My short article titled A Big Fat Lie – Busting the Myths About Fats and Oils published in the September / Octoer 2011 issue of Organic NZ magazine has triggered a great deal of interest from readers and I felt motivated to share a wonderful blog that provides insight and answers to many people's questions. It's written by Denise Minger who is known for her incisive re-analysis of the China Study. Here she critiques a movie called Forks Over Knives. It's a long indepth witty read, rich in important information. Thank you Denise!
22 09 2011
Welcome to my “Forks Over Knives” analysis, AKA the longest movie review you’ll ever attempt to read. Thanks for stopping by! In case you aren’t yet convinced that I’ve made it my life’s mission to critique everything related to T. Colin Campbell, this should seal the deal.
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 on 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.
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
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.
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.)
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.
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.)
In a similar attempt to reduce the waste of food resources in Norway, the home economics institutes focused on how to exploit the local resources from the sea and from wild plants in a more efficient manner. This involved exploring the boundaries for what was commonly perceived as food, by experimenting with uncommon ingredients such as wild sea birds (including sea gull) and wild plants including moss.
Who needs Lean Cuisines when you can have seagulls and moss for dinner?
This paper also remarks that ”herring and potatoes represented the mainstay of the Norwegian crisis diet,” which certainly agrees with the graphs and tables we looked at earlier. But those rascally Scandinavians took their herring consumption one step further. Fish eggs, or “roe,” also became a staple:
For instance, the food labs tried to find new uses for the nutritious and plentiful fish roe. … The institutes created a number of recipes using fish roe as a substitute for flour. … The most basic recipe simply recommended using equal amounts of roe and flour, then mix with water and some yeast to bake bread or rolls. But there was nothing wrong with using roe in finer foods either; for instance in waffles mixed with milk, sugar, some regular flour and essence of vanilla and cardamom.
We’ve got to give those Norwegians props for being resourceful. Substituting fish eggs for flour? Serving herring roe waffles? Who would’a thunk it? (This actually makes me wonder if, despite bread consumption going up during the war, actual flour intake could have gone down due to substitution with other ingredients. But maybe that’s just my suspicious-of-wheat bias creeping in.) Apparently, a popular dessert was also “herring roe bread pudding,” made mostly from fish eggs and potatoes*:
350 g. herring roe; 1 tbs potato flour; 1 tbs bread flour; 5 tbs breadcrumbs; 4 boiled potatoes; 4 dl. milk; 1 tsp currants (made of dried blueberries); 2-3 tbs sugar; essence of almond; Served with sweet red sauce (saftsaus).
*Hey ancestral-eating folks, this is totally tweakable to be paleo. The first person to modify this recipe and actually eat it will earn my lifelong respect.
Lastly, some cool info on the fruits and vegetables Norwegians were eating. By the end of 1942, most fruits and veggies were done near gone from the markets and tremendously hard to get through rationing. So the government gave housewives throughout the country a list of “valuable wild plant supplements” to use for vegetables, which included “nettles, goutweed, and dandelions … as excellent sources of iron and vitamin C.” Foraging for wild edibles became common. And even before that, Norwegians earned their stripes as deft berry-pickers:
Already in August 1940, the public provisions office in Oslo [Forsyningsutvalget] launched a publicity campaign to get the city dwellers out in the forests surrounding the capital picking berries. The simple slogan “Pick berries! There is plenty in the forests!” printed on a poster of a girl carrying a big basket of berries was meant to tempt the city consumers to supplement their own supplies of food. As the war progressed, berries became an increasingly treasured resource. By 1943, the authorities had introduced a limit for when one was allowed to start picking different sorts of berries, and there are accounts of masses of consumers spending the night in the forests waiting for the official start date for when the berries were ripe.
How cute! Like rabid fans camping outside the theater for Harry Potter, Norwegians would line up in the forest, waiting for berry season to commence.
But back to the point of this thing. In “Forks Over Knives,” Esselstyn cites Norway’s war experience as a remarkable example of a plant-based diet leading to rapid improvements in cardiovascular disease. But as we can see from the exhaustive (and probably excessive; sorry) information above, the real Norwegian war-time diet was:
- Based on marine foods, particularly omega-3-rich herring and its eggs (which are super high in cholesterol… just sayin’)
- Supplemented with a variety of foraged foods, including berries, moss, and wild greens—which tend to be much higher in antioxidants and nutrients than their commercial counterparts
- Based on potatoes as the main source of starch
- Remarkably low in sugar and added fats, including vegetable oils/margarine
Those are a lot of positive changes—and as we saw earlier, the increase in fish intake more than made up for the drop in meat and dairy, in terms of total animal product consumption. Plant based? Only if fish is a vegetable.
…And now that I’ve stolen a big chunk of your day yapping about war-time Norway, I’ll add a warning that everything above may be moot. The apparent decline in cardiovascular disease could easily be confounded by the major rise in infectious disease that happened during the war, including a full doubling of pneumonia deaths. Just because cardiovascular disease mortality drops doesn’t prove cardiovascular disease itself has truly declined. Sometimes, it just means faster-acting diseases are snatching lives before heart attacks or strokes have a chance to claim their victims.
Hat tip to Chris Masterjohn for passing along this snippet from Broda Barnes’ book, “Solved: The Riddle of Heart Attacks.” Barnes reviewed 70,000 Austrian autopsy protocols from the years 1930 to 1970, and found—just like in Norway—that cardiovascular disease mortality dropped significantly during World War II. But instead of ascribing the change to diet, Barnes had a different hypothesis. He writes (emphasis mine):
At Graz, heart attacks dropped 75 percent between 1939 and 1945, and it is true that people were not eating cholesterol foods during the war. … A look at the arteries of the entire series of 2000 autopsies in 1945 revealed that the number of the individuals with damage to their coronary arteries (arteries to the heart) was approximately doubled in 1945 compared to 1939, and the degree of damage to each one affected was about twice as great. … Adult patients, dying from tuberculosis during the war, had a very severe degree of damage to the arteries of their hearts. … Two years later the conditions were reversed. The antibiotics against tuberculosis had become available, and deaths from this disease fell like a lead pipe. Immediately deaths from heart attacks started to rise. The autopsies gave us the answer: the adult dying from a heart attack had healing tuberculosis in his lungs. (Pages 2 and 3)
In contrast to Esselstyn’s theory, Barnes found that actual arterial damage was about twice as great by the end of the war as it was before the war, at least in Austria. But because infectious diseases shot up during the war years, a person’s official cause of death was more likely to be tuberculosis, pneumonia, or another acute illness, even in folks who actually did have cardiovascular disease. For Austria, the decline in cardiovascular disease mortality didn’t reflect the true state of Austria’s heart health. (And it’s possible the infections themselves, with accompanying inflammation, actually helped worsen cardiovascular disease.)
This doesn’t mean that Norway’s war-time diet had no impact on mortality, of course—just that we ought to look at death statistics in the context of total mortality.
Whew! How was that for a long discussion of something that only took one minute and fifteen seconds in the film? Let’s move on.
Hammer Dougall time
Next up, Dr. John McDougall makes an appearance to remind us once more that animal foods are terrible. We hear exactly how the McDougall of yore evolved into his current pro-plant, anti-animal-foods position.
The story goes like this. In the 1970s, McDougall was working as a doctor on a sugar plantation in Hawaii. He noticed that the older generations of Japanese (and other Asian) immigrants were free from modern diseases—they were slim, active into old age, didn’t get heart disease or arthritis or breast cancer or diabetes, and generally evaded the maladies plaguing most Westerners. McDougall attributes this to the fact that the older generation “learned a diet of rice and vegetables in their native lands,” and carried this diet with them when they set sail for the US. Their kids and grandkids, on the other hand, were a different story: They started getting fat and suffering from the same diseases other Americans do—and according to McDougall, the reason was simple:
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.
Among other things, this paper records the differences in eating habits between native Japanese and Japanese who moved to Hawaii—and provides us with my favorite thing ever: graphs. I’m posting copies of the relevant ones below. The black bars represent Japanese who moved to Hawaii; the white bars represent Japanese who still lived in Japan when the data was recorded (a few years before McDougall was working on the sugar plantation). The three sets of bars for each graph show what percent of the population ate that particular food for the specified frequency (in most cases: less than two times a week, two to four times a week, and seven or more times per week). If that’s a little confusing, don’t worry—we’ll discuss what these graphs show in a moment.
(FYI: Each row of graphs is a separate image. I made them huge on account of the spotty, barely-readable text, which was even spottier and more barely-readable when the pictures were normal sized.)
For starters, look at the middle row with three graphs. See how the center and right-hand graph have black and white bars that follow a similar distribution? That means the intake of those foods wasn’t massively different between the native Japanese and the Hawaii-dwelling Japanese. Now look at the labels on those particular graphs: Meat and Ham, Bacon, Sausage. As you can see, the majority of both native and Hawaii-dwelling Japanese were eating regular meat two to four times per week, and ate processed meats less than twice per week. Out of all the foods documented, the ones with the smallest difference of intake between native and Hawaiian Japanese populations were flesh foods.
How ’bout that.
Now look at the bottom left graph that says Fish. The white bars, representing the native Japanese, show that about 40% of Japan’s population ate fish at least seven times per week—compared to only about 8% of Japanese living in Hawaii, who were apparently unaware of their islands’ marine bounty. In sharp contrast to their native diet, over half of the Hawaiian Japanese ate fish a maximum of once per week.
The tally so far: the native Japanese on their “traditional” diets ate a lot more fish (which, c’mon, is totally an animal product) than Hawaiian Japanese, and ate slightly less meat, ham, bacon, and sausage… but the difference wasn’t huge.
Now for the fun stuff. Check out that top row of graphs. The Hawaiian Japanese didn’t swap out rice for animal foods—they swapped out rice for bread! Whereas the native Japanese almost all ate rice two to three times per day (and most ate bread less than twice a week), the vast majority—almost 90%—of Hawaiian Japanese ate bread more than seven times per week. As we saw in an earlier blog post, wheat-based diets seem to have different effects than rice-based diets in at least one other Asian country.
The other major change, along with a drop in traditional soy intake, was “butter, cheese, and margarine.” I’ll definitely agree with McDougall that Hawaiian Japanese seem to be eating more dairy than their native counterparts, although throwing margarine into the mix makes it difficult to determine just how much.
At least based on this data, the “Americanization” of Japanese immigrants in Hawaii didn’t involve a newfound guzzling of flesh foods: it involved picking up America’s wheat habit and abandoning the native staples of fish and rice. If “sugar” had been included in the above graphs, I have no doubt we’d see major changes with that, too. The only animal food that did strongly increase among the immigrants was dairy, although in this paper, it was pooled together with margarine (which no one considered bad yet back in the groovy ’70s).
Does this invalidate McDougall’s observations? Not necessarily. Maybe the patients he treated on the sugar plantation were skewering wild pigs and snacking on bacon all day.
After the tale of sickly Hawaiians, “Forks Over Knives” segues back into the research Campbell embarks on after his experience in the Philippines. In ’75, Campbell was working at Cornell University, conducting a battery of experiments on dietary protein and aflatoxin-induced liver cancer in rats. I’ll let the movie sum it up:
Minute 25:03—Just like the Indian researchers, Campbell fed half the rats in his study a diet of 20% casein, the main protein in dairy products. The other half was fed only 5% casein. Over the 12 weeks of the study, the rats eating the higher protein diet had a greatly enhanced level of early liver cancer tumor growth. On the other hand, all of the rats eating only 5% animal protein* had no evidence of cancer whatsoever.
*Notice the sneaky interchange of “casein” with “animal protein”? Rest assured, folks, that casein is an animal protein, but not all animal proteins are casein. This movie falls into the same trap I mentioned in my “China Study” critique last year, and that many other people (Dr. Harriet Hall, Chris Masterjohn, and Anthony Colpo, to name a few) have taken issue with as well: extrapolating the effects of casein to all forms of animal protein. As I discussed in that critique, casein seems to be the strongest cancer-promoter among the isolated proteins (with whey, the other major protein in milk, being decidedly anti-cancer). Not only that, but the effect of specific protein sources on tumor growth can vary dramatically depending on the types of fat and carbohydrate also included in the lab diet. Both in the movie and in his book “The China Study,” Campbell makes an unjustified leap from “isolated casein in rat studies” to “any animal protein in a real-world human diet. Shazam!”
But those are small potatoes compared to what’s coming next. First, take a look at something Campbell himself noted in the movie (emphasis mine):
Minute 26:05—[Campbell:] “This was so provocative, this information. We could turn on and turn off cancer growth, just by adjusting the level of intake of that protein. Going from 5% to 20% protein is within the range of American experience. The typical studies on chemical carcinogens causing cancer are testing chemicals at levels maybe three or four orders of magnitude higher than we experience.”
Although Campbell is trying to explain why his rat studies have relevance for humans, this statement actually highlights why they usually don’t. In Campbell’s experiments—as well as the Indian study that inspired him all those years ago—the rats received very high doses of aflatoxin to initiate cancer in the first place. Protein only appeared to work as a cancer promoter in his studies, not an independent carcinogen. And even though the range of protein was reasonable for a real-life situation, the amount of aflatoxin exposure would be really hard to replicate unless you had a death wish and a bottomless stomach. Quoting Chris Masterjohn’s “Curious Case” article again, to get the sort of aflatoxin exposure that caused even a “barely detectable” response in Campbell’s rats, you’d have to eat about 1,125,000 contaminated peanut butter* sandwiches over the course of four days. I don’t know about you, but I doubt I could eat a lick over 900,000. More than that is just gluttony!
*Contaminated with aflatoxin at a level of 20 parts per billion—the maximum allowed by the FDA.
So what would happen if the animals were exposed to lower, more realistic levels of aflatoxin? Would different levels of protein still have the same effect?
Luckily, we have an answer to that question. In the late 1980s, more researchers from India were conducting experiments with casein and cancer—but this time used different doses of aflatoxin, and studied rhesus monkeys instead of rats. In one intriguing paper titled “Effect of Low Protein Diet on Chronic Aflatoxin B1-induced Liver Injury in Rhesus Monkeys,” the researchers describe something that undermines the conclusions Campbell drew from his own research.
I’ll let the paper speak for itself. Here are the first three paragraphs:
And a bit later:
Okay, I’ll speak too. Let’s decode the science jargon.
Basically, the researchers are talking about an experiment they conducted feeding monkeys diets that had either 5% or 20% casein. These monkeys were given a hefty dose of aflatoxin each day—1 part per million. Just like in the rat studies, the monkeys in the low-protein group suffered from massive cell death (but no cancer), while the monkeys in the high-protein group got pre-cancerous growths called “preneoplastic lesions.” So far, this is consistent with everything Campbell found.
But here’s where it gets interesting.
The researchers reference an earlier study they did with the same setup—rhesus monkeys, aflatoxin exposure, and either 5% or 20% casein in each diet. But in that study, they used a much more moderate dose of aflatoxin: 0.16 parts per million. And guess what happened? In this situation, it was the low-protein group that grew tumors, while the high-protein group was perfectly healthy and cancer-free! Oh, snap.
The results of this earlier experiment were published in a paper called “Effect of Low Protein Diet on Low Dose Chronic Aflatoxin B1 Induced Hepatic Injury in Rhesus Monkeys” in 1989. Indeed, the researchers weren’t pulling our legs: This study really did show that a low-protein diet was both more “cancer promoting” and more deadly than a high-protein diet when the dose of aflatoxin was lower. When the dose was 0.16 parts per million, the low-protein monkeys were stricken with liver lesions while the high-protein monkeys were fine. When the does was raised to 0.5 parts per million, the low-protein rats didn’t get tumors—mainly because every single one of them died when they were less than one-and-a-half years old! And I quote:
Monkeys on low protein diet [with 0.16 ppm aflatoxin] surviving for 90 weeks or more show foci of preneoplastic lesions, whereas those on high protein diet reveal no such alterations at the corresponding time interval.
(Translation: The low-protein monkeys on a low dose of aflatoxin had pre-cancerous growths in their livers (at least, the ones that weren’t already dead did). The high-protein monkeys were A-OK.)
The hepatic injury again is more accentuated in the low protein group as compared with the high protein group [with 0.5 ppm aflatoxin]. No preneoplastic lesions are observed, possibly due to a poor survival (less than 70 weeks) in the low protein animals with this dose. The animals in the high protein group surviving even beyond 90 weeks do not show any preneoplastic/neoplastic lesions. It appears that in the simian model used by us, the liver injury caused by AFB1 is accentuated by simultaneous restriction of dietary protein and in animals on such combined regimen preneoplastic lesions appear around 90 weeks of experiment.
(Translation: When the aflatoxin dose was raised a bit, the low-protein monkeys still suffered from a lot more liver injury than the high-protein monkeys. They all died too soon to develop any precancerous tumors—in contrast to the high-protein monkeys, who had a better survival rate and still didn’t have any tumors growing at the 90-week mark.)
And here’s the researchers’ (perhaps more digestible) discussion of it all; emphasis mine:
In contrast to innumerable studies on aflatoxin induced hepatotoxicity in rats, very few studies have been done in monkeys and in most of these studies large doses of aflatoxin have been used. The important feature of the present study is the low level of intoxication ingested as contaminated meal, a situation more likely to be encountered in natural exposure to human and animals.
(In other words, this study—at least in theory—has more real-world relevance than Campbell’s rat experiments.)
The study shows that small doses of aflatoxin (0.16 and 0.5 ppm) on chronic administration induce injury in the liver. However at both the dose levels and at all time intervals the injury is more severe in animals on low intake of proteins.
(Whether the aflatoxin does is low or moderate, the low-protein monkeys are worse off than the high-protein monkeys.)
These observations suggest a synergism between protein calorie malnutrition and aflatoxin induced hepatocarcinogenesis and may explain the higher incidence of hepatocellular carcinoma in certain areas of the world where contamination of foods with aflatoxin and malnutrition are prevalent.
Remember when Campbell was talking about how, in the Philippines, it seemed to be the well-nourished affluent folks who were getting liver cancer? This paper presents the opposite perspective. Here, the researchers are noting that liver cancer tends to be higher where there’s aflatoxin contamination and malnutrition (most notably protein-calorie malnutrition), rather than affluence and high animal food consumption like Campbell observed. According to the researchers, their experiments suggest that malnutrition increases the liver damage and cancerous growths associated with aflatoxin exposure—explaining why liver cancer, for instance, is highest in areas where malnutrition runs rampant.
But enough of this monkey business. When we compare the above study to the ones using an extremely high aflatoxin dose, it’s clear we’ve got a paradox. In this study, it was the low-protein monkeys getting tumors. In the other studies, it was the high-protein monkeys (or rats) getting tumors. So what’s going on here? Why would a low-protein diet protect against cancer at high doses of aflatoxin, but promote cancer at low doses of aflatoxin?
The answer, it seems, lies in protein’s effects on both growth and detoxification.
Although this isn’t discussed in “Forks Over Knives,” Campbell spends a few pages of “The China Study” talking about an enzyme responsible for metabolizing aflatoxin—a lil’ somethin’ called “mixed function oxidase.” This enzyme is key for turning aflatoxin into metabolites that can mess up DNA and initiate cancer. And as Campbell discovered through his research, a diet of 5% casein can turn this enzyme down faster than you can say “hepatocellular carcinoma.” Here’s how he describes the process on page 52 of his book:
Decreasing protein intake like that done in the original research in India (20% to 5%) not only greatly decreased enzyme activity, but did so very quickly. What does this mean? Decreasing enzyme activity via low-protein diets implied that less aflatoxin was being transformed into the dangerous aflatoxin metabolite that had the potential to bind and to mutate the DNA. … We now had impressive evidence that low protein intake could markedly decrease enzyme activity and prevent dangerous carcinogen binding to DNA. These were very impressive findings, to be sure. It might even be enough information to “explain” how consuming less protein leads to less cancer.
This is a strangely happy portrait of something that’s actually deadly.
Why does your body want to detoxify aflatoxin in the first place? How ’bout because it’s… well… a toxin? Even though slashing enzyme activity does reduce cancer-causing metabolites, it also leaves more aflatoxin in its original, toxic form—which can damage organs and start to promote cancer in another way, which is exactly what happened with the low-protein monkeys. Here’s how.
In aflatoxin studies, we’ve seen that low-protein diets cause some unfortunate problems for lab animals—one being an increased toxicity of aflatoxin. That’s because the reduced enzyme activity from low-protein diets prevents the body from properly detoxifying stuff. (Campbell even acknowledges in some of his earlier papers that a low-protein diet makes rats more susceptible to liver injury from aflatoxin, even when they don’t get cancer from it.) So what happens when aflatoxin toxicity goes up? Apparently, it makes liver cells start dying like crazy in a process called necrosis. At low levels of aflatoxin, the necrosis only occurs in low-protein animals, because the high-protein animals still have their detoxifying enzymes in working order.
Here’s where the trouble starts for our low-protein friends. Because their liver cells are facing mass genocide, their bodies rush to make new cells to help the liver regenerate. According to the authors of the monkey studies, this rapid death/proliferation cycle is one of the very things that encourages pre-cancerous lesions to form—especially when cells are proliferating at the time of aflatoxin exposure (which is what would happen to a malnourished human eating aflatoxin-contaminated food). At mild aflatoxin doses, the low-protein monkeys still had enough dietary building blocks to regenerate their liver cells and feed early tumors—hence why they began developing lesions. (The authors also note that low-protein diets slow down the cell cycle, causing more cells to hang out in the “S phase” where their replicating DNA is vulnerable to attack—another potential pathway to cancer.)
Once the aflatoxin dose is raised, though, something new happens. Cell death increases even further for the low-protein animals, so much that their poor bodies can’t keep up with it all. The result is that the liver starts facing major injury—gettin’ fatty, exhibiting bile duct proliferation—but avoids developing tumors because there’s just not enough construction material (protein) to build a bunch of new cells. Healthy cells are dying left and right, and pre-cancerous ones don’t even stand a chance. It’s at this point that a lot of lab animals—both in Campbell’s studies and with the monkeys—keel over and die, despite having tumor-free corpses.
For the high-protein animals, not much happens until aflatoxin dosing is raised through the roof. At lower doses, their bodies do a fine job of detoxifying the aflatoxin, cell death isn’t increased, and there apparently aren’t enough cancer-causing metabolites yet to do much harm. It’s only when aflatoxin exposure gets cranked way up that the high-protein animals experience the same liver necrosis that plagued their low-protein counterparts. Although the extra protein improves the animals’ ability to detoxify aflatoxin and regenerate their livers, it also provides more tissue building-blocks—giving both healthy cells and pre-cancerous lesions the stuff they need to proliferate. The protein that prevents high-protein animals from dying from necrosis overload is the same thing that lets them develop tumors. Quite the catch-22, huh?
At least, that’s the explanation suggested by the authors of the monkey papers over two decades ago. I haven’t done an exhaustive search of the literature, so it’s possible there’s more current research explaining the paradox of low-protein diets increasing tumor growth at low doses of a carcinogen, but preventing tumor growth at higher doses.
As much as Campbell condemns “reductionism”—which refers to looking at a singular nutrient or pathway instead of how various components work in harmony—Campbell’s interpretation of his protein research falls into this very trap. By looking at only the positive effects low-protein diets seem to have on cancer, he misses out on the many detrimental effects they have on other aspects of health, including the fact that they seem to invite early death.
Important note: One important difference between Campbell’s rat studies and the monkey studies above is the use of continuous versus acute dosing. In the monkey studies, the animals got small, daily doses of aflatoxin throughout the experiment. That’s like what would happen if you lived in a humid climate where some of the food supply was growing aflatoxin-containing mold. By contrast, in Campbell’s studies, the rats got a giant dose of aflatoxin at the beginning of the experiments. That’s like what would happen if you accidentally ate 80,000 jars of aflatoxin-contaminated Jif in one sitting (oops!).
With all that said, let’s return to “Forks Over Knives” and see what else Campbell has to say.
Minute 26:29—Even more surprising, Dr. Campbell found that a diet of 20% plant proteins from soybeans and wheat did not promote cancer.
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 the omega 3/omega 6 ratio, down goes inflammation, down goes some 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.
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.”
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.
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.
Why isn’t that nasty meat congealing in China’s collective aortas? Why does wheat seem like a less-than-heart-healthy grain? Why are we told that a plant-based diet “is always associated with lower mortality of … coronary heart disease” in the China Study data, when it’s the folks eating the most animal foods who get less heart disease? It’s quite a mystery. (And in case you’re wondering, it’s not because the animal-eaters were croaking from strokes instead: Non-fish animal protein correlates at only 0.05 with stroke mortality; fish protein correlates at -0.11, and plant protein correlates at 0.12.)
Of course, in the vast sea of potential ways to die, cardiovascular disease is only one tiny, plaque-bound droplet. We’ve still got cancer to think about! And indeed, a cursory glance at the China Study data makes the animal food-cancer relationship seem massively confusing: Meat and dairy have zero statistically significant positive correlations with any form of cancer, eggs are associated only with colorectal cancers, but fish—which we’re usually told is healthy for us—is strongly associated with a number of major cancers, including leukemia and liver cancer. What gives?
This, my friends, is why correlations can lead us astray.
A closer analysis of the fishy data shows us that the “cancer clusters” mostly occur in prosperous coastal areas, where more people are eating refined starch and sugar, drinking beer, eating refined vegetable oil, smoking manufactured cigarettes, working at indoor industry jobs instead of doing manual farm labor, and experiencing other aspects of urbanization. In fact, the variable “percentage of employed population who are in industry” is highly associated with nearly every common cancer, including male lung cancer (0.62), female lung cancer (0.47), leukemia (0.53), liver cancer (0.47), colon cancer (0.41), stomach cancer (0.25), breast cancer (0.24), brain cancer (0.21), and death from all cancers (0.31). It just so happens that the more industrialized counties are near bodies of water, where fish consumption is frequent. (Incidentally, humid coastal regions also have a higher prevalence of both aflatoxin and the hepatitis B virus, which are major risk factors for liver cancer.)
Unless there’s something uniquely cancer-promoting about fish protein in comparison to other meat protein, it seems likely that the fish/cancer links are confounded by other elements of industrial lifestyles. Indeed, when we look at the variable “non-fish animal protein intake,” the correlation with “death from all cancers” is a measly 0.03, which is even less than the correlation with plant protein (0.12).
Feel free to peruse my full China Study critique for more details about the lack of straightforward correlation between animal foods and disease (or plant foods and good health). You can also check out some earlier posts on individual animal foods and their correlations in the China Study:
That should cover it, right? Moving on…
Just kidding. How could I be done with this section when I haven’t posted a single graph, table, Bigfoot photo, or liberally-screen-shotted article excerpt? We’re far from finished here, folks.
Although Diet, Life-style, and Mortality in China is crazy-expensive and out of print (and I returned my library copy long ago, so I can’t scan pages), I still want to post some direct charts* to prove I’m not just making stuff up. Lucky for us, the results of China Study II are posted online as a series of PDFs. The China Study II is basically a follow-up to the first China Study, except the researchers plopped 20 more counties onto the list and recorded even more variables than they did for the first round. Because China Study II includes regions with a much greater degree of urbanization than the first China Study, some of the correlations are a little different. Meat, for instance, is now more popular in industrialized coastal counties instead of mainly pastoral areas, and as a result, has some of the same disease associations that fish did in the first China Study. Even though the data between the two studies aren’t identical, China Study II is still useful for a couple things I’m going to show you.
*I realize I can overdo it with the graphs. It isn’t because I want to bore you or turn your eyes into blurry, computer-screen-induced globes of pixelation—but rather, because I suffer from Liberal Arts Complex.
lib•er•al arts com•plex: n. Subconscious desire to compensate for poor choice of collegiate studies by over-explaining, over-referencing, and over-graphing material in attempt to gain credibility; form of mild neurosis.
So let’s take a look at some pages straight out of the second China Study monograph—more specifically, the mortality section. (If you’re worried the meat industry bribed me to Photoshop the following images to make them look anti-vegan, by all means, download the full PDF straight from Oxford’s website by clicking here.)
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).
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.)
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 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 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 diabetes.” Strong inverse associations with milk, meat, red meat, and animal fat; strong positive associations with fruit and eggs:
And lastly (no, seriously, this is the last thing): Since we already know collections of plane-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.
- “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”
- Meat, fish, and green vegetables are associated with higher levels of sex hormone-binding globulin, indicating greater insulin sensitivity/less insulin resistance
- Wheat has the strongest positive association with insulin resistance out of any food
- “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”
- “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”
- Even after adjusting for other factors, animal foods are negatively associated with death from cervical cancer
- “Our finding that the highest blood cholesterol levels in the Chinese were associated with … the lowest risk [of heart disease] is also a contradiction of what might be expected”
- “Consumption of green vegetables, rice, meat, and fish was associated with reduced mortality [from stomach cancer]“
- “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.”
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:
- 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.
- 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.
- 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.
- 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 graph, 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?