Why I’m Not Dismissing the Latest “Animal Protein is Bad” Study (But Not Losing Sleep Over It, Either)

I keep doing this thing where I stand in the shower writing blog posts in my head, emerging from the suds giddy and prune-fingered, feeling strangely accomplished about the words I have not yet typed. And then I squeegee the fog off the bathroom mirror and tell myself you can do it Denise! and think about how awesome it will be to actually update my blog after so much horrible silence. And then I load WordPress and think I’m blogging, I’m blogging, I’m finally blogging, it’s really happening.

And then suddenly it’s three hours later and I’ve opened 800 new browser tabs in Firefox and have become distracted by something shiny, Facebooky, or delicious, at which point all hope is lost.

This madness must end. Today, we blog.

So now I stand before you here in Cyberland, up on my soapbox, rantin’ muscles ready to flex. In case you haven’t heard, the world just got slammed with a new “meat is bad” tsunami—and it’s a doozy. We’ve got the familiar swirl of headlines designed to strike fear in our hearts (“That chicken wing you’re eating could be as deadly as a cigarette!” – The Financial Express), and pretty much every mainstream outlet caught it on their radar (hello ABC, Fox, The Guardian, Scientific American, Washington Post, and any other big-hitters I left out). The actual study, which is decidedly less popular than the press releases heralding its existence, is available here: Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger but Not Older Population. Go take a gander. The gist is that animal protein will (purportedly) shorten your life and increase your risk of chronic disease—at least if you’re eating a bunch of it before you turn 66. (Once you’re in your golden years, though, the study implies animal protein is a good thing. Tricky, eh?)

So what’s really going on here? Should we all go vegan until we retire?

To be honest, I get weary blogging about what seems like the same study repackaged and regurgitated every few months under a different name (and it appears I’m not the only one). Observational meat studies are a dime a dozen. The media-viral ones seem to pop up at least a few times per year (I’ve already dissected a few). Ultimately, there’s only so much you can say about a study that uses wobbly survey methods, tries to squeeze causation from correlation, and falls victim to the confounders plaguing most epidemiological projects involving food. So whenever I see a new Meat Is Gon’ Kill Ya Dead study hijacking the airwaves, I feel kind of  like


except with more sadness, and less nostril flare.

But this latest study grabbed my attention for a few reasons.

For one, it doesn’t orbit around the usual meat-damning suspects—saturated fat and cholesterol—but instead looks at animal protein, which I’m rather fond of discussing due to my previous shenanigans on this blog. And two, the researchers padded their observational study with some follow-up work on mice and cells, which at least earns them an A for effort. It’s still not the sort of research that should keep you awake at night, but at least in my mind, it’s interesting enough to warrant a closer look.

And perhaps more importantly, I think there might be some truth to the researchers’ findings. Yep, I said it. Gasp shock horror!

So let’s plow into this thing, shall we?

The Study Low-Down

Here’s the gist. The study itself was a two-parter: half human, half mouse (I realize that sounds like some kind of weird centaur). The human part grabbed the most media attention, so let’s start with that.

For this leg of the study, the researchers analyzed data from NHANES III—a giant survey of the health and nutritional status of American adults and kiddos, which churns up reams of info about what the good folks of this country eat. Basically, the researchers pulled data from almost 6,400 NHANES III participants aged 50 and over, looked at their food consumption (gleaned from a 24-hour recall survey they answered two decades ago), divided them up based on reported protein intake, and followed their disease and mortality outcomes for up to 18 years. (As best I can tell, that single recall survey was the sole source of the study’s dietary data.)

Those eating less than 10 percent of their calories from protein were scooted into the “low protein” group; those eating between 10 and 19 percent of their calories from protein comprised the “moderate protein” group; and those eating at least 20 percent of their calories from protein became the “high protein” group. Simple enough.

Initially, the only visible pattern was a much higher death rate from diabetes among the moderate- and high-protein groupers—not really worth sweating, though, because the sample size was too small to draw any meaningful conclusions. Other than that, protein consumption didn’t seem to be doing anything statistically noteworthy for the group as a whole: it was unrelated to all-cause mortality, death from cancer, and death from heart disease.

But here’s where it gets interesting. Instead of keeping all the participants lumped together, the researchers tried stratifying folks based on age—with the 50 to 65 year olds ushered into one group and the 66+ folks into another. The goal was to test for an age interaction, where a variable behaves differently depending on how old the participants are.

And it turned out “age interaction” was there in spades. Suddenly, a whole slew of diet-disease links cropped up—highlighting a trend for high protein to be bad news for middle-aged adults (50 to 65 years) but a boon for anyone older than that. Weird, right? It’s why protein didn’t have many meaningful correlations for the participant pool as a whole: its positive effects in the older crowd were canceled out by the negative effects in the younger crowd, creating the illusion of neutrality.



Anyway, the most interesting findings of that age stratification included:

  • The 50 to 65 crowd had a 74 percent greater risk of death from all causes for the high-protein group compared to the low-protein group (hazard ratio: 1.74), and a 433 percent greater risk of dying from cancer (hazard ratio: 4.33).
  • Folks aged 66 and older had a 60 percent lower risk of cancer mortality for the high-protein group compared to the low-protein group (hazard ratio: 0.40), and a 28 percent decrease in deaths from all causes (hazard ratio: 0.72).

In other words, the middle-aged adults eating the most protein faced higher rates of cancer mortality and deadness in general. Meanwhile, the 66-and-older crowd was apparently benefiting from all things proteinaceous, and those eating the most were living longer and more cancer-freely. And because I can’t not: here’s a friendly reminder that this is an observational study, and we can’t slap a cause-and-effect label on any of these relationships.

* Important caveat: both in the media hoopla and throughout the text of the Cell Metabolism paper, the results are reported as relative risk (e.g., “five-fold greater chance of getting heart disease”) rather than absolute risk (e.g., “3 percent died of heart disease”)—a great way to make findings seem wildly more dramatic and scary than they really are. For instance, this study found that among the NHANES III participants who were diabetes-free at the study’s onset, those eating the most protein were 73 times more likely to die of diabetes (yikes!). But if we look at the absolute numbers, which are tucked away in a little PDF supplement accompanying the study, we’d see that 0.2 percent of the low-protein group died of diabetes (one person) versus 2.0 percent of the high-protein group. That’s an absolute difference of 1.8 percent, which no longer sounds quite as horrifying.

The researchers also added another layer to their analysis: percent of calories from animal protein and percent of calories from plant protein. Here’s where the plot thickens. When adjusting for animal protein, all those links between protein intake, cancer mortality, and all-cause mortality went poof into the abyss—with the protein-cancer connection significantly diminishing, and the protein-total-mortality connection disappearing entirely. But when the researchers tried adjusting for plant protein in the same way, nothing happened.

So what does that mean? In a nutshell, that animal protein specifically was driving those disease links, whereas plant protein didn’t elicit an effect one way or another. (That rules out the possibility that plant protein had special mortality-slaying superpowers that made animal protein look bad by comparison.)

Should You Freak Out?

To figure out how seriously we should take this, let’s look at the study’s lifeblood: its dietary intake data. Although the Cell Metabolism paper is strangely silent about how people’s food intakes were gauged (a bit unnerving, considering how heavily this study depends on that data being sound), we know that NHANES collects its information via 24-hour recalls. The CDC website has a file discussing the whole process. Basically, participants get phoned by an interviewer, are asked to name everything they ate from midnight to midnight of the previous day, get prodded to make sure they didn’t forget any snacks or butter pats or late-night cookie nibbles, and then receive some follow-up questions about tap water and salt and other fun things. According to the CDC file, the participants also answer a short questionnaire “to ascertain whether the person’s intake on the previous day was usual or unusual.”

After looking over that questionnaire, I’ve got to say the word “ascertain” seems a bit optimistic to me. Keep in mind, the 24-hour recall is the sole source of dietary data in this study—so it darn well better strive for accuracy. And indeed, the NHANES survey employs a five-step strategy to help participants remember every bite they ate, described in “Nutrition in the Prevention and Treatment of Disease” (PDF) as follows:

  1. An initial “quick list,” in which the respondent reports all the foods and beverages consumed, without interruption from the interviewer;
  2. A forgotten foods list of nine food categories commonly omitted in 24-hour recall reporting;
  3. Time and occasion, in which the time each eating occasion began and what the respondent would call it are reported;
  4. A detail pass, in which probing questions ask for more detailed information about the food and portion size, in addition to review of the eating occasions and times between the eating occasions; and
  5. Final review, in which any other item not already reported is asked.

As far as boosting reporting accuracy, that’s all a great help. But it appears the interviewers only asked one question to gauge how typical each participant’s reported diet was, relative to what they generally eat: “Was the amount of food that you ate yesterday much more than usual, usual, or much less than usual?”

That’s it. No qualifier for what “much more” or “much less” actually meant; no queries about specific foods; no prodding to see whether yesterday happened to feature a birthday barbeque, thus skewing the day’s frankfurter-to-kale ratio in a meatier direction than usual. Just one vague question about total food quantity, whose answer could only ever be subjective. (After the diet recall, each person’s reported intake was converted into food codes and nutrient components—so any flaws in that initial reporting trickled upstream to the final statistical analysis.)

And it gets worse. While it’d be nice to suspend disbelief and pretend the NHANES III recall data still manages to be solid, that’s apparently not the case. A 2013 study took NHANES to task and tested how accurate its “caloric intake” data was, as calculated from those 24-hour recall surveys. The results? Across the board, NHANES participants did a remarkable job of being wrong. Nearly everyone under-reported how many calories they were consuming—with obese folks underestimating their intake by an average of 716 calories per day for men and 856 calories for women. That’s kind of a lot. The study’s researchers concluded that throughout the NHANES’ 40-year existence, “energy intake data on the majority of respondents … was not physiologically plausible.” D’oh. If such a thing is possible, the 24-hour recall rests at an even higher tier of suckitude than does its cousin, the loathesome food frequency questionnaire.

(And in case that’s not enough to make your blood boil: the NHANES data is what the US government uses to determine what the country is eating, formulate dietary guidelines, and divvy up funding. Your tax dollars hard at work!)

If it’s that bad with calories, can we really expect the protein data to be much better?

In case you’re wondering why anyone uses such a destined-for-failure way of determining food intake, the answer is simple: it’s a heck of a lot cheaper (and easier) to ask people what they’re eating than to hellicopterishly stalk them all day long, weighing and measuring every morsel of food headed for their lips. When it comes to massive surveys like NHANES that track thousands of enrollees, affordability and convenience reign supreme. And sometimes that means cutting corners with precision.

Bottom line, it’s almost a given that the recall data here is less than stellar. And despite all the magical things math can do, no amount of statistical wizardry will heal numbers that are wrong from the start.

And to add insult to injury, keep in mind that this was the only diet information collected for each participant over the course of 18 whoppin’ years. Even if the recall managed to be accurate for the time it was recorded, there’s no way to know whether the participants’ diets evolved over the next two decades, and how any changes in their noshing habits impacted mortality outcomes.

That’s a lot of trust to put in one day’s worth of self-reported eating!

Diamonds Among Coals?

Now that I’ve bashed the NHANES diet survey to the moon and back, let’s look at why it might actually have some legitimacy. Bear with me!

While combing through the Cell Metabolism paper, one thought kept tickling my brain. Typically, if we dig into an observational study about meat, we see the heavy meat eaters—particularly those daredevils mowing down on red and processed varieties—engaging in a variety of lifestyle practices that spell I AM NOT HEALTH CONSCIOUS loud and clear: more smoking and drinking, less exercise, higher calorie intake, fewer fruits and vegetables each day, the works.

In turn, all those health-defeating behaviors tend to confound the true relationship between meat and various diseases and mortality. It’s hard to decipher whether meat itself is increasing cancer and heart disease and early death, or if reckless-with-their-health folks—already on a crash course towards chronic illness—just eat more of it because they don’t heed any conventional advice about diet and lifestyle.

If a situation like that was at play in this study, and protein intake was a surrogate for health-unconsciousness the same way meat tends to be, we’d expect to see the folks in the high-protein group fitting a similar anti-health profile—poorer diets overall, more risky behaviors. In turn, that would mean the study’s results could’ve been biased against the high-protein consumers due to all that residual confounding.

So was that the case?

Unfortunately, the paper doesn’t make it very easy to answer that question. There’s no data for biggies like drinking or exercise in the paper’s “participant characteristic” list. But we can see that the high-protein group actually had relatively fewer smokers than the low-protein group (18.2 percent versus 21.8 percent for current smokers; 37.8 percent versus 39.8 percent for former smokers), and that the high-protein group reported a lower calorie intake than the low-protein group (though heaven knows if that’s accurate). In addition, more people in the high-protein group than the low-protein group reported trying to lose weight during the past year (43.9 percent versus 37.5 percent), as well as changing their diet for health reasons (29.3 percent versus 15 percent). But it’s hard to say whether that’s a reflection of greater health awareness or poorer health when the study started.

What can we piece together from that?

Here’s my take. Contrary to what we might assume, the deck probably wasn’t stacked against the high-protein eaters from the start. If anything, the study’s confounders should have given them an advantage in their health outcomes. And I think that possibility is supported by more than just the (admittedly sparse) participant characteristics.

Here’s why. When the researchers took their protein correlations and adjusted for fat and carbohydrate intake (as percent of total calories), the numbers didn’t budge. That’s pretty interesting, because this batch of NHANES III surveys happened at the height of the nation’s fat-phobia, when mainstream thought was that all fat was bad—regardless of whether it came from something hooved, winged, or rooted in the dirt. Since adjusting for fat intake didn’t dissolve the links between protein and mortality, it reduces the likelihood that fat was acting as a confounder here.

Likewise, protein—at least until this study came out and ignited terror in omnivorous hearts near and far—has been the only macronutrient not demonized by any popular diets or mainstream health authorities. Fat and carbs have received more than their fair share of bashing over the years, but protein, as far as conventional thought goes, has clung tightly to its health halo—emerging unscathed from even the bloodiest of diet wars. (And the perception of “good protein” certainly includes that from animal sources, thanks in large part to the USDA’s push to consume our meat and dairy lean. How many egg-white omelets and and skinless chicken breasts have been choked down in the name of health?)

So again, if we were going to find any bias in the survey data, it’d probably lean towards protein being a good thing—at least in the eyes of the health-conscious crowd. The fact that a non-stigmatized macronutrient had such defined links with mortality cranks up its relevance, in my mind.

Of Mice and Rodent Chow (And Growth Factors and Protein)

Is your brain full yet? Save room, because there’s still another piece of the study to run through our wringer—and this one’s a lot more rambunctious and furry. To understand why protein might be linked to cancer and overall mortality as their human study suggested, the researchers conducted a series of experiments on mice, feeding them a range of protein levels mirroring that of the NHANES III participants—4 percent to 18 percent of calories. The prime goal was to see whether tweaking those protein levels would impact levels of insulin-like growth factor 1 (IGF-1) circulating in the mice’s bodies, as well as cancer incidence and progression.

But first, lets back up for a moment and get some context on this whole IGF-1 thing and why it’s so relevant.

As you might’ve seen in some of the news reports, the lead researcher of this study was Valter Longo—the director of the University of Southern California’s Longevity Institute, who already has a scroll of really cool studies under his belt (mostly on fasting and cancer). And he was profiled on “Through the Wormhole” with Morgan Freeman, which ups his awesomeness quotient considerably. Because science.


And in the world of aging research, IGF-1 is a bona-fide spotlight stealer. As its name implies, insulin-like growth factor 1 is a hormone molecularly similar to insulin, with its modus operandi being “grow, grow, grow!” It promotes growth for nearly every cell in your body—building muscle, making young’uns get taller, creating new brain cells, repairing nerve damage, and doing other awesome things that keep your body cranking like the fabulous machine it is. But IGF-1 is kind of a double-edged sword. And the bad-slicey side plunges right through the heart of longevity.

Part of the problem is that, while fulfilling its growth-promoting duties, IGF-1 doesn’t distinguish between healthy cells and damaged ones—potentially spurring cancer proliferation and contributing to tumor growth, if the conditions are right. High levels of IGF-1 have been linked to breast cancer, prostate cancer, bladder cancer, colorectal cancer, endometrial cancer, and lung cancer (though most of that research is observational, so there’s always the possibility of tumors increasing IGF-1 levels instead of the other way around, or a third unmeasured variable raising both). On the flip side, folks with a genetic deficiency in IGF-1 appear nearly immune to cancer—a phenomenon Longo himself has investigated.

Apart from the potential cancer connection, IGF-1 plays a huge role in the aging process. After all, the cycle of cells growing, dividing, and repairing is just a fancy way of explaining that they’re aging—so IGF-1 is pretty much orchestrating how rapidly that happens.

And the evidence comes from more than just the usual rat and test-tube studies. As far as human data goes, there’s some interesting research showing a connection between IGF-1 levels and lifespan when we look at the oldest of the old. A disproportionate number of centenarians have mutations affecting their IGF-1 receptor activity, which probably plays a role in their long-livedness. Likewise, the offspring of centenarians have lower IGF-1 levels than others of their age, gender, and BMI—suggesting the hereditary component of longevity could be due to reduced IGF-1 tricking through a family’s bloodline. (It’s less useful to look at IGF-1 levels in centenarians themselves, since the hormone naturally declines with age and will be pretty low in anyone who reaches the century mark.)

For longevity researchers, there’s an ongoing quest to “hack” all this life-extending genetic stuff and help us average Joe Shmoes reap the same benefits. Quite a few things can influence your body’s levels of IGF-1 beyond genes—everything from your stress level to your ethnicity to your estrogen status to the time of day—but diet is a huge determinant, and perhaps the easiest to tweak and control. So it’s not too surprising that food gets so much attention in this field. And as Longo was keenly aware of, protein is chief among the IGF-1 governors we consume.

But the life-extension hunt is still a work in progress. For at least 60 years, the darling of longevity seekers was calorie restriction (CR)—with the first case of its life-extension properties appearing in 1935, when an experiment showed that rats lived longer if their energy intake was reduced. Ditto for mice, flies, crustaceans, and yeast, more studies revealed. And subsequent research showed the same longevity effect in calorie-restricted ringworms, who idled in their larva’s “dauer” stage instead of catapulting towards maturity like usual. (Which made their lives longer, but not necessarily more enjoyable: the dauer stage consists mostly of not eating, not reproducing, and sitting like a lump on a bump until food supply becomes abundant. Even if we humans had a dauer stage, I can’t imagine wanting to stay there for very long. It sounds too much like high school.)


Please, come join me in existential limbo.

The reasons behind calorie restriction’s perks? A biggie was thought to be its suppressive effect on growth hormone and IGF-1—essentially slowing down aging and age-related diseases. Calorie-restricted organisms had much lower levels of IGF-1 than their more abundantly fed counterparts, at least in the creatures and fungi that’d been studied up to that point. And those reduced IGF-1 levels seemed to help protect cells from DNA damage—a boon for warding off cancer. It made sense: there’s a huge evolutionary and survival advantage to halting growth in times of food scarcity.

Although there wasn’t controlled data available for humans (we live too darn long to make lifespan studies an easy feat), the benefits of calorie restriction were expected to be universal. And thus emerged an era of books, gurus, theories, and research funding all pouring towards the promising new field of “CR.”

But soon cracks in the calorie-restriction theory started appearing. More comprehensive rodent studies, including one looking at 41 different strains of mice, found that calorie restriction shortened the lifespan in more strains than it extended. Likewise, in wild mice opposed to massively lab-domesticated ones, a lower energy intake did nada for average life expectancy (though it did curtail cancer rates). A 25-year rhesus monkey study—which the longevity world had waited with baited breath for completion—failed to show any life-extension benefit from feeding them less. And while studies on calorie-restricted humans weren’t far enough along to offer mortality data, the existing numbers showed their IGF-1 levels were pretty much the same as everyone else’s, casting doubt on the hope those earlier rodent and yeast and worm studies would be translatable to humans.


Well, f%@#.

What the heck was going on?

Eventually it emerged that calorie restriction, for most species, was only effective if it also restricted protein intake. And as the study gods breathed more and more research into being, it seemed all that deliberate hunger might be for naught. Protein restriction alone could push down IGF-1 levels and spark a cascade of longevity-enhancing changes. (In case you’re wondering, neither fat restriction nor carbohydrate restriction seemed to increase lifespan, at least in rodent models.)

But it didn’t end there! A new wave of studies zeroed in on methionine, a sulfur-containing amino acid abundant in muscle meat and eggs. In mice, restricting methionine—without reducing calories—was enough to increase lifespan and induce health perks like slowing down immune aging, improving blood glucose, reducing IGF-1 and insulin levels, and protecting organ cells from oxidative damage. The reason? It appeared to be twofold: methionine tends to generate toxic byproducts—

And then the plot turned once more! Seriously, this saga had more twists than a pretzel factory. A fascinating but woefully little-known study in 2011 showed that in mice, supplementing with glycine—an amino acid found abundantly in connective tissue and gelatin and bone broth—had the exact same life-extending effect as restricting methionine. Without reducing calories or other amino acids, glycine supplementation increased the rodents’ lifespan, reduced fasting glucose and insulin, decreased IGF-1 levels, and nearly halved their triglycerides—the very perks that’ve variously been attributed to calorie restriction, protein restriction, and methionine restriction.

Let me make it abundantly clear: THIS IS HUGE. If the glycine finding translates over to humans (which I strongly suspect it does), life-extension-seekers may be barking up the wrong tree—or at least an unnecessarily complicated one—by trying to selectively reduce animal protein in order to live longer, as Longo seems to support. A wiser method could be simply getting a more “biologically appropriate” balance of amino acids than the standard Western diet typically provides. That means eating more of the glycine-rich foods that’ve been gradually stripped from our menus—things like skin, bones, tendons, tripe, feet, hooves, ears, connective tissue, and some organ meats—and less of the muscle meat typically dominating our fridges and freezers.

So to put all that in a Reader’s Digest version, the history of life-extension research went something like this:

“Calorie restriction extends rats’ lifespans. We must eat less to live longer!”

“Wait… reducing protein without reducing calories does the same thing. We must eat less protein to live longer!”

“Well I’ll be darned! The whole ‘life extension’ thing works just by limiting methionine. Methionine bad. Other amino acids okay! Down with meat!”

And now, it seems we’re at yet another crossroads—one where methionine intake may become less important than its balance and interaction with other nutrients, especially glycine.

*Note: This is deliberately oversimplified and lots of other really interesting discoveries happened. But heaven knows this blog post doesn’t need to be even longer than it already is.

Now back to Longo’s mice.


Exhibit A: Denise has inserted yet another cute animal picture to distract you from the fact this blog post is horrifyingly long and word-full.

In a nutshell, the researchers put groups of mice on different experimental diets: one relatively high protein (18 percent of total calories) and one very low (4 to 7 percent of total calories). Then the mice were injected with cancer cells—melanoma for one experiment, breast cancer for another—in order to kick off the tumor-growing process.

Now brace yourself for some China Study déjà-vu. Fifteen days after getting their melanoma implants, all of the mice on the high-protein diets had developed measurable tumors—compared to only 80 percent of the low-protein group. (Over the course of the experiment, that number rose to 90 percent, but never got any higher.) What’s more, the low-protein group’s tumors seemed to grow at a much slower rate: by the final day of the experiment, the average tumor size in the high-protein group was 78 percent bigger than in the low protein group.

When that experiment was repeated with breast cancer cells, the results were pretty similar—except the tumor rate of the low-protein group maxed out at 70 percent of the mice, while the high-protein group was universally tumor-stricken.

And to tie IGF-1 back into the picture, the low-protein mice—as we might expect—had significantly lower levels than their protein-gorging brethren.

So there’s the gist. Is it a legitimate strike against eating lots of protein?

There’s one major reason I’m reluctant to draw any conclusions from all this (apart from the whole we aren’t mice thing). And that reason is called “AIN-93G standard chow.” That’s the name of the lab diet used for the high-protein mice, according to some notes in the paper’s supplement. You can download the AIN-93G specs here, but if you’d like to save yourself the effort (and hard drive space), here are the top six ingredients:

  • Corn starch (397 g)
  • Casein (200 g)
  • Maltodextrin (132 g)
  • Sucrose (100 g)
  • Soybean oil (70 g)
  • Cellulose (50 g)


A lot of things are wrong with this picture, such as “where are the food things?”—but for the sake of brevity, I’m just going to focus on that second ingredient: casein. It’s one of the major proteins in milk, and it’s got an awful track record for promoting tumor growth more than other types of protein, including its dairy-derived cousin whey.

I’ve already written tomes on casein, cancer, and rodents in previous blog entries—including my Fork’s Over Knives critique and China Study critique—so I won’t torture you by rehashing it all here. Chris Masterjohn also has some awesomesauce posts on the subject, so hop on over there if you’re insatiably curious about it all. The bottom line is that when we look at the mice-and-protein studies outlined in Longo’s paper, this is what we’re dealing with: a cocktail of purified ingredients, with the protein component being a well-known promoter of cancer in rodents. It’s not at all surprising that the mice eating the most of it sprouted tumors like mad. But it’s impossible to say how much of that’s due to protein per se, or to casein—especially casein that’s been stripped of all the other goodies in dairy and tossed into a party bag of refined junk.

Putting It All Together

For those of us in the ancestral, paleo, “real food,” low carb, and other related communities, there’s a tendency to see a study like this and be like RAAWRRR KILL IT BEFORE IT BREEDS at the first whiff of its correlation-is-causation tone. And as someone who generally places epidemiology in the ninth circle of Research Hell, I’ve certainly been guilty of that myself. But one of the biggest gifts of observational studies like this one is the opportunity to explore new hypotheses and test out perspectives that challenge what we believe.

I think that’s definitely the case here.

Think of it this way. For most of human history, dietary consistency was a fairy tale. Famines struck. Periods of scarcity tangoed with those of abundance. We gorged on energy-dense foods like meat when they became available, knowing full well we might not be so lucky the next day or week. And to be sure, we ate the whole freakin’ animal after a kill—not just the skeletal muscle.

Constant abundance and pickiness is absolutely new to our bodies, even for those of us eating foods we deem ancient or ancestral. So it’s really not all that far-fetched to think that America’s animal protein habits—heavy on the methionine-rich muscle meats, scant on the glycine, swimming in ceaseless surplus instead of punctuated with scarcity—could be a problem for our health.

Perhaps it’s not a coincidence that many of the world’s longest-living populations eat fairly low-methionine diets or periodically abstain from protein-rich foods (like in Ikaria, where the predominantly Orthodox Christian residents cyclically fast from animal products). And perhaps just as relevant as the types of foods we eat is the manner in which we eat them—nose-to-tail for animals, with some plant-only days thrown in for good measure.

That doesn’t mean the solution is to go vegan. Nor is it necessarily to eat a low-animal-protein diet. But perhaps it’s time to seriously explore options like protein cycling, periodic fasting, or just cooking up heaps o’ bone broth to get that glycine down our gullets.

Just to be clear, nothing I’ve written here—even my moments of quasi-defending this study—changes the fact that the NHANES III data is observational and the diet recalls are basically handicapped from the start, thanks to the history-revising sinkhole that is the human mind. As always, correlation isn’t causation. It’s pretty disappointing that the study’s own researchers seemed to forget that. The reason I’m not sliding this study straight into the slush pile is because regardless of its validity, it at least opens the door to some important discussion. The bigger point is that the trends it excavated and hypotheses it explored could feasibly be real—evolutionarily, biologically, logically. In my opinion, the greatest value of this study, then, is its role as a springboard for breaking out of the comfort zone of what we think—and want—to be true.

Otherwise, I guess it could make a nice doorstop.


  1. OMG, a rational response to all this stupidity. I am officially in love. Can I connect in LinkedIn. Iget so tired of responding to the many variants of stupidity that poses as rational nutrition discussions.
    From now on I am just referring people to your blog.

  2. If the takeaway from this is what I think it is, namely that an ancestral diet including gristle, bone, and organ meats should serve to balance the possible negative effects of too much methionine from animal protein, I still find it confusing that these negative effects do not seem to exist in the older age group, if that NHANES-based observational study is any indication.

    1. Great question! Pure speculation here, but I wonder if the age difference also implies a difference in how the participant prepared meats. My grandmothers were both constantly making soups, bone broths, lamb on the leg etc. My mum, not so much.

    1. Ivor, thank you for reminding me of this fact:

      The study is NOT very sound or solid -due at the very least to how it is INCONSISTENT:

      You point out that this study shows that “Low protein” is associated with *more* cancer for ages 65 years … LOL.

      While I don’t remember the exact text of the study (I’m taking your word for these claims), I **do** VERY vividly remember that it showed that one age group was *more* healthy for low protein, and another, ADJACENT age-group was *less* healthy -and since there is no rational thing that can explain this, it stands to reason that the factor under observation (protein intake) was NOT as “bad” a problem (or as “good” a cure) as anyone might otherwise have said – or else, why would it “help” one cohort, but “harm” a similarly-situated cohort?

      Gordon Wayne Watts, LAKELAND, Fla., U.S.A.
      BS, The Florida State University, Biological & Chemical Sciences,
      double major with honours
      AS, United Electronics Institute , Valedictorian

      1. maybe the old guys have less teeth and prefer the juicier tender parts while the younger ones like to chew on the muscle meat :-) just kidding

      2. Hi Gordon

        I’ll save you picking through the faeces that is the report proper, below is taken directly from the author’s Abstract/Summary:

        “Respondents aged 50-65 reporting high protein intake had a 75% increase in overall mortality and a 4-fold increase in cancer death risk during the following 18 years. These associations were either abolished or attenuated if the proteins were plant derived. Conversely, high protein intake was associated with reduced cancer and overall mortality in respondents over 65”

        By the way, the “4-fold increase” they quote was based on 6 (yes 6) deaths total in the low protein group – the overall death rate for low protein (averaged across all ages) was higher than for moderate or high. So the researchers DID need to go picking through their ordure to get something fruity.

        As I said…………..faeces.

        See Zoe Harcombe’s nice piece earlier today:


        1. http://www.zoeharcombe.com/about/

          Zoë is a qualified nutritionist with a Diploma in Diet & Nutrition and a Diploma in Clinical Weight Management, but she is first and foremost an obesity researcher.

          Where exactly did she get her diplomas from? Why does she not list the university?

          1. HI Charles

            I’d say her scholarship-enabled Mathematics and Economics from Cambridge is equally (if not more) salient to her fundamental capability in this arena. I have a Chemical Engineering degree (biochemical stream), and over 25 years of Engineering & Management roles specializing in Complex Technical Problem Solving and Statistical Inference. This capability is hard won, believe me, and I see a depressing dearth of it out there in the medical and nutritional research fields. As I said earlier – faeces abound, but there are good guys too in fairness; it’s a tremendous tragedy that the media don’t evhibit positive discrimination in focusing on them, rather than the extruded “movements” of the obfuscators ……

            Best Regards

  3. Thanks for this great post Denise. Please blog more often if you can, and please write another book soon. The people I trust in the diet world are down to precious few, and you top the list!

  4. ok, that was the coolest article i’ve read all year, I can’t believe this is the first i’m hearing about the role of glycine in longevity, i’m experiencing a nutrition-nerd rhapsody as I type :)

  5. Denise, don’t ever apologize for long posts. Your commitment to lending balance and perspective while remaining accurate is greatly appreciated in a world dominated by reductionist thinking. Unfortunately the Dr. Oz effect has people hopscotching from one sensational study to the next and they remain blind to the holistic perspective that can truly save them and repair their health. Thanks for all you do and thanks for such a great book!! I’ve been spreading the word as it was so impactful. To our health!

    1. Avishek is right. I don’t think this can be evaluated at all in the absence of presentation of the primary data. How many people died of which disease when?

  6. Love it! I was hoping you’d take on this study when it came out. Very helpful analysis. I wish I could get you to teach all my dietitian colleagues how to think for themselves!

  7. Thanks for your great analysis, Denise. Also, thanks for your wonderfully funny writing style–I was laughing many times as I scrolled down. Great job!

  8. Everybody that has read this post by Denise should also google “glycine cancer”. It seems to be pretty well established that cancer cells consume much greater levels of glycine than healthy cells. It was even suggested that the suppression of glycine may be a treatment for cancer.

    1. That may be the case in vitro but not in vivo.

      Dietary glycine inhibits angiogenesis during wound healing and tumor growth.

      Dietary glycine prevents the development of liver tumors caused by the peroxisome proliferator WY-14,643.

      Dietary glycine inhibits the growth of B16 melanoma tumors in mice.

      This makes sense as glycine lowers the growth factors IGF-1 and Insulin. It also lowers glucose which is probably an even better fuel for cancer than glycine itself.

          1. Chupilo, none of the human data cited on Valtsus’ blog had anything to do with glycine counteracting the negative effects of methionine.

  9. sign me up to the fan club of those officially in love with your intellect. hey, the good looks don’t hurt either :-)

  10. So I have to admit I had to read this in a few sittings lest my eyes dry out and I miss something :) BUT learned so much. Thank you for taking the time to break it all down. I knew some of the flaws/challenges with the studies but this was super enlightening. Great work, keep it up!

  11. One of the major take-home messages here — and, from what I’ve read, one of the major reasons that this blog exists — is that nutritional research is not really research. The VAST majority of it is marketing and bias-confirmation masquerading as research. Notes from this thread:

    1) At least one of the authors of the primary study in question (Levine et al) has a major conflict of interest. Three other authors MAY have an undeclared conflict of interest. See #2.

    2) As pointed out in Zoe Harcombe’s blog, three other authors on the Levine et al paper *may* have an undeclared conflict of interest, in that they work on the L-Nutra scientific team. That does not necessarily mean diddley-squat, though. “Conflict of Interest” in the scientific world means (in brief; a full discussion is complicated) that you are a significant stakeholder or officer in a company which stands to gain from your research. Being an employee does not give you a conflict of interest; being President of the company or having a major share does. Zoe does not differentiate, and those same authors have been on numerous other publications without declaring any conflicts, so they probably don’t have one by official definition. So, about Zoe…

    3) Zoe Harcombe sells diet books; she has half a dozen of them so far. She has also been caught fibbing in the past about her qualifications: http://carbsanity.blogspot.com/2013/01/zoe-harcombe-credentials-ii.html (I haven’t bothered to look up the author of the “Carb-Sane Asylum” website, but I would be amazed if that person didn’t have a conflict as well. Lord knows he obviously has a tremendous bias.)

    4) The lead author of the study Denise quoted showing a cancer-protective effect of glycine just happens to be CEO of a company that sells a glycine supplement, and he also just happens to be a major proponent of the reasonably well-debunked claim that abortion increases breast cancer rates. (http://en.wikipedia.org/wiki/Joel_Brind).

    5) For entertainment value, I have to point out the failed politician who QUOTES HIMSELF as an authority, and then points out that his qualifications are that he got a Bachelor’s degree (“double major with honors”! Whoopdy-friggin’-do! I’ll see your Bachelor’s and raise you my MD!) and that he was Valedictorian for his *associate’s degree*. It’s hard not to laugh. (NB: I’m no degree-snob; neither Gary Taubes nor Denise Minger have more than a bachelor’s, and I think they’re both brilliant. They’re just not as douchey as Mr. Didn’t-get-the-vote.)

    Finally, I have to point out that basically what happens in a “debate” like this (in quotes because there’s so little reliable data on which to conduct a real debate; it’s basically dogma vs dogma) is that everybody finds a sufficient reason to distrust an article they don’t like; sufficient suspicion of conflict of interest for the people with whom they disagree; sufficient support of their own biases & dogma; and everybody goes back to their Happy Place, where life is simple and they don’t have to question their own beliefs. I love, for example, how people who hate the Levine et al study decry the study, and then claim that it would have been different if they had used Organic, Grass-fed beef. Please show me one iota of evidence that such products increase human health. Not an in-vitro study, not a study of the contents of the beef, but an actual study that shows that it makes one go***mn bit of difference to actual human health. Can’t do it? I didn’t think so.

    Just to stir the pot (‘cuz I’m that much of a d**k), here’s a link to a “grass-fed beef is crap” article:


    1. Born in Rochester, New York, Taubes studied applied physics at Harvard and aerospace engineering at Stanford (MS, 1978). After receiving a master’s degree in journalism at Columbia University in 1981…

      1. OOPS! My bad, thanks for the correction. :)

        Anyway, my point was that I wasn’t discriminating against people who have “just” a bachelor’s, which is what I thought he had. It doesn’t matter, really, I think his work is recognition-worthy, regardless of letters after his name. I was basically just razzing the dude who signed his post thusly:

        Gordon Wayne Watts, LAKELAND, Fla., U.S.A.
        BS, The Florida State University, Biological & Chemical Sciences,
        double major with honours
        AS, United Electronics Institute , Valedictorian

        It’s pretty douchey, if you ask me, to try to flaunt your credentials when they’re not really very extraordinary. That was not in any way meant to demean otherwise smart people who haven’t felt the need to pursue “advanced” degrees. You can be a critical thinker without having a university title. You can also be a very poor/NON-critical thinker and have a big title…

        1. Personally I think it’s douche-y to quote Wikipedia anymore since they’re basically a tool of the Quackwatch people. I trust people who sell supplements more than Wikipedia that’s for sure.

          Lots of research has to be carried out by interested parties instead of “independent” people. We all like to think that there is some robotic emotionless person doing research on our behalf, but that simply isn’t how it works. Bias begins with the funding process. If you can’t get your idea funded, you’ll have to do something to find funding. Anyone who isn’t familiar with the concept should subscribe to just one journal and find out. Reading the commentaries for a year will reveal the process quite well. I’m grown up enough to look for bias in the work of researchers. I don’t expect them to be angels and neither should you.

          Plus those arguments you made were not on the merits.

        2. It’s all good, David :) – yes, I have “just” a bachelor’s degree – BUT it’s a double major – AND with honours -AND also an AS degree in Electronics Technology (Valedictorian of UEI), etc…

          The bigger point, though, is this: was what I posted correct on the merits?

          Also, Lee, who were u referring to? Another Gordon Watts, maybe the Washington professor of Physics here? http://d0.phys.washington.edu/~gwatts/
          and here
          and even here??

          I’m “this” Gordon Watts:



  12. Hi Denise,
    I liked a lot you China Study analysis and The death of the food pyramid. As for this study: since you can the statistics, you should also be interested in Zoe Harcombe’s new info on the splitting of the groups in Longo’s study. It has not been given out elsewhere, and it seemed to be hard to get also this time. With the figures given I’m not surprised of that, either.

    Here’s the link: http://www.zoeharcombe.com/2014/03/animal-protein-as-bad-as-smoking-headlines-based-on-6-deaths/


  13. Surely this study says that middle-age people should eat MORE protein?

    It says that there is a relationship between the protein that you ate 18 years ago and your current health. If you are 50-65, the ‘effect’ of protein is bad, if you are 65+ the effect is good.

    Most people have taken away from this that people should eat less protein during middle age (ie 50-65). But surely people should start eating more protein 18 years before they hit 65, ie from age 47… ?

    (The people who showed a benefit from eating a lot of protein (i.e. the over 65s) had reported what they ate when they were 47, whereas the other had reported war they ate from age 32.)

  14. Denise,

    That mouse study started with 30 diets and nearly 1000 mice. The final pro-LP results consider the results for only 25 diets and 854 mice. Huh?

    Yes, before declaring that low-protein diets boost longevity in mice, the researchers excluded five LP diets and 100+ sick/dying mice from the calculations. It’s all here: (Comment 5) http://www.abc.net.au/radionational/programs/healthreport/high-protein2c-low-carbohydrate-diet/5309616#transcript

    Excluding 5 killer LP diets from longevity results before “finding” LP diets boost longevity seems outrageous, at least to me.

    Am I wrong? Readers, any thoughts. Anyone?

  15. Another good analysis and some good info nuggets…

    “The idea of laying blame on a single dietary factor such as protein intake in the pathogenesis of cancer – or any disease for that matter – is absurd,” adds Aragon. “The adverse potential of not getting enough protein (sarcopenia, compromised glucose control, lower immunity, brittle bones), especially in the aging population, far outweighs the risks of getting too much.“

    There was no consideration of food sourcing. No consideration of exercise. No looking at what other foods the participants consumed.
    Yes—the researchers will point out that they controlled for carbs and fats. But again, this was just bottom line and didn’t consider what types of food were consumed. Would anyone doubt that green + grains + organic chicken ≠ fast food burger + mayo + fries?
    Those macronutrients (proteins, carbs, and fats) could be matched in those two meals, but if two different people ate those identical meals year-over-year for 18 years, I’m pretty sure I know whom I would bet on for better health.

    Schoenfeld was also quick to point out that most people who eat red meat tend to consume it at fast food restaurants. (Just look at the sheer volume of sales to understand how much red meat is devoured at all of these establishments.) And while it’s not a hard rule, most people who eat fast food consistently have other lifestyle factors that could impact overall health.
    Maybe the most important takeaway is an increased awareness that the needs of your body might change during different phases of your life.
    The main thing we have to realize—or at least entertain—is that the things that make us ‘jacked’ or ‘ripped’ may not also be the best thing for longevity,” says nutrition researcher, Brad Pilon, author of Eat Stop Eat. “Even optimal health guidelines when you’re young may not be the best for longevity, as longevity is all about maintaining a status quo by reducing cumulative cellular damage and debris.”
    Pilon suggests that the biggest push from this research could be a greater investigation into whether there simply might be different protein needs throughout your life cycle.

    The response is not necessarily to overreact and cut all protein, but instead consider what your body needs given it’s activity levels and goals, and then consider the sourcing of your foods and all other factors that lead to health.

    – See more at: http://www.bornfitness.com/do-high-protein-diets-cause-early-death/#sthash.mpscJZ3Y.dpuf

  16. Some good points Brad, especially about the fast food. And what goes together with fast food?: hamburger buns, ketchup, french fries, sodas….(high fructose corn syrup, soy oil, soy protein, additives, sugar…..maybe it’s not the animal protein after all…..)
    Another point I’d like to make is, did they ask the people what medications they took? That could be another factor, as certain medications can cause illness (I don’t know if they include that in NHANES data). Some people in the 50-65 aged group might have been on statins, which are known to be a factor in diabetes and cancer.

  17. Someone else may have mentioned this but there are a lot of comments and I can’t read them all, so just in case:

    Several of the people involved in the study all work for the same company, which Valter Longo apparently founded (http://www.l-nutra.com/index.php/about/team.) That company, L-Nutra sells completely plant based products. Conflict of interest perhaps?

    And to piggy-back on Brad’s comment above, the whole singling-out-a-single-nutrient study model needs to be retired. The human body and how it utilizes nutrients is way too complex for sweeping macronutrient claims.

    Love your work and writing style Denise!

  18. Very thought provoking post, thank you. I kept thinking about the CR people and how they often intersect with the vegan and raw vegan communities, probably because of this protein issue. I spent many “retreats” with groups of these people in San Diego for a period of about 6 years. Willowy is a kind description of the body type. So the thread that’s hard to pinpoint in this discussion is the muscle mass issue. How can you look healthy, maintain strength and your own muscles while gaining CR benefits? Is it enough to just increase glycine or glycine rich foods? And…. ahem… when are we going to see the Denise Minger Meet Your Meat Cookbook? Heheh..

  19. There are at times certain information that crops up which runs contrary to all that you’ve always held to be true. Something like this comes up … what do you do? Heck .. I do some research and see whether this new data has got any basis at all.

  20. Have attempted several times on Amazon to leave a review on your book. Tried different words making your excellent book even less desirable than I found it. None were put through.

    Couldn’t help but wonder if the person(s) reviewing the review for Amazon rules were fans of Campbell.

    Maybe I will make another attempt to get it through today?

    1. Mary — so sorry you’re running into trouble with that! Quite a few people have reported the same thing. Did you use my last name anywhere in the review? “Minger” is a derogatory term in the UK (“someone who fell out of the ugly tree and hit every branch on the way down,” according to Urban Dictionary :( ), and Amazon flags it as a swear word. A few people had success by deleting Minger and just writing “Denise” or “the author” instead. Let me know if that works or not!

  21. Teeny weeny correction: C.elegans is a round worm, I believe, not a ring worm (which isn’t actually a worm at all. It’s a fungus.) I get the bottom line, though: more broth, skin (which I love and do eat anyway) and organ meats, less muscle meat. I’ve got a pot of broth cooking right now. :) Thank you. Love your posts, long or otherwise.

  22. Hi Denise, Thank you for your amazing posts – I’m becoming addicted. They go deep, and are clear at the same time.
    Just to give my 2 cents: in my opinion, if it’s true that glycine counterbalances the bad deed methionine might do in our body, there’s that easy solution you mentioned on your post – let’s just consume it from the other parts of the animal. We focus (obsess?) too much about lean animal protein, but the rest is important too, everything balances each other! (sorry for the bad english?) Let’s eat the skin, let’s drink the bones’ broth, let’s eat the crunchy cartilage – in case you’re not a vegetarian of course. [Foods highest in glycine: http://nutritiondata.self.com/foods-000094000000000000000.html ]

  23. I’ve been waiting with bated breath to post this: proofreading alerts!

    “waited with baited [sic] breath”

    “including my Fork’s [sic] Over Knives critique” — grocer’s apostrophe

  24. I really don’t understand the enthusiasm for Brind’s glycine study. Aside from the various criticisms raised above (Brind’s conflicts of interest, the fact that it was a study in rats not humans, the fact that it was merely a meeting presentation not a peer-reviewed study etc), the glycine used in the study was in it’s isolated (ie non-wholefood) form. I seem to recall Campbell being raked over the coals for allegedly making conclusions about whole foods based on isolated nutrient feeding studies, and yet that’s exactly what you appear to be doing here.

  25. Methionine causes a flushing reaction very similar to what many people of Asian or Finnish genome experience with alcohol (the “Asian flush”). I experience both.

    That latter flush is related to our genetically inherited alcohol dehydrogenase deficiency (ALDH2). To put it over-simply, this is a flawed alcohol metabolism pathway; those who have it do not metabolize alcohol efficiently and end up with a mess of (highly toxic) acetaldehydes floating around in our systems. For some of us (SE Asian and American Indian, e.g.), it means going from one sip to totally drunk or sick, very fast. For others (esp. Finns) it means being able to drink enormous amounts without “feeling it” until literally nearly fatally poisoned (a huge public health issue in Finland, btw).

    Take a look at this, on the relationship between methionine synthase and acetaldehyde:


    Surprise–candida albicans also produces acetaldehyde.

    The glycine connection is spot on IMO. But in the metabolic view at the link above, other micronutrients also come into play…and even more so, inherited alleles.

    [The Web site is targeted toward people who have MTHFR mutations. “The MTHFR gene provides the instructions for making the MTHFR enzyme, which plays a role in converting the amino acid homocysteine to methionine.”]

    Think we’ll live to see the day when dietary “scientists” pay attention to genomic differences in recommending diets? I’m afraid that political correctness will rule that one out. But we’re on the verge of finding out that what you eat is less important than who your parents were. It’s getting harder every year to deny the inherited genomic role in wellness and disease.

  26. I’m glad you gave this study a fair hearing. I too think the glycine / methionine ratio is important, but when you go into the pathways, glycine and serine fairly freely interconvert, and cysteine spares methionine requirements. A useful article regarding this is Fukada et al. 2008. Effects of various amino acids on methionine-induced hyperhomocysteinemia in rats. So I believe the ratio of interest in proteins is (glycine + serine) / (methionine + cysteine). Here are some averages of that ratio for food groups:

    Among “supplemental” proteins, collagen and and its rendered product gelatin still reigns: gelatin (36.0), soy (3.4), pea (3.2), casein (2.1), egg whites, whey (1.8).

    Among more common foods, beans have the highest ratio:
    legumes (4.1), nuts (3.0), mollusks (2.8), grains (2.5), tubers, red meat, poultry (2.4), dairy, pork (2.3), fish, eggs (2.1).

    Generalized protein restriction and methionine restriction seem to be working by slightly different pathways. Protein restriction downregulates the IGF-1/PI3K/mTOR pathway, reducing protein synthesis and increasing autophagy. Methionine restriction does this as well, but excess free methionine floating about in cells appears to marked increase mitochondrial ROS generation and DNA damage.

    Personally, I’ve chosen to rely on beans and nuts for most of my lysine, ensuring a relatively low (G+S)/(M+C) ratio, but its possible omnivores may benefit from adding rendered connective tissue (in stocks etc) and gelatin to their diet.

  27. http://www.sciencemag.org/content/336/6084/1040

    This would imply caution for people with active cancer considering glycine / bone broths.

    “Metabolic reprogramming has been proposed to be a hallmark of cancer, yet a systematic characterization of the metabolic pathways active in transformed cells is currently lacking. Using mass spectrometry, we measured the consumption and release (CORE) profiles of 219 metabolites from media across the NCI-60 cancer cell lines, and integrated these data with a preexisting atlas of gene expression. This analysis identified glycine consumption and expression of the mitochondrial glycine biosynthetic pathway as strongly correlated with rates of proliferation across cancer cells. Antagonizing glycine uptake and its mitochondrial biosynthesis preferentially impaired rapidly proliferating cells. Moreover, higher expression of this pathway was associated with greater mortality in breast cancer patients. Increased reliance on glycine may represent a metabolic vulnerability for selectively targeting rapid cancer cell proliferation.”

    1. Hey Ben, I was about to post this. A great a well-thoughout publication! It’s very interesting work, and as it states, 2/3rds of the glycine used to create cancer DNA purine rings is actually synthesised in vivo. Only 1/3 come from the extracellular environment (i.e. could come from the food we eat).

  28. “Eat the whole buffalo”, like the Native American Indians, but only occasionally, when the hunt is good. The rest of the time, rely on the “3 sisters”, corn, beans and squash, and probably some wild greens. All your needs provided.

  29. Adding 10-12 g / day of glycine as a supplement may be indicated. See “A weak link in metabolism: the metabolic capacity for glycine biosynthesis does not satisfy the need for collagen synthesis” (google it) The authors show that synthesis of glycine in animals is sub-optimally rate-limited.

  30. If I remember, much of Campbell’s ‘aha!’ moments in the China study came from observing a negative effect of animal protein v.s. plant protein, in any amounts. Wonder what difference knowledge of the glycine/methionine factor would have made to Campbell, et all, and their study.

    1. I wonder what difference it might have made if Campbell, et all, had not been so biased that they were will willing to ignore any evidence that might have contradicted their religion(*), and were willing to make stuff up.

      (*) The China “Study” certainly resembles religion more closely than it does science.

    2. The negative effect of animal protein was specifically a negative effect of casein, a protein from milk, that was never a part of the Chinese diet. It would probably not have such a bad effect on people for whom it a part of their traditional diet.

  31. Bravo! Great write-up. I am currenly a vegetarian with a open mind about everything. I am happy to see a candidly thorough and upbeated-ly written report on studies that the laymen, (me), can actually appreciate and benefit from. The IGF-1 should have been the real headline; guess it doesn’t have that scary vibe that the news likes. Well please keep the blogs-a-coming

  32. The real thing is that you can live perfectly with a whole plant based diet among with exercise absence os smoking drinking etc and of course minimize or at best annihilate stress (which is the emperor of all killers).Meat nowdays is NOT IN WHATEVER POINT YOU CAN SEE IT like it was maaaaaaany years before.Truth is that meat its not nessecary to live a quality life.I could explain also the whole methionine thing and igf1 mtor1 and all the rest metabolic pathways and why especially people who do not train seriously they need low to normal levels of protein but we will not find the golden solution.People get sick and die all the time,and the reasons are MANY,from low levels of melatonin,to even very high (not nessecary protein) but very high animal protein from todays livestock which are full with deadly substances.Also many people they eat meat and in most cases they don not tend to pay attention to vegetables,fruits,nuts,legumes etc,cause they think that eating meat makes them higher in their social status.Really the reasons are many for certain its not the problem just the meat,but for certain also meat has its contribution to the whole health story.

  33. Thank God I have a understanding between healthy protein and cholesterol vs the unhealthy, do yourself a test, next time you have lab’s drawn, go out the night before (12-18 hours) and have a ribeye steak with double butter and double sour cream on the baked potatoe, then a dressing mix of blue cheeze and ranch, YUM, your levels will be off the charts, Now before you go on statins, do a 2 week spinach and green clean out 1-3 lbs per day and limit your fat intake, you numbers will drop to normal, (I have done this to my doctor)
    Now I have started (slowly building up) to eating 4 raw egg’s shells and all, wash em, toss in blender mix with 2 bananas and a scoop of vanalla ice yogurt, just Yummie !, even on the day of my labs my cholesterol levels while a tad high were nothing of that of the steak dinner and no point In changing just for having lab’s drawn, 1st the steak, grease, butter sour cream dressing contain fats that will solidify at room temp’s, the egg’s will not solidify even at 45 degrees cold in fridge, what’s the difference, well 1st the egg’s contain cholesterol your body needs and needs badly, and helps take a burdon off liver (our liver expends up to 25% of our daily energy reserves just to make the 3,000mg of cholesterol we need to be healthy, and our brain needs 25% of that) so cutting back on one type may show one result while intaking more of another type is a totally bird of a different feather, when tested after eating 4 raw egg’s just 3-4 hour’s that morning, labs on cholesterol were just a tad above normal range’s for me,
    You can google health benefits of egg’s (raw egg’s) but a warning of note, do not use any information older than august of 2012, FDA revised CFR went into effect, and their has been no egg recalls or cdc reports in 5 years on contamantaion’s involving fresh egg’s, ( when you touch the egg’s, you contamanate them , they do not contamanate you)

    1. One other point of Note, with Veganism at all time high’s and Autoimmune at all time high’s, this is one big Money business boom for big pharma, so obviously it is not in their best interest for you to eat healthy cholesterol, or healthy collagen bot found in the egg’s, (egg’s = superfood)

  34. I have read your blog, and, as others, I´m amazed by that critical thinking that you show. But some of the things you say like this make me uncomfortable:

    “The bottom line is that when we look at the mice-and-protein studies outlined in Longo’s paper, this is what we’re dealing with: a cocktail of purified ingredients, with the protein component being a well-known promoter of cancer in rodents. It’s not at all surprising that the mice eating the most of it sprouted tumors like mad. But it’s impossible to say how much of that’s due to protein per se, or to casein—especially casein that’s been stripped of all the other goodies in dairy and tossed into a party bag of refined junk”

    But after reading the China Study, and seeing here some really good arguments against it, I wonder if some of your statements have practical value.

    I have a sister with type 1 diabetes, and another member of my family with type 2. None of then are fat or eat a lot. But the thing is: If milk has Casein, and even if it is is true that it is “impossible to say how much of that is due to protein per se or casein”.

    In the case of my sister, assuming of course her genetic predisposition and that I can´t do much to revert this extremely problematic disease, I wonder:

    Why on earth should I tell her about that “impossible to say” that role of Casein might have on her future, and not tell her instead just NOT to drink milk or anything with Casein? She is more than thirty years old!

    Is it casein or whatever Cow milk can add that essential as a nutrient to a person with a condition like her´s?

    Let me put it another way: I am pretty sure I am not going to ruin her life by telling her not to drink cow milk anymore (while looking for some other nutrients for her bones, for example), but I could well do that if I start questioning everything.

    And since Cow milk is associated with so many diseases, even if we agree that is never is a cause by itself (as it happens with smoking, for example) that “impossible to say” becomes simply a non-possibility the moment one takes that source of protein (Cow milk) out of the equation.

    When you analyzed the TUOLI case, I could not find in any graph “Diabetes”. Why? No data?

    1. Isolated casein is linked to increase tumor development. But whey, which makes up the other half of cows’ milk protein package, has cancer protective qualities.

      I think you could in good conscience tell your sister not to eat isolated casein.

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