I’m talking about the late, great Ancel Keys, and his equally late (but maybe not as great) role in the history of heart disease research. The oft-repeated tale goes something like this:

Once upon a time, a scientist named Ancel Keys did an awful thing. He published a study about different countries that made it look like heart disease was associated with fat intake. But the truth was that he started out with 22 countries and just tossed out the ones that didn’t fit his hypothesis! When other researchers analyzed his data using all the original countries, the link between fat and heart disease totally vanished. Keys was a fraud, and he’s the reason my mom made me eat skim milk and Corn Chex for breakfast instead of delicious bacon and eggs. LET HIS SOUL BURN. BURN! BUUUUUURN!

Depending on who tells the story, some of the details (and wishes for eternal hellfire) may differ. But in many cases, Keys’ infamous cherry-picking is attributed to his Seven Countries Study, a landmark project that helped sculpt our common beliefs about fat. Even the Seven Countries Study page on Wikipedia—the first hit when you Google “Seven Countries Study”—says that Keys shamelessly erased the data he didn’t like:

The study began with a great many more countries … but Keys deleted the countries whose results did not match his pre-conceived conclusions, leaving him with only Japan, Italy, Great Britain, Australia, Canada and the US. Full disclosure would have made a great deal of difference.

Ditto for the page on Ancel Keys himself:

Keys collected data on deaths from coronary heart disease and fat consumption from 22 countries. Despite the fact that 22 countries provided statistics, Keys cherry-picked the data from the 7 countries which supported his theory that animal fat was the main cause of coronary heart disease in order to publicize his opinions. The results of what later became known as the “Seven Countries Study” appeared to show that serum cholesterol was strongly related to coronary heart disease mortality both at the population and at the individual level.

…And we all know Wikipedia would never lead us astray. Other big-hitters in the nutrition blogosphere have repeated this version as well, dismissing the Seven Countries Study as manipulated bias, and claiming Keys’ theory fell apart once some discarded countries were added back in—making it all the more troubling that the study became so influential.

This, we’re told, is Keys’ cherry-picked graph:

The upward curve of doom.

And this, we’re told, is the graph with all 22 countries and a diminished fat-and-heart-disease association:

And this, we’re told, is the man who ruined the world:

Unfortunately, reality sometimes infringes on the things we’d prefer to consider “facts.” This is one such occasion.

The Truth:

• Ancel Keys did not drop any countries from the Seven Countries Study. His most famous graph—the first one up above—is from a different paper he presented at a World Health Organization (WHO) conference in 1955. The Seven Countries Study didn’t even launch until 1958, and entailed much more than just plopping numbers into a pretty curve. (That said, the Seven Countries Study had plenty of problems too; some are mentioned on this site.)
• Contrary to popular belief, the cherry-picked graph didn’t convince everyone that fat was evil. In fact, Keys was pretty much ridiculed for the weakness of his fat/heart disease theory by other scientists at the WHO meeting, and whenever his graph was cited in medical journals later on, it was usually paired with some criticism. Although Keys’ work definitely shaped our current beliefs about fat, this graph didn’t exactly take the world by storm. (More on this later.)
• When all 22 countries were analyzed, the association between fat and heart disease did not go away. It actually remained statistically significant (meaning it probably wasn’t due to chance). And to make matters worse, the paper frequently cited as a “rebuttal” to Keys shows pretty clearly that animal protein had an even stronger association with heart disease than total fat did. The China Study was right all along! Time to go vegan, you guys. (Just kidding. But this part is the most interesting of all, and we’ll examine it in excruciating depth in a moment.)

Although some of his saga has been misconstrued, Keys was still far from perfect—and his eventual role in demonizing saturated fats (while glorifying polyunsaturated fats) has led us down an unfortunate road. In fact, it was his glossed-over portrayal in a recent series of anti-paleo YouTube videos that inspired me to write this post. My goal is neither to nudge Mr. Keys into sainthood nor to perpetuate his villain status—only to lay out the history and data as objectively as possible.

Here’s the more detailed scoop.

The six-country graph

Let’s look at this sucker again—smaller now, to symbolize its diminished importance (and to ease the burden of scrolling):

Keys published this graph in 1953 in a paper called called “Atherosclerosis: A problem in newer public health” (which is apparently so brilliant that neither the abstract nor full text is allowed to exist online). It was simple, really: he graphed fat consumption alongside heart disease mortality in men from six different countries—and voila! The data points landed in a tidy little line. Keys first unveiled his Wonder Curve to a handful of people at Mt. Sinai Hospital in New York, but his most famous presentation was at that WHO conference a few years later.

Curiously, instead of rolling around on the floor possessed by fat-phobia demons, his WHO audience reacted with skepticism. One report says another researcher challenged Keys to describe his “best piece of evidence” for the diet-heart idea, and effectively squashed Keys’ argument with his Oxford-educated debate tactics. As a result, poor Keys never got to show all the WHOs down in WHOville the full reasoning behind his theory, and left the conference rather defeated. (At least he didn’t steal Christmas.)

But the debate humiliation was small potatoes compared to what came next. In 1957, Jacob Yerushalmy and Herman Hilleboe—Berkeley statistician and New York State Commissioner of Health, respectively, who’d both attended the WHO meeting with Keys—wrote a scathing critique of Keys’ beloved graph. Their paper was titled “Fat in the diet and mortality from heart disease: A methodological note.” This, my friends, is the rebuttal that gets cited near and far as proof of Keys’ fraudulence, and is the source of that “original 22 countries” graph we saw a bit ago.

It’s a pretty good paper, almost clairvoyantly identifying problems that would plague epidemiology for decades to come. And like most pretty good papers, I can’t link to it for free anywhere online. Which means I’ll be screen-shotting excessively from a copy Peter at Hyperlipid kindly sent me a few months ago. (Thanks, Peter!)

It starts out with a nugget of wisdom about “indirect” studies (e.g., playing connect-the-dots with observational data):

It is well known that the indirect method merely suggests that there is an association between the characteristics studied and mortality rates and, further, that no matter how plausible such an association may appear, it is not in itself proof of a cause-effect relationship. But quotation and repetition of the suggestive association soon creates the impression that the relationship is truly valid, and ultimately it acquires status as a supporting link in a chain of presumed proof.

True that, Yerushalmy and Hilleboe. True. That. But I realize we’re not here for wisdom nuggets; we’re here to learn the truth about Ancel Keys and his picking of cherries. Here’s where the paper gets interesting:

Since no information is given by Keys on how or why the six countries were selected [for his graph], it is necessary to investigate the association between dietary fat and heart disease mortality in all countries for which information is available.

That’s right, folks. At the time he made his six-country graph, Keys actually had access to a much larger database of food intake and mortality statistics for 22 countries. Why he chose only six will forever remain one of life’s great mysteries.

And thusly, we’re presented with this. The graph with all the original countries in their non-manipulated glory. Drumroll, please. (For purposes of suspense and unbridled excitement, pretend you didn’t already see this graph a few minutes ago.) Here we have…

…a less defined, but existent upward trend. Yeah, it’s still there.

But wait! Wasn’t this graph supposed to demolish the association between fat intake and heart disease among the 22 countries? Aren’t we told that was the epic discovery of this paper? Yerushalmy and Hilleboe concede that although Keys’ six countries “greatly exaggerated the importance of the association,” the full graph still shows that there’s “some association in the conventional sense between the two variables.” And as we’ll see shortly, that “some association” was actually quite large—a statistically significant r-value of 0.59 (p < 0.02), which is pretty hefty in math-speak.

So here’s what we’ve got so far:

1. Keys cherry-picked six countries and never told us why.
2. The cherry-picking was shameful and terrible and unscientific, but the fat/heart disease association among his six countries was also present in the full set of data. Keys didn’t just make it up.

I’m not going to pat Keys on the back for deliberately choosing countries to make his case look stronger, but in terms of historical accuracy, we can’t say that he actually lied. His biggest error, in fact, had less to do with data-deletion and more to do with tunnel vision. Along with failing to explore reasons why fat might be linked to heart disease in a non-causal way, it seems Keys had his eyes locked so tightly on his lovely lipids that he didn’t notice the role of other dietary factors.

And indeed, this is where Yerushalmy and Hilleboe really hammer the heck out of Keys (he could surely never open a door again). In their paper, they explain that—in order to gauge whether the fat-heart disease relationship is really noteworthy—we also have to look at the relationship between heart disease and other elements of diet. Is fat as a category really the strongest link? Certain subsets of fat? A different macronutrient altogether? What’s the deal?

Luckily, the paper supplies us with a chart answering those very questions, using the same data Keys drew from. Apologies for the crookedness of it all. (Edit: A huge thank-you to Tynan Smith for removing said crookedness and emailing me the improved version below!)

There’s a lot going on here, so for now, let’s just look at that first column that says B-26. That’s neither a vitamin nor a rock band: it’s the official classification for “arteriosclerotic and degenerative heart disease,” which is the mortality category Keys used in his six-country graph.

To make it a little easier to prune through, here’s the B-26 column typed out. Values higher than about 0.43 (or less than -0.43) are considered statistically significant, meaning the association is very likely to be valid and not just due to random chance. Positive numbers indicate a positive correlation—heart disease goes up hand-in-hand with the food variable. Negative numbers indicate an inverse correlation—heart disease goes down as the food variable goes up.

• Total calories: 0.723
• Total calories from fat: 0.659
• Total calories from animal fat: 0.684
• Total calories from vegetable fat: -0.236
• Total calories from protein: 0.709
• Total calories from animal protein: 0.756
• Total calories from vegetable protein: -0.430
• Total calories from carbohydrate: 0.305
• Percent of calories from fat: 0.587
• Percent of calories from animal fat: 0.677
• Percent of calories from vegetable fat: -0.468
• Percent of calories from protein: 0.172
• Percent of calories from animal protein: 0.643
• Percent of calories from vegetable protein: -0.651
• Percent of calories from carbohydrate: -0.562

No use in beating around the bush. After statistic-ifying all 22 countries, Yerushalmy and Hilleboe found that not only was “fat as percent of total calories” still associated with heart disease (r = 0.59), but animal fat was clearly driving that correlation. In fact, plant fat had a negative association with heart disease (-0.47) while animal fat was uber positive (0.68). And to rub salt into the wounds of omnivores everywhere, the animal protein/plant protein division was equally stark: animal protein as a percent of total calories had a correlation of 0.64 with heart disease, while plant protein had an inverse correlation of -0.65.

In number-free language, this means the countries eating more animal foods were—as a general trend—reporting more deaths from heart disease.

As with any observational data, this doesn’t tell us diddly squat about cause and effect. Drawing correlations between countries is particularly risky because of massive confounding that’s almost impossible to account for. But if we’re going to be honest about these specific numbers, a heart disease/animal food relationship is very much there.

Oh, the irony. The fat Keys focused on for his 1953 graph was basically a reflection of meat and dairy. We’ve lambasted him for not using all the available data, but if he had, he might’ve turned his “correlation is causation” laser-gaze onto animal foods and plumb gone vegan.

Come join us, Ancel.

In fact, the relationship with heart disease and animal foods rather than “fat as a percent of total calories” becomes even more obvious when we improve the data a bit. Yerushalmy and Hilleboe—those perceptive fellas—note that the countries with the lowest rates of “death from arteriosclerosis and degenerative heart disease” had suspiciously high rates of “death from other diseases of the heart” (or B-27, if you want to get fancy):

Odd, oui? Yerushalmy and Hilleboe offer the most logical reason:

…unless there is a reasonable explanation for the high rates in these countries in this less definitive group of “other diseases of the heart,” it may be safer to operate on the assumption that in these three countries [Chile, Mexico, and France] some deaths from arteriosclerotic and degenerative heart disease are being recorded under the broad group of “other diseases of the heart.”

Indeed, classifying heart disease deaths was pretty inconsistent in the mid-1900s—and even today, “death coding” practices vary widely between countries. To get a more accurate picture, Yerushalmy and Hilleboe recommend combining the “death from arteriosclerotic and degenerative heart disease” with “other diseases of the heart,” instead of using only B-26 like Keys did. And when we do that, our correlations shift a bit. Here’s the “B-26 + B-27″ column from two charts ago:

• Total calories: 0.593
• Total calories from fat: 0.470
• Total calories from animal fat: 0.562
• Total calories from vegetable fat: -0.282
• Total calories from protein: 0.694
• Total calories from animal protein: 0.695
• Total calories from vegetable protein: -0.153
• Total calories from carbohydrate: 0.423
• Percent of calories from fat: 0.390
• Percent of calories from animal fat: 0.557
• Percent of calories from vegetable fat: -0.509
• Percent of calories from protein: 0.465
• Percent of calories from animal protein: 0.608
• Percent of calories from vegetable protein: -0.483
• Percent of calories from carbohydrate: -0.386

Nearly all the correlations got weaker, but Keys’ favorite variable—”percent of calories from fat”—dropped off into statistical-insignificance land. Animal fat and protein, however, remained strongly associated with heart disease deaths. (Gasp shock horror!)

(Note: Even though adding “other diseases of the heart” to the mix probably gives a better picture of heart disease trends, it’s quite possible—maybe inevitable—that the mortality data is still skewed for some of the “healthiest” looking countries. A WHO paper called “Miscoding and misclassification of ischaemic heart disease mortality” (PDF) points out that countries like Japan, France, and Portugal have historically been “high ill-defined coders,” meaning they dump a large portion of heart disease deaths into the wrong category. This is typically because of insufficient diagnostic methods (especially for low-income countries), local medical practices (such as Japan’s tendency to write off coronary heart disease as “heart failure”), or simple physician error. Interestingly, the WHO paper also notes that the apparent rise in heart disease as countries become “more developed” is probably due to better classification on death certificates rather than an actual increase in the disease.)

But the story’s not over yet, folks.

Yerushalmy and Hilleboe ramp it up a notch by posing the question: “How does fat (and by extension, animal food variables) relate to other causes of death?” We’ve seen what happens with heart disease, but there are certainly many other ways for the human body to perish. Are the folks eating more fat, animal fat, and animal protein generally dropping faster than their more plant-focused counterparts?

Time for another table. Omnivores, wipe away your tears. Vegans, put away your kazoos. The playing field’s about to change.

Let’s look, first, at that middle column—deaths from everything other than diseases of the heart. Notice a pattern?

• Total calories: -0.530
• Total calories from fat: -0.674
• Total calories from animal fat: -0.466
• Total calories from vegetable fat: 0.296
• Total calories from protein: -0.398
• Total calories from animal protein: -0.505
• Total calories from vegetable protein: 0.452
• Total calories from carbohydrate: 0.172
• Percent of calories from fat: -0.657
• Percent of calories from animal fat: -0.481
• Percent of calories from vegetable fat: -0.090
• Percent of calories from protein: -0.080
• Percent of calories from animal protein: -0.405
• Percent of calories from vegetable protein: 0.521
• Percent of calories from carbohydrate: 0.671

We’re basically staring at the reverse image of that earlier heart disease chart. Fat now has the strongest negative association with mortality out of any variable—a whopping -0.674 for “total calories from fat” and -0.657 for “percentage of calories from fat” (highlighted in purple). Animal fat and animal protein, but not plant fat or plant protein, are also strongly negatively associated with non-heart-disease mortality. You may notice, too, that the folks with a higher percent of calories from carbohydrate had the greatest mortality in this age range.

Even if we look at the first column for “death from all causes”—which is a little less impressive, because none of the numbers reach statistical significance—we see that all of the animal food correlations are negative. The only positive correlations, weak as they may be, are with plant protein and carbohydrates.

The results are clear. When we look at “non-cardiac deaths,” it’s the folks eating more animal fat and animal protein who are stayin’ alive. And when we look at overall mortality, animal foods sure don’t seem like stealthy killers.

Out of curiosity, I tried graphing the life expectancy for the countries in 1950 against their fat intake to see what would happen. Considering that the bulk of each nation’s fat intake came from animal sources, plotting animal food against life expectancy would probably turn out similar. (Life expectancy data taken from EarthTrends.)

Although the dots are pretty scattered when fat intake is below 25% of calories, the trend becomes unmistakable once that number passes 30%: countries with higher average fat intake had the longest life expectancies.

But does any of this—the life expectancy graph and the “death from other causes” table—prove that eating more fat and animal foods makes you live longer, or eating more carbohydrates makes you die sooner? Heck to the no. Same goes for interpreting the animal food/heart disease relationship in this data as a reason to go veggie. Yerushalmy and Hilleboe explain precisely why we shouldn’t assign a cause-and-effect relationship to anything we’ve seen so far (emphasis mine):

Table IV shows that fat calories and animal protein calories, which were seen above to be positively associated with heart disease, are here negatively associated with noncardiac diseases. A … plausible explanation is that the dietary components which according to the rank correlation coefficients appeared to be positively related to heart disease are indices of the various countries. That is, it may be that the amount of fat and protein available for consumption is an index of a country’s development, industrially, nutritionally, medically, and no doubt in other respects as well.

Bingo. Intake of fat and protein—particularly from animal sources—is usually a proxy for a country’s development. These foods goes hand-in-hand with other features specific to industrialization, making their relationship with disease likely to be confounded. Continuing on:

It may also be that countries with more abundant diet are more high developed and diagnostic acumen is greater. Hence, it is possible that in some of the countries in which less protein and fat are available, a certain percentage of deaths from arteriosclerotic and degenerative heart disease are recorded under the non cardiac groupings.

Bingo again. As we saw in the WHO paper I referenced earlier (PDF), diagnostic patterns vary tremendously between countries. This paper even points out that the countries with the highest apparent rates of coronary heart disease often have the most valid death classifications as well. In fact, if we X-out the countries with the worst track record for classifying heart disease and circle the countries whose accuracy was nearly perfect, our 22-country graph looks pretty striking. (Mexico gets an X because it didn’t even have a death-certificate system until the late 1950s. Ceylon/Sri Lanka and Chile—numbers 4 and 5 at the bottom—aren’t mentioned in the WHO paper one way or another, but I imagine they deserve some Xs too.)

Keep in mind that the WHO paper looks at mortality data for the ’70s through ’90s, while the graph above uses mortality data from 1948 and 1949. It’s possible that some of the countries improved their death-classifying practices in the decades between, so this graph should be taken with a grain of salt. Especially if you have low blood pressure.

Moreover, as Table IV shows, there are appreciable negative correlation coefficients between dietary components and death rates from B-45 (“senility, ill-defined and unknown causes”). The latter category may be considered a rough index of the accuracy of cause of death certification in the different countries. The negative association with protein and fat is further evidence of the non-”specificity” of the presumed association.

Indeed, if we glance at that third column from a couple graphs ago (click here to open it in a new window so you don’t get lost in scrolling-limbo), we’ll see that animal food variables have strong inverse associations with this death category, while the plant food variables have strong positive associations with it. Senility, ill-defined, and unknown causes are the equivalent of a doctor saying “Gee, I dunno why this person died so I’ll just file them away under one of these vague, essentially meaningless categories!” Such a scenario is much more likely in an under-developed area with shoddy medical care than an industrialized country with more diagnostic precision.

I wanted to explore this issue even further, so I dug up some data for each country’s gross domestic product (GDP) per capita in 1950. This is the measure of a country’s economic output divided by the population, and is a pretty good way to estimate standard of living. (Numbers taken from NationMaster; Israel and Ceylon/Sri Lanka are omitted because I couldn’t find their data from this year.)

So there we have it: more kindle for the idea that fat intake generally reflects a nation’s economic status and level of industrialization, and is hence vulnerable to confounding. (Or maybe correlation really is causation, and inhaling sticks of butter will make your country richer! Only one way to find out…)

One final, super-important point that could quite possibly render everything else useless: The diet data for our 22 countries comes from F.A.O. food balance sheets—which show how much food was available for consumption in each country, rather than how much food was actually consumed. If this sounds like a totally weird and unreliable way to measure what people eat, that’s because it is. Yerushalmy and Hilleboe explain the problem further:

These indices were constructed by the Food and Agriculture Organization of the United Nations from statistics on production, imports, exports, and on the proportion of available food used for purposes other than human nutrition. The underlying data are stated by F.A.O. to be subject to great limitations. Moreover, there are no doubt great differences in food “scraps” in the various countries compared. For example, it is highly probable that far more edible dietary fat is thrown into waste cans in the United States than in less fortunate countries.

That about covers it for the Yerushalmy and Hilleboe paper. Isn’t it neat that we just did a deeper analysis of the 1950s data than Keys himself probably did? Here’s a summary of the major points in case your eyes glazed over for any of that:

Keys on dietary cholesterol: one thing he got right

Although Keys was staunch in his belief that saturated fat causes heart disease by raising blood cholesterol, he was one of the brave few who insisted that dietary cholesterol was pretty much irrelevant. Thanks to a slew of early animal experiments—such as Nikolai Anitschkow’s famous rabbits—that used dietary cholesterol to induce atherosclerotic lesions, implicating dietary cholesterol with heart disease was all the rage for a while. For a long while, actually, considering how many folks today still to dump their egg yolks down the drain.

But Ancel didn’t buy it. In his paper “Human atherosclerosis and the diet” (PDF), he writes that “from these animal experiments only, the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.” Likewise, in some of his metabolic ward studies, Keys found that altering dietary cholesterol in the context of a normal diet had only minor effects on blood cholesterol, concluding that “attention to this factor alone accomplishes little.” And in his paper “The relationship of the diet to the development of atherosclerosis in man,” Keys is pretty clear about his views:

The evidence—both from experiments and from field surveys—indicates that the cholesterol content, per se, of all natural diets has no significant effect on either the serum cholesterol level or the development of atherosclerosis in man.

Good for him.

And since I probably won’t write any more blog posts until 2012 (unless someone surgically implants a new month between December and January), I want to use this final paragraph to tell everyone who reads this blog that I love you and appreciate your readership more than you could possibly imagine. I’m continually astounded that you guys not only bear with me through my sporadic blogging habits, but also create such awesome dialogues in the comment section. You people rock my world. If I were wearing socks right now, those would be rocked, too. I really mean it. Have a wonderful new year, everyone!

As most of you probably know, a documentary called “Forks Over Knives” recently hit the theaters after months of private screenings. Vegans everywhere are swooning, giddy that their message is now animated, narrated, and on sale for $14.99. Proud meat-eaters are less enthused, sometimes hilariously so. The film’s producers call it a movie that “examines the profound claim that most, if not all, of the degenerative diseases that afflict us can be controlled, or even reversed, by rejecting our present menu of animal-based and processed foods.” Roger Ebert calls it “a movie that could save your life.” I call it a movie that deftly blends fact and fiction, and has lots of pictures of vegetables.

Vilification of animal products aside, “Forks Over Knives” highlights something I strongly believe in—the power of diet and lifestyle to trump illness. When I first heard about this movie, I thought the title described a salad fork conquering a steak knife, but it turns out the imagery actually refers to diet (fork) and medicine (knife, or scalpel). Forks over knives. Food over medicine. Hey, I can get on board with that!

And along those lines, I have a weird confession. I kind of loved this movie. Not because of its scientific accuracy (which was sketchy) or because of its riveting narrative (it’s no Brave Little Toaster), but because I’m a sap when it comes to seeing sick people get healthy. “Forks Over Knives” had no shortage of personal stories from folks who, with a tearful glimmer in their eye, recounted how they evaded death by ditching their pill-popping, fast-food-noshing, insulin-injecting lifestyles. Toss in some animated graphs and gross surgery pictures, and I’m in 96 minutes of nerd heaven.

But there’s a reason I’m a health blogger and not a film critic, and I realize not everyone likes to see coronary arteries slashed open or a hear slew of personal stories intended to pluck at our heartstrings. So this won’t be your standard movie review. In fact, it isn’t a “review” so much as a chronological critique of the scientific claims made throughout the movie. My criticisms are limited to the stuff presented as evidence rather than those weepy personal stories, the filming quality, or other features I’ve got no talent in reviewing.

Why am I doing this? Am I evil?

For the record, I’m not dissecting this movie because I think everything in it is terrible. Quite the opposite, in fact. I believe the “plant-based diet doctors” got a lot of things right, and a diet of whole, unprocessed plant foods (i.e., Real Food) can bring tremendous health improvements for people who were formerly eating a low-nutrient, high-crap diet. Especially short term. But I also believe this type of diet achieves some of its success by accident, and that the perks of eliminating processed junk are inaccurately attributed to eliminating all animal foods. So the goal of this critique is to shed light on the areas where the “plant-based science” is a little, um, wilted.

Some other observations about the movie, both positive and negative, before we dive into the real critique:

• Word choice. This film was very careful about avoiding the term “vegan” and using “plant-based diet” instead—and frankly, it was a smart move. Even though the movie made it clear that no animal foods are good for you ever, the phrase “plant-based diet” sounds flexible, non-dogmatic, and limited to the realm of edible things. “Vegan,” on the other hand, is loaded with ethical and political connotations—evoking images of pamphlet-pushing PETA members, rubbery soy cheese, and Walter Bond.

• You’re good men, Charlie Browns. I’ve written (and spoken) about the “plant-based diet doctor squad” in the past—our enthusiastic Team Asparagus comprised of Dean Ornish, John McDougall, Neal Barnard, Caldwell Esselstyn, and Joel Fuhrman (although he’s a bit of a rebel, eschewing grains and allowing more fat than the rest). In this movie, Esselstyn and McDougall get plenty of camera time, and I’ve got to say, I really like these guys. No joke. They’re sincere, they’re well-intentioned, and they’re passionate about what they do. The world needs more doctors who want their patients to get off their medication, who prescribe food instead of drugs, and who have a sincere interest in changing lives. Way to go, dudes.
• Hey, fatty. A major component of Esselstyn’s heart-disease-reversal diet is the massive reduction in fat—not just from animal sources, but also the elimination of nuts, seeds, avocado, olives, olive oil, canola oil, coconut, and any other forms of concentrated plant fat. Unless I dozed off for something important, this movie barely mentioned this part of Esselstyn’s program, which I think is critical one. By keeping fat under 10% of total calories (which we also see in the disease-fighting programs of McDougall, Ornish, Pritikin, and Barnard), omega-6 intake—particularly the problematic linoleic acid—sinks like a gondola shot with a machine gun. Although these plant-based-diet doctors have a different view of fat than I do (Esselstyn, for instance, believes that any dietary fat damages the endothelial cells and promotes heart disease), it still would’ve been useful to hear about this in the movie, if only for the sake of full disclosure. I almost wonder if the movie’s creators dodged the “uber low fat” message to avoid freaking out the audience. What? We can’t even put olive oil on that ten-pound salad?!
• Go fish. As we’ll see later in this critique, some of the anecdotes used to support a plant-based diet (such as Norway’s war-time cuisine and the traditional Japanese diet) actually point to marine foods being a great addition to your menu. For some reason, no one in the movie says a gosh darn thing about fish. Are they lumping fish into the same “meat” category as Oscar Mayer Weiners? Have they forgotten that fish exists in the food supply? Are they ignoring the health benefits of marine foods that nearly everyone—even the folks who swear on their momma’s grave that red meat will kill you—agrees on? What’s going on here? I sure don’t know, but it seems awfully… fishy. (You totally saw that coming.)
• Welcome to False Dichotomyville—population: you. According to this movie, “plant-based diet” and “Standard American diet” are the only two ways you can possibly eat, and an egg is exactly the same as a bag of Cheetos. A recent pingback led me to this review at DoingSpeed.com (it’s not what you think), which nicely sums up the movie’s flip-flopping description of America’s cuisine: “the definition of the Western diet changes suddenly, one second referring to cake and donuts and the next [to] animal products.” Animal foods, it seems, are synonymous with the Western diet, and meat exists only in industrialized countries. Non-Westernized populations like the Masai, traditional Inuit, Australian aborigines, and countless hunter-gatherers have conveniently vanished for the duration of this movie. It must be awesome to selectively choose reality like that!
• Fast forward. For me, the most interesting part of this movie happened around the 30 minute mark. First, the film discusses a 1973 corn subsidy bill that encouraged a massive increase in corn production—which pretty much explains why so many foods these days are injected full of high-fructose corn syrup or other cheap, corn-based ingredients. It’s all about the money. Shortly after that, the movie gives some camera time to evolutionary psychologist Dr. Doug Lisle, who tells us about a concept called the Pleasure Trap—a motivational triad of “seeking pleasure, avoiding pain, and conserving energy” that all our years of evolution have hardwired us for. Because our modern, processed foods are so rich in calories and easy to access, they provide a high degree of dietary reward with almost no effort. Our bodies freakin’ love this. So much, in fact, that our brains say “eat eat eat!” in the presence of such foods and our natural hunger signals get overridden. That worked well in the wild, when periods of food abundance were interrupted with periods of famine. But these days, it just makes it easy to get fat. And the Pleasure Trap applies to much more than just food. Indeed, we’re biologically driven to seek the easy way out, to avoid pain, and to pursue things that make us feel good.

Critique time!

After a collage of soundbites about how awful and unhealthy Americans are (ya think?), the fun begins around the 13-minute mark, when we get a brief biology lesson on the C-word: cholesterol. Props to the scriptwriter for at least noting that cholesterol is a “natural and essential substance” (per some descriptions, you’d think the stuff was toxic sludge), but the narration goes downhill from there. After outlining cholesterol’s important biological functions, the movie states:

13:06—But when we consume dietary cholesterol, which is only found in animal foods like meat, eggs, and dairy products, it tends to stay in the bloodstream. This so-called plaque is what collects on the inside of our blood vessels and is the major cause of coronary artery disease.

Yikes! Did we slip and fall back into the ’80s?

For starters, cholesterol from animal foods does not have some magical ability to set up permanent camp in your bloodstream and turn into plaque, just by sheer virtue of its animal-foodness. This was a common line of thought decades ago, but as research progressed, we figured out that the body is actually pretty awesome at regulating cholesterol production in response to what we ingest from food. As this paper from 2009 explains, the supposed link between dietary and serum cholesterol stems from studies that had fundamental design flaws, failed to separate the effects of cholesterol different types of fat intake, or were performed on animals that are obligate herbivores (hey there, rabbits!). The doctors in “Forks Over Knives,” it seems, are among the few stragglers who still believe dietary cholesterol is harmful.

Most people (about 70% of the population) are “hypo-responders” when it comes to cholesterol intake—meaning the cholesterol they eat from food has a negligible effect on the total cholesterol in their blood. A smaller slice of the population (“hyper-responders”) see a greater rise in blood cholesterol after eating high-cholesterol foods, but the change is because both LDL and HDL increase proportionally, preserving the cholesterol ratio and leaving heart disease risk the same as what it was before. (As more evidence, a similar study (PDF) found no change in LDL/HDL ratio in either they hypo-responders or hyper-responders, even when feeding folks an extra 640 mg of cholesterol per day.)

Not only that, but some cholesterol-rich foods like eggs have actually been shown to make LDL (the so-called “bad” cholesterol) less atherogenic by increasing its particle size. And in one study of diabetics, a high-protein, high-cholesterol diet improved HDL more than a similar high-protein diet with a low cholesterol content (though it was likely other components of the foods involved, rather than the dietary cholesterol itself, that caused this). It’s a weird, wobbly stretch to paint animal foods as a death knell because they contain cholesterol.

Enter: T. Colin Campbell

Minute 17:01—"We learned that animal protein was really good in turning on cancer." There's an inappropriate joke buried somewhere in there.

Now we’re talkin’! To anyone who’s read (or is moderately familiar with) the book “The China Study,” the next part of the movie is a trip down memory lane. We learn about Campbell’s work in the Philippines, where he was trying to improve the lives of malnourished children by filling their diets with more protein. It was here that the trajectory of his career made its first wild turn:

Minute 15:42—But then Dr. Campbell stumbled upon a piece of information that was extremely important. … The more affluent families in the Philippines … were eating relatively high amounts of animal-based foods. But at the same time, they were the ones who were most likely to have children susceptible to getting liver cancer.

(Gasp! Shock! Horror! Let me insert the requisite “correlation isn’t causation” warning before we continue.)

Minute 16:10—Shortly afterward, Dr. Campbell came across a scientific paper published in a little-known Indian medical journal. It detailed work that had been done on a population of experimental rats that were first exposed to a carcinogen called aflatoxin, then fed a diet of casein, the main protein found in milk. [Campbell:] “They were testing the effect of protein on the development of liver cancer. They used two different levels of protein: They used 20% of total calories, and then they used a much lower level, 5%. Twenty percent turned on cancer; 5% turned it off.”

Although the above is true, it’s only one (misleading) part of the story. We’ll explore exactly what’s wrong with this summary later on, when Campbell’s own research comes to the fore in the film. But for now, let’s just look at one spot where the film lets a figurative cat (err, rat?) out of the bag.

The paper from India that Campbell found is called The Effect of Dietary Protein on Carcinogenesis of Aflatoxin, which appeared in the Archives of Pathology in 1968. Indeed, the researchers discovered that rats fed 5% of their diet as casein were generally free from cancerous growths, whereas the rats fed 20% casein were riddled with ‘em. But at the 16:37-minute mark, we get to see a snippet of this paper that shows us something equally important:

Don’t get distracted by those red letters! What we’re interested in is the sentence near the bottom, which the film’s producers apparently didn’t notice: ”In all, 30 rats on the high-protein diet and 12 on the low-protein diet survived for more than a year.”

Let that sink in for a moment. Maybe it’ll hit a little harder if I told you that in the “high protein vs. low protein” experiments discussed in this paper, 10 low-protein rats died prematurely while all the high-protein rats stayed alive. In other words, the overall survival rate for the 20% casein group was much better than for the 5% casein group, despite the fact they had liver tumors. The low-protein rats were dying rapidly—just not from liver cancer. And as we’ll see later, the reason the non-dead, low-protein rats didn’t get tumors was partly because their liver cells were committing mass suicide. 

In his article “The Curious Case of Campbell’s Rats: Does Protein Deficiency Prevent Cancer?“, Chris Masterjohn explores this oddity further by plowing through the Indian research Campbell talked about. If you haven’t seen this article yet, you owe it yourself to read it now, because it’s kind of mind-blowing—both for Chris’s analysis of the Indian research and his takedown of Campbell’s own rat studies. (And for anyone who’s going to gripe about this article being posted on the Weston A. Price Foundation site (I know you gripers are out there), I encourage you to read it anyway, use your noggin, and check the references for yourself rather than dismissing it sight unseen.)

Regarding that paper from India that sparked Campbell’s “aha protein evil!” moment, Chris notes that “Campbell never tells us … that these Indian researchers actually published this paper as part of a two-paper set, one showing that low-casein diets make aflatoxin much more acutely toxic to rats.” This second paper is called The Effect of Dietary Protein on Liver Injury in Weanling Rats, and indeed, it shows that rats on low-protein diets experience much more actual liver damage than rats on high-protein diets when they’re exposed to aflatoxin. They don’t get cancer, but they’re sicker overall because they’re less capable of detoxifying aflatxoin—leading to fun stuff like fatty liver, liver necrosis (cell death), proliferation of bile duct tissue, and early death. As Chris puts it:

Somehow, I doubt many people would read this study and shout “sign me up!” for a low-protein, plant-based diet if it is going to save them from cancer at the expense of killing them in their youth.

Indeed! As we’ll see later in this critique, Campbell’s own low-protein rats weren’t a rosy picture of health, either. Even more exciting, we’ll look at some more studies conducted in India showing that low-casein diets—but not high-casein diets—promote cancer when aflatoxin dosage is at a lower, real-world-applicable level. Fun times ahead! (If you’re impatient, you can skip to that section right now by clicking here.)

Esselstyn: From operating table to kitchen table

Next up, we get a bigger peek into the life of one seriously cool cat: Dr. Caldwell Esselstyn, physician at the Cleveland Clinic. Although Esselstyn noted—in an earlier segment of the movie—that he loved surgery for its ability to neatly remove a problem from the body, he faced some disillusionment as his career progressed. In 1978, when Esselstyn was chairman of Breast Cancer Task Force at Cleveland Clinic, he was unhappy that he was only treating people who were already ill and doing diddly squat for the “next unsuspecting victim.” He wanted to focus on prevention. So he put on his sleuth cap and set off to investigate—first by shoveling through global statistics for cancer.

Only YOU can prevent forest fires. And heart disease.

For the next few minutes, we get to hear about the alarming discoveries this investigation uncovered. Don’t want breast cancer? Then move to Kenya, where the rates are 82 times lower than in the US (well, at least they were in 1978). Got prostate cancer? Japan doesn’t: In 1958, there were only 18 autopsy-proven deaths from prostate cancer in the whole country. Compare that to the 14,000 in the US for the same year. Heart disease, too, was lower outside of America:

Minute 19:21—Dr. Esselstyn also discovered that in the 1970s, the risk for heart disease in rural China was 12 times lower than it was in the US. And in the highlands of Papau New Guinea, heart disease was rarely encountered. The link he noticed between all the areas he studied was simple. [Esselstyn:] “Virtually the Western diet was nonexistant. They had no animal products. No dairy, they had no meat.”

…And there it is. Again, we have the conflating of “Western diet” with “animal products,” as if meat and dairy are the major dietary difference between Westernized and non-Westernized populations. Oy! (By the way, here’s a friendly reminder that in rural China—at least based on the China Study data—heart disease mortality was actually inversely associated with meat intake, meaning the folks eating the least meat actually died more frequently of heart disease. It doesn’t mean too much as a lowly correlation, but it does fly against the assumption that animal foods are always linked with heart disease.)

Next is where it really gets interesting. About 20 minutes into the movie, we get a fascinating historical tidbit about diet and heart disease in war-time Norway:

Minute 19:50—In World War II, the Germans occupied Norway. Among the first things they did was confiscate all the livestock and farm animals to provide supplies for their own troops. So the Norwegians were forced to eat mainly plant-based foods.

In the movie, Esselstyn eagerly explains how cardiovascular disease went kerplunk when the Germans invaded in 1939, only to zip back up as soon as the war was over—perfectly coinciding with their supposed near-vegan period. How obvious it is! The Norwegians went veggie and healthied up; they returned to their lamb and gjetost and re-clogged their arteries. As Esselstyn puts it: ”With the cessation of hostilities in 1945, back comes the meat, back comes the dairy, back comes the strokes and heart attacks.”

Here’s the graph the movie walks us through. The Nazi flag marks the arrival of the Germans; 1945 is when they left. (Right below it is a similar graph from a 1951 issue of “The Lancet” that’s even more dramatic. After adjusting for an unequal age distribution (and unrealistically low mortality in the ’20s and ’30s), we can see that death from cardiovascular disease really did nosedive to a lower rate than Norway had seen in the past few decades.)

War! What is it good for? Reversing heart disease, apparently.

Oh, Norway; how close you were to cardiovascular salvation! Nice job screwing it up.

The intended point, of course, is that the dip in mortality was from giving up animal foods. When the Germans swiped all sentient creatures from the food supply, Norwegian hearts pumped with atherosclerosis-free ease—proving that going “plant based” will save your ticker. It sounds convincing enough, and the graph is compelling*… but is there more to the story than meets the eye?

*Note: If you look at the numbers on the right side of the graph, you’ll see mortality dropped from 30 to 24 deaths per 10,000—a difference of only six people per 10,000. That’s still nothing to sneeze at (especially if one of the saved was your great-grandpa Bjørn who helped you exist), but the graph gives an exaggerated view of the actual change in mortality.

Luckily, there are a few resources out there that track the war-time diet changes in more detail. One is a paper discussing how nutrition affected Norwegian youngsters during the war, which you can read as a PDF here (spoiler: the kids were shorties). But the part we’re interested in is the table estimating how food intake changed during the war. The numbers represent how much each food increased or decreased during the war (percentage wise) compared to the pre-war values.

Did meat and milk intake go down? Fo’ sho’ (although clearly not to zero). But look what else happened. Sugar consumption was chopped in half. Both butter and margarine intake decreased significantly. Veggie intake shot up. And perhaps most significantly, fish consumption increased by a whopping 200%, a bigger change than seen with any other single food item. Need I mention the eighty gazillion studies showing the benefits of fish, DHA, and an improved omega-3/omega-6 ratio for cardiovascular health?

The paper also notes that total calorie intake decreased by about 20% compared to pre-war levels and weight loss was common. Did calorie restriction and sinking body mass play a role in mortality changes? Definitely maybe.

Oh, but it gets better. There’s a section in a super old issue of “Proceedings of the Nutrition Society” called “Food Conditions in Norway During the War, 1939-45” with even juicier details. I couldn’t find any free copies to link to, so I’ll type out the relevant bits. But first, take another look at that “circulatory disease” graph from the movie and verify with your own eyes that the first (and biggest) drop in mortality happened in 1941.

Now read this:

During the first year [starting in spring of 1940] the rationing included all imported foods, bread, fats, sugar, coffee, cocoa, syrup, and coffee substitute. In the second year [starting in late 1941] all kinds of meat and pork, eggs, milk and dairy products were rationed…

See the problem?

Animal foods didn’t really dwindle from Norwegian kitchens until the end of 1941. Even if we ignore the fact that changes in mortality would naturally lag behind changes in diet, it’s hard to blame the 1941 drop in cardiovascular disease on something that mostly happened in 1942! D’oh. Time-wise, there’s a stronger link between the mortality tailspin and the previous year of food rationing: “imported foods, bread, fats, sugar, coffee, cocoa, syrup, and coffee substitute.” (Or maybe it was just the anticipation of ditching meat that made everyone healthier.)

Despite the dismal record keeping, a few studies were “secretly performed” in Oslo to track changes in food intake during the war. Between 30 and 50 families were surveyed three times annually from 1941 to 1945, giving us a nice little diet portrait encompassing not only rationed food, but also the “black market” items people were eating. Although it’s hard to say how accurately this represents the food intake of Norway’s whole population, it’s at least a place to start. And unlike the last table, it breaks down food consumption year by year, rather comparing only war-time and pre-war values. (Note that the top row is for the years 1936-7 and the next is for 1941—it seems there isn’t any data for the gap between.)

I pity da fool who doesn’t enlarge this image.

From "Proceedings of the Nutrition Society," 1947. Volume 5, issue 4, page 264.

Numbers, numbers, everywhere! Let’s distill the major stuff from that chart so you don’t have to squint at it forever:

• Cod liver oil became a standard addition to war-time diets. (Interestingly, the paper later notes a huge improvement in Norwegian dental health between 1940 and 1945: By the end of the war, the average number of cavities was less than half of what it was before the war. Vitamin A and D, anyone?)
• As we saw earlier, fish intake increased massively. So did ‘taters, roots, and vegetables, particularly in 1942 and 1943.
• Intake of whole milk was actually higher in 1941 compared to before the war, but then gradually diminished.
• Intake of skim milk was higher throughout the war than before it.
• Cheese, cream, and condensed milk started dropping off the radar at the end of 1941.
• Meat hit a major low in 1943 and 1944.
• Added fats like margarine and butter declined, particularly in 1942 and 1943.
• Flour, meal, groats, and bread intake went up slightly, mainly from black-market sources.
• Intake of sugar, coffee, and chocolate declined significantly.
• Fruit also declined significantly, and as we’ll see later, mainly came in the form of locally picked berries.

There’s no doubt about it: In 1941, when cardiovascular disease started plummeting, Norwegians were eating more total dairy (light blue line) than they were before the war, when the death rate was higher.

How about flesh foods? Again, this is in grams per day for your average Norwegian man:

For the families surveyed in Oslo, fish and meat consumption were almost exactly inverse: Fish intake rose in perfect step with the decline of meat. And at its peak, the average man was consuming almost three-quarters of a pound of fish a day! That’s a decent chunk o’ seafood. Because meat and fish intake were so tightly correlated, it’s hard—maybe impossible, given the sparse data available—to separate any mortality effects of meat reduction from the huge spike in marine foods.

One more gem from this paper. In another table, we get yearly data for Norway’s daily intake of total animal protein (in grams) for 1936-7 and then from 1942 to 1945. This should  be fun, right? Here’s a graphed version of that data, paired up with the cardiovascular disease mortality rates from those same years. (To make it easier to see the interplay between the lines, I doubled the mortality figures to make them “per 20,000 people” instead of “per 10,000.”)

Well, golly. In both 1942 and 1943, when mortality made its steepest descent, animal protein intake was actually higher than it was before the war! The major decline in total animal protein intake didn’t happen until 1944 and 1945, well after Norway had already seen cardiovascular disease plummet. Again, this data isn’t rock-solid because of poor record keeping, and correlation isn’t causation anyway, but it sure doesn’t support the argument that Norway got healthier due to a plant-based diet.

For comparison’s sake, this is what a graph would look like if these variables were tightly linked:

One more thing before we emigrate from Norway. After poking around the interwebs, I found a gem of a paper called Food rationing during World War two: a special case of sustainable consumption? The whole thing’s pretty interesting, but the best nuggets are the details about actual foods eaten in Norway during the war (and the reiteration that “sugar rations [were] restricted to 3 kilos per household per year,” which is less than 2% of what a four-person Norwegian family consumes today.)

Minute 21:56—[McDougall:] Their kids, they started to give up the rice and replace it with the animal foods, the dairy products, the meats… and the results were obvious. They got fat and sick. I knew, at that point, what causes most diseases.

The movie goes on to explain that animal protein has some mystical, inexplicable, yet very real ability to promote disease—a property that plant protein lacks. Referencing Campbell’s rat studies, we’re told that “the results were consistent: Nutrients from animal foods promoted cancer growth, while nutrients from plant foods decreased cancer growth.” And yet…

Minute 29:20—Campbell hadn’t identified a specific biological mechanism that caused the effects he observed. “It finally occurred to me that there was no such thing as the mechanism. What we were looking at was a symphony of mechanisms,” he said.

Out of all the moments in the movie, this might have been the biggest face-palmer for me.

It just so happens that Campbell did identify exactly why casein behaved differently than plant proteins in his rat studies. Decades ago. In 1989. The discovery emerged from a study he conducted on “protein quality” and liver tumor growth, which you can find here. Although regular wheat protein didn’t spur tumor growth like casein did,* wheat protein behaved exactly like casein as soon as Campbell added lysine, the amino acid wheat is low in. Basically, any complete set of amino acids—whether from the animal kingdom or plant kingdom—is going to have the same cancer-promoting effects. (At least when aflatoxin dosing is very high. At lower aflatoxin dosing, that same complete protein will protect against oft-deadly liver damage. In fact, in the paper cited above, Campbell notes that the unsupplemented gluten groups and low-casein group—despite getting fewer “foci” that mark the start of cancer—had far worse liver injury than the high-casein group. He writes: ”All animals developed bile duct proliferation, which characterizes the acutely toxic response to aflatoxin B1 (data not presented). The most severe lesions occurred in the experimental groups with the lowest response of foci [5% casein and 20% unsupplemented gluten].”)

*Note: Campbell actually used casein diets that were supplemented with methionine (test diet PDF here), an amino acid that casein is low in. This made the casein a more “complete” protein and may have influenced the cancer-promoting abilities of the casein diets. If we’re going to compare apples and apples, we could look at the casein-supplemented-with-methionine diet right next to the gluten-supplemented-with-lysine diet. And when we do that, we find that both are equally powerful at promoting tumor growth.

The reason this finding is so important is that it shows, fairly convincingly, that Campbell’s findings only apply in a lab setting—where rats are fed a single source of protein for their entire lives. The rats that stayed cancer-free on an unsupplemented gluten diet were the equivalent of a human eating nothing but wheat, every single day, from the moment they’re weaned off Momma’s teat until the day they die. A vegan eating a mixture of plant foods will naturally end up consuming complementary amino acids, and their body will synthesize the “complete protein” that Campbell says is cancer-promoting. For instance, in the common combination of rice and beans, beans supply extra lysine that rice is low in—the same effect as supplementing gluten with this amino acid.

It’s not like Campbell forgot about his discovery, either. In his 2009 response to a critique by Joseph Mercola, Campbell wrote:

The adverse effects of animal protein, as illustrated in our laboratory by the effects of casein, are related to their amino acid composition. … There have been many different kinds of studies for well over a half century showing that the nutritional responses of different proteins are attributed to their differing amino acid compositions. … These differences in nutritional response disappear when any limiting amino acids are restored.

Wheat protein, unlike casein for example, did not stimulate cancer development but when its limiting amino acid, lysine, was restored, it acted just like casein. There have been literally thousands of studies going back many decades showing a similar effect on body growth and other events associated with body growth—all resulting from differences in amino acid composition of different proteins.

Enough said. Let’s look at one more snippet from this segment before we move on:

Minute 29:00—Over the next several years, Campbell initiated more extensive lab studies using various animal and plant nutrients. The results were consistent. Nutrients from animal foods promoted cancer growth, while nutrients from plant foods decreased cancer growth.

Beep! False. Campbell actually discovered that certain animal fats are superior to certain plant fats in terms of cancer protection. In a study published in 1985, he found that fish oil tends to inhibit cancer, and in a couple other studies, found that corn oil appears to promote it (such as here).

Esselstyn: The study cogs start turnin’

But enough about rats and vegetable protein. Next up, the movie returns to one of our movie’s shining (human) stars, Caldwell Esselstyn. In the 1980s, with “prevention!” flashing relentlessly in his mind’s eye, Esselstyn finally got the chance to do what his years of surgery never allowed: Fix heart disease with food instead of scalpels.

Minute 44:11—In the mid-1980s, Dr. Caldwell Esselstyn was struggling to organize a study on coronary artery disease. His plan was to put a group of patients on a diet of low-fat, plant-based foods along with small quantities of low-fat dairy products and minimal amounts of cholesterol-reducing drugs.

Indeed, that’s the gist of it: a low-fat, plant-based diet with a scoop of statins for dessert. But since the film doesn’t dive into the finer details of the diet, let’s look at how Esselstyn describes his program in his book, “Prevent and Reverse Heart Disease.” From pages 5, 6, and 72, we  can see that the diet eliminates:

• Anything with a “mother or a face,” including meat, fish, and poultry
• All dairy*
• All nuts and avocados
• All oils, such as soybean oil, olive oil, corn oil, cottonseed oil, canola oil, and anything else with “oil” in the name
• All solid fats like margarine and butter
• All foods—whether pre-made or prepared at home—that contain even a drop of added fat
• Any grains that aren’t cross-your-heart, swear-on-your-grandmomma’s-grave, 100% whole. According to Esselstyn, this includes eliminating items that have healthy-sounding ingredients like “multigrain, cracked wheat, seven-grain, stone-ground, 100 percent wheat, enriched flour, or degerminated cornmeal”

On the flip side, the diet allows:

• All vegetables, including leafy greens, root veggies, and other veggies encompassing all the beautiful colors of the rainbow
• Legumes such as lentils, peas, and beans
• Whole grains ranging from the commonplace (whole wheat, corn, wild rice) to the exotic (quinoa, millet, amaranth, teff, kamut, spelt, rye)—but only if they contain no added fat, high-fructose corn syrup, or even a smidgen of refined grain
• All fruit

And if you think this diet is flexible and allows some cheat-meal wiggle room, you’re sadly mistaken. Esselstyn is a self-admitted stickler, and insists that a fundamental rule of his program is that “it contains not a single item of any food known to cause or promote the development of vascular disease.” Which, to him, means a life permanently devoid of pot roast, Nutty Buddies, or butter on your endless bowls of steamed kale.

Although his program doesn’t specifically forbid processed foods, adhering to his rules pretty much ensures everything you eat will be Real Food. For instance, his diet manages to eliminate even the “fat free” replacement products we’ve all seen at the store:

If you see any of the following words or phrases on a label—glycerin, hydrogenated, partially hydrogenated, mono or diglycerides—avoid the product. These are all sneaky forms of fat. Snackwell’s devil’s food “fat-free” cookies* list 0 grams of fat on the nutritional chart required on all packages. But if you read the ingredients, you notice that glycerin is listed fifth among them. Similarly, Kraft’s zesty Italian fat-free dressing and Wishbone’s fat-free ranch both list soybean oil and dairy products among their ingredients. But because the portion sizes are small, these products can still be called “fat-free,” under the government’s standard. Read the ingredients. (Page 124)

*Forget glycerin! How ’bout avoiding this junk because the first four ingredients are sugar, refined flour, high-fructose corn syrup, and corn syrup?

Indeed, Esselstyn’s diet categorically eliminates most “fat-free” Frankenfoods—many of which were wildly popular when he conducted his study in the ’80s and ’90s. Apparently, he nixes them not because they contain ingredients so awful they’d make a billygoat puke, but because their microscopic amount of fat is still too much. In a lipid-phobic era when dieters swapped fat for refined carbs, Esselstyn accidentally ‘rescued’ his patients from junk-filled replacement foods, which we now know are often worse than the originals. He got it right for the wrong reasons.

And lastly, despite what it may seem, Esselstyn’s diet is not a whole-grain free-for-all. His book describes the diet as decidedly vegetable-based, and notes that you may need to scale down on the starches to avoid unwanted pounds:

If you are eating a plant-based, no-oil, whole-grain diet filled with leafy greens and all the colorful vegetables, you don’t need to worry about weight. … However, if you let whole grains, starchy vegetables, and desserts dominate, weight can begin to creep back. If that happens, simply cut back on grains and starches, increase your consumption of leafy greens and colorful vegetables, and cut out desserts. (Page 126)

As we can see, Esselstyn’s program entails a lot more than a simple shift to plant foods. Here are the likely culprits behind his success:

• By completely eliminating oils, Esselstyn’s diet causes a massive reduction in the omega-6 fats—particularly linoleic acid—running wild in Western diets. (And more broadly, it slashes intake of polyunsaturated fats, which are the type of fat most likely to promote LDL oxidation because of their unstable chemical structure.) Boom! Down goes polyunsaturated fat intake, down goes omega-6 intake, down goes inflammation, down goes some major components of heart disease. Although Esselstyn achieves this by giving the boot to all fats, the same thing could be achieved by just eliminating foods and oils high in polyunsaturated fats, particularly industrial seed oils like soybean oil and corn oil. (If you’re thinking, “But those are the types of oils the government tells us are healthy,” please read this.)
• Due to its strict no-added-fat rule, Esselstyn’s program eliminates 99% of what you’d find in a gas-station convenience store, a vending machine, or a crinkly silver Frito-Lay bag. In other words, this is a no-junk diet. Sure, animal foods are out—but so are the even wider range of low-nutrient snacks, processed desserts, convenience foods, and other manufactured items that usually fill American kitchens.
• By allowing only 100% whole-grain foods with no added fat or sugars, Esselstyn makes it pretty tough to eat processed wheat products like bread, pasta, cereal, bagels, pastries, crackers, and other grainy goodies. In his book, Esselstyn acknowledges how hard it is to find bread that fits into his diet plan, and endorses sprouted grain products by companies like Ezekiel. As a result, the main starches in this diet are likely to be from roots, starchy vegetables, legumes, squash, and grains that still look like they did when they came off the plant—like corn or wild rice. The movie showed the following display as an example of an Esselstyn-approved feast.

Behold: plants.

Now that we have a better idea of what Esselstyn’s diet entails, let’s hop back into the movie.

Minute 44:32—[Esselstyn:] “Slowly, over the next 18 months, I got the patients that I’d asked for. But the ones they sent me were a little bit sicker than I’d thought! These were patients who had failed their first or second bypass operation, they had failed their first or second angioplasty, and there were five who were told by their expert cardiologist that they would not live out the year.”

We then get to meet one of those so-called lost causes: Evelyn Oswick, who’d been one of Esselstyn’s most “gravely ill” patients. Not only had she already suffered from two heart attacks by the age of 59, but her doctors thought her situation was so hopeless that they told her—quite literally—to go home, sit in a rocking chair, and wait to die. But as evidenced by the fact she appeared in “Forks Over Knives,” she’s not only alive, but quite the bright-eyed and bushy-tailed survivor. Woohoo, Evelyn! Woohoo, Dr. Esselstyn! Woohoo, plant-based diet!

Although we don’t have enough data to really analyze her success, I’ve got to wonder if ditching meat—or even the fat—was really the thing that helped. Here’s how she describes her previous diet:

Minute 45:00—[Oswick:] “I ate all the chocolate I could eat, I ate every doughnut I could get my hands on… oh, I just loved things like that. A lot of gravy.”

"It was that drop of glycerin in the candy that did me in."

Esselstyn then describes how his study was performed. For a full five years, he met with his patients once every two weeks to draw blood, take their blood pressure, measure their weight, and endure the nickname “Dr. Sprouts.” We know Mrs. Oswick is alive, but what happened to the other 23 study subjects? Did they end up back on the operating table, wads of carrots lodged in their veins? Did they miraculously heal? We’ll have to wait to find out, because now it’s time to learn about…

The China Study

I’ll admit it: I was pretty excited to see what “Forks Over Knives” had to say about the China Study—a massive epidemiological project and namesake for Campbell’s bestselling book. Would we get an elaborate, attempted indictment of animal foods by blaming all woes of the human body on high cholesterol? Would the producers sacrifice accuracy for simplicity and just say “animal foods made bad things happen?” Would Campbell warn the audience not to Google around for critiques of his study, because they’re all written by shills for the meat industry, or—worse—liberal arts majors?

Finally, we get to find out. After nearly 50 minutes of nail-biting anticipation for our China Study segment, we see T. Colin Campbell and his colleague, Junshi Chen, thumbing through a copy of “Diet, Life-style, and Mortality in China“—the 900-page tome showcasing the data they spent so many years gathering. Oh, sweet reminiscence! This is the same book that sat on my desk for three months last year, collecting blood, sweat, and sticky-notes.

"Orange you glad I didn't say banana?"

Campbell briefly explains how this study generated a whopping 8,000 to 9,000 statistically significant correlations. “This means that if 19 out of 20 are pointing in the same direction, it’s highly significant, and likely to be true,” he says. (I’d add that “true” isn’t the same as “meaningful”—variables can be strongly and legitimately correlated, but not actually have a cause-and-effect relationship.) After learning a bit more about how the data was presented in that giant book, we get to the good stuff. The summary of it all. The fruit of international labor. The culmination of those 9,000 statistically significant correlations. Are you ready?

Minute 49:30—[Chen:] “I think the major message we got out of this correlation analysis is only one message: The plant-food based diet—mainly cereal grains, vegetables, and fruits, and very little animal food—is always associated with lower mortality of certain cancers, stroke, and coronary heart disease.”

That’s a pretty simple message to get from such a big, complicated study! Too bad it’s baloney.

What Campbell and Chen imply in this movie clip is that all those correlations are, serendipitously, singing the same tune: That plant foods offer protection against diseases, while animal foods tend to promote them. Alas, the trends in this study are anything but straightforward—and as Campbell himself has pointed out, the unadjusted correlations can be quite misleading:

“Use of these correlations … should only be done with caution, that is, being careful not to infer one-to-one causal associations. … First, a variable may reflect the effects of other factors that change along with the variable under study. Therefore, this requires adjustment for confounding factors.”

Agreed, good sir. But since we’ve just been told in “Forks Over Knives” that these correlations generally point in the same direction (and reinforce the idea that animal foods cause disease), let’s put relevance aside and see if that claim is up to snuff.

Note for anyone needing a math catch-up: A correlation is basically a relationship between two things—meaning they both go up at the same time (a positive correlation) or one goes up while the other goes down (a negative or “inverse” correlation). For example, your age is positively correlated with the number of wrinkles on your face, but your age is negatively correlated with the amount of time you spend Googling “Justin Bieber.” Correlations are usually expressed as numbers between 1 and -1, with zero indicating that there’s absolutely no relationship between the variables. The farther away the number is from zero, the stronger the relationship—so a value of 0.54, for instance, would be stronger than a value of 0.12. In the case of our China Study data, strong positive numbers indicate that a certain food is associated with more of a certain disease, while strong negative numbers indicate the food is associated with less of that disease.

Get it? Got it? Good!

In my China Study critique last year, I pulled a bunch of data directly from “Diet, Life-style, and Mortality in China”—the same book Campbell and Chen are huddled around in that last picture—showing just how inconsistent the “plant-based diet is healthier” message really is. For instance, we’ve got peculiar things like this:

• Plant protein has a correlation of 0.21 with heart disease (positive)
• Non-fish animal protein has a correlation of 0.01 with heart disease (neutral)
• Fish protein has a correlation of -0.11 with heart disease (inverse)
• Meat intake has a correlation of -0.28 with heart disease (strongly inverse)
• Fish intake has a correlation of -0.15 with heart disease (inverse)
• Egg intake has a correlation of -0.13 with heart disease (inverse)
• Wheat has a correlation of 0.67 with heart disease (really flippin’ high!)—which is not only the strongest association between any food and heart disease, but remained sky-high even when I tried adjusting for anything that might be confounding it.*

*Our grain-happy “conventional wisdom” might scoff at the idea of wheat being atherogenic, but there’s at least one cardiologist out there who has great success treating his patients’ heart disease by eliminating wheat (and not going low-fat)—and he recently published a fantastic book showing why modern wheat is so problematic.

First, let’s look at how various foods correlate with “death from all medical causes” for adults age 35 to 69. This variable is more interesting to me than “all-cause mortality” because it excludes things like drowning, car accidents, getting mauled by a pack of rabid wolves, and other modes of death that have nothing to do with diet (unless the wolves found you because they smelled your nitrate-free liverwurst).

Correlations with death from all medical causes, ages 35 to 69.

All aboard the Abbreviation Train! Choo-choo. For reference, PLNT =  plant, ANIM = animal, PROT = protein, and CHOL = dietary cholesterol. The variables preceded by the letter “M” are mortality statistics; the ones preceded by “P” are plasma measurements; the ones preceded by “U” are urine measurements; the ones preceded by “D” are foods from the diet survey; and the ones preceded by “Q” are from a questionnaire.

I’ve highlighted the food variables specific to either the plant or animal kingdom, so let’s take a gander at how they correlate with “all medical deaths.” Total plant food, percent of diet as plant protein, and wheat? All strongly positively associated with death from all medical causes, meaning that as intake of these things goes up, so does the risk of keeling over from something body-related. Total animal protein intake, percent of total calories as animal protein, egg intake, meat intake, red meat intake, fish intake, and consumption of dietary cholesterol? All strongly negatively associated with death from all medical causes, meaning that as intake of these foods goes up, medical mortality rates decline. Again, many of these associations may be—and probably are—totally meaningless, but they describe an important trend: For whatever reason, in China, the animal-food-eaters are living longer than their more plant-based counterparts.

…Which brings us to another problem. As we saw with heart disease in Norway, high rates of infectious disease can sometimes obscure the true prevalence of chronic disease—because folks are getting wiped out by short-term illness before they have a chance to die from things like cancer, strokes, or heart attacks. Even if their arteries are plaqued up the wazoo or their bodies riddled with tumors, it’ll be the tuberculosis, or the pneumonia, or the other infectious disease that shows up on the death certificate (and, subsequently, in the data). In the China Study, low animal food intake tends to be associated more with poor counties where malnutrition, unsanitary conditions, less education, and acute “diseases of poverty” prevail. For instance, here are some charts for three mortality variables associated with lower quality of living: death from all respiratory disease, death from all digestive disease, and death from pregnancy and childbirth complications. In each case, you can see the strong inverse associations with animal foods (except milk), and strong positive associations with a greater portion of the diet as plant foods. (For a complete key to all the variable abbreviations, check here.)

Correlations with death from all respiratory diseases, ages 35 to 69.

Correlations with death from all digestive diseases, ages 35 to 69.

Correlations with death from pregnancy and childbirth, women aged 34 and under.

Based on the above, we’d actually expect to see areas with higher animal food consumption also experience higher mortality from long-term diseases. Not because they actually have more of those diseases, but because there are fewer “diseases of poverty” to kill them off prematurely. Again, it’s all about what the death certificate says. And to quote a paper Campbell himself co-authored: “it is the largely vegetarian, inland communities who have the greatest all-risk mortalities and morbidities and who have the lowest LDL cholesterols.”

While we’re at it, here are some other relevant pages from the China Study II monograph—some “diseases of affluence.” If you’re sick of these charts, just keep scrolling ’til it’s over. I won’t be offended! Once again, correlations really don’t mean diddly squat here, but they do paint an interesting picture of how diet and mortality patterns interact… and again, it’s far from damning of animal foods.

Correlations with “death from all cancers.” Strong inverse associations with animal fat (ANIMFAT) and saturated fat (%SATFA); strong positive associations with millet and eggs:

Correlations with death from all cancers, ages 35 to 69.

Correlations with “death from heart disease.” Strong inverse associations with animal fat, rice, legumes, and green vegetables; strong positive associations with wheat flour, light-colored vegetables, fruit, and eggs:

Correlations with death from heart disease, ages 35 to 69.

Correlations with “death from stroke.” Strong inverse associations with percent of diet as animal protein, rice, poultry, fish, dietary cholesterol, legumes, and green vegetables; strong positive associations with wheat, percent of diet as plant protein, and percent of total calories from plant food:

Correlations with death from stroke, ages 35 to 69.

Correlations with “death from diabetes.” Strong inverse associations with milk, meat, red meat, and animal fat; strong positive associations with fruit and eggs:

Correlations with death from diabetes, ages 35 to 69.

And lastly (no, seriously, this is the last thing): Since we already know collections of plain-jane correlations can be totally misleading, here are some of the findings from researchers who analyzed the China Study data beyond the raw correlations—including adjustments for confounders. I wrote about these studies in greater depth in my one-year China Study Anniversary post, but here’s the Reader’s Digest version.

From “Erythrocyte fatty acids, plasma lipids, and cardiovascular disease in rural China” (PDF):

• “Within China neither plasma total cholesterol nor LDL cholesterol was associated with cardiovascular disease”
• “There were no significant correlations between the various cholesterol fractions and the three mortality rates [coronary heart disease, hypertensive heart disease, and stroke]“
• “The consumption of wheat flour and salt … was positively correlated with all three diseases [cardiovascular disease, hypertensive heart disease, and stroke]“
• “Red blood cell total polyunsaturated fats, especially the n-6 fatty acids, were positively correlated with coronary heart disease and hypertensive heart disease”

Just because.

Esselstyn: It’s a plant-based miracle!

Now that we have The One Message from the China Study neatly tucked into our brains, we turn our attention back to Dr. Esselstyn and his revolutionary research.

Minute 52:00—While Dr. Campbell was publishing his China Study, Dr. Esselstyn was getting some powerful data from the research he’d started in 1985. He began with 24 patients. But six had dropped out in the first year, leaving him with a total of 18. [Esselstyn:] “At the end of five years, we had follow-up angiograms, and 11 of the group had halted their disease. There was no progression. And there were four where we had rather exciting evidence of regression of disease.”

As the movie notes, this is pretty darn exciting. Even the most experienced, uber-credentialed doctors often believe that heart disease progression can only be slowed down—not stopped, and certainly not reversed. I salute you, O mighty broccoli!

But there’s something majorly funky with the movie’s description of this study. We’re told that Esselstyn ultimately ended up with 18 patients, 11 of whom halted their disease. Four folks regressed their disease, but we don’t know if these people are included in the 11 who didn’t get worse. And at any rate, 11 plus 4 doesn’t equal 18, so some folks have mysteriously vanished from the head-count. What’s up with the weird math?

After poking around for more detailed results of Esselstyn’s study, I found that—quite fortuitously—he posted the full text his papers right on his website. The five-year results are discussed here: A Strategy to Arrest and Reverse Coronary Artery Disease: A 5-Year Longitudinal Study of a Single Physician’s Practice. (Note the line of links near the top of the article for the full description of methods, results, discussion, and conclusion.)

In contrast to what we’re told in “Forks Over Knives,” Esselstyn’s paper says that he started with 22 patients, five dropped out, and six stayed on the diet but never came back for data collection—leaving Esselstyn with only 11 people in the study. (We’ll talk about why this is a problem in a moment.) Of those 11 folks, all had an “overall” stabilization of their heart disease, although four people did have lesions that slightly progressed. Depending on the method of analysis used (“mean percent stenosis” or “minimal lumen diameter”), either eight people or five people had evidence of regression in some of their arterial lesions. Aye, numbers!

No disrespect to Dr. Esselstyn and his work, but right off the bat, we can see there are some big problems with this study:

1. The drop-out rate was crazy high! Since the initial 22 patients got slashed down to 11, we have to consider why the other half of the group slipped off the radar. Was it because they were feeling bad on Esselstyn’s program? Did they experience repercussions from a plant-based diet that they perceived were even worse than heart disease? Were they sick of getting celery strings stuck between their teeth? When studies have a significant drop-out rate, the folks who stick around tend to be the ones having the most success, while the failures slink away—which ends up skewing the results to make the intervention look more effective than it may have truly been.
2. It was an uncontrolled intervention trial. That means there was a no control group to compare against the folks who got dietary and statin intervention, so we can’t estimate how many of their health changes were due to Esselstyn’s program and how many were due to chance.
3. It was a non-randomized study. The patients volunteered rather than being randomly assigned to treatment, creating a problem called “selection bias.” In this type of research, we know that folks who elect themselves for study may have different characteristics than the rest of the population, which is why many researchers use randomization to choose study subjects instead of letting people choose themselves.
4. A whole bunch of variables changed. This wasn’t a study that examined the effects of one component of diet; it did a complete menu overhaul, changing total fat intake, animal food intake, processed food intake, sugar intake, vegetable oil intake, and about ninety gazillion other things. Combined with that lack of a control group, it’s impossible to determine exactly which diet components had an effect on heart disease, and which were neutral (or even negative).

In addition, some effects of Esselstyn’s diet are a little alarming. In the “results” section of his paper, he displays the following table, which shows how his study subjects’ blood values changed during the intervention.

Let’s ignore the fact that those super-low total cholesterol levels are associated with higher rates of cancer, mental illness, infection, and other fun stuff (yes, your cholesterol can be too low) and focus instead on the other values. Holy triglycerides, Batman! Although Esselstyn’s diet helped lower most of his patients’ triglycerides, a couple still have values in the major danger zone (362?). Some of those HDL numbers are looking pretty sorry as well.

All in all, Esselstyn’s study shows that a whole-foods, plant-based diet is probably infinitely better for cardiovascular health than the junky cuisine many folks eat. But it’s far from conclusive evidence that this diet is the best we can do for reversing heart disease, or that it would generally be effective in a population beyond his 11 self-selected subjects. A diet that reduces triglycerides and increases HDL more than his did, for instance, might have an even better outcome.

That’s all, folks

For sure, “Forks Over Knives” has some other areas I could nitpick, such as Campbell’s statement that “animal protein tends to create an acid-like condition in the body called metabolic acidosis” and leads to osteoporosis (minute 1:03:20)—an unfounded belief that I already debunked in the “dairy” section of this post. But I think this critique covers the meatiest points. (Pun definitely intended.) And if you made it this far, hats off to you!

Now if you’ll excuse me, I have to go tend to my feedlot cows and cash my Meat Industry checks. Oops, did I say that out loud?

Don’t worry; I’ll vanish again soon. I’m mostly here to pass on the link to a guest post I wrote for Mark’s Daily Apple about the “fatty food gives you diabetes!” study that came out this month:

• Do High-Fat Diets Cause Diabetes?

If you read the link above, you’ll notice that a major component of the “high fat” mouse diet was hydrogenated coconut oil. After the article went up on MDA, I got an email from Sally Fallon with some neat background on the role of this ingredient rodent studies:

Just a clarification on fully hydrogenated coconut oil.  This is used in experiments because it is the only fat that can be fully hydrogenated and still be soft enough to eat–because the fatty acids are short.  If you fully hdrogenate lard, it will be hard as a rock, even at room temperature.

Full hydrogenation just produces saturated fatty acids–partial hydrogenation produces trans fats.  So technically fully hydrogenated fats are not such a bad thing, they are just saturated fatty acids (usually esterified with unsaturated fatty acids).  But of course, there will be lots of impurities and chemicals from the processing, so this begs the question of why not just eat regular saturated fats.

Fully hydrogenated coconut oil was developed so researchers could test fatty acid deficiency. . . . not the effects of saturated fats.  If the only fat given to rats or mice is fully hydrogenated coconut oil, researchers can bring on EFA deficiency.  Today most researchers don’t have a clue about what the product was developed for, and fully hydrogenated coconut oil is sold and used in all sorts of experiments that have nothing to do with fatty acid deficiency.

How interesting! Hydrogenated coconut oil is incredibly common in lab diets for rodents, but its original purpose was to induce EFA deficiency—not to represent the effects of saturated fat in the diet. (In the context of this particular study, Chris Masterjohn noted that EFA deficiency probably wasn’t a factor because the mouse diet was supplemented with soybean oil. But it’s good info for future reference, nonetheless.)

Ancestral Health Symposium videos are up!

In case you haven’t seen ‘em yet, the presentations from the Ancestral Health Symposium are now viewable on Vimeo. Check ‘em out here, and see the accompanying PowerPoint slides here. (My “How to win an argument with a vegetarian” speech is here. In retrospect, especially after reading the comments on an article that summarized my talk, a more appropriate title might’ve been “How to win an argument with a vegetarian who thinks they’re healthier than you because they don’t eat meat, but not with vegetarians who only avoid meat for ethical reasons and think you’re scum no matter what you tell them about health.” Alas.)

As I understand it, the current videos will be edited sometime in the future to incorporate the PowerPoint slides.

AHS, meet WFF.

To balance out the paleo-ness that rocked the West Coast this month, New York just hosted the week-long Woodstock Fruit Festival—essentially the low-fat, raw vegan counterpart of the Ancestral Health Symposium, featuring less beef jerky and a whole lot more durian. Dietary disagreements aside, there seems to be a shared paleo/fruity emphasis on fitness—and after perusing some photos of the event, I noticed at least one person wearing Vibram FiveFingers. Will minimalist footwear be the bridge that unites these rival communities? Only time (and forefoot strikes) will tell.

Sinister Involvement in Wikipedia!

Despite what it may seem, I honestly don’t spend all day refreshing the China Study Wikipedia page, hungrily waiting for drama to emerge. But I do snoop around there whenever I see blog traffic coming from Wikipedia.com, since it usually means someone added my critique and the vegan moderators haven’t yanked it out yet.

Indeed, a wave of Wiki traffic last night led me to a new “Criticism” section with this interesting blurb (that link will probably stop being valid very quickly):

There is some criticism for the book, as well. Dinise Minger has written several times, including her Formal Analysis and Response, about her interpretation of the data presented in the book, and makes the claim that many of the conclusions drawn by Campbell are ill-founded.

I don’t know who Dinise is, but apparently she’s trying to pass this blog off as her own. But that’s not the exciting part. I also checked out the China Study “talk” page and found a paragraph full of impeccable insight and wisdom. I don’t trust things to not magically disappear from Wikipedia, so I took a screen to preserve this epic moment:

If you don’t feel like adding an extra mouse click to your day, here’s the relevant bit; emphasis mine:

Sinister involvement in Wikipedia

I think there is something seriously wrong going on with regard to this article. It has been put up for deletion and has also been marked as relatively unimportant. This is quite surprising, since the book talks about the most important epidemiological study ever undertaken. I hate to be a conspiracy theorist, but there is a deeper issue her [sic] of sinister interests manipulating Wikipedia articles. In particular, in the case of this article, Wikipedia is highly vulnerable to sophisticated manipulation by the pharmaceutical industry and the meat industry. Such anti-vegetarian economic interests may be subtly suppressing this article. –Westwind273 (talk) 21:52, 22 August 2011 (UTC)

Now it all makes sense. The nomination for deletion, the removal of all China-Study-related criticism, the seemingly biased patrolling of vegan moderators… it’s all been carefully orchestrated by the meat industry! Such an elaborate scheme must be financially draining, though. I wonder if that’s why Farmer Bob stopped sending me my checks?

But seriously, you should have been there because this thing was all sorts of awesome.

For anyone who hasn’t read the smorgasbord of blog posts chronicling the symposium (or the live Tweeting from fast-fingered folks like Lindsay Starke, Diane Sanfilippo, and Jimmy Moore), here’s the gist. Six hundred attendees and an impressive lineup of speakers converged at UCLA for an epic two days of presentations. Superstars Brent Pottenger and Aaron Blaisdell deserve mega kudos for putting this thing together, and for extending their generosity in more ways that can reasonably expected of mortal beings (Brent played chauffeur for disoriented, diva-like presenters, and Aaron opened his lovely home to a bunch of paleo loonies who dribbled wine and steak juice all over the floor).

Fifty volunteers—whipped into docility by the fabulous Gavin Impett—manned the cameras, conducted interviews, endured merciless teasing, and otherwise ensured that nothing went kaboom during the event. These folks worked incredibly hard behind the scenes and somehow, by either elbow grease or sorcery, made the whole symposium run with nary a hitch. Considering this is the first time this event took place and no one really knew what to expect, the seamlessness of it all was pretty amazing. Great job, guys.

The pre-symposium potluck for presenters and volunteers was also fantastic. Here’s a picture of me and interviewer-volunteer Alyssa Rhoden, which is the sole piece of visual evidence I have that I was there. For anyone who needs more proof of my existence, there are other pictures floating around the interwebs too, in which I’m half-blinking or doing weird things with my face.

Photo credit to Alyssa Rhoden's phone, and to whichever Mystery Photographer snapped this.

Seeing as I’m fashionably late to the AHS blogging parade, I’ll try not to rehash too much of what’s already been said. The recorded presentations are being uploaded here for your viewing pleasure, and if you want a detailed account of each lecture, other bloggers have already done a nice job of capturing the fine points.

Stuff I really, really liked about the symposium:

Diversity. I was pleasantly surprised by the range of ancestrally-inspired diets represented there. If you’ve read much of this blog, you probably know that my own diet is an unconventional blend of raw foods, paleo, and Weston A. Price principles—and up until now, I was never quite sure there was room for me within the “ancestral health” umbrella. This symposium changed my mind about that. Some speakers (and attendees) were of the low-carb persuasion, like Michael Eades and Gary Taubes. Others were either macronutrient-agnostic or welcomed a higher-carbohydrate approach, like Stephan Guyenet and Don Matesz. I shared a fructoselicious grapefruit lunch with Danny Roddy, whose own diet experiments led him to an eating style much like mine. I met an intriguing fellow named Lex Rooker who’s been eating but nothing but raw meat for the past decade, and on the other end of the spectrum, a “lacto-ovo paleo” dieter who eats no meat or fish (more on him in a moment).

All in all, the symposium reflected a major element of the ancestral health community, which is that there is no single ‘paleo’ diet. I’m confident in saying that the symposium would be a great experience for anyone interested in using an ancestral framework to improve their health, whether or not you consider yourself “paleo” by the popular definition. There was very little of the unchallenged groupthink sometimes infusing this type of event, and plenty of encouragement to question convictions about diet and fitness. Some intellectual dueling even occurred between two well-respected figures, Stephan Guyenet and Gary Taubes. The overall vibe was more “tribe” than “cult.” And that is a very good thing indeed.

People. As much as I enjoyed watching the presentations, I think the biggest perk of the symposium was the social aspect—having so many amazing people in one place, and being able to meet them in person. If you read this blog, chances are good that there’s something not-quite-mainstream about you. Maybe you’re like me—a food outcast who picks strawberries off appetizer plates at parties while everyone else eats the pizza and cake. Maybe you feel secretly sickened walking through the food court in malls, seeing various vegetable-oil-fried meals sliding down the throats of the masses. Maybe you really like to be barefoot… all the time. Whatever your quirks are, you’re probably a misfit to some degree, and you’ve probably just learned to suck it up and live with it.

Now imagine being in a room with 600 people who are just as weird as you are. They read the same blogs you do. They loved that same podcast you listened to last week, where the one dude interviewed the other dude. They wouldn’t be caught dead taking the elevator instead of the stairs unless both their legs fell off. All you have to do is say the word “No…” and they interject with “gluten.” It’s like being surrounded with clones of yourself, except your clones happen to be awesomer, cooler, and way more interesting than you are, so conversation with them is outrageously fun.

This is what the symposium was. A gathering of like minds. A community. It was a rare and wonderful experience.

Also, everyone was really good looking. I know that’s been mentioned a few times in other blogs, and there’s a reason for that. The people at AHS looked the way humans are supposed to look: vibrant, glowing, and as alert as one can be when running on four hours of sleep. Holy hotness, Batman!

Some of the new, wonderful people I got to connect with include:

• Melissa McEwen, who is whip-smart and almost unbearably adorable;
• Chris Masterjohn, who’s a rare blend of genius and modesty;
• Stephan Guyenet, who is every bit as zen-like and intelligent as you’d expect from his blog;
• David Csonka, who is not only a hoot, but managed to rise to eminence despite his questionable upbringing as a trumpet player;
• Robb Wolf, who announced his return to low-fat veganism and spent the whole symposium eating rice cakes (just kidding, he’s legit);
• Nora Gedgaudas, who is one of the sweetest and warmest people I’ve ever met;
• Tom Naughton, who (amazingly) remained in good spirits despite sleep deprivation, LA disgruntlement, and a battery of travel snafus;
• Don Matesz and his beautiful wife, both of whom are incredibly kind and polite;
• Richard Nikoley, in all his barefooted glory, who I finally got to thank face-to-face for sailing my China Study critique all over the ‘net (also, his wife is one foxy lady);
• Danny Roddy, lover of raw fish and tropical fruit, who stole my diet but is so cool that I won’t even consider suing him over it;
• Paul and Shou-Ching Jaminet, who are as intelligent and approachable in person as they are on their blog (and whose book clearly influenced the shift towards a greater acceptance of starch among many attendees);
• Andrew Badenoch (AKA Evolvify), who rocks a kilt and has a subtle Evil Genius vibe;
• Debbie Young (AKA Grassfed Momma), who can best be described as the human equivalent of sunshine;
• John Durant, whose laid-back demeanor conceals his weird obsession with hair accessories and galoshes;
• Emily Deans, who is not only brilliant but also incredibly lovely and down to earth;
• J. Stanton, who is a smarty pants with an impressive ponytail mohawk (which I’m convinced is where he stores his smarty-pantsness);
• Jack Kruse (AKA the Quilt), who is a powerhouse of ideas and knowledge, and will no doubt be making tsunami-sized waves in the health world;
• and Diane Sanfilippo, who I only saw from afar but was wearing sweet boots and had arms so magnificent they could make a grown man weep (before crushing his head with their brute strength).

Add to that list the 50 volunteers and quite a few of the amazing attendees. I’m so excited to finally have faces to put on the names of some of the blog readers here. Meeting you guys seriously made my year. To quote Stephan Guyenet: “This is like being in the internet.”

Paleo and vegetarianism: let’s be friends!

My symposium presentation was called “How to Win an Argument With a Vegetarian”—which was a play on a similarly-named Vegsource article called “How to Win an Argument With a Meat Eater.” In general, I don’t recommend debating with vegetarians who haven’t picked a fight with you first, or thumping your chest screaming “MEAT! Rawwwwr!” in an effort to drag them back onto the animal-food bandwagon. Not only is diet-proselytizing obnoxious, but when your victim is sitting unobtrusively in the corner with cup of green tea and a Thich Nhat Hanh book, attacking them makes you look like a dipwad.

Heck, the vast majority of vegetarians I know (and I know lots) are totally awesome people, whose dietary choices stem from the desire to live a compassionate life, save geriatric ol’ Mother Earth, and hopefully improve their health in the process. Even though I don’t agree that shunning animal products will make you healthier or even make your diet more sustainable, I understand the motivations for going veggie (I was one for ten years), and don’t think war-like “conversion” efforts from omnivores are warranted. As Robb Wolf commented at the end of my speech, it’s better to spend your time helping people who are already receptive to change—otherwise, you can waste a lot of time shouting into deaf ears.

But that’s not really what I want to talk about in this post.

There’s a small but existent portion of the population that will always be vegetarian. Always. Maybe their motivation is ethical. Maybe they just can’t separate the sight of steak from the image of Daisy the cow mooing tragically at the slaughterhouse. Maybe their religion mandates meatlessness. Maybe it’s an ingrained part of their culture. Maybe they share a roof with T. Colin Campbell. Or maybe they just have an aversion to animal flesh and are drawn more to the bounty of the plant kingdom. Whatever their reason, no amount of evolutionary history, Lierre Keith quotes, or “population XYZ eats meat and is healthy!” arguments will un-vegetarianize them—so issues of optimality aside, a meat-free diet is what they have to work with.

I think, up until this point, the paleo community has either ostracized these folks or dismissed them as lost causes. How could a diet that defines itself by meatlessness be compatible with an ancestral framework, in which meat has always been present and perhaps even pivotal in our evolution? How can paleo folk see eye-to-eye with the vegetarians and their grain love, soy fixation, and neolithic mock-meats made from hunks of pure gluten?

Although I’ve generally seen more “us vs. them” vitriol coming from the meat-free community than from the paleosphere, the animosity definitely goes both ways. Which brings me to the point of all this. At the Ancestral Health Symposium this month, I had the pleasure of meeting a bona-fide meat-free, lacto-ovo paleo dieter. For real. This brave soul (let’s call him Aravind, because that’s his name) came to the symposium not because he wanted to freeload off beef jerky samples, but because he tailors what most people would consider a “vegetarian” diet into an ancestral framework. No grains except white rice for him. No excess fructose. No industrial seed oils. No soy—only small amounts of traditionally-prepared legumes. The only thing that separates him from the rest of the crowd is that his sole animal products are eggs and high-quality, grass-fed dairy.

And indeed, Aravind appeared to be in mighty fine health. When I shook his hand, he neither fell over nor crumbled into a pile of sawdust. You couldn’t distinguish him from the omnivores in the room—and had he not outed himself, we’d be none the wiser to his meatlessness. He was a stark contrast to the stereotype of “pale, sunken-eyed vegetarians” we’ve all seen wandering the aisles of Whole Foods.*

*I hate using this description, I really do—because I’ve also known “regular” vegetarians who looked fantastic, and junkfoodarians who get sick less often than their health-conscious counterparts, old people who stay bright and youthful eating their daily Maple Bars, and countless other examples of where diet doesn’t seem to correlate with appearance. But as someone who spent a whole lot of time around vegetarians and vegans in the past, there’s definitely a “look” about some of them that I like to call the Veg*n Deterioration Glaze. It doesn’t strike everyone… but you know it when you see it.

Aravind represents a rare, under-discussed intersection between ancestral eating and vegetarianism. And the more I’ve been thinking about this, the more I’ve realized how lame it is that this converging point is so neglected. By bashing vegetarians because of their meat avoidance, we’re alienating a chunk of the population that would probably be really, really receptive to other principles of ancestral eating, because they’re already likely to be health conscious. Instead of giving up when someone tells you meat is a no-go, why not discuss other areas they can improve on standard vegetarianism—like switching from gluten grains to “safe starches” like tubers and rice; eliminating processed meat replacements and soy products; avoiding added sugars; reducing omega-6 intake and replacing industrial seed oils with coconut oil, grass-fed butter, or ghee; emphasizing full-fat, raw-when-possible dairy; eating shellfish if it’s not an ethical concern; sourcing eggs from pastured hens; preparing grains or legumes traditionally to reduce toxins and anti-nutrients; and so forth?

I think Aravind summed it up well in a post on Paleohacks:

Paleo is about toxin avoidance. It is not about being a meatasaur, low carber, re-enactor, etc. I am a very proud member of this community and a very strong supporter of the movement. … This community is squandering a huge opportunity to gain the support of a crowd (like me) that is completely on board with the virtues of avoiding neolithic toxins and actually would lend support to our movement.

So back to the whole “win an argument with a vegetarian” thing. If you encounter a committed vegetarian who’s sincerely interested in being healthy, debating them about meat is probably the worst thing you can do. A better approach is to seek out areas of commonality and help them make changes they’re comfortable with, helping them design the best possible diet within the bounds of vegetarianism.

(By the way: There’s a reason I’m talking about vegetarianism rather than veganism here. As I mentioned in my presentation, I think the difference between veganism and vegetarianism is much greater than the difference between vegetarianism and omnivorism, both psychologically and in execution. I think it’s possible for many folks to pull off being a vegetarian with enough planning and high-quality, non-meat animal foods, but veganism is a lot trickier to stay healthy on.)

“Neolithic Agents of Disease”: the common denominator

In the spirit of emphasizing similarities, I also want to expand on something I talked about in my AHS presentation. A common anti-paleo argument from vegans and vegetarians is that plant-based diets—particularly the low-fat, starch-based ones advocated by Dean Ornish, Neal Barnard, John McDougall, and Caldwell Esselstyn—have been “proven” to prevent or reverse chronic conditions like heart disease and diabetes. (“So neener, neener, nah nah; we win!”) These diets eliminate animal foods, sharply limit fat, and embrace whole grains—making them the apparent antithesis to paleo eating. Ouch! Score one for the vegans, right?

Indeed, if we look at a starch-based diet and, say, a low-carb paleo diet in terms of what they both include, we won’t find much in common. Vegetables and… well, that’s about it. But if we look at them from the perspective of what both diets systematically exclude, that’s where some interesting similarities pop up. Whether you eat a nearly-carnivorous diet or a low-fat, plant-based one advocated by Dean Ornish, you’ll be avoiding:

• All forms of processed, refined sugar, including high-fructose corn syrup
• All industrial oils (including high-omega-6 varieties like soybean and corn oil)
• Refined grains like white flour
• Fruit juice and other sugary beverages
• Industrially processed foods*

* In his book “Eat More, Weigh Less,” Ornish recommends avoiding all processed or “convenience” foods with over 2 grams of fat per serving. I can’t say that I spend a whole lot of time reading the backsides of Hungry Man dinners and Little Debbie snacks, but my limited knowledge on the subject tells me most processed foods have way more than 2 grams of fat.

Now let’s compare that “avoid” list with what Kurt Harris refers to as the three neolithic agents of disease—the modern nasties driving many of our health woes:

• Excess fructose
• Excess linoleic acid (typically from high-omega-6 oils like soybean oil)
• Wheat or gluten

Ancestral or “paleo” diets specifically eliminate all three. Incidentally, the near-vegan diets with a track record for fighting disease eliminate the first two. And in many cases, they inadvertently slash wheat intake by promoting a more diverse spectrum of grains, tubers, and legumes than the average person on an industrialized diet consumes (in which grain products are overwhelmingly wheat-based).

For example, check out this McDougall Program health clinic menu and play “spot the starches.” Notice—first of all—the liberal use of potatoes, squash, and legumes rather than grains as the meal centerpiece. But even among the grain-containing items, how many use wheat? Only nine out of 26. Instead of seeing an endless stream of bread, crackers, pretzels, bakery items, cookies, and other common wheat-based foods, there’s an abundance of rice, barley, quinoa, and corn. And that accidental reduction of wheat (if it really is uniquely problematic among grains) may contribute to the success of whole-foods, plant-based diets in treating disease.

Moving on to one final thing:

Clarification. After my presentation, I noticed the quote “Salad is what food eats” started fluttering around on Twitter, attributed to me. This was actually said by an audience member and I just repeated it into the mic for everyone else to hear. Yeah, it’s a cute phrase. But considering I eat salad and have already been “outed” as a meat-based organism, I’m not sure I really like its implications.

The end!

First item of business: The Ancestral Health Symposium. Due to some serendipitous events, it turns out I’ll be presenting at this hyperventilation-inducingly-awesome event next week. My lecture is at 10:00 AM on August 6th in the Rolfe 1200 auditorium. If you’re lucky enough to have a ticket, I hope to see you there, and to verify my existence for anyone who still thinks I’m a meat industry puppet. Otherwise, unless PETA pops in and sets fire to UCLA, all the presentations should be available online for free shortly after the symposium is over. Woohoo!

Second item of business: Now that he’s outed the project himself, I feel safe in announcing that Mark Sisson is going to be publishing the book I mentioned working on in an earlier blog post, and that it’ll be released mid-2012. I’m super excited, and couldn’t ask for a better publisher to work with. Or one with more impressive abs (see link above). More details to come in the near future.

Now on to the real point of this post.

One year ago, this happened:

Those are the monthly visits to this blog, according to my top-secret WordPress dashboard. And that crazy jump last July is when I posted my critique of the China Study, which is probably the only reason most of you know this blog exists. Thanks to Richard Nikoley’s smackdown roundup, the critique got passed along by a lot of cyber-hands, eventually reaching Campbell himself.

With the release of the movie Forks over Knives, Campbell’s recent appearance on the Bill Maher show, and continued Wikipedia drama about the peculiar lack of criticism on its “The China Study” page, it seems the China Study is back in the spotlight for awhile.

Since I’m not a vegan anymore, I figure it’s okay for me to beat dead horses. And also to resurrect the ones I buried last year and wallop on their half-rotten, fly-infested carcasses with my fists a few more times. So wallop I will: This post is dedicated to driving a couple more nails into the China Study coffin—and is aimed particularly at the folks out there who would rather listen to peer-reviewed research than some girl with a blog.

So my dear readers, hecklers, and spambots, I present to you a collection of peer-reviewed papers based on the China Study data that contradict or conflict with Campbell’s interpretation in his book, “The China Study.” Some studies you may have seen before; others will be new. Regardless, you can rest assured that these papers—some co-authored by Campbell himself—are by folks generally considered qualified in their field, and that, contrary to the “animal foods are harmful and cholesterol is associated with all Western diseases” message we received in “The China Study,”* other perspectives of the data abound.

*It’s also worth noting that”The China Study”—the one written by Campbell and published by BenBella Books—is not peer reviewed. Shockingly, neither are BenBella’s other books, including “You Don’t Talk About Fight Club,” “Seven Seasons of Buffy,” and “The Psychology of Harry Potter.” Contrary to what’s apparently popular belief, books—even health books—don’t have to pass under the scrutiny of peer review before they hit the stands. Hence why this exists.

But first, a few words on peer review

I want to burst the Peer-Review Bubble of Perfection before we get much further.

Peer review might be the best we’ve got right now—but it’s far from infallible, and its biases are no secret. In an article from 2000, Richard Horton—editor of the uber-peer-reviewed journal “The Lancet”—wrote some rather scathing comments about the peer-review system, stating that it is “biased, unjust, unaccountable, incomplete, easily fixed, often insulting, usually ignorant, occasionally foolish, and frequently wrong.” Even peer-reviewed journals have published papers on the problems with peer review (e.g., this article in “Nature”).

To top that off, history is speckled with some disturbing cases of research fraud that slipped right through the peer-review system. The best example is Scott Reuben, once considered a pioneer in the field of anesthesiology and pain management, who concocted at least 21 “studies” that were pure works of fiction—and managed to get all of them published in peer-reviewed journals. Over the years, he accepted big bucks from pharmaceutical companies to conduct studies on drugs like Celebrex and Effexor, but instead of actually enrolling patients, he made up some numbers and slid his nonexistent findings into major publications. And as it turns out, many of the drugs he convinced the world were beneficial were either ineffective of downright harmful. (You can see a list of his falsified peer-reviewed papers here.)

That’s an extreme example, but it illustrates the point. Even peer-reviewed papers should be taken with a grain of salt instead of held as gospel.

And with that, here are some papers to mull over. The bolded parts within quotes are to highlight the relevant bits.

Erythrocyte fatty acids, plasma lipids, and cardiovascular disease in rural China by Fan Wenxun, Robert Parker, Banoo Parpia, Qu Yinsheng, Patricia Cassano, Michael Crawford, Julius Leyton, Jean Tian, Li Junyao, Chen Junshi, and T. Colin Campbell.

A study involving fat, cholesterol, and cardiovascular disease? Surely they must be talking about how all that nasty saturated fat in animal foods clogs your arteries, right? Oh, snap:

Within China neither plasma total cholesterol nor LDL cholesterol was associated with CVD [cardiovascular disease]. … The results indicate that geographical differences in CVD mortality within China are caused primarily by factors other than dietary or plasma cholesterol.

There were no significant correlations between the various cholesterol fractions and the three mortality rates [coronary heart disease, hypertensive heart disease, and stroke]. In contrast, plasma triglyceride had a significant positive association with CHD and HHD but not with stroke.

We’ve even got a cameo appearance from wheat again:

The consumption of wheat flour and salt (the latter measured by a computed index of salt intake and urinary sodium excretion) was positively correlated with all three diseases [cardiovascular disease, hypertensive heart disease, and stroke].

And for those of your leery of industrial oils and polyunsaturated fats, check this out:

Unlike what might be expected from studies on Western subjects, there was no significant inverse correlation between RBC-PC total PUFAs and CVD mortality; in fact, RBC-PC total PUFAs, especially the n-6 fatty acids, were positively correlated with CHD [coronary heart disease] and HHD [hypertensive heart disease].

That one was a little acronym-y, but basically it says that higher levels of polyunsaturated fats (especially omega-6 fats) in red blood cells was associated with more heart disease.

So if you don’t want to take my word for it, take the word of this peer-reviewed paper: The China Study data showed no correlation between cholesterol and heart disease, but did find wheat and polyunsaturated fats to be mighty suspect.

Association of dietary factors and selected plasma variables with sex hormone-binding globulin in rural Chinese women (PDF) by Jeffrey R. Gates, Banoo Parpia, T. Colin Campbell, and Chen Junshi.

Wheat-fearers, you’ll enjoy this one.

This study focuses on sex hormone-binding globulin (SHBG), a molecule sometimes used to test for insulin resistance. (Higher levels are associated with better insulin sensitivity; lower levels are associated with insulin resistance and diabetes.) After fishing out associations between SHBG, fasting insulin, triglycerides, testosterone, and a number of diet and lifestyle variables, the researchers found:

The principal positive food-SHBG correlates in order of magnitude were rice (0.61, P < 0.0001), green vegetables (0.49, P < 0.001), fish (0.42, P < 0.001), and meat (0.38, P < 0.05). The strongest negative food correlate with SHBG (positively correlated with insulin) was wheat (-0.57, P < 0.0001).

In other words, the foods associated with higher SHBG (and lower insulin) were rice, green veggies, fish, and meat. The main food associated with lower SHBG (and higher insulin) was… dun dun dun… wheat. Not only do we have vindication of some animal foods, but we also have another red flag whipping up over our favorite glutenous grain. Although the link with meat diminished in more sophisticated statistical models, the other foods kept their associations with SHGB—and wheat proved to be the strongest predictor of low SHBG, while rice was the strongest predictor of higher SHBG. In discussing their findings, the researchers note that wheat seemed to accompany a number of markers for poor health:

Significant differences in the diet of rural Chinese populations studied suggest that wheat consumption may promote higher insulin, higher triacylglycerol, and lower SHBG values. Such a profile is consistent with that commonly associated with obesity, dyslipidemia, diabetes, hypertension, and heart disease. On the other hand, the intake of rice, fish, and possibly green vegetables may elevate SHBG concentrations independent of weight or smoking habits.

It looks like the post I wrote on wheat and heart disease in the China Study was old news: Campbell and his colleagues already spotted the link back in 1996! But why would wheat have such a vastly different effect than rice? The paper offers a possible explanation:

The effect of rice and wheat on SHBG was remarkable and unexpected. … Nevertheless, there is some evidence to suggest that rice and wheat can have significantly different effects on the biochemical variables we measured. Panlasigui et al (58) found that the high-amylose rice varieties had blood glucose responses that were lower than those of wheat bread. Other varieties, particularly “converted” rice, gave considerably higher values. Miller et al (59) in comparing rice and wheat varieties found that the insulin index (II) was unusually low on the relative scale compared with the glycemic index (GI) of the same foods. For example, Calrose brown rice had a GI = 83 but an II = 51. White bread was used as the reference food (GI = 100, II = 100). Wheat may be unique in its relative capacity to stimulate insulin. Most recently, Behall and Howe (60) reported a significantly lower insulin response curve area in both normal and hyperinsulinemic men consuming a high-amylose diet. The relative differences in the fatty acid proportions and/or amylose content for wheat and rice may thus be responsible for modulating serum SHBG, triacylglycerols, and insulin.

Although it’s still speculative, the amount of amylose (a component of starch) and relative proportion of fatty acids in wheat might make it more problematic than other grains like rice—especially in terms of raising triglycerides and fasting insulin while lowering SHBG. Which is particularly interesting in the context of this paper, because in one of his responses to my critique, Campbell stated:

[The] correlation of wheat flour and heart disease is interesting but I am not aware of any prior and biologically plausible and convincing evidence to support an hypothesis that wheat causes these diseases, as you infer.

Go figure!

Prolonged infection with hepatitis B virus and association between low blood cholesterol concentration and liver cancer (PDF) by Zhengming Chen, Anthony Keech, Rory Collins, Brenda Slavin, Junshi Chen, T. Colin Campbell, and Richard Peto.

This one’s a doozy. But first, some background info to help us understand the full extent of its doozydom.

One of the prevailing themes in “The China Study” is a supposed link between cancer and animal protein (and subsequently, blood cholesterol). Campbell first started chasing this association after finding that casein, a milk protein, raised cholesterol and promoted liver cancer growth in rats exposed to aflatoxin. After reviewing the China Study data, Campbell concluded this link held true in humans: He states that animal protein, as reflected by higher cholesterol levels, promoted liver cancer in folks already at risk for it (namely those who carried the hepatitis B virus). Straight from the book:

In addition to the [hepatitis B] virus being a cause of liver cancer in China, it seems that diet also plays a key role. How do we know? The blood cholesterol levels provided the main clue. Liver cancer is strongly associated with increasing blood cholesterol, and we already know that animal-based foods are responsible for increases in cholesterol. … Individuals who are chronically infected with HBV and who consume animal-based foods have high blood cholesterol and a high rate of liver cancer. The virus provides the gun, and bad nutrition pulls the trigger. (Page 104)

People chronically infected with hepatitis B virus also had an increased risk of liver cancer. But our findings suggested those who were infected with the virus and who were simultaneously eating more animal-based foods had higher cholesterol levels and more liver cancer than those infected with the virus and not consuming animal-based foods. (Page 105)

Seems clear enough. According to Campbell, the data showed that liver cancer went hand-in-hand with high cholesterol in the China Study data.

…Which is what makes this particular study (co-authored by Campbell, nonetheless) so interesting. Campbell et al. set out to investigate “the association between low blood cholesterol concentration and liver disease by studying blood lipid concentrations about middle aged men in rural China.” Already seems fishy, huh? Before even discussing the study results, the paper includes some sections that contradict the notion that high cholesterol is linked with liver cancer:

Several prospective epidemiological studies … have found an inverse relation between cholesterol concentration and the subsequent risk of cancer. … A prospective observational study in a Chinese population … found a significant inverse association between blood concentration of cholesterol and subsequent mortality from non-malignant liver disease or from liver cancer. More recently significant excess risk of death from liver cancer and chronic liver disease has been reported among North Americans with a low blood cholesterol concentration.

In the largest study in a Western population (the multiple risk factor intervention trial) 100 deaths from liver cancer were recorded during the follow up period, and a significantly increased risk of death from liver cancer was found among people in the group with the lowest cholesterol concentrations.

In our previous prospective study of another Chinese population the subsequent risk of death from liver cancer was shown to increase significantly with decreasing blood concentrations of cholesterol.

Whether low cholesterol is a cause or a consequence of cancer is a different story—but either way, there’s no mistaking it: Liver cancer looks pretty solidly linked with low cholesterol in other relevant studies. And this study does nothing to refute that:

We have now shown that prolonged infection with hepatitis B virus is an additional factor contributing to the inverse relation between cholesterol concentration and liver cancer. Chronic hepatitis B, which usually starts in early childhood in China, leads not only to liver disease but also to a lower blood concentration of cholesterol in adulthood. This produces, as observed elsewhere, an inverse relation between cholesterol concentration and the risk of death from liver cancer or from other chronic liver disease. This result may also help to explain, at least in part, the inverse association between cholesterol concentration and liver disease observed in Western populations.

So why did Campbell repeatedly state in “The China Study” that liver cancer was associated with higher cholesterol? Probably because it was—but only after the (more reliable) individual data was aggregated at the county level, which made it easy to succumb to a little somethin’ called the “ecological fallacy.”

Let me explain. The publicly available China Study data—the stuff I used for my critique, and that Campbell pulled correlations from in his book—consists of averaged values for 65 counties, instead of the thousands of data points originally collected. But this particular study used the individual data, before any of it was combined and diluted by averaging. And as the paper explains, that makes this study much more reliable than the ones using aggregated data:

In this study there was a negative correlation between chronic infection with hepatitis B virus and blood concentrations of cholesterol (and apolipoprotein B) when people living in the same village were compared with each other, but the correlation was reversed when average values for different villages were compared with each other.

Correlations between populations based on average measures in groups are subject to the “ecological fallacy” (whereby these correlations may not represent the correlations that would be seen among individual subjects). … In general, comparisons within populations are much more reliable than comparisons between populations when assessing association of variables and diseases in individual subjects. So, in the present instance, the negative correlation observed when people living in the same village were compared with each other provides the most reliable evidence as to the real relation between chronic infection with hepatitis B virus and lipid concentrations in individual subjects.

This is kind of fascinating. Here we’ve got a China-Study-based paper—again, co-authored by Campbell—that explicitly describes why aggregated data can be unreliable, and why positive links between liver cancer variables and cholesterol are probably backwards. This also begs the question of how many other associations in the aggregated data would be reversed at the individual level. (Or whether any seemingly neutral relationships are actually correlated—such as liver cancer and the carcinogen aflatoxin, which are paradoxically unassociated in the aggregated data.)

Here’s an example to help illustrate the concept of “ecological fallacy” as it relates to liver cancer in China.

Say we’ve got two counties, each with 1000 residents. Folks in the first county have total cholesterol ranging from 130 to 150, with the average being 140. These lucky ducks are free from liver cancer or hepatitis B infection! The second county has total cholesterol ranging from 120 to 190, with the average being 170. Much more liver cancer and hepatitis B infection in this place, but the afflicted folks all have cholesterol at the bottom end of the spectrum, around 120.

What happens if we look only at the aggregated data? We’d see that the county with the lower average cholesterol (140) had lower rates of liver cancer, and the county with higher average cholesterol (170) had higher rates of liver cancer. Thus, a liver cancer/higher cholesterol relationship is born. But what happens if we look at the individual data instead? We’d see that the people with liver cancer had lower cholesterol than any of the healthy folks—the exact opposite of what the averaged data showed.

See how tricky numbers can be?

At any rate, this (peer-reviewed!) study blatantly contradicts some of the claims made in “The China Study,” especially the concept that cancer goes hand-in-hand with high cholesterol.

Dietary calcium and bone density among middle-aged and elderly women in China (PDF) by Ji-Fan Hu, Xi-He Zhao, Jian-Bin Jia, Banoo Parpia, and T. Colin Campbell.

True to its title, this paper examines the role of calcium in bone density in the China Study data—with a special focus on the effects of dairy calcium versus plant calcium. Campbell et al. zoomed in on five counties with “distinct lifestyles and diets”: the dairy-and-meat-loving Xianghuangqi, the infamous dairy-full Tuoli, and the rural, nearly-vegan farming towns of Jiexiu, Cangxi, and Changle.

But before we look at the paper itself, let’s see how Campbell summarized its findings in a Cornell Chronicle article in 1994:

Animal protein, including that from dairy products, may leach more calcium from the bones than is ingested, said Campbell, professor of nutritional biochemistry at Cornell and director of the Cornell-China-Oxford Project, the most comprehensive project on diet and disease ever conducted.

Campbell [and other collaborators] analyzed the role of dietary calcium in bone density by following closely the diets of 800 women from five counties that have very different diets in China. … Analyses of these data suggest that increased levels of animal-based proteins, including protein from dairy products, “almost certainly contribute to a significant loss of bone calcium while vegetable-based diets clearly protect against bone loss,” Campbell reported.

Sounds pretty clear: The dairy-eating counties must have had poor bone health due to their animal protein habit, whereas the more plant-based dieters were skeletally superb. In other words, milk does a body bad! But do the summaries above match up with this paper actually found? First, let’s look at what the women in each county were typically eating:

*Lest I get the “you’re trying to justify your dairy addiction” line and/or accusations of dairy industry affiliation, I’d like to remind everyone that dairy hasn’t been part of my diet in over six years, and I believe the dairy most people consume (low-fat, ultra-pasteurized, etc.) is downright nasty stuff. But that doesn’t mean I won’t defend dairy when the science warrants it.

As you can see, Xianghuangqi ate a pretty shabby diet as far as whole-foods veganism is concerned: We’ve got dairy galore, beef, mutton, wheat flour, a mere smattering vegetables, and millet. Their bones should be snapping like peanut brittle! Tuoli’s not much better, what with their milk tea, animal flesh, and decided lack of green leafy veggies. More bone snappage, right?

I’ll let the paper speak for itself:

Analysis by individual for all counties combined showed that [bone mineral content] and [bone mineral density] were correlated positively with total calcium (r = 0.27-0.38, P < 0.0001), dairy calcium (r = 0.34-0.40, P < 0.0001), and to a lesser extent with nondairy calcium (r = 0.06-0.12. P = 0.001-0.100), even after age and/or body weight were adjusted for. The results strongly indicated that dietary calcium, especially from dairy sources, increased bone mass in middle-aged and elderly women by facilitating optimal peak bone mass earlier in life.

Did you catch that? Dairy calcium—far more than plant calcium—was linked with stronger bones. Moreover, the paper notes that “nondairy calcium … showed no association with bone variables after age and/or body weight were adjusted for.”

Continuing on:

Comparison of results in Table 7 reveal that calcium from dairy sources was correlated with bone variables to a higher degree than was calcium from the nondairy sources, probably resulting from the higher bioavailability of dairy calcium.

A comparison of the bone mass of women in the five counties revealed that 20% greater bone mass at the distal radius was observed for all age groups of women in county YA [Xianghuangqi], a pastoral county with high consumption of dairy foods, as compared with the nonpastoral areas with lower calcium intakes.

I’ll add my own unsolicited 2¢ and speculate that calcium probably wasn’t the only protective factor in the dairy-eating counties. Aged cheese, likely consumed at least in Xianghuangqi, is high in vitamin K2—a nutritional superstar when it comes to bone health (among other things). K2 isn’t present in plant foods except for a fermented soy product called natto (not everyone’s cup o’ tea). As the paper notes, the dairy-eating counties also had a higher intake of fat (25% of daily calories, opposed to 9.9 – 13.6% for the other counties), potentially increasing the absorption of fat-soluble vitamins necessary for bone health.

So how did Campbell conclude from this study that “increased levels of animal-based proteins, including protein from dairy products, almost certainly contribute to a significant loss of bone calcium”? The dairy part is unfounded no matter which way you spin it, but the rest of his statement probably stemmed from this:

The associations between bone mass and other nutrients, like dietary protein and phosphorous, were also examined. However, none of these nutrients showed an association with bone mass as significantly as did dietary calcium, although an inverse correlation was observed consistently for nondairy animal protein.

Unfortunately, that’s the only blurb in the entire paper that mentions animal protein in relation to bone mass, so we can’t see the data behind the “consistent inverse correlation.” In the context of this study, though, it makes sense: Protein has a complex relationship with bone formation, serving as a synergist when calcium intake is adequate, but as a potential antagonist when calcium intake is low. In other words, the effects of protein on bone health depend on how much calcium you’re taking in.

So for the counties in this study that ate more animal protein but sparse calcium—such as Changle, which had the highest non-dairy animal food consumption and also the lowest calcium intake (averaging a mere 230 mg per day)—I wouldn’t be surprised if an animal protein/weaker bones connection showed up. Whether that trend would hold at higher calcium intakes is a different story. And either way, this finding doesn’t jive with most other research done on this topic: Most studies show a protective association between animal protein and bone density, formation, and retention:

• Prospective study of dietary protein intake and risk of hip fracture in postmenopausal women. “Protein from animal sources was the nutrient variable with the strongest negative association with risk of hip fracture in this prospective study of Iowa women. Protein from vegetable sources did not appear to protect against hip fractures.”
• Effect of Dietary Protein on Bone Loss in Elderly Men and Women: The Framingham Osteoporosis Study. “Contrary to expectations, elders with animal protein intake up to several-fold greater than the RDA also had the least bone loss after controlling for known confounders. Nonanimal sources of protein were not related to BMD. These results suggest that typical population intakes of animal protein, within the range commonly consumed, do not result in bone loss. Rather animal protein intake appears important in maintaining bone or minimizing bone loss in elderly persons.”
• Protein Consumption and Bone Mineral Density in the Elderly. “Multiple linear regression analyses … showed a positive association between animal protein consumption … and BMD. Conversely, a negative association between vegetable protein and BMD was observed in both sexes. … This study supports a protective role for dietary animal protein in the skeletal health of elderly women.”
• Controlled High Meat Diets Do Not Affect Calcium Retention or Indices of Bone Status in Healthy Postmenopausal Women. “Calcium retention is not reduced when subjects consume a high protein diet from common dietary sources such as meat.”
  

In addition, if animal protein was such a bone-killer and plant protein was bone protective, we’d see vegetarians or vegans having the best outcomes in the bone department. But this just ain’t the case. At best, non-meat-eaters are equally matched with their omnivorous counterparts; at worst, they’re more prone to fracture:

• Veganism and osteoporosis: A review of the current literature. “The findings gathered consistently support the hypothesis that vegans do have lower bone mineral density than their non-vegan counterparts.”
• A Comparison of Bone Mass Measurements of Vegetarians and Omnivores. “In this review of 9 cross-sectional and 1 longitudinal study, little statistical significance between bone density and bone content was found between vegetarians and omnivores.”
• Effect of vegetarian diets on bone mineral density: a Bayesian meta-analysis. “The results suggest that vegetarian diets, particularly vegan diets, are associated with lower BMD, but the magnitude of the association is clinically insignificant.”
• Long-Term Vegetarian Diet and Bone Mineral Density in Postmenopausal Taiwanese Women. “Long-term practitioners of vegan vegetarian were found to be at a higher risk of exceeding lumbar spine fracture threshold … and of being classified as having osteopenia of the femoral neck.”

So, although the “calcium-leeching” properties of animal protein is a common battle cry in the vegan world, the research just doesn’t support it. There are even some interesting (and peer-reviewed!) papers out there looking at how belief systems influence the interpretation and misrepresentation of bone/protein studies. Read that link because it’s awesome.

But back on topic. This paper, with Campbell’s own name on it, suggests a strongly bone-protective role for dairy in the diet. Not quite the message we heard in “The China Study.”

Reply to TC Campbell by Frank B. Hu and Walter Willett.

Short n’ sweet, this one speaks for itself. Frank Hu and Walter Willett responded to Campbell’s criticism of their findings in the Nurses’ Health Study*, and in so doing, offered their take on the China Study.

Campbell questioned the validity of our findings because they contradict the results of international correlation studies on animal product consumption and disease rates. … Correlational studies conducted within a country can usually provide more credible data than international comparisons because of relatively homogeneous populations and the possibility of collecting data on potential confounding variables at individual levels. A survey of 65 counties in rural China, however, did not find a clear association between animal product consumption and risk of heart disease or major cancers.

*The Nurses’ Health Study has its share of problems, and I actually agree with Campbell’s assessment in some cases, but that’s a story for a different day.

Correlation of Cervical Cancer Mortality with Reproductive and Dietary Factors, and Serum Markers in China by Wan-De Guo, Ann W. Hsing, Jun-Yao Li, Jun-Shi Chen, Wong-Ho Chow, and William J. Blot:

As this paper notes, cervical cancer is the second leading cause of cancer-related deaths among Chinese females. There are a few known risk factors (especially herpes infection), but other than that, the reason for its variation across China is a big mystery. Can we blame animal foods for this one?

After identifying the variables that had the strongest correlations with cervical cancer in the China Study data—including herpes infection, serum ferritin, body mass index, cigarette smoking, age at first birth, green vegetable intake, and animal food consumption—the researchers ran multiple regressions to see which correlations were legit. The results?

When these variables were considered in the multiple regression analysis, early age at first birth and higher BMI were positively associated with cervical cancer mortality, while consumption of green vegetables and animal foods were negatively correlated.

Simply put, animal foods were inversely associated with death from cervical cancer—meaning the folks eating more animal products had fewer deaths from this disease. If it were true that animal protein promotes the growth of cancer cells, as Campbell theorized based on his research with casein and liver cancer, then we’d expect to see the opposite. What an anomaly.

Risk Factors for Stomach Cancer in Sixty-Five Chinese Counties (PDF) by Robert W. Kneller, Wan-De Guo, Ann W. Hsing, Jun-Shi Chen, William J. Blot, Jun-Yao Li, David Forman, and Joseph F. Fraumeni, Jr.

In this paper, the authors pulled out variables that had strong correlations with stomach cancer in the China Study data, and then analyzed them in greater depth using some regression models. The most significant associations involved plants—but since the focus of this post is animal foods, let’s see what the researchers uncovered on that front:

Consumption of green vegetables, rice, meat, and fish was associated with reduced mortality. … On the other hand, salt-preserved vegetables, potatoes, wheat, and millet, plus combinations of wheat, corn, and millet, were correlated with significantly increased mortality.

Our finding of a significant inverse association for meat is consistent with a recent case-control report from Turkey. Meat is a common source of selenium, which showed the strongest protective effect among all the plasma micronutrients.

Say what? Not only did meat not seem to increase stomach cancer rates (which we might expect if Campbell’s “animal protein spurs cancer growth” hypothesis held true), but it actually showed the opposite trend. Perhaps the selenium was enough to counteract meat’s general evilness. Also interesting is that the foods associated with increased stomach cancer mortality were mainly of plant origin. Including wheat.

However, this paper did uncover a relationship between stomach cancer and one animal food: eggs. Given the known associations between stomach cancer and salt-preserved foods (and lack of association with any other animal food), I’d wager this link has something to do with the way eggs are eaten in China rather than anything inherent in the eggs themselves. China is known for dishes like salted duck eggs, which are preserved with salt or charcoal, and century eggs, which sit for weeks or months in a mixture of ash, salt, clay, and other ingredients, gradually becoming glossy balls of ammonia stench. It seems likely that preserved eggs could increase stomach cancer risk for the same reason preserved vegetables do.

Century egg. Nom, nom, nom.

The researchers also note that they “know of no previous reports linking egg consumption to increased [stomach cancer] risk” and that the counties with high egg consumption had other confounders not accounted for—including a tendency to be in coastal areas, have a higher percent of industry-employed workers, and have higher indexes of socioeconomic status. In addition, the range of egg intake in China may be too narrow to determine anything meaningful: The eggiest county ate the equivalent of only two or three chicken eggs per week, and the average for all counties was about 1/15th of an egg per day.

Nonetheless, no other animal foods, nor animal protein as a whole, contributed to stomach cancer risk in this analysis. Which is pretty interesting, because Campbell still links stomach cancer with animal foods via blood cholesterol in his book (pages 78 – 79):

What a surprise we got! As blood cholesterol levels decreased from 170 mg/dL to 90 mg/dL, cancers of the liver, rectum, colon, male lung, female lung, breast, childhood leukemia, adult leukemia, childhood brain, adult brain, stomach and esophagus (throat) decreased.

Yet as meat consumption increased, stomach cancer decreased. How curious!

Fish consumption, blood docosahexaenoic acid and chronic diseases in Chinese rural populations by Yiqun Wang, Michael A. Crawford, Junshi Chenb, Junyao Li, Kebreab Ghebremeskel, T. Colin Campbell, Wenxun Fan, Robert Parker, and Julius Leyton.

As an animal food rich in protein, fish should top the list of health villains—at least according to the animal protein/disease theory. Was that the case in this study? From the full text (not linked above):

Our finding that the highest blood cholesterol levels in the Chinese were associated with DHA and fish consumption but with the lowest risk [of heart disease], is also a contradiction of what might be expected.

The higher blood LDL cholesterol levels associated with the marine coastal and lacustrine communities in China as compared with their inland neighbours, needs to be seen as starting from very low levels. In this context, it is the largely vegetarian, inland communities who have the greatest all risk mortalities and morbidities and who have the lowest LDL cholesterols. It could well be that there is a minimum level of LDL cholesterol below which cell membranes are adversely affected.

Translations: In the China Study data, fish-eaters (with higher cholesterol, to boot) were generally healthier than the more vegetarian populations that didn’t consume seafood.

And here’s a nice table showing the associations between red blood cell concentration of DHA (which the researchers determined was mostly due to fish intake) and chronic diseases. (The bars to the left of the center line indicate a negative or “protective” correlation; the bars to the right are positive.)

The researchers note that the liver cancer correlation has a likely explanation:

[It] is not difficult to visualise the reason for the link with liver cancer. The coastal, estuarine and lacustrine regions with the high fish and sea food intakes are also those with the highest humidities. Storage of food in regions of high humidity is known to encourage the spread and growth of hepatitis B virus and Aspergillus flavus which produces aflatoxin, both are major causes of primary carcinoma of the liver.

Diet and Blood Nutrient Correlations with Ischemic Heart, Hypertensive Heart, and Stroke Mortality in China by Wande Guo, J.Y. Li, H. King, and F.B. Locke.

Here we’ve got a paper reporting some of the correlations between blood markers, food intake, and cardiovascular disease in the China Study data. Yep, cardiovascular disease! We should see animal products splattered all over this one, right?

Five variables were positively correlated: triglycerides and herpes antibodies with ischemic heart disease; salt and phosphorus (females) with hypertensive heart disease; and only albumin (males) with stroke. … Some findings confirm those observed in the West (salt, triglycerides, herpes, legumes, oleic acid, and liquor), but molybdenum and age at first pregnancy have not been emphasized previously. Still others significant in the West have not been observed here, such as cholesterol and smoking.

This bears repeating: This correlative study (the kind Campbell drew heavily from to link animal products and disease in the China Study data) found no association between cardiovascular diseases and cholesterol. Nada. Or smoking, which is also pretty interesting. How peculiar that one of the most monstrous “diseases of affluence” was unrelated to blood cholesterol.

Okay, folks: That should be enough to chew on for now. I hope to see some of you at the Ancestral Health Symposium in a few days!

For those looking at evolution for clues about the optimal human diet, fruit is often regarded with suspicion. On one hand, few foods are “intended” for consumption in the way fruit is: In a lovely act of symbiosis, plants offer nourishment to the animal kingdom in trade for seed dispersal. But on the other hand—the one purpled with blackberry stains—we humans are famous for playing Food God, turning once-healthy things into gross abominations. For hundreds (and in some cases, thousands) of years, we’ve been selectively breeding certain fruits to become bigger, prettier, easier to eat, and easier to transport thousands of miles away from their mothering trees. As a result, the waxed apples and seedless watermelons lining store aisles are a far cry from their wild ancestors.

And for the health minded, this is a predicament. How can we reconcile this year-round supply of modern fruit with the wild stuff we encountered in the past?

Especially in the paleo/ancestral diet communities, statements like these tend to be widely accepted in a common sense, no-reference-needed sort of way:

• “Fruits in the Paleolithic would have been tart and smaller, and you may want to limit modern fruit because of this.” (From here)
• “The problem is that the fruits our paleo ancestors ate no longer exist. While they had mostly bitter fruit, we’ve bred ours over the past 200 years to be extremely sweet and sugary. It’s thus become something akin to candy plus a mediocre multivitamin.” (From here)
• “Bear in mind that the fruits that paleolithic man ate, while still being, say, apples, bore almost no resemblance to today’s apples. Modern fruit is bred to be HUGE and sweet. Most fruits are packed with a particularly bad sugar, fructose…”(From here)
• “Fruits have been selectively bread to contain massive amounts of sugar compared to how they used to be. Eating a bunch of tropical fruit is not in the spirit of Paleo.” (From here)

At first glance, that all seems logical enough. Virtually all the food we have available today—from plant and animal kingdoms alike—has been selectively bred for both flavor and ease of eating, and fruit is certainly no exception. It seems reasonable to conclude that, apart from the rare batch of honey or seasonal berry bushes popping up outside, humans didn’t get much exposure to sugar during our evolution, and modern fruits are completely unlike anything we encountered in the past.

But are these assumptions truly accurate? Let’s take a look at the facts.

(Note: This isn’t a post about how much fruit we should or shouldn’t be eating, or how much fruit we’ve eaten in the past, or how many apples it’ll take to turn your liver into a ready-to-explode fructose grenade. Those are some hot issues, and I’m not sure they can be reasonably addressed with current research (for instance, there are virtually no studies on the effects of fruit-derived fructose in healthy humans, and quantifying historical fruit consumption is extremely difficult). My intent here is to shed light on some of the myths surrounding wild and ancestral fruit, since some of the most common beliefs are also the most inaccurate.)

Wild fruit: small, bitter, and low in sugar?

Contrary to popular belief, wild fruit—including the stuff we would’ve had access to during our evolution—is not necessarily any of the above. In fact, it can be bigger, tastier, and sweeter than anything you’ll ever find in the aisles of your grocery store.

Fruit is decidedly sparser once you get out of the tropics, but considering we were stationed in Africa until about 50,000 years ago, the flora of a backyard in Michigan might not be a great reflection of the plant life we encountered for the majority of our evolution. As a result, comparisons of cold-climate fruits to their wild ancestors (for instance, a Red Delicious versus a crab apple) tend to be misleading, and tropical fruits may offer more insight. Although we’ll probably never get a clear picture of the exact fruits available to early humans, we can look at the wild fruits growing today to get an idea of what nature is capable of producing on its own.

There’s a great book called “Lost Crops of Africa” (readable online) that has a brilliant section on wild fruit. The authors start by describing the vastness of Africa’s wild fruit supply:

Most of Africa’s edible native fruits are wild. One compilation lists over 1000 different species from 85 botanical families and even that assessment is probably incomplete. Among all those fruit-bearing plants, many of the individual specimens growing within Africa are sheltered and protected, some are even carefully tended, but few have been selected to bring out their best qualities, let alone deliberately cultivated or maintained through generations. They remain untamed. … Africa’s wild-fruit wealth is essentially unknown to science.

So what kinds of “wild fruits” are we talking about here? Let’s take a look at some.

Monkey orange: a tasty fruit enjoyed by more than just primates. Photo by Douglas Boldt of boldt.us.

Nope, that’s not a cross between brains and canned peaches: It’s a monkey orange, a wild species native to Africa. Far from small, these fruits can weigh up to 2.5 pounds each—but untouched by the sweet-seeking hands of humans, is their flavor bitter and unpalatable? Quite the opposite:

In organoleptic taste tests, people were requested to compare the monkey orange fruit with familiar fruits; the most common answers were, orange, banana, and apricot, and all possible combinations among them. The fruits emit a delicate aroma reminiscent of the spice clove. … Over 90% of the panel claimed that it was very tasty.

Nom nom nom. Moving on:

Junglesop: a giant, ugly ball of deliciousness. Photo from SkyfieldTropical.com.

Junglesop. Photo from Lost Crops of Africa: Volume III: Fruits.

Next up, we have the truly wondrous junglesop—a wild member of the same “sop” family that gives us cherimoyas, soursops, sweetsops, sugar apples, and other uber-sweet delicacies common in the tropics. If any uncultivated fruit can blast the “wild fruit is tiny” myth, it’s this sucker: Junglesops average 15 inches in length and weigh around 12 pounds each, with some of the larger fruits clocking in at 30 pounds or more. (Yes, these fruits are even heavier than your obese cat.) And folks lucky enough to live in the junglesop’s native regions seem quite fond of it:

It is so well liked in the regions where it occurs, that for example, in the Central African Republic, some people pay up more than one day’s salary for a single large fruit. A fruit of this size is several meals worth of food. In addition to being an important and widely liked fruit in equatorial Africa, it is also a very important staple for wildlife, especially primates.

Indeed, part of the reason the junglesop hasn’t been messed with by humans is because it does so darn well growing on its own. These fruits pop up like weeds in their homeland (West and Central Africa), and reach their enormous size without any human intervention. Looks like we should give nature more credit for making megafruits without our help.

Other wild fruits in this family are equally scrumptious:

One, the African custard apple, has been called “the best indigenous fruit in most parts of tropical Africa.” Another, the junglesop, produces probably the biggest fruits in the whole family—as long as a person’s forearm and as thick as a person’s thigh. A third—perhaps the strangest of all—“hangs like a bunch of sausages,” each fruit a bright scarlet link. At least two more produce small tasty fruits that make people’s mouths water at just the remembrance from a long-ago childhood. And this group includes a tangy fruit borne on a plant so strange that it barely rises above ground level.

African custard apple, mentioned above: scent of a pineapple, taste of an apricot.

You get the picture. And here are some more:

Soursop. Image from KaieteurNewsOnline.com.

Inside of a soursop. Photo from MedicoNews.com.

The soursop is an often-gigantic fruit of the Annona family that grows wild, but is now being increasingly cultivated in the tropics due to its awesome flavor. I’ve had the pleasure of trying these monsters in Hawaii, and they taste vaguely like the sour-apple gummy snacks I devoured in my youth. (I’ve also heard them described as a mixture of strawberry and pineapple.) The inside is moist, creamy white, and full of seeds. One of the few wild fruits with a documented nutrition profile, they’re decidedly high in sugar (30 grams per 150-calorie serving).

Canistel, also known as egg fruit. Photo from MarketManila.com.

This fruit is as delicious as it is beautiful. The canistel—also called an “egg fruit”—is rich and dense, tasting like a cross between pumpkin pie and sweet potato. The name comes from its texture, which is a bit crumbly and resembles cooked egg yolk. Although bigger, prettier strains are being grown commercially these days (after being introduced to other parts of the world in the mid 1920s), the canistel still grows wild in Mexico, Belize, Guatemala, and El Salvador, where it retains its distinctive flavor. With 37 grams of sugar per 100-gram portion, this is another fruit that’s naturally sweet without human help.

Masuku fruit. Photo by Douglas Boldt of boldt.us.

Those are masukus, another wild fruit renowned for their sweet, delicious flavor. They might not be as visually pleasant as the store-bought fruit we’re used to seeing, but they’re highly sought after throughout Africa due to their taste.

Gingerbread plums. Image from "Lost Crops of Africa."

Gingerbread plums are a wild African fruit with sweet, crunchy flesh reminiscent of strawberries. They’re considered one of the yummiest wild foods in Malawi. When they’re in season, many communities rely on gingerbread plums as a dietary staple, according to “Lost Crops of Africa.”

Pedalai. Photo from SkyfieldTropical.com.

A distant relative of jackfruit (a giant that tastes like Juicyfruit gum), pedalai is a softball-sized wild fruit from Southeast Asia with soft, sweet white pegs of flesh inside.

Jaboticaba, or Brazilian grape tree. Photo from OddityCentral.com.

An open jaboticaba. Photo by Jacob Katel of the Miami New Times.

Contrary to what it may seem, this wacky looking tree isn’t sprouting purple marbles: It’s a jaboticaba, AKA a Brazilian grape tree. This plant produces sweet, big, grape-flavored fruits that grow directly on the trunk—an evolutionary maneuver allowing non-climbing creatures to pick the fruits and disperse the seeds.

Bacupari.

And this is a bacupari—a wild-growing fruit native to South America, with a very sweet, slightly acidic flavor.

Abiu. Photo from CloudForest.com.

Abiu, the Amazon-native wild fruit pictured above, is said to be pretty tasty: Their “delicious flavour is reminiscent of crème caramel and it is sometimes used to flavour ice cream and make other desserts,” according to Daleys Fruit Nursery.

So there you have it: just a small sampling of the many wild fruits that can be sweet, flavorful, and (sometimes) doggone big without us humans breeding them for centuries. Interestingly, one reason wild fruits have a reputation for being more sour than cultivated kinds isn’t because they have less sugar, but because they have more vitamin C, which imparts an acidic flavor. According to a paper about wild fruits in South Africa that I’ll be discussing in the next section:

The composition of these [wild] fruits does not appear to differ much from the better-known domestic fruits except in so far as their vitamin C content is substantially higher than that of domestic fruits. The high vitamin-C content of the wild fruits must undoubtedly contribute to their characteristic acidity.

Nutrient profile of wild fruit

A common belief about wild fruit is that it’s generally lower in sugar and digestible carbohydrates than our modern varieties. Although most of the world’s wild fruits are relatively unstudied (making it difficult to analyze this claim), we do have information on some of ‘em. For instance, a paper published decades ago in the South African Journal of Nutrition, called “The nutrient composition of some edible wild fruits found in the Tansvaal” (PDF), documents the nutrient breakdowns of some of southern Africa’s most popular wild fruits. Here’s a table from the paper:

Wondering why the protein, fat, and carbohydrate percentages look so funny and don’t add up to 100? These measurements are based on dry weight rather than caloric yield like we’re used to seeing—so those are just the relative weights of each macronutrient, with moisture and ash (basically a measurement of mineral content) making up the rest. You can still get a sense of which macronutrient dominates in each type of fruit by looking at that chart, but to make it easier, I went ahead and converted those numbers into “percent of total calories” for all the fruits and graphed ‘em. This is using only non-fiber carbohydrate so we don’t inflate these figures with indigestible carbs (we’ll cover fiber a bit further down). The first monkey orange values are for the flesh surrounding the seeds; the second values are for the flesh on the inside of the shell.

These puppies range from 78 to 92% of calories from carbohydrates. How does that measure up with some of the fruits more likely to find their way onto our kitchen counters? Let’s compare:

Pretty consistent, right? The biggest difference is that some wild fruits are a bit higher in protein than cultivated varieties, but in general, the macronutrient breakdowns are pretty similar. With the exception of durian (and avocado, which I didn’t graph), cultivated fruits—including berries—tend to hover around 85 to 95% of calories from carbohydrate. (Unfortunately, the data set for wild fruit doesn’t tell us how much of the carbohydrate content was from sugar versus starch, so this comparison is still incomplete.)

It’s quite possible that the macronutrient breakdown of wild fruits is more diverse than indicated by the sample above, but studies from other geographical locations offer similar data. For instance, a paper on Australian Aboriginal plant foods found that indigenous fruits had a similar or higher carbohydrate content compared to domestic fruits.

Fiber

So what about the claim that wild fruits are much higher in fiber than cultivated varieties? Going back to the data set above, let’s look at the ratio between fiber and total carbohydrate in various fruits. These ratios can be read as “1 part fiber for every X parts total carbohydrate”—so the lower the second number, the greater the relative fiber content of that fruit.

Fiber:total carbohydrate ratio in wild fruits

• Wild plum: 1:6
• Marula fruit: 1:15
• Wild apricot: 1:42
• Monkey orange, flesh around seeds: 1:4
• Monkey orange, flesh around shell: 1:4
• Amatungulu: 1:11
• Baobab: 1:10
• Sour plum: 1:17
• Red gherkin: 1:11

Fiber:total carbohydrate ratio in cultivated fruits

• Papaya: 1:6
• Guava: 1:3
• Strawberries: 1:4
• Cantaloupe: 1:10
• Oranges, Valencia: 1:5
• Apricots: 1:6
• Grapefruit: 1:7
• Pear: 1:5
• Banana: 1:9
• Grapes, American: 1:20
• Nectarines: 1:6
• Peaches: 1:7
• Blueberries: 1:6
• Honeydew melons: 1:12

Basically, we have quite a bit of fiber variation among both wild and cultivated species. Of the wild fruits listed in the paper above, the fiber-to-total-carb ratio ranges from 1:4 for monkey oranges to a whopping 1:42 for wild apricots (meaning the monkey orange has a decent amount of fiber, while the wild apricot has relatively little). Similarly, the sampling of cultivated fruits here range from 1:3 for guava to 1:20 for American grapes. At least from this data, it seems that wild fruit isn’t universally higher in fiber than cultivated varieties, at least not when we look at the edible portion of the fruit.

The fructose factor

If you’ve been keeping up with the latest health news, you’ve probably noticed fructose stealing the spotlight as a potential factor in obesity, non-alcoholic fatty liver, metabolic syndrome, and other health woes (for instance, see Robert Lustig’s “Sugar: The Bitter Truth“). Although most of the finger-pointing has been at high-fructose corn syrup and other refined sweeteners, fruit has also taken a whooping because of its natural fructose content. Modern fruit, in particular, has been accused of being higher in fructose than ancestral and wild strains and thus less healthy than it was in the days of yore. In my frequent internet lurks, I often see unreferenced advice to limit fruit consumption to berries, which are supposedly lower in fructose than other varieties of fruit.

But is there truly a significant difference in fructose between wild and cultivated fruits?

Once again, wild fruits are terribly understudied in terms of nutrients (especially sugar composition), but we do have a few resources out there to mine for clues. One is the paper “Phytochemicals, vitamin C and sugar content of Thai wild fruits” published in Food Chemistry in 2011. This article has a nice breakdown of the sugars in 19 wild fruits from Southeast Asia. I’ve graphed them out below.* If you’re not a botany buff, don’t worry about the gibberish-esque Latin names: Just look at the pie charts to get a visual feel for what sugars are abundant in some wild species.

*For the fruits that had a listing for both “ripe” and “raw” (not ripe), I only graphed the “ripe” data.

(Note: Maltose and galactose made up a minor portion of the sugars in some of these fruits, but for the sake of keeping things simple, I’m only graphing the three major sugars—sucrose, glucose, and fructose. And since sucrose cleaves into equal parts fructose and glucose in your body, all the blue pie slices below could be viewed as contributing half fructose and half glucose.)

If there’s any pattern here, it’s that most of these fruits are comprised of at least half glucose and a hefty dose of fructose—but three are actually sucrose-dominated, so there aren’t any set-in-stone rules regarding sugar distribution in wild fruits. Likewise, human-bred fruits are all across the board in terms of sugar. Berries (both wild and cultivated) tend to be about half fructose with only minimal amounts of sucrose, while other commercial fruits contain more sucrose and proportionately less fructose and glucose. Take a look at some common varieties as an example:

Whether you’re looking at straight-up fructose or fructose derived metabolically from sucrose, there’s really no basis for the claim that wild fruit is lower in fructose than cultivated varieties—at least in terms of sugar breakdown. After digestion, both wild and cultivated fruits seem to yield about 50% fructose.

Seasonality

Although many wild fruits do have a limited harvesting period, this doesn’t mean early humans would only have access to fruit for only a few weeks or months per year (as is sometimes stated). Particularly in tropical climates, different plant species tend to bear fruit at different times annually—and even plants of the same genus or species can have staggered fruiting periods within the same region. Although a single fruit might not have been available year-round, different species would certainly provide access to fruit beyond a single season.

On top of that, some species remain edible for months after they ripen, and others naturally sun-dry on the plant, making them easy to store for later consumption. For example:

• The monkey orange, mentioned earlier: “These three special monkey orange trees are widely enjoyed and have the amazing capacity to stay edible in tropical heat for months after maturity.”
• Sand apples can be easily dried and formed into a long-lasting “cake.”
• Australian aborigines dry a number of desert fruits to eat throughout the year, including the raisins Solanurn centrale and S. ellipticurn and the bush tomato.

On the flip side

Despite all of the above, there are some notable differences between wild fruits and cultivated ones:

• The ratio of pulp vs. inedible stuff. Wild fruits tend to have thicker peels and bigger seeds, strings, rinds, cores, and other gnarly bits relative to the amount of edible flesh they yield. Even when sugar composition doesn’t differ dramatically between the edible parts of wild versus cultivated species, a single wild fruit will generally provide a lot less edible material than a cultivated fruit of the same size. This is one area where humans have definitely left our signature in fruit breeding: We like our cultivated fruits to be seedless (or at least low in ‘em), easy to bite into, easy to peel, and abundant in edible flesh. Due to their extra roughage (and sometimes-scary exteriors), wild fruits can be more of a challenge to eat. (This doesn’t just apply to sweet fruits, either: See my earlier post on wild avocados.)
• Water content. Interestingly, wild fruits are often calorically denser than cultivated fruits due to their lower water content. Whereas humans seem fond of fruits with a juice-dribbling-down-your-chin effect, wild fruits are sometimes (but not always) dry, crumbly, crunchy, mushy, and otherwise non-juicy. The higher water content of cultivated fruits makes them appear relatively lower in protein and fat than wild varieties (as primate-diet-expert Katharine Milton points out in many of her publications), even though this isn’t usually the case when viewed from a calorie perspective.
• Fruiting cycles. On an individual-species basis, the fruiting cycles of wild versus cultivated fruit tend to be very different. In the wild, plants can have variable fruiting periods depending on climate, season, rainfall, and even the specific year (some plants are biennial, bearing most of their fruit once every two years), leading to inconsistent fruit yields. Farmers, on the other hand, may deliberately control or extend fruiting periods so that a particular fruit stays in season longer or hits the grocery store shelves earlier than nature dictates.
• Dangerous natural substances. Although most cultivated fruit is pretty safe from a toxicity perspective, wild fruits—especially under-ripe ones—can contain an array of natural toxins causing everything from an upset stomach to death. Alkaloids, tannins, cyanogenic glycoside (which turns into cyanide), and a variety of other compounds can exist in some types of wild fruit, making it imperative to know which parts are safe to eat. These substances can also make some types of wild fruit difficult to eat in large quantities without feeling queasy.
• Flavor variability. Because flavor is influenced by soil quality (among other things), wild fruits of a single species can sometimes vary tremendously in taste. The junglesop, for instance, can span a wide range of flavors—not all of them pleasant. According to Lost Crops of Africa: “In some varieties [the junglesop flesh] is deliciously sweet and very good to the taste; in others, it can be not only sour but downright awful. Just how mature the fruit was when picked can affect the sweetness, but genetics also plays a part, and locals know individual trees that are always sweet and others that are always sour.”
• Micronutrients. Some wild fruits are far more nutritious than the conventionally-grown ones we throw into our shopping carts, although the vitamin and mineral content of wild fruit fluctuates almost as much as flavor. I initially planned to write a separate section on this subject, but the papers I found were so inconsistent (some showing high levels of certain micronutrients in wild fruits, others showing low levels compared to cultivated fruit) that it seems impossible to say anything definitive.

In addition, if you rounded up every single wild fruit species in the world (not just ones preferred by primates with somewhat-similar digestive anatomy to ours), the majority likely would be small and unpalatable. Wild sweet fruits are a favored minority. This isn’t necessarily a blow against fruit, though. You could also argue that if you rounded up every animal, every vegetable, or every seed in the world, the majority would be small and unpalatable. Across the board, humans have distinct preferences within each food category, such a for sweeter fruit, fattier meat, and less-bitter vegetables.

Take-home points

If you’re in brain-burnout mode and didn’t absorb all that (I can empathize!), here’s the Reader’s Digest version of this post.

• Although not all wild fruits are as big and sweet as our modern cultivars, at least some are, and certain varieties even surpass our deliberately-bred fruits in size and flavor. Nature—especially with selection pressure from other fruit-eating creatures—is perfectly capable of producing sweet (and sometimes massive) fruits without human intervention. It seems unlikely that early humans only ever encountered berries or other “small, bitter” fruits, and avoiding sweeter fruits on the basis of evolutionary history may be misguided.
• Based on the limited research we have, wild fruits aren’t considerably different from cultivated fruit in terms of carbohydrate content, fructose content, or fiber content. Both wild and cultivated fruit seem to average around 90% of calories from carbohydrates, and have a sugar composition that yields roughly equal parts glucose and fructose. And both wild and cultivated fruit can be relatively high or low in fiber.
• Although berries are often lauded as being lower in fructose compared to other fruits, from a calorie/energy standpoint, this just ain’t true!
• Early humans may very well have had access to fruit for most or even all of the year. The fruiting seasons we witness in cooler climates—with most fruit appearing in the summer—doesn’t necessarily apply to our evolutionary homeland closer to the equator.

I blame the “wild fruit is bitter and small” belief on our woeful state of food education. Most people can name more types of candy than they can of fruit, even though there are literally thousands of edible varieties across the globe—a great many of them wild. With the exception of raw foodists, well-traveled gourmands, and anyone who hangs out at Asian markets, most people’s concept of “fruit” is limited to the standard grocery store staples, with little idea of what else is out there.

Again, this post is only intended to be descriptive, not prescriptive. Fruit is a regular part of my own diet, but I also believe dietary context and individual health history plays a big role in how people react to nature’s proverbial candy. If you avoid modern fruit on the basis that only “small, bitter, fibrous” fruit was available in the past though, it might be time for a paradigm shift.

Nutrition information in this post was taken from the USDA Nutrient Database and Fruits of Warm Climates by Julia Morton.

As some of you’ve already seen, a major study came out this week with some unexpected findings about DHA, an omega-3 fat abundant in fish. The study linked high blood levels of DHA to aggressive prostate cancer (and trans fats to lower prostate cancer rates). To date, it’s the biggest fat-and-prostate-cancer study of its kind—which makes these findings all the more peculiar. Given the widespread use of fish oil supplements for quelling inflammation and boosting cardiovascular health, it’s a little spooky to think DHA is really a double-edged sword. But is this study really a slam against fish fat?

This analysis wound up as a guest post for Mark’s Daily Apple, so head over there to read the full thing:

• Is Fish Oil Linked to Prostate Cancer?

Overall, the study itself isn’t too shabby—and the researchers readily admitted their findings surprised them. But this study is far from a harbinger of doom for seafood lovers. The take-home points, and some additional thoughts:

• Serum fatty acids aren’t a perfect mirror of diet—and the men with higher levels of DHA weren’t necessarily eating more fish. In fact, it seems low-fat diets can actually increase DHA status in the blood the same way omega-3 supplementation can.
• The “highest levels of serum DHA” reported here were based on percentage of fatty acids—not absolute value. Here’s a great explanation of why percentage-based measurements may be misleading in studies like these.

Another major study, the European Prospective Investigation into Cancer and Nutrition, also found a slight (but non-statistically-significant) link between prostate cancer and DHA levels in the blood—but at the same time, found zero association between dietary fish fat and the disease. And as I wrote in the post on Mark’s Daily Apple, nearly all previous studies have shown fish consumption to have either a neutral or protective association with prostate cancer. Blood levels of DHA and dietary intake don’t seem to follow the same pattern in relation to this disease.

That said: I’m pretty weary of long-term mega-dosing of fish oil for other reasons. Thanks to all their double bonds, omega-3s are relatively unstable and prone to oxidation, just like other polyunsaturated fats. It’s quite possible that the anti-inflammatory benefits appearing short term could eventually collide with a new set of problems that take longer to appear: those stemming from oxidative stress. Moderate supplementation probably won’t cause harm, but regularly taking huge doses of fish oil should probably be done with caution. The best strategy for achieving a great omega-3/omega-6 ratio is reducing your intake of high-omega-6 foods like grains and industrial oils, rather than simply chugging back more omega-3 to compensate.

Edit: Paul at Perfect Health Diet has a more technical discussion of omega-3s, angiogensis, and cancer that does make DHA seem a little fishy. Highly worth reading!

• Omega-3 Fats, Angiogenesis, and Cancer: Part I
• Omega-3s, Angiogenesis and Cancer: Part II

Actually, I’ve had my hands tied lately with things other than death—the biggie being a book I’m writing. (A real one, contract and all!) More details to come. And, like a frustratingly slow-to-ripen fruit, the promised “wheat and heart disease” post is nearing completion. I don’t expect anyone to believe me anymore, but it’s true. A huge thank-you to those of you who’ve had the patience to keep checking back here for that. Your page-refreshing efforts will soon be rewarded.

Other stuff:

Wise Traditions Conference 2011: I’ll be speaking at The Weston A. Price Foundation’s annual conference in Dallas this year—about the China Study, veganism, and anything else they’ll let me gush on about. I hope to see some of you there! The theme this year is “Mythbusters,” and it’s guaranteed to be a great experience.

For those of you who can’t attend that, come hang out with me at the Ancestral Health Symposium coming up in August, which I’m going to try my darnedest to attend. Check out that awesome lineup of speakers! It’s like all the coolest people from the internet will be crammed together in the same building.

Time to give up fish if you’re a dude? A new study came out this week showing that high blood levels of DHA—the omega-3 fat abundant in fish—are linked to aggressive prostate tumor growth. Check out the abstract here and a regurgitated news story here. It’s the largest prospective study so far to examine serum fatty acids and prostate tumor occurrence, so this is one to pay attention to. But as usual, there’s more to the study than the media’s reporting. Check back here tomorrow for a closer look at the full text.

Sucky Science Award of the Day goes to an article by Dr. Tim Harlan at Huffington Post, titled Low-Carb Diets Linked With Type 2 Diabetes:

I can’t imagine why anyone would follow a diet — any diet — that takes entire food groups away from you. There’s no reason to give up great foods like pasta, potatoes, beans and corn to lose weight or to be healthier. Giving up these foods is one of the main reasons that the Atkins diet is not a diet that can be sustained for the long term. Further, such diets seldom prepare people for eating real food. …

Hear that, low-carbers? Your diet doesn’t prepare you for eating real food. Time to practice for Reality with some Twinkies.

There’s been concern for years about the long term health risks of such diets. We’ve seen that those eating higher protein diets that are also high in saturated fat were more likely to develop heart disease than those whose higher protein diet came from vegetable protein sources.

No we haven’t!

The rest of the article is pretty entertaining, too. Read it and weep.

Some housekeeping. I added a subscription button to this site (was it seriously not there before? What a blogging failure I am!). That should make it easier to deal with my chaotic posting schedule. And despite dragging my feet for years, I finally woman-ed up and joined Twitter. I don’t understand it yet, and that makes me nervous. I promise I won’t post 80 million daily updates about when I blink and brush my teeth.

That’s all for now. More posts to come very soon!

Nah.

Contrary to my title, though, the new guidelines aren’t total hogwash. Just mostly. A few of their recommendations are passable, like these:

• Prevent and/or reduce overweight and obesity through improved eating and physical activity behaviors. (Duh.)
• Increase physical activity and reduce time spent in sedentary behaviors. (Duh.)
• Keep trans fatty acid consumption as low as possible by limiting foods that contain synthetic sources of trans fats, such as partially hydrogenated oils. (Duh.)
• Limit the consumption of foods that contain refined grains, especially refined grain foods that contain solid fats, added sugars, and sodium. (Yes!)

Unfortunately, the rest of the guidelines are the regurgitated—and often unsubstantiated—snippets we’re already inundated with. Case in point:

• Consume less than 10 percent of calories from saturated fatty acids by replacing them with monounsaturated and polyunsaturated fatty acids.
• Consume less than 300 mg per day of dietary cholesterol.
• Consume at least half of all grains as whole grains. Increase whole-grain intake by replacing refined grains with whole grains.
• Increase intake of fat-free or low-fat milk and milk products, such as milk, yogurt, cheese, or fortified soy beverages.
• Use oils to replace solid fats where possible.

According to the guideline packet, these recommendations provide ”information and advice for choosing a healthy eating pattern” and are ”based on the most recent scientific evidence review.” If you’ve read anything else on this blog, you probably know by now that I’m weary of trusting second-hand interpretations—the original data often tells a different story than the mouths claiming to interpret it. So instead of taking the USDA’s word as gospel, why not see what they’re basing their recommendations on?

Luckily, the USDA has a Nutrition Evidence Library, where they’ve compiled the studies they used to create their latest guidelines. Let’s dig in.

Saturated fat: true killer or whipping boy?

Here’s what the USDA has to say about saturated fat:

A strong body of evidence indicates that higher intake of most dietary saturated fatty acids is associated with higher levels of blood total cholesterol and low-density lipoprotein (LDL) cholesterol. Higher total and LDL cholesterol levels are risk factors for cardiovascular disease.

Ah, the lipid hypothesis in all its unproven, scientifically-feeble glory! We’ll look at the evidence they cite to bash saturated fat in a moment. But for now, let’s see their specific 2010 recommendations regarding this oft-feared nutrient:

To reduce the intake of saturated fatty acids, many Americans should limit their consumption of the major sources that are high in saturated fatty acids and replace them with foods that are rich in monounsaturated and polyunsaturated fatty acids. For example, when preparing foods at home, solid fats (e.g., butter and lard) can be replaced with vegetable oils that are rich in monounsaturated and polyunsaturated fatty acids.

Time to start frying your (yolk-free) eggs in soybean oil. Never mind that polyunsaturated fats actually increase oxidative stress (a major player in heart disease and cancer) and become particularly hazardous when heated, especially compared to heat-stable saturated fats. And never mind that most vegetable oils are disproportionately high in omega-6 fatty acids, aggravating the omega 3/6 imbalance that’s already rampant in American diets. If the USDA guideline team could peel off those lipid-hypothesis goggles for a minute, maybe they’d realize that the vegetable oils they’re recommending are likely to wreak some serious health havoc, regardless of what they do to cholesterol levels.

Worse, the new dietary guidelines give the green light to eat some of the worst industrial oils out there:

Oils that are rich in monounsaturated fatty acids include canola, olive, and safflower oils. Oils that are good sources of polyunsaturated fatty acids include soybean, corn, and cottonseed oils.

From page 38 of the 2010 USDA Dietary Guidelines for Americans

From this graph, we should learn that soybean oil and corn oil (for example) are more healthful options than coconut oil and butter, because they’re lower in saturated fat. It doesn’t matter that we have studies showing high-omega 6 oils like corn oil may promote tumor growth while—using the same study design—saturated fats do not. As long as the USDA is on board with the “cholesterol causes heart disease” theory, the only thing that matters about fats is how they affect lipid profiles.

Besides, saturated fat is saturated. And saturated things kill us.

Here’s something else that’s interesting. Let’s hop over to the fatty acid page in the Evidence Library for a second. Under the subheading called “Needs for Future Research” (AKA “Stuff We Don’t Really Understand Yet”), they wrote:

1. Determine the benefits and risks of MUFA vs. PUFA as an isocaloricsubstitute for SFA. Confirm the metabolic pathways through which dietary SFA affect serum lipids, especially as some SFA (e.g., stearic acid) do not appear to affect blood lipid levels.

Basically, they’re recommending we swap saturated fat for unsaturated varieties without being sure what the effects are, and that we slash all saturated fat consumption without being sure whether the reasons are biologically justified. I guess by the time the next tome of guidelines is released, the USDA will get to see whether their lipid recommendations helped or killed us off faster. Welcome to America, land of 300 million guinea pigs.

But could the USDA be onto something we don’t know about—especially with the “strong body of evidence” they mentioned linking saturated fat to heart disease? The answer may lie in their evidence summary page, which recaps the 12 studies they looked at to assess saturated fat. As best I can tell, these studies are the main pieces of research the USDA used to back up their “replace saturated fat with unsaturated fat” recommendation.

For the sake of being thorough, here’s a rundown of all those studies. You can click the article name for a link to the study (full text for most).

1. Particle size of LDL is affected by the National Cholesterol Education Program (NCEP) step II diet in dyslipidaemic adolescents.

This one looked at a group of 46 adolescents who had high cholesterol. One group continued chowing down on their normal diet (the only instructions: “eat as usual”), and the other group ate the “National Cholesterol Education Program Step II Diet.” At the end of the study, the Step II kiddos had lower total cholesterol, lower LDL cholesterol, and larger LDL particle size.

So how did the Step II diet differ from the control group? Was a shift in fat sources the only change? Let’s take a look:

As you can see, the Step II dieters ate significantly fewer sweets, fewer fats and oils, more vegetables, more fruit, more poultry and fish, more fiber, and more dairy products (mostly low-fat) than the eat-whatever group. They also ate less saturated fat (7 percent compared to 14 percent) and more monounsaturated fat. The researchers note that the higher fiber intake of the Step II diet “could explain its beneficial effects on lipid concentrations and particle size,” at least to some extent.

But what did the USDA, in their infinite wisdom, conclude from this? That the improved lipid profiles resulted solely from reducing saturated fat and replacing it with unsaturated fats. At least that’s what it seems like, since “type of fat” is the only changed variable they mention in their summary in the Evidence Library.

In other words, this study is fairly useless for isolating the effects of saturated versus unsaturated fat—but that’s exactly what the USDA team tried to do.

2. Comparison of monounsaturated fat with carbohydrates as a replacement for saturated fat in subjects with a high metabolic risk profile: studies in the fasting and postprandial states.

This study rounded up 85 adults—mostly folks with low HDL and high triglycerides—and made them consume three consecutive diets: an “average American diet” (with 15.6 percent of calories as saturated fat), a high-monounsaturated-fat diet (replacing 7 percent of the saturated fat with monounsaturated fat), and a high carbohydrate diet (replacing 7 percent of the saturated fat with carbs). The carbohydrate-heavy diet also added a significant amount of fiber. Unfortunately, the study doesn’t document what else changed between the diets in terms of specific food intake, nor what the actual sources of fat were.

The results? Both of the low-saturated-fat diets reduced HDL levels (bad, bad, bad—these folks had low HDL to begin with!), and the carby diet produced higher triglycerides than both the average American diet and the mono-fatty diet. The total cholesterol/HDL ratio worsened when carbs replaced saturated fat, and none of the diets produced any differences in glucose or insulin response. It’s hard to say why the USDA thought this study supported their recommendation to cut saturated fat and replace it with unsaturated varieties. Even though the high-monounsaturated fat diet reduced LDL levels, it did so roughly in proportion to reducing HDL (not something you want to see happen in folks who are predisposed to insulin resistance)—and the effect on triglycerides was negligible. If anything, this study shows that it’s generally better to eat saturated fat than replace the saturated fat with carbohydrates. But even then, there aren’t enough specific diet details to get a sense of all the factors involved. In a nutshell: It’s a long, painful, joint-busting stretch to say this study supports the USDA’s fat recommendations.

3. Macrophage cholesterol efflux elicited by human total plasma and by HDL subfractions is not affected by different types of dietary fatty acids.

In this study, the researchers compared the effects of eating diets with either 30 percent trans fat, 30 percent polyunsaturated fat, or 30 percent saturated fat for four weeks (using hydrogenated soybean oil, rapeseed oil + sunflower oil, and palm oil + a little olive oil, respectively). The results? Maybe the title should tip us off, especially the “not affected by different types of dietary fatty acids” part. Total cholesterol and triglycerides didn’t change over time with any of the fat types, and the researchers conclude that “differences in the cell cholesterol efflux with these diets were not observed.” In the USDA’s summary, they note—looking closer at the study’s details—that the polyunsaturated fat diet seemed to have some favorable effects compared to the saturated fat diet, such as clearing more LDL cholesterol after meals. Unfortunately, they overlook the artery-clogging elephant in the room, which is that—based in the markers in this study—the trans-fat diet produced better results than the polyunsaturated or saturated fat diets.

Is this really a good study to use for saving the health of America?

4. Consumption of an oil composed of medium chain triacyglycerols, phytosterols, and N-3 fatty acids improves cardiovascular risk profile in overweight women.

This one’s a head-scratcher—not because of the study itself, but because it somehow became evidence for replacing saturated fat with unsaturated varieties. In this study, the researchers compared the effects of a control diet supplemented with beef tallow versus the same diet supplemented with “functional oil”—a combination of medium-chain triglycerides (abundant in coconut oil and palm oil), phytosterols (substances in plants that stop or slow cholesterol absorption), and omega-3 fatty acids. The goal was to see whether the phytosterols and omega-3 fats would keep lipid profiles lookin’ good.

By the end of the experiment, the “functional oil” diet did well enough to please any cholesterol-fearing doctor: Total cholesterol, LDL, the HDL:LDL ratio, and the HDL:total cholesterol ratio all improved significantly compared to the baseline measurements and to the beef tallow diet. The beef tallow diet didn’t produce any statistically significant changes except for a reduction in triglycerides. So what does this tell us about saturated fat, and the effects of replacing it with polyunsaturated fats? Almost nothing. The baseline measurements reflected the participants’ normal diets, not the study diet sans fat supplement—so it’s impossible to isolate the effect of beef tallow or of any specific component of the “functional oil.” In fact, the “functional oil” diet had more saturated fat (63.8 grams versus 50.9 grams) and less monounsaturated fat (24.4 grams versus 41.9 grams) than the tallow diet, the opposite of what the USDA recommends. If anything, this study shows that the USDA could still appease their cholesterol fixation by recommending a diet loaded with coconut products, butter, and palm oil (the best sources of medium-chain fatty acids) along with fish and phytosterol-containing vegetables. That’d roughly mimic the “functional oil” supplement used in the study, but with real foods. Ya hear that, USDA? It’s the sound of saturated fat busting out of jail. And it goes something like this: “Neener-neener.”

5. Phytosterol intake and dietary fat reduction are independent and additive in their ability to reduce plasma LDL cholesterol.

Here we have another study that does nada to support lowering saturated fat. In this one, researchers wanted to see if the effects of plant sterols differ depending on the dietary context—so they compared four diets: a typical American diet (13.2 percent saturated fat), an American diet supplemented with plant sterols, a reduced-saturated-fat Step I diet (7.7 percent saturated fat), and a Step I diet supplemented with plant sterols. The diets consisted of pretty much the same foods, just with different fat levels.

Compared to the Step I diet, the higher-saturated-fat American diet (without plant sterols) produced higher values for all the lipoproteins and plasma lipids measured—except for triglycerides, which were the same. It also yielded a slightly prettier total cholesterol:HDL ratio, since the lower-saturated-fat diet reduced both LDL and HDL. Once the phytosterols were thrown into the mix, the results showed that the sterols have an additive effect rather than an interactive effect with their diet context—meaning there were no special benefits from adding plant sterols to the American diet versus the Step I diet. Okay. That’s interesting and all, but how does it show that saturated fat ruins your heart health? Why did the USDA find it relevant enough to use in their uber-selective Evidence Library to answer the question “What is the effect of saturated fat intake on increased risk of cardiovascular disease?” Even if you ignore the fact that this study was about plant sterols and try using it to gauge the effects of the typical American diet vs. the Step I diet (where the only major difference is saturated fat content), it definitely doesn’t show the reduced-saturated-fat diet coming out ahead.

6. Contribution of postprandial lipemia to the dietary fat-mediated changes in endogenous lipoprotein-cholesterol concentrations in humans.

This is a study examining the effects of a high-polyunsaturated-fat diet versus a high-saturated-fat diet on postprandial lipemia (lipids in the blood after eating). Compared to the saturated-fat diet, the polyunsaturated-fat diet resulted in faster clearing of cholesterol and triglyceride-rich lipoproteins from the blood—which is generally considered a good thing. However, given the potential for polyunsaturated fat to contribute to oxidized LDL, quicker clearance time doesn’t automatically make polyunsaturated fat a friend of the heart. Nor does this study offer hard evidence that saturated fat contributes to cardiovascular disease.

7. Moderate intake of myristic acid in sn-2 position has beneficial lipidic effects and enhances DHA of cholesteryl esters in an interventional study.

Next up is a study looking at myristic acid, a type of saturated fat found in coconut, palm oil, butter fat, and nutmeg (which has the scientific name Myristica fragrans—where the word “myristic” actually comes from). The researchers gave a group of French Benedictine monks two diets: one with 30 percent fat (8 percent saturated, 0.6 percent myristic acid) and one with 34 percent fat (11 percent saturated, 1.2 percent myristic acid). The extra saturated fat came mainly from whole milk.

Did that added dairy fat do ‘em in? Au contraire. Both diets improved lipid measurements across the board. But compared to the lower-saturated-fat diet, the higher-saturated-fat diet produced a greater drop in triglycerides and a higher boost in HDL from the baseline measurements, without comparatively raising LDL or total cholesterol.

This, of course, baffled the researchers. Here’s a blurb straight from their paper, emphasis mine:

Many questions are raised by comparing diets 1 [lower saturated fat] and 2 [higher saturated fat]. If one accepts the conclusions of Gaggiula and Mustad, Clarke et al., Howell et al. and Verschuren et al., the better results should have been obtained with diet 1 and not diet 2. The MUFA and PUFA intakes are identical in both diets, while the PUFA/SFA ratio is 1 in diet 1 and 0.75 in diet 2. The predictive equations of [long list of lipid hypothesizers] point to the superiority of diet 1 over diet 2. The main difference between the diets is that there is twice as much myristic acid in diet 2. … Moreover, the decrease in carbohydrates in diet 2 (51.2%) vs. diet 1 (55.2%) should have worsened the lipid results. Yet at these levels which are pertinent in clinical terms and are widely accepted, the present findings are in contradiction with the various theories based on explanatory equations and on certain studies performed at levels not encountered in daily life.

In other words: “Oops! We found something that contradicts the lipid hypothesis. Let’s air our cognitive dissonance on paper.”

Again, this is a study straight from the USDA’s Evidence Library, on the page dedicated to the saturated-fat-causes-heart-disease issue. If the USDA deemed it a high-quality study, why did they continue universally condemning saturated fat?

8. Effect of protein, unsaturated fat, and carbohydrate intakes on plasma apolipoprotein B and VLDL and LDL containing apolipoprotein C-III: results from the OmniHeart Trial.

This study looks at the effects of a carb-heavy, protein-heavy, and unsaturated-fat-heavy diet on apo-B levels. As much as I love to yammer on about this stuff, I’ll keep this one short: The most interesting outcome was that, compared to the carby diet, the protein-rich diet had a much more favorable impact on apolipoprotein and lipoprotein profiles. The unsaturated-fat diet was also an improvement over the carby diet, but not significantly so.

Unfortunately, this study can’t tell us diddly squat about saturated fat because none of the test diets used saturated fat as an independent variable, or even indirectly measured its effects. Next, please.

9. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies.

Finally! A paper that actually involves saturated fat and heart disease and a link between the two (maybe). It’s a miracle! Oh USDA, you’ve almost redeemed yourself.

Here we have a review of 11 studies concerning diet and heart disease, with a special focus on what to do once we succumb to conventional wisdom and scoot the saturated fat off our plates. Should we fill the calorie void with carbs? With polyunsaturated fat? With monounsaturated fat? With Soylent Green*?

*Not suitable for vegans

Indeed, this study found some interesting trends. Reducing saturated fat by 5 percent and replacing it with monounsaturated fat was associated with an increase in coronary events (hey USDA—why not vilify olive oil, too?). Although carbs were a mixed bag in the pooled analysis, a newer study led by the same researcher, Marianne Uhre Jakobsen, found that the type of carbohydrate plays an important role: Increasing high-glycemic carbs by 5 percent in place of saturated fat was associated with a 33 percent greater risk for having a heart attack. (Funny how the new USDA recommendations, while censuring saturated fat, still allow up to half your daily grain intake to be refined.) Low- and medium-glycemic-index carbs fared more favorably, but in Jakobsen’s second study, neither were associated with a statistically significant improvement in heart health when displacing saturated fat.

Interestingly, from the USDA’s cited study, replacing saturated fat with polyunsaturated fat seemed to be associated with reduced deaths from heart disease. I say “seemed” because of a reply Martijn Katan wrote shortly after this study was published, which you can read here. This is the point worth noting (emphasis mine):

Jakobsen et al (1) found that a low intake of saturated fatty acids and a proportionally higher intake of omega-6 polyunsaturated fatty acids was associated with a significant reduction of coronary heart disease. Confounding was again a problem: diets low in saturated fatty acids and high in polyunsaturated fatty acids are rich in vegetable oils, polyunsaturated margarines, lean meats, and low-fat dairy. That is what health-conscious people eat. Indeed, correction for smoking, body mass index, and other risk factors diminished the effect from a risk reduction by 31% to a risk reduction by only 13%, if 5% of energy from saturated fatty acids was replaced by that from polyunsaturated fatty acids. Is this 13% due to residual confounding by imperfectly measured aspects of a healthy lifestyle, or is it real?

Given what we know about the biological effects of polyunsaturated fats (especially their contribution to oxidative stress), it sure seems possible that their apparent health perks could be a result of confounding. Especially since polyunsaturated fats are pushed so firmly by health authorities.

Public diet guidelines have a spooky tendency to create self-fulfilling prophecies: As soon as specific foods are slapped with a “healthy” label by the white-coat-sporting experts, they’re more likely to appear beneficial in studies. That’s because health-conscious folks are often the only people who actually heed the advice of the USDA and other nutrition authorities, so they integrate foods like low-fat dairy and vegetable oils into their tangled web of healthy habits—creating a massive ball of confoundment that’s nearly impenetrable with statistical tools. (Of course, healthy foods can appear deadly by this same mechanism. If the health-indifferent folks are the only ones brave enough to eat a declared “artery-clogging” item—say, butter—then statistical analyses are generally going to show that food being hazardous, because the people consuming it are damaging their health in other ways.)

But I digress. If the USDA had kept its eyes peeled for research a little longer before finishing the 2010 guidelines, maybe they would’ve seen the newer meta analysis on saturated fat and heart disease reviewing almost twice as many studies as the one above. What did this bigger analysis reveal? I’ll let the researchers say it for me:

In conclusion, our meta-analysis showed that there is insufficient evidence from prospective epidemiologic studies to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD.

As meta analyses often do, this paper also examined the pooled studies for publication bias—an all-too-common tendency to publish studies based on their results rather than on their theoretical or design quality. Indeed, the researchers found that—in the realm of saturated fat and heart disease—studies showing a strong relationship were more likely to get published than studies showing a neutral relationship.

Our results suggested publication bias, such that studies with significant associations tended to be received more favorably for publication. If unpublished studies with null associations were included in the current analysis, the pooled RR estimate for CVD could be even closer to null.

All in all, the USDA’s chosen study—the pooled analysis by Jakobsen—is their strongest “evidence” so far to support replacing saturated fat with polyunsaturated fat. But that study is far from conclusive, especially since it 1) seems to warn against monounsaturated fat (one of the USDA’s darling lipids), 2) was followed by another study showing that many carbohydrates are more convincingly associated with heart disease than saturated fat, and 3) had its findings challenged by a newer, bigger meta analysis.

But maybe the USDA has some more compelling studies up it’s sleeve. Let’s look at the next one.

10. Replacement of dietary saturated FAs by PUFAs in diet and reverse cholesterol transport.

In this study, researchers took 14 male volunteers and studied the effects of a high-saturated-fat diet versus a high-polyunsaturated-fat diet on cholesterol efflux from macrophages—your body’s mini-vacuum cleaners. (When macrophages can’t get rid of the cholesterol they slurp up, they can turn into foam cells, which is one of the earliest steps in atherosclerosis). Since diets high in polyunsaturated fat tend to decrease HDL, the researchers wanted to see if this type of diet would be detrimental for transporting cholesterol to the liver for catabolism. The results? The high-saturated-fat diet and high-polyunsaturated-fat diets didn’t produce any differences in cholesterol reflux. In other words: This study isn’t a strike against polyunsaturated fat, but it’s also not a strike against saturated fat.

11. Individual variability in cardiovascular disease risk factor responses to low-fat and low-saturated-fat diets in men: body mass index, adiposity, and insulin resistance predict changes in LDL cholesterol.

Here we have a study looking at three diets with differing fat levels: The Average American Diet (38 percent fat, 14 percent saturated fat), the Step I diet (30 percent fat, 9 percent saturated fat), and the Step II diet (25 percent fat, 6 percent saturated fat). The Step diets, by the way, were designed by the American Heart Association to help combat heart disease. Since all meals were provided for the participants, there was a high degree of control

Was there a trend between lower saturated fat intake and better lipid profiles (and, by association, better heart health)? Nope. Both of the saturated-fat-reduced Step diets significantly raised triglycerides, lowered HDL, and worsened the total cholesterol:HDL cholesterol ratio.

This is bad news, folks.

Because the changes in apo-B and apo-A1 were (percentage-wise) less than the changes with LDL and HDL cholesterol, the researchers speculate that the lower-fat diets increased the proportion of small, dense LDL particles (the ones most associated with atherosclerosis) as well as decreasing HDL2 relative to HDL3 cholesterol (HDL2 is the more protective subfraction).

Basically, slashing fat resulted in lipid profiles more likely to promote heart disease.

On top of that, the men who were overweight (and insulin resistant) suffered the most from the Step diets: For them, cutting down fat caused a much steeper drop in HDL relative to LDL, resulting in a more dangerous total cholesterol:HDL ratio than folks of a healthier weight. The researchers conclude that:

[P]ersons who may already be at increased risk of CVD because of their underlying insulin resistance, and thus who are prime candidates for dietary intervention, may be less likely to benefit from dietary changes.*

*”Dietary changes” = reducing total and saturated fat. Because obviously, this is the only kind of dietary change in existence.

The Step I diet is pretty close to what the USDA recommends, in terms of total and saturated fat percentage, but eating this way only made things worse compared to the higher fat diet. Again, I ask: how does this study support the USDA’s fat-lowering recommendations? How, how, how? Did they even read the stuff they crammed into their Evidence Library?

12. Novel soybean oils with different fatty acid profiles alter cardiovascular disease risk factors in moderately hyperlipidemic subjects.

This one’s easy-schmeasy. In this study, researchers compared the effects of five experimental diets, all with 30 percent fat: one with soybean oil, one with low-saturated-fat soybean oil, one with high oleic-acid soybean oil, one with low-alpha-linolenic-acid soybean oil, and one with partially hydrogenated soybean oil.

None of the diets produced significant changes in very-low-density lipoprotein, triglycerides, lipoprotein(a), C-reactive protein, or ratios between cholesterol fractions—except for the hydrogenated soybean oil diet, which yielded a higher total cholesterol:HDL ratio than the rest. The take-home point? Non-hydrogenated soybean oils are better than hydrogenated soybean oils. Thanks for the study, Captain Obvious USDA. Too bad this one’s completely irrelevant to the saturated fat guidelines.

…And that’s it, folks. These 12 studies are what the USDA used to evaluate the connection between saturated fat and heart disease.

Why does saturated fat seem evil in studies?

Quite by accident, the USDA does a rockstar job of proving saturated fat goes hand-in-hand with a junky cuisine—making it a nightmare to untangle in epidemiological studies, and more likely to be “guilty by association” when it comes to disease. Check out this pie graph of the most common sources of solid fats (AKA saturated) hitting America’s collective dinner plate:

From page 28 of the 2010 USDA Dietary Guidelines for Americans

Here’s the lowdown. “Grain-based desserts” (think cookies, cakes, pies, pastries) are the second-largest contributor to America’s saturated fat intake—right behind the rather ambiguous “all other food categories.” In fact, grainy desserts are a bigger source of saturated fat than butter, eggs, and whole milk combined. What’s after grain-based desserts? Pizza. Then cheese. Then processed meats. Then french fries. Then dairy desserts.

In fact, if you add it all up, 45 percent of our saturated fat intake comes from starch-based meals, sugary desserts, or processed meat, whereas only 32 percent comes from whole foods traditionally associated with saturated fat (butter, milk, unprocessed meat, eggs). The remaining 23 percent is that mysterious teal slice on the pie chart.

Think of it this way: When a study looks at someone’s saturated fat intake in relation to disease, is it really measuring foods like animal products and coconut oil, or is it actually recording stuff like deep-dish pizza and Oreos—markers for an I-don’t-give-a-hoot-about-my-health lifestyle? I’ll let you be the judge.

Polyunsaturated fat: mmm-mmm good, or uh-uh bad?

If you’ve made it this far in this article, you’ve probably noticed that the USDA is awfully fond of polyunsaturated fats—especially in the form of vegetable oil. For the sake of argument, let’s assume that it’s not because the USDA is a mouthpiece for the soybean and corn industries, but rather, because their collection of Evidence Library studies proves this fat is healthy for us. Here’s their page dedicated to answering the question: “What is the effect of dietary PUFA intake on health and intermediate health outcomes?”

Let’s just look at heart disease for now, since the USDA is so intent on telling us vegetable oils will keep our arteries squeaky clean. Of the 10 polyunsaturated fat studies in the Evidence Library, not all were relevant to heart disease, and one was a re-citation of the Jakobsen meta-analysis we already scoured. Here are the ones worth looking at:

1. Prediction of cardiovascular mortality in middle-aged men by dietary and serum linoleic and polyunsaturated fatty acids.

This study confirms what we suspected all along: that polyunsaturated fats are associated with a healthy lifestyle, and therefore massively confounded. In a cohort of 1,551 middle-aged men, the folks who died from cardiovascular disease by the 15-year follow up had been eating less polyunsaturated fat, but they were also far more likely to smoke (54 percent versus 31 percent in the entire cohort), drank more alcohol, had a lower socioeconomic status, had higher blood pressure, had higher BMIs, were more often on blood pressure medication, and had higher fasting insulin. Polyunsaturated fats as a whole, as well as serum linoleic acid, were inversely associated with BMI, fasting insulin, fasting glucose, alcohol intake, and age.

Interestingly, there was virtually no difference in the total fat or saturated fat intake of those who died from cardiovascular disease versus the cohort as a whole.

Not surprisingly, polyunsaturated fats appeared inversely correlated with death from heart disease (as well as death from all causes), but the associations often diminished after accounting for lifestyle factors or using different statistical models:

Dietary linoleic acid intake was associated with a lower overall mortality during follow-up after adjustment for age and examination year … but not significantly after adjustment for lifestyle or dietary factors. Total PUFA intake was not significantly associated with overall mortality. Men whose
-linolenic acid intake was in the upper third were 15% to 33% less likely to die of any cause than men whose intake was in the lower third, but the trend at best approached significance. The association of the dietary PUFA/SAFA ratio with overall mortality was significant, … but the association was not significant in models 2 through 4.

Serum fatty acids showed more robust associations, but we’re more interested in the effect of actual fat intake on heart health. All in all, this study doesn’t exactly give us a compelling reason to inject our diets with industrial oils.

2. Interplay between different polyunsaturated fatty acids and risk of coronary heart disease in men.

I’ll make this one short. The title explains the study, and this excerpt explains the outcome:

In this large prospective cohort study, modest dietary intake of long-chain n-3 PUFAs (≥ 250 mg/d) was associated with a 40% to 50% lower risk of sudden death, regardless of background intake of n-6 PUFAs. This lower risk was observed after adjustment for a variety of cardiac risk factors, lifestyle characteristics, and other dietary habits. These results suggest that n-6 PUFAs neither greatly counteract nor greatly augment the cardiovascular benefits of a modest intake of long-chain n-3 PUFAs from seafood.

Basically, this study found that omega-3 fats were beneficial, but omega-6 fats—the kind vegetable oils are chock full of—didn’t offer any special health perks. Moral of the story: Seafood is good for you, industrial oils are unnecessary. Nice job shooting yourself in the foot with this study, USDA.

3. Dietary fat intake and risk of coronary heart disease in women: 20 years of follow-up of the nurses’ health study.

Here we have another study where polyunsaturated fat looks cardio-protective—thanks to its entanglement with healthy lifestyle choices. In following almost 79,000 women for 20 years, this study (a Nurse’s Health Study follow-up) found that polyunsaturated fat was associated with lower heart disease risk for the gals with the highest versus lowest intake. And it’s no big surprise: Out of all the fat types, polyunsaturated fat was the only one where unhealthy habits decreased as consumption rose.

See exhibit A. (Each fat type is divided into quintiles, with the folks in quintile 1 eating the least amount of the specified fat and the folks in quintile 5 eating the most.)

For saturated fat, monounsaturated fat, and trans fat, the women with the highest intake were smoking more, had a greater history of hypertension, had lower use of multivitamins and hormones (eg, birth control), had lower use of aspirin, and had a higher intake of cholesterol (indicating less concern with our trustworthy governmental guidelines). In contrast, the women with the highest intake of polyunsaturated fats were smoking less than the women with the lowest intake, had less history of hypertension, were more likely to be using hormones and taking aspirin, were eating only a negligibly higher amount of cholesterol, and had a much smaller change in fiber intake. Collectively, those trends point to an overall higher interest in healthy living—including, no doubt, some daily portions of the polyunsaturated-fat-rich foods we’re told are good for us.

Indeed, this study produced some apparent fat-heart disease correlations that vanished after adjusting for other factors:

In age-adjusted analyses, total fat intake was significantly associated with increased risk of CHD. However, in the multivariate analyses, the association was attenuated and was not significant. For specific types of fat, intakes of saturated fat, monounsaturated fat, polyunsaturated fat, and trans-fat were each significantly associated with risk of CHD in age-adjusted analyses. … Intakes of saturated fat and monounsaturated fat were not statistically significant predictors of CHD when adjusted for nondietary and dietary risk factors.

Even though polyunsaturated fat was still associated with lower heart disease after some adjustments, the relationship was closer to neutral for women who weren’t overweight. And given the entanglement of this fat with healthier living in general, it’s pretty much impossible for a study to record all the factors needing adjustment—making it hard, if not downright futile, to attempt isolating the effects of polyunsaturated fat itself.

4. Snack chips fried in corn oil alleviate cardiovascular disease risk factors when substituted for low-fat or high-fat snacks.

No, this study isn’t a joke. The researchers took 33 adults and dragged them through three controlled feeding phases: one where they ate a low-fat/higher carb diet (30 percent fat, 10 percent saturated fat), another where they ate a high-polyunsaturated-fat diet (36 percent fat, 9.7 percent polyunsaturated fat), and a third where they ate a general high-fat and trans-fat diet (38 percent fat, 11 percent saturated fat, 2.7 percent trans fat). All the diets reduced total and LDL cholesterol, although the low-fat and high-polyunsaturated-fat diets had the greatest effect. Considering one of the diets was higher in processed carbs and one of the diets was higher in trans fats, it shouldn’t be a shock that the remaining diet—the one with the greatest proportion of polyunsaturated fats—fared the best, reducing some markers associated with heart disease compared to the other diets. The researchers concluded that it’s better to eat corn chips fried in corn oil than corn chips fried in trans-fatty oil.

5. Stearic, oleic, and linoleic acids have comparable effects on markers of thrombotic tendency in healthy human subjects.

This study examined the effects of two unsaturated fats (oleic and linoleic acids) and a saturated fat (stearic acid) on thrombotic—or blood-clotting—tendency. Long story short:

In conclusion, our results do not suggest that stearic acid is highly thrombogenic compared with oleic and linoleic acids.

Another redeeming point for saturated fat, and another “this doesn’t support guzzling vegetable oils” point against the USDA.

6. Small differences in the effects of stearic acid, oleic acid, and linoleic acid on the serum lipoprotein profile of humans.

After feeding a group of 45 people three randomly-ordered experimental diets, this study found no statistically significant differences between the effects of the unsaturated fats (oleic and linoleic acid) versus the saturated fat (stearic acid):

In this well-controlled crossover study of healthy subjects, we found that the differences in effects of stearic, oleic, and linoleic acids on the serum lipoprotein profile were less than expected. Although total and LDL-cholesterol concentrations tended to decrease with the increasing degree of unsaturation, the changes between the 3 diets were not significant.

Once again, we’ve got a string of studies that do little to validate the USDA’s love-fest for vegetable oils.

Dairy: low-fat or bust?

The new USDA guidelines don’t waste any time pushing dairy—but, despite some earlier hoopla about encouraging cheese consumption, staunchly warn against consuming anything other than low-fat or fat-free milk products. Apart from the saturated-fat phobia, is this recommendation justified?

I probably don’t need to explain that dairy in general isn’t a necessary food, that your bones won’t crumble into sawdust if you forgo milk with breakfast, and that factory-farmed dairy is laden with all sorts of nastiness. That’s been covered in a billion ways on a billion blogs. But dairy—real dairy, the stuff from pastured animals who aren’t squished into feedlots—may very well have some health perks, especially when left in full-fat form. (At least for those who tolerate it.)

Don’t believe me? Consider this:

A recent Dutch study showed that full-fat fermented dairy was inversely associated with death from all causes and death from stroke. A large study of Australians, published in 2010, showed that full-fat dairy appears protective against cardiovascular death. Yet another study, this one from 2005, showed a significant inverse association between full-fat dairy consumption and colorectal cancer. Another study still linked vitamin K2 from full-fat cheeses to reduced risk of death from all causes, as well as a reduction in aortic calcification. And a review from 2009, examining 10 different dairy studies, noted that some types of saturated dairy fat have a neutral effect on LDL, and full-fat cheese—compared to other dairy products—seems to have the strongest inverse relationship with heart disease.

The vilification of dairy fat is mostly linked to the anti-saturated-fat craze—but given the evidence above and the fact that some of the most beneficial components of dairy are concentrated in the fat (vitamins A, D, E, K2, and medium-chain triglycerides), it seems that for milk drinkers, going skim defeats the purpose.

Healthy Whole Grains: a mandatory health food, or the lesser of two evils?

Per the new guidelines, the USDA recommends eating six (or more) servings of grains per day—half of which ought to be whole. For the mathematically challenged, there’s even a graphic to help you see what this looks like visually, bread-slice style:

How helpful!

I contemplated writing a giant take-down of the “healthy whole grain” studies in the USDA Evidence Library, but soon realized it’d be pointless (and would raise this blog post to an even greater degree of mammoth). Virtually all studies showing the benefits of whole grains do so in a specific context—when whole grains are displacing refined grains or other bottom-of-the-totem-pole foods. There’s nary a study out there looking specifically at the effects of a diet with whole grains versus no grains, and the USDA’s recommendation for everyone to eat at least six servings per day is arbitrary (at best). Emerging research on paleo and low-carbohydrate diets—many of which yield improved lipid profiles and risk markers for disease—are showing that, yes, humans can live without bread.

That said, the USDA does have some interesting stuff on their carbohydrate summary page, under the “Needs for Future Research” subheading:

“Develop and validate carbohydrate assessment methods. Explore and validate new and emerging biomarkers to elucidate alternative mechanisms and explanations for observed effects of carbohydrates on health. Rationale: Studies of carbohydrates and health outcomes on a macronutrient level are often inconsistent or ambiguous due to inaccurate measures and varying food categorizations and definitions. The science cannot progress without further advances in both methodology and theory.”

Hmm. Despite their firm assertion that “healthy diets are high in carbohydrates” (page 42 of the guideline packet), they seem to concede here that the evidence supporting it is weak.

While we’re on carbs, here’s another surprising admission about fruits and vegetables, also from the “Needs for Future Research” section:

“Determine whether the effects of vegetables and fruits in the overall dietary pattern are due to displacement of other foods in the diet or to the action of vegetables and fruits, per se, on specific health outcomes. Rationale: The mechanism(s) of action for the effects of vegetables and fruits have not been determined and, therefore, may vary for different health outcomes. The observed effects could be a simple displacement of these foods with other foods that cause poorer outcomes, or vegetables and fruits may contribute specific benefits or a combination of the above may explain the observations made thus far in the literature. Only further research can provide more definitive answers.”

In other words: “We aren’t actually sure that fruits and vegetables are good for you… even though we’re telling everyone to eat lots more of them.”

In conclusion…

Although some of the new USDA guidelines are just watered-down common sense (“be more active, eat less junk food”), a few of the recommendations are downright harmful: the idea that polyunsaturated fats are universally healthy, the perpetuated fear of saturated fat, the encouragement of low-fat dairy, and the notion that everyone needs a carb-heavy, grain-based diet to thrive. Unfortunately, the 2010 recommendations parrot the same misinformation that’s been keeping Americans fat and sick for so long—all stemming from a flawed understanding of cholesterol and disease, as well as decades of research biased to please the gods of Conventional Wisdom.

Bottom line: These guidelines will guide you alright—straight to your spot in the pharmacy line. Look elsewhere for advice if you’re serious about your health.

High Fat Diet Linked to Breast Cancer?

And because this feels a little too much like a link-and-run crime, here’s some stuff this post would’ve had if it were longer:

Get it? Because I’m kind of cheesy and corny? I’m here all night, folks.