I was looking for official guidelines and they were doing my head in – they weren’t really telling me what specifically I need to know for my child.

21 04 2012
Richard

No problem. Here’s Michael Greger’s nutrition guidelines for vegan nutrition. He updates them every year as he reads every single nutrition research article published in english-language journals.

For example, Greger used to recommend 5000IU vitamin D doses (as do Minger) but since compelling new studies on all-cause mortality and vitamin D showed up, the recommendation changed.

Optimum Nutrition Recommendations (by Greger MD)

http://nutritionfacts.org/blog/2011/09/12/dr-greger%E2%80%99s-2011-optimum-nutrition-recommendations/

29 04 2012
Marty

Thank you so much for this link. I really appreciate it!

17 05 2012
Richard

Sotimes simple observations can be powerfull:

1) William Clifford Roberts, American Journal of Cardiology, editor in chief:

“Because humans get atherosclerosis, and atherosclerosis is a disease only of herbivores, humans also must be herbivores”

http://ncp.sagepub.com/content/23/5/464.full

2) National cholesterol education program, third expert panel :

“Only populations that maintain very low levels of serum cholesterol, eg. total cholesterol below 150mg/dl throughout the life do we see a near-absence of clinical CHD”.

3) William Castelli, Framingham study, principal scholar:

“You know, we know that if I can get your total cholesterol down around let’s say 100 to 130 or so, and I have maybe not quite a billion people on the earth like that, and those people cannot get atherosclerosis. You know in the China Study, for example, when Chou En-lai was dying of cancer he started a study in China just like the Framingham Study. The only difference was it was in 880,000,000 people so it was a little larger than the Framingham Study. But you know they found these villages in China where you couldn’t get a heart attack or you couldn’t get diabetes and the women couldn’t get breast cancer and you know their total cholesterol were 127, but the chances we could ever get Americans down that low with diet and exercise are not good”.

“KIRK HAMILTON: But what would the diet be if you didn’t have drugs and you could get everybody to do exactly what you wanted diet-wise in the United States? How would you reverse the heart disease?”

“DR. WILLIAM CASTELLI: Well you’d have them on a pure vegetarian diet and not getting fat on the vegetarian diet.”

17 05 2012
Richard

This one came out today (Lancet, 2012)

The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials

“…..This benefit greatly exceeds any known hazards of statin therapy. Under present guidelines, such individuals would not typically be regarded as suitable for LDL-lowering statin therapy. The present report suggests, therefore, that these guidelines might need to be reconsidered”.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960367-5/fulltext

At this point, it’s clear that the number one supplement in every paleo-omnivore adherents toolbox should statin.

“…Only pure vegetarians for practical purposes do not need statins, most of the rest of us do”

William Roberts, Evaluating lipid-lowering trials in the twenty-first century.

Minger babe,

Maybe you could illustrate the hazards of “carefully designed” omnivore diets in a seperate section

“I don’t think any person on the planet needs to have any of their lipoproteins or cholesterol tested ever. I think it’s all worse than useless because, what happens is – and I get these emails all the time – you know, eating Paleo, feeling great, blood pressure decreased, no longer on medication, no longer have diabetes… bench press 250, and then they say, but, but, my total cholesterol is now 290 or 300 …

My answer to that is, well, you were doing fine until you got your cholesterol measured.”

–Kurt Harris, MD

20 05 2012
Doug Spoonwod

Richard, I find you a positive presence in the comment section. Thank you for your input and pointing out information from useful sources!

21 05 2012
Richard

Dude, that was the biggest compliment I’ve ever received online. -Thanks :)

1 07 2012
mokshasha

Hi Richard dude,

i find your presence obnoxious, overbearing, mis-guided and most of all – disrespectful and demeaning to Denise and i would be happy if you would go away. since i respect Denise and her blog, i will not list the other things i think of you and your input. (thanks for listening, “Richard-babe”….)

20 09 2013
Charles

Richard is probably the most disrespectful person on the internet and that is saying a lot.

19 05 2012
Yasmin

Richard, you are a horribly negative presence in the comment section. your ruthless rebuttals left a bad taste in my mouth. I wonder what your own agenda is? Mabye you should start your own blog with your own views instead of vindicating others observations. The above article is great for people who are struggling with finding out pathways to better health. I am Paleo and for the first time in my life, feel healthy. My sister, who is bordering on veganism is really struggling with a multitude of health issues that doctors cant seem to find the cause of. She has had blood tests done, seen specialists, had x rays and scans, all to no avail. From watching her eating patterns over her whole life, (Sotimes simple observations can be powerfull) the times she has been healthiest (both in looks and mood, her skin is clear and she is not depressed or easily run down and stressed out by life’s bumps in the road) is when she has consumed a varied diet including meats. I am not a scientist nor do I profess to know a lot about it but I have done a bit of my own research over the years and have even considered vegetarianism/veganism at one time. All I know is that I know less than when I started looking. Its not a competition about who is the most correct, nor is it a fight which will ever be resolved with a decisive winner. Soon there will be 11 billion of us on this planet. Chances are, some people will thrive with veganism genetically whilst others wont. I am more concerned with how we use our resources and I think that our lifestyle at present is unsustainable. The whole world will never be Vegan or Veggo. It is better to find best practices in ALL industries (after all, vegans on a grain based monocrop diet do just as much damage to the environment and sentient beings as do meat eaters, (Sotimes simple observations can be powerfull) the grainfields of the nations do not hold much diversity of life that I have seen. I think it is better to be mindful of all things you eat. For meat eaters, eat only grassfed, free range and organic, for vegans and meateaters alike, avoid monocrop frankenfoods and eat only local, homegrown, in season produce. I hope you find the validation you are craving. Peace to you.

1 07 2012
ravi

i’ve tried that Yasmin – he won’t go away. like those really horrid horse-flies that bite and draw blood. he has a chip on his shoulders as big as new jersey but not nearly as attractive (not…)

i would be **very** happy if he would start a blog and create his own 30 jackfruits a day following and leave denise’s blog to those who are sincerely pleased and interested in contributing in a positive manner. denise is too goody to cut off his sorry spammin ass, so what to do…

and i don’t think there are many chances that some people will “thrive” on a vegan diet – those that claim to do so have not had enough time for the subtle and not so subtle deficiencies to totally drain this or that essential nutrient from their systems (and get cancer at not-so-old ages perhaps….) Just look at denise’s advice – one would have to spend all day every day in intense compensatory nutritional planning to thrive on a vegan diet.

but take heart – the more vegans there are, the more low-fertility females there will be, and although it breaks my heart as a father, the more children that are fed vegan diets, the fewer of them will make it to reproduce successfully especially if times on the planet will get tough.

if successful veganism is not possible without the extraordinary dietary planning and supplementation only available in a complex, consumerist society – does it really qualify as a valid, human-appropriate nutritional choice?

no

6 12 2012
Pablo

wow, I am asking why my wife and my daughter, and myself are alive now. Maybe we are genetic freaks (it would be ver y good, but I fraid it isn’t the case)
But, of course, we are living in the tropics. who knows the reason

27 10 2012
daniel

your sister needs to eat beans and lentils. what genetic predisposition prevents that?

20 05 2012
Doug Spoonwod

“13. Look into “bivalveganism,” a combination of plant foods and non-sentient shellfish. It’s unfortunate this one ended up as unlucky #13, because I honestly think it could be a solution for a lot of struggling vegans. Bivalves—such as oysters and clams and mussels—are incredibly rich in nutrients that are absent or hard to get from plant foods. Oysters in particular are a great source of iron, B12, zinc, selenium, copper, and vitamin D, and have a small amount of true vitamin A as well. Bivalves don’t have a central nervous system and are generally not considered sentient by traditional criteria, so vegans who avoid other animal products may be more ethically comfortable consuming a few oysters per week. (If you want to hear about the potential role of bivalves in vegan diets from someone else’s mouth, here’s a very relevant article by Christopher Cox.)”

1. Iron is NOT hard to find on a vegan-type of diet. See Vegan for Life by Norris and Messina, or here: http://www.vrg.org/nutrition/iron.htm

2. Zinc isn’t all that hard either, especially if you eat grains, legumes, and seeds. Here’s just one source I found online: http://vegetariannutrition.net/docs/Zinc-Vegetarian-Nutrition.pdf

3. Selenium isn’t hard either: http://food.vegtalk.org/minerals//selenium.html

4. Copper isn’t hard either (the RDA is 2 mg) http://www.veganpeace.com/nutrient_information/nutrient_info/good_sources/good_sources_copper.htm

5. Cox’s piece doesn’t indicate anything of substance about the potential role of bivalves in vegan-type diets. What do *the bivalves* that Christopher Cox eats do *for him*? Well, first I’ll remark that his *consumption* of them does make it seem like he understands his ethical position, and thinks that consuming bivalves doesn’t lead to their suffering since it doesn’t cause them pain. But, this does not tell us what role the bivalves as food have in a vegan-type of diet, since the consumption of a food is not even close to the totality of how the food acts with respect to your body.

The role of bivalves in a “bivalveganic” diet comes as simple in one respect. They will provide a source of dietary cholesterol. So, if one has health concerns about consuming and digesting cholesterol for any reason, bivalves are not appropriate to eat.

I find it irresponsible to give advice *for vegans* to consider eating bivalves, while NOT pointing out that bivalves do contain cholesterol.

22 05 2012
Richard

Very good points, Dough. Besides, why would someone who is well-informed even eat stuff that carries high risk for food poisoning. This stuff contains loads of human-pathogens even after well-done cleaning.

Scientists unlock mechanism behind food poisoning from bivalves

http://www.foodnavigator.com/Science-Nutrition/Scientists-unlock-mechanism-behind-food-poisoning-from-bivalves

And dietary cholesterol, no thanks. Jenkins review article.

Dietary cholesterol increases the susceptibility of LDL-C to oxidation, vascular inflammation, oxidative stress, and postprandial hyperlipemia and potentiates the harmful effects of saturated fat, impairs endothelial function, and increases cardiovascular events.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/

@Yasmin,

in order to avoid your sister becoming a muppet for Weston Price Foundation, why don’t you give her a link to Ginny Messina’s website? Contains plenty of nutritional non-nonsense information.

Tasha’s story

Do Ex-Vegans’ Stories Make the Case Against Vegan Diets?

http://www.theveganrd.com/2010/11/do-ex-vegans%E2%80%99-stories-make-the-case-against-vegan-diets.html

23 05 2012
Richard

“George Lundberg MD was Editor-in-Chief of the Journal of the American Medical Association (JAMA) and its Archives publications for 17 years. Today he admits he has gone vegan after reading Dr. McDougall’s new book, “The Starch Solution,” and he calls it “the diet book to end all diet books.” It is the definitive book out there and culmination of years of research and successful treatment of thousands of patients”.

Vegsource, 5.23.2012

24 05 2012
Carolyn Trammell

Hi Denise,

Your work continues to amaze me and reaching out to the vegans was a beautiful thing. Thank you so much for being a great resource of truthful health information we can trust.
I think this article is good for everyone regardless of eating style. I will be using it and sharing it with family. I love the vegan ideals but feel the need for animal protein and I am trying to be responsible and buy the best I can find.
Thanks again for your hard work helping a tremendous number of people of all persuasions and for your very entertaining and fun style.
Hopefully we will all learn that nutrition and health can and should be fun and not a source of anxiety. There is good food out there, we just have to find it, or grow some of it.
I think I will go to the store and look for oysters!

Sincerely,
Carolyn

28 05 2012
Richard

Minger,

sorry this is slightly off-topic, but one question. You write that “lipid-hypothesis is a bonk”. Are part of these Southern religious sects that deny the connection of human to other mammals or the so-called “paleo”-movement which harbours similar line of though and, inter alia, blindly refuse to accept any animal models as valid for humans. Do you support intelligent desing hypothesis? Is human above the Darwinian evolutionary model that dictates our current biomedical research paradigm

This is what I think

Cholesterol denialism = creationism / intelligent desing hypothesis.

Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. This can’t be explained away by stress, inflammation or some infectious agent

Malinow MR. Atherosclerosis. Regression in nonhuman primates. Circ Res. 1980 Mar;46(3):311-20.

11 07 2012
Erik Danielsen

So by what you’re saying, humans need to find a diet that lowers their total cholesterol to reduce risk of aethersclerosis. Also acknowledged is that while some animals experience higher TC on some diets, while others experience higher TC on others.

So well-studied groups of humans consuming high amounts of cholesterol and saturated fat and experiencing low TC levels follow your advice perfectly. Let’s give a big hand to african herdsmen and traditional northern cultures like the inuit and sami. Let’s hear another round for chinese peasants and isolated mexican indian tribes, also experiencing low total cholesterol but on a diet high in cereals and starches.

Oh dear, it appears we have a conflict here. Let’s backtrack.

Herbivorous mammals experience high TC when fed a diet inappropriate to their digestive system, high in saturated fat and etc. Carnivorous mammals do not have high TC on such diets, nor do omnivores like rats. What probably WOULD raise their TC, aside from chemical intervention in a research setting (you never told us just how they went about raising those cholesterol levels), might include beer, poor air quality, chronic stress, working in a chair all day, eating frankenfoods stuffed with preservatives, getting their gut bacteria destroyed by antibiotics, showering in hot chlorinated water every day, or any number of other things that have shown a strong correlation with blood cholesterol levels.

Given that humans can experience low TC on diets high OR low in saturated fat, certain populations have happily consumed grains for millenia, or dairy, or fish, or whatever, I think it reasonable to infer that 1) humans are omnivores with a digestive system adapted to a variety of food materials, and 2) different populations may do better on different foods (what’s best for a rural chinese woman may not be best for me, a suburban scandinavian male) thanks to generations of different diets.

I know, I know. You want for their to be a “right” diet, and the internet gives you more tools than ever to cherry-pick the experts with all the technical talk you could ever dream of to support your Chosen One. But if expert one studies the chinese, and expert two studies the masai, and they both say the exact opposite about how dietary components affect the human, might it be, perhaps, that they are both right? After all, while they are saying different things, they are also talking about different people.

18 07 2012
Doug Spoonwood

“So well-studied groups of humans consuming high amounts of cholesterol and saturated fat and experiencing low TC levels follow your advice perfectly.”

How do you define low TC here?

“Oh dear, it appears we have a conflict here.”

Nope, no conflict. The different groups live under different environmental conditions.

“Given that humans can experience low TC on diets high OR low in saturated fat…”

They aren’t the same humans. Given that human group 1 can experience low TC on diets high in saturated fat, and given that human group 2 can experience… except you haven’t written that. You wrote as if they consisted of the same group. I don’t know why you wrote there in such a misleading way.

“1) humans are omnivores with a digestive system adapted to a variety of food materials”

Not necessarily, because even some herbivores get recognized to consume animal flesh. Additionally, the classification here doesn’t mean much at all, since it applies to the species. It doesn’t say anything about the potential of individuals.

“2) different populations may do better on different foods (what’s best for a rural chinese woman may not be best for me, a suburban scandinavian male) thanks to generations of different diets.”

I don’t think anyone denies that, but you also have to factor in environmental conditions (including the microbrial environment). You have to consider what works best for humans in a highly sanitized, modern, industrial environment when talking about this stuff usually. Talking about traditional cultures such as the Masai or rural people in Mexico almost surely isn’t all that relevant, because your intended audience simply is NOT living under those sorts of conditions (environment) with that sort of line of descent.

“But if expert one studies the chinese, and expert two studies the masai, and they both say the exact opposite about how dietary components affect the human, might it be, perhaps, that they are both right?”

They can both come as right, technically, yes. However, one group, no doubt, lives under conditions more similar to ours than another, at least in certain respects. One can easily argue, I suspect, that the conditions of Chinese, even rural Chinese, more similar to ours than that of the Masai or Eskimos. So, the information given by the Masai study would NOT be as relevant to us as the information given by the Chinese study. In other words the Chinese study would work out as “better” (for us in terms of learning what to do in terms of diet), even though, yes, they both “are right” (see how the notion of “right” can mislead you here?).

20 09 2012
Caba

What you say makes sense, however it seems to me that almost all low-fat vegan eaters see their TC fall to very low levels, and almost all paleo and low carb eaters within the West see theirs rise or at least not diminish, not to the 100-150 level which is the desirable one. Therefore, almost all Westerners would do better to eat a low fat vegan diet. Am I wrong?

5 03 2013
Leon Nel

Interesting. this is what i think
Lipid Theory / Sutured Fat is bad for you = Flat earth Society / Everything Resolves around the Sun.
But let me keep quiet, before you send the Inquisition after me :)

28 05 2012
Richard

Are you part of these…..that is.

28 05 2012
Nan

What does a vegan eat if dropped on an isloated unpopulated island or mountain top?

7 06 2012
co

Same thing as anyone. What they can find. Keep dreaming if you believe humans can catch animals without guns and enslaving them.

9 06 2012
Wyatt

hahhahaha ladies and gentlemen, I am pleased to present the most ridiculous comment on Denise’s entire blog. Co, thank you.

11 06 2012
Wyatt

Denise, I know you are busy but maybe you could write your next post on the prevailing ridiculous notion that we could catch animals without the use of guns and enslaving them. Well I mean, aside from all those bugs we humans eat and all that fishing we do. And, well, aside from our rich history of hunting animals before guns existed. Please awake us from our dogmatic slumber.

1 07 2012
ravi

the Lapp people of norway – a semi-nomadic tribe has been herding and milking WILD reindeer for eons without the use of guns. Goats have, for time immemorial, accompanied humans of nomadic/pastoral tradition – no guns necessary – goats actually seem to like the company of humans. Vegan claims denying co-evolution of humans and animals, often in very symbiotic relationships – are inane.

12 07 2012
Suzanne Ubick

It’s pretty damned easy to catch animals without guns and without enslaving them – we’ve been doing it for some 5 million years. Chimpanzees do it regularly and shamelessly. There are nets, snares, pits, corrals, blowpipes, buffalo jumps, birdlime, spears, bows and arrows, fishtraps, directed fires. Birdsnesting will provide tasty fledglings. Tidepooling will provide crabs, shrimps, sea urchins, and more. Poisonous roots, pounded up and dropped into river pools, will stun or kill fish. And that’s the short version!

12 07 2012
Suzanne Ubick

By the way, it’s pretty darned easy as well to tame animals without “enslaving” them. Food will do it. Every time. Bambi will always renounce the proud free life of the forest if there’s a good source of salt and fodder…that’s why national parks forbid the feeding of animals…

8 06 2012
Davene

I truly want to thank you for all your hard work. I am a vegan myself and have been following Dr Campbell. I have been struggleing because ever since becoming vegan I have been experiencing hunger all the time. I never felt this way on vegetarian diet so I know something is up. No one has been able to give me an answer and I recently have up gluten with the hopes that would help. My first thought has been I need more fat. Do you know anyone else who has experienced this ? Also what supplements besides b12 do you feel are essential. Okay one more question :) most of the veggies I eat are kale and cabbage. What kind of veggies should I be eating if those you mentioned can have long term affects.

I want to thank you again

1 07 2012
ravi

visit some paleo blogs like Marks Daily Apple for example, NOT for the meat eating in your case, but for the oh so remarkably more accurate information about the problems and some solutions for many vegetables, nuts and roots.

the ignorance, misinformation or totally muddled information you get from most idiotic vegan blogs will lead you to a miserable health. for all the aggressive ranting that denise puts up with (vegans are more aggressive due to the lack of many fat-soluble nutrients not making it to their brains…) it is unforgivable in the light of her sincere efforts to dispense what is very good solid information.

even if you still cling to your veganism, you should get some really solid information about how the central elements of your diet should be balanced and treated. your biggest problem is that you will now have to depend on either high sugar fruit or non-human grains if you won’t eat what you are biologically/genetically predisposed for – animal products.

20 09 2012
Caba

Davene, you probably just need more CALORIES – it’s that simple. If you used to eat calorie rich dairy products on your vegetarian diet, the moment you give up those products you need to increase your consumption of other calorie rich foods, otherwise you’ll feel HUNGRY all the time. It’s actually a typical phenomenon which newcomers to the plant based diet experience all the time. You may believe that you’re getting enough food because your food looks bulky, but ultimately it’s the calories that feed you and give you energy, not the bulk. And the best and way to get calories is to rely on well cooked whole grains. Eat more of those. Way more. Believe me, a normal consumption of grains in a low fat diet is somewhere between one and two pounds a day – often it’s around one and half pounds – and if you aren’t eating like that, then you are in danger of feeling starved and tired and depressed – so don’t be afraid of volume! Also you might consider lowering a bit your consumption of certain foods (fruit, potatoes, sometimes legumes due to the protein content – remember grains should be the basis, not beans) that give you an excessive sense of satiation thus making it harder to get the grains you need. Have a good carb binge!

20 09 2012
Caba

Oh and don’t believe the grain bashers. Contrary to what they believe, grains are among the natural foods for us – they are the staple food for many very healthy people, they were eaten during the Paleolithic, and certain hunter gatherers eat them even in the present time. If you have doubts about that, start here:

http://donmatesz.blogspot.it/2011/06/gathering-wild-grains.html

27 10 2012
daniel

you need to eat beans and lentils

13 06 2012
Misguided Slander about Denise Minger from Vegans & I Just Won’t Have It This Time // 30 Bananas a Day… Sucks!

[...] it all comes down to personal choice. She even wrote this article to help any vegans out there!For Vegansrawfoodsos.comI promise this page isn’t scary or mean! Despite rumors to the contrary, I’m [...]

21 06 2012
Long-term on a raw plant-based diet and healthy … anyone ? // 30 Bananas a Day… Sucks!

[...] healthy teeth and bonesMain reason why people fail on 80/10/10and this external article:  For vegansand these resources:  http://jacknorrisrd.com/    [...]

21 06 2012
If I Were Still a Vegetarian… | Critical MAS

[...] a much better article on this topic, please read For Vegans by Denise Minger. She is way smarter than me and brings up a few issues I was unaware [...]

27 10 2012
daniel

if minger is way smarter than you, that doesn’t say much about you.

30 10 2012
andrea

go away, fat soluble vitamin deficient, angry, misguided vegan. ms. minger is obviously far smarter than you.

28 06 2012
Can A Vegetarian Be Paleo? | Paleo Plan

[...] and you’d be eating WAY too many nuts, which wouldn’t end up being very Paleo anyway.Here’s a piece from Denise Minger, a former vegan and current Paleo eater, that describes what you can do as a [...]

1 07 2012
2 07 2012
Ramora

I was wondering if anyone has experienced yellowing on 811 diet. I have yellow undertones to my skin naturally but this is not normal. On the 811 diet I got yellowing particularly prominent around my mouth. I think I have had it from around a year or so in…although that’s when I noticed it…can’t be sure if I had it sooner or not. I have followed that diet for 4 years or so now. Besides the yellowing around my mouth, my skin tone did even out on the diet. I do have a better colour to me overall – before eating this way I was very pale. However I have this blotching.
Now I know that you can get colouring from eating so much fruit/veg but the yellowing round my mouth its like a big blotch and does not look healthy at all..and I don’t think its to do with the fruit/yellow colouring me..but something awful lying underneath like something is wrong with my liver. Of course I have no clue..but I don’t think its right..so want to rectify it. I am hoping my dietary changes over the course of the next few months help. I still intend to eat lots of fruits/vegetables but I don’t think I should be eating the 811 way.

Anyone,please…

27 10 2012
daniel

you need beans and lentils

30 10 2012
andrea

you need to read some non-vegan biased nutritional info.

30 10 2012
andrea

never mind, I see what you’re doing in the thread. hahaha!

(it’s late, what can I say?)

2 07 2012
Richard

People,

remember to take lessons from China:

“In 1940, I confirmed De Langen’s results . . . by the observation that in North China, coronary disease, cholesterol [gall]stones and thrombosis were practically nonexistent among the poorer classes. They lived on a cereal-vegetable diet consisting of bread baked from yellow corn, millet, soybean flour and vegetables sautéed in peanut and sesame oil. Since cholesterol is present only in animal food, their serum cholesterol content was often in the range of 100 mg. per cent. These findings paralleled the observation of De Langen that coronary artery disease was frequent among Chinese who had emigrated to the Dutch East Indies and followed the high fat diet of the European colonists (Snapper 1963, 284)”.

Cornelis de Langen: Diet-Heart Theory, 1916

http://www.epi.umn.edu/cvdepi/essay.asp?id=111

3 10 2012
Eve Kendall

Yes, and those colonists were also eating lots of white flour and sugar!!

Association is not causation. Obvious, but needs to be repeated often.

And I’m not saying that it was fat, or flour, or sugar that was the culprit. The point is, it’s *impossible to know* from this kind of observational study.

15 03 2014
samhuff96

There was endemic pellagra on that diet, perhaps they died earlier for that reason and that level of cholesterol is not healthy there is a minimum death rate around 200-240. At 100 one would expect death by infection and violence.

2 07 2012
Bass Master B

Results speak for themselves. Due to various chronic health problems i became a vegan. My health deteriorated to a ridiculous level as a supplementing vegan for six years despite careful dietary planning and pro-vegan nutritional research. My health stabilised and slightly improved on a health-food oriented Western diet with lots of supplements over many years. My health improved noticeably (without supplements) in three months on a paleo diet. My health improved RADICALLY in only a month on the GAPS diet (a paleo-like diet that minimises complex carbs) and without supplements. At three months it continues to improve radically. I’m 35 and my doctor recently told me my blood work was now better than most 18 year-olds and one of the healthiest he had ever seen!

I know various GAPS dieters and all of them are experiencing obvious noticeable gains in their heath, and they’re coming from serious chronic health problem backgrounds including autism, ADHD, IBS and CFS. I know various vegans who started quite healthy and all are going downhill.

I know what diet i’ll be following thanks!
.

20 09 2012
Caba

I tried the GAPS diet and it destroyed my health. It made me look like a concentration camp inmate. I’m doing quite well on the low fat vegan diet.

3 10 2012
Eve Kendall

Ditto on GAPS. I went vegan for 2 years because I fell in love and then I, a year later, I started feeling badly, and a year after that, became extremely ill. I did not to any research or supplement for all the nutritional deficiencies one develops if not eating meat. I think that one’s ability to tolerate a vegan diet probably varies greatly between individuals, but as an individual who has an extremely sensitive/fragile brain & central nervous system, it was catastrophic.

After two long years of declining health, I am now no longer bed-bound or wheelchair dependent. What did it? Five months of eating a low-complex carb, low sugar (and by that I mean not overdoing the fruit–I haven’t eaten processed sugar or flour in years), paleo diet.

We all have our own personal stories, and I think it’s incredibly important to keep and open mind and most of all, listen to our bodies. What might work for one person may not work for everyone. I cannot infer from my own sample of one, personal story to anyone else.

That said, personally, the more I read about the possible deficiencies created by a vegan diet, the more I am convinced that we evolved eating meat and cannot live (healthfully) without it. Even if you can supplement all of the vitamins, amino acids, and other compounds you cannot get in sufficient quantities from a vegan diet, what about all the compounds that have yet to be discovered or understood?

Nature has its secrets but it is complete. Science is the man groping for his keys under the lightbulb.

27 10 2012
daniel

obviously you weren’t eating beans and lentils.

go get checked for parasites now

4 07 2012
Chris Heppner

Hi, Denise–another great blog–I really want to see that book, so don’t waste too much time here! But a couple of things: John McDougall’s latest newsletter has some good stuff, including links to some recent anthropological papers that push back our consuming grasses and other things a long long way before that 10,000 year mark so often quoted as the beginning of the agricultural revolution and its alleged destruction of our health. I am going to discount the a. sediba paper because it is not yet clear enough just where this new species fits. But the evidence for grasses, I think legumes, and also cooking seems pretty strong.

Also in his recent book, “The Starch Solution,” which on the whole I found thin and disappointing–and if I buy one more book on food issues that is half filled with recipes I shall never use, I shall ask for half my money back–there is yet one thing that caught my eye–the attack on methionine, now classed as an “enemy” along with cholesterol (I think he just slipped up there, but never mind). I chases up the refs he gives, and it looks like a very important story. We all know that CR, caloric restriction combined with a nutritious choice of food, is the best sure way to extend life, reduce oxidation, etc . Turns out that researchers have first zeroed in on lowering of protein as the primary agent of this effect, and then in turn on lowering of methionine as the responsible agent.
Methionine levels are much higher in most animal protein than in veg protein. But–and I think you have already noted this–they are lower in shellfish than in fish or most animals. You may have written about this somewhere already, but it is interesting, and I now do eat–and enjoy –scallops. Will experiment with oysters too, but shucking is a chore, and distrust the packaged ones.

Behind this I strongly suspect an evolutionary program deeply distributed among our genes that runs something like this: when food abundant (including lots of juicy animal food), rev up the metabolism, rev up sex hormones, reproduce fast, the hell with longevity; when food scarce (digging for roots, eating grass and bark) slow down the metabolism, slow reproduction, engage long-life gear, and wait it out till food is abundant again and then start reproducing again. There are obviously programs like this widely distributed among the animal kingdom–and we are animals.

So to repeat a point I made long ago on your main blog, there may not be a “one suits all and all desires” way to eat. I can imagine following the first route for the first 35-40 years of life and getting maximun bangs out of life, and then switching gears to the second slower program to enjoy those more mature years. I am too old to follow that, but …
Anyway, just thoughts of an old brain in a dry season–and keep up the great work of threading an intelligent path between / among the paleo/ vegan propaganda machines.
One of your faithful admirers, Chris

4 07 2012
Barrett Reznick

I find it quite interesting that so many people are willing to put their opinions out there, yet are afraid to use their real name. (First and last) Who are you all hiding from?

6 07 2012
Richard

“John McDougall’s latest newsletter has some good stuff, including links to some recent anthropological papers that push back our consuming grasses and other things a long long way before that 10,000 year mark so often quoted as the beginning of the agricultural revolution and its alleged destruction of our health”.

Interesting thoughts, from the latest piece in NY Times:

Benjamin H. Passey, a geochemist at Johns Hopkins University:

“One thing people probably don’t realize is that humans are basically grass eaters,” Dr. Passey said in a statement. “We eat grass in the form of the grains we use to make breads, noodles, cereals and beers, and we eat animals that eat grass. So when did our addiction to grass begin? At what point in our evolutionary history did we start making use of grasses? We are simply trying to find out where in the human chain that begins.”

http://www.nytimes.com/2012/06/28/science/australopithecus-sediba-preferred-forest-foods-fossil-teeth-suggest.html?_r=2

6 07 2012
Chris Heppner

Hi, Richard–I omited the Sediba paper from my comments because it deals with a newly discovered species classified as an australopithecine, 2 million years old, and apparently adapted to a forest environment–rather distant from our species, generally thought to have arisen around 200,000 years ago and adapted to a more open landscape offering different food sources. It is also unclear whether they belong in the line leading to sapiens–they may represent a side branch that disappeared.

But it does seem clear from the other evidence that the 10,000 BC year date put on sapiens use of grains and legumes for food is way too late, and other evidence seems to point to a more rapid evolution in handling new food sources than the Paleo people assume. I am trusting Denise to thread a path through the evidence from both history and biological science to make sense out of this dietary thing for us all.
Chris

11 07 2012
Richard

Dennis/Cavewoman,

perhaps a warning page for paleo-dieters should be in place. The host of Safe & Effective Crohn’s Disease Treatment -blog, a fervent paleo-dieter died last week as the result of sudden cardiadic death at the age 53.

http://crohnsdad.com/2012/07/09/only-the-good-die-young/

another completely unnecessary death. A person who ought to have been on a strict statin-supplemented Esselstyn diet was lost to pseudoscience. Paleo diet is based on appeal-to-nature fallacy & design fallacy thus it’s by default pseudoscience. These unnecessary deaths occur when simple people think it is a good idea to bring some imaginary meat-based HG diet to their own parasite-free eco-niche (all hunter-gatherers are inflicted by high parasitic burden which is very efficient in lowering serum cholesterol, parasites have even reversed cardiovascular disease in animal models).

23 01 2013
Terry Victory

Firstly Richard, let me just say, that after reading hundreds of your comments on here, i’ve come to the only conclusion possible….that you’re a tosser!!

Wow, that feels better.

Now, regarding the very sad passing of Crohns Dad. What makes you think that he was even following a paleo diet himself? And if he was, how could you possibly know how long he had been on the diet? Maybe he was a vegan until the age of 50, who knows. But one thing i will say as a crohns sufferer myself, that the work this great man did, a medical professional remember, was born out of the love for his daughter who was also suffering with the disease, and the extensive research he did has improved the health of hundreds of people.

Can you say you’ve done the same?

11 07 2012
Vicky

I know this article is REALLY old but it’s really good. I was wondering if you have any more info/reading material on incubation as a determining factor in health. Like how you said what your mom ate while you were in the womb is really important.. I’d like to know more about that!

11 07 2012
Heidi

Fabulous last line:

As much as veganism roots itself in compassion, please consider that you, as a living breathing human, also deserve your own kindness.

This is it in a nutshell for me, a former vegetarian for 10 years although never completely vegan.

12 07 2012
Tim

A very wise friend once wrote a song that included the lyrics “after all the arguments, everybody’s wrong.” Having said that, we should all eat less processed foods and do what works best for our own bodies, regularly reevaluating what that best dietary practice is. Isn’t it that simple? Of course, deciphering what that means for a specific individual is not always so simple. Anyway, I’m pretty certain surprising and tragic deaths occur across all diet types and should not be used as evidence to discredit any one food lifestyle in particular. Mortality is the great equalizer.

13 07 2012
Richard

People stay away from saturated fat: A great new video by Michael Greger MD,

14 10 2012
Mel

The studies in this video by Michael Greger are really unconvincing. The high-fat meal in the first study is an egg or sausage mcmuffin – the Egg McMuffin for example contains 12g of fat and 30g of carbs. The ingredients are: Egg McMuffin®: English Muffin, Egg, Pasteurized Process American Cheese, Canadian Style Bacon, Liquid Margarine
Sausage McMuffin®:
English Muffin, Sausage Patty, Pasteurized Process American Cheese, Liquid Margarine.” Liquid margarine – yum.

In the article looking at the effects of cream, the cream they used had the following ingredients: Heavy Cream, Sugar, Contains 2% or less of each of the following: Nonfat Milk, Artificial Flavor, Sorbitan Monostearate, Carrageenan, Mixed Tocopherols (Vitamin E) to protect flavor, Propellant: Nitrous Oxide. “Animal fat” was hardly the only thing ingested and is really not the only possible cause of the increase in LPS concentration and TLR-4 expression.

The ‘high-fat meal’ in the last study by Erridge is the best. ”The high-fat meal, which provided ≈900 kcal, consisted of a cup of tea and 3 slices of toast spread with a total of 50 g butter.’ The controls were no meal or cigarettes. Wow, I don’t really know what to say. The endotoxemia was clearly caused by the animal fat, unless it was caused by the toast or tea.

Any monkey can do research. It’s really important to critically evaluate the quality before citing conclusions as evidence. People should definitely not ‘stay away from saturated fat’ based solely on this shoddily researched video.

14 07 2012
Perfekthälsa » Blog Archive » RAW food SOS – vad du bör tänka på som vegan

[...] dra fördel av om de vill förbli veganer. Inlägget är en översättning av Denise Mingers råd För veganer med en del kommentar från mig. Denise Minger har en riktigt bra blogg för den som tycker om att [...]

23 07 2012
Staraby

I just want to say that vitamin K2 can be found in sauerkraut and other fermented foods like already mentioned natto, tempeh, miso etc. And who said natto has to be gooey and hard to swallow. Some people do find it to be quite tasty. Tempeh is my favorite, a soft bite of tempeh makes my mouth water so much my cheeks start to hurt, lol! Appetizing food btw is good for the digestion.

Good tips overall on vegan nutrition, especially the bean soaking method, I also – like you – own the book “Wild Fermentation” by Sandor Katz, it really is a great addition to anyone who is interested in fermentation.

Yes, we vegans can be a little hard on ourselves. You are right that some little amount of animal foods is not the end of the world, if one feels that something is missing in ones vegan diet. But it’s important to keep the movement going, do our research, keep strong and healthy and do what we can to help the environment. Peace out!

26 07 2012
Richard

A great assesment of the paleo pseudoscience nonsense by a biologist, published by Scientific American.

Human ancestors were nearly all vegeterians

“Paleolithic diets have become all the rage, but are they getting our ancestral diet all wrong?”

http://blogs.scientificamerican.com/guest-blog/2012/07/23/human-ancestors-were-nearly-all-vegetarians/

A good one from McDougall as well:

The Paleo Diet Is Uncivilized (And Unhealthy and Untrue)

http://www.drmcdougall.com/misc/2012nl/jun/paleo2.htm

Best,
Richard

26 07 2012
Chris Heppner

Richard, thanks for the link to that Sci Am article–a nice piece, though it does leave things rather up in the air–which is perhaps where they belong for the time being. Maybe Denise will make all things clear!
Best, Chris

6 08 2012
Richard

Chris,

Denise making thing clear is rather wishfull thinking. After all, Denny is cholesterol denialist and climate change skeptic. She is in the same basket with creationists and 9/11 conspiracy theorists and other people who are opposing questions where great scientific consensus is established. Doubt & confusion is what these folk are good at. Denise is the merchant of doubt & denial!

I feel pety for those people who actually think that an untrained denialist, pushing appeal-to-nature fallacy, paleo dietary bogus has something constructive to say about the data sorted out by Sir Richard Peto, Oxford professor, the inventor of meta-analysis concept and member royal society. I am referring to the China Study.

6 08 2012
Richard

This was the correct video I meant to copypaste:

Denise trolling her anti-science:

6 08 2012
Richard

Youtube screwing things up:

28 07 2012
Rachel

When did vegan ism stop being about the animals…..

2 08 2012
Aaron

Denise-

You clearly do a lot of research and everything… but what I think you might be overlooking is that if you did a critical review on yourself.. it could be just as compelling as anything for Dr. Campbell’s book or the Forks over Knives Movie.

I don’t find you citing your sources much and you pretty much state things based on your own logic (and for people to believe you.. just because). You definitely aren’t able to be attacked as easily because you don’t name your sources and how you fully come to your conclusions.

Do you have anything to say for this?

6 08 2012
Chris Heppner

Hi, Richard; I did not know that Denise is a cholesterol sceptic–but so are a good many researchers–that is in my mind an ongoing legit debate, to which I am not competent to contribute. But she is also a climate change denier? That would be disturbing indeed, but on what evidence do you make that charge? Please share… Chris

7 08 2012
Richard

There’s not a single scholar who is expert in atherosclerosis/lipid research and opposing lipid-theory, why? Because distancing from the lipid-theory equals creationism. It’s a statement for saying that the Darwinian foundation of out biodemical research is invalid. According to many atherosclerosis/lipid expert the cholesterol theory is the only theory in medicine which is bullet-proof. Every single expert in the branch all over the world including every every public-health organization embraces it. Cholesterol theory has similar consensus behind it as many widely recognized ideas such as evolution, climate change, the theory of gravity, etc.

Confusionist are good at confusing regular joe’s and giving the impression that things are unclear when they are not. The cigarette industry always maintained that people need to hear equal, balanced view. Equal view is a good basis for bi-partsan politics, but not for science where opinion’s do not matter, what matter is the evidence, and evidence from multiple directions. The evidence for lipid-theory not only comes from epidemiology and clinical interventions but from bile-acid research, surgical studies, animal models, statin trials, genetic studies, etc.

Read this book and see if you place Denny in a proper context: learn f.ex about the greatest “expert” and physicians who were opposing cigaret-cancer link, obviously no of them had any background in cancer research. Also, learn what being expert equals in science.

18 01 2013
Mary Ellen

I would use this book to make the opposite argument… I would compare the physicians opposing the cigarette-cancer link to the physicians who promoted the lipid hypothesis while on the Puritan Oil payroll back in the 50′s! You say not a single scholar/expert in lipid research denies the lipid hypothesis… you’re absolutely wrong. Mary Enig, PhD, lipid researcher is one of the biggest opponents of the lipid hypothesis. She has been smeared for years by the big industries profiting from heart disease, cholesterol meds, obesity, etc. Before you make ANY replies, I would ask that you read “The Oiling of America” http://www.westonaprice.org/know-your-fats/the-oiling-of-america. She worked at the University of Maryland and they are largely responsible for getting public awareness of trans fats to where it is and labeling of such on products.

The BEST expert that I will listen to over everyone is: MY BODY. You can try to dismiss anecdotal evidence, but that is truly foolish. I dislocated my knee as a teenager and had two surgeries (1977 & 1980) back when it was more like medieval butchery. I was told by orthopedic surgeons in the 1980′s that I had little cartilage and would develop arthritis. I was told I would need a knee replacement, but that I should wait as long as possible. Two years ago, I was afraid the time had come. I was having a lot of knee problems and other joint problems. I’m going to skip the longer story of joint supplements and my withdrawal, but I did go through a very painful detoxification from joint supplements. However, I knew that my knees would get worse without the supplements. I was right. Last spring I wasn’t sure how long I could hold out on knee replacement.

Coincidentally, I started taking coconut oil eight months ago. I took it because of some claims about cholesterol. An amazing thing happened… within days, I not only had more energy, but my knees felt “lubricated”! I was truly amazed. When I went down the back porch steps using both knees instead of one at a time, I knew something amazing had happened.
I started reading more about coconut oil. I also started reading about the harmful affects of polyunsaturated seed oils… which are pushed on everybody, by doctors, as the “healthy” choice. Even before I started reading this, I was starting to notice a correlation between meals with a lot of sunflower oil and my joint pain. So, after a month of adding coconut oil, I became obsessed with removing seed oils from my diet. I also looked up PUFA contents of nuts and limited myself to nuts with lower amounts (cashews, hazelnuts, pistachios). Actually, I found avoiding nuts altogether for the first 3 or 4 months worked best. I’ve lost 43 pounds in these past 8 months. I have NO joint pain. EVER. My husband and I both began using only coconut oil or some EVOO or organic pasture fed butter. Mostly coconut oil. It is amazing.

Richard, you can tell me all about scientific proof. I challenge you to read the article mentioned and look at the 66 references cited. I have seen more recent references in other places, too. There are thousands of scientific (and contradictory) studies… some good, some bad. The quality is usually NOT what determines whether they languish in university basements or are spread through medical schools and media to become irrefutable “fact” that people believe without question. Money and power determine these things. Now, however, this wonderful internet has allowed communication from sources other than mainstream media. They can’t “control” the dialog any more. You can bash Dr. Enig all you want. The proof is in the pudding… And I won’t buy a seed oil for the rest of my life. You can say my life will be shorter. I disagree. I have jumped out of the hamster wheel of the medical/pharma/agricultural industries… I actually believe if I keep doing what I’m doing, I may never need a knee replacement. Feeling good, energetic, no joint pain for 8 months straight, is all the proof I need.

7 08 2012
Richard

Look for primitivenutrion-serie on youtube (including the new response serie) and browse through sub-segments called “The futility of cholesterol denialism”, “Anything but LDL”, “The infamous Ancel Keys” and “Playing games with your health”. There’s no on-going debate, the lipid theory is nailed, those opposing it are basically intellectual dwarfs and denialists cranks who are not to be taken seriously on scientific platform. The same goes with the paleo-dietary movement which is nearly 100% pseudoscience based on appeal-to-nature fallacy and grotesque misunderstanding of evolution.

7 08 2012
Richard

Look for scientific consensus chances are much higher that they got it right over Stephen “dietarary cholesterol does not raise your cholesterol, and my TC cholesterol of 250 is healthy” Guynet.

I discussed with one of these cholesterol confusionists whackjobs under the pseudoname “Bog” and “Peter”, the mind of a confusionist is a funny indeed: it’s just that you need to be much beyond talanted elementary school kid to refuse this cholesterol denialism nonsense:

http://wholehealthsource.blogspot.fi/2012/05/beyond-otzi-european-evolutionary.html

Many of these cranks have a formal education in a given branch which happens to be the only branch where they do not harbour pseudoscientific non-sense ideas, but for the idea’s they are willing to discuss outside their own expertise the same cannot be said.

7 08 2012
Richard

It’s just that you do NOT have to much more talented than a talanted elementary school kid to refute this cholesterol denialism nonsense.

10 08 2012
i miss cheese, but don't like tummy aches

This is certainly all overwhelming for me. I started eating [mostly] vegan after watching Forks Over Knives and reading Crazy Sexy Diet (great book despite its name), and I’m tempted to initially say: girl – how do you find yourself on the same playing field as people who’ve been doing research on this for decades longer than you’ve been alive? but also i know research is often skewed and we can’t possibly know everything (good and bad) about a field of study. So again, i’m overwhelmed! I used to do a lot of reading about nutrition b/c it’s a big interest for me, but after all this back-and-forth and fierce debate to the point of disrespecting each other, I’ve almost decided to follow the nutrition theory of my own body. Still hard to tell what will happen to me long term (which makes me want to turn to research studies done over long periods of time) but there are just too many that totally contradict others. And it’s not like people are somewhat agreeing with each other. It’s DIRECT disagreements and contradictions. Like the research on soy: some say it causes cancer, others say it cures it. What am I supposed to do with that?!?! ah!

27 10 2012
daniel

you need to start eating beans and lentils, in that higher state of being you’ll know whats good.

14 08 2012
Tom

Richard, You would benefit greatly from watching Mathieu Lalonde’s Science of Nutrition seminar. If you want accurate science from an academic source then it’s definitely worth watching.

@Denise, this a great page with some really good advice. It’s a shame that a few vegans have to come on here and insult you even though you are trying to help them

15 08 2012
A

Wow. People on this site are MEAN.

As a vegan, I really appreciate that you took the time to post this, Denise. Thanks for the suggestions.

15 08 2012
Aaron

Denise-

You clearly do a lot of research and everything… but what I think you might be overlooking is that if you did a critical review on yourself.. it could be just as compelling as anything for Dr. Campbell’s book or the Forks over Knives Movie.

I don’t find you citing your sources much and you pretty much state things based on your own logic (and for people to believe you.. just because). You definitely aren’t able to be attacked as easily because you don’t name your sources and how you fully come to your conclusions.

Is there a reason you don’t cite many of your sources? It seems of utmost importance when you review others statements?

I know I sound a bit harsh but I really am curious too..

15 08 2012
The Real Food Lifestyle "Diet" - All In Paleo - Big Tim's Primal Journey

[...] I look at it like this.  Choose not to eat them because you don’t feel it’s healthy for YOU, but do not tell me that it isn’t healthy for me, or it’s bad for the environment when the facts and science clearly state otherwise.  My friend Denise Minger has put together an outstanding article to assist Vegetarian/Vegans in making better choices if they still choose not to eat meats, complete with supplements you should be taking if you have chosen that lifestyle.  You can find that post here at her blog.  [...]

16 08 2012
Richard

Tom,

Denise Minger denies the lipid-theory, she is a religious anti-darwinist, a creationist, that is. I don’t take dietary advices from anti-science -crowd. Dennis recommends the diet of Kurt Harris: you can look here the lipid-responses people following her diet advices receive in their clean, parasitic-free eco-niche:

http://perfecthealthdiet.com/2011/03/low-carb-paleo-and-ldl-is-soaring-%E2%80%93-help/

Denial of the “lipid hypothesis” is an implicit denial of evolution. If it applies to other mammals, why shouldn’t we expect it to be true of ourselves? Based on homology, evolutionary theory would predict a similar effect in humans, and the burden of proof lies with those claim the contrary.

Would Denise Minger blog about this study, f.ex I might take her seriously some day:

The plasma lipids, lipoproteins, and diet of the Tarahumara indians of Mexico

“Since in the experimental dietary cholesterol is sine qua non for the development for the experimental atherosclerosis, especially among the sub-human primates, the finding of linear association of dietary cholesterol intake and plasma cholesterol concentrations in man further undergirds the evidence relating dietary factors to hypercholesterolemia and atherosclerotic coronary heart disease”.

http://www.ajcn.org/content/31/7/1131.long

16 08 2012
neisy

Richard, you’re free to post here with valid criticisms, but I am in no way a creationist (many of my posts talk about evolution!), nor am I a “religious anti-Darwinist” (I don’t adhere to a specific religion), nor do I deny that cholesterol plays some role in heart disease (though I think it needs to be viewed through the lens of oxidation, thyroid status, etc. instead of the usual “high cholesterol causes heart disease”). Where are you getting this stuff?

27 10 2012
daniel

Denise failed veganism because she thought a soy candybar was a bean, and popcorn was a lentil.

99.9% of mostly plant based diet cultures eat beans and lentils almost daily.

Septuagenarian vegan body builder Jim Morris puts it in laymens terms

27 10 2012
daniel

16 08 2012
Aaron

Ok.. please let her decide on the evolution debate without- ipso facto conclusions.

Denise: Are you a creationist or believe in evolution? It’s a pretty important question.

If she has talked about this before- I’d be curious of what she had to say.

16 08 2012
tlg

SOME role in heart disease? Heart surgeons talk about opening a heart and valves and seeing the them lined with cholesterol. I am still having a hard time taking information from you when you don’t have formal education or research training.

16 08 2012
robroy777

Most serum cholesterol is formed from endogenous cholesterol made by the liver in response to a low-cholesterol diet. The more cholesterol you eat, the less you have in your blood usually (if refined, acellular carbs are low).

This is why low-fat, high carb diets (cholesterol trends with fat) are so good at generating plaques and heart disease.

16 08 2012
tlg

I absolutely need to see multiple studies and reports saying the more cholesterol you eat, the less you have in your blood aka in your heart thus less risk for heart disease. Heart Disease is the #1 killer in this country, and we happen to eat more cholesterol than most other countries. Not that correlation always means causation, but there is a DIRECT relationship between the cholesterol you eat, and your risk of heart disease because of plaque buildup. Any case against that sounds like the unfounded reports coming out of the Weston Price Foundation.

16 08 2012
el-bo

>>”I am still having a hard time taking information from you when you don’t have formal education or research training.” <<

then don't

this whole nutrition thing is an open game with everything to play for

only the most foolish of your 'educated' scientists would claim that it was all known

many folk have found that denise presents more than a compelling angle on some of this, but that doesn't mean you have to…there are many thousands of blogs, some of which will likely support your bias

16 08 2012
tlg

“educated” scientists? since when are we downplaying the role of education? there is a huge difference between engaging in a discussion about nutrition and the role it plays in our lives and the effects we feel of certain foods, and trying to play in the same field as people with decades of experience and education and knowledge in the field. i’m not saying you need to be part of the ivory tower to engage in a discussion, but the people up there spend their lives up there studying and researching and reviewing. we live in a society that affirms truth through research and studies and education and experience. Just because Denise spends hours a day reading, that means she’s qualified? I just think it’s insulting to try to match up to someone like T. Colin Campbell who actually grew up on a dairy farm believing milk was the perfect food, then through research found contrasting facts about the affects of certain nutrition on your body. His research spans decades. Shouldn’t we respect that and stop putting quotations around words like scientist and expert? this is just extremely frustrating. humans by nature want to be in control and display “know it all” attitudes about things, the innate desire to be someone and matter. That’s great, and we all have that, but if you’re serious, go to school and be a real part of the field.

16 08 2012
el-bo

i’m not downplaying anything..you seemed to be making the point that denise has nothing valuable to offer (or at least giving you a hard time), because she lacks qualifications

and campbell ?? you couldn’t have given a better example of someone who seemed to allow an agenda to make him act in a very un-scientist-like manner, despite his qualifications….

it doesn’t matter that he grew up on a dairy farm, nor does it matter how qualified, nor how many years of research…the only thing that matters is he’s being ‘straight’ with his findings

>>”Shouldn’t we respect that and stop putting quotations around words like scientist and expert?<<"

respect is earned, not assumed…so, no, not all scientists are 'scientists'…not all experts are 'experts' , but in campbell's case the quotations are valid…if i knew internet code those quotations would have been in bold, italics and covered in glitter

my point is that it's not the qualification that's the important part

do you think that being qualified would make denise any more determined, any more focused, any more intelligent or any less dedicated to finding the truth in all of this ??…and denise, "know it all" ?? where'd she say that

i agree, though, that her getting qualified would at least get her more attention from those that think that's important

i doubt this is the first time you've read her blog, nor have you just discovered she is not traditionally qualified to do this, so it's a bit late to be pulling the 'yeah, but you aint qualified' card

you either find something of worth here or you don't…if you have queries or doubts, that's cool, but argue your case without the campbell-esque cheap shots

16 08 2012
tlg

campbell-esque cheap shots? he’s not a scientist? isn’t THAT a cheap shot? ok i again sense a strong disrespect for the academic community from you. qualifications and years of research dont matter? more education doesn’t make you more intelligent or qualified?

i’m not finding these discussions to be respectful or useful because this is clearly not a place where the science is a priority. its abrasive and again, disrespectful. try telling someone to his/her face, who’s worked for years in a field, that he/she is not a scientist b/c you disagree with methodology. try saying that to your doctor. or anyone.

has anyone heard of the straw man argument? that’s what campbell is being used as here – easy target. i dont praise him, but if i were to look to either him (or any actual scientist who has lab experience and peer-to-peer discussions and someone mentored by professors) or denise, obviously it wouldnt be denise. i’m disappointed by the dialogue here and i wont be returning.

16 08 2012
el-bo

>>”i wont be returning.”<>”i again sense a strong disrespect for the academic community from you”<>”qualifications and years of research dont matter?”<>”more education doesn’t make you more intelligent or qualified?<<"

seriously ??

well, i reckon more education would lead to more qualifications, but intelligence is something that can be defined and exist on many different levels, even outside the realms of formal education

—————-

it was just very convenient that you mentioned campbell, as he is someone who i think does science a disservice, not only by his methodology but also his real world interactions that are full of puffed-up, self importance and arrogance buoyed on the very same sentiment and automatic respect that you bestow upon him

it is not valid to be attacking others who question your findings because they are not qualified…in a world where everyone with an interest can get hold of the data, i bet it boils his blood that someone without his qualifications can question him

any scientist truly interested in making progress towards finding truth would welcome fresh insight, even challenges without the "DO YOU KNOW WHO I AM !! " histrionics

so yeah, i don't really think too much of campbell

i'm out

16 08 2012
el-bo

for some reason the top came out real funky…

i know you won;t be returning, so wont actually read it, but…….

>>”i wont be returning”

yeah you will :)

i think i made it quite clear that qualifications are moot to me….

that doesn’t mean that i give automatic respect or disrespect to someone who is or isn’t qualified

>>”i again sense a strong disrespect for the academic community from you”

not at all…you didn’t really read my answer did you….

i find clever people with that aptitude and determination inspiring…but here’s the thing, i include denise under the academic umbrella

>>”qualifications and years of research dont matter?”

they matter if you want to be able to say you have a lot of qualifications and have completed years of research

neither qualifications nor years of study mean anything on their own

>>”more education doesn’t make you more intelligent or qualified?”

seriously ??

well, i reckon more education would lead to more qualifications, but intelligence is something that can be defined and exist on many different levels, even outside the realms of formal education

16 08 2012
The most obvious reason veganism is not good for long term health | Primal Bodybuilding and Health

[...] the healthiest human you can be. It’s more like a religion. So here’s an excerpt from Raw Food SOS I thought was worth digging [...]

16 08 2012
Aaron

“many folk have found that denise presents more than a compelling angle on some of this”

I am sorry but I am unsure what everyone sees as so compelling from this blog. It seems like she has become known mainly through her critiques of others… which is fine. But I have the feeling this has given her undeserved credit or an honorary ‘strong background/scientific knowledge’ if you will.

I have commented several times that I have not found compelling resources and citations that back ‘Denise’s’ claims and she holds others to a much higher standard than her own it seems (through her reviews).

I have commented that if she was to do a review of herself, she would blow herself apart too… with her quips and fact checking.

Does anyone else disagree with this…? and does Denise have a moment to comment on the seeming lack of adequate citations (references) and background to back up her claims (that doesn’t have references)?

Am I missing something?

16 08 2012
tlg

I too would love to see citations and a self-criticism of herself. until then, my source is going to be NIH.

16 08 2012
neisy

Could you give some examples of claims that are missing citations? I try to link abundantly to outside studies and articles (which appear as underlined text in my blog posts) for any claim that may be controversial — if there’s anything I’ve written that seems unsubstantiated, feel free to point it out so I can reference it.

16 08 2012
el-bo

i said “many”, not “everyone”…i also used the word ‘angle’ to denote an alternative viewpoint

no one is suggesting that the fat lady has sung (nor even yet reached the theatre), so why is everyone setting themselves up as some kinda david to her goliath

it is worth making the distinction between others bestowing praise and merit where some might feel it undeserved, and her blowing sunshine up her own arse

just ask her for more info without the warpaint and battle-cry

19 08 2012
Tom

Richard,

No-one is denying that cholesterol plays a role in heart disease.It’s just not as simple as you want it to be.

Mat Lalonde explains it well

“Cholesterol is not whats going to determine whether or not you get heart disease. What you want to look at is whether or not the lipoprotein molecules are oxidized. So you want to look at oxidized LDL, LDL particle size, triglycerides, markers of inflammation etc. All of which are going to be better predictors of heart disease than total cholesterol”

“Blaming cholesterol for heart disease is like going into a bank where theres a heist and arresting all the customers becuase they are there in greater numbers”

The whole notion that saturated fat causes disease is quickly being abandoned by the top researchers. Even Walter Willet and Frank Hu are no longer anti-saturated fat.

I suggest you read Stephan Guyent’s blog posts about cholestrol and heart disease

http://wholehealthsource.blogspot.co.uk/search/label/cholesterol

He writes in an academic manner and comes to the same conclusons as Denise.

19 08 2012
Tom

Oh and Richard,

Ronald Krauss is possibly the leading lipid researcher in the world. He was anti fat for many many years but now his research shows that the problem isn’t saturated fat and it isn’t as simple as “more cholesterol, more heart disease”

20 08 2012
Richard

Denise, as I stated you are a creationist and bogus artist.

This “cholesterol plays some role in heart disease” is grotesque understatement and nothing but a pseudoscientific half-truth. Lunatic stuff you only you only see in online blogs that are tied to the new neo-carnivore movement.

Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis.This can’t be explained away by stress, inflammation or some infectious agent.

We have extremely well-done animal models to show that cholesterol is all that is required for heart disease. These models can show us direct cause-and effect relationships. We can induce heart disease in a mouse by feeding it an athrogenic diet and transplant the damaged arteries to low-cholesterol environment where the damaged arteries simply heals. We can also simply turn-of and turn-on athrosclerosis in a mouse by simply altering its cholesterol feedback mechanism through the genes that dictates it efficiency. Nothing else is needed. We some exceptionally good primate models as well.

Creationists hate animal models and think we humans are biblical creatures, beyond other animals. Judged by your comments you oppose darwinism and think something else beyond cholesterol is needed to induce heart disease on humans (thyroid function, etc).

In addition, we see increased heart disease risk in people who have genetic defect in their cholesterol feedback mechanism. These people die in heart disease irrespective of what other biomarkers (or thyroid function) would suggest. Elevated cholesterol is all what is needed. It works the other way around too, people who have inherited extremely effecient cholesterol cleaning mechanis and have the rare genetic defect the other way around live about 9-12 years longer than their lifestyle would suggest. It’s all comes down to cholesterol.

We also have extremely good epidemiologic data as well. Currently only 5-6 people have died in heart-disease out of those who kept their TC cholesterol under 150mg/dl in a 40-year time frame. I’m talking about the Framingham study. Cardiovascular disease has traditionally been non-existent in Central-Africa. Rural Africans have their serum cholesterol around 116-135mg/dl. The China Project included a cohort from Guizhui county, 250 000 people and zero death through fatal stroke during the 3-year follow-up, mean serum cholesterol were 127mg/dl.

The epidemiology of coronary heart disease in South Africa

http://archive.samj.org.za/1999%20VOL%2089%20Jan-Dec/Articles/02%20February/4.2%20THE%20EPIDEMIOLOGY%20OF%20CORONARY%20HEART%20DISEASE%20IN%20SOUTH%20AFRICA.%20A.R.P.%20Walker.pdf

Drug-trials are a great tool as well

A meta-analysis of 108 randomized controlled trials of various lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, whereas modifying HDL provided no benefit after controlling for LDL cholesterol.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf

You should introduce yourself to primitivenutrition video-serie, he has a good additional serie as well, and more is about to come.

The Futility of Cholesterol Denialism, Part 1: How Much LDL?

20 08 2012
Richard

Ronald Krauss warned low-carbers about the dangers of SFA in his recent article. People citing Krauss in the SFA issue are a bit behind their times.

Cholesterol denialism made some sense in the 1930′s. Not anymore.

20 08 2012
Richard

In a nutshell, the we can prove the lipid theory through the context of animal models, diet intervention, bile-acid research, surgical trials, yeah we only need to need to bypass operate the ileal which results in lower LDL and thus reduces atherosclerosis progression (POSCH trial), genetic data, drug trials, epidemiology, research on parasites, etc.

Who you are going to believe, un-trained amateur pushing diets based on appeal-to-nature/primitivism fallacy (Denise Minger) or the people who actually know the science and the big picture?

The Masai make a great example in favour of lipid-theory as well. In contrast to the popular online idea that Masai eat lot of fat, they don’t eat lot of fat, they eat very little anything and due to their genetic peculiarity and their chronic low-calory context their serum cholesterol are very low which follows that atleast Masai women are quite well-off in terms of cardiovascular disease protection. An average Masai women does not consume even a single egg worth of dietary cholesterol per day. Diseases like rheaumatoid arthrisis and cancers are ofcourse pretty popular among Masai, unlike among their Central-African tribes that comsume low-fat, plant-based, quasi-vegan diets. Check out PrimitiveNutrition:

1) The Masai of East Africa: some unique biological characteristics

http://www.ncbi.nlm.nih.gov/pubmed/4103135

2) “In contrast to white-americans who have a limited maximal absorption capacity of 300mg of cholesterol, the Masai could absord more than 650mg cholesterol. Compared with the 25% suppression of synthesis found in white Americans, the Masai could suppress 50% of their endogenous cholesterol synthesis”.

Cardiovascular disease in the tropics. IV. Coronary heart disease

3) Lipid intakes of Maasai women and children

“Cholesterol intakes were below 220 mg/day. Energy intakes were inadequate and were between 65% and 80% of the recommended daily intakes based on body weight, or 50% and 60% of the RDI based on age/physiological status. It is suggested that this is the reason why serum lipid levels are not high”.

http://www.tandfonline.com/doi/abs/10.1080/03670244.1993.9991299

Everything you’ve learnt about diet online is flawed. Saving good science from pseudoscience,

Best,

Richard

9 01 2013
Dani

Amen, brother!

20 08 2012
Tom

“Who you are going to believe, un-trained amateur pushing diets based on appeal-to-nature/primitivism fallacy (Denise Minger) or the people who actually know the science and the big picture? ”

I think guys like Lalonde, Guyenet, Kresser, Masterjohn and minger etc do see the big picture.

20 08 2012
Richard

I hate to break it to you, but these people do not know the big picture. Just like Denise Minger, they are not too good with the co-founders (I am referring to Mingers “Green veggie paradox”). These people are religious and blinded in their appeal-to-nature fallacy. You’ll get a good second opinion on these people through PrimitiveNutrition -serie on youtube. It’s free, use your freedom of choice.

A research on parasites add to the nearly never ending cascade of lines of evidence suggesting that cholesterol theory is one of few theories that is bullet-proof in medicine.

Denny Minger suggests people to follow Kurt Harris -style paleo/primal diet, a similar diet his book publisher recommends. As a second opinion, I would suggest that anyone who follows such a diet in their own clean, parasite-free eco-niche take a potent daily statin (atorvastatin, or preferably rosuvastatin, judged bythe lipid responses many paleo-dieter get you need a good share of lipid lowering, a daily apple won’t cut the deal anymore). How do the real primal/paleo people still living in their stone-age manages it? This comes to an important co-founder the appeal-to-primitivism -crew don’t talk about. Parasites! The primitive tribes all have them, and they have them a lot. What do they do, they eat up the LDL in your intima. Statins have less side-effects.

1) Role of cholesterol in parasitic infections

http://www.ncbi.nlm.nih.gov/pubmed/15882457

2) An anti-atherogenic effect of Schistosoma mansoni infections in mice associated with a parasite-induced lowering of blood total cholesterol.

“Observations on S. mansoni-infected conventional laboratory mice indicate that patent schistosome infections could be counteracting the effects of an atherogenic diet by modulating host lipid metabolism and inducing a reduction in blood total cholesterol concentrations”.

http://www.ncbi.nlm.nih.gov/pubmed/12458825

Email these papers to Chris Masterjohn and ask for him to explain these finding that contradict his grand idea of the allaged additional “beyond LDL” properties of statins.

1) A meta-analysis of 19 studies (81,859 participants in all) that lowered LDL and measured clinical disease or death, including 5 diet trials, 3 bile sequestrant trials, 1 surgery trial and 10 statin trials concluded that: “The pleiotropic effects [effects apparently unrelated to lowering LDL] of statins do not seem to contribute an additional cardiovascular risk reduction benefit beyond that expected from the degree of LDL-C lowering observed in other trials that primarily lowered LDL-C.”

Robinson JG, Smith B, Maheshwari N, Schrott H. Pleiotropic effects of statins: benefit beyond cholesterol reduction? A meta-regression analysis. J Am Coll Cardiol. 2005 Nov 15;46(10):1855-62.

.2) It looks like Masterjohn is just pushing you corporate propaganda

Low-density lipoprotein cholesterol reduction and prevention of cardiovascular disease

“There was little question after the first major statin trials that the reduction in CVD was related to lipid lowering and was totally consistent and supportive of the lipid hypothesis. However, stimulated by funding from the pharmaceutical industry, in which competition was fierce for market share and was driven mainly by the efficacy of lowering LDL-C levels, manufacturers of less-effective agents for lowering LDL-C levels helped propagate “beyond LDL-C” theories; these theories were that statins reduced CVD events by means other than lipid reduction, often termed pleotropic effects, usually shown in in vitro laboratory studies or small, poorly standardized surrogate marker trials. This belief culminated in an RCT by a pharmaceutical company that was designed to show that more LDL-C reduction with a competitor’s statin achieved no greater benefit. However, the results of that study clearly and convincingly showed otherwise, with additional reduction in CVD events with the drug that lowered LDL-C levels more. Even with this evidence, and perhaps with an even more powerful statin about to be approved, the investigators suggested that the reduced events were due to pleotropic effects of the more efficacious statin. However, the trial was soon followed up with results from another head-to-head RCT, with the same drug at different LDL-C lowering doses, which eliminated the pleotropic potential and rein-forced that lower is better”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665973/

You can also ask why Masterjohn does not advocate a vegan diet since he is so fond with the oxidation of LDL -story:

1) Gluten-free vegan diet induces decreased LDL and oxidized LDL levels and raised atheroprotective natural antibodies against phosphorylcholine in patients with rheumatoid arthritis: a randomized study

http://arthritis-research.com/content/10/2/R34

2) Dietary cholesterol increases the susceptibility of low density lipoprotein to oxidative modification

http://www.ncbi.nlm.nih.gov/pubmed/10704618

3) Dietary cholesterol increases the susceptibility of LDL-C to oxidation, vascular inflammation, oxidative stress, and postprandial hyperlipemia and potentiates the harmful effects of saturated fat, impairs endothelial function, and increases cardiovascular events.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/

and when you are at it, you might also ask Masterjohn about the relevance of particle size to people who do not have metabolic syndrome in the light of the new panel report of lipid/atherosclerosis specialists:

Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

Minger & Co are behind their times and after the new follow-up of primitivenutrition -serie that will be lauched during the upcoming september these people won’t be looking too good. To me, these people remind me of the attacks Darwin received from the behalf of the creationist. The Minger -crew is hoplessly uneducated about the biological mechanisms/pathophysiology of atherosclerosis along with the multiple of lines of evidence supporting the lipid-theory. What they have left with are their imaginary weaknesses in epidemiologic data and diet-interventions. These people are good in confusing people. With primitivenutriion -serie, we try to act a bit like whistle blowers. The good times of Minger -crew are soon to be done. Be prepared for the new era.

Ornish et al. demonstrated in an intervention trial that lowering LDL was associated with increased telomerase activity, which in turn is associated with longevity.

http://www.ucsf.edu/media/pdf/nobel/blackburn_and_ornish_lancet_2008.pdf

Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

Richard

20 08 2012
Tom

So richard, you think if LDL is increased, risk for heart disease increases no matter what happens to other biomarkers ?

I think this is interesting from stephan guyenet

Now let’s swim over to the island of Tokelau, where the traditional diet includes nearly 50% of calories from saturated fat from coconut. This is the highest saturated fat intake of any population I’m aware of. How’s their cholesterol? Men in the age group 20-24 had a concentration of 168 mg/dL in 1976, which was lower than Americans in the same age group despite a four-fold higher saturated fat intake. Tokelauans who migrated to New Zealand, eating half the saturated fat of their island relatives, had a total cholesterol of 191 mg/dL in the same age group and time period, and substantially higher LDL (J. Chron. Dis. 34:45. 1981). Sucrose consumption was 2% on Tokelau and 13% in New Zealand. Saturated fat seems to take a backseat to some other diet/lifestyle factor(s). Body fatness and excess calorie intake are good candidates, since they influence circulating lipoproteins.

Btw, you should email them papers to chris masterjohn

20 08 2012
Richard

@Tom

not quite, so. You miss the context. LDL alone is sufficient to orchestrate the opera as we can see very well thanks to genetic data. People with defect in their cholesterol feedback mechanism develope atherosclerosis even despite other biomarkers (and thyroid) would be perfectly ok. In population consuming atherogenic diets, such as the WHI-trial intervention group who took 3/4 of their protein from animal sources and put only 16gram fiber intake, other biomarkers matter. When your LDL is really low, like it is among Central-Africans, rural Chinese or many HG-population, none of the biomarkes matter. With LDL under 70mg/dl you ain’t getting atherosclerosis even if you tried.

All this Tokelaun, pukapukan nonsense is already refuted long time ago, as said, the creationists are a bit behind their times, find this primitivenutrition video:

RaCCG5: The Tokelauans, and more on the Masai

Interesting blog-posts:

Forks Over Knives and Healthy Longevity: Perhaps the Science is Legit After All

http://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity_17.html

Forks Over Knives and Healthy Longevity: A Missed Opportunity for the Cholesterol Skeptics

http://healthylongevity.blogspot.com/

20 08 2012
Tom

Heres what Krauss says on the saturated fat matter

“Yeah. I like to think the world has come around but obviously that’s not true. We looked carefully at the saturated fat effects. With more saturated fat in the diet, we did see a signal for an increase in the overall amount of cholesterol in their blood. But when we looked more carefully, that slightly increased amount of total cholesterol was not being carried by more of the dangerous, small particle LDLs. It seemed to be carried more by larger particles. Actually, in the people eating more fat, and fewer carbs, the total particle concentration, which most people in our field think is a stronger signal of risk that total cholesterol, the total number of particles did not go up.”

“In our 2006 Study in the American Journal of Clinical Nutrition, we included one branch of the study that involved eating a really high saturated fat diet, with lots of dairy fat, which is the main dietary source of saturated fat for most people. Beef also contains some saturated fat, but in dairy, it’s much higher. That higher amount of saturated fat seemed to cause no adverse increases in LDL particle numbers, compared to feeding people higher monounsaturated fats, such as olive oil. And in our 2006 study, the blood work was better when feeding people higher fat diets, than when feeding them lower fat and more carbohydrates. But keep in mind, this was in the setting of lower carb and a mixed protein diet, proteins from various sources from white meat and dark meat and chicken and fish and beef.”

From a personal experience, when i increased my cholesterol and saturated fat consumption, my total cholesterol actually dropped slightly, my HDL went a little up and my LDL dropped. My markers of inflammation didn’t go up and haemoglobin A1C decreased slightly. I know it’s just an n=1 experiment and maybe my biomarkers will change in the long term but at the moment i am not seeing devastating outcomes from eating a reasonably high amount of saturated fat and cholesterol.

I also think that it’s interesting that observational studies, time and time again show no link between saturated fat consumption and heart disease and that populations such as the kitavans and the french eat a diet high in saturated fat and have low rates of heart disease. It’s only observational but there has got to be much more important factors at play (refined carbohydrates ? vegetable oils ? grains ?)

20 08 2012
Richard

@Tom

I am not even bothering to go to the nonsense by Krauss, find out his fresh article in the leading magazine for diabetics in US. You are behind your times.

Krauss is against SFA. Plain and simple. Krauss own paper: very interesting thoughts from a lipid specialist paid by the Egg board, Atkins-foundation, Cattlemen’s beef association, Pork board, etc.

”Plasma total, LDL, and non-HDL cholesterol as well as apoB concentrations were lower after the low-carbohydrate, low-saturated fat diet period than after the low-carbohydrate, high-saturated fat diet period. Given our previous observations with mixed protein diets, the present findings raise the possibility that dietary protein source may modify the effects of saturated fat on atherogenic lipoproteins”

http://www.ncbi.nlm.nih.gov/pubmed/22031660

Observational studies are just part of the puzzle. Read Jeremiah Stamlers views of the paper by Siri-Tarino, Stamler was in the first congress where meta-analysis concept was ever used, he knew the game and had a thing and two to say about the meta-regressioncurve used in Siri-Tarino paper. Stamler pointed about 14 methodological flaws in the paper paid by Dairy Counsil. BTW meta-analysis conceot was developed by Sir Richard Peto, the same guy who sorted the data for China Study, and BTW here’s what the co-author of the Siri-Tarino paper, Frank Hu had to say about SFA in february 2012:

”Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”

http://harvardmagazine.com/2012/01/a-diabetes-link-to-meat

“The ability to detect an association between a dietary variable and disease require adequate interindividual variation in that dietary factor. This implies that the likelihood of detecting a risk associated with specific food or nutrient among homogenous population who are characterized by little variation in food or nutrient studied will be low”

Nutrition In Pediatrics, 4 (Textbook

Don’t miss the blog posts refuting Mingers nonsense about Fork over Knives.

Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

Richard

20 08 2012
Richard

“It’s about cholesterol, stupid” (William Clifford Roberts, American Journal of Cardiology, editor-in-chief).

Cholesterol cannot be too low, the lower the better

“In view of the 10 to 1 gradient between concentrations of LDL in plasma and interstitial fluid, a level of LDL-cholesterol in plasma of 25 mg/dl would be sufficient to nourish body cells with cholesterol. This is roughly one-fifth of the level usually seen in Western societies. Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”.

–Nobel winners, Brown & Goldstein

Furthermore, individuals born with extremely rare conditions that cause life-long LDL levels of <15 mg/dl display normal growth and actually experience increased longevity

More Minger nonsense refuted here:

http://healthylongevity.blogspot.com/2012/08/forks-over-knives-and-healthy-longevity_17.html

20 08 2012
Tom

Well the Krauss quote was from march 2012, way after the study you referenced.

So you believe that if LDL levels increase, regardless of particle size and other biomarkers, you are heading straight for heart disease ?

20 08 2012
Tom

Heres the thing i don’t get Richard,

LDL is only problematic when it is oxidized, small-dense LDL particles are a lot more susceptable to oxidation and small-dense LDL particles pretty much always show up with low HDL and high triglycerides. I don’t see the mechanism by how eating saturated fat causes low HDL, high triglycerides and small-dense LDL. I haven’t seen enough evidence to convince me that saturated fat causes dyslipidemia. Don’t you think refined carbohydrates and vegetable oils (consumption has increased substantially in the last 100 years) are far more likely culprits?

20 08 2012
Tom

PUFA vegetable oils have been shown to lower LDL in humans, does that mean that consuming more vegetable oil will protect us against heart disease.

This is an interestng quote from Stephan Guyenet

“Saturated fat does not influence LDL in humans in the long term. This is contrary to the mainstream consensus, but is an inevitable conclusion if you carefully consider the evidence from controlled trials and observational studies”

It’s interestng that you have came to the complete opposite conclusion, someone must be cherry picking data.

20 08 2012
Tom

This graph is a little weird.

21 08 2012
Richard

@Tom,

I know you love your denialists. However, pay attention that what I am saying is shared by every single health institution in the world along with every single non-industry sponsored lipid researcher. The consensus on these matters among experts is similar to that the consensus in regards to evolution among biologists.

LDL has direct causal role in the pathogenesis of atherosclerosis. However, a direct causal role does not imply that all with high x will get y. Most smokers do not end up with lung, however many of them do. Watch primitivenutrition’s segments “Anything but LDL” and “Futility of Cholesterol denialism”.

As I’ve already indicated Stephen Guynet is one of the most ardent denialists on the web and is completely off the track. He has his expertise in obesity research and that’s the only issue where he do not harbour any pseudoscientific nonsense ideas. He thinks his own TC cholesterol 250 is fine, because his HDL is high. LOL. Guynet thinks that dietary cholesterol does not raise serum cholesterol even despite hundreds of metabolic-ward feeding experiments that show it does. He bases his notion on cohorts of extremely high risk American patients, among high risk patients consuming atherogenic diets dietary cholesterol does not raise serum cholesterol, when the starting point is healthy completely different pattern emerges.

http://www.blogger.com/comment.g?blogID=1629175743855013102&postID=1401573240583600968

Denise Minger think Esselstyn should have focused more on raising his patients HDL and lowering their triglycerides. Do you realiaze what a mess these people are?

1) Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function

http://www.ncbi.nlm.nih.gov/pubmed/16904539

2) NY times (may 16th)
Doubt Cast on the ‘Good’ in ‘Good Cholesterol’

“I’d say the HDL hypothesis is on the ropes right now,” said Dr. James A. de Lemos, a professor at the University of Texas Southwestern Medical Center..”

“The current study tells us that when it comes to HDL we should seriously consider going back to the drawing board, in this case meaning back to the laboratory,” said Dr. Lauer, who also was not connected to the research. “We need to encourage basic laboratory scientists to figure out where HDL fits in the puzzle — just what exactly is it a marker for.”

http://www.nytimes.com/2012/05/17/health/research/hdl-good-cholesterol-found-not-to-cut-heart-risk.html?_r=2&hp

3) ‘Good’ HDL Cholesterol Can Also Be ‘Bad’ (2012)

“the HDL amplified inflammatory reactions several times over and could explain the latent chronic inflammation that is associated with high cardiovascular risk,”

“Lowering the LDL level is therefore still even more important than raising the HDL level.”

http://www.sciencedaily.com/releases/2012/01/120113210207.htm

4) Some HDL, or “Good” Cholesterol, May Not Protect Against Heart Disease (2012)

http://www.hsph.harvard.edu/news/press-releases/2012-releases/hdl-cholesterol-heart-disease.html

5) HDL Not Always the Good Cholesterol We Think Says University of Chicago Study (2008)

http://seniorjournal.com/NEWS/Health/2008/20081201-HDLNotAlwaysTheGood.htm

Email this paper to Guynet. Another good one from Sir Richard Peto

Meta-analysis of 395 metabolic ward experiments concluded that in typical British diets replacing 60% of saturated fats by other fats and avoiding 60% of dietary cholesterol would reduce blood total cholesterol by about 0.8 mmol/l (that is, by 10-15%), with four fifths of this reduction being in low density lipoprotein cholesterol

Clarke R, Frost C, Collins R, Appleby P, Peto R. Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ. 1997 Jan 11;314(7074):112-

21 08 2012
Richard

Lipid scholar paid by the Dairy Counsil, Egg Board, Pork Board, Cattlemen’s Beef Association and Atkins foundation see polyunsaturated fats healthier choice as a opposed to SFA and warns against the dangers of red meat

2012 ADA Diabetes Dispactch

“similar study using red meat as a primary source of protein found that high intake of beef and saturated fat had an effect that was not observed with either of these dietary components alone: all types of LDL particles, including small particles, increased significantly. On the basis of this finding, the National Institutes of Health recently funded a study comparing the effects of high- and low-saturated fat on diets containing red meat, white meat, and nonmeat as the major sources of protein”.

“The bottom line,” Dr. Krauss said, “is that you can go high on fats and if you go low on carbs, especially sugars and white starch, and limit red meats, you don’t have to worry too much about saturated fat, although foods rich in polyunsaturated fat are a healthier choice. For most people, saturated fat is not the top priority in managing atherogenic dyslipidemia.”

http://www.nxtbook.com/tristar/ada/day3_2012/index.php#/8

Minger, Guynet, etc think SFA and red meat is if not good, at least harmless. Go figure. These denialists are even behind the industry scientists.

ooh…btw the red meat – cancer link is also very strong in places such as Uruguy where all beef is grass fed and antibiotics banned.

21 08 2012
Richard

1) Measuring apolipoproteins does not help risk prediction (June 19, 2012)

“The study, published in the June 20, 2012 issue of the Journal of the American Medical Association, found that measuring a combination of apolipoprotein B (apoB) and apoA1, lipoprotein (a) (Lp[a]), or lipoprotein-associated phospholipase A2 (Lp-PLA2) gave worse predictions of risk than current lipid measures—total and HDL cholesterol. In addition, the study showed that measuring these alternative biomarkers added little information when added to conventional risk factors”.

“Grundy adds that recommendations for statin use in primary prevention may need to be revisited now anyway, highlighted by the recent meta-analysis from the Oxford group that showed benefits of statins in much lower-risk individuals than those for whom treatment is currently advised. And he suggests that risk assessment may in the future move away from measuring many biomarkers and instead focus on subclinical atherosclerosis with imaging methods or simple risk projection based on age, sex, LDL levels, and perhaps another major risk factor”.

http://www.theheart.org/article/1417589.do?utm_medium=email&utm_source=20120622_topStories_dreamail&utm_campaign=newsletter

2) More evidence for lowering LDL to below 70

“LaRosa, who wrote an editorial [3] accompanying Lee’s study, expanded on his views to heartwire: “I used to be skeptical about the idea of trying to achieve very low cholesterol levels, but now I am more accommodating. As cholesterol levels are coming down, we are seeing much lower rates of bypass surgery and elective angioplasty. I think elective angioplasty will eventually disappear altogether.”

“Chimpanzees eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis. He noted that levels of LDL below 70 are on a par with those of nonhuman primates who don’t develop atherosclerosis, adding that, like these primates, humans were designed to be vegetarians. “Our dental anatomy suggests that we are not meant to be meat eaters. Animals that eat meat have sharp tearing teeth, while we have flatter teeth more similar to vegetarian animals. I believe humans are not anatomically or metabolically designed to be meat eaters, and because we do consume animal fat that’s why we get atherosclerosis. Chimpanzees don’t eat meat; they eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis. Maybe we wouldn’t get atherosclerosis either if we had levels this low.”

http://www.theheart.org/article/1290061.do

21 08 2012
Tom

Why don’t YOU email all those papers you reference to Guyenet, Masterjohn, Lalonde etc ? Or post on one of their blogs.

See what responses you get :)

wholehealthsource@yahoo.com

ChrisMasterjohn@gmail.com

lalonde@fas.harvard.edu

23 08 2012
Richard

Minger thinks warnings against dietary cholesterol are something from the 1980′s. Not quite so. Oxidized Omega6 does not oxidize LDL, but dietary cholesterol does. So much for the free-range eggs.

The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis (2005)

http://www.ncbi.nlm.nih.gov/pubmed/16270280

Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation

http://www.ncbi.nlm.nih.gov/pubmed/9001684

When Minger says she is not a creationist, it’s like someone is saying I don’t believe in god, but Intelligent design is an astute theoretical framework.

23 08 2012
Richard

Some of that 80′s science still coming (2009)

The effect of dietary cholesterol on macrophage accumulation in adipose tissue: implications for systemic inflammation and atherosclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/19133410

Cholesterol oxides and carcinogenesis.

http://www.ncbi.nlm.nih.gov/pubmed/2061746

23 08 2012
Tom

Richard

“This hypothesis is supported by our feeding experiments in animals. When rabbits were fed oxidized fatty acids or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. Moreover, dietary oxidized cholesterol significantly increased aortic lesions in apo-E and LDL receptor-deficient mice. A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population.”

Don’t you see a massive problem with that statement ?

23 08 2012
Richard

Now, I don’t, and I can hardly think that you can either.

If you want to believe untrained bloggers with TC cholesterol 250mg/dl instead of listening the IOM about the dangers of dietary cholesterol, then have it!

Rainy-day reading for creationists:

Even small amounts of dietary cholesterol were shown to increase atherosclerosis without evidence of a threshold beyond which a lower intake did not provide additional benefit

Intimal Thickening in Normochoiesterolemic Rhesus Monkeys Fed Low Supplements of Dietary Cholesterol

http://circres.ahajournals.org/content/34/4/447.full.pdf+html

Atherosclerosis. Regression in nonhuman primates.

http://circres.ahajournals.org/content/46/3/311.citation

Arterial lesions and blood lipids in rhesus monkeys fed human diets.

http://www.ncbi.nlm.nih.gov/pubmed/6832336

Claiming that these experimental animal models are not relevant for humans would be like saying that the Darwinian foundation of our biomedical research is invalid. Do we any evidence in non-religous literature to make such a postulation, no we do not have!.

A study on humans showed that dietary cholesterol was associated with increased carotid intima-media thickness, a marker of atherosclerotic independent of other risk factors

Influence of lifestyle modification on atherosclerotic progression determined by ultrasonographic change in the common carotid intima-media thickness.

http://www.ncbi.nlm.nih.gov/pubmed/9094885

23 08 2012
Richard

I provided a small glimpse to some of the best kept secrects of cholesterol denialists. No need to thank me. Use your freedom of choice.

I am having a bit of break. I’ll be back soon.

Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

Richard

23 08 2012
Tom

If you feed a rabbit cholesterol, what do you expect to happen ? Rabbits do not consume cholesterol, they are herbivores.

Look at the masai, they consume MASSIVE amounts of cholesterol and have a low serum cholesterol. Humans have mechanisms to deal with dietary cholesterol and the liver can manufacture 10-20 times more cholesterol per day than you could ever get through diet.

24 08 2012
Richard

Tom,

I covered the Masai already. Use the search function and type Masai.

24 08 2012
Richard

Primitive nutritions excellent “anything but LDL” and “The futility of cholesterol denialism” -segments from his primitivenutritions -serie are recommended for lay people.

Primitive Nutrition 45: Anything but LDL, Part III

The best kept secret of Chris Masterjohn and Stephen Guynet. Our detailed understanding of the cause-and effect relationship of dietary cholesterol to plaque build-up in the artery walls.

NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals.

http://www.ncbi.nlm.nih.gov/pubmed/20428172

Molecular processes that handle — and mishandle — dietary lipids

http://www.jci.org/articles/view/35206

24 08 2012
Tom

I’ve just read Anthony Colpo’s post about primitve nutrition and yourself. I’m sorry but Colpo completely exposed you and your sources. Just like primitive nutrition, you just present cherry-picked, biased, irrelevent studies that fail to address the big picture.

Having read thorugh all of your posts in this blog, it amazes me how many ad hominem attacks and logical fallacies you use. The way you refer to Densie as a “creationist” is offensive and downright stupid.

I’m not going to post in here again as your shear presence raises my cortisol levels. I just want to thank Densie for taking the time to help vegans who are constantly being lied to by people like you.

The only person in here presenting pseudo-science is you.

25 08 2012
Richard

LOL

Incase you put your email here, I can forward you our whole discussion and you judge yourself tell who is cherry-picking. PlantPositive replied to Colpo in a lenght of 10 videos, Colpo responded to him in regards to one video, and in which he had terrible lie in it, something that is about to be revealed soon.

Look for the denialists tactiques, when I pointed out to Colpo the epidemiologic data, people who maintain consistently TC cholesterol under 150mg are immune to heart disease, Colpo used an example of a dead person to show this premise as false, as if TC cholesterol levels at the age of lifespan would matter anymore, as if serum lipids would not lower about 10% already immeadiately after death, as if they was not co-founded by cancers, lipid lowering drugs, diabetes, blood pressure medication, heroin, rapid weight loss induced by detoriating health, chemotraphy, etc.

When I addressed the lack of chronic disease among population who maintain very low cholesterol levels, Colpo started talking about total mortality as if having access to toilet, vaccines, and hospital to a give birth to the child would not be co-founded by these factors.

Wacth out primitivenutritions response serie. Colpo did not even know that he was dealing with wikipedia’s parody page, he confused the term confusionist to confucian and apologist to apology. And no, he has not exposed anything except his own sillyness. His amateur status and lack of basic education is apparent.

25 08 2012
Tom

I think any educated person would come to the conclusion that primitive nutrition is the one cherry picking and has a blatant agenda. I’llcontinue to learn off people like Mathieu Lalonde, Denise Minger, Stephan Guyenet, Chris Masterjohn, Chris Kresser, Anthony Colpo, Robb Wolf etc. It’s funny how most of them guys were vegan at some point in their life and stopped due to poor health or lack of scientific evidence.

25 08 2012
Richard

@Tom

don’t be ridiculous. What primitivenutrition showed to you was the role of multiple lines of evidence in shaping our health policy. The denilaists including Minger cover only epidemiology and diet trials with imaginary weaknesses they are able crunch out of them. That’s about 1/5 of lipid theory, and as Daniel Steinberg showed that the diet trial data is powerfull but not “airtight”. However, the denialists don’t talk you about the powerfull genetic data or the animal models that has accumulated over the years. No talk about bile-acids, surgery data, etc. They are stuck in their RCT -la la la land. LDL has a direct causal role in pathophysiology of atherosclerosis. This is the view that is shared by every major health institution in the world. If you to heartwire.org (theheart.org) you’ll notice that 100% the cardiologists and lipid specialists in the US are on board with LDL lowering “the lower, the better”. There’s no debate, the creationists have lost. What they have left is fooling stupid lay people.

When Stephen Guynet with his TC cholesterol of 250 tells you dietary cholesterol and SFA does not have role in your serum lipids, you cannot but laugh. Just to give some perspective (Coronary heart disease was virtually non-existent in Central Africa):

1) “As to the risk factors in predominantly rural African populations in southern Africa, the principal dietary sources of energy were in the past and still are to an extent cereals (maize and kaffir corn or sorghum) and their products, wild spinaches, and a variety of legumes (cowpeas, sugar beans, Jugo beans), along with relatively low intakes of most vegetables and fruits and infrequent consumption of small quantities of milk and meat”.

“Serum cholesterol levels of rural Africans in the past ranged from about 3.0 to 3.5 mmol/l and remain low. The range of mean serum cholesterol levels of urban Africans was 3.5 to 4.40 mmol/l and later increased to 4.0 to 5.0 mmol/l” (3 mmol/l = 116)

Nutrition and Heart Disease Causation and Prevention Edited by Ronald Ross Watson and Victor R . Preedy

2) The epidemiology of coronary heart disease in South Africa

“…..Soweto (which now has a population of 3 – 4 million), according to records of the Department of Cardiology at Baragwanath Hospital (3 200 beds), 35 blacks were diagnosed with CHD in 1992,51 in 1993, and 62 in 1994. However, of the latter number only 36 were Sowetans; the rest lived elsewhere.I’ Clearly CHD remains very uncommon in urban blacks in South Africa. To afford perspective, it could be asked how uncommon CHD is in urban blacks, compared with its occurrence in Western populations? Of the population of Soweto, almost all attend Baragwanath Hospital when serious illness occurs. If it is assumed that all the 36 patients with CHD mentioned ultimately died from the disease, CHD would be responsible for only about 0.2% of the roughly 20000 deaths occurring annually in Soweto, an extremely low proportion even allowing for uncertainties. In Europe, in the Seven Countries Study,16 for those in the Mediterranean countries and inland the age-standardised 25-year CHD mortality percentages were 4.7% and 7.7%, respectively. The proportions reported for countries in Northern Europe and for the USA were far higher, namely 16.0% and 20.3%, respectively. These comparisons with Western populations underline the very low occurrence of CHD in urban blacks”.

Anthony Colpo was put on statins by his doctor. Guynet, Colpo etc. These are young defect people. Young guys should not have elevated cholesterol. People do not like to be diagnosed as malfunctional. Hence, the childish rebellion.

ATP 3rd expert panel:

“Any LDL cholesterol above 100 mg/dL appears to be atherogenic. The prevalance of elevated levels in large part accounts for the near universal development of coronary atherosclerosis in the United States and the high attendant risk for developing CHD over a lifetime—49 percent for men and 32 percent for women”

http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

25 08 2012
Richard

Denise Minger made a big mistake by attacking the lipid theory. She shouldn’t have gone there. I don’t have problems with her anti-vegeterian agenda, I have problem with her denialism. She screwed up a big time and she is going to pay for that.

What she did to Colin T Campbell she will receive 10-fold back, no less.

25 08 2012
Richard

@Tom

Stephen Guynet claimed to me poker-face that LDL cannot be lowered significantly without drugs. He probably still thinks this is so, because that’s what denialists with creationists mind-set do.

Patients who participated in the 12 week Ornish program showed statistically significant improvements in their total cholesterol, LDL cholesterol, and triglycerdies. In fact, patients lowered their LDL-cholesterol levels by an average of 40%.

The effectiveness and efficacy of an intensive cardiac rehabilitation program in 24 sites.

http://www.ncbi.nlm.nih.gov/pubmed/20232608

The LDL numbers of various low-carbers, these numbers are outright horrible, one can legitimately ask whether paleo-diet offers long-term health improvements over the SAD. I believe that this is not so. Cordain himself is obese these days.

http://perfecthealthdiet.com/2011/03/low-carb-paleo-and-ldl-is-soaring-%E2%80%93-help/

25 08 2012
Richard

One of the best kept secrets of cholesterol denialists.

Email this to creationists end you will be replied “that’s not double-blinded RCT, it can’t prove anything”. The science community does not agree.

High cholesterol per se causes heart disease, and low cholesterol per se heals heart disease, animal models are killers when it comes to establishing cause-and effect. The reseachers transplanted atherosclerotic, damaged artery from a mouse with high cholesterol to a mouse with a low cholesterol. Low cholesterol is all that is required from the environment for the atherosclerotic lesions to fully heal. Inflamation, thyroid function, etc cannot be an independent cause for atherosclerosis. “It’s all about cholesterol, stupid”.

1) Dramatic remodeling of advanced atherosclerotic plaques of the apolipoprotein E-deficient mouse in a novel transplantation model

http://www.ncbi.nlm.nih.gov/pubmed/11533609

Daniel Steinberg, a man who has authored over 400 on lipid metabolism.

2) Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia (2008)

“Armstrong et al and Armstrong and Megan showed that in cholesterol-fed nonhuman primates, virtually total regression could ultimately be achieved, but it took 40 months after return to a cholesterol-free diet to undo the damage done during 17 months of prior cholesterol feeding. The remarkable thing about these studies is that not only was almost all of the lipid gone from the arteries but also virtually all signs of the inflammatory process were gone. The remains of the lesions were basically scar tissue with no signs of cellular infiltrates. In other words, it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining. Simply arresting the hypercholesterolemia by reverting to a normal monkey chow diet caused virtually complete lesion regression without the need for intervention directed specifically at the inflammatory process, results recently confirmed in an elegant series of studies in rabbits.”

“Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences. Consequently, early and aggressive correction of hypercholesterolemia may be sufficient. On the other hand, if hypolipidemic therapy is initiated at, say, 40 or 50 years of age, optimal intervention will no doubt also require attention to inflammation, thrombosis, and hemodynamic factors”.

http://circ.ahajournals.org/content/118/6/672.full

3) Excellent study for Denise Minger to blog about:

Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity.

“These results demonstrate a continuous, graded relationship of serum cholesterol level to long-term risk of CHD, CVD, and all-cause mortality, substantial absolute risk and absolute excess risk of CHD and CVD death for younger men with elevated serum cholesterol levels, and longer estimated life expectancy for younger men with favorable serum cholesterol levels”.

http://www.ncbi.nlm.nih.gov/pubmed/10891962

28 08 2012
michaelphillipjagger

Richard, I don’t need to refute your various insane statements because everyone else already has, but I will say this: I don’t mean to be a total dick (…Dick), but please, for the love of all that is good, would you stop saying ‘serie’!?!? I realize English probably wasn’t your first language, but there is no such word as ‘serie’. It’s SERIES. SERIES, SERIES, SERIES. GAH.

28 08 2012
Tom

It’s probably the lack of B12

25 08 2012
Tom

It’s funny how you posted the perfect health diet link. You should read Pauls follow up to that post

http://perfecthealthdiet.com/2011/03/answer-day-what-causes-high-ldl-on-low-carb-paleo/

and then listen to this podcast for Mat Lalonde’s response to pauls article at the 50 minute mark

http://chriskresser.com/the-healthy-skeptic-podcast-episode-8

It’s not just Denise who has problems with the lipid theory.

31 08 2012
Richard

Denise Minger = Creationist

Evolution predicts that the shared derived features of a clade will affect all members of that clade in similar ways, because of their recent common ancestry. It predicts that the things which induce atherosclerosis in other hominoids probably do so in us, and for the same reasons. The same lipid-eating parasites that co-evolved with them also did so with us, and therefore have similar effects on us.

This is why primate studies — especially those that focus on the hominoids — are relevant, and why they undermine the paleo/creationist diet paradigm. To argue that humans aren’t burdened by highly similar trade-offs as other hominoids is to argue that evolutionary theory has no predictive power. It is a denial of evolution, implicitly rejecting what it explicitly seeks to co-opt.

If humans aren’t hominoids, then evolution is false. Mingers arguments on lipid theory implicitly denies this hominoid heritage, and it therefore rejects evolution itself. That’s why it’s appropriate to her position creationist.

Even small amounts of dietary cholesterol were shown to increase atherosclerosis without evidence of a threshold beyond which a lower intake did not provide additional benefit

Intimal Thickening in Normochoiesterolemic Rhesus Monkeys Fed Low Supplements of Dietary Cholesterol

http://circres.ahajournals.org/content/34/4/447.full.pdf+html

Atherosclerosis. Regression in nonhuman primates.

http://circres.ahajournals.org/content/46/3/311.citation

Arterial lesions and blood lipids in rhesus monkeys fed human diets.

http://www.ncbi.nlm.nih.gov/pubmed/6832336

31 08 2012
Tom

No, just no

1 09 2012
Richard

Tom buddy,

I got another great secret of cholesterol confusionists for you:

This may explain why no one in the biomedical community take seriously the LDL-particle size nonsense. Aall particles in the LDL fraction are atherogenic, independent of size.

1) LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

“Thus, smallLDL was a strong confounder of the association of largeLDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic”.

“After accounting for particle correlations, we demonstrated that the magnitude of association between small LDL and carotid atherosclerosis became equal to large LDL (on a per 1-S.D. basis) or less than large LDL (on a per particle basis). Failure to account for the strong negative correlation between small and large LDL and their different associations with other lipoproteins may underlie the belief that small LDL particles are a more potent atherogenic subclass than large LDL”.

“There are several mechanisms that may underlie the atherosclerotic effect of both large and smallLDL[5]. At both extremes of LDL size, there is decreased receptor-binding affinity for LDL receptors [27]. Small LDL may be oxidized more rapidly and have been associated with endothelial dysfunction and metabolic dyslipidemia [28]. In comparison, large LDL predominate in patients with familial hypercholesterolemia [29] and those consuming high saturated fat diets. Large LDL have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls [30], a speculation supported by our finding a greater IMT difference for large compared to small LDL on a per particle basis”.

http://www.nypcvs.org/images/MESA.pdf

2) Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

Everything you’ve learnt about diet online is flawed. Rescuing good science from pseudoscience,

Richard

1 09 2012
Tom

“What is the physiological rationale for the link
between HDL subfractions and adverse CV
outcome?

HDL particles are involved in reverse cholesterol transport
and have additional antioxidant and anti-inflammatory
properties believed to be antiatherogenic”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

The financial disclosures list of that paper is horrifying, 90% of the researchers have recieved major funding from drug companies.

“Everything you’ve learnt about diet online is flawed”

You are online, primitive nutrition is online, all the paers you reference are online.

I think you have been brainwashed by that vegan oddball primitve nutrition, the guy has a blatant agenda. Possibly works for a major vegan organization or statin manufacturer. The loser has nothing better to do than make videos about anthony colpo or denise minger. Heres an idea for you Richard, if you are so convinced that heart disease is all about total cholesterol and LDL, why don’t you put your effort into publishing a paper so we can stop wasting our time looking at other biomarkers such as HDL, triglycerides, LDL particle size, LDL oxidation, HA1C, CR-P, IL-1 beta, Homocysteine. That way we can carry on eating even less saturated fat and cholesterol, we can chug bottles of vegetable oil (proven to lower LDL cholesterol), we can all start taking statins to lower our LDL even more.

3 09 2012
Richard

LDL independent, causal factor in atherogensis. HDL = Leap of faith is required. All other risk factors matter in universally high risk Western population. The other risk factors matter less in a low-risk population, since atherosclerosis cannot developed independently if LDL is low enough (below 80mg/dl), an orchestra cannot perform without the conductor. At this point I’m sure you’ve heard about the immunity of CVD with TC cholesterol below 150mg/dl.

Chant with me, babe: “Correlation does not equal causality”!

The HDL hypothesis: does high-density lipoprotein protect from atherosclerosis?

“It should be noted, however, that the associations between elevated LDL-C and blood pressure and increased CVD risk reflect causal relationships, whereas such a relation between low HDL-C levels and increased CVD is not undisputed”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903818/

3 09 2012
4 09 2012
Richard

^Complete nonsense.

Low-cholesterol in elderly people in high risk cohorts usually just means bad thngs, it co-founds with cancer, aggressive medication, muscle degeneration etc. Why would we care about what happens in high risk populations.

The cholesterol-denialist are not aware of J-curve (reverse causation) and troll about low cholesterol being hamrfull because it suggest higher total mortality in epidemiologic studies, this is correct, but it does not follow, that we should not be having low cholesterol, it just follows that the cholesterol of sick, elderly Western people plummets during the last years of the their life-span due to chronic diseases and aggressive lipid lowering agents. Cholesterol levels at the age of life-span tells very little.

Show Ray Peat these.

1) From the Framingham

“Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling–perhaps due to diseases predisposing to death.”

http://www.ncbi.nlm.nih.gov/pubmed/3560398

2) Low cholesterol, mortality, and quality of life in old age during a 39-year follow-up

“More dispute has arisen regarding the association of low cholesterol and mortality in elderly persons. For example, in the Honolulu Heart Program (5) low cholesterol was associated with greater mortality risk. Obvious explanations for the association are intervening factors that both increase mortality risk and decrease the cholesterol level. In the nine-year follow-up of the Helsinki Aging Study, mortality risk was associated with both lowered cholesterol synthesis and lowered cholesterol absorption (20), which reflect terminal decline and lead to lower serum cholesterol levels. These associations are not identified, and the relationship between cholesterol and mortality becomes distorted unless the follow-up is long enough”

http://content.onlinejacc.org/cgi/reprintframed/44/5/1002

3) Ornish et al. demonstrated in an intervention trial that lowering LDL was associated with increased telomerase activity, which in turn is associated with longevity.

http://www.ucsf.edu/media/pdf/nobel/blackburn_and_ornish_lancet_2008.pdf

4) A meta-analysis of 108 randomized controlled trials of various lipid modifying interventions found that lowering LDL cholesterol significantly decreased the risk of coronary heart disease and all-cause mortality, whereas modifying HDL provided no benefit after controlling for LDL cholesterol.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf

LDL over 50mg/dl is only Western luxury that very few Hunter Gatherer could ever afford.

4 09 2012
Tom

Are there grey clouds in the sky when it rains ? Yes

Does it rain everytime there are grey clouds in the sky ? No

Ornish’s intervention shows that excercise, stress reduction and increased consumption of anti-oxidants are beneficial. The LDL number on it’s own is of little importance as seen in the Lyon diet heart study.

What is your opinion of excess linoleic acid and seed oils? Don’t you think they are somewhat responsible for heart disease rates ?

4 09 2012
Richard

There are some indications in the literature that veggie oil induce strokes (and do not provide protection for atherosclerosis) but, apart from high SFA trophical oils, they are not part of pathogensis of atherosclerosis. Remember not all strokes are due to atherosclerosis, although most are. So, strokes can occur due to other mechanism, besides atherosclerosis.

I use veggie oils very sparingly, occasionally I use virgin canola oil for preparing chantarelle mushrooms along with whole-grain pasta.

Saturated fats are harmfull to health, they cause elevated LDL, if isocaloric diet is maintained, this is an undisputed fact. Opposingt this is religious, not scientific at this point anymore.

4 09 2012
Tom

ok then.

What does your diet look like ?

4 09 2012
Charlie

Normal cholesterol panel . . . no heart disease?

http://blog.trackyourplaque.com/2011/06/normal-cholesterol-panel-no-heart-disease.html

Small LDL particles and increased HbA1c–An evil duo

http://blog.trackyourplaque.com/2011/10/small-ldl-particles-and-increased-hba1c-an-evil-duo.html/comment-page-2#comment-14685

“Small LDL particles are triggered by consumption of carbohydrates. Eat more “healthy whole grains,” for instance, and small LDL particles skyrocket. ”

Cholesterol Myths that May Surprise You

http://health.yahoo.net/experts/dayinhealth/cholesterol-myths-may-surprise-you

5 09 2012
Richard

Nobel winners Brown & Goldstein in Stockholm, 1988

Brown & Goldstein in Stockholm, 1988.

A receptor mediated pathway for cholesterol homeostatis

“Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl (Fig. 16 and ref. 120). In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels (9,119). Second, the LDL level in newborn humans is approximately 30 mg/dl (121), well within the range that seems to be appropriate for receptor binding (Fig. 16). Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies” (116,122)”

6 09 2012
Vegan Dietary Guidelines | Justin Penoyer

[...] For Vegans [...]

8 09 2012
Richard

Minger’s playschool China data-”analysis”. LOL

This Swedish blog post is the best kept secret of the oaleo/real food -crew.

1) http://translate.google.com/translate?hl=en&prev=/search%3Fq%3Dhttp://michelblomgren.blogspot.com%26hl%3Den%26biw%3D2133%26bih%3D1105%26prmd%3Dimvns&rurl=translate.google.co.jp&sl=sv&u=http://michelblomgren.blogspot.jp/2012/01/vete-och-china-study.html

2) http://translate.google.com/translate?hl=en&prev=/search%3Fq%3Dhttp://michelblomgren.blogspot.com%26hl%3Den%26biw%3D2133%26bih%3D1105%26prmd%3Dimvns&rurl=translate.google.co.jp&sl=sv&u=http://michelblomgren.blogspot.jp/search/label/chinastudy

Minger is a DIET-HEART theory denialis/creationist who thinks Darwins homology is a flawed premise. She also think the WHO has pulled an international conspiracy for daring to recommend plant-based diets (obs. Minger makes a big fuss for not recommending any specific diet as long as it is not vegan, except he recommends Kurt Harris archevore diet, doesn’t make any sense, but, hey, don’t blame me)..

The World Health Organization / Food and Agriculture Organization of the Unit Nation asserted in regards to diet that:

“Households should select predominantly plant-based diets rich in a variety of vegetables and fruits, pulses or legumes, and minimally processed starchy staple foods. The evidence that such diets will prevent or delay a significant proportion of non-communicable chronic diseases is consistent.”

http://www.fao.org/docrep/004/Y2809E/y2809e00.HTM

11 09 2012
Richard

1) What Can Human Genetics Teach Us About the Causes of Cardiovascular Disease?

“If one still did not believe that LDL-C is a causal factor influencing CHD, a report in this issue of the Journal could help convince the persistent skeptic”

Journal of the American College of Cardiology Vol. 55, No. 25, 2010

2) PCSK9 R46L, Low-Density Lipoprotein Cholesterol Levels, and Risk of Ischemic Heart Disease: 3 Independent Studies and Meta-Analyses

Conclusions: The PCSK9 46L allele was associated with reductions in LDL-C from 20 to 80+ years in the general population. The reduction in risk of IHD was larger than predicted by the observed reduction in LDL-C alone. This could be because genotype is a better predictor of lifelong exposure to LDL-C than LDL-C measured in adult life.

http://content.onlinejacc.org/article.aspx?articleid=1142928

Goldstein (Nobel prize winner for the work of LDL receptors)

“The studies on PCSK9 mutations that lower LDL levels over a life time, as mentioned above (see answer to Question 2), show a superior effect in decreasing coronary disease as compared to the 5-year lowering of LDL levels achieved in statin trials. For example, a 15% lowering of LDL achieved after 5 years of statin treatment leads to a 15% reduction in coronary events, whereas the same 15% lowering of LDL achieved over a life time as a result of having a PCSK9 mutation leads to a 45% reduction in coronary events”.

http://www.afernandezcruz.com/en/uncategorized-en/jl-goldstein/

11 09 2012
Richard

Minger maintains that it’s is not just so that cholesterol per se causes CAD. Well, Minger, it is just so. Coronary artery disease is multifactoral disease only in uniformly high risk society where most show non-physiological cholesterol levels due to life-long digestion of SFA and dietary cholesterol together with low-fibre context. The one gets the disease gets down to factors such as genes, smoking, diabates, issues that do not have significance in development of CAD in low-risk population.

1) Cardiovascular Benefits of Aggressive Cholesterol-Lowering Therapy

“In a recent editorial, William Roberts, MD, editor of the American Journal of Cardiology, succinctly summarized this complex issue into a simple phrase: “It’s the cholesterol, stupid!”

“..in individuals with lifetime LDL-C levels reduced by approximately 28% (about 40 mg/dL) due to a nonsense mutation of PCSK9 gene, a reduction of up to 88% in the rate of coronary heart disease events has been reported.10 This 88% reduction is quite different from the 30% reduction predicted by a similar decrease in LDL-C levels noted in a meta-analysis of statin trials.11 Individuals with the PCSK9 mutations have lower LDL-C levels throughout their entire lives, which may actually triple their risk reduction compared with those whose LDL-C levels are lowered similarly but are measured for only a 5-year span”.

http://www.jaoa.org/content/111/4_suppl_3/i.full

2) Diagnostic Criteria for Dyslipidemia

“Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

3) Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia (Steinberg, 2008)

“Armstrong et al and Armstrong and Megan showed that in cholesterol-fed nonhuman primates, virtually total regression could ultimately be achieved, but it took 40 months after return to a cholesterol-free diet to undo the damage done during 17 months of prior cholesterol feeding. The remarkable thing about these studies is that not only was almost all of the lipid gone from the arteries but also virtually all signs of the inflammatory process were gone. The remains of the lesions were basically scar tissue with no signs of cellular infiltrates. In other words, it appeared that in the absence of continuing hypercholesterolemia, the inflammatory process was not self-sustaining. Simply arresting the hypercholesterolemia by reverting to a normal monkey chow diet caused virtually complete lesion regression without the need for intervention directed specifically at the inflammatory process, results recently confirmed in an elegant series of studies in rabbits.59–61″

“Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences. Consequently, early and aggressive correction of hypercholesterolemia may be sufficient. On the other hand, if hypolipidemic therapy is initiated at, say, 40 or 50 years of age, optimal intervention will no doubt also require attention to inflammation, thrombosis, and hemodynamic factors”.

http://circ.ahajournals.org/content/118/6/672.full

4) LDL = independent, causal factor influencing CAD. Paleo-Diet = High LDL in making. The mechanism what lowers LDL is irrelevant. Genes, surgical bypass operation of illeal (POSCH-trial), statin, excersise, diet pattern, etc they all result in lowered risk for CAD.

5) The cause of Atherosclerosis (William Roberts, American Journal of Cardiology, editor-in-chief:)

“In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”

“Because humans get atherosclerosis, and atherosclerosis is a disease only of herbivores, humans also must be herbivores”

http://intl-ncp.sagepub.com/content/23/5/464.full

11 09 2012
Richard

The large majority of the decline in serum cholesterol in the pre and early statin period in developed nations in the second half of the 20th century is explained by diet, and resulted in some of the largest declines in cardiovascular disease mortality in the world.

A recent meta-analysis of mendelian randomized controlled trials including over one million individuals found that inheriting one of the nine studied genetic variants associated with life-long reduced LDL, but do not alter other known risk factors equally predicted a three-fold greater decreased risk of coronary heart disease per unit lower of LDL than statins do when started later in life. This study also found that individuals who inherit a variant of the statin drug targeted HMGCR gene that is associated with life-long reduced LDL, have an equal degree lower risk of coronary heart disease as individuals who inherited any of the other 8 studied gene variants. This provides further evidence that the primary mechanism in which statins lower coronary heart disease can be explained by its ability to lower LDL cholesterol.

These findings demonstrates that the benefit of lowering LDL depends on both the timing and the magnitude of the LDL reduction, and that the benefits associated with lower LDL are largely independent of the mechanism in which LDL is lowered. This in-turn provides strong evidence indicating that dietary changes to reduce serum cholesterol will result in similar results as other medical based lipid modifying interventions (ie. the meta-analysis of 108 lipid modifying interventions), as has been observed in a number of nations that experienced some of the largest declines in cardiovascular disease mortality in the world.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199603/pdf/1471-2458-11-641.pdf

http://eurheartj.oxfordjournals.org/content/32/10/1187.full.pdf

http://www.bmj.com/content/344/bmj.d8136

http://www.unilever-pro-nutrition-sante.fr/wp-content/uploads/2012/06/Importance-of-reducing-SAFA-to-limit-CHD-BJN-2011-Pedersen-et-al.pdf

13 09 2012
Charlie

http://omega-6-omega-3-balance.omegaoptimize.com/2010/12/03/meta-analysis-reveals-heart-healthy-omega-6-fat-increases-risk-of-heart-disease.aspx?ref=rss

Meta-analysis Reveals “Heart Healthy Omega-6 Fat” Increases Risk of Heart Disease

Bottom Line: The research upon which the American Heart Association based their “eat-your-omega-6-fat” advisory, is fatally flawed, according to the results of a meta-analysis study, which showed that a steady diet of omega-6 polyunsaturated fatty acids increases the risk of heart disease and death, especially for women [1]. British J Nutr. Dec 2010.

Background: Omega-6 fats are the most commonly eaten polyunsaturated fatty acids (PUFA) in westernized countries. The top three sources are corn oil, soybean oil and cottonseed oil, which are the main ingredients in margarines, salad dressings, and mayonnaise. Many studies have shown that PUFA lower cholesterol.

Prior to industrialization, no population has been exposed to the current high levels of omega-6 polyunsaturated fats. We evolved on a diet with a balanced proportion of omega-6 to omega-3 fats of about 1:1. Today, that ratio in westernized countries is out of whack, near 20:1 of omega-6 to omega-3 fats. Different farming practices, new food processing and the urging by health authorities to use vegetable oils in place of animal fats for heart health, triggered an onslaught of omega-6 fats into the food we eat.

While it’s true that PUFA lowers cholesterol, cholesterol is not they key culprit in heart disease. Inflammation is the “new cholesterol” in matters of eating to protect the heart (and other chronic diseases for that matter).

15 09 2012
Jason P. Miller

Hey, Richard, give is a rest, will you? Why don’t you find another hobby?

18 09 2012
Richard

Evidence from over 100 randomized controlled trials, mendelian randomized control trials consisting of over one million individuals, and prospective studies consisting of several million individuals have firmly established a causal relationship between lowering LDL and non-HDL cholesterol and a decreased risk of coronary heart disease, cardiovascular disease and all-causes mortality (references below). The counter-evidence that Guynet f.ex provided is generally from studies with a significantly lower participant size without being of higher methodological quality, or some observational study that failed to sufficiently account for reverse causation.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988224/

http://circ.ahajournals.org/content/118/6/672.long

http://www.staessen.net/publications/2006-2010/07-44-P.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284229/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488755/

http://www.ncbi.nlm.nih.gov/pubmed/19349632

22 09 2012
bill

Richard, what do you think about the study referenced here at the 3.35 mark ?

23 09 2012
Abby

I would ask about the amount of K2 you recommend. On the brand you listed, is 5mg where as other brands listed is typically around the “50 mcg 30 Sgels” range. I was wondering if you take such a high concentration because of your need for recovery and if the lower concentration would be sufficient enough for prevention?

Also, fun-fact: I get my vitamins and supplements from http://www.swansonvitamins.com they carry their own brand in addition to most popular brands and usually at a fraction of the cost. The K2 brand that you use is listed ***$20 cheaper*** through them rather than Amazon.

30 09 2012
phil

lol, “eat real food” then the rest is anything but real food..a list of friggen supplements. if you honestly believe nature is so simple that 6 billion years can be replicated with 50 years of supplement experience then you are insane.

30 09 2012
Tom

Ignorant ^^^^^^

I’m sorry but if you are deciding to be a vegan then you WILL need to supplement. There are many nutrients (some essential, some not) in animal products that are not found in plant foods.

30 09 2012
Experimenting with vegetarian diets: Finding your own way | Surgically Enhanced Mannequin

[...] up her concerns and recommendations for those who may want to follow a strict vegan diet.  Go here to read her [...]

1 10 2012
curtis

Umm… K2 is synthesized in the gut from K1, so there isn’t a need to supplement K2 i you are getting enough K1. This is easily attainable information.

27 02 2013
onemoretime

http://en.wikipedia.org/wiki/Menatetrenone

Am I the first one on this comment feed to notice the wiki article mentions that K1 conversion is not dependent on gut bacteria?!?

3 10 2012
raspberryink

do remember that whatever diet you choose, most doctors recommend a supplement/vitamin. meat eater or veggie. in the end do what makes you feel the best and consult your doctor. i’m a recent veg head. i was doing low carb high protein lots of veg, but for me i felt bad. i gained a lot of weight, skin looked bad, hair was limp. changed that to a vegetarian diet high in leafy greens, a daily b12 and calcium supplement, nuts with breakfast daily, beans bean beans, fruit daily, whole grains (quinoa!!!!) and veggie “junkfood” only when i have no other option. i am supervised by a cardiologist at hopkins and she thinks i look wonderful, and should keep doing what i am. I feel great and look great. so it works for me. but mind you it wouldn’t work for everyone. and that is where everyone needs to know who they are and how they feel. you are your best doctor.

6 10 2012
Raw Food DietRawGosia

[...] [4] For vegans [...]

9 10 2012
Leandro

Hey “ex-vegan girl”! You’re so beautifull! But, stop trying to unveganize the world! Your only reason to do that, is that you missed animal foods. We don’t need any “cientist” to tell us what our diet is. We feel all the benefits in ourselves. ;)

18 04 2013
Robin

Agreed. Husband and I are vegan athletes in our mid-50s. All health prblems (asthma, arthritis onset, breast lump, etc.) subsided after switching to vegan diet (mostly plants, fruits, seeds/flaxseeds/quinoa, beans…very little processed grains) supplemented only with vitamin B12 ten years ago. Never have been healthier, and have more energy and endurance than most athletes half our age.

10 10 2012
10 10 2012
Ask a Vegan - Page 11

[...] [...]

11 10 2012
Charlie

Everything You Know About Saturated Fat Is Wrong

One of the most prominent proponents of rewriting the book on saturated fat is cardiologist Dariush Mozaffarian, an associate professor of medicine at Harvard Medical School and the author of more than 100 scientific papers on nutrition and health. We asked him to explain why the conventional wisdom on saturated fat is misleading—and how eating it, in moderation, can sometimes be the healthiest move you could make.

http://www.more.com/health/healthy-eating/saturated-fat-good

Q: What has been the effect of the move to cut down on saturated fat in the United States?

A: In the last few decades, total-fat and saturated-fat consumption has gone down, but consumption of refined carbohydrates has soared. Low-fat versions of packaged foods, loaded with refined carbohydrates, sugars and salt, now flood the market. When people replace saturated fat with refined carbohydrates, they are unlikely to improve their health and may worsen it. That’s because these kinds of carbohydrates are more likely than saturated fat to raise the risk of heart disease and type 2 diabetes.

12 10 2012
Richard

Avoiding SFA is a no-brainer. Just because an item a is perceived to be better than item b, does not establish that item a is good.

1) Jeremiah Stamler wrote an excellent piece over the ideas harboured by Krauss and Mozzafarian, it’s here:

http://ajcn.nutrition.org/content/91/3/497.full

2) The co-author of Siri-Tarino Meta-Analysis in 2012:

“Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”

http://harvardmagazine.com/2012/01/a-diabetes-link-to-meat

3) Harvard School of Public Health:

“Choose foods with healthy fats, limit foods high in saturated fat, and avoid foods with trans fat”

http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-and-cholesterol/

4) Fresh paper about the Inuits:

Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”

http://www.ncbi.nlm.nih.gov/pubmed/18054937

4) Denise Minger wants us to believe that malfunction in the thyroid is the CAUSE of coronary artery disease. That’s is ridiculous nonsense and based on really old & poorly presented speculations. If even small but relavent bunch of those who died as result of CAD got first problems with thyroid, then this would be reflected in the large body of high quality prospective studies that have corrected for regression dilution bias. There’s absolute no hint of such events taking place. Even the few who develope malfunction in the thyroid and end up dyeing due to CAD develope CAD because of elevated LDL.

Increased Oxidizability of Low-Density Lipoproteins in Hypothyroidism

http://jcem.endojournals.org/content/83/5/1752.short

5) CAD is shown to be develope in linear relationship to serum cholesterol concentration even within population that have low cholesterol concentration to begin with, and even in the context regression dilution bias has been corrected with follow-up blood-lipid measurements.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670480/?page=1

Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

“Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women”

http://ije.oxfordjournals.org/content/32/4/563.long

6) Elevated total cholesterol: its prevalence and population attributable fraction for mortality from coronary heart disease and ischaemic stroke in the Asia-Pacific region.

“Conventional methods for estimating disease burden severely underestimate the effect of TC. Cholesterol-lowering strategies could have a tremendous effect in reducing cardiovascular deaths in this populous region”

http://www.ncbi.nlm.nih.gov/pubmed/18677162

7) According to the anti-darwinist denialists such as Denise Minger we should eat the “archevore diet” ala Kurt Harris and have total and LDL cholesterol levels far exceeding those found in wild animals, human infants, and groups of people well-documented to have no atherosclerosis. They want to believe that adult humans need /benefit from having TC more than 50% and LDL at least 200% above known required and physiologically normal levels. LOL

For some reason, they clearly understand that a blood sugar level 50-200% above physiological levels is harmful, and that a body fat level 50+% above physiological levels is harmful, but they believe that a blood lipid level 50-200% above physiological levels is not only not harmful, it is, according to them, positively beneficial. LMAO.

12 10 2012
Richard

Tell me Dennis,

if significant proportion of those who died in CAD had malfunction in thyroid, then why high quality prospective cohorts corrected for regression dilution bias have failed to show this? How is this possible? Instead these high quality cohorts have firmly establish the independent, continuous, positive and log-linear, nature of the associations between TC and both CHD and Ischemic Stoke even within population that have very low serum cholesterol concentrations compared to Westerners!

In fact, this great review discusses eloquently how regression dilution (systematic error) has failed to show the real association of serum cholesterol concentrations to coronary heart disease in many Western cohorts characterized with very high population-wide cholesterol concentrations.

http://aje.oxfordjournals.org/content/150/4/341.full.pdf

12 10 2012
BB

First let me say that this article is a very nice summary and has good information.

But I also wanted to make a general point. The vegan diet is scrutinized so much and people are obsessed with “if their doing it right” and if their daily fluctuations in how they feel is a result of their diet changes.

For some reason people think meat is some multi-vitamin of something. If you have dietary issues eating meat is not a magical cure. People walk around deficient in all kinds of things because of a poor diet and that doesn’t have to do with eating meat or not, its about eating right or genetic issues (which the author mentions briefly). There are tons of things we could do to be at PERFECT health. Eating all of these supplements might get you closer to that. But this article makes it seem like if you don’t supplement with all these things then you can’t be vegan and feel fine. This would be a fallacy.

12 10 2012
BB

I should also comment to Denise that “squashing out bad science” with opinions or reinterpretations of data that themselves have no data doesn’t make any sense.

15 10 2012
Richard

Creationist-minded debators like Minger deny the independent & causal role of LDL in coronary artery disease.

Atherosclerosis can be induced in a great variety of animal species including vegetarian and carnivore species (e.g. insects, birds, cats, dogs, non-human primates etc.) by raising serum cholesterol high enough and maintaining it long enough. Atherosclerosis can also be reversed by lowering TC enough and maintaining it long enough. The lipid deposits and foam cells disappeared but some fibrous tissue remained. Some species, such as the dog and rat, do not get elevated TC from a diet high in saturated fat and cholesterol. But when a way was found to elevate their TC they also developed atherosclerosis. This is so consistent no matter which species is tested that it appears to be a scientific law that elevated LDL can cause atherosclerosis. ) This can’t be explained away by stress, inflammation or some infectious agent. In clinical trials, Dr. Esselstyn’s group did better than Dr. Ornish’s group even though Dr. Ornish used stress reduction and Dr. Esselstyn didn’t. However Dr. Esselstyn’s patients had lower LDL. And although inflammatory factors like infection can speed up atherosclerosis, oxidized LDL, foam cells and cholesterol crystals inside the artery wall provide their own inflammation

Here are findings from reviews that demonstrate that LDL concentration is a causal risk factor for coronary heart disease and all-cause mortality:

Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

Similarly, we found no association between change in triglycerides and risk of coronary heart disease events whenever the model included an adjustment for the change in low density lipoprotein cholesterol (data available from the authors). Change in low density lipoprotein cholesterol, however, remained a significant predictor in a multivariable model adjusting for change in high density lipoprotein cholesterol, change in triglycerides, and class of intervention, with a 7.4% (4.4% to 10.4%; P <0.001) relative risk reduction for coronary heart disease events.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/

A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

Number of participants in meta-analysis = 1,003,207

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

16 10 2012
Richard

Campbell & Junshi reported,

“There appears to be no treshold of plant-food enrichment or minimization of fat intake beyond which further disease prevention does not occur”

“Mean intakes of animal protein (about one-tenth of the mean intake in the United States as energy percent), total fat (14.5% of energy), and dietary fiber (33.3 g/d) reflected a substantial preference for foods of plant origin. Mean plasma cholesterol concentration, at approximately 3.23-3.49 mmol/L, corresponds to this dietary life-style”

“These findings suggest that even small intakes of foods of animal origin are associated with significant increases in plasma cholesterol concentrations, which are associated, in turn, with significant increases in chronic degenerative disease mortality rates”.

Minger does not believe that LDL-cholesterol concentrations of +200% above physiological levels can cause problems per se. LDL-cholesterol concentrations of +200% above physiological levels are the norm in Western societies. Physiological LDL-levels are those levels we are designed to have by evolution, which are essentially the levels found in all mammalian species that do not develope atherosclerosis, healthy neonates and those societies that face absence of coronary artery disease as well as other chronic disease. Campbell & Junshis findings may be provocative, but essentially the authors observed that even small amount of animal products can cause abnormal cholesterol concentration in human in the studied eco-niche. In turn, abnormal cholesterol concentrations may a catalysator for chronic disease. Observe that high quality prospective cohorts that have adjusted for regression dilution bias have firmly established positive, inpendent, continuous and log-linear association of serum cholesterol to coronary artery disease and ischemic stroke for both sexes even among populations that have low cholesterol concentrations as a base-line. These associations opf seum cholesterol to coronary heart disease are inpendent of thyroid function.

Minger claim that she has refuted the findings in China. I find these claims outrageously ridiculous. Everyone can clinically observe for themselves how much animal foods they can tolerate in order to hit the 3.23-3.49 mmol/l the cholesterol treshold observed in rural Chinese villages. The values observed matches nicely to the cholesterol concentrations observed in Western people consuming whole-food, plant-based diets.

16 10 2012
Charlie

Confirmed Again: Statin Drugs Accelerate Cardiovascular Disease

http://articles.mercola.com/sites/articles/archive/2012/10/15/statin-drugs-on-coronary-disease.aspx

What You Need to Know About Cholesterol in Order to Understand the Dangers of Statins

Statin drugs work by preventing the formation of cholesterol and reduce LDL cholesterol, which is considered the “bad” cholesterol. There is no argument that these drugs can effectively lower your cholesterol levels. However, what has NOT been proven is that they significantly lower your risk of dying from heart disease. In no way, shape or form do they treat the underlying cause of your problem. They are nothing more than a toxic band-aid.

So just what makes statins so dangerous, and why are they not the answer for managing your cholesterol levels?

First you need to understand the biological workings of cholesterol. In fact, there is no such thing as “good” or “bad” cholesterol. Both HDL and LDL cholesterol perform vital functions in your body, which is why it’s actually dangerous to bring your LDL levels down too low.

HDL (high density lipoprotein) and LDL (low density lipoprotein) are actually proteins that transport the cholesterol to and from your tissues. Cholesterol in turn is a precursor to your steroid hormones, bile acids, cell membrane walls and vitamin D. For example, cholesterol is essential for you to make testosterone or estrogen, cortisol, DHEA or pregnenolone, or a multitude of other steroid hormones that are necessary for health, without cholesterol. Even more importantly, your cells cannot regenerate their membranes without it.

The reason you have LDL to begin with is to transport the cholesterol to the tissues in order to make new cells and repair damaged ones. However, there are different sizes of LDL particles and it’s the LDL particle size that is relevant, and statins do not modulate the size of the particles. Unfortunately, most people still don’t know about that part, and very rarely, if ever, get tested for particle size. The particles are sticky, so very small LDL’s can easily get stuck in different areas, and the build-up eventually causes inflammation and damage.

The only way to make sure your LDL particles are large enough to not cause damage is through your diet. In fact, it’s one of the major functions of insulin.

Conveniently enough, a healthy diet is also the answer for type 2 diabetes, so by focusing on what you eat, you’re treating both your diabetes and your cholesterol levels, and reducing your associated risk of heart disease. If you eat properly, which is really the only known good way to regulate LDL particle size, then it does the right thing; it takes the cholesterol to your tissues, the HDL takes it back to your liver, and no plaque is formed.

17 10 2012
Richard

LOL!

Don’t you think it’s perfectly natural that those prescribed to statins have most plaque? Second, calcium-dense plaques are the most mild form of plaque, the lipid-dense plaque are the real nightmare. Statins have an ability to stabilize the plaque and change its composure.

You didn’t seriously think statin shave cause-effect relationship in increasing plaque-build up? As Minger would say: “correlation does not equal causation”. What would be the biological mechanism which would cause HMG-CoA inhibitors to produce more plaque?

17 10 2012
Richard

View this picture:

You can see that Rosuvastatin produced significant changes to the plaque composure. Altering its constitution from more lipid-dense to more fibrous as well slightly more calcified. Lipid-dense plaques are the most rupture prone. Calcified and fibrous plaques more stabil and safer. Moreover, pay attention that Rosuvastatin not only produced changes in the plaque form but significantly reduced its size as well.

Early intervention with rosuvastatin decreases the lipid components of the plaque in acute coronary syndrome: analysis using integrated backscatter IVUS (ELAN study).

http://www.ncbi.nlm.nih.gov/pubmed/21266787

I find it weird that the cholesterol denialist/creationist -fringe online neglect these findings. The take-home message is that low LDL does a lot of good things for us.

17 10 2012
Charlie

http://blog.trackyourplaque.com/

Why small LDL particles are the #1 cause of heart disease in the US

9/15/2011, Dr. William Davis

Ask your doctor: What is the #1 cause of heart disease in the US?

Let’s put aside smoking, since it is an eminently modifiable risk and none of those crazies read this blog anyway. What will your doctor say? Most like he or she will respond:

High cholesterol or high LDL cholesterol
Too much saturated fat
Obesity

Pfizer, Merck, AstraZeneca and their kind would be overjoyed to know that they can add your doctor to their eager following.
I’d tell you something different. I would tell you that small LDL particles are, by far and away, the #1 cause for heart disease. I base this claim on several observations:

–Having run over 10,000 lipoprotein panels (mostly NMR) over the past 15 years, it is a rare person who does not have a moderate, if not severe, excess of small LDL particles. 50%, 70%, even 90% or more small LDL particles are not rare. Over the course of a year, the only people who show no small LDL particles are slender, athletic, pre-menopausal females.

–In studies in which lipoproteins have been quantified in people with coronary disease, small LDL particles dominate, just as they do in my office. Here’s a 2006 review.

–Small LDL is largely the province of people who consume carbohydrates, such as the American population instructed to “cut fat and eat more healthy whole grains.” Conventional diet advice has therefore triggered an explosion in small LDL particles.

–When fasting triglycerides exceed 60 mg/dl, small LDL particles increase as a proportion of total LDL particles. This includes the majority of the US population. (This ignores postprandial, or after-eating, triglycerides, which also contribute to small LDL formation.)

If you were to read the data, however, you might conclude that small LDL affects a minority of people. This is because in most studies small LDL categorize it as either “pattern B,” meaning exceeding some arbitrary threshold of percentage of small LDL particles, versus “pattern A,” meaning falling below that same arbitrary threshold.

Problem: There is no consensus on what percentage of small LDL particles should mark the cutoff between pattern A vs. pattern B. In many studies, for instance, people with 50% small LDL particles are called “pattern A.”

If, instead, we were to set the bar lower to identify this highly atherogenic (atherosclerotic plaque-causing) particle at, say, 20-30% of total, then the number or percentage of people with “pattern B” small LDL particles would go much higher.

I see this play out in my office and in the online program, Track Your Plaque, every day: At the start eating a low-fat, grain-filled diet with lots of visceral fat (“wheat belly”) to start, they add back fat and cut out all wheat and limit carbohydrates. Small LDL particles plummet

17 10 2012
Richard

Scientific outlook on the views expressed by William Davis. Everything this whackjob manage to say can be taken with a pinch of salt.

http://www.aaccnet.org/publications/plexus/cfw/pastissues/2012/OpenDocuments/CFW-57-4-0177.pdf

See my sources from various expert panels over the ideas of LDL particle-size pushed by Atkins-Foundation funded Ronald Krauss. I posted already quite a few of them in this thread.

17 10 2012
Richard

This large study found that all LDL particle sizes are atherogenic and big fluffy particles, those carried by FH patients, were even more atherogenic, partly because of its abilty to deliver more cholesterol per particle to arterial walls.

1) LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

“Thus, smallLDL was a strong confounder of the association of largeLDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic”.

“After accounting for particle correlations, we demonstrated that the magnitude of association between small LDL and carotid atherosclerosis became equal to large LDL (on a per 1-S.D. basis) or less than large LDL (on a per particle basis). Failure to account for the strong negative correlation between small and large LDL and their different associations with other lipoproteins may underlie the belief that small LDL particles are a more potent atherogenic subclass than large LDL”.

“There are several mechanisms that may underlie the atherosclerotic effect of both large and smallLDL[5]. At both extremes of LDL size, there is decreased receptor-binding affinity for LDL receptors [27]. Small LDL may be oxidized more rapidly and have been associated with endothelial dysfunction and metabolic dyslipidemia [28]. In comparison, large LDL predominate in patients with familial hypercholesterolemia [29] and those consuming high saturated fat diets. Large LDL have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls [30], a speculation supported by our finding a greater IMT difference for large compared to small LDL on a per particle basis”.

http://www.nypcvs.org/images/MESA.pdf

——————————————————————————————–
This expert panel reviewed the data and did not recommend particle-size count for any patient group. Particle number count was recommended for diabetics, in order to define the degree of intensiveness of LDL-lowering theraphy for them.

2) Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

19 10 2012
Charlie

Anyone who wants to put their faith on the many monetary interest on the promotion of grains, statins and the “official” advice can do so. But the simplistic approach to arthrosclerosis is foolish this is a disease that is just a superficial label for a cluster of symptoms not yet fully understood by medical science. You can have studies pointing in multiple directions because the science is very complex and has yet to be settle, regardless of what you may hear. The reality is that what little is known about the cholesterol theory has been changing with time.

If you want to read how complex the science is read:

http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i

19 10 2012
Charlie

Potato, tomato and rice lectins may cause as much inflammation as wheat

http://www.naturalnews.com/037597_wheat_lectins_inflammation.html

Inflammation and osteoarthritis common

Sayer Ji, founder of GreenMedInfo.com, says tomatoes, rice and potatoes are particularly lectin-heavy. That’s especially problematic, he says, because “while the ‘nightshade’ (potato and tomato) connection with inflammation has been known about for quite some time anecdotally, rice has rarely been considered problematic and has become something of a poster child for the wheat/gluten free industry which often substitutes it for gluten-containing ingredients.”

“The discovery that chitin-binding lectin is broadly distributed throughout cereal grasses sheds light on how the grain-free diet produces health results superior to that of eliminating wheat and gluten containing grains alone,” he continued.

These three foods are extremely prevalent in the West’s diet, which could help explain another phenomenon: why the incidence of osteoarthritis, a degenerative joint disease, is so widespread, Ji says.

It all begins with gluten, however.

“Gluten’s inflammatory effect in the gut causes intestinal cells to die prematurely and causes oxidation on those cells,” writes health enthusiast Sebastien Noel at Paleo Diet Lifestyle. “This effect creates a leaky gut and a leaky gut can allow bacterial proteins and other toxic compounds to get in the blood stream, which can also lead to autoimmune attacks on the body. A leaky gut also means that food as not digested properly and nutrients are not absorbed fully, which can lead to nutrient deficiencies.”

20 10 2012
Richard

@Charlie,

the nonsense about “little is known” was very well utilized by the cigarette and asbestos industries. Peter Attia is another anti-science figure and is on par with William Davis. Typically the societies where atherosclerosis does not exist show very low levels of serum cholesterol which are maintained throughout the life. These cultures are almost essentially grain-cultures where staple food is maize, sorghum, rice, millet, wheat, etc.

While you are doing your succesfull “research” on the pathophysiology of atherosclerosis, I leave you with these two reviews. I personally have the statin and grain industries anytime over obese, anti-science low-carb/paleo spin-doctors.

LDL-cholesterol is the direct, causal factor influencing artery disease. This notion has similar consensus among the biomedical community as any great idea has within its respective experts, e.g. the theory of evolution.

1) Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis

The meta-regression analysis included 108 randomised trials involving 299 310 participants at risk of cardiovascular events. All analyses that adjusted for changes in low density lipoprotein cholesterol showed no association between treatment induced change in high density lipoprotein cholesterol and risk ratios for coronary heart disease deaths, coronary heart disease events, or total deaths. With all trials included, change in high density lipoprotein cholesterol explained almost no variability (<1%) in any of the outcomes. The change in the quotient of low density lipoprotein cholesterol and high density lipoprotein cholesterol did not explain more of the variability in any of the outcomes than did the change in low density lipoprotein cholesterol alone. For a 10 mg/dl (0.26 mmol/l) reduction in low density lipoprotein cholesterol, the relative risk reduction was 7.2% (95% confidence interval 3.1% to 11%; P=0.001) for coronary heart disease deaths, 7.1% (4.5% to 9.8%; P<0.001) for coronary heart disease events, and 4.4% (1.6% to 7.2%; P=0.002) for total deaths, when adjusted for change in high density lipoprotein cholesterol and drug class.

To take into account non-lipid effects of specific drugs (such as potential pro-thrombotic effects of hormone therapy), we included a categorical variable of drug class in the meta-regression model and did a meta-regression analysis stratified by drug class. We used R2 to measure the proportion of the variability in the log risk ratio of an outcome explained by the statistical model.

Similarly, we found no association between change in triglycerides and risk of coronary heart disease events whenever the model included an adjustment for the change in low density lipoprotein cholesterol (data available from the authors). Change in low density lipoprotein cholesterol, however, remained a significant predictor in a multivariable model adjusting for change in high density lipoprotein cholesterol, change in triglycerides, and class of intervention, with a 7.4% (4.4% to 10.4%; P <0.001) relative risk reduction for coronary heart disease events.

http://www.ncbi.nlm….les/PMC2645847/

2) A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

Number of participants in meta-analysis = 1,003207 million

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life ( p = 0.00000000000000000843, Mean age at randomization in statin trials: 63 years;)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

3) "The most commonly used statins are off patent, which means the drug companies no longer have any financial incentive expanding the market. It's the medical community who is pushing for wider use of statins since they are convinced by the evidence this will reduce heart attacks and strokes in the future"

–Peter Weissberg, British Heart Foundation

20 10 2012
Richard

The links to the two above reviews

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/

23 10 2012
Richard

Here’s a nice textbook on atherosclerosis:

Dyslipidemia & Atherosclerosis Essentials (2009). The authors note that normal cholesterol in Americans is twice that of physiological levels. In the page 8 they have picture showing mean cholesterol levels in various hunter-gatherer groups (which are similar to those found in quasi-vegan agriculturalists in rural Asia, South-America and Afrika), wild primates and other mammals.

Most people realize that blood pressure above 200% of physiologicl levels are harmfull. We also realize that BMI 50% over physiological levels can be harmfull as such. Dennis Minger is a denialist who thinks tht LDL -cholesterol levels 200% above physiological levels, the “normal” ,cannot be harmfull as such. According to her we need to explain heart disease through thyroid function & oxidation independent of elevated cholesterol. Big LOL!

Dietary cholesterol oxidizes LDL:

The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/16270280

Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation

http://www.ncbi.nlm.nih.gov/pubmed/9001684

“Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”.

–Brown & Goldstein, Nobel lecture

Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

“The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/

Diagnostic Criteria for Dyslipidemia

Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

23 10 2012
Richard

This quote went in as erranous: here’s the correct citation

Of the various atherosclerotic risk factors, which one is an absolute prerequisite for development of atherosclerosis?

“The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/

23 10 2012
Richard

Very weird, the text still came as flawed. Hopefully this one works. If not check out the original source: P

The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100— and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis.

23 10 2012
Richard

Extremely weird, but the this platform just screws the whole above citation. Minger, can you removed the above two posts. As everyone can see the tesxt is completely illogical because of the artificial cut-point of the text. Perhaps this happens because of the frequent use of symbols in the original text.

“The answer is hypercholesterolemia. What level of total cholesterol and specifically LDL cholesterol is required for atherosclerotic plaques to develop? Symptomatic and fatal atherosclerosis is extremely uncommon in societies where serum total cholesterol levels are <150 mg/dL and serum LDL cholesterol levels are <100 mg/dL (8). If the LDL cholesterol level is <100 – and possibly it needs to be 150 mg/dL and the LDL cholesterol is >100 mg/dL, the other risk factors clearly accelerate atherosclerosis”.

23 10 2012
Bill

“A typical Western diet is rich in oxidized fats and therefore could contribute to the increased arterial atherosclerosis in our population”

Thats very true. This supports low temperature cooking and avoiding excess PUFA consumption. How many healthy populations have a high consumption of PUFA’s, especially linoleic acid ?

Cooking with vegetable oil is a bad idea.

It’s worth noting that the Lyon diet heart study was the most successful CVD intervention of all time and serum lipids did not differ between the control group and intervention group.

Focusing on biomarkers like LDL and total cholesterol may not be an optimal measure to prevent and reverse heart disease unless the levles are supraphysiological which could indicate FH or other diseases. Eating a diet rich in fruits, vegetables and quality meats and balancing the omega 3 to 6 ratio is a good enough intervention

As Lalonde explains at the 3.30 mark, you can use drugs to lower LDL to really low levels but you can still get progression of atherosclerosis and the methods by which statins work when they do work is still up for debate. They have anti-inflammatory properties, antioxidant properties, anti-clotting properties and the interfere with Rho signalling.

24 10 2012
Richard

Lyon trial showed difference in LDL between intervention group and the control, this difference was very small, though. Not a single one participated in the Lyon intervention group had the progression of their coronary artery disease halted let alone regressed. What happened was that the disease progressed slower in the intervention group as opposed to control group. These are not really good results compared to the work of Ornish and Esselstyn, who is soon out with a larger study involving over 200 patients. Last, the Lyon intervention group based their diet in lacto-ovo-vegeterian style mediterranian diet rich in canola oil. This approach clashes pretty much 180-degree with approach chosen by the spindoctors around the internet, including Dennis Minger and yourself.

24 10 2012
Richard

If you can show me a (animal) model where coronary disease was regressed without the change in LDL, I’d like to see that, so far I’ve encountered on such papers.

24 10 2012
Richard

Great paper by O’Keefe and Loren Cordain.

Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

http://www.sciencedirect.com/science/article/pii/S0735109704007168

Good luck for those who’ve read the paleo-solution and think they can show off equally healthy metabolic-parameters as been observed in Hadza, f.ex. Eating meat in parasitic-rich, non-sanitized eco-niche is different than eating meat in an eco-niche where cholesterol lowering parasites do not exist.

I am glad to know my diet has resulted in physiological LDL -cholesterol for me. Whole-food vegan diet seems to do the trick.

24 10 2012
Richard

“Lalonde explains at the 3.30 mark”….LOL

The mean age of randomization in statin trials is 63-years of age. The mean lenght of the trial is 5-year. By the age of 63-year most hypolipidemic individuals have managed to accumulate an atherosclerotic burden where LDL-lowering drug theraphy alone may not be enough, especially if a potent statin is not used. Even though, potent statins can induce slight regression in the plaque and change its composure from more lipid-dense to more fibrous and calficied, the plaque even when smaller and more stabile can cause a ruprure in these people. In order to tackle the residual risk, health bureacrats want people to start taking statins earlier. Because the benefits of LDL-lowering theraphy depends on both magnitude and durance.

Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581–90

Give statins to all over-50s: Even the healthy should take heart drug, says British expert

http://www.dailymail.co.uk/health/article-2194892/All-50s-statins-regardless-health-history-says-Oxford-professor.html

When you keep your LDL-low throughout the life you get more benefits than statins can give when started at the mean age of 63. (60% reduction per each 1mmol/l reduction in LDL-fraction as opposed to 20% reduction with a statin)

A Mendelian Randomized Controlled Trial of Long Term Reduction in Low-Density Lipoprotein Cholesterol Beginning Early in Life

Number of participants in meta-analysis = 1,003207 million

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life ( p = 0.00000000000000000843, Mean age at randomization in statin trials: 63 years;)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

24 10 2012
Bill

Actually the thing that makes the lyon diet heart study unique is that it reduced lionoleic acid consumption to minimal levels. I’m sure denise and many others would agree that this is a good idea. The intervention group also ate fruits, vegetables, poultry and fish. I don’t see a major clash.

What do you think about the rose corn oil trial ?

“Eighty patients with ischaemic heart disease were allocated
randomly to three treatment groups. The first was a control
group. The second received a supplement of olive oil with
restriction of animal fat. The third received corn oil with
restriction of animal fat. The serum-cholesterol levels fell in
the corn-oil group, but by the end of two years the proportions
of patients remaining alive and free of reinfarction (fatal or
non-fatal) were 75 %, 57 %, and 52 % in the three groups respectively”

Does saturated fat increase LDL number in the long term ?

“The low-carbohydrate group had a lower
intake of carbohydrates (P<0.001) and higher
intakes of protein (P<0.001), total fat (P<0.001),
saturated fat (P<0.001), and total cholesterol
(P = 0.04) than the other groups."

What happened to their lipids by the end of the study ?

After 6 months LDL levels were higher in the low carb group but by 24 months they dropped.

The authors conclude

"Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions."

There is a reason why harvard now agree that saturated fats are not the problem. Taking all the observational studies and RC'sT into account, saturated fats do not cause dyslipidemia and dietary interventions should now focus on the reduction of refined carbohydrates and reduction in central adiposity.

24 10 2012
Bill

“Thus, although recommendations to replace SFA with PUFA appear appropriate, the much larger CVD burdens caused by other dietary factors (e.g., low omega-3, low fruits and vegetables, high trans fat, and high salt appear to warrant much more attention”

Dariush Mozafarrian

I very much agree with this except the evidence supporting substituting SFA for PUFA is far from conclusive as shown in a 2010 christopher ramsden paper

25 10 2012
Richard

There are some preliminary evidence that oils can induce heart disease with a mechanism that the LDL-cholesterol (and HDL) fail to track. Pay attention that not all heart disease is of atherosclerotic in origin, although most are.

As Bill Roberts, the editor in chief of American Journal of Cardiology put it:

“….The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! It’s the cholesterol, stupid!”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3012294/

25 10 2012
Richard

“I don’t see a major clash”

Really? You don’t see the hefty use of canola oil-laden margharines and the removal of SFA’s such as butter as a major clash to the recommendations made by the spin-doctors? And, no the intervention group in Lyon did not consume heart-disease causing palm and coconut oils recommended by Minger.

1) Differences in all-cause, cardiovascular and cancer mortality between Hong Kong and Singapore: role of nutrition.

“The ratio of animal to vegetal fat was higher in Singapore (2.24) than in Hong Kong (1.08). Singapore had higher serum concentrations of total cholesterol and low-density lipoprotein cholesterol than Hong Kong, but the opposite result was observed for high-density lipoprotein cholesterol”.

“There are striking differences in all-cause and cardiovascular mortality between Hong Kong and Singapore. These differences can be most reasonably and plausibly explained by their differences in dietary habits, for example, a higher consumption of coconut and palm oil, mainly containing saturated fat, in Singapore”

http://www.ncbi.nlm.nih.gov/pubmed/11855581

2) Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”.

http://www.ncbi.nlm.nih.gov/pubmed/18054937

25 10 2012
Bill

In response to the hong kong and singapore study

http://www.ncbi.nlm.nih.gov/pubmed/9066473

“•
Mortality from coronary heart disease in 50-54 year old men is four times higher in Lithuania than in Sweden


Differences in traditional risk factors for coronary heart disease in 50 year old men in LinkÖping (Sweden) and Vilnius (Lithuania) were small–systolic blood pressure was higher in men from Vilnius, but total and low density lipoprotein cholesterol concentrations were lower and smoking habits similar


The resistance of low density lipoprotein to oxidation was lower in men from Vilnius and remained after adjustment for antioxidant vitamin concentrations


Plasma concentrations of the antioxidant vitamins, ß carotene, lycopene, and lipid adjusted tocopherol were lower in men from Vilnius; tocopherol did not differ

Mechanisms related to antioxidant state may be important in explaining the much higher mortality from coronary heart disease in Lithuanian compared with Swedish middle aged men”

Do you buy Esselstyn’s argument that you are heart attack proof below 150 ?

26 10 2012
Richard

A huge blow to cholesterol nihilist. No matter what the mechanism is used, they all work differently in lowering circulative LDL-C in serum, however the end result is highly identical.

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease
A Mendelian Randomization Analysis

Results: All 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD per unit lower LDL-C, with no evidence of heterogeneity of effect (I2 = 0.0%). In a meta-analysis combining nonoverlapping data from 312,321 participants, naturally random allocation to long-term exposure to lower LDL-C was associated with a 54.5% (95% confidence interval: 48.8% to 59.5%) reduction in the risk of CHD for each mmol/l (38.7 mg/dl) lower LDL-C. This represents a 3-fold greater reduction in the risk of CHD per unit lower LDL-C than that observed during treatment with a statin started later in life (p = 8.43 × 10−19).

Conclusions: Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.

Importantly, we evaluated 9 polymorphisms located in 6 different genes, including polymorphisms in the genes that encode for the targets of both statins and monoclonal antibodies directed against PCSK9. Although each of these polymorphisms presumably affects circulating LDL-C levels by a different mechanism, and the per-allele effect of these SNPs on LDL-C levels varied by more than 6-fold; all 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD when measured per unit lower LDL-C. This finding suggests that the effect of long-term exposure to lower LDL-C on the risk of CHD appears to be independent of the mechanism by which LDL-C is lowered. Therefore, the method of lowering LDL-C is likely to be less important than the magnitude and timing of LDL-C reduction. As a result, diet and exercise are probably as effective at reducing the risk of CHD as are statins or other treatments that lower LDL-C when started early in life (and when measured per unit lower LDL-C).

http://content.onlinejacc.org/article.aspx?articleid=1379036

Do I buy Esselstyns idea? Esselstyn hasn’t come up with any ideas of heart disease immunity with TC cholesterol under 150, kept consistently! This is what biomedical community at large maintains, he merely echoes the message. This not about buing, this is about consistency of evidence, science that is. Atherosclerosis is a cholesterol problem, and when cholesterol levels are maintained low (TC cholesterol under 150 and LDL preferably under 80) the disease cannot iniate or progress despite of glucose abnormalities, cigarette smoking, stress, etc. They factors can only exacerbate the problem, not cause the artery disease.

National Cholesterol Education Program, ATP- third expert panel:

“Only populations that maintain very low levels of serum cholesterol, eg. total cholesterol below 150mg/dl throughout the life do we see a near-absence of clinical CHD”.

“Any LDL cholesterol above 100 mg/dL appears to be atherogenic”

http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf

Diagnostic Criteria for Dyslipidemia

“Low-density lipoprotein cholesterol (LDL-C) is identified in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) report as the most abundant and clearly causal atherogenic lipoprotein on the basis of many observational and experimental studies over several decades.1 Guidelines from the American Association of Clinical Endocrinologists (AACE) are in agreement with NCEP ATP III that LDL-C is central in the diagnosis of dyslipidemia. Any LDL-C level above 100 mg/dL appears to promote atherogenesis”

http://www.lipidu.com/Pillars.aspx?PillarID=2&ChildID=2

1) This great review discusses eloquently how unadjustment for regression dilution (systematic error) has failed to show the real association of serum cholesterol concentrations to coronary heart disease in many uniformly high-risk Western cohorts characterized by very high population-wide cholesterol concentrations.

http://aje.oxfordjournals.org/content/150/4/341.full.pdf

2) High quality prospective cohorts which have corrected for regression dilution bias have firmly establish the independent, continuous, positive and log-linear nature of the associations between TC cholesterol and both CHD and Ischemic stoke even within population that have low serum cholesterol concentrations to begin with!

Cholesterol, coronary heart disease, and stroke in the Asia Pacific region

“Numerous other observational studies, particularly in men, have demonstrated a strong, continuous, graded, and independent association between cholesterol and the risk of CHD.1–,6 The current data clearly extend these findings to Asian populations with substantially lower average levels of cholesterol, and confirm that effects are similar in men and women”

http://ije.oxfordjournals.org/content/32/4/563.long

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670480/?page=1

3) Elevated total cholesterol: its prevalence and population attributable fraction for mortality from coronary heart disease and ischaemic stroke in the Asia-Pacific region.

“Conventional methods for estimating disease burden severely underestimate the effect of TC. Cholesterol-lowering strategies could have a tremendous effect in reducing cardiovascular deaths in this populous region”

http://www.ncbi.nlm.nih.gov/pubmed/18677162

26 10 2012
Richard

Cholesterol denialist refer to cross-sectional studies and observational studies on saturated fat and serum lipids, the nonsense often mentioned by the denialists were already refuted several decades ago.

It was estimated over four decades ago that in order to estimate within 20% of the actual dietary intake, there is a requirement of at least 22 days of 24-hour dietary recalls for saturated fat. Inaccurately measuring intraindividual variation has been shown to lead to a miss-classification of subjects into ranges of usual dietary intakes, and biasing correlation coefficients towards null. The majority of the observational studies cited by denialists used single 24-hour dietary recalls and therefore a null association between saturated fat and serum cholesterol is to be expected. Furthermore, the denialists often fail to cite numerous observational studies that used higher quality dietary measurement methods with a larger participant size that found a positive association between saturated fat and serum cholesterol.

Another issue with the observational studies that you and others have cited is that many only used single measurements of serum cholesterol. Several measurements of serum cholesterol are required to measure mean cholesterol due to the substantial intraindividual variation in concentrations, and therefore would have likely biased the association between saturated fat and serum cholesterol towards null.

One more major issue with observational studies, as was noted in the Chicago Western Electric Company study is that the cross-sectional association between saturated fat and serum cholesterol can be biased towards the opposite direction due to participants lowering intake of saturated fat in response to elevated serum cholesterol, which is similar to the “sick quitter effect”, this would have likely biased the association between saturated fat and coronary heart disease towards null in meta-analyses of prospective studies.

http://ajcn.nutrition.org/content/24/3/304.full.pdf

http://ajcn.nutrition.org/content/37/6/986.full.pdf

http://www.ncbi.nlm.nih.gov/pubmed/7041632

http://ajcn.nutrition.org/content/65/5/1597S.full.pdf

http://www.ncbi.nlm.nih.gov/pubmed/17982164

Cholesterol denialists try to mislead their readers into believing that a hand-full of poor quality cross-sectional studies are more informative to address the association between saturated fat and serum cholesterol than that of hundreds of controlled feeding trials which have produced an irrefutable strong positive association.

Now, are suggesting to me that people in Lithuania with mean LDL -choelsterol of 127mg/dl had healthy, physiological cholesterol levels to begin with? In fact the LDL-fraction of the Lithuanian men was about 200% above what is physiologically normal LDL cholesterol present in healthy neonates, wild mammalians who not develope atherosclerosis and among people living in societies where chronic disease are near absent.

26 10 2012
Richard

Anyways,

couple word about your Sweden-Lithuania paper. Both cultures had huge amount of CHD. The fact that Lithuania had lot more, was because people, especially men in post-Communist socities live more plaque-rupture prone lifestyle, alcoholism, stress, lack of medical care, (and perhaps a poor antioxidant status). Moreover, th cross-sectional study did not even control the amount of care received by Swedish high risk patients, assuming that most poor high risk Lithuan were left out from such medical care.

Instead of uniformly high risk cross-sectional studies from Western societies where non-physiological cholesterol concentration are the norm, I find studies on low-risk people much more beneficial from the standpoint of healthy lifestyle decisions.

Studying pooulation with very low serum cholesterol concentration as a baseline, Campbell and Junshi (1994) reported that the chief correlate to all diseases of affluence was elavated TC cholesterol (p = 0.01), which in turn was associated with intake of meat & total fat and inversely associated with intake of legumes and certain fiber extractions

http://ajcn.nutrition.org/content/59/5/1153S.full.pdf+html

26 10 2012
Richard

Cholesterol theory is one of the few theories in medicine which is bullet-proof.

In fact it would not even require much evidence. LDL -cholesterol levels over 200% above to what is physiologically normal is a norm in Western socities. By physiological levels is meant by those LDL- levels which are seen in healthy neonates, all wild mammalians who do not develope atherosclerosis and members in socities where chronic disease including atherosclerosis is near absent.

Normal, non-retarded humans are perfectly able to gather that blood-pressure or BMI above 200% of the physiological norm is harmfull. Normal non-retarded people are also able to conclude and deduce that LDL +200% above to what is physiologically normal cannot be too good.

IMO very good paper by O’Keefe and Loren Cordain:

Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

“People with heterozygous hypobetalipoproteinemia have total cholesterol levels as low as 80 mg/dl and LDL cholesterol levels as low as 30 mg/dl (30). This condition is associated with longevity (31), presumably due to the absence of atherosclerosis, but the lack of other adverse effects that might have accompanied a low LDL level suggests that such low levels of LDL are safe”.

http://content.onlinejacc.org/article.aspx?articleid=1135650

26 10 2012
Bill

Is this the same T colin campbell who said

“The highest blood cholesterol levels in the Chinese were associated with DHA and fish consumption but with the lowest risk of heart disease”

and

“it is the largely vegetarian, inland communities who have the greatest all risk mortalities and morbidities and who have the lowest LDL cholesterols”

Why don’t you post this kind of stuf on masterjohn’s blog ? You will probably get a much better debate out of him

26 10 2012
Richard

LOL! Cholesterol denialists haven’t advanced much from the 1970.s. All risk mortality in China correlated with wealth and access to antiobiotics, well sanitized loo’s and health care. All that was lacking in the plant-based rural parts where LDL levels were low. The idea of China Study was not to study all-cause mortality but diseases of affluence. In other words, the scholars weren’t too interested in 12-girls with low cholesterol dying because of infection. This because of diet had no role in it. Lack of antibiotics had.

High fish consumption protects high risk communities. The benefits of fish consumption becomes less clear in low-risk groups.

“Shekelle et al. [382] reported a significant inverse correlation between fish consumption and 25 year CHD mortality in Chicago. This also appeared to be independent of other risk factors (The 30-year follow up of this cohort, with the same overall result was reported in detail in 1997) [383]. Eleven cohort studies had reported by the end of the century. They were critically reviewed by Marckmann and Gronbaek [384], who concluded: “Of 4 studies judged to be of high quality, the 2 largest were performed in populations at low risk of CHD. They found no protective effect of fish consumption. The other two high-quality studies were relatively small and included individuals at higher risk. They found an inverse relationship between fish consumption and CHD death, suggesting that 40–60 g fish/day is optimal and associated with a risk reduction of 40–60%. Results of 4 studies of intermediate quality support that fish consumption is inversely associated with CHD mortality in high-risk populations only”

Stewart Truswell., Cholesterol & Beyond (textbook)

If you are worried about LDL peroxidation as Masterjohn is, I advice a cut on the fish department

Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men

“These data suggest that a high intake of mercury from nonfatty freshwater fish and the consequent accumulation of mercury in the body are associated with an excess risk of AMI as well as death from CHD, CVD, and any cause in Eastern Finnish men and this increased risk may be due to the promotion of lipid peroxidation by mercury”

http://www.ncbi.nlm.nih.gov/pubmed/7828289

27 10 2012
Richard

2 11 2012
Richard

Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet

“In summary, our results clearly show that the HCHF (high cholesterol and high fat) diet resulted not only in increased serum cholesterol concentrations but also in inflammation and endothelial dysfunction”

http://www.ncbi.nlm.nih.gov/pubmed/16210703

7 11 2012
Bill Smith

We are not baboons. Although I’m pretty certain you may be a baboon, although infinitely less intelligent and definitely not as charming.

7 11 2012
Bill Smith

Richard, you total A55HOLE,

http://fora.tv/2010/11/06/Teresa_E_Steele_The_Evolution_of_Human_Diet

I would hardly say that this woman is not qualified to comment.

8 11 2012
Richard

Passwater: Is it accurate to say that only oxidized-LDL starts the plaque process?

Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.

Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.

Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).

So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.

http://www.healthy.net/scr/interview.aspx?Id=197

12 11 2012
Toni

Richard,

You should really write these to your own blog / free-online-book. This is great work you are doing. I just wonder how somebody manage to write so much! Keep up the great work! Example blogspot.com is great and very simple platform.

13 11 2012
Bill Smith

It’s not great work that Richard is doing, it’s propagating utter nonsense, spouted by a closed minded individual with an agenda.

Read this, all parts of it:

http://eatingacademy.com/nutrition/the-straight-dope-on-cholesterol-part-i

14 11 2012
Toni

Bill,

In the other hand there’s Peter Attila, who has studied lipids 9 months, saying “All cholesterol is good!” and in the other hand there’s T. Colin Campell proving with the best studies in nutrition world that cholesterol kills… hmm wonder who’s right.

14 11 2012
Richard

Thanks Toni,

why would anyone listen to denialists spindoctors such as Masterjohn or P. Attia who aim to confuse and sabotage the truth around cholesterol and heart disease by spreading infantile nonsense that everyone abobe the age 12 can easily debunk by using google, when one can just listen real scientists who do actual research on the given topic. Daniel Steinberg has authored over 400 articles on cholesterol metabolism and served in several expert panels and review board of scientific journals.

Anyways, that was great interview with Steinberg who revealed us that oxidized LDL is just one form of modication process that can ininiate the foam cell formation together with the two of three additional modification process where one is simply the aggregation of LDL with itself.

14 11 2012
Richard

Cholesterol denialists such as Denise Minger/Colpo/Masterjohn/Guyenet wants mislead our attention from a meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs to a epidemiologic studies that are either cross-sectional and suffer from a signficant regression dilution bias and/or or show major weakness in the form of imprecise dietary assessment methods without even mentation the limitations and shortcomings of these kind of studies. In short, denialists often recite studies without a discussion about the methdologic strenght/weakness inherent in these studies and thus confuse their readers into believing that all studies are made equal.

Moreover, denialists such as Denise Minger/Guyenet wants to confuse their audience into believing that TC cholesterol as risk marker is not relevant by citing studies that are cross-sectional by nature and suffer from a signficant regression dilution bias. Simultaneously, the cholesterol denialists miss the opportunity of discussing studies that have used superior methodology by adjusting for regression dilution bias and showed a powerfull, consistent, independent, positive and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke, even within populations that have very low cholesterol as baseline compared to high risk Western populations.

Lastly, cholesterol denialists such Denise Minger fail to discuss the evidence from mendelian randomized controlled trials consisting over the one million people that have showed highly consistent and major reduction in coronary heart disease risk, independent of mechanism by which LDL cholesterol is lowered, in people who’ve born and maintained low LDL cholesterol levels throughout the life, without showing any other inherent differences in other biomarkers.

Finally, cholesterol denialist like Denise Minger wants to confuse her readers into believing that thyroid dysfunction is a root cause for coronary heart disease independent of cholesterol levels (eventhough elevated cholesterol are part of the pathology of thyroid malfunction) without the evidence from high quality prospective cohorts that would indicate that the majority of coronary heart disease patients FIRST developed thyroid dysfunction prior to the diagnosed heart disease. The lack of such evidence from high quality prospective cohort studies consisting millions of people, and showing the independent and causal nature of elevated cholesterol to coronary heart disease risk, strongly indicates that Denise Minger utilizes the common tactiques of denialists as described by Diethelm (2009)

http://eurpub.oxfordjournals.org/content/19/1/2.full

References:

http://content.onlinejacc.org/article.aspx?articleid=1379036

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/pdf/bmj.b92.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2988224/

http://circ.ahajournals.org/content/118/6/672.long

http://www.thelancet.com/journals/lancet/article/PIIS0140673607617784/abstract

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3284229/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488755/

http://www.ncbi.nlm.nih.gov/pubmed/19349632

http://ije.oxfordjournals.org/content/32/4/563.long

http://www.ncbi.nlm.nih.gov/pubmed/18677162

14 11 2012
Richard

Couple typing and grammatical errors there. English not my first language, anyways, I am sure the message will be understood by those who do not posses the typical denialist/crank psyche.

14 11 2012
Richard

Continues…

Elevated LDL cholesterol induces atherosclerosis and coronary artery disease mortality in every mammalian specimen (birds and insects included). Humans in Western societies typically show LDL cholesterol levels that are +200% above to what is physiologic, that is, levels that has been observed in a) free-ranging mammalians that do not develop atherosclerosis, b) healthy neonates and c) members living in societies where chronic disease including atherosclerosis is near-absent.

In free-ranging non-human primates, consuming only food founds in their natural habitat higher cholesterol concentrations (LDL > 70mg/dl) have been associated with atherosclerosis despite having cholesterol concentrations that are much lower than in humans living in Western societies and despite consuming a diet rich in antioxidants.

Perhaps the considerations expressed above influenced this article, published in a peer-reviewed scientific journal.

Cholesterol myth club on par with flat earth society

http://www.ncbi.nlm.nih.gov/pubmed/2296560

Dennis Minger does not want to share the opportunity for her readers to find about the +100 hundred experiments demonstrating that dietary cholesterol induces experimental atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small, this includes omnivorous non-human primates. There was no evidence of a threshold for dietary cholesterol with respect to an adverse effect on arteries. This persisted even when researchers made sure that micronutrient intake requirements were being met.

Dennis Minger who is mentally invested in the appeal-to-nature fallacy, is suggesting that virtually all the major health authorities around the world who warn against the dangers of dietary cholesterol, saturated fatty acids and elevated serum LDL concentrations are participating in a worldwide conspiracy. For Denise Minger, LDL cholesterol level that is +200% above to what is biologically normal and (unfortunately) a norm in societies where saturated fats and dietary cholesterol are customarily ingested in every meal, cannot cause harm as such. Her arguments are based on imaginary science and denialism, shunning the evidence from over one hundred randomized controlled trials and animal models.

14 11 2012
melkoppelman

Richard, the article ‘Cholesterol myth club on par with flat earth society’ may have been published in a ‘peer-reviewed scientific journal,’ but it’s an editorial . . . written by a medical student . . . in 1990.

Your skepticism is healthy, however I do not understand why a) you make your attacks so personal (it really detracts from your arguments) b) you use such lousy references and bad science to support your arguments. If the question were so clear cut, you wouldn’t have to and c) if you are indeed a man of science, I don’t understand how you can be so confident that you are right. Scientific understanding, particularly where it comes to health and disease, is changing literally all the time. In my experience, the key attribute that separates the truly scientific mind from the angry amateur is humility. After all, we’re all trying to explain something that none of us fully understands.

14 11 2012
Richard

@melkoppelman

I don’t need humility nor patience since I am not pushing a fringe beliefs in regards to first class theories that are globally accepted by every major health organization. Thus, it’s clear that I can afford to be more confident than cholesterol denialists such as Denise Minger who advocate the consumption saturated fat laden trophical oils for vegans.

Please, provide a detailed explanation why my references are lousy. My references include a) meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs, b) high quality prospective cohort studies including millions of participants showing a positive, independent and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke even within population with very low serum cholesterol levels as the baseline, c) mendelian randomized controllod trials consisting over million people showing the causal nature of LDL cholesterol to coronary heart disease risk, and d) evidence from over 100 experimental models, including evidence from omnivorous non-human primates, demonstrating that dietary cholesterol induces experimental atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small. In addition, my sources include the findings from Campbell and Junshi (1994) showing that elevated TC cholesterol is the most important correlate to all chronic disease (p=0.01) in a low-risk population with low serum cholesterol concentrations as the baseline.

I am not angry I simply try to do atleast 0.01% of that what Dennis did to Colin T Campbell.

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease:

Number of participants in meta-analysis = 1,003,207

Prolonged exposure to lower LDL-C beginning early in life associated with 3-fold greater clinical benefit for each unit lower LDL (1mmol/l) than treatment with a statin started later in life (Mean age at randomization in statin trials: 63 years; p = 0.00000000000000000843)

Absence of Heterogeneity: Suggests the effect of each of included SNPs on risk of CHD is mediated largely or entirely through effect on circulating levels of LDL-C, rather than through some other pleiotropic effect.

The increased clinical benefit associated with lowering LDL-C beginning early in life appears to be independent of the mechanism by which LDL-C is lowered. Diet and exercise are probably as effective as other therapies at reducing the risk of CHD (per unit reduction in LDL-C)

http://content.onlinejacc.org/article.aspx?articleid=1379036

20 11 2012
melkoppelman

Hi Richard,

I think the biggest issue I have with your references (aside from you citing them inconsistently, it’s helpful to start with the author and year so everyone is singing from the same hymn sheet, or at least this is generally how it’s done int he academic community), is relevance. Most of your references seem to link high LDL and heart disease. I may have missed it, but I didn’t see where in this article Denise claims otherwise. If she’s done so elsewhere, I’d love to see what she says accurately quoted and in context.

What most of your references do not do is link the diet advice that Minger actually recommends to elevated cholesterol or, more importantly, CVD, in any convincing way. This is a diet blog, after all. You realize that dietary cholesterol has very little effect on serum cholesterol? I’m pretty sure at this point (2012), you’d no longer considered this a ‘fringe belief’?

I’m sure some of your points are valid but their effect gets lost in your misquoting and ranting. Is your point that a vegan diet is safer or better for your health than an omnivorous diet?

21 11 2012
Richard

The impact of dietary cholesterol to serum lipids is not pronounced for most people who already have suprafysiologic levels to begin with. Dietary cholesterol as a dose-dependent, linear relationship to serum lipids for all who follow low-cholesterol diets. This is a well established fact. Moreover, there’s evidence showing that dietary cholesterol damages arteries independently of their effect to serum lipids. To make a case for dietary cholestrol and pretending its health promoting substance for humans is nothing pushing fringe beliefs.

21 11 2012
Richard

Dietary cholesterol has a dose-dependent…

To make a case for dietary cholestrol and pretending its health promoting substance for humans is nothing BUT pushing fringe beliefs.

16 11 2012
Richard

According to Denise Minger, Caldwell Esselstyn shoul’ve focused in raising the HDL in his patients. Denise Minger, mentally invested in the appeal-to-nature fallacy, clearly forgor her “correlation is not causation” mantra. While HDL function may be causally related to coronary heart disease (still unclear) there’s no indication that HDL volume is.

The causal nature of LDL cholesterol volume was established not only in meta-analysis regression curve consisting of 108 randomized controlled trials showing that lowering LDL cholesterol significantly reduces coronary events and all cause mortality independent of changes in triglycerides, HDL or the non-lipid lowering effects of various drugs and high quality prospective cohort studies including millions of participants showing a positive, independent and log-linear association of TC cholesterol and coronary heart disease and ischemic stroke (starting from somewhere around 3.2mmol/l/122mg/dl) even within population with very low serum cholesterol levels as the baseline, but also in mendelian randomized controlled trials consisting of over million genotypes and showing 55% reduction for heart disease per every 1mmol/l (38mg/dl) reduction in LDL fraction beginning early in life. The independence of mechanism (each of the studied mutations in different SNPs lower LDL with different mechanism) and lack of heteogenity suggest that dietary patterns and excerise have similar effect.

While similar mendelian randomized trial was performed on HDL cholesterol, what happened? No indication of causality.

CONCLUSION: “Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction”.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract

17 11 2012
Richard

Cholesterol denialists invested in appeal-to-nature fallacy and pushing for diets that elavate serum LDL cholesterol such as Denise Minger argue that Ancel Keys cherry picked countries from the 22-country data set that the FAO had collected without a good and justified reason. While claiming so, Denise Minger fails to provide explation why Keys left Finland and Guatemala out from his landmark speech in 1953. Finland showed the highest comsuption of saturated fats which correlated with very highest cardiovascular mortality,where as Guatemala showed the lowest SFA consumption and lowest cardiovascular mortality rate of the data set. Leaving out the two countries showing the strongest case for lipid theory, is not supportive for the cholesterol denialists agenda against Keys.

Denise Minger claims that Denmark did not experience decrease in cardiovascular mortality during the WW2 unlike the other Nordic countries. While aiming to sabotage and confuse the truth around global cardiovascular disease epidemiology, Denise Minger does not disclose that Denmark with its huge life stock industry, did not show decrease in the animal food consumption during the WW2 unlike the other Nordic countries without such powerfull live stock industry.

While aiming to fabricate the truth around Seven Country Study, the cholesterol denialists fail to discuss the prospective nature of the cohorts used:.

HOMOGEMEITY IN THE RELATIONSHIP OF SERUM CHOLESTEROL TO CORONARY DEATHS ACROSS DIFFERENT CULTURES. 40-YEAR FOLLOW-UP OF THE SEVEN COUNTRIES STUDY

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2642008/

Instead, cholesterol denialists like Denise Minger aim to sabotage and confuse her readers into believing that LDL levels +200% above to what is physiologic, observed customarily in people living in Western societies, are not harmfull. Denise aims to confuse the unlucky reader with issues such as LDL oxidation, inflamation, thyroid function instead of seeing these as complimentary to the lipid theory.

Denise Minger reminds me of a classic example of a denialist that will look under every pebble to make up some sort of excuse and refuses to consider the overwhelming preponderance of evidence presented before him.

All large meta-analyses of randomized trials essentially show the same thing, that lowering LDL reduces the risk of CHD and all-cause mortality. As a denialist Denise would have others believe that scientists have somehow forged the results of dozens of trials as well as the meta-analyses, and that there is some mass conspiracy amongst the scientists and health authorities who have come to the conclusion that there is a causal association between LDL and CHD, in order in to what seems to be to promote an LDL raising diet. This reminds me of how the Flat Earth Society claims also of some mass conspiracy amongst scientists and that the satellite photo’s showing earth as a sphere is “a fraud, a fake, a piece of trickery or deceit.

17 11 2012
Richard

William Roberts, Americn Journal of Cardiology, editor-in-chief:

“..In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet”.

“Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”.

19 11 2012
Richard

To understand the background against saturated fats, one need to understand the well-established causal role of LDL cholesterol to CHD:

To understand those pushing for SFA consumption, one needs to understand appeal-to-nature-fallacy and denialism as described by Diethelm (2009).

20 11 2012
Richard

HealthyL’s updated blog-account on the Minger scam is amazing.
Part 2

http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-healthy-longevity_17.html

1 12 2012
Ralph

Great post!
Please, I’ve one question: Why do you say that lentils and split peas should be soaked for 7 hours, but WITHOUT any vinegar or lemon juice added. Why not add acid?
An interesting website about phytic acid: http://www.phyticacid.org/

Thank you!
Ralph

2 12 2012
kahmen

HI denise! I’ve been following you since I saw you on youtube with the rawbrahs and have been so taken by your wisdom, your grounded nature and your ability to communicate. It is so inspiring to me! I am following you from Melbourne Australia :o)
You mention a lot about supplementing things like B12, iron and Vit D.. I was introduced to raw organic blend of liquid aloe vera and 9 seaweeds 2 1/2 years ago.. It’s called body balance. Have you heard of it?
I had 10 weeks of postpartum bleeding after I had my son 3 years ago followed with fortnightly periods until he was 6 months old. 2 years later besides a 80% plant base diet and body balance I have completely reprogramed my genetics in my family of long heavy painful overdue periods.. My girlfriend who is (predominately raw) vegan and pregnant had low iron and b12, the only choice she had from the Dr was B12 shot in the bum! (contraindicated to pregnancy!)… 4 weeks on aloe and seanine and her levels were normal again. She is about to birth in a week or so… All with no synthetic supplementation, doesn’t that just rock?!
I feel so called to share this information with you and would love your feedback if you have the time?
http://www.abundantsource.com.au
Thanks again, you are such an inspiration and really enjoy how you deliver the information.
Kahmen xxx

6 12 2012
Evan

Rescuing good health from bad science? How does an English major know what even science is? This is such B.S. Only in the Internet age can this occur.

10 12 2012
Richard

Good one Evan.

Denise’s most recent cup of tea is to distort the findings in regards to the 7th Day Adventists cohort. Her “secret” “recent reanalysis” of the all-cause mortality among the fish eating and lacto-ovo vegetarian Seventh Day Adventists is the 1999 paper she cites Very little in it supports Minger’s pseudoscience.

The data for all-cause mortality across all of the Seventh Day Adventists vegetarians by itself is misleading as all-cause mortality was greatly dependent on the length of adherence to a vegetarian diet. For example, the risk ratio in one of the Adventist studies found that those Adventists that adhered to a vegetarian diet for >17 years compared to <5 years was 0.70 after controlling for non-dietary risk factors.

http://ajcn.nutrition.org/content/78/3/526S.full

As the authors of this study reported elsewhere:

“Thus, when interpreting the findings from these studies, there remains the possibility of bias due to changes in diet. Of particular concern is that a subject’s baseline diet reflects a change in dietary pattern due to illness. In the Adventist studies, the author had the opportunity to relate two reports of diet (in 1960 and in 1976) to the subsequent risk of all-cause mortality and found that subjects who reported changing from weekly meat intake in 1960 to no meat intake in 1976 experienced a non-significant 20% increase in risk relative to those who remained as weekly meat-eaters over the 17-year interval. This finding is contrary to all other findings from the Adventist populations, indicating decreased risk for very low meat intakes. One possible explanation for this unexpected effect might be that subjects may have quit consumption of meats due to an illness that was ultimately fatal. This is similar to the “sick quitter effect,” shown among smokers in which those who quit smoking in response to illness were likely to have biased the protective effect of quitting the smoking habit toward the null.

Minger used absolutist language in her claims regarding the lower rates of mortality among the vegetarian Seventh Day Adventists being unrelated to a decrease in animal food intake, despite the fact that the researchers found a lower rate even after controlling for non-dietary risk factors, and also found that egg and meat intake was independently associated with an increased risk of all-cause mortality in one of the studies.

http://www.ncbi.nlm.nih.gov/pubmed/6720674

10 12 2012
neisy

Richard:

I assume you’re talking about something I mentioned in my AHS speech a year and a half ago, so I have no idea why you’re calling it my “most recent cup” of anything. That info has nothing to do with any papers from 1999 — it came from Brian Bull of Loma Linda University where they conduct the Adventist Health Studies, sent via private email. He listed out the numbers from an interim analysis. I have no idea if the numbers will be formally published or not, but you’re welcome to email him yourself and confirm that the Adventist fish-eaters were doing better than any other diet subclass, including the vegans:

http://www.llu.edu/pages/faculty/directory/portfolio_activity.php?uid=bbull&catid=19

11 12 2012
Richard

Hey Denise the beauty,

good that you clarified this, so that I do not spread non-validated claims about science or people (including you) around. Do you have any ideas why fish eaters did better than vegans? Length of adherence, baseline risks, possible sick quitter effect, etc. Well, that doesn’t really matter, the new Seventh Day Adventists cohort on mortality has already been presented, and should be in print by now. The paper on cancer just appeared. This time the fish eaters did not perform too good (within a low-risk healthy population-wide context)

VEGETARIAN DIETS AND THE INCIDENCE OF CANCER IN A LOW-RISK POPULATION.

http://www.ncbi.nlm.nih.gov/pubmed/23169929

10 12 2012
Claudia

I’ve been following Dr. Essy with a vegan diet
for the past year, exept for egg whites. I have bad genes and
Have had high cholesterol and triglycerides
Since my youth. My cholesterol is still over
250 and I’m discouraged. Have you got any
Advise? I feel great but sure would like to be heart attack proof without using statins.

12 12 2012
Richard

I don’t think it’s responsible to advocate the consumption of highly saturated plant fats to vegans.

1) Saturated fat and heart disease

Major weakness of the meta-analysis is the imprecision of dietary assessment methods used in the underlying studies. About half of the studies used 1-d dietary assessments or some other unvalidated method. Food intake varies from day to day, and there is a substantial literature showing that a single 24-h recall provides a poor estimation of the usual dietary intake of an individual (5). Such methods cannot reliably rank individuals by their long-term intake, especially within populations with a uniformly high saturated fat intake. Such imprecision in the assessment of disease determinants systematically reduces the strength of association of determinants with the disease. This is referred to as attenuation (6) or regression dilution bias (7). Observational studies that used such dietary assessment methods failed to show an association between diet and serum cholesterol concentrations (6). This shows the shortcomings of such dietary methods, because the effect of diet on serum cholesterol concentrations has been well established in randomized controlled trials (2, 8). Thus, the lack of a significant association between saturated fat intake and CHD may well reflect the consequences of regression dilution bias”

We believe that the conclusions of Siri-Tarino et al are invalid and are likely to mislead the general population” .

2) Dietary lipids and serum cholesterol level: change in diet confounds the cross-sectional association.

Shekelle RB, Stamler J, Paul O, Shryock AM, Liu S, Lepper M.

“In the Chicago Western Electric Company study, diet was assessed at the initial examination, in 1957-1958, of 1900 middle-aged men and again at their second examination about one year later. At the first examination, lipid composition of the diet, as summarized by a score based on the formula of Keys, Anderson and Grande, was positively associated with level of serum cholesterol. Between the first and second examinations, however, hypercholesterolemic men were more likely than others to have reduced intake of dietary saturated fatty acids and cholesterol. As a result, at the second examination the cross-sectional linear association between the diet score and serum cholesterol concentration was significantly positive for men with initial levels of serum cholesterol less than 250 mg/dl, significantly negative for men with initial levels of 250 mg/dl or higher and not significantly different from zero for all men together. The bias introduced by change in diet among hypercholesterolemic men differs importantly from bias due to unreliability of measurement and to interindividual differences in intrinsic level of serum cholesterol, because it can produce statistically significant but spurious correlations”..

3) Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs

http://www.ncbi.nlm.nih.gov/pubmed/18054937

4) Differences in all-cause, cardiovascular and cancer mortality between Hong Kong and Singapore: role of nutrition.

“There are striking differences in all-cause and cardiovascular mortality between Hong Kong and Singapore. These differences can be most reasonably and plausibly explained by their differences in dietary habits, for example, a higher consumption of coconut and palm oil, mainly containing saturated fat, in Singapore”.

http://www.ncbi.nlm.nih.gov/pubmed/11855581

5) “The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”.

–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]

12 12 2012
Richard

And Finally, the best kept secret of cholesterol denialists such as Denise Minger: Jeremiah Stamler.

Based on Siri-Tarino Meta-analysis, Stamler calculated that saturated fat increase the risk of fatal CHD by 32% (weighted by person-years of exposure) despite the regression dilution bias and sick quitter effect.. Jeremiah Stamler is well acquainted with the meta-analysis concept as he was present when the concept was first introduced to a biomedical community in the 1984 by its “inventor” Sir Richard Peto who also worked out the China Project raw data.The differences in the findings may be partly explained by the fact that Siri-Tarino meta-analysis was the product of the Dairy Association and one of its lead authors Ronald Krauss enjoys hefty grants from Pork Board, Egg Center, Veronica & Atkins Foundation, Cattlemen’s beef association, etc. Studies have shown that whenever dairy or soft drink industry is involved the interpretation is likely to be in favor of the product as opposed to independent research. .

Stamler works out the meta-analysis piece by piece and points out in regards to dietary cholesterol:

To neglect this fact in a review about humans is to imply that the Darwinian foundation of biomedical research is invalid and/or that there is a body of substantial contrary evidence in humans. Neither is the case. Dietary cholesterol (as well as SFA) adversely influences human serum lipid concentrations, per cited equations. And several prospective epidemiologic studies found direct relations of dietary cholesterol to CHD independent of serum total cholesterol (6).

http://ajcn.nutrition.org/content/91/3/497.full

Denise Minger obviously have religious allegiances as she is willing to overlook the detrimental effects of dietary cholesterol for long term health. Doesn’t Darwin’s homology have any predictive value for humans? I believe it does, but then again I am pro-evolution.

The co-author of Siri-Tarino Meta-Analysis, professor Frank Hu in regards to saturated fats (february, 2012):

“Why is red meat harmful? “Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,” explains Hu”

http://harvardmagazine.com/2012/01/a-diabetes-link-to-meat

Forks Over Knives and Healthy Longevity: A Missed Opportunity for the Cholesterol Skeptics
http://healthylongevity.blogspot.fi/2012/08/forks-over-knives-and-healthy-longevity.html

12 12 2012
Chris Heppner

Richard, while I find many of your links and quotes interesting and valuable, I am tired of your repeated–and repetitive, gratuitous, and altogether immature–insults to Denise very, very tiresome. Why don’t you wait for that book to appear, like the rest of us? Chris

12 12 2012
Richard

@Chris,

you are right, I am afraid. I’ve been pretty rough on Denise. I believe its important to tackle denialism, however one must always give a humane treatment, which I’ve occasionally forgot. Sorry a lot, Denise.

Anyways, I was a bit puzzled why Denise claimed that Esselstyn should’ve focused in raising the HDL of his patients. A rudimentary glimpse to literature would have helped here. Less WAPF more science! We shouldn’t pretend that, inter alia, randomized controlled trials with over 1,000 000 genotypes did not exist.

LDL-C = causal factor influencing CHD
HDL-C = Not causal factor in CHD

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease: A mendelian Randomization Analysis

“Background: LDL-C is causally related to the risk of CHD. However, the association between long-term exposure to lower LDL-C beginning early in life and the risk of CHD has not been reliably quantified”

Conclusions: Prolonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life.

http://content.onlinejacc.org/article.aspx?articleid=1379036

Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study

Background: High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal .

Interpretation: Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)60312-2/abstract

Prevention of heart disease: LDL reduction is the outcome of choice? Absolutely yes.

“There is only one well-established relationship between blood cholesterol lipid fraction and coronary artery disease (CAD) That meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fraction, only LDL cholesterol satisfies These criteria”

http://www.ncbi.nlm.nih.gov/pubmed/16674358

Besides,

Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function.

http://www.ncbi.nlm.nih.gov/pubmed/16904539

Doubt Cast on the ‘Good’ in ‘Good Cholesterol’ (May, 2012)

For purposes of comparison, the researchers also examined inherited variations in 13 genes that determine levels of LDL, the so-called bad cholesterol. It is well known and widely accepted that lowering LDL levels by any means — diet and exercise, statin drugs — reduces risk. Clinical trials with statins established with certainty that reducing LDL levels is protective. So, the researchers asked, did people who inherited gene variations that affected their LDL levels, have correspondingly higher or lower heart disease risk?

The study found, as expected, that gene variations that raise LDL increase risk and those that lower LDL decrease risk. The gene effects often were tiny, altering LDL levels by only a few percent. But the data, involving tens of thousands of people, clearly showed effects on risk.

“That speaks to how powerful LDL is,” Dr. Kathiresan said.

But the HDL story was very different” .

http://www.nytimes.com/2012/05/17/health/research/hdl-good-cholesterol-found-not-to-cut-heart-risk.html?_r=0

12 12 2012
Richard

I also have problem with Denise’s glutein alarmism, this is just plain appeal-to-exception fallacy. For those +90% of vegans who have no problem in metabolizing glutein, whole-grain wheat products are excellent. Glutein lowers LDL-C cholesterol as metabolic ward experiments have demonstrated

In one of the most long-living communities in Europe, in Greek Ikaria island, people base their diet largely on potatoes, beans and high-fiber bread made from stone-ground wheat.

http://www.nytimes.com/2012/10/28/magazine/the-island-where-people-forget-to-die.html?pagewanted=all

It would be awesome if Minger could write a scientific book instead relying on pseudocientific & infantile nonsense spread by Masterjohn, Guyenet, Ravnskov and other professional cholesterol confusionists. My hope are not high, but I am easily to be surprised.

*BTW, the causal relationship of LDL-C cholesterol to heart disease is not only demonstrated in bile-acid sequestrant research, high quality epidemiologic studies, statin trials, genetic evidence, animal experiments and diet trials but also with surgical experiments. Even bypass of intestine to lower circulating LDL-C works in decreasing CHD events.

http://www.medscape.com/viewarticle/732829

*Did you know that the the REVERSA-mices clearly demonstrate that atherosclerosis can be turned on and off as a plain function of serum cholesterol. There’s huge board of experimental models that demonstrate this also in non-human primates. Steinberg sums up the animal experiments and inflammation:

“Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences”.

http://circ.ahajournals.org/content/118/6/672.long

In terms of cause-effect elevated LDL-C comes always before the inflammation.

Scott Grundy, The Chaiman of ATP-3 Guidelines highlights the risk modelling in future.

Measuring apolipoproteins does not help risk prediction (June 19, 2012)

“Grundy adds that recommendations for statin use in primary prevention may need to be revisited now anyway, highlighted by the recent meta-analysis from the Oxford group that showed benefits of statins in much lower-risk individuals than those for whom treatment is currently advised.And he suggests that risk assessment may in the future move away from measuring many biomarkers and instead focus on subclinical atherosclerosis with imaging methods or simple risk projection based on age, sex, LDL levels, and perhaps another major risk factor”

http://www.theheart.org/article/1417589.do

The discordance with LDL-P to LDL-C is pretty much solely observed in people with metabolic syndrome. The separate assessment of LDL-P informs doctors about the extent and aggressiveness of the LDL-C lowering theraphy to which diabetics are put by default now days, independent of their baseline LDL-C levels. There’s no upside having any more than 15mg/dl in the LDL fraction.

Clinical utility of inflammatory markers and advanced lipoprotein testing: Advice from an expert panel of lipid specialists (2011)

“All lipoprotein particles in the LDL fraction are atherogenic, independent of size”

http://www.lipid.org/uploads/300/Expert%20Panel%20Paper.pdf

Denise wants you to focus on oxLDL and forget your circulating LDL-C levels, which may not be entirely wise thing to do since oxLDL is just one modification process that gives you atherosclerosis, better just focus on eating a diet that result in low LDL-C levels:

Passwater:Is it accurate to say that only oxidized-LDL starts the plaque process?

Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation.Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.

Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.

Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).

So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.

http://www.healthy.net/scr/interview.aspx?Id=197

*Bonus; did you know that people with rare genetic condition and showing extremely low LDL-C levels since birth (<15mg/dl), but without any differences in other biomarkers, end up living 9-12 longer than their peers and are immune to heart disease.

http://circ.ahajournals.org/content/118/6/672.long

12 12 2012
Richard

^Unfortunately youtube wires the wrong video.

The video on glutein appears in PrimitiveNutrition response-serie:

The Futility of Cholesterol Denialism, Part 3: A Process of Elimination

http://www.youtube.com/user/primitivenutrition

12 12 2012
Richard

The biomedical community including American Heart Association was in large convinced that the relationship between serum cholesterol and CHD was causal already in the 1970′s long before statin industry became existent. However, the double-blinded, placebo controlled large-scale statin trials provide the most staggering evidence for lipid theory. The denialists such as Chris Masterjohn tries to use every imaginable argument to sabotage the truth and confuse the laypeople before the preponderance of evidence. One of these arguments are that statins lower CHD risk due to mechanism other than lipid lowering. This is dead alley, because:

a) There exist ridiculously linear relationship between LDL-C lowering and the decrease of cardiovascular events observed in 5-year statin therapy initiated at mean age of 63. 15% reduction in LDL-C = 15% reduction in events, 45% reduction in LDL-C = 45% reduction in events, and so forth.

b) A meta-analysis on mendelian randomized controlled trials with over 1,000,000 genotypes have shown that people with inherited LDL-C lowering mutations in the statin targeted HMG-CoA gene showed no heterogeneity between other studied SNPs with regard to the decrease in CHD risk per unit of LDL reduction, which suggests that the effects of statin to the risk of CHD is mediated largely or entirely through effect on circulating levels of LDL, rather than through some other pleiotropic effect.

It appears that the effects often denoted as pleitrophic are mostly related to LDL lowering itself and would accrue independent of the mechanism used. A meta-regression curve accumulated from 108 randomized controlled trials of various medical and dietary based lipid modifying interventions has established that lowering LDL cholesterol significantly decreases the risk of coronary heart disease and all-cause mortality, independent of changes to HDL cholesterol and triglycerides, and non-lipid effects of specific drugs

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645847/

1) Low-density lipoprotein cholesterol reduction and prevention of cardiovascular disease

“There was little question after the first major statin trials that the reduction in CVD was related to lipid lowering and was totally consistent and supportive of the lipid hypothesis. However, stimulated by funding from the pharmaceutical industry, in which competition was fierce for market share and was driven mainly by the efficacy of lowering LDL-C levels, manufacturers of less-effective agents for lowering LDL-C levels helped propagate “beyond LDL-C” theories; these theories were that statins reduced CVD events by means other than lipid reduction, often termed pleotropic effects, usually shown in in vitro laboratory studies or small, poorly standardized surrogate marker trials. This belief culminated in an RCT by a pharmaceutical company that was designed to show that more LDL-C reduction with a competitor’s statin achieved no greater benefit.13 However, the results of that study clearly and convincingly showed otherwise, with additional reduction in CVD events with the drug that lowered LDL-C levels more. Even with this evidence, and perhaps with an even more powerful statin about to be approved, the investigators suggested that the reduced events were due to pleotropic effects of the more efficacious statin. However, the trial was soon followed up with results from another head-to-head RCT, with the same drug at different LDL-C lowering doses,14 which eliminated the pleotropic potential and rein-forced that lower is better”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665973/

2) A meta-analysis of 19 studies (81,859 participants in all) that lowered LDL and measured clinical disease or death, including 5 diet trials, 3 bile sequestrant trials, 1 surgery trial and 10 statin trials concluded that: “The pleiotropic effects [effects apparently unrelated to lowering LDL] of statins do not seem to contribute an additional cardiovascular risk reduction benefit beyond that expected from the degree of LDL-C lowering observed in other trials that primarily lowered LDL-C.

The statins have helped the biomedical community to redefine what is normal. In other words, having a “normal” cholesterol in a society where saturated fats and dietary cholesterol are ingested at every meal may not be optimal. Normal is culturally related and does necessarily imply that something biologically normal. The president of SUNY Downstate Medical Center and author of several large-scale statin trials sums up the evidence of statin trials in regards to dietary recommendations:

More evidence for lowering LDL to below 70 (2011)

“LaRosa, who wrote an editorial [3] accompanying Lee’s study, expanded on his views to heartwire: “I used to be skeptical about the idea of trying to achieve very low cholesterol levels, but now I am more accommodating. As cholesterol levels are coming down, we are seeing much lower rates of bypass surgery and elective angioplasty. I think elective angioplasty will eventually disappear altogether.”

“Chimpanzees eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis.He noted that levels of LDL below 70 are on a par with those of nonhuman primates who don’t develop atherosclerosis, adding that, like these primates, humans were designed to be vegetarians. “Our dental anatomy suggests that we are not meant to be meat eaters. Animals that eat meat have sharp tearing teeth, while we have flatter teeth more similar to vegetarian animals. I believe humans are not anatomically or metabolically designed to be meat eaters, and because we do consume animal fat that’s why we get atherosclerosis. Chimpanzees don’t eat meat; they eat very little fat. They have LDL levels in the range of 40 to 70, and they don’t get atherosclerosis. Maybe we wouldn’t get atherosclerosis either if we had levels this low.”

http://www.theheart.org/article/1290061.do

*Interesting statin studies published this year (2012):

1) Cholesterol Treatment Trialists’ (CTT) Collaborators. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet 2012;380:581–90.

2) Statins reduce cardiovascular events and all-cause mortality in women: Meta-analysis

http://www.theheart.org/article/1347045.do

12 12 2012
Richard

A scientific look at wheat-alarmism: claims made by William “robust” Davis at closer scrutiny:

What do real scientists think?

http://www.aaccnet.org/publications/plexus/cfw/pastissues/2012/OpenDocuments/CFW-57-4-0177.pdf

13 12 2012
Bogi

Great blog, thanks a lot Denise Minger.

13 12 2012
Jeff

Great blog,keep up the good work Denise.

13 12 2012
Rich-ard

“It’s the cholesterol stupid”.

The real deal-breaker in China-Project was serum cholesterol levels. Campbell & Junshi (1994) reported that the chief correlate to all chronic disease was elevated serum cholesterol concentrations (p= 0.01) within in population with significantly lower serum cholesterol levels compared to Western societies. Diet became important, but only as the function of serum cholesterol levels. Campbell and Junshi observed that even small amounts of animal foods are associated with elevated cholesterol levels. They noticed that plant-based diets based on whole-foods and fat intake minimization will provide optimal cholesterol levels for long-term health for most people:

“Mean intakes of animal protein (about one-tenth of the mean intake in the United States as energy percent), total fat (14.5% of energy), and dietary fiber (33.3 g/d) reflected a substantial preference for foods of plant origin. Mean plasma cholesterol concentration, at approximately 3.23-3.49 mmol/L, corresponds to this dietary life-style

These findings suggest that even small intakes of foods of animal origin are associated with significant increases in plasma cholesterol concentrations, which are associated, in turn, with significant increases in chronic degenerative disease mortality rates”.

“There appears to be no treshold of plant-food enrichment or minimization of fat intake beyond which further disease prevention does not occur”

http://ajcn.nutrition.org/content/59/5/1153S.full.pdf+html

Campbell & Junshi (1994) are basically saying that serum cholesterol levels above to what is observed in free-ranging mammalians, healthy neonates and people living in cultures where chronic disease is near-absent, are unhealthy. Denise Minger wants us to believe a raw data sorted out by Sir Richard Peto does not support Campbell’s message when everyone can in fact try for themselves how much foods of animal origins they can include in their diet in order to get serum cholesterol levels down under 130mg/dl. Elevated serum cholesterol levels in midlife has been associated with not only to CHD but to alzheimer disease, prostate cancer and impotence in Western cohorts where elevated cholesterol including LDL-C cholesterol +200% above to what is biologically normal is the norm thus weakening the statistical power of these cohorts.

13 12 2012
Richard

Thank for patience Denise, this will be my last post.

Best,.
Richard

21 12 2012
Richard

I am back:

the associations of elevated cholesterol with aggressive, fatal prostate cancer is likely to be causal. Your arteries and prostate do not care about you feeling good about eating “a natural diet”. Dennis Minger’s dietary recommendations are likely to lead to severe hypocholesterolemia and thus put you in an increased risk for cancer, CHD, alzheimer, etc. But you would’t mind because you’d know you would get enough vitamin K2.

Cholesterol and Cancer: Answers and New Questions

“Considerable evidence supports the plausibility of an association between low cholesterol and reduced risk of high-grade prostate cancer. Several studies have reported an association between statin use and reduced risk of advanced or high-grade prostate cancer (15, 16). In addition, an inhibitory effect of low cholesterol on prostate cancer progression is biologically plausible. Laboratory evidence suggests that lowering cholesterol levels could inhibit cell-signaling pathways that are important for prostate cancer progression (17). This hypothesis is supported by experiments in mice in which lowering serum cholesterol with dietary modification or a cholesterol-lowering drug reduced the cholesterol content, size, and vascularity of human xenograft prostate tumors (18).”

http://cebp.aacrjournals.org/content/18/11/2805.full

21 12 2012
Richard

Even paleo-author’s have know the difference between “normal” and biologically normal. Denise Minger does not want to accept that LDL-C cholesterol +200% above to what is really normal cannot be harmful. She thinks AHA has got it wrong when warning vegetarians not to eat a vegetarian diet with too much SFA.

Optimal low-density lipoprotein is 50 to 70 mg/dl: Lower is better and physiologically normal

“The average total cholesterol level in American adults today is 208 mg/dl (corresponding to an LDL of approximately 130 mg/dl) (13). In this case, average is not normal because atherosclerosis is present in up to 40% to 50% of women and men by age 50 (14).Atherosclerosis is endemic in our population in part because the average person’s LDL level is approximately twice the normal physiologic level(Figure 1)”

http://content.onlinejacc.org/article.aspx?articleid=1135650

Some people try to rationalize their LDL-C elevating diet with the notion that atherosclerosis is an inflammatory disease. If you poke a stick to your finger there will be inflammatory reaction, which is eliminated while the stick is removed from the finger. This is exactly what happens in high-tech animal models. Daniel Steinberg summarizes that most amazing models in atherosclerosis which show that atherosclerosis can be turned on & off as simple function of serum cholesterol. These models provide us the direct cause-effect answers. Elevated cholesterol provokes the inflammation. Cholesterol denialists confuse the cause & effect. ,

Evidence Mandating Earlier and More Aggressive Treatment of Hypercholesterolemia

“Taken together, all of these findings suggest that the inflammation associated with atherogenesis is not sufficient in itself to cause further lesion progression or even to maintain lesions at a steady state once the hypercholesterolemia has been fully corrected. In other words, many (or even most) of the inflammatory processes in the advancing lesion are downstream responses ultimately traceable to hyperlipidemia and its consequences”
ttp://circ.ahajournals.org/content/118/6/672.long

The chief editor for American Journal of Cardiology challenges the whole notion of inflammation as a part-definition in atherosclerosis. W. Roberts has written 1300 scientific articles about atherosclerosis and 12 textbooks. He is trained pathologists specialized in cause & effect in CHD.

“In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”

In summary, the connection between cholesterol elevation and atherosclerotic plaques is clear and well established. Atherosclerosis is a cholesterol problem! If one has elevated cholesterol, has an elevated blood pressure, smokes cigarettes, or has an elevated blood sugar, these additional factors serve to amplify the cholesterol damage but they by themselves do not produce atherosclerotic plaques! Societies with a high frequency of systemic hypertension or a high frequency of cigarette smoking but low cholesterol levels rarely get atherosclerosis”.

“….The lower the LDL cholesterol the better, and this principle has been established repeatedly despite the voices of the anticholesterol, antistatin fallacy mongers! It’s the cholesterol, stupid!”

21 12 2012
Richard

Just like Denise Minger does today, cholesterol denialists around 100 years ago aimed to dismiss mechanism models of atherosclerosis by pointing out that rabbits are obligatory herbivores and thus results from cholesterol feeding expiriments have no relevance to humans. The scientists replied by designing an experiment where serum of the cholesterol fed rabbit was transferred to another rabbit eating its herbivore diet. The cause of artery disease was demonstrated to be abnormality in the serum lipids, as expected.

+100 hundred experiments demonstrates that dietary cholesterol induces experimental atherosclerosis in virtually any animal model that it elevates serum cholesterol in, even when the elevation is considered to be small, this includes omnivorous non-human primates. There was no evidence of a threshold for dietary cholesterol with respect to an adverse effect on arteries. This persisted even when researchers made sure that micronutrient intake requirements were being met,

If Dennis Minger was right, it would mean that homo-sapien is not only race and specimen on the face of this planet which is immune to the harms of elavated cholesterol. Makes sense. NOT!

23 12 2012
Richard

In a huge Korean prospective cohort elevated TC cholesterol strongly associated with cancer:

Total Cholesterol and Cancer Risk in a Large Prospective Study in Korea

Results Over follow-up, 53,944 men and 24,475 women were diagnosed with a primary cancer. Compared with levels less than 160 mg/dL, high total cholesterol (≥ 240 mg/dL) was positively associated with prostate cancer (hazard ratio , 1.24; 95% CI, 1.07 to 1.44; P trend = .001) and colon cancer (HR, 1.12; 95% CI, 1.00 to 1.25; P trend = .05) in men and breast cancer in women (HR, 1.17; 95% CI, 1.03 to 1.33; P trend = .03). Higher total cholesterol was associated with a lower incidence of liver cancer (men: HR, 0.42; 95% CI, 0.38 to 0.45; P trend < .001; women: HR, 0.32; 95% CI, 0.27 to 0.39; P trend < .001), stomach cancer (men: HR, 0.87; 95% CI, 0.82 to 0.93; P trend ≤ .001; women: HR, 0.86; 95% CI, 0.77 to 0.97; P trend = .06), and, in men, lung cancer (HR, 0.89; 95% CI, 0.82 to 0.96; P trend < .001). Results for liver cancer were slightly attenuated after additional adjustment for liver enzyme levels and hepatitis B surface antigen status (men: HR, 0.60; P trend < .001; women: HR, 0.46; P trend = .003) and exclusion of the first 10 years of follow-up (men: HR, 0.59; P trend < .001; women: HR, 0.44; P trend < .001). Total cholesterol was inversely associated with all-cancer incidence in both men (HR, 0.84; 95% CI, 0.81 to 0.86; P trend < .001) and women (HR, 0.91; 95% CI, 0.87 to 0.95; P trend < .001), but these associations were attenuated after excluding incident liver cancers (men: HR, 0.95; P trend < .001; women: HR, 0.98; P trend = .32).

Conclusion In this large prospective study, we found that total cholesterol was associated with the risk of several different cancers, although these relationships differed markedly by cancer site.

http://jco.ascopubs.org/content/29/12/1592.abstract

In high risk Western cohorts association of low cholesterol and cancer is often observed. In this paper the scholars note that besides cancer cells sucking up the LDL, patients with high cholesterol are usually already passed away due to CHD before their cancer is diagnosed.

Time-dependent association of total serum cholesterol and cancer incidence in a cohort of 172,210 men and women: a prospective 19-year follow-up study.

http://www.ncbi.nlm.nih.gov/pubmed/19164459

26 12 2012
Corner Shelves

I stopped counting them long ago, but I would guess that there are somewhere around 4
- 5,000 volumes of one kind or another, both hard covers
and paperbacks in my home. One of the greatest benefits of
buying used books is the fact that it means that less new books need to be printed,
therefore there is less harm to the environment.

Complete games ‘ Halladay.

28 12 2012
Laura

I have been a vegetarian (vegan but for honey) for years, and don’t take any supplements or worry about any oils or anything. I just eat tons of fruits, vegetables, whole grains, legumes, coconut fats, etc. I am now in my 30′s and feel amazing. Much better than when I was in my teens. My husband, in his 40′s now, is better in bed than when we married. Just saying. :)

31 12 2012
Richard

PlantPositive is setting the record straight with revisionists. His 3rd and most compelling serie on nutrition, denialism and distortion

1 01 2013
Richard

Chris Masterjohn and PUFAs oxidize.

It’s the video number 41 of the new serie, incase the video does not come right.

3 01 2013
Richard

Denise Minger aimed to distort and sabotage the truth around Ancel Keys. PlantPositive has found the original source in where A. Keys explain himself over why left countries away from the 22-data set that was collected by the FAO. Why did Keys left out Finland and Guatemala which were perfect examples of lipid theory with their opposite realities? Thumbs up for Yerushalmy and Hilleboe, two whackjobs fond of bad science.

3 The Journalist Gary Taubes 3: Ancel Keys Was Very Bad 1

Minger thinks lipid theory/diet-heart theory is nonsense. While it’s very unlike that LDL cholesterol is the only substance found in the body that cannot cause harm in excess and while it’s very unlike that human is only specimen in the face of this planet which is immune to the dangers of elevated lipids, I am really wondering if Minger has a theory of her own. Since it’s well established that animal fats and dietary cholesterol elevates serum cholesterol ( I have referenced to meta-analysis of 395 metabolic ward feeding experiments), I think Minger has some kind of explanation of why SFA intake are not harmful despite their well-known ability to elevate LDL cholesterol by suppressing messanger RNA synthesis for the LDL receptor. I think Minger owns us explanation. Otherwise, I feel myself fooled by her.

4 01 2013
Richard

The story around Yerushalmy and Hilleboe. Denise Minger is an anti-darwinist who just like the Cremlin marxists aims to rewrite history in an attempt to distort and sabotage the truth around the diet-heart science.

4 The Journalist Gary Taubes 4: Ancel Keys Was Very Bad 2

4 01 2013
Richard

Denise Minger thinks we’ve slipped back to the 1980s when warning against dietary cholesterol. “Second opinion” is provided by PlantPositive.

23 Cholesterol Confusion 6 Dietary Cholesterol (And the Magic Egg)

4 01 2013
el-bo

seriously man, why don’t you just fuck off

all everyone is getting in their inbox is updates from you, whining

if you have anything of interest other than just spamming and making us party to your plant positive wankfest then make your points in a concise post, asking whichever questions you need (with some kind of civility)

you are being ignored not because people don’t have any interest in finding the truth, but because you are acting like a raging fucking idiot

6 01 2013
Tor

I’m a vegan trying to incorporate more raw and I really appreciate this page! Lately I’ve had huge issues with fatigue, concentration, mood swings and weight that just won’t go away – I had a blood test that showed elevated TSH, but my doctor can’t test me for hypothyroid for another 6 months. For a long time I’ve thought it was because I just messed up my metabolism with disordered eating (bulimia for 5 years) but reading this, I realised that I pretty much live on foods like broccoli, kale, sprouts and strawberries. I also ate a lot of soy until a few weeks ago. I don’t tend to eat any cruciferous vegetables when I’m on raw and then I have incredible energy, to the state of restlessness – I feel like I suddenly have the missing link. I will scale back on the goitrogenic foods and hopefully I’ll find a happy medium!

7 01 2013
Richard

Plant Positive Strikes Back: Nutrition Past and Future

“It is ignorant to suggest that Ancel Keys cherry-picked these six countries without giving the reason for the selection criteria. In Denise Minger’s post regarding Ancel Keys 1953 paper where she attempted to plagiarize Plant Positive’s work, like Yerushalmy and Hilleboe, Minger ignorantly claimed that ‘Keys cherry-picked six countries and never told us why.’ It is clear that Minger has either simply not read or is ignorant of the data presented in the Keys paper that she criticized, yet still claimed that she ‘did a deeper analysis of the 1950s data than Keys himself probably did’.3 This is the same level of ignorance that Minger applied to her criticisms of the China Study”

http://healthylongevity.blogspot.fi/2012/12/plant-positive-strikes-back-nutrition.html

30 10 2014
shanarose

in addition to all this, Ancel Keys lived until a healthy 101 years old …. he was the grand-daddy of the ‘Mediterranean Diet’ …. and he ate that way – low fat/low protein/high whole carb – for over 60 years until the end …. how many high fat/high protein/low carb people do we know who lived healthy and productive lives until 101 years old? talk is cheap …. i would rather see a sermon than hear one ….. this man’s healthy 101 years is enough sermon for me ……..

7 01 2013
Richard

Denise Minger, making no exception to her deceitful character, aimed to (once again) sabotage and distort the truth around diet-heart by falsely claiming that Keys never explained why he chose 6 countries out of a data set that was produced by the FAO. Keys explained himself, and PlantPositive has the original source in his videos. Keys used data quality control and believed that only six countries data was subjected to International standards. That was the reason he leaved aside, inter alia, Finland and Guetemala which were the best examples of the diet heart theory. Jerushalmy and Hilleboe did not use any quality control, not using quality control is akin to cherry picking since just like cherry picking, lack of quality control leaves us at risk of missing opportunities for important trends. Keys wasn’t into cherry picking. Keys was selective and showed high standards.

9 01 2013
Richard

A fresh new RCT from the print:

Causal Relevance of Blood Lipid Fractions in the Development of Carotid Atherosclerosis: Mendelian Randomization Analysis

CONCLUSIONS: “Our findings confirm a causal relationship between LDL-C and CIMT but not with HDL-C and triglycerides. At present, the suitability of CIMT as a surrogate marker in trials of cardiovascular therapies targeting HDL-C and triglycerides is questionable and requires further study”

http://www.ncbi.nlm.nih.gov/pubmed/23275344

12 01 2013
Richard

Denise Minger, a question! Given PrimitiveNutrition’s video “PUFAs oxidize” is there something that might have changed your mindset over LDL oxidation? Second opinion in regards to paleo-broscience around PUFAs and LDL-oxidation provided by PlantPositive. Amazing video.

41 PUFAs Oxidize!

Masterjohn and Kresser making their mommies proud. LOL

22 Cholesterol Confusion 5 Cholesterol Is Necessary for Life

15 01 2013
Richard

Denise Minger, you think that “cholesterol has something to do with CHD”. Perhaps you’d understand the causal link of LDL cholesterol to CHD if you were looking CHD in terms of causal exposure model (see Sniderman, et al 2012). Here’s a fresh study from Helsinki that highlights this very nicely. Pay attention to the very long follow-up and the fact that the authors were not just looking CHD but mortality and quality of life. TC cholesterol is an excellent predictor of mortality and quality of life up to late mid-life until the association gets co-founded. The cholesterol levels of Western people start to rapidly plummets due to metabolic changes in the liver and intestine leading to weaker cholesterol absorption and synthesis.

Effect of cholesterol on mortality and quality of life up to a 46-year follow-up

“A strong and graded relation was found between the cholesterol level and total mortality, with the men with a cholesterol level ≤4 mmol/L (154 mg/dl) having the lowest mortality. In all, the men with the lowest cholesterol gained the most life years. However, no association was found with the cholesterol level in 2000 (when 16% were using statins) and subsequent mortality. The lowest (≤4 mmol/L) cholesterol value in midlife also predicted a higher score in the physical functioning scale of RAND-36 in old age. In conclusion, a low total cholesterol value in midlife predicts both better survival and better physical functioning in old age”.

http://www.ncbi.nlm.nih.gov/pubmed/21714947

23 01 2013
Richard

Dennis Minger had the golden opportunity the set the record straight with the denialist Keys bashers, she missed her chance and instead resorted to distortion. Minger claimed Ancel Keys never explained himself over the fact that he choose six countries from the 22-country data set: Minger was dead wrong. Minger even displayed her total ignorance while claiming she dug deeper over the diet-heart studies than Keys ever did :)

“Broadly speaking, death rates ascribed to specific causes are not very reliable under the best of circumstances. Certainly it would be difficult to insist that the values in Table 3 for “degenerative heart disease” in the different countries are stricktly comperable nor would it be reasonable to suggest that the values listed for all circulatory diseases are actually precise.”

“The list in Table 2 includes the countries with good vital statistics which are reasonably compared in race, climate, culture, medical services and vital statistics. The omissions are Western Germany and Finland, because of major population shifts and other effects from the war, and Iceland, Luxemburg and some colonies and semi-independent states with very small populations. (…) So far it has been possible to get fully comparable dietary and vital statistics from 6 countries.”

–Ancel Keys, 1953

Minger has a beef with with dietary recommendation that encourage to keep an eye on SFA consumption. Why?

A review of 248 tightly controlled metabolic ward feeding trials showing that SFA has an adverse effect on serum lipids

http://www.ncbi.nlm.nih.gov/pubmed/8503356

Meta-analysis of 395 metabolic ward studies showing the deleterious effect of animal fats to serum lipids.

http://www.ncbi.nlm.nih.gov/pubmed/9006469

Meta-analysis of 60 controlled trials on SFAs.

http://www.ncbi.nlm.nih.gov/pubmed/12716665

Is Minger suggesting we humans are the only specimen on the biosphere that is immune to dislipidemia? Is she really saying that LD-lipoproteins are the only substance in human body that does not cause harm in excess? Is she suggesting that evolution has “designed” our LDL receptors not to work most efficiently with the very similar & low serum cholesterol concentrations that are observed in free-ranging mammalian species, especially those who do not develop artery disease? I hop Minger shed some light on these issues.

9 03 2014
Philippe

I think it’s time to stop quoting or even mentioning Minger, a lady who can’t tell a molecule of starch from a protein is shown one. I’ll remind everybody that she has no background in basic science. Not in science, in BASIC science. Just a degree in English. Please, forget Minger. She’s just somebody trying to make money from her website.

25 01 2013
john staunton

i really appreciate the stance you take as an educated ex vegan. Might I trouble you with a question. I’m 14 years pescetarian and have on and off suffered from depression/moods potentially with a strong wheat/gluten link or just GL Mania from my grain consumption. Anyway I’d like to ask you do you think I’m missing out on something as a fish eating egg eating uhm person :)? You didnt mention anything about Creatine or Carnitine does that mean you are not concerned with them or the list would just have been too long?

27 01 2013
Richard

“Ah, the Lipid hypothesis, in all its unproven, scientifically feeble story”

–Denise Minger

It would be so awesome to inject LDL directly to Denise’s veins. I am sure an intelligent creator made all animal fundamentally very different from human, and thus nothing bad would not happen to Dennis with this experiment.

1 02 2013
Richard

Stephan Guyenet and Denise Minger are both in pathological denial. HealthyL provides a second opinion to Stephan Guyenets nonsense about SFAs, serum lipids and diet-heart theory in his excellent 2-piece serie. After reading these you are equipped with a powerfull tool to navigate through the online cholesterol/diet-heart denialism.

Diet-Heart: A Problematic Revisit,

http://www.healthylongevity.blogspot.fi/2013/01/diet-heart-problematic-revisit.html

Diet-Heart: Part II – Saturated Fat and Blood Cholesterol

http://www.healthylongevity.blogspot.fi/2013/01/diet-heart-problematic-revisit-part-ii.html

8 02 2013
Richard

I hate to break the field trip of anti-darwinist kooks like Minger, but, no the Syndey Diet-Heart trial does not vindicate butter. The secondary intervention that took 12-months was not too rigorous. TC cholesterol in the intervention arm was 243 vs. 266 in the controls. Here are some excellent pieces of critique:

“The authors state that the study assessed the effects of replacing saturated fat in the diet with omega 6 polyunsaturated fats, but it doesn’t.
The study used Miracle margarine as a source of polyunsaturated fat. In the 1960s, when this study began, Miracle margarine contained approximately 15% trans fatty acids, which have the worst effect on heart disease risk of any fat. The adverse effect of the intervention in this study was almost certainly due to the increase in trans fatty acids in the diet. Recent, well conducted studies indicate that replacing saturated fat with polyunsaturated fats lowers heart disease risk and this is widely accepted. Trans fatty acids were largely removed from Australian margarines in the mid-1990s when their adverse effects on heart health became apparent.”

–Bill Shrapnel

“This is a very small study with only 63 total deaths. The 5.8% difference between groups for total mortality represents a difference of 10 deaths between groups (p=0.051) computed from the % deaths which does not meet conventional statistical significance. Figure 1 though only shows a difference in 6 deaths between groups. Certainly there is no evidence of benefit but the evidence of harm is relatively weak. Although dismissed by the authors trans fats are likely to be responsible for the lack of benefit. The margarine would have contained at least 20% trans fatty acids and if the participants were eating 25g/day of margarine then they would be consuming 5g of trans which might represent about 2% of calories. From the Nurses Health study this could reduce heart disease by 40-50% which would almost completely remove the apparent increased risk from the N6 margarines. The more margarine eaten the greater the risk. The test margarine would have mostly supplanted butter rather than other margarines. The fall in total cholesterol seen not only reflects a fall in LDL cholesterol but also a trans induced fall in HDL cholesterol.

“The fact that an increase in PUFA in the control group (90% of which would have been N6) was not associated with harm suggests the findings in the intervention group are confounded by the trans fats.”

–Peter Clifton

http://www.smc.org.au/2013/02/round-up-dietary-fats-and-heart-disease-bmj-experts-respond/

Moreover, Peter Clifton replied to Ramsden and showed the flaws in his reasoning in a comment that applies more or less well to the new study or rather the interpretation of the old study as well:

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8376167

12 02 2013
Richard

The relationship of dietary cholesterol to serum lipids. From Daniel Steinbergs book:

,Serum cholesterol concentration is clearly increased by added
dietary cholesterol but the magnitude of predicted change is
modulated by baseline dietary cholesterol. The greatest response
is expected when baseline dietary cholesterol is near zero, while
little, if any, measurable change would be expected once baseline
dietary cholesterol was > 400-500 mg/d. People desiring maximal
reduction of serum cholesterol by dietary means may have
to reduce their dietary cholesterol to minimal levels (< 100-150
mg/d) to observe modest serum cholesterol reductions while
persons eating a diet relatively rich in cholesterol would be expected
to experience little change in serum cholesterol after adding
even large amounts of cholesterol to their diet. Despite modest
average effects of dietary cholesterol, there are some individuals
who are much more responsive (and others who are not responsive).
Individual degrees of response to dietary cholesterol
may be mediated by differences in cholesterol absorption efficiency,
neutral sterol excretion, conversion ofhepatic cholesterol
to bile acids, or modulation of HMG-CoA reductase or other
key enzymes involved in intracellular cholesterol economy, each
ultimately resulting in changes of plasma LDL cholesterol concentration
mediated primarily by up- or down-regulation of LDL

Denise Minger is anti-darwinist who thinks the lipid-theory is bogus, according to her logic:

a) Human is the only mammalian specimen on whole biosphere that immune to dyslipidemia, elevation of LDL cholesterol in particular

b) LD-lipoproteins are the only substance in human body that cannot cause harm in excess.

Free-ranging mammalians typically have their LDL cholesterol way under 80mg/dl.

15 02 2013
Richard

Brown & Goldstein:

How LDL receptors influence cholesterol and atherosclerosis.

“If the LDL receptor hypothesis is correct, the human receptor system is designed to function in the presence of an exceedingly low LDL levels. The kind of diet necessary to maintain such levels would be markedly different from the customary diet in Western industrial countries (and much more stringent than moderate low-cholesterol diets of the kind recommended by the American Heart Association). It would call for total elimination of dairy products as well as eggs, and severely limited intake of meat and saturated fats”.

18 02 2013
Richard

Creationist Minger thinks the lipid theory is unproven, not so fast.

31 03 2013
Evan

Do you realize you’ve made over 150 comments here, most of which are demeaning? So she doesn’t have a science degree. Do you not understand how science works? Plenty of credentialed experts have screwed up the science while nerdy amateurs have given us advances. Do you really think calling her a creationist and throwing out demeaning sexist names is going to convince anyone of anything other than the fact that you’re a mean-spirited person?

If I were to delve into the science, I may find you to be right or wrong. I don’t know. But as a rule of thumb, when witnessing an argument about a topic on which I lack expertise, I tend to think the sneering condescending one is coming from a position of weakness. After all, why talk this way if you’re coming from a position of confidence? You may be right, but you’re certainly not acting like it.

6 03 2013
Amber

Denise, I’m wondering if you have any advice for a former paleo/gaps girl that HAS to eat a more vegan low-histamine diet due to histamine intolerance. I try to incorporate a small amount of fish once a week and just grin and bear some mild histamine effects, but any more than that and I get chronic hives, debilitating migraines etc. I don’t beleive a totally vegan diet is healthy for me either and will try to incorporate some oysters once a week perhaps instead of the fish. Any suggestions?

20 01 2014
Sarah

Are you taking supplemental quercetin?

11 03 2013
Mattheworbit @ James and Matt

Thank you so much for this post, I’ve sent it to someone I care about a lot. I’m currently renegotiating my diet after 5 years as a vegan, but it’s so tough. Your advice is a great start to cover my bases while I begin figuring out where to go from here. And yep – epic Jack Norris love. I think he probably saves a lot of lives, and people’s health. So great to have an honest, unbiased vegan providing nutrition advice – sadly, a lot of the vegan “experts” spout just as much misleading crap as the meat and livestock industry-endorsed “experts”. In seeking to label ourselves and extremism, I think we often find – the best way is the middle path.

16 03 2013
Heretic

Even though everybody is entitled to his/her opinion, I cannot stand by observing this debate, without submitting my input.
The human race is cancerous to this planet’s well-being. Even if the vegan diet was the most unhealthy out there, it is the best choice, as we do not possess the divine right to massacre, torture, rape, confine, breed, castrate, molest, orphan other living things.
Denise, may I impregnate you artificially, lock you up for 9 months, take your infant post-birth, slaughter it immediately, so I may feast on fresh & tender meat, milk you, so I can eat cheese and then do that same thing all-over again until I realize that you aren’t providing as much dairy as you used to and your offspring isn’t as well-built as it was when you were yet fertile?This would lead me, the consumer, to the decision of having to put you down, so a new, younger female could take your place. I love cheese & meat, my body demands it. What can I do? I am simply powerless to my cravings! Let me eat meat! I love myself some tasty limbs to chew on. Delicious. I crave corpses, always have, always will.
Determination, there is no free will. Placebo’s triumph! Standardize standards. Your case, it’s implications, a beacon of truth in this herbal mayhem. Devil’s avatar, thirsty prophet. Amen

21 03 2013
Karly

I have heard it is okay to cook with macadamia nut oil. Am I wrong to believe this?

21 03 2013
What to tell those who claim being vegan is "heart healthy"? - Page 3 | Mark's Daily Apple Health and Fitness Forum page 3

[...] tell them you care about them and want to make sure their nutritional bases are covered. Point them here and hope they figure it out before they do irreparable damage to their health. Because veganism is [...]

26 03 2013
How My Primal Instincts Led Me to... Veganism - Page 34 | Mark's Daily Apple Health and Fitness Forum page 34

[...] you read some pro-vegan blogs or books or articles. Will you do me and yourself a favor and read one pro-vegan article written by someone who cares more about your wellness than your ideology? Reply With [...]

4 04 2013
Richard

Pedersen et al paper (2011), co-authored with 13 prestigious European nutrition scholars, deliver a massive blow against diet-heart denialism.

“..That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. in Finland. CHD was also almost non-existent in rural China when mean cholesterol levels were approximately 3·5 mmol/l (1350 mg/l), with total fat intakes only about 15% of energy and extremely low intakes of SFA(10,11). These observations, replicated in many other countries, should not be ignored even if meta-analyses of prospective cohort studies suggest no independent associations of SFA intake with CHD risk(2). The null results of the latter studies(2) probably reflect measurement error, residual confounding, over-adjustment by covariates on the causal pathway and large variations in plasma cholesterol compared to variations in intake of dietary fat(3,12 – 15).The role of SFA risks may also be overlooked, given the strong emphasis on TFA(16) and the incorrect proposition that the CHD epidemic in affluent societies has been primarily linked to a high consumption of TFA(17)”

Jeremiah Stamler pointed out in his response to the meta-analysis of Siri-Tarino et al (2010) that the RRs for the SFA – CHD link of the various sub-studies in the meta-analysis was highly depended on the quality of dietary assessment used. For example, it has been estimated that it requires 22 replication of 24-hour dietary recalls to asses the mean consumption of SFAs within 20% accuracy. Most studies in the S-T meta-analysis only used one dietary recall. In addition it is widely known that there’s substantial spontaneous intraindividual variation (5 to 10%) of serum cholesterol levels. Hegstedt & Nicolosi estimated that atleast 3 measurement is needed at the beginning of the survey. Because of inadequate number of dietary assessments and cholesterol measurements at the baseline, people were often classified into incorrect categories in older studies. These older studies often failed to find an association between SFA and serum cholesterol concentrations; thus null finding of SFAs to CHD was nothing but expected. Stamler showed that out of the 16 CHD studies used, 4 relied on one 24-h dietary recall which is considered invalid dietary assessment method these days; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Only five studies used the most modern dietary assessment methods available (dietary history or multiday food record) and the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids.

Vegans, stay away from saturated fat laden oils:

Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) Study

“Wall thickness was measured with B-mode ultrasound. After adjustment for age and energy intake, animal fat, saturated fat, monounsaturated fat, cholesterol, and Keys’ score were positively related to wall thickness, while vegetable fat and polyunsaturated fat were inversely related to wall thickness. These associations persisted after further adjustment for smoking and hypertension and were consistent across the four race and sex groups. Thus, elements of habitual dietary intake were consistently associated with carotid artery wall thickness, compatible with their putatively atherogenic and antiatherogenic properties”.

4 04 2013
Richard

It looks like that the link to article by Pedersen et al is currently not working (The Importance to Limit SFA consumption). Anyways, the article was response to the attempts to downplay the importance of SFA reduction as a public health measure by certain American scholars. The authors pointed out that a) elevated LDL cholesterol can initiate atherosclerosis in experimental models even in the absence of other risk markers and b) saturated fat with its peculiar carbon atom form is the most potent single substance to elevate LDL-C cholesterol. The authors also noted that the IMPACT-models by Simon Capewell and others are very important part of the evidence. The IMPACT -models have shown that the age-adjusted CHD mortality has declined 80% in Finland since the1960s, and +50% of this positive development in public health can be attributed to the decrease in mean cholesterol levels; decreased SFA consumption explains almost all the observed decrease in serum cholesterol levels in Finland. Similar observation in other parts of Europe.

In their re-response to diet-heart denialism, Pedersen et al noted that the HDL sales pitch (often used by Harvard professor Willett) ain’t goin’ nowhere anymore. While there are many biomarkers in the lipid-fraction that are associated with CHD, causal link has only been observed between LDL cholesterol and CHD.

“People with mutations that cause life-long elevated LDL levels have higher risks of CHD, but mutations that lower HDL levels do not cause such excess risk of CHD(4). Moreover, randomised trials of statins have demonstrated that substantial reductions in LDL of about 2 mmol/l are associated with about a halving in the risk of CHD and ischaemic stroke(5). Other drugs and surgical intervention to lower LDL also reduce the incidence of CHD. In contrast, recent trials of drugs that raise HDL failed to reduce the risk of atherosclerosis and CHD(6) and a recent metaanalysis of 108 randomised lipid-lowering trials could not document that altering HDL-cholesterol by drugs or diet influences the risk of CHD(7). Several other ongoing large-scale trials are currently assessing whether raising HDL will reduce the risk of CHD and ischaemic stroke. Pending the results from these ongoing HDL-raising trials, the available evidence is still consistent with HDL levels being a marker of CHD rather than being causally related to CHD. Although the drug intervention trials do not, of course, provide a definitive answer on the impact of lifestyles, including diet, on HDL metabolism and the risk of atherosclerotic vascular diseases known to associate with low HDL levels, they currently do not provide strong support for interventions to raise HDL. Consequently, the primary target for risk reduction by dietary fat should still be LDL- or total cholesterol(7), thus reinforcing the overwhelming importance of reducing the intakes of SFA. PUFA might be a preferred replacement for SFA because it lowers LDL more and has less of an effect on HDL than carbohydrate”.

4 04 2013
Richard

1) The importance of reducing SFA to limit CHD

2) Response to Hoenselaar from Pedersen et al.

10 04 2013
Some long overdue book reviews - discountBlogs

[...] than be inclusive and understanding with our vegetarian/vegan friends, like Denise Minger7 is, he uses study after study to tell you why vegetarianism/veganism is wrong and how many ways [...]

12 04 2013
Richard

Denise Minger is a de facto creationist who thinks the lipid-theory is flat out bogus. I am afraid, she has managed to overlook a hundred years of experimental research.

A great peer-reviewed response article was recently published in the journal of Lipids in Health and Disease by a young vascular biochemist and a PhD. student. It was a response to a Dutch supplement merchant and his alternative hypothesis. The key points of response article are:

1) There seems to be several factors besides oxygen radicals that contribute to the oxidation of LDL such as enzymatic reactions

2) It has been demonstrated that macrophages are able to take up LDL particles even in their unmodified form

3) If apoB protein is modified so that it doesn’t bind to artery wall, even a marked increase in LDL-C does not promote significant atherogenesis.

In nuthshell, experimental atherosclerosis can be induced by using various pathways, exogenous LDL infusions, hypercholesterolemic diet and/or genetic modifications.

I’ve already expressed my wish to see Denise having LDL cholesterol injected directly into her veins. I would certainly not have problems with glucose injections, especially after a hard work-out, for experimental purposes. Denise should walk the walk.

13 04 2013
ZM

The only creationist here is you Richard. You display a similar lack of critical thought. You also seem paranoid with your incessant posting of BS.

Quickly:

His first few references (2-5) are basically speculation as to what initiates atherosclerosis.

Reference (6) is a Merck meta-analysis which includes Statin, Diet and other interventions which are confounded by pleiotropic effects and the multi-interventional nature of some of the trials yet they attribute the benefits to “cholesterol reduction”. Similar can be said of Reference (7) which also includes an interesting conflict of interest statement.

Nothing needs to be said of Reference (8): “Campbell TC, Parpia B, Chen J:Diet, lifestyle, and the etiology of coronary artery disease: the Cornell China study”

Reference (9) is compatible with the oxidative hypothesis.

14 04 2013
Richard

@ZM,

The studies you and I referred were based on mechanical models, there was nothing speculative in them, everyone can replicate the findings themselves. Why do you think nothin’ needs to say about the China Study? China study showed the rural Chinese had once their TC cholesterol less than 130mg/dl and that they were practically immune to heart disease. This is exactly what is expected based on global epidemiology and statin trials. This is very powerfull evidence.

The large meta-analysisl of LDL reduction by Gould et al is essentially an update of the prior meta-analysis (1998) which was co-authored with Curt Furberg who happens to be a reknown critic of the medical industry. So, I don’t think your Merck notions bears much of a significance unless your attempt is to confuse the reader.

The benefits of statins happens to accrue in a ridiculously linear relationship with the amount of LDL being lowered, reinforcing the fact that the main mechanisn by which statins work is their ability to lower LDL cholesterol. The benefits of LDL reduction are independent of mechanism used, anything that lower LDL (without having negative effects of reverse cholesterol transfer) seem to work: bypass of the intestine, statins, bile-acid sequestrants, genes, diet, etc.

I leave you with one of the top-snotch atherosclerosis expert in world, Evan Stein who is currently conducting studies with a new LDL lowering drug, REGN727 which targets PSCK9 (as opposed to statins that are HMG-CoA reductase inhibitors).

Prevention of heart disease: is LDL reduction the outcome of choice? Absolutely yes.

There is only one well-established relationship between blood cholesterol lipid fractions and coronary artery disease (CAD) that meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fractions, only LDL cholesterol satisfies these criteria.

Low-density lipoprotein cholesterol reduction and prevention of cardiovascular disease

“There was little question after the first major statin trials that the reduction in CVD was related to lipid lowering and was totally consistent and supportive of the lipid hypothesis. However, stimulated by funding from the pharmaceutical industry, in which competition was fierce for market share and was driven mainly by the efficacy of lowering LDL-C levels, manufacturers of less-effective agents for lowering LDL-C levels helped propagate “beyond LDL-C” theories; these theories were that statins reduced CVD events by means other than lipid reduction, often termed pleotropic effects, usually shown in in vitro laboratory studies or small, poorly standardized surrogate marker trials. This belief culminated in an RCT by a pharmaceutical company that was designed to show that more LDL-C reduction with a competitor’s statin achieved no greater benefit.13 However, the results of that study clearly and convincingly showed otherwise, with additional reduction in CVD events with the drug that lowered LDL-C levels more. Even with this evidence, and perhaps with an even more powerful statin about to be approved, the investigators suggested that the reduced events were due to pleotropic effects of the more efficacious statin. However, the trial was soon followed up with results from another head-to-head RCT, with the same drug at different LDL-C lowering doses,14 which eliminated the pleotropic potential and rein-forced that lower is better”

16 04 2013
ZM

Richard, it’s called hypothesis generating data. They were not studies done on humans. I have nothing against it as it is an important part of science but it has to be realized for what it is.

In case you didn’t realize you are commenting on a site that has that has thoroughly examined the China Study which is essentially a poor observational study.

Given the dubious activities of the pharmaceutical industry and given that studies funded by a pharmaceutical companies are more likely to give favorable results I have every right to be skeptical. Furthermore that wasn’t my main criticism. Just something to keep in mind. Richard, you and creationists share yet another quality – gullibility.

As for Stein’s review. It’s more rubbish. No one, and I mean no one knows how much the pleiotropic effects of stains are responsible for its benefits. They usually base this around other non-statin trials that supposedly showed benefits independent of pleiotropic effects. There is one massive problem with this. These non-statin drugs or procedures (eg. cholestyramine or partial ileal bypass) do have pleiotropic effects just not as extensive as statins and are in fact consistent with the oxidative hypothesis.

Keizer supplied plenty of evidence for his hypothesis most of which was ignored by Ohukain.

13 04 2013
Why I’m no longer Vegan: Hardcore Vegan to Primal Paleo | Primal Nutritionist

[...] Denise Minger: http://rawfoodsos.com/for-vegans/ [...]

15 04 2013
Richard

Denise Minger had the golden opportunity to bust the myth around Ancel Keys but unfortunately she did not use her chance. In order to demonstrate the futility of diet-heart denialism (Stephan Guyenet, Taubes, etc), I’ll bring in few key themes which are crucial for understanding the diet-heart history.

1) Interindividual varition; individual differences in the response to the dose

The differences in fat intake are usually minor in homogeneous cultures. However, the cholesterol levels in every population follows a normal distribution: a same diet will lead to wide variety of cholesterol levels between individuals, even though everything else is kept constant. If the differences in the fat intake are small in a given population, it cannot explain the large differences in serum cholesterol levels in a model. Jacobs et al showed mathematically that null association is expected between diet and serum cholesterol levels in cross-sectional population studies (even when there exist cause and effect): despite the null associations in such studies, the intake of saturated fats is one of primary determinants of serum cholesterol levels of an individual (Pedersen et al 2011).

2) Intraindividual variation (regression dilution bias); spontaneous variation within individual

”Similar lack of attention to intraindividual variability is frequent in surveys and epidemiological studies and leads to error, controversy, and waste of time and money.” (Keys, 1988)

For a long time, Keys held an intellectual monopoly over this theme. In the past, the researchers didn’t properly understood that there’s a substantial, spontaneous day-to-day (5 to 10%) variation of cholesterol levels within individual, even though the diet is held constant. Hegstedt & Nicolosi (1987) showed that it takes at least 3 blood cholesterol measurement at the baseline of the survey in order to reliable assess the serum cholesterol level of an individual. In addition, twenty-two randomly collected 24-h dietary recalls are required to estimate the true individual mean intake of saturated fat within ±20 %, while most studies have only one recall or a food frequency measure of saturated fat intake available (Kromhout et al). In older studies, participants were often misclassified in wrong categories of both SFA intake and serum cholesterol levels because of inadequate emphasis on intraindividual variation. In other words, an inadequate number of cholesterol measurements and dietary recalls were performed for the participants at the baseline of the survey. This resulted often in null associations of both diet and serum cholesterol levels and eventually between diet and the risk of CHD.

The Seven Countries Study

When Keys (1988) decided to analyze the participants of the large Israel Ischemic Heart Disease study in the form of small groups based on place of birth, he found a strong correlation between the intake of saturated fat and serum cholesterol levels. This association did not exist when the participants were analyzed as an individual basis. This was the whole point of the 7CS. Information is always lost when using medians, However, by using and comparing medians, the researchers can effectively eliminate the effect of spontaneous variation within individuals (part 2) and the large individual differences in dose-response and the statistical fallacy brought by such large differences between individuals (part 1). Keys understood these two key concepts of diet-heart research already in the late 1950′s. He was several decades ahead the curve. The differences in the intake of saturated fat explained 89% of variation in the serum cholesterol levels between the 16 different cohorts used in the 7CS. The differences in the intake of SFAs was large, from 3% (of calories) to 22% (of calories). The lowest mean serum cholesterol levels at the baseline was measured in one of the Japanese cohorts (3,7mmol/l, 143mg/dl) and the highest in one of the Finnish cohorts (6,7mmol/, 262mg/dl). These ecologic correlations described the real world in much greater accuracy than did the poorly conducted population studies from homogeneous cultures. The ecologic correlations between diet and serum cholesterol levels were similar to the results of tightly controlled metabolic-ward feeding trials. Neo-diet-heart denialists such as Guyenet and Taubes attempt to confuse the reader by showing a cascade of old cross-sectional and prospective cohorts in order to demonstrate that the intake of SFAs do not affect the risk of CHD: The poor audience is left out with an impression that the science is a democracy where every study bears an equal value*

*Bonus

It has been pointed out that regression dilution bias dilutes the real association of serum cholesterol concentration and the risk of CHD in several large-scale prospective population studies such as the Framingham and Whitehall. Moreover, the infamous meta-analysis by Siri-Tarino et al used mostly outdated sub-studies that did not pay adequate attention to regression dilution bias and/or were adjusted for serum cholesterol levels (see Stamler 2010; Katan et al 2011; Scarborough 2010; Kromhout et al 2011 and Pedersen et al 2011). Modern forward-looking studies, with sophisticated dietary recall technology, paying careful attention to intraindividual variation, such as the Health Professional’s Follow-up found that saturated fat intake was associated with a statistically significant 72% increased risk of fatal coronary heart disease for high compared to low intake (after maximum adjustment).

16 04 2013
ZM

You have to be really, really, really, really desperate to cite the The Health Professionals as evidence against saturated fat. After maximum adjustment there was no association with Total MI (in fact it found a non-significant reduced risk) . For fatal CHD there was no significant association in any of the quintiles excepting the highest which was barely significant. Furthermore the trend for fatal CHD was non-significant. The associations with cholesterol wasn’t significant either. Yep this is the (observational) study Richard would have you believe shows the harm of saturated fat.

Stamler, Katan and friends can complain all they want but the bottom line is that none of them have yet to provide any convincing evidence that there is even an ASSOCIATION between saturated fat and CHD. Complaining about things like “Regress Dilution Bias” and “Interindividual varition” does not change that.

17 04 2013
Richard

@ZM,

Richard, it’s called hypothesis generating data. They were not studies done on humans

1) Well, yes. Our biomedical research paradigm relies on the darwinian foundation. Experimental models allow the study of cause & effect. Creationists and their lipid-theory denying brethren have a huge problem with this. How do you think the oxLDL hypothesis was generated? Experimental atherosclerosis can be induced in every specimen on the face of this planet simply by keeping their LDL cholesterol elevated. This on the other hand can be done by feeding dietary cholesterol and saturated fat, manipulating cholesterol metabolism (genetics), using surgery or by using exogenous LDL injections.

it’s about totality of evidence, I addressed the problems of saturated through multiple lines of evidence, ultrasound measurements (artery wall), epidemiology, biological mechanism (SFAs interact with the LDL receptors). Health Professional’s follow-up is just a one piece of evidence. The marginals of SFA intake were very modest between the quintiles. The intake of SFA in the lowest fifth of Health Professionals study was 3g more (per day) than the intake of SFAs in the highest range of consumption (quartile) in rural Japan in the 1970′s.

2) You are wrong in your conclusions with Stamler. Jeremiah Stamler pointed out in his response to the meta-analysis of Siri-Tarino et al (2010) that the RRs for the SFA – CHD link of the various sub-studies in the meta-analysis was highly depended on the quality of dietary assessment used. Stamler showed that out of the 16 CHD studies used, 4 relied on one 24-h dietary recall which is considered invalid dietary assessment method these days; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Only five studies used the most modern dietary assessment methods available (dietary history or multiday food record) and the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids. Moreover, Stamler reported that saturated fat increased the risk of fatal heart end poin by 32% despite the regression dilution bias, over-adjustment for lipids, and sick-quitter effect.

3) The idea that China Study is debunked is as ridiculous as the idea that Ancel Keys cherry-picked countries for the 7CS:

4) What were the pleitrophic effects on the surgery trial that used bypass of the intestine to lower LDL-C levels and thus the risk of CHD?

A meta-analysis of 19 studies (81,859 participants in all) that lowered LDL and measured clinical disease or death, including 5 diet trials, 3 bile sequestrant trials, 1 surgery trial and 10 statin trials concluded that: “The pleiotropic effects [effects apparently unrelated to lowering LDL] of statins do not seem to contribute an additional cardiovascular risk reduction benefit beyond that expected from the degree of LDL-C lowering observed in other trials that primarily lowered LDL-C.”

Robinson JG, Smith B, Maheshwari N, Schrott H. Pleiotropic effects of statins: benefit beyond cholesterol reduction? A meta-regression analysis. J Am Coll Cardiol. 2005 Nov 15;46(10):1855-62.

5) Since you do not like observational studies, I’ll leave you with Brown & Goldstein and the Inuits.

“The molecular basis for the effects of dietary saturated fat on plasma LDL cholesterol levels is well understood. Saturated fat influences the LDL receptor activity of liver cells as described by Brown and Goldstein, dietary saturated fat suppresses messanger RNA synthesis for the LDL receptor. This decreases hepatic LDL receptor activity and slows the removal of LDL from the blood, thus increasing the concentration of LDL cholesterol in the blood. Dietary cholesterol augments the effects of saturated fat further suppressing the hepatic LDL receptor activity and raising the plasma LDL cholesterol levels”.

–Heart Disease, Environment, Stress and Gender [proceedings of the NATO Advanced Research Workshop on Increase in Coronary Heart Disease in Central and Western Europe: Stress and Gender Related Factors, 20-24 May, 2000, Budapest, Hungary]

Consumption of omega-3 fatty acids is not associated with a reduction in carotid atherosclerosis: the Genetics of Coronary Artery Disease in Alaska Natives study

“Dietary intake of omega-3 FAs in a moderate-to-high range does not appear to be associated with reduced plaque, but is negatively associated with IMT. The presence and extent of carotid atherosclerosis among Eskimos is higher with increasing consumption of saturated FAs”

http://www.ncbi.nlm.nih.gov/pubmed/18054937

17 04 2013
ZM

Wrong. Experimental models help to generate HYPOTHESES about cause and effect. Even many types studies done on humans are hypothesis generating. The oxidative hypothesis is just a much better hypothesis looking at the totality of evidence.

The Health Professional’s follow-up is a piece of evidence? To call a study that overall was not supportive as “evidence” is bizarre. I urge the reader to look at Table 2 – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2351515/pdf/bmj00550-0026.pdf

No I’m right about Stamler. Stamler states -

“Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies” and “Only five studies used the most modern dietary assessment methods available (dietary history or multiday food record) and the RR was >1.00 in all 5 studies”

So what. 4 of the FFQ studies were less than 1 and most importantly 5 out of the 7 were not significant.
For the 7-d diet records Fehily et al (which had no adjustments at all) was nowhere near statistical significance. Jakobsen et al found a pathetic RR of 1.03 and was nowhere near statistical significance. Following the pattern Tucker et al was nowhere near statistical significance. Siri-Tiriano dealt with this with a “quality score”. they also dealt with the cholesterol over-adjustment issue in a secondary analysis. Stamler criticizes the dietary recall methods without realizing that these same criticisms apply to every study that claims to support the diet heart hypothesis.

You ask “What were the pleitrophic effects on the surgery trial that used bypass of the intestine to lower LDL-C levels and thus the risk of CHD”

I assume you are reffering to the POSCH study.

http://www.medscape.com/viewarticle/564952_2 -
“partial ileal bypass resulted in a 60% reduction in cholesterol absorption; an increase of 380% in the fecal sterols, both in the neutral sterols and in the bile acid fraction; a 450% increase in cholesterol synthesis; a 300% increase in cholesterol turnover and a 35% reduction in the body cholesterol pools, including the slowly miscible pool, which contains the arterial wall”

This is consistent with the oxidative hypothesis. Also according to the author (http://jrnlappliedresearch.com/articles/Vol3Iss2/Buchwald.htm) – ” In addition, the intervention group at 5 years had significantly lower body weights and significantly lower systolic and diastolic BP”. Also it seems that there was no attempt to measure any dietary or lifestyle changes after the surgery.

“5 diet trials, 3 bile sequestrant trials, 1 surgery trial and 10 statin trials”

This includes trials I’ve already discussed.

18 04 2013
Richard

@ZM,

1) What you refer as pleitrophic effect is simple what is followed after reduction of LDL cholesterol itself. Once LDL cholesterol is lowered the inflammation is also normalized. If statins would work through other than their lipid lowering mechanism, one should explain the linear relationship between the LDL-C being lowered and the risk of CHD being reduced.

2)The very fundamental reason why mechanic animal models are being performed is because they allow the test of cause & effect. It’s about principles, not about hypothesis. Read the story about PSCK9 published in nature. The exact principles established in a mice worked identically in humans. http://www.nature.com/news/genetics-a-gene-of-rare-effect-1.12773

You probably confuse this issue with dietary experiments with animals.

3) Siri-Tarino et al never addressed anything else except the question of over-adjustment for lipids. There were two kind of studies in the meta-analysis in regards to cholesterol:

a) Studies that were adjusted for lipids
b) Studies that had no information about lipids

Scarborough et al pointed out the meta-analysis had lot studies of the part a). Siri-Tarino et al responded by reporting the results in regards to only to part b) kind of studies.

4) “… these same criticisms apply to every study that claims to support the diet heart hypothesis.

This is absolute rubbish. The 7CS for example avoided the issue altogether (intraindividual variation) because of the use of medians.

In regards to regression dilution bias, Kromhout et al made nice notions in their rebuttal of the Siri-Tarino paper:

“Parallel to the lack of association between saturated fat intake and CHD risk, as shown in the meta-analysis, is the lack of association between dietary saturated fat and serum cholesterol in cross-sectional analyses of the Framingham, Tecumseh and Zutphen studies(6-8). Keys(9) explained the lack of an association between dietary saturated fat and serum cholesterol in cross-sectional studies by the large day-to-day variation within individuals in both saturated fat intake and serum cholesterol. He showed that the intra-individual variance of the SFA palmitic acid was more than twice as large as the inter-individual variance, based on two measurements. He also found that in healthy adults on an ostensibly constant diet, the average intra-individual standard deviation of serum cholesterol was approximately 200 mg/l (20 mg/dl), about half the total standard deviation(9)”.

If the within-person variation is larger than the between-person variation, which is common in homogenous populations where everyone consumes a similar diet, then this will especially bias the findings towards a null association. For example, in a homogenous population with a between-person variation of between 2 to 6 eggs per week on average, the variation of intake of an individual consuming on average 4 eggs per week maybe between 1 to 7 eggs per week. If this person’s diet is measured at a high or low point they will be misclassified into a high or low range of intake, typically biasing the results towards a null association.

Another concern is related to the fact that observational studies addressing the association between diet and blood cholesterol and cardiovascular disease dating back to at least the early 1950s have been complicated by reverse causation. It is well documented that people will lower intake of cholesterol and saturated fat in response to elevated blood cholesterol. This is known to bias studies towards finding an association between a higher intake of cholesterol and saturated fat and lower blood cholesterol levels. This would also likely similarly bias the results for the association between intake of cholesterol and saturated fat and the risk of cardiovascular disease.

Let the co-author of Siri-Tarino meta-analysis, professor Frank Hu (2012) have a word:

“Why is red meat harmful? ‘Saturated fat, which can lead to cardiovascular disease, is really just the beginning of the story,’ explains Hu”

Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) Study

“Wall thickness was measured with B-mode ultrasound. After adjustment for age and energy intake, animal fat, saturated fat, monounsaturated fat, cholesterol, and Keys’ score were positively related to wall thickness, while vegetable fat and polyunsaturated fat were inversely related to wall thickness. These associations persisted after further adjustment for smoking and hypertension and were consistent across the four race and sex groups. Thus, elements of habitual dietary intake were consistently associated with carotid artery wall thickness, compatible with their putatively atherogenic and antiatherogenic properties”

18 04 2013
Richard

The Health Professional’s follow-up is a piece of evidence? To call a study that overall was not supportive as “evidence” is bizarre.

Not bizarre at all. A global perspective might help you out with your interpretation of the data. Consider the following:

A Group with very high saturated fat consumption at the baseline is compared to a group with even higher saturated fat consumption.The risk of fatal heart event is increased by 72% in the with even higher intake. As said, the rural Japanese in the 1970s had lower intake of SFA in the highest category of consumption compared to the intake of SFA in the lowest category of Health-Professionals follow-up.

oxLDL is a mess at this point. See PlantPositive’s video “PUFAs oxidize”, he refers to, among other, to Heinecke who is top-snotch cholesterol researcher working at the same institution with Stephan Guyenet. Maybe you should post Guyenet about it. He should be updated with these issues. Also, read one more time the post by Ohukainen who is an atherosclerosis researcher.

I’l quote Daniel Steinberg:

Passwater: Is it accurate to say that only oxidized-LDL starts the plaque process?

Steinberg: No, it seems to me very likely that other modified forms of LDL are involved in plaque formation. What we know so far is that the use of antioxidants can decrease the rate of progression of lesions by 50-80%. That would speak to a major involvement of oxidation, but other things can also lead to foam cell formation. Studies by Dr. John C. Khoo in my laboratory have shown that aggregation of LDL with itself markedly increases the rate of uptake by macrophages. [15] The uptake in that case occurs by way of the native LDL receptor, not the acetyl LDL receptor or oxidized LDL receptor.

Studies by Drs. J. S. Frank and A. M. Fogelman at UCLA have demonstrated the generation LDL aggregates in the subendothelial space. [16] Aggregation does not depend upon prior oxidative modification. So here is a quite distinct mechanism by which LDL uptake into the macrophages can be accelerated and can perhaps initiate the fatty streak lesion.

Studies by Dr. Joseph L. Witztum and others in our laboratory have shown that minor modifications in the structure of LDL can render it immunogenic. Autoantibodies against oxidized LDL have been demonstrated in rabbits and in humans as well. Therefore, a complex of a modified LDL particle and an antibody against it can be taken up into macrophages by way of a completely different receptor, the receptor for immunoglobulins (the FC receptor).

So, there are at least two or three alternative modifications of LDL that could account for foam cell formation. These have not yet been studied in vivo as intensively as oxidative modification, and so we are not in a position to say with any confidence how important they may be.

http://www.healthy.net/scr/interview.aspx?Id=197

18 04 2013
ZM

I’ve spent enough time responding to your nonsense. At this point I’d much rather spend my time elsewhere than arguing with a troll who enjoys spamming the board and whose arguments consist of logical fallacies and poor scientific
standards.

18 04 2013
ZM

“What you refer as pleitrophic effect is simple what is followed after reduction of LDL cholesterol itself”

Having lower LDL CAN reduce oxidation. However it’s a very poor method. Having lower LDL does not necessarily mean lower oxidation.

“one should explain the linear relationship between the LDL-C being lowered and the risk of CHD being reduced”

Repeat one thousand times every night before you go to bed – Correlation does not imply causation. Furthermore there are numerous studies which contradict that idea.

“The very fundamental reason why mechanic animal models are being performed is because they allow the test of cause & effect”

and there is a reason why Randomized Contolled Trials are the highest form of evidence and non-human studies of any kind are at the bottom. This is not controversial. Only vegans seem to be confused by it.

“Read the story about PSCK9 published in nature.”

Again, it’s consistent with the oxidative hypothesis.

“The 7CS for example avoided the issue altogether ”

Huh, I never mentioned the 7CS study once.

As for saturated fat, it’s quite amusing seeing Scarborough, Katan and friends criticizing observational studies. Talk about a double standard. Every single observational study has legitimate criticisms against it.

Repeat this one thousand times before you go to bed – Pointing out weaknesses in studies with saturated fat is not equal to providing evidence against saturated fat.

“Dietary fat intake and carotid artery wall thickness: the Atherosclerosis Risk in Communities (ARIC) Study”

Waiting for Stamler and friends debunking of this observational study. Should be fun.

18 04 2013
Richard

@ZM

1) You enunciate that all observation studies are of equal value.

2) The linear relationship between statin induced LDL reduction and plummeting risk of CHD has been established in multiple randomized, double blinded trials. The results are consistent with the findings of Mendelian randomized controlled trials with +300 000 genotypes. People with inherited mutation that cause life-long exposure to low LDL are protected from CHD by reduction of risk of the magnitude of 55% per each 1mmol/l lower LDL. Each of the studied nine mutations lower LDL with mechanism of its own, but the end result is identical which refutes the idea of pleitrophy. LDL cholesterol is the direct causal factor influencing CHD, LDL is “the master switch” to CHD, strokes, premature death and aggressive fatal prostate cancer.

3) RCT’s are for drugs. They are not for chronic disease prevention, We are dealing with diseases that take decades to manifest themselves. We don’t have a single RCT that would prove that smoking or asbestos exposure is harmful. With smoking we have rely on evidence from metabolic ward, pathofysiology and epidemiology. The same applies pretty much to SFA.

As already concluded, it has been demonstrated in experimental models without a reason of doubt that that macrophages are able to take up LDL particles even in their unmodified form. Creationist should not put their heart on the oxLDL story only.

4) “Correlation does not imply causation”.

^The favourite line of creationist low-carbers. What Gary Taubes did not tell you is that scientist are bound to the rules of logic, whenever there is strong, consistent association that is biologically valid and supported by experimental evidence, we should not overlook it. By overlooking such correlation may result in a missed opportunity for long-term health.

18 04 2013
ZM

Blah blah blah

“bound to the rules of logic”

Coming from someone who is illogical and denying a basic statistical principle.

“RCT’s are for drugs”

No. RCT’s are based on simple inductive reasoning principles. It applies to anything.

“smoking or asbestos”

Comparing smoking or asbestos to Saturated Fat is one of the most idiotic comparisons. It takes an airhead like yourself to do something like that.

19 04 2013
Richard

RCT’s were designed for drug context. To have bunch of fat & sick people randomized for a short-term trial and have them do what they after they’ve been handed out manuals for a diet. These studies are not well controlled and usually lack adequate counselling. These kind of diet trials just create confusion. They provide very little information for long-term life-style factors that have a potential to reduce the risk of chronic disease.

LDL cholesterol is probably a causal factor for fatal prostate cancer, meaning that elevated cholesterol increases the risk for dying in prostate cancer and decreasing cholesterol levels reduce the risk of prostate cancer.

“Considerable evidence supports the plausibility of an association between low cholesterol and reduced risk of high-grade prostate cancer. Several studies have reported an association between statin use and reduced risk of advanced or high-grade prostate cancer (15, 16). In addition, an inhibitory effect of low cholesterol on prostate cancer progression is biologically plausible. Laboratory evidence suggests that lowering cholesterol levels could inhibit cell-signaling pathways that are important for prostate cancer progression (17). This hypothesis is supported by experiments in mice in which lowering serum cholesterol with dietary modification or a cholesterol-lowering drug reduced the cholesterol content, size, and vascularity of human xenograft prostate tumors (18)”

http://cebp.aacrjournals.org/content/18/11/2805.full.

19 04 2013
ZM

Let’s recap Richard’s illogical position on science –

He thinks that “Correlation does not imply causation” is a phrase of Gary Taubes when in fact it’s a basic statistical principle (known way before Taubes was even born) used in science all the time and is logically solid.

He thinks that non-human “experimental models” provides proof of cause and effect in humans.

He thinks “RCT’s were designed for drugs” when in fact the principles that experiments and by extension RCT’s are based on was formally set out in the 1800′s. Later Fisher made experiments on humans possible with his concept of randomization.

He thinks Diet RCT trials are “not well controlled” and “creates confusion” but has no problem with observational studies like “The China Study” and the “7CS” which are rife with confounding and bias and creates the most confusion.

He uses an absurd analogy to
compare smoking to saturated fat (two completely different
substances) when in fact there isn’t
convincing evidence of even an
association between saturated fat and has not even come close to
satisfying Hill’s criteria.

Science denial at it’s finest.

15 04 2013
Richard

Minger,

I screwed it up with the HTML-codes, that’s why the 3 posts in a row. Please, delete the first two and spare the last one with codes intact.

Best,

Richard

20 04 2013
Richard

@ZM

let me clarify myself. Diet RCT’s are usually not very well controlled compared to let say studies done in metabolic ward. For example, the participants in the WHI-trial received 20 min personal counselling. It’s easier to ask fat & sick people to take a pill or a placebo than to ask them to do profound changes in their life-style. What did the new PREDIMED trial proved?

“Correlation is not causation” is much basic concept that is so ridiculous to point about it. Denialists such as Denise Minger misuse this phrase in order to create confusion among the lay people. Consistent and strong correlations such as that with elevated cholesterol and prostate cancer seen in epidemiology probably are causally related (see Bradford-Hill) since they are biologically plausible and easily backed with experimental evidence.

I compared smoking to SFA in the sense we can never perform perfect RCT to demonstrate the harmful effects of these substances to long-term health. And, that is just fine. We don’t need that kind of evidence.

The 7CS was the last diet-heart study that was able to study people who were not trying to alter their risk markers (sick-quitter effect, statin usage, etc). It’s well known from the tobacco epidemiology that those who are in the highest risk of dying are the ones who are the first to make drastic changes in their lifestyles, such as quitting smoking thus biasing the association of tobacco smoking to cancer mortality towards the null. It’s also widely known that people with elevated cholesterol and thus at high risk of stroke and CHD are the ones who cut back on SFAs and dietary cholesterol. The 7CS done in pre-statin era (also pre-McDonald’s era) when people had no idea of risk markers was much less distorted by potential confounders compared to more recent studies on diet heart.

BTW, I have great paper for you. This is what Keys and Stamler did for a living. in case you are going to say something contrarian to the prevailing diet-heart theory, I suggest you start with educating yourself with PhD level medical statistics.

“Statistical methods to asses and minimize the role of intraindividual variability in obscuring the relationship between dietary lipids and serum cholesterol” (J Chron Dis Vol 31 1978)

20 04 2013
ZM

Richard, you are basically sinking yourself.

“Correlation is not causation”

That is not the phrase. It’s “Correlation DOES NOT IMPLY causation”. Do you know what “does not imply” means Richard? the fact that some people misuse or misunderstand it does not make it any less valid. The phrase has nothing to do with Denise Minger or Gary Taubes.

“I compared smoking to SFA in the sense we can never perform perfect RCT to demonstrate the harmful effects of these substances to long-term health.”

Richard I know exactly what you are doing. You are trying to create a sort of guilt by association. Since smoking is seen in such a negative light you compare it to saturated fat to suggest that saturated fat shares similar negative qualities. If the evidence against saturated fat is so strong it should stand on its own merits and you would have no need to even make such an absurd comparison.

“This is what Keys and Stamler did for a living”

Maybe you should call Stamler and tell him that while statistical analyses are important they cannot compensate for poor study designs.

16 04 2013
Richard

After few years, low-carb dieters are getting injection leading to dramatic reductions to their elevated cholesterol.

“You’re not supposed to be so healthy!’.”

“It wasn’t just that her LDL cholesterol measured 14. As a person with two dysfunctional copies of the gene — including a new type of mutation — Tracy was effectively a human version of a knockout mouse. The gene had been functionally erased from her genome, and PCSK9 was undetectable in her blood without any obvious untoward effects. The genomics community might have been a little slow to understand the significance, Hobbs says, “but the pharmaceutical companies got it right away”.

““My first reaction was, ‘This must be wrong. How could that be?’And then it hit me — these people had low LDL from the day they were born, and that makes all the difference.” Steinberg argues that cardiologists “should get off our bums” and reach a consensus about beginning people on cholesterol-lowering therapy in their early thirties”.

http://www.nature.com/news/genetics-a-gene-of-rare-effect-1.12773

21 04 2013
Richard

Ellsworth Wareham; 98-year old vegan. Heart surgeon who operated still at the age of 95. Has been vegan over half of his life. He is very acquainted with the science and stresses the importance of very low cholesterol levels (under 140). His own digits have been around 117.

30 05 2013
Antiqua Tours (@AntiquaTours)

this guy is great!

22 04 2013
Vegan | Mark's Daily Apple Health and Fitness Forum page

[...] Minger dealt with this pretty thoroughly For Vegans | Raw Food SOS Reply With [...]

24 04 2013
Primal Vegetarian/Vegan ? | Mark's Daily Apple Health and Fitness Forum page

[...] convince him to add animal products to his diet, here are some primal nutrition tips for vegans: For Vegans | Raw Food SOS Reply With [...]

27 04 2013
On estic ara mateix pel que fa a tendències nutricionals? La Paleo Dieta | Diari de l'Albert

[...] naturalment, podria donar per un altre post – veure aquest genial de na Denisse a RAW Food SOS, crec que és [...]

6 05 2013
Filipe Castro

Hello, how do you eat “raw-eggs”? Mono-meal? Combined with something? Thanks a lot! Nice page!

11 05 2013
Jeff Puhek

Try to understand the whole blog….do you notice a hint in the name of the blog? “Raw Food SOS” – Denise once WAS a raw food vegan, but that doesn’t mean that she advocates eating all food raw. Some eggs are OK to eat raw, but I (personally) find it too unappealing. Humans, some anthropologists theorize, made their biggest advancements in evolution when they began cooking, which releases some nutrients that were not bio-available in the raw state. Not to mention the benefits of destroying micro-parasites by cooking food…..

21 05 2013
vegetarian | Mark's Daily Apple Health and Fitness Forum page

[…] thing ever written for insistent vegetarians: For Vegans | Raw Food SOS I know you didn't say vegan, but it applies to you. Please read it. It doesn't say "Hey, stop […]

30 05 2013
Antiqua Tours (@AntiquaTours)

Thank you so much for this post. I am a vegan for ethical reasons, mostly my deep love of animals ( i live with 11 rescue animals). i felt a lot of improvement in my health after giving up dairy (esp anything from a cow)because I have Crohn’s disease d have only 1/3 of my large intestine in tact. In terms of digestion, eating a low fat low protein diet has been great for me, but after 4 years, I realize that I need more, because I feel very tired lately. I have started fermenting my own veggies and kombucha and have already started feeling better. I am very interested in VIT D. Coming from San Diego it has never been an issue, even with this diet, but now I live in Italy. It is usually sunny here nd I am outdoors with my job so it has never been an issue either, but this year…the spring never arrives. It has been the cloudiest spring in 200+ years and we are all feeling it, myself as a vegan and my meat eating friends. Anyway, I think it is possible to live weel as a vegan as long as you eat real food, though i do admit that even when I ate meat I loved tofu, it has the best texture! I hae to be honest, if i were to add animal product I would never add dairy. It has always seems very unnatural and disgusting to take the milk meant for another animls for my use, esp cow’s milk. I will never agree that mill that is meant to make a mammal grow hundreds of pounds in a short amount of time could ever be healthy for human children raw or not.

I have my own vegetable garden, fruit trees and 23 olive trees which I produce olive oil from. Somehow, Italians seem to have been eating the right way without making it an issue.

31 05 2013
Philippe

So if I eat brussels sprouts, kale and broccoli every week, several times a week, I’ll get in trouble, thyroid wise, I mean?

3 06 2013
Pescovegan – Adding Oysters to My Diet | Canadian Veggie

[…] got the idea after reading 13 Tips for Vegans by Raw Food SOS. There’s also this Slate article, Consider the Oyster – Why even strict […]

24 06 2013
Liesl

Great article! I agree with almost everything. Two suggestions:
#1 why suggest not eating grubs and insects, which can be high in K2, B12 and other nutrients that are hard to impossible to get in a strict vegan diet? All other primates do it.
#2 Seeds are also high in phytic acid and must be soaked and dehydrated before consumption.
Excellent information and I admire how careful you are to respect vegans.

24 06 2013
Liesl

‘why not suggest’

25 06 2013
Newbie Vegetarian Primal | Mark's Daily Apple Health and Fitness Forum page

[…] Eat Toxins 5) Yeah looks like it. Denise Minger wrote a guide for vegans that you might For Vegans | Raw Food SOS but if you are eating eggs that should help a lot. Apathy is tyranny's greatest ally. […]

9 07 2013
Are we really supposed to eat animals? Fruit seems a more natural choice - Page 4 | Mark's Daily Apple Health and Fitness Forum page 4

[…] just denying that living things (even apples and bananas) require death to exist. First, read this, then read this. I hope you can avoid ruining your health, but I truly doubt it. Reply […]

12 07 2013
Is it Possible to be Healthy on a Vegan Diet? [Part One] | Truthbutter

[…] D3. It’s easy to get your vitamin D levels tested with a quick blood draw, and Denise Minger recommends supplementing with a vegan form of D3 to get your blood levels up to at least 35 ng/mL. However, […]

21 07 2013
Presentació de la Denise Minger al AHS12: Coneix la carn que menges! | Diari de l'Albert

[…] camí que havia seguit la Denise em va donar moltes pistes per a analitzar punts forts i dèbils. Recomano MOLTISSIM llegir el següent post per als vegetarians/vegans que estiguin llegint ara mateix això. Cadascú ha de fer el que cregui més convenient, però […]

14 08 2013
Sandra

Hi Denise,
I enjoy reading your blog! very informative! I actuallyl just became a Vegan not long ago… and I’ve been reading reading reading, watching documentary after documentary. I’ve found that there’s opponents to everything! But I was already living a “healthy” lifestyle when I was including lean meats, greek yogurt, etc etc… in my diet. I turned vegan for more ethical reasons. I live in a low income community, my nearest whole food is like 30 minutes away, so me and my family do what we can to eat nutritiously. Plus, being a meat eater left a lot of open space for overindulging in a lot of crappy food!

My question is this..would you rather be a healthy typical “healthy” meat eater (a standard diet, of lean fish, chicken, eggs and fish..cooked and factory farm grown), or a “healthy” vegan (using most of the recommendations you have mentioned above)?

The reason I ask is because those are the most doable options for me… of course my mind is pretty much set, I want to be the healthiest vegan I can be… but I’d love to hear your opinions on both semi-healthy lifestyles.

I hope you get a chance to respond.

thanks!

13 09 2013
8/15/2012 The Real Food Lifestyle "Diet" | All In Paleo (Big Tim's Primal Journey)

[…] I look at it like this.  Choose not to eat them because you don’t feel it’s healthy for YOU, but do not tell me that it isn’t healthy for me, or it’s bad for the environment when the facts and science clearly state otherwise.  My friend Denise Minger has put together an outstanding article to assist Vegetarian/Vegans in making better choices if they still choose not to eat meats, complete with supplements you should be taking if you have chosen that lifestyle.  You can find that post here at her blog.  […]

21 09 2013
Stephen Campbell

Wow, an article full of animal ag lobbyist misinformation. Typical. You make me even more sure about being strictly vegan, getting all my needed K2 from plenty of green leafies with K1, and getting everything else I need easily and with a little B12 supplement, not like that insanely impossible looking rocket-science type formula you recommend for vegans who eat plenty of fruits, veggies, nuts, beans & grains. While you say little or nothing directly to the pop tart/cheese log/juice box/bacon&egg/pancake/hamburger brigade.
No one ever lectured me about nutrition when I partook in the animal slaughter insanity, never warned me of the severe constipation from cheese/meat/flour, the obesity caused by milk/cheese/ice-cream, the severe processed carb cravings from the high-protein plant-deficient diet, the very high blood pressure, etc.. But once I became really healthy & normal weight for the first time by eating only plant foods, all the fear mongering in the world is thrown at me. But I’m immune to BS. Strong. Vegan.
Shame on you, slaughterhouse promoter.

5 10 2013
Evan M

Reading comments like this, I’m tempted to think some vegans like you want people to think you’re insane. I’m glad the vegan diet works so well for you, but for many people, it’s works horribly and she’s only trying to help them make it work. I would think vegans would appreciate the effort (and some obviously do reading these comments), but for some reason, people like you just insult her and sneer. Why?

30 10 2014
shanarose

you can’t make a vegan diet work by recommending oysters …. it wouldn’t be a vegan diet anymore and the person who is eating those oysters would no longer be a vegan ….. a truly knowledgeable person knows that vegans are vegans because they eat only plants …. only plants …. let me repeat this: an all plant diet, without any animal products whatsoever, is the correct definition of a vegan diet ….. it’s what defines vegans …… if Ms. Minger believes an oyster can pass as a plant …… well then ….. we might all be overestimating her capabilities here …..

10 10 2013
Steve

Let’s respect that different folks have different body types and needs. Me, I’ve been vegetarian and 95% vegan for 22 years. My nonvegan moments primarily involved spinach pizza or infrequently pastries while traveling. About 5 years ago my system became quite acidic. This is easy & cheap to test for, testing saliva or urine with 5-8 Ph strips on waking and after eating specific foods. I was able to normalize in two months by eating lots of melon and apples. The asthma / acidosis symptoms went away completely. I liked the Ph strips as an objective indicator of specific foods that were not working for my system, though they do not indicate completeness nor vitamin/mineral deficiency. I have noticed times when my sleep has not been solid, and then taking a broad colloidal multimineral and/or a multi-B vitamin has had immediate positive effect on my sleep. Parenting also helps me sink quickly into deep deep sleep. :)

10 12 2013
Sky (NZ)

What brand of colloidal multi-mineral do you find good?

6 11 2013
Julia

I’m sorry but you didn’t do your homework well here. Coconut oil for cooking? Seriously? Coconut oil is not heat stable. And only slightly better than extra virgin olive oil. Use extra virgin olive oil in salads or to add to cooked foods, but not for high temperature cooking. Unrefined walnut oil is also good, but again only for low temperature uses.

You can use virgin coconut oil (high in beneficial saturated fats and medium chain triglycerides) for most mid-temperature cooking. However, coconut oil has a smoke point of about 350 degrees F (171 C), which means it is not suitable for high temperature cooking. Other choices include virgin olive oil and even butter in small amounts.

Use avocado oil for high temperature cooking. Avocado oil has a very high smoke point by comparison to other cooking oils. It will not burn or smoke until it reaches 520 F (271 C), which is ideal for searing meats and frying in a Wok. Another good cooking oil is rice bran oil 495 F(257 C). Again, look for organic, cold-processed oil.
- See more at: http://www.jonbarron.org/article/healthiest-cooking-oil-chart-smoke-points#sthash.c90joIcS.dpuf

10 12 2013
Sky (NZ)

Is it correct that you take a K2 supplement even though you eat eggs etc? If so why is that?

I’ve ended up in somewhat of a corner in terms of a long term health situation and extreme sensitivity to a wide range of healthy foods so I particularly appreciate your general attitude that we each need to find what works for our own bodies, rather than following someone else’s supposedly ideal diet.

My irises have changed colour simply from eating as well as I can, rather than from eating a raw diet. All sorts of things seem to contribute to that kind of “cleansing”.

Thanks for the great website and loads of useful information. You probably already do them at times but I would really welcome more brief summaries and bullet points in your posts as I don’t have the brain stamina at present to read the detail.
best wishes

24 12 2013
CJ

With all due respect, I don’t think you’re unbiased in the least. It’s just that 95% of the world likes what you have to say, so you look more objective. Nice trick!

9 03 2014
Jason

With all due respect, I agree 100% XD

9 03 2014
Jason

But I guess all we can do is respect the bits of objective information that IS presently here, and then start our own blogs and websites, in order to spread the knowledge we wish to share.

28 01 2014
Rob Bissell

Want to learn more. Awesome foods.

1 02 2014
harnessedinslums

This is a great post. I wish I didn’t learn this the hard way after years of veganism.

11 02 2014
Theresa

I tried vegan for 6+ months. Gave up when my eye sight and memory began failing, and thyroid problems were diagnosed. I did follow all the guidelines, supplementation, seaweed. My Norse genes just needed fish to get back on track. If vegan works for you, wonderful, just please pay attention to your body. Humans are varied, and humans usually have eaten animal products through our evolution. Stay tuned into your own bio-feedback, and remain humble in your ideology.

16 02 2014
marika

Hi! Wow haha I love the way you write it! :)
Im really happy I found this because I recently went Vegan
and BAM I cant sleep anymore and I think I lost my period
and I don’t know why, ive always had period issues like I lost it
for a whole year. So I was thinking of going to a Vegetarian or Prescatarian but which of the two diets do you think would help my period?

9 03 2014
Jason

Great read… would love for you to check out these plant-based athletes! Torre Washington https://www.facebook.com/ThaVeganDread — Frank Medrano http://www.youtube.com/watch?v=mvJHw64fxgQ — Alexey Voyevoda http://www.pledgevegan.com/watch-vegan-arm-wrestling… — Michael Arnstein http://www.thefruitarian.com/ — Mac Danzig http://www.ufc.com/fighter/Mac-Danzig — and last but not least (not really a notable “athlete” per se, but a nearly 80 y/o hot mama by the name of) Mimi Kirk http://youngonrawfood.com/

9 03 2014
Jason

The following paragraph is taken from the article that you cited in your article above. Are you in agreement with it? “There are dozens of reasons to become a vegan, but just two should suffice: Raising animals for food 1) destroys the planet and 2) causes those animals to suffer. Factory farms are the worst offenders, but even the best-run animal operations can’t get around the fact that livestock are the largest contributors to global warming worldwide and that the same amount of land used to feed one beef-eater can feed 15 to 20 vegans. Animals are terribly inefficient machines for turning plants into food, and an inefficiency of this scale is disastrous. The animal welfare argument is even simpler: While there are limitless ways in which humans are different from nonhuman animals, one thing we share with most is the ability to feel pain. Since I consider it unethical to cause you, dear reader, undue pain, there’s no reason—other than simple preference for my own species—to have a separate standard for mammals, fish, and birds.”

9 03 2014
Michael G. Morris

Jason, your two questions avoid THE question: what food does the human body expect and thrive best on. If our ancestors had not eaten animals for millions of years, few of us would be here.
It would be nice to live as a species that didn’t ever cause pain to another, but that’s a rarity here on Earth. And we didn’t evolve to what we are today by being harmless. That’s just the reality we’re stuck with.

24 04 2014
Kika

And maybe, just maybe, part of evolution is we no longer need to eat meat? Just a thought…since I want to believe that we did evolve since we came out of caves….

10 03 2014
Ellen

Hi Denise,

Thank you for taking the time to publish your thoughts and findings. My diet has evolved over many years to be much as you described in this article. The K2 is my last puzzle piece (I hope) and I am grateful to you for it.

Peace and happiness :)

31 03 2014
Gene

I don’t know any vegans who eat oysters, including myself. Why would you advise that?

24 04 2014
pathancock

yes I did read the link you provided for Dr McDougall, am I missing something?

“On average, for someone raised on the Western diet, about 2 to 5 milligrams of B12 are stored, mostly in the liver. This means most people have at least a three year reserve of this vital nutrient. Conservation of B12 by the body boosts the time this supply lasts by 10-fold. After excretion through the bile into the intestines most of the B12 is reabsorbed by the ileum for future use. As a result of this recirculation it actually takes, on average, 20 to 30 years to become deficient after becoming a strict vegan. That is if no vitamin B12 were consumed—which is impossible, even on a strict vegan diet, because of bacterial sources of B12 from the person’s bowel, contaminated vegetable foods, and the environment.”

2 05 2014
Rayca

I’ve ridden on every horse of this merry-go-round. Here’s my take: if I have to do this, take that, swallow those, avoid these and MAYBE (fingers crossed) I’ll get all the nutrients I need to thrive then I’m not doing it. And don’t forget to rotate everything you eat daily/weekly. Especially if all I have to do is: eat tons of vegs. w/some fruit (everyone seems to agree on this much), nuts/seeds, whole grains (not bread), then treat the rest like condiments (dairy, protein) –then I think I’m covered for not having to pop this useless vitamin or make sure I get out of the sun just short of burning. Enough already. Also what I don’t quite understand about The China Study (still reading it), Fuhrman (who I follow the most), etc. is why cancer and heart disease seem to be new chronic diseases, say 100-150 years. Meat’s been around a whole lot longer than that. So, what gives? Why would it be the scapegoat for science? Also, I’ve done so much reading where children have suffered terrible health experiences from their vegan/vegetarian parents (some reversible, some not). I know adult needs are different from children but it’s enough to scare the bajesus out of me.

2 05 2014
Rayca

I forgot to add the reason I think the big killers, heart disease and cancer have increased exponentially in the last 100 years or so –two words– JUNK FOOD. I believe that’s the whole problem in a “nutshell.”. But who can write a book, sell vitamins or conduct more useless studies on a problem that already has an answer. Nobody.

5 05 2014
Steph

Hi! I’m looking forward to reading your book – will be ordering from Amazon today. And while I understand you aren’t out to preach that there is one, perfect diet for all – I was curious what a typical one week’s diet of your own includes? For instance percent of fruit/veggie, meat/fish, grains and dairy? I am fascinated by nutrition. I tend to limit any red meat in my diet – occassionally I will have a meatball or hamburger. I do eat fish/chicken and dairy and veggies/fruits. I don’t typically think too hard about what I eat – so I think there is definitely room for improvement. I exercise regularly, am at a healthy weight, and feel very good at 45 years old. A very close family member is 100% vegan and she is raising her 3 small children the same. Her husband however is not vegan. While I feel what she is doing is comendable solely on the cruelty aspect because I am a BIG animal lover – I find some of the information she shares regarding the animal cruelty to be so incredibly upsetting and offensive. So much so that I avoid thinking about it or reading the info she supplies on her facebook. It’s a tough call – sure I’d like to think I am not responsible for ANY animal suffering – but is eliminating all the pleasure and NUTRIENTS i receive from a varied diet being kind to ME? Or am I just being selfish along with millions of others on this earth? How do you rationalize what animal products you do eat? :)

16 05 2014
Trent Black

I bought 3 books. I don’t need them, but for support.

If somebody does not want to eat meat, then just take amino acids with you vitamins vitamins. The FDA allows chicken poop to be fed to cows.

http://www.motherjones.com/environment/2013/12/we-feed-cows-chicken-poop

The link to disease is NOT MEAT. What was gone up in consumption is SUGAR over the last 50 years. If you get cancer, they take you off sugar. If you go raw greens for cancer, like at hippocrates, they take you off sugar. But the INSURANCE companies are your best source. They pay for it all. And they say that CANCER FOLLOWS DIABETES, almost perfectly, in the 4 states they looked at locally here. I did not even ask it. They brought it up in a metting explaining why the companies health care costs are skyrocketing.

The Paleo diet is now showing links to autoimmune diseases and leaky guy via, you got it, sugar. An average USA kid will eat as much sugar by the age of 8 as a grand parent did his whole life. Ketogenic diets don’t have many of the sugar diet diseases

SUGAR IS THE LINK.

I was watching a film of some raw people taking diabetics out in the New Mexico desert, and putting them on raw sprouts (sugar free). Many of the diabetics were cured. They say is it the RAW. But I have seen the same thing done on ketogenic diets, and even McDougall after they lose weight. It is not the RAW, like they endless say. It is getting rid of…. SUGAR.

26 05 2014
Céline

Thank you so much for all your fascinating articles! I’ve been vegan for two years, vegetarian for ten years before that and I’m noticing now that my teeth are decaying (I’ve eaten a lot of raw fruits and vegetables lately). Some people noticed also that I look quite pale. I’ve probably some deficiencies. Therefore, I’ve begun eating eggs again as soon as I read your blog and I think I will follow your advice: taking K2 and maybe cod liver oil. Your blog is amazing, you’re very honest, kind and compassionate. I will definitely keep following you :)

29 05 2014
Marianne

Thank you, Denise, everything you say makes sense.

I eat high good fats, whole foods, mostly plants and some organic pastured meat/fish, hardly any fruit, no sugar, no grains, some soaked nuts/legumes. It works for me.

I am amazed at how much negative energy the Richards of this world can expend, trying to rain on someone’s parade. In the face of that I must admire your courtesy, grace and restraint!

29 05 2014
rawraj

K1 is converted to K2 in the body, So its pretty stupid to take k2. How did the animals get K2 in the first place. Oh are you going to give the “dirt” theory?
So much bullshit on this blog wow!
I bet all your fans are those who are simply frustrated with the vegan movement. Nice niche u have created. I hope you are making money in some way. Otherwise you really have to by crazy psychotic to be doing this as an inspiration (or maybe just deluded & ignorant)

29 05 2014