Nah.

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

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

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

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

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

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

Saturated fat: true killer or whipping boy?

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

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

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

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

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

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

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

From page 38 of the 2010 USDA Dietary Guidelines for Americans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

*Not suitable for vegans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This is bad news, folks.

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

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

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

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

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

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

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

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

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

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

Why does saturated fat seem evil in studies?

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

From page 28 of the 2010 USDA Dietary Guidelines for Americans

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Dairy: low-fat or bust?

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

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

Don’t believe me? Consider this:

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

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

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

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

How helpful!

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

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

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

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

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

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

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

In conclusion…

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

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

(Not only is this woefully, frustratingly, absurdly belated, but it’s also not yet finished. But I hate being a blog tease, so here’s part one!)

If you’ve been following along with the previous China Study entries (and the wild drama that ensued), you know that I’ve been promising an entry on wheat for a while now, mostly because this little snippet snagged so many eyes:

Correlation between wheat flour and coronary heart disease: 0.67

That’s a value straight from the original China Study data. Could the “Grand Prix of epidemiology” have accidentally uncovered a link between the Western world’s leading cause of death and its favorite glutenous grain? Is the “staff of life” really the staff of death? Bwah ha ha.

Damning as it seems, a single unadjusted correlation isn’t enough to make that leap. Actually, nothing in this post will be enough to make that leap, because A) it’s epidemiological data and not a controlled study, and B) correlation isn’t causation anyhow. You know the drill.

So my goal here isn’t to prove anything about wheat. Mostly, I want to see if I can find a confounder that’s creating a false association between wheat and heart disease in the China Study data. Something wheat-eating regions have in common that makes them more susceptible to ticker troubles. Because really, folks, this is serious business:

And when we pluck out the wheat variable from the 1989 China Study II questionnaire—which has more recorded data—and consider potential nonlinearity, the outcome is even creepier:

Wowza! By the way, wheat flour also correlates significantly with hypertensive heart disease and stroke, but I’m mainly going to look at coronary heart disease in this post. (And although wheat looks like it could have a nonlinear relationship with heart disease, with the highest wheat eaters having disproportionately steeper rates than non-wheat eaters, I’m going to treat it as linear for the sake of this analysis. That way, the worst that’ll happen is we’ll underestimate the potential effect of wheat, which—for now—is better than overestimating it.)

Since I’m not trying to dissect our friend Campbell’s claims anymore, I’ll be using the China Study II data (from 1989) because it recorded more descriptive variables about diet and blood samples.* And because it’s already available online. (Not that I don’t love typing thousands of numbers onto my computer by hand. Three cheers for data-entry-induced carpal tunnel!)

*Quickie note: If you want to play with the China Study numbers yourself, I recommend not just using the “all vascular diseases” variable, because it includes rheumatic heart disease—a condition spawned by rheumatic fever and generally unrelated to diet. Lumping diseases with different etiologies together dilutes the strong correlations you can find by looking at each disease independently. Try checking out stroke (M065 STROKE), ischaemic heart disease (M063 IHD), and/or hypertensive heart disease (M062 HYPTENS)  along with all vascular diseases (M059 ALLVASC).

Here’s the problem with looking at wheat and heart health. Along with correlating pretty darn strongly with heart disease, wheat-eating regions boast  a number of other factors possibly involved as well—some as protective agents and some as causative. For instance, wheat flour correlates significantly and inversely with:

• Plasma folate concentrations (and consequently, homocysteine status)
• Fish intake and DHA levels
• Yearly green vegetable consumption
• HDL cholesterol
• Vitamin C intake

And it correlates significantly and positively with:

• Height, weight, and BMI
• Blood pressure
• Latitude (as a possible marker for vitamin D status)
• Yearly milk intake
• Polyunsaturated fatty acid intake

Since all of these variables also associate (inversely or positively) with heart disease, it’s possible they could be confusing the “0.67″ figure we’ve cited for wheat. Could some other, non-grain component of the wheat eaters’ diets predispose these folks to heart disease?

On the bright side, China’s wheat eaters are less likely to drown than the wheat-shunners (r = -0.68 for the youngsters under 34). Maybe they’re all buoyant from celiac bloat.

And in case you’re wondering, here are some heart disease risk factors (the ones Conventional Nutritional Wisdom likes to toss around) that don’t positively correlate with wheat. That means we probably can’t blame ‘em for wheat’s dirty deeds. Out of curiosity, though, I’ll still include them in some of my models just to see how they behave in relation to wheat with heart disease.

• All meat intake (r = -0.35)
• Red meat intake (r = -0.30)
• Animal fat intake (r = -0.35)
• Saturated fat intake (r = -0.40)
• Total animal protein intake (r = -0.27)
• Total fat intake (r = -0.43)
• Fat as a percentage of total calories ( r = -0.41)
• Total cholesterol (r = -0.05)
• Apolipoprotein B (r = 0.02)
• Daily alcohol intake  (r = -0.37)

Mostly, what I’m looking for is a little somethin’-somethin’ that both wheat flour and heart disease have in common. A shared variable that could be slyly—and wrongfully—framing wheat as our heart-harming villain.

So how do we untangle all these variables? I’m using two methods: multiple regression analysis and stratification. Multiple regression is a handy way of looking at two or more variables and seeing how each one behaves when the others are held constant, and stratifying data can work similarly by divvying up data into groups that share or exclude a certain variable. (For the stats junkies out there, I’m using ordinary least squares for the regressions, and I’m running each model two times: once with the data as-is, and once with any non-normally-distributed dependent variables transformed (via natural log) for more reliable statistical significance testing. I’m also checking for linearity between the variables before creating each model, since a nonlinear relationship will be underestimated with linear regressions.)

And for anyone not familiar with statistics terminology, here’s a really quick rundown of what you need to know to understand the numbers in this post:

• r = the Pearson product-moment correlation coefficient  between two variables. It can range from -1 to 1. When it’s zero or close to zero, there’s pretty much no relationship between the variables. When it’s a negative number (like r = -0.50), there’s an inverse relationship between the variables, meaning one increases as the other decreases. When it’s a positive number (like r = 0.50), there’s a positive relationship between the variables, meaning they increase and decrease hand-in-hand. The closer to -1 or 1 r is, the stronger the association. R can never prove cause and effect, though—it only indicates an relationship of some sort.
• beta = the standardized coefficient for each variable in the multiple regressions I’ll  be running. This is a lot like r, in the sense that it shows how well a specific variable is predicting the outcome (eg, heart disease) and also ranges from -1 to 1. But in the case of beta, we’re also controlling for the effects of other variables, so this number tends to be more accurate than r.
• p = the probability that our results are just a fluke. P indicates how likely it is that we’d get a value of a test statistic that’s as extreme (or more extreme) as the one we have based on chance alone. Having a p-value of less than 0.05 indicates a high level of significance and means that our results are pretty sound. The lower the number, the more confident we can be that we’ve got something legit.
• r-squared = percent of variance explained. This number shows what proportion of the outcome (eg, heart disease) can be explained by the variables in a particular model (eg, wheat and HDL cholesterol). The higher the number, the more successfully the variables are predicting the outcome. (“Predicting” is a misleading way of putting it, though, since we still aren’t looking at proof of cause-and-effect—only a relationship.)

Preliminary theories

It’s no secret that I’m less-than-enamored with wheat. We parted ways long ago (he got me allergic and then ran off with some floozy—classy, eh?). Nonetheless, I don’t like pointing fingers where they shouldn’t be pointed, so I’ll entertain some alternative theories that could explain wheat’s apparent association with heart disease.

1. Folate deficiency. In northern China, about 40% of the population qualifies as folate deficient (compared to only 6% in the south)—a geographical trend that corresponds nicely with wheat consumption. Being low in folate tends to elevate homocysteine, which—you guessed it—is an independent risk factor for heart disease. So maybe it’s not the wheat itself causing mischief, but the fact that low-vegetable, wheat-centered diets in China tend to breed folate deficiency and hike up homocysteine.

On top of that, in the China Study II data, wheat flour positively correlates (r = 0.30, p<0.05) with childhood death from neural tube defects—a category of birth defects often related to folate deficiency. Although the China Study data didn’t document homocysteine levels (darnit), the 1989 data did measure plasma folate. That means we’ll be able to test whether folate levels could be obscuring the true relationship between wheat and heart disease.

2. Vitamin D deficiency. For the most part, wheat-eating regions in China are in the northern half of the country—a hotspot for vitamin D deficiency, which is strongly linked to heart disease. Given the pretty convincing correlation between latitude and heart disease mortality, it’s possible that vitamin D is playing a role in this mess. Are the wheat-eaters merely suffering from low levels of the ol’ Sunshine Vitamin due to their unfortunate geographical placement, and getting more heart disease as a result? Sure seems possible.

3. Low intake of DHA. In an earlier publication, Campbell and his crew already determined that fish and DHA intake appears protective against heart disease in the China Study data. Not too surprising, since DHA reduces blood viscosity and can lower other factors associated with heart disease (like triglyceride levels). And considering wheat-eating regions don’t consume much seafood (r = -0.43 for daily fish intake), perhaps DHA deficiency—rather than wheat consumption itself—is to blame for higher rates of heart disease.

4. Combo-abombo. Maybe a mix of low folate, vitamin D deficiency, and DHA deficiency are swirling together into a doomful vortex—some horrible, Bermuda-Triangle-esque zone of heart disease. A zone that just happens to overlay areas of wheat consumption.

5. Unexpected mystery variable. If none of the above can explain the wheat-heart disease link, we’ve still got a verdant jungle of China Study variables to plow through. So plow we shall. I’ll try running a number of common-sense models to see if I can find something that explains heart disease better than wheat alone.

Multiple regression results

Folate. Ah, theory numero uno! Like wheat, folate has a strong, statistically significant correlation with heart disease (r = -0.40, p<0.001), so what happens when we run a model using both folate and wheat as exposures? Initially, it looks like wheat clobbers folate as a predictor (beta = 0.59, p<0.001 versus beta = -0.06, p = 0.39)—which would suggest that, although China’s wheat-eaters tend to have lower folate levels, folate deficiency itself isn’t enough to explain the link with heart disease.

But I’m not ready to dismiss this one just yet. As often happens with plasma measurements and health conditions, folate may have a nonlinear relationship with heart disease—which means multiple regressions (of the linear variety) won’t show the full picture. Indeed, when I make a scatter plot for folate levels and coronary heart disease, it looks like a bit of a curve emerges, with folate being most strongly associated with heart disease when the county average dips below 10 micrograms per liter (or thereabouts). Above that, the correlation is far less dramatic.

So how do we deal with this statistical monkey wrench? For starters, I tried transforming the folate data to make it more suitable for linear regressions, but that didn’t do diddly squat to the results: The numbers were beta = 0.58, p<0.001 for wheat and beta = -0.06, p = 0.31 for folate. So then I tried stratifying the data based on “low” and “high” folate levels (10 or less micrograms/liter versus 10.1 or more micrograms/liter), but both subgroups continued showing wheat as strongly and significantly correlated with heart disease while folate was off the hook.

Just to cover my bases (and because I’m a stubborn son-of-a-gun), I kept playing  with the numbers for a while longer to see if I could excavate anything new. Nope. Bottom line: It looks like wheat is predictive of heart disease whether or not folate levels are low, whereas folate is mostly predictive of heart disease only in the presence of high levels of wheat consumption.

So, theory #1 doesn’t pan out. Bugger. But bear in mind, we’re using folate mostly as a marker for elevated homocysteine, so these results don’t mean that homocysteine itself isn’t playing a role. Other causes of high homocysteine, such as B12 deficiency, weren’t documented in the China Study data. So this is an issue that’ll have to remain annoyingly unresolved. Another bugger!

Onto the next theory: latitude. Could the folks living in northern wheat-eating regions have lower vitamin D levels, leading to more heart problems—and creating a false link between wheat and cardiovascular disease? I admit, this was my favored theory after folate, but it ain’t holdin’ water. When I run wheat and latitude together as potential contributors to heart disease, wheat remains strongly predictive (beta = 0.65, p<0.001), while latitude diminishes (beta = -0.01, p=0.96). It’s pretty clear that the raw correlation between heart disease and latitude (which is 0.43, p<0.01) is just an echo of the relationship between heart diseases and wheat-eating regions, which are typically northern.

Okay, so that’s two strikes for Denise’s heart disease theories. What about fish and DHA? Are the wheat eaters suffering due to their fishless (and low-in-DHA) diets rather than from wheat itself? Alas, it doesn’t look likely. When I run these things together as exposures for heart disease, wheat stays strongly predictive (beta = 0.68, p<0.001) while the fishies do not (beta = 0.08, p = 0.47). Likewise, DHA teeters out into statistical insignificance (beta = 0.06, p = 0.30) when used in a model with wheat.

(Wait, I know what you’re thinking! “Why does it look like fish and DHA contribute positively to heart disease?” It’s because many of the fish-eating regions are more industrialized, and—in the absence of wheat—the fish-heart disease relationship is confounded by other factors like more desk work, more smoking (especially manufactured cigarettes), less physical activity, more vegetable oil consumption, and so forth. When we add some more variables to the model that take away the “city effect” associated with fish—such as apo-B, tobacco use, or percentage of the population employed in agriculture—then both fish and DHA turn inverse again. Although wheat, it should be mentioned, stays rock-steady in its high coefficient and statistical significance.)

Other stuff

Milk. Is moo juice a cardiovascular foe obscuring the relationship between wheat and heart disease? Probably not, according to the data—which isn’t surprising, given how few counties even drink the stuff. When running daily milk intake alongside wheat intake, wheat keeps its positive correlation (beta = 0.67, p<0.001) and milk actually turns a bit inverse, though not significantly so (beta = -0.07, p=0.47). No model shows a significant association between milk and cardiovascular disease, so I’m crossing this one off the list of potential confounders.

Blood pressure, BMI, corn, millet, sorghum, rice, added animal fat, added vegetable fat, total fat, total animal food, total carbs, total protein, percent of calories from animal protein, and all the smoking/tobacco variables I tried became statistically nonsignificant (in relation to heart disease) when thrown into a model with wheat.

Income is positively associated with heart disease when wheat is held constant, but it still doesn’t put a ding in wheat’s association with heart disease.

Models with more variables

So apparently comparing wheat + one other independent variable isn’t enough to explain the Wheat Effect. Not even a little bit. But maybe, just maybe, a bigger combination of variables will do the trick. Perhaps wheat-eating regions just host a collection of heart-harming factors (low folate, low vitamin D, low EFAs, and so forth) that, together, are more powerful predictors of disease than the variable wheat.

Here are the variables I’m interested in looking at. Some could be causative and some could be preventative:

• Wheat consumption
• Corn consumption
• Millet consumption
• Rice consumption
• Total blood cholesterol
• LDL cholesterol
• HDL cholesterol
• Apolipoprotein-B
• DHA levels
• Folate levels
• Latitude
• Added vegetable oil
• Blood pressure
• Weight
• BMI
• Total fat intake
• Total monounsaturated fat intake
• Total polyunsaturated fat intake
• Total saturated fat intake
• Percent of calories as fat
• Percent of calories as carbohydrates
• Total animal protein intake
• Total plant food intake (by weight)
• Total animal food intake (by weight)
• Green vegetables (daily, not yearly)
• Vitamin C intake
• Total sodium intake
• Poultry consumption
• Egg consumption
• Red meat consumption
• All meat consumption
• Fish consumption
• Dietary cholesterol intake
• Percent of the population currently smoking
• Percent of the population who have ever smoked tobacco
• Percent of the population smoking manufactured cigarettes
• Percent of the population pipe smoking
• Percent of the population smoking cigars
• Percent of the population working in industry (typically less physical activity)
• Percent of the population working in agriculture (typically more physical activity)

I won’t bore you with the results of every single combination I tried (over 100), so here’s the gist. No matter what model I use, wheat always adds unique variance. That means wheat (or an undocumented variable associated with wheat) is contributing something to heart disease that these other variables can’t account for. No combination out of the above bumped the association between wheat and heart disease out of the “statistically significant” zone.

Incidentally, one model had the best fit out of all the others for explaining heart disease:

1. Wheat consumption (beta = 0.62, p<0.001)
2. Apolipoprotein B (beta  = 0.38, p<0.001)
3. Total cholesterol (beta = -0.22, p<0.05)

Note that the number for total cholesterol is inverse, meaning higher cholesterol was associated with less heart disease—at least in this specific model. Unless you’re an Ancel Keys groupie, this may actually be quite plausible.

Anyway, here’s the important point. No matter what variables I adjust for, I can’t make the correlation between wheat flour and heart disease go away. Sorry, wheat! Neener neener.

Cardiovascular disease: The only “Western” problem without “Western” risk factors

Here’s a mystery for ya.

In the China Study data, most Western diseases (such as breast cancer, colon cancer, lung cancer, and diabetes) are concentrated in areas that share some key characteristics: more industrial employment, less agricultural work, greater population density, and often higher levels of schooling. Folks here eat more processed starch and sugar, use more polyunsaturated vegetable oils, chug down more beer, smoke more manufactured cigarettes, and typically get less physical activity than their neighbors in pastoral communities.

In other words, the Western-disease-prone-regions are like baby Americas—slowly waddling, diapered and naive, towards the motherly lap of disease.

Most likely, these Western ailments aren’t spawned from a single food or activity, but from a tragic mix of diet choices, lifestyle habits, and environmental factors. For problems like breast cancer and colon cancer and lung cancer, it’s pretty easy to see what the matrix of risk-raisers are from looking at the data: It’s the same combination of things spurring disease in Western nations.

But oddly enough, this isn’t the case for heart conditions. The factors shared by other Western illnesses are not, in most cases, associated with heart disease in this data set. If you’ve read some of the earlier China Study posts, you might remember that I took issue with Campbell’s disease-clustering strategy because heart disease doesn’t fit cleanly with the “diseases of affluence” group, despite his insistence on sticking it there anyway. Unlike the other Western problems, heart disease isn’t associated with eating more sugar, working in industry, drinking more alcohol, using vegetable oils, having higher apo-B levels, or any of the other variables uniting the Western diseases and mirroring the traits common to industrialized countries.

What’s the only thing heart-disease-prone regions have in common with Westernized nations? That’s right: consumption of high amounts of wheat flour.

Food for thought. Kinda spooky.

Wheat eaters: fatter with fewer calories

Here’s some more weirdness. In both China Study I and II, wheat is the strongest positive predictor of body weight (r = 0.65, p<0.001) out of any diet variable. And it’s not just because wheat eaters are taller, either, because wheat consumption also strongly correlates with body mass index (r = 0.58, p<0.001):  

How odd! This aligns with a post Stephan Guyenet at Whole Health Source wrote about wheat consumption and obesity in China, speculating that wheat might wreak metabolic havoc wherever it goes—a trend that becomes apparent when comparing similar populations of wheat eaters and non-wheat eaters, such as in China. But perhaps there’s some confounding going on. What about calorie intake? Are the wheat eaters just scarfing down more food in general, leading to higher weight regardless of wheat consumption? Doesn’t look like it. Running wheat and calorie intake together as predictors with BMI as the outcome, wheat takes the weight-gaining gold:

• Wheat: beta = 0.56, p<0.001
• Calorie intake: beta = 0.13, p = 0.19

Unfortunately, we have no way of accounting for energy expenditure through physical activity—but considering wheat-eating regions tend to be pastoral and dominated by agricultural work, it seems they’d be burning through a greater wallop of calories than more sedentary regions. Indeed, independent of calorie intake, there’s a clear association between agricultural work and weight (lower) versus industry work and weight (higher), suggesting these things could be approximate measures of calorie expenditure. So once again, we’ve got a paradox: The wheat eaters are consuming lower or average levels of calories, doing more physical labor, and yet… they’re fatter.

Out of curiosity, I ran a stepwise regression on a bunch of relevant variables to see what combination would best predict BMI. (In statistics, stepwise regression is a really cool, but sometimes totally misleading method for building a statistical model. It involves adding (or winnowing away) variables one by one based on how they behave together and contribute to the outcome—BMI, in this case—until you’ve got a model where each variable offers significant variation and the highest possible percent of explanation (represented as r-squared). Unfortunately, since this process is automated and computers usually don’t understand the whole “biological plausibility” thing, you can wind up with weird models that don’t make sense in the real world. Nonetheless, it can be a worthwhile method if used with caution.)

Setting BMI as the outcome, I chose the following variables as potential exposures:

• Total calories
• Total fat
• Total carbohydrates
• Total plant food
• Total animal food
• Total plant protein
• Total animal protein
• Total monunsaturated fat intake
• Total saturated fat intake
• Total polyunsaturated fat intake
• Red meat
• All meat
• Fish
• Poultry
• Eggs
• Wheat flour
• Corn
• Millet
• Legumes
• Starchy tubers
• Green vegetables (daily, not yearly)
• Agricultural employment
• Industrial employment

(I left out milk because so few counties consumed it.)

The best-fitting model for predicting BMI (at 95% confidence)? Drum roll please. Three variables made the cut.

1. Eating more wheat flour (beta = 0.48, p<0.001)
2. Eating more polyunsaturated fat (beta = 0.44, p<0.001), and
3. Eating fewer green vegetables (beta = -0.29, p<0.01).

This model has an r-squared value of 0.53, meaning it predicts a little over half of the variation in BMI—at least in theory. That’s actually pretty high, considering we haven’t directly factored things like physical activity into the equation.

Interesting, eh? All animal foods and total dietary fat, by the way, were completely insignificant in terms of BMI.

Of course, there could be other variables involved that the China Study didn’t cover. Were the higher-BMI folks also more heavily muscled (perhaps from more physical labor), increasing their body weight but not body fat? Are the wheat eaters, some of whom are ethnic minorities in China (especially Turkic and Mongolian), genetically “bigger” than the Han Chinese? There are plenty of unknowns, and alas, no way to clarify them based on this data.

I guess we’ll leave it as a question mark for now.

Grain damage: Do other studies back it up?

But don’t those peer-reviewed, scientific studies tell us wheat is healthy? Alas, the vast majority of studies on grains—especially wheat—showcase at least one of the following problems:

• They look at the effects of whole grains versus refined grains—not whole grains versus the same diet with no grains at all.
• Study subjects increase their consumption of whole grains, and this displaces some portion of yuckfoods (processed junk, white-flour products, sugary things, and so forth). As a result, it’s hard to tell whether any health perks are due to the addition of whole grains, or from the reduction of truly-awful-for-you foods. This is particularly true in studies that scout out disease patterns in populations rather than controlled studies that measure specific changes that occur with the addition of whole grains.
• They don’t adequately account for other factors that often accompany whole-grain consumption, like a greater level of health consciousness, more exercise, other positive diet choices, and so forth.

However, a few gems are lurking in the massive slush-pile of irrelevant studies. This one’s pretty doggone interesting, and it’s from all the way back in 1959: “Comparisons of atherogenesis in rabbits fed liquid oil, hydrogenated oil, wheat germ and sucrose.” You can click on that for the full-text PDF.

As you might guess from the title, this study examines the effects of diet on the development of atherosclerosis—AKA hardening of the arteries. The researchers took cholesterol-infused rabbit food and supplemented it with liquid corn oil (yuck), hydrogenated corn oil (double yuck), wheat germ (mystery murderer?), and sucrose (sweet poison!). Sorry, I dig hyperbole. Anyway, part of the goal was to create an experiment testing the hypothesis that “the geographic differences in the incidence of coronary disease might be related to selective hydrogenation of polyunsaturated fatty acids or to degermination of cereals.”

So now, the moment of truth: Which group had the most severe atherogenesis? Perhaps the one fed the nasty hydrogenated oil, as hypothesized? Ladies and gentlemen, place your bets. From the article:

The most severe atherogenesis occurred in the animals on the wheat germ diet.

Was it a fluke? Probably not:

In an earlier study, we maintained 5 groups of 5 rabbits each for three months on 500 mg of cholesterol daily and rabbit chow supplemented with different fats or with wheat germ. Here also, the animals on the wheat germ diet showed a significantly greater degree of atheromatous lesions than the animals on rabbit chow plus 20% corn oil, cottonseed oil or hydrogenated cottonseed oil, whereas no significant difference was found between the various fats.

So what made the wheat germ contribute to atherogenesis? The researchers state that it’s “difficult to speculate” about the mechanism, which is a scientific way of saying “We dunno.” They suggest the extra dietary protein from wheat germ could be the cause, but from the literature I’ve skimmed so far, it looks like plant proteins don’t have much effect on bunnies (although animal protein does).

Of course, rabbits are truly terrible models for anything that happens in the human body. They’re hardcore herbivores. A mere billowing of the wind is practically enough to spike their cholesterol. But what explains the specific effect of wheat germ on their poor arteries? Could this have implications for humans?

My answer: It’s “difficult to speculate.”

Other studies

Prefer human studies? Me too. Here’s one that initially looks totally irrelevant but is actually pretty interesting: Flaxseed and cardiovascular risk factors: Results from a double blind, randomized, controlled clinical trial. (This also a stellar example of why it’s important to read full-text articles instead of just abstracts, which often don’t tell you diddly about the stuff you want to know.)

This particular study charted the effects of flaxseed on adults with high cholesterol. One group got food with ground flaxseed; the other group got food with added wheat bran. Other dietary elements were the same. (Low fat, low cholesterol. Fun times!)

The results? Ye Olde Flaxseed Group did pretty well: Compared to their baseline measurements, these folks had lower insulin, lower blood glucose, lower C-reactive protein (a marker for inflammation), and better insulin sensitivity (as calculated by HOMA-IR).

But poor Wheat Group was less fortunate. Since the study was about flaxseed, the results of wheat aren’t specifically discussed, but check out “Table 4″ in the link above to see the numbers for yourself. The wheat-bran eaters had a 14.9% increase in insulin resistance (calculated by HOMA-IR) and a 9.3% increase in C-reactive protein. In other words, they lost some insulin sensitivity and gained some inflammation—two risk factors for heart disease. Hmm. Was the wheat bran to blame? Some other element of the control diet? It’s impossible to say for sure based on this study, but considering the wheat group’s adverse effects were more dramatic than the flaxseed group’s benefits, it seems a little suspect.

(A rather abrupt end of part one! The next post will have some more studies and speculations on potential mechanisms for wheat as causative of heart disease.)

View from the Kalalau Trail, 4/27/2010

Aloha from Kauai!

First and foremost, my apologies for the shortage of blog entries this month—and the sluggish replies to emails. I’m currently exploring the balmy islands of Hawaii, expanding my repertoire of exotic fruit while gifting the mosquitoes with two sacrificial offerings of flesh (my legs). Holy insect swarms, Batman! Expect a steadier stream of updates once I’m back on the mainland and not spending half of my waking hours itching.

Here’s a subject near and dear to any raw foodist’s heart: organics. Given the amount of produce most of us scarf down, it’s only logical that the quality of our food—and any chemical residue it ushers into our body—should be a major concern. It would be wonderful if everything we put in our mouths was free from pesticides, untouched by toxins, and grown in a way that was healthy for both the land and for our bodies.

Most people assume that means buying organic.

Unfortunately, for your average non-millionaire Joe Schmoe raw foodist, organic foods have two obvious strikes against them. One: they typically bear a higher (sometimes astronomically so) price tag than their conventional counterparts, and two: some towns and cities have limited availability of organic produce—which means less variety and sometimes less freshness for you.

Alas, it doesn’t end there. For those of us seeking a squeaky-clean diet that won’t stab Mother Earth in the back, organics are not necessarily the holy grail we’re looking for. Check out these misconceptions.

Myth 1. Buying organic means you’re supporting small farms, family-owned businesses, your next-door neighbor Hank who grows chemical-free cucumbers, and all those other nice people who battle big, evil, pesticide-spraying corporations.

If only this were true! The reality is that most producers of organic food also crank out billions of dollars worth of conventional items. Rather than caring tenderly for the earth and its inhabitants, some of these companies simply realized that they can make a prettier penny cashing in on the organics niche, selling less product for a higher cost.  Take Cascadian Farm, for example—maker of the organic frozen fruit you’ve probably seen lining the shelves of your grocer’s freezer. Far from a quaint family-run farm, Cascadian Farm is owned by General Mills. Yep, that’s right: the same mega-corp that makes fruit roll-ups, Haagen-Dazs ice cream, Gushers candy, Lucky Charms, Hamburger Helper, and a laundry list of other foods that don’t belong near anyone’s lips.

Cascadian Farm organic blueberries... brought to you by the makers of the Pillsbury Dough Boy

Bottom line: unless you’re getting your organic food straight from a farm or at a farmers’ market, chances are you’re still padding the pockets of those giant unsavory companies.

Myth 2. Organic food doesn’t contain any harmful or toxic substances.

Unfortunately, this is not only a common myth, but a potentially dangerous one because it implies organic food is safe to eat without washing. How far from the truth this is! Organic does not mean “pesticide free” or “chemical free.” Organic growers do shun synthetic chemicals, but many make liberal use of organic fungicides and pesticides—often at much higher concentrations than conventional growers use, since organic pesticides are generally less effective than synthetic ones. Organic produce can carry residues of nicotine (used as an insecticide), pyrethrum (“a likely human carcinogen,” according to the Environmental Protection Agency), rotenone (a potent carcinogen)… the list goes on. About half of the most common organic pesticides used have cancer-causing properties, according to Bruce Ames (inventor of the famous Ames toxicology test), and the ones that don’t are frequently harmful or lethal to birds, fish, and small mammals.

Myth 3. All conventional produce has pesticide residue when you eat it.

Thanks to the wonders of technology, this is no longer the case. Some modern synthetic pesticides (known as “non-persistent pesticides”)  have such a rapid break-down rate that by the time they leave the farm, they’re no longer detectable on the fruits and vegetables they originally coated. Depending on where your food is sourced, conventional produce may have even less pesticide residue than organically-grown varieties.

Why does everyone say organic food isn’t as toxic as conventional?

For many years, it was simply assumed that organic, botanically-derived pesticides wouldn’t cause any harm to the human body—the whole “natural is healthy” mantra. In fact, organic pesticides weren’t even the subject of toxicology studies until fairly recently; only synthetic pesticides were examined for their damaging and carcinogenic effects. Once the research spotlight fell on organic chemicals, their own dangers became apparent—but due to pervading myths and pressure from the highly lucrative organic niche, this information hasn’t received the attention it deserves.

In other words…

Don’t freak out if you can’t afford a completely organic diet. Although organic foods do seem to taste better much of the time and are often grown in better soils (which is the reason for the better taste), you aren’t dooming yourself to a toxic overload if you eat some—or even entirely—conventionally grown food. And when it comes to nutritional content of your fruits and veggies, organic-versus-conventional matters less than freshness—the total transit time from the tree or bush to your dinner plate. Spinach, for instance, loses half of its folate within a week of being picked. Yikes, right?

Bye-bye, toxins

Whether your purchases are organic or conventional, you can remove some lingering pesticide residue with a homemade or store-bought produce wash. Try spritzing your fruits and veggies with a mixture of 90% water and 10% food-grade hydrogen peroxide, then scrub those puppies clean with a sponge or vegetable scrubber. Alternatively, you can use a spray made from a mixture of water (1 cup), baking soda (2 tablespoons), vinegar (1 cup), and grapefruit seed extract (20 drops)—or even double the recipe, pour it into a pot, and let your food sit in it for a few minutes before washing it off thoroughly with warm water. If you can find a chemical-free fruit and veggie wash containing grapefruit seed extract at the store, that can do the job as well.

Be aware, though, that as soon as you wash any produce in this manner, it won’t store for very long before going bad—so wait until you’re ready to eat your fruits and veggies before giving them the de-pesticiding treatment.

What’s safest to eat?

Some foods generally require less pesticides and fungicides than others, whether grown conventionally or organically, simply because pests don’t attack them much. The absolute safest raw foods to eat, in terms of low pesticide residue, are…

(Drum roll please)

• Asparagus
• Avocados
• Bananas
• Blueberries
• Broccoli
• Cabbage
• Corn (fresh/raw)
• Kiwi
• Mangoes
• Onions
• Papaya
• Pineapple
• Sweet peas
• Sweet potatoes
• Watermelon

Some other not-so-bad choices include:

• Cauliflower
• Grapefruit
• Honeydew melons
• Plums
• Raspberries
• Tangerines
• Tomatoes

And on the flip side, the most pesticide-laden raw foods include:

• Apples
• Bell peppers
• Carrots
• Celery
• Cherries
• Nectarines
• Peaches
• Pears
• Strawberries

Note: you don’t need to completely give up the foods on the last list (I’m definitely never bidding farewell to my beloved strawberries), but it’d be wise not to center your diet on them—unless you have a source of truly pesticide-free varieties.

Additional tips

Get to know your source. If you shop at a co-ops or farmers’ market, you’ll be able to track down specific farms fairly easily—meaning you can contact your food source directly and inquire about their pesticide and fungicide use.

Grow your own and forage. Whenever possible, take your food production into your own hands: pick wild edibles, grow herbs or greens on your windowsill, plant strawberries in your garden—whatever your climate and living situation allows.

A 100% chemical-free diet might not always be practical or possible, but with proper planning, we can choose our produce wisely to minimize the damage.

Did we adapt to cooked food, or is that idea—ahem—half-baked?

In part 1 of this “optimal human diet” series, I mentioned that there is no single, exact diet that will deliver perfect health for everyone. We’re tough cookies, us humans—and we only made it as far as we did by adapting to whatever happened to land on our evolutionary dinner plates. Mastodon meat, sweet little figs, plant roots—we made food of it all.

Even so, there’s a notion in the raw food world that we’re still best-suited for the type of diet we ate back in the good ol’ days. You know, before we exited the tropics, conquered all corners of the planet, and invented the deep-fried Krispy Kreme (which surely triggered the downfall of humanity). Maybe you’ve heard claims that we haven’t adapted to cooked food at all, that we’re designed to be vegan or vegetarian, and that our digestive systems still look like those of other fruit-munchin’, leaf-chompin’ primates.

But do those beliefs hold up to reality? Let’s take a look.

Digestive anatomy

There’s no doubt that we have plenty of anatomical similarities with other primates. We do share a good chunk of their genes, after all—especially chimpanzees, bonobos, and orangutans. In fact, some researchers have argued that chimpanzees should be reclassified under the same Homo genus as humans because we’re so similar, although this is pretty controversial and it’s been challenged by more recent research.

All in all, humans have the same general digestive structure as apes: a single-compartment stomach, a small intestine, a cecum and appendix, and a colon. Pretty simple.

But the devil is in the details, as they say. When you look closer, our digestive tracts have some major differences compared to other primates—differences that pose dietary consequences. The most significant is the size of our small intestine versus our colon. In chimpanzees, gorillas, and orangutans, the colon is about two to three times the size of the small intestine. But in humans, those figures are reversed: the small intestine dominates, clocking in at over twice the size of the colon.

A visual representation for your viewing pleasure (humans are the striped bar):

As you can see, there’s not much difference in relative stomach volume—but other primates have a whole lotta’ colon, and we’ve got a whole lotta’ small intestine.

So what does that mean?

In simple terms, a big colon is good for handling “low-quality” foods like tough leaves, stems, and fibrous fruits—things that require a lot of digestive work to break down. Primates that eat boatloads of greens, like gorillas, have a whole army of microbes in their colon that digest cellulose and convert it into an energy source. That’s a process called “hind-gut fermentation.” Humans aren’t so lucky; we can digest some forms of fiber, but much of it passes right through us without delivering nutritional value. Our colons aren’t big enough to host enough little organisms to ferment things as effectively as other primates do.

On the flip side, a big small intestine (is that an oxymoron?) is perfect for digesting high-quality foods that are dense, smaller in volume, and easy to break down. That includes soft fruits, animal foods, cooked foods, tender leaves, and perhaps items that have been pre-processed through chopping or grinding. Even our modern-day blended and juiced foods make our small intestines happy, because that pre-processing translates to less digestive work.

In other words, humans are adapted to a softer, more compact diet than other primates. Our bodies have moved away from extremely high-fiber cuisines and are better suited for foods that require less digestive effort.

What caused the change in colon and intestinal size?

This is one of those mysteries that researchers like to argue about, but no one has a definite answer for. What we do know is that the change was sparked by a shift to more energy-concentrated diets. It could have been:

• A higher reliance on meat, fish, and other energy-dense animal foods
• The advent of cooking and the subsequent “shrinking” of our food size
• Consumption of more nutrient- and calorie-dense plant foods
• The invention of tools for chopping, grinding, and other forms of processing plant matter

More likely than not, it was one (or both) of the first two. Our shrinking colon size is pretty clear evidence that our bodies started adapting to the energy-dense structure of cooked food and meat, since we no longer had to rely primarily on bulky, super-fibrous plant foods.

Does that mean we should all be cooked omnivores?

Even though our bodies have grown accustomed to denser diets than our primate friends, that doesn’t mean cooked food is mandatory or  that veganism is impossible. What it does mean is that the most successful human diets are going to have some form of concentrated nutrition. On a completely raw vegan diet, the options are very sweet or fatty fruits, nuts, sprouted grains, coconut, seeds, juices, or blended foods. Although I don’t recommend a lot of gourmet-style raw meals and dehydrated snacks in general, those fit in here as well. On a raw non-vegan diet, those dense items could be animal products like raw dairy, fish, eggs, honey, or raw meat. On a high-raw diet, you could opt for steamed root vegetables, grains, cooked legumes, and so forth.

Basically, what we can’t do is live off of leaves and occasional fibrous fruit for extended periods of time like most primates can. Thanks to our dwarfed colons, we would starve.

Shouldn’t we be vegan because meat causes disease?

I’ve said it before and I’ll say it again: veganism is an ethical choice, not a dietary ideal. Today, we know enough about nutrition to plan or supplement a vegan diet to avoid deficiency, but eschewing all animal products won’t necessarily make you healthier than eating a diet containing a portion of high-quality animal foods.

Part of the reason animal foods get a bad rap these days is because of our farming practices. Agricultural products like dairy, farmed meat, and eggs from grain-fed chickens are a far cry from anything we encountered in the 2 million years prior to agriculture. And the state modern animal products (along with the often-horrific way farm animals are treated) is particularly disconcerting. Along with carrying high levels of growth hormones, pesticide residue, and other harmful substances, grain-fed animal products have a far different nutritional composition than wild animals eating their natural diets. And that spells trouble for the humans who eat such foods.

For instance, grain-fed cattle is significantly lower in omega-3 fatty acids and higher in omega-6 fatty acids than grass-fed cattle—an imbalanced ratio that numerous studies have linked to cardiovascular disease, cancer, and autoimmune diseases.

From G.J. Miller, "Lipids in Wild Ruminant Animals and Steers," published in the Journal of Food Quality, 9:331-343, 1986; image courtesy of EatWild.com

Total fat composition is also much different between commercial, grain-fed meat and wild game:

For more information on the differences between pastured animal products and commercial, grain-fed animal products, visit the Eat Wild site.

It’s certainly no surprise we find high rates of disease linked to these foods. Although animal products and byproducts have been components of our diets for quite a while, “franken-meats” pumped full of hormones and antibiotics are the equivalent of space aliens in our digestive systems. They just don’t belong there. At all.

A word on cooking

Although we have adapted to the energy density of cooked food, we haven’t necessarily adapted to all the new substances cooking produces. Charred meat, for instance, contains compounds called heterocyclic amines (HCAs) known to contribute to cancer in humans. Acrylamide, another human carcinogen, occurs when many starch-based foods are heated. Maillard molecules and glycotoxins crop up in browned foods, and these suckers contribute to inflammation and other unpleasant conditions (research here is still in its infancy). And eating high-temperature cooked food may also accelerate aging due to advanced glycation end products.

In other words, there’s good reason to include plenty of fresh, raw foods in your diet even if you don’t jump on the 100% raw bandwagon. And high-temperature cooking seems to stir up all sorts of trouble, so if you prefer to eat some cooked food, gentle methods like steaming are the safest way to go.

In conclusion…

There might not be a single optimal diet for humans, but health-producing cuisines—especially ones with a reputation for healing ailments and reversing chronic conditions—typically have a few things in common.

• Elimination of refined sugar, high fructose corn syrup, and other nutritionally-devoid sweeteners
• Avoidance of man-made ingredients and fake foods—such as artificial sweeteners, soy-based meat replacements, chemical additives, nitrites, preservatives, artificial flavors, dyes, margarine, and hydrogenated fats
• The inclusion of mineral-rich foods (dark greens, seaweed, animal organs, green juices, or produce grown in well-mineralized soil)
• No pasteurized, homogenized cow dairy
• An emphasis on eating foods in their whole state
• An emphasis on some or all pre-agricultural foods (fruit, vegetables, meat, fish, nuts, seeds) rather than post-agricultural foods (grains, potatoes, dairy, vegetable oils)
• A large portion of fresh, raw foods and/or “living” foods (kombucha, fermented vegetables, kefir)
• High nutrient density

If you eat a diet that fits the above description, raw or otherwise, you’re probably well on your way to staying healthy. Even though I prefer a completely raw diet for the level of clarity and surging energy it brings, I have no reason to think that a 100% raw diet will extend a human’s lifespan or offer more immunity to disease than a mostly raw diet with well-planned cooked foods.

But regardless of what you put in your mouth, remember that an optimal diet is one you can sustain—and that doesn’t knock your whole life off kilter by making you socially, mentally, or emotionally imbalanced. Diet is only one component of health and should never become the driving force in your life.

Does this fella offer us nutritional clues?

Part of what first led me to raw foods was a curiosity about our “optimal diet.” It seemed like such a simple concept: a combination of foods that our bodies are best adapted to, that we could easily discern by looking at our anatomy, that evolutionary history supported, and that would lead to the best health possible. It shouldn’t be rocket science, right?

Unfortunately, it kind of is.

Why there is no single “best” diet