The New USDA Dietary Guidelines: Total Hogwash, and Here’s Why

A few days ago, the USDA finally unveiled their (fashionably late) 2010 dietary guidelines—the first update they’ve made since 2005. Are you as excited as I am? Can we live without bread yet? Leave the fat on our dairy? Ditch the rancid vegetable oils? Gobble down butter and coconut oil without fearing imminent death? By golly, has the USDA finally pulled its head out of the soybean fields and given us something useful, emerging as a reliable authority instead of a food industry puppet?


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.



  1. “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.”

    AMEN! Who would trust the GOVERNMENT for dietary advice anyway?

  2. At the risk of stating what will surely be dead obvious to anyone who reads it, as long as grain farmers remain a powerful political force, the USDA (or any other Federal government entity) will never issue dietary recommendations that don’t include their products, science be damned.

  3. As Max Planck put it:”A scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it.”
    Great article, congratulations for your approach.

  4. I don’t think the recommendations herein are “all stemming from a flawed understanding of cholesterol and disease”. Actually, it seems they are manipulated and controlled (like stats) to please the corn syrup, corn oil, pharmaceutical and ‘garbage foods’ industry. We are being read the ‘current’ rules of eating by ‘Big Brother’ for the best profit equation. The only variables in the equation, unfortunately for we Guinea Pigs, are maximum profit visa vie extended average life expectancy. The former being the ultimate priority. The people at the top want the hordes to live as long as possible, gobbling up as much of their products as they can and then, when decreased health dictates, move from the garbage food line to the garbage pill line and last as long as possible there until they keel over. Notice I make no mention of quality of life or maximum possible life, only maximum profit. If it improved the bottom line, they wouldn’t care if millions dropped dead…that would just mean less traffic, which would mean less carbon monoxide pollution and again yaaay PFA and MFA. Our only chance is to take care of ourselves, get rest, get exercise and ‘whatever’ it is we consume…do so in moderation.

    Good luck everyone. ~Dan

  5. Of course the government would issue guidelines which are ridiculous considering they are beholden to the industries which lobby them into power. However, the answer is not to jump to the other end of the spectrum and advocate a diet full of coconut oil, meat and raw everything. Humans have never eaten like that. We need to eat like our modern ancestors and base our diet on properly prepared whole grains and legumes (soaked, fermented, sourdough, etc.), seasonal and locally available fruits and vegetables both cooked and raw, tubers, nuts/seeds, good unrefined whole fats in reasonable amounts (butter, virgin oils), and from time to time we can indulge and eat meat and other rich animal foods either at feast times or in condiment size amounts in our everyday diet. This is truly a proper diet of an agrarian, urban civilized society.

    1. Agreed. Look at populations like the Okinawans who have the highest number of (legitimate) centenarians per capita of any country in ther world. Their diet is highly plant based with modest amounts of animal foods like fish and pork.

      1. There’s a lot of disagreement over how the Okinawans actually eat. Some say it’s mostly plants, some say pork is a staple.

        Besides, Okinawans also live more stress-free lives than most Westernerns, so it’s difficult to pinpoint diet as the reason they live longer.

    2. Actualy, very likely humans ate much like that throughout most of the paleolithic. Fossil bone isotope analyses show a diet high in, possibly entirely composed of, meat. Middens show a lot of butchered ungulate bones, and also animals like hippos and crocodiles that were eaten.

      An urban civilized society should use sustainable techniques to to provide the diet most suitable to humans, not the diet that is cheapest and most profitable for agribusiness.

    3. Man has only been eating grain for less than 10k years. In the scheme of evolution, that’s nothing. Most indigenous people eat copious amounts of meat and fat. The Inuit are a prime example of nothing but meat all the time.

      In fact, in most climates, man probably would have eaten primarily meat, since he didn’t have a grocery store to go to to pick up fruits and vegetables. Nor did he have refrigeration. He would have eaten things in season. The only thing in season in the middle of winter is wild game. There’s plenty of evidence that ancient man ate a lot of it.

    4. And where is the evidence that the diet of our ancestors was optimal for longevity? Selection pressure is for reproduction, not longevity.

      And whole grains, seriously? Why do we “need” to eat prepared whole grains? Where did you find that our ancestors ate whole grains, prepared or unprepared? Unless by “ancestors” you mean agricultural societies, which begs the question why such a diet would be healthy in the first place.

  6. This is an excellent post, thank you for summarizing and providing links to all of the source material. Like you said, it’s always important to read the actual studies and look at the actual data in order to form our own conclusions. I get so frustrated by people who don’t understand (or at least don’t mention/report) the confounding effects of a generally healthy lifestyle on risk of disease. Now I’m going to go stock up on some full fat yogurt 🙂

  7. Thanks for another fantastic and thorough review of bullsh*t studies! I’m sick and tired of all the bad researchers out there who make strange conclusions. We just got new dietary guide lines here in Norway too and they’re obviously looking to the US because they’re telling us the same thing. Sigh.

      1. Eduardo, if I had any malicious intent why would I post that initial comment AND clearly link this page with a trackback attached to “Denise Minger” in the middle of a complement. If that’s not the proper way to credit a blogger than forgive me but you can’t say I tried to steal this content and call it my own. I’ll take feedback but not name calling please.

      2. You seem to be unaware that re-posting with proper attribution of credit is an honest, widespread and widely accepted practice on blogs. Many authors enjoy the increased visibility coming from it.

        1. It’s honest and accepted if the author has given permission. People repost with permission.
          Why is the idea to ask for permission before you grab someone else’s stuff so inconceivable?

          The fact that reposting without permission is widespread doesn’t make it right. It’s about basic respect for someone else’s intellectual property. Someone else’s property.

          If I want to borrow something of a friend, even though I know very well that they will say yes, I still ask!

  8. delicious, full fat review – spot on!

    Thank you Denise yet again for your efforts – i want to re-read this when i get my 3 year old out of my ear…( how many times can a human adult here the ABC song without going totally insane??)

    1. Ned, there are two varieties of safflower oil out there. There are high oleic versions of both safflower and sunflower oil. The graph must show the high oleic safflower, which I think is about 70% oleic acid. Their labeling could be more specific.

  9. The only goal of the USDA to promote and sell agricultural products subsidized by tax payers, not the health of US citizens. Taking any evidence that shows the harmful and obesity-promoting effects of wheat, corn and soybeans seriously would compromise their sole mission.

  10. My high school science teachers always emphasize the importance of reducing the effect of controlled variables i.e. confounding factors whenever we perform experiments. It is sad to see basic science thrown aside on many of those so called ‘scientific’ nutritional studies.

    1. Sadly, the last 30-40 years of big nutrition studies have been exactly this paradigm. No controls, self-reports, 500 dietary/lifestyle confounders. Hence the whipsaw of “Eggs kill you! Eggs are good for you! You get too much D! Too little! D prevents cancer! No, it doesn’t! E prevents cancer! No, it doesn’t! Fruits are super-foods! No, wait, fruit juice makes us obese!” Etc.

  11. OK slogged through it (no really Denise – a fun, if dense, read…)

    2 things – first can someone tell me why these oils are referred to as “vegetable” oils? i’ve never run across broccoli oil, celery oil or eggplant oil. They are SEED oils and as such – have all the wondrous don’t-digest-me baddies that seeds have and there is NEVER any thought of adjusting for phytates, anti-digestive enzymes, etc that are going to be raging in oils pressed from seeds. and secondly – if they really want to “prove” sat fat is bad – why not design a simple straight forward study with identical diets (perhaps a couple versions with different % of carbs) and give one group hugely more sat fat and one group hugely less sat fat – and measure – ?

    course this is most certainly not their intention – keep it utterly oblique to the layman and even pretty much anyone not willing or able to do the kind of analysis Denise has done here. big ag financiers like it really really muddy and convoluted…

    The dairy results Denise has posted don’t surprise me a bit – even as a layman, i will stand up and tell Cordain (master-paleo-diet-man) that to use CW anthropological assumptions about dairy being only a neolithic development is as weak – or weaker than the sat-fat claims of the USDA – (Cordain is kinda against sat fats too – look to Dr Eades for better guidance on that). I’m just doing a 3part-er on why anthropological data supporting the fertile crescent domestication of animals – goats specifically – is flawed and suspect. Just as the estimates of the time-line domestication of dogs is all over the place (12,000 years ago to some claims of over 100,000 years ago) many other factors – like Denise’s evidence of the benefits of full fat dairy (and raw better i’m sure) indicate something of a longer history of consumption. Since there is actually no hard evidence – and lots of conflicting assumed evidence about domestication in general and goats in particular, I believe we’ve kept goats – and dogs – a hell of a lot longer back into paleo era when we consumed goat dairy to great nutritional benefit – and those benefits are evident in studies today – dairy IS paleo – at least for a large percent of our human populations –

    thanks for that paragraph Denise – i will use in in my part 3 with full credits and a link to this study!

    Ravi, DaiaSolGaia, Discoveries for a Full Life

    1. ///like Denise’s evidence of the benefits of full fat dairy (and raw better i’m sure) indicate something of a longer history of consumption.///

      It would make sense that people hunting large mammals like mammoths would have consumed any milk present if they took down a lactating female. So the keeping of animals isn’t necessary for consumption. I personally figure that we are born to drink it, so continuing to drink it isn’t a problem. However, their pasteurized homogenized crap you can buy at the store isn’t even close in taste or composition to raw milk. Just try some raw and you’ll see what I mean. I didn’t even like milk before I tried raw.

  12. Very good analysis!

    Here are some more studies you may find useful and interesting:

    Skeaff and Miller’s meta-study:

    More links to studies are here:

    SciAm article:

    Holmberg study:

    Tarino, Sun, Hu and Krauss’ meta-study: ttp://

    Please write more!

    Different subject – cancer! Any thoughts, ideas?

  13. Very nice.

    Here is a paper that reviews the proposed 2010 Dietary Guidelines for Americans:
    Hite A.H., et al. In the face of contradictory evidence: report of the Dietary Guidelines for Americans Committee. Nutrition. 2010 Oct;26(10):915-24. Full text:

    From the abstract: “Although appealing to an evidence-based methodology, the DGAC Report demonstrates several critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science.”

    Chris Kresser also discussed the paper at


  14. Great work; thank you. As you know, the 1980 Dietary Guidelines were based on the same type of science, especially: “drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science.”

    So, what happened? Thirteen (13) university professors from across the country conduct over two years of meeting and deliberations and then come up with the same 1980 recommendations? Or, did bureaucrats (registered dietitians) in USDA trump the 13 PhD’s who actually knew better? Someone, please help? Is Kafka around somewhere?

  15. Pingback: 10% fat
  16. Hi Denise! (and everyone else!)

    Just a little misprint, I think: “This study examined the effects of two polyunsaturated fats (oleic and linoleic acids)” polyunsaturated -> unsaturated.

    This time you are not pinning down a simple (reduced group) person’s work (The China Study case), but a room full of bureaucrats. Since there seems to be already available published articles on the weaknesses of these guidelines, I would love you to be invited to expose this nonsense in a major media, since you do superb on interviews. It seems to me that to shake the establishment on dietary guidelines worldwide, the best starting point is going to be your country.

    And thanks for all the links about cheeses ;-). After years of lipid-hypothesis-induced deprivation, I’m going down on hard cheeses with a vengeance. I’m sorry you can’t tolerate it.

    Keep up the good work!


    1. Thanks for the poly/unsaturated typo catch! Fixed it.

      Indeed, I like cheese more than cheese likes me. At least that leaves more for everyone else. 🙂

  17. OK, so we should eat less hydrogenated oils. But then look at the oils we hydrogenate: Canola, soy, corn. Any wonder why cutting those out is better for us?

  18. If the nytimes had any sense, they would get down on their knees and beg you to take six figures to be their lead nutrition writer.

    Oh, well.

    1. To write for the NY Times, one must worship The Obamessiah. If one worships The Obamessiah, one will almost certainly advocate a low-fat, grain-laden, ideally vegan diet–the kind that kills brain cells in such numbers that one will…worship The Obamessiah.

      In all seriousness, the clustering of “compassionate” diets and “compassionate” public policies is an interesting phenomenon. Papers like the Times seem curiously resistant to abandoning their Jane Brody-oid diets because they cannot stomach the notion–with food as with politics–that seemingly “crueler” approaches can lead to “kinder” outcomes.

      1. Where did all you Bircher wackjobs come from, anyway?

        You are the unwitting footsoldiers in the Koch brothers’ army (and you don’t even know who they are.)

    2. That’d put a dent in their advertising dollars, so I doubt we’ll see that any time soon. After all, what would big food sell us if we all ate paleo?

  19. 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.

    Ouch. So basically cakes+cookies (hello, Type 2 diabetes) and processed meats which have once again been linked to colon cancer?! (And may lead to heart disease due to high sodium?) Also cheese, which leads to weight gain in many people, pizza (major source of gluten + more processed meats + too much sodium … although I personally don’t believe pizza is all that bad for you, assuming you can digest wheat), and fries. Fries which may contain trans-fats because of the frying process. Yum, trans-fats.

    Good catch.

    1. I’d be willing to bet that a huge portion of that mysterious 23 percent slice consists of crappy breakfast cereals and salty (vs. sweet) grain & starch-based snacks (like crackers & chips.)

      Those items fill multiple aisles of the supermarket yet don’t seem to fit into any other category.

      What an amazing horror show that pie chart is!

      1. Oh, good call. I decided I didn’t want to end up obese like my mother and avoid those aisles in the supermarket with a vengeance (except to pick up coffee ^_^). What I’ve found after many years is that I don’t have a taste for those items any more. Especially crackers. Some friends have brought them over with cheese when visiting. Eat the cheese; the crackers collect dust. They just don’t taste good.

    1. Denise, Bobby Fernandez (above) has indeed stolen this entire post and put it on his blog.

      For the benefit of the Goog, I’d just like to point out that Orange County personal trainer Bobby Fernandez is an unbelievable jerk who steals content because he ain’t smart enough to write his own.

      1. I’m lost here. Isn’t a trackback link stating her name in the middle of a complement proper citation? The first portion of the post is my philosophical exploration of the topic. I clearly state that Denise can do the technical critique of the new Dietary Guidelines better than I. Please let me know how better to spread her work and properly give her credit?

        1. By not copying her content without permission.
          Citing short passages with a link is considered fair use and is ok. Copying a whole article without asking for permission is copyright violation. Also known as stealing other people’s hard work.
          You appear to have done it in good faith, but it’s copyright violation all the same.

          1. By not copying Denise’s content without permission.
            Geez, where is the edit button. Sorry, Denise, didn’t mean to talk about you as if you weren’t in the room.

      2. Follow-up. Denise has now officially approved my use of her work. She was even so gracious as to apologize for her readers attack on me. I’d like a public apology from you too Eduardo. If you have the courage to libel me here in public, you should have the courage to apologize to me. Thank you.

        1. Bobby, you weren’t libeled dude. You have to get “official approval” first before copying someone else’s work entirely. Don’t start acting like you were the offended party – that makes you sound like a douche-bag.

          Normally it is better to just quote select portions of someone else’s work and direct your readers to the original source to read the bulk of the material. Many people that produce original content want the web traffic too, not just the “credit”.

        2. Bobby, you infringed a copyright. That Denise has — incredibly — permitted it after the fact speaks to who she is, not the rightness of your act.

          There are people who would sue you for $150k + your domain based on what you did yesterday. (They are very aggressive, yes, but the law is on their side.)

          Be grateful you took Denise’s content, rather than theirs:

      3. Thanks for watching my back, Eduardo and Birgit! Bobby edited his post to make it clear I was the original author, and I gave him permission to keep it up that way. Thanks for pointing it out, though — I’m traveling right now and not able to monitor the blogosphere too closely. 🙂

        1. Thanks Denise. As I said to you privately, I truly see it as such a positive that so many people have your back like this. I hope to be honored with such a readership someday. My intention was made clear in a comment above dated 2/4. I had not heard back from Denise yet so I went with my instincts and added her material to my content making sure to give her proper credit. My suspicion is that perhaps you saw the trackback comment I generated on Denise’s blog and didn’t read my post well enough to see that A) I had 1,000 words of original content B) I credited her as well as paid her a nice self-deprecating complement. Either way, I have chosen to further change my post to only provide an excerpt of Denise’s wonderful post.

          My request for an apology from Eduardo is also based upon what he said to me in private rather than his public defense of Denise. His public attempt to attack my personal training business and my intelligence was uncalled for IHO. If you all don’t agree, fine. Sorry for the ruckus Denise. Great post!

          1. Bobby, I do apologize for those remarks. I get that you weren’t aware of the copyright issue.

            Denise, please remove my remarks as there is no edit button.

            1. hey – easy solution folks – just announce the important info, give the link – problem solved. If someone does not have interesting content on their site other than the link to someone else’s interesting content – well – the readers will decide and come back… or not, yes?

              forces all us bloggers to be creative and better at what we do if we want to sincerely share and get traffic…

  20. [off topic]
    Eduardo Tegucigalpa, Birgit,

    My point of view on this is totally different!

    You are legally correct but I would like to point out, that United States’ copyright law that you are defending so vigorously, is one of your problems rather than being a beneficial thing. I think it’s time to change this “law”! It causes your lawyers eager to pursue some teenage kids downloading songs rather than your oligarchs “downloading” trillions of your own wealth!


    If you have an apple and I have an apple and we exchange these apples then you and I will still each have one apple. But if you have an idea and I have an idea and we exchange these ideas, then each of us will have two ideas.- George Bernard Shaw

    1. I don’t want to turn this into a copyright discussion, but I wholeheartedly disagree with you.

      The only things wrong with current US copyright law are the absolutely ridiculous term lengths (life + 70 years?!!) and select portions of the DMCA that nullify fair use.

      Your quote at the bottom is exactly why copyright exists. We would not have professional authors or professional songwriters without it, as there would be no way for them to reliably earn a living off their work. This is because ideas, by their very nature, can be stolen but not taken away. If an author spends a year on a book and is only able to sell a handful of copies because everyone else knows to get their copy for free from those who purchased it first, what author in his right mind would continue writing books?

      This is the problem with abolishing copyright law, it is an incredibly short-sighted idea.

      1. It is a necessary evil nonetheless. If you wanted to live in some purist utopia then the idea of intellectual “property” would seem like an abomination. Institutionalized selfishness for the sake of greed. Owning one of nature’s most fundamental forces, information.

        I’m not speaking for the previous commenter nor am I saying I believe all that I have characterized above, but I have heard this type of reasoning in many circles. Mainly Buddhism and related…

        Yet in the world that we have created, as you point out, the practical application and defense of copyright law is one of the many things that keep our world turning. If you want to find out how the universe works, you study its laws, guess society is the same way.

  21. The US dietary guidelines will change once Monsanto genetically engineers a soybean that produces stearic acid…

    …and not one day before.

    Nutrition policy is 100% determined by farm policy, which is to shovel billions of dollars at Monsanto, ADM, Cargill, and other agribusiness behemoths in return for overproducing corn, soy, and wheat.

    Those grains aren’t going to eat themselves. Get to work, America!


    1. The carbohydrate chair on the 13-member Dietary Guidelines Advisory Committee was Prof Joanne Slavin, University of Minnesota. Corn syrup-maker Cargill and General Mills – sugary cereal – are headquartered in MN and have given millions to Prof Slavin’s employer, the nutrition department at the U of MN. It was Slavin who said we should not “grade” carbohydrates (good and bad) and that it was perfectly okay to consume up to 25 percent of calories as sugar. I wonder, how was she selected to be on the DGAC and how was she able to appoint herself carbohydrate chair?

    2. Genetically modified soybean and cottonseed oils are here:

      Spencer MM, “Mapping the Fas locus controlling stearic acid content in soybean”, Theoretical and Applied Genetics, 2003

      Lin Q, “High-Oleic and High-Stearic Cottonseed Oils: Nutritionally Improved Cooking Oils Developed Using Gene Silencing”, Journal of the American College of Nutriiton, 2002

  22. As several have stated, government nutrition policy is determined by farm interests.

    However, that doesn’t mean farming can’t be affected by nutrition information. If it becomes clear that say, beef that can be grown on land turned to pasture is nutritionally more valuable than grains which can be grown on that land – clear enough that the economics reflect it – the use of much land will change from farming of grains to grazing of cattle. Then the USDA will be free to change their recommendations accordingly.

  23. Denise,

    You sure are going to make more Americans fat and sick. After reading your blog, the already astound population is going to eat more meat, dairy and saturated fat.

    on the side note

    I’m not the PETA activist and would consume animal product as a therapeutic agent.

    But picture yourself instead of those animals who are butchered mercilessly when the other choices are readily available. And this require no so called science or statistician. There is no way you can gain anything valuable at the cost of some-other life. It is impossible.

    If you need attention and cookies, play it with your own life!

    1. The ethical aspect to vegetarianism is one not entirely thought through. One simple way I approach any moral issue is to ask the question, “what if everybody did x, y or z?”. The answer to this question in regards to vegetarianism is that we’d have to destroy much, if not all, of the natural habitats of said spared animals in order to calorically compensate for the sustaining of the population of humans on meat substitutes from the soil. So if this vegetarian utopia were thought out beyond the first stage where everybody gets to feel noble, its reasonable to predict that there would be massive reduction in population of either wild animals with no home, or humans with no food.

    2. Butchered meat is already dead. If you’re talking about slaughtering, some very smart people, like Dr. Temple Grandin, have worked very hard to make slaughter as humane a practice as possible.

    3. mark,

      Can you actually point to a valid study that confirms that meat, dairy, or saturated fat make people fat and sick? In my view, this article did a pretty neat and tidy job of pointing out the lack of scientific underpinning of the current dietary recommendations.

      In general, I’m confused by the second portion of your argument. Humans evolved as omnivores, just like pigs, raccoons, crows, hedgehogs, and a myriad of other species. Certainly, it is our responsibility to ensure that the animals we eat have been raised and slaughtered in the most humane, ecologically responsible way possible. But I just don’t see how eating my biologically appropriate diet is unethical.

    4. Nature is not a Disney movie. In nature there are predators and prey. Life and death everyday. At least we kill our prey before eating it, unlike some animals that start eating before their prey is even dead. And we try to do it as humanely as possible. That’s what separates us from the rest of the predators.

      Tearing up land for agriculture is not good for this planet. I daresay agriculture was the worst thing humanity could have done to this planet. We should be eating more free range game, and less genetically engineered plants.

    5. Hi Mark,

      This blog focuses on the science behind human health and nutrition — dietary ethics is an entirely different subject, one that plenty of other sites are covering. I hope that people can find useful information here and then apply that knowledge in whatever way fits with their ethical beliefs. But I have no interest in telling people what those ethical beliefs should be.

      “There is no way you can gain anything valuable at the cost of some-other life.”

      No matter what you eat, something has to die. Even vegans non-intentionally (but inevitably) leave a “death footprint” from eating vegetables grown in animal-based fertilizer, plant foods grown with pesticides, grains whose harvest involved massacring small animals with wheat threshers, crops grown in areas where natural habitats were destroyed, etc. Every single person on earth lives “at the cost of some other life.” The only way to remove yourself from the death cycle is to not exist.

      That doesn’t excuse the brutal treatment of most factory-farmed animals (which I don’t personally support — pastured or wild-caught animals live better and are much healthier for human consumption), but it does obscure the issue of a plant-based diet always resulting in less harm than an omnivorous one.

      1. HOLY COW!!!!

        “””…vegans non-intentionally (but inevitably) leave a “death footprint” from eating vegetables grown in animal-based fertilizer, plant foods grown with pesticides….”””

        I had a dream about talking to some vegans two nights ago and THAT is almost verbatim what I told them….in my dream! I’m a bit scared now.

    6. “Morality” issues have nothing to do with the health aspects of what one eats. You claim Denise is going to make people fat and sick, but your reasoning offers no proof other than a complaint about butchering animals.

    7. Marks has got a (valid if unsettling) point. Denise’s carefully picked and chosen findings will only further fuel the hamburger munching brigade’s feelings of entitlement when it comes to feeding with impunity on stuff which ultimately is an endorsement of the SAD. The sad irony of it all is that this nutrition blog, which started (or at least posed) as a smart and highly interesting /irreverent writing seems to end up as yet another bland(ish) conformist, safe, unadventurous pro-carnivore take on things. Your average Joes will rejoyce…

  24. That said, I’m totally against CAFOs and believe that if you chose to eat meat, you should be responsible for knowing that the animals are treated properly and killed in an appropriate manner. I’d also love to have a picture of the actual animal on the packaging in the store so that the consumer fully appreciates the life they are taking in to their own.

  25. If at all Americans need to hear anything then it is to consume less and less of animal products. Any responsible person would agree with that. Instead Denise is giving them all the more reasons to eat more of these products. Like I said, you can not be happier by making someone else miserable, same way , nothing good can ever come out by brutally killing be it “stupid” animals. You can argue as much as you want. She can make use of her excellent communication skills in a way that is positive. Those who want to include small portion of animal products in their dietry habit, let them do so..I don’t understand the need for the glorification and incitation.

  26. If we did not eat cows, chickens, pigs, etc. they would not be here; they would have no life – no one could afford to provide food and water for them. (Unless we set up token Disneyland zoos here and there and people volunteered to care for them.)

    There are no traditional peoples who consumed a strictly vegetarian diet. If we all became vegetarians, farm animals would disappear from the planet. We would follow shortly thereafter. Only animal foods , as an example, provide Vitamin B-12 critically necessary for human life.

    In a vegan world – there would be no farms and there would be no farm animals! Since we’re all sacrificed in the end, the real issue is raising animals outdoors, in pastures, and providing them a social life. We all must die! Life and death are inescapable and killing for food and nourishment is simply part of this great cycle of sacrifice that we share with all forms of life.

    (Keep in mind, the monoculture of soybeans and corn are destroying the soil – also very much a living thing. In contrast, small mixed farms that include properly-raised animals help sustain the soil to provide food for future generations.) Herbicides and pesticides are not needed to raise beef and diary cows – they eat grass!

    Isn’t it time for meat-eaters and vegans to work together to end Industrial Agriculture in all its grizzly forms – the destruction of living soil, the spraying of herbicides and pesticides that kill everything in their wake, and the inhumane treatment of animals, such as dairy cows living on cement floors?

  27. Denis, this is wonderful and helpful research. You have admirable energy and you seek the truth. I am so full of these useless studies that I cannot bear to do what you do.

    Do note the Medical Hypotheses, only an hypothesis but convincing nonethe less, in Milk – The promoter of chronic Western diseases Bodo C. Melnik that speaks to the chronic elevation of the Insulin/IGF pathway and human health.

    1. Arthur I noticed you called Mrs. Minger Denis. Now maybe you know something I don’t know but my brother Stanley is a fan of rawfoodsos and he works for The Security Agency or TSA and he got a really good look at Mrs Minger as she was waiting to get on a plain and he is convinced that she is not a guy at least not yet. Stanley says even through the machine its sometimes its hard to tell if its a girl or a guy tucking his junk but in this case he said I’m sure she was a chick and saved the pictures on his laptop. He says she didnt have any tatoos or piercings which is so weird for Portland he almost wondered if she was a secret moslem terrier but she didnt have a bomb so they let her through.

  28. Gee Denise, another great post. You’ve really opened my mind to how miserable a job science is doing for us right now….I’ve been thinking for awhile about all the important nutritional studies that aren’t being done. Gary Taubes mentions this on a fairly regular basis. I wonder – how hard can it be? There are many thoughtful people out there who could be conducting these studies with volunteers. Is it not possible for a smart person like you or others within the nutritional community to design some studies and then get volunteers to conduct them? It would seem that as long as proper monitoring were done – results should be credible. Perhaps it would save the 40 or 50 years of waiting around for the powers to be to get around to it…..

  29. So now the consensus is we need more properly designed study perhaps designed by someone as intelligent as Denise or Denise herself. I’m flabbergasted here, why do you need more studies? I thought Denise has already proved it that animal protein is not the part of the problem. So why we need yet more ” properly designed” studies is beyond me.

    Listen folks, long laundry list doesn’t prove anything. If science/research was that easy everyone would have been the scientist!

  30. ///”Welcome to America, land of 300 million guinea pigs.”///

    I think that with the rise in obesity and diabetes, that their research is panning out for them. Quite a change from the under-powered studies they cite as proof of their dogma.

    ///”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)”///

    Mmmm, mammoth… I bet they were tasty. I get so hungry reading about all this food LOL

    1. Mammoth will once again be on the menu. Question is…Will you eat it?

      (Jan. 13, 2011)

      “””Mammoths, which went extinct about 10,000 years ago, may once again walk the Earth.

      A team of researchers will attempt to resurrect the species using cloning technologies after obtaining tissue this summer from the carcass of a mammoth preserved in a Russian mammoth research laboratory. It has already established a technique to extract DNA from frozen cells.

      “Preparations to realize this goal have been made,” said Prof. Akira Iritani, leader of the team and a professor emeritus of Kyoto University.

      Under the plan, the nuclei of mammoth cells will be inserted into an elephant’s egg cells from which the nuclei have been removed to create an embryo containing mammoth genes.”””

  31. Okay, I need someone to educate me here. I drink 16 ounces of soybean milk (organic and unsweetened). Is this a dumb thing to do? Exactly how bad is soy milk compared soy oil? What I have read on my own has been pretty confusing (what nutritional information is not confusing?). If I hear some serious concerns, I will dump it where my other grains went!


    1. I guess the first question is why not cows milk? Raw, whole, un-homogenized milk is available in many states. If you are allergic to dairy, I would reccomend is almond milk.

      Honesly, I haven’t looked in to the means of production too much because to me, soy is not an edible food in the first place. I wrote a little blog post about it a couple years ago. Here it is If you’d like my $0.02:

      If you need more science, read “The Ploy of Soy” by Sally Fallon or better yet, “The Whole Soy Story” by Kaayla T. Daniel

      1. Thanks. I just read the blog post. I have looked at the USDA nutrition site and it has pretty low carbs, good calcium and other minerals. I have switched from cow’s milk for reasons of provoking insulin response. Soy is one of those things which is too hard to figure out given all the hype – both positive and negative.

        1. Well thank you for reading my blog post. I honestly just became aware of the insulin issue with cows milk after listening to a podcast interview with Dr. Arthur DeVany (I think he’s on this comment thread a few spost above this, 02/08/11). I would have to do more research but I would also invite Dr. DeVany to chim in here. Are you talking about raw, whole, un-homogenized cows milk? And if I’m not mistaken Dr. Devany, you mentioned the insulin response in conjunction with other simple carbohydrates/fat bombs like french fries.

          I try not to micromanage my macronutrients (if I can say that). I tend to look at what I eat with an intuitive consciousness. I think that’s what this whole “hogwash” aspect to these new guidelines is about; moving away from common sense and giving far too much creedence to the research du’ jour. I know for some this logic, vis a vis cows milk, brings about the conclusion that it’s purpose is to grow a big, dumb animal. To that I say, that if we were to have nothing but milk then veggies in our lives, we would be big, dumb animals. We use milk as a component of our diet. If that still doesn’t convince you, go for raw goats milk. I’ve also heard seal milk is really healthy but good luck getting it.

          1. To reduce the sugar content of milk, make yoghurt out of it. The longer you leave the yoghurt to set, the more sugar is used by the bacteria culture, so you get a more sour yoghurt. Soy milk without sugar in it tastes really awful, so read the labels and you will see a high sugar content.

    2. Soy milk is delicious/nutritious, as long as you can fit it into your macros – it is a little sugar-y.

      Making soy your main protein (as some vegetarians do) can imitate the effects of estrogen. So as with a lot of foods, mix it up and don’t over-do it.

    3. Hi Phil — I second (or third, or fourth?) the recommendations to read the info folks linked to above. I’m pretty leery of unfermented soy (and more-than-modest amounts of fermented soy) due to the issue of goitrogens, other anitnutrients, high omega-6/polyunsaturated fat content, etc. If you can’t do mammal milk but need something white and creamy, I’d opt for diluted coconut milk, or possibly almond milk in small amounts.

  32. @PhilM

    Soy is actually quite dangerous to chronic drinkers. The Soy Bean Oil is full of omega-6s which can upset your omega 6:3 balances which will cause chronic inflammation which in turn creates everything from Diabesity to Alzheimers.

    On the other hand, the milk is full of toxic soy proteins which cause leaky gut and inflammation. This is not to mention the other things in soy such as plant estrogens, goitrogens, and a laundry list of anti-nutrients. You definitely should read the “The Whole Soy Story” that Mr. Fernandez linked to above and make a decision to keep this industrialized processed “food product” out your body.

    1. I didn’t know why all of a sudden I was getting migraines every day for a month and discovered that the soy milk I was drinking was causing them. For those who suffer migraines from any cause(s), soy is a huge trigger for many people. I can’t remember what compound it was in soy that triggers the headaches, but I’m sure you can google it.

  33. A while back a reporter went to the leading governmental nutrition official in the UK to find out the justification for their recommendations for intake of fruits and vegetables, which was half what is recommended in the US. She admitted there was no scientific basis for making any specific recommendations, and then cut off contact with the reporter.

    1. Hi Sue — I listened to all the nights except the Daniel Vitalis/David Wolfe one. Interesting stuff! Donna Gates rekindled my interest in fermenting. I was disappointed that only one round was an actual debate format and the rest were just interviews (I wanted to hear ’em duke it out — especially Campbell versus Fallon!), but I understand that many speakers would only agree to the interview format, so Kevin Gianni had to do it that way. Props to him for bringing so many unique voices together in one place.

      Did you listen? What were your impressions?

      1. Daniel Vitalis was really good. Also liked the Mike Adams and Sean Croxton which retained the debate format. I think the debate format better as long as speakers didn’t hold back with the points out of politeness to other party. Campbell was included as a bonus. Didn’t listen to him – can’t bare to – especially after reading your review(s) on China Study.

        1. Darn, I knew I’d regret not listening to the Vitalis/Wolfe one! I heard Campbell’s bonus interview last night and was surprised that I agreed with a lot of his food philosophy (just not the “animal protein = every conceivable illness” part). Gianni asked him at one point to explain correlation vs. causation, and Campbell used the example of “breast cancer rates tend to go up as fat consumption rises, but that doesn’t mean fat causes breast cancer.” It made me happy to hear him say that. But he also mentioned that he didn’t feel like getting in debates with his critics because they all just make stuff up and shout obscenities at him.

          1. I may listen to the Campbell bonus if I get an opportunity. I wonder if he sees you as one of his critics? A very smart one at that.

  34. Is there any mention of fructose (and hence sucrose) as just possibly being somewhat less than the very nicest carbohydrate, and maybe even worthy of some special attention of some sort?

    1. Hey Ed — As far as I saw, the guidelines didn’t distinguish between sugar types and lumped all “added sugar” into the same category. As long as the government is subsidizing corn –> high fructose corn syrup, I doubt fructose will get any special negative attention. Woe!

      1. It’s scary to see all the apologetics for HFCs coming from the mainstream. I got this “free supplement” that read more like a press release in my winter IDEA Fitness Journal that was written by an Registered Dietician. She went on about how the anti-Fructose crowd are all riled up simply because High Fructose Corn Syrup is un-natural. She said we shouldn’t be concerned with it because, afteral, it’s almost 50/50 Fructose/Glucose…hardly should be called “high” in her opinion. Just Google all the mainstream stuff on it. It’s truly Orwellian the way the industry is trying to re-name and re-brand with the help of the US government and medical establishment.

  35. Denise,

    Interesting that the guidelines don’t distinguish between different kinds of sugar. There’s an old story that has a bearing on this.

    It concerns the building of the Panama Canal 100 years ago. It seems that many people from the sugar-growing Dominican Republic applied to work on the canal, and they were all tested for diabetes. None was found to have it. This was a surprise, and further investigation revealed that only the rich Dominicans had diabetes. The rich ate white sugar, and the poor chewed sugar cane.

    In other words, you can chew as much sugarcane as you like and you won’t get diabetes. The juice has all the minerals that metabolism of the sugar needs. Diabetes is caused largely by deficiencies of these minerals, without which the pancreas can’t go on producing insulin, and other tissues can’t go on responding to insulin.

    1. 500g of Sugar Cane will have about 100ug of Chromium in it. I have been wondering for a while though, would merely adding back the proper ratio of Chromium to refined sugars be enough or because of over-consumption would both end up being toxic?

    2. I believe that as sophisticated as our biochemical field of study is, we can only yet form opinions on such things as sugar. The overexamination of the individual parts of the whole is best applied to Physics, computers and Mathmatics. That said, my opinion of sugar is that it is natures grand ruse. It’s the only way any of us would climb a tree and pick an orange. It’s not something to fear to the extent that we substitute it with other sweet chemicals however it should be avoided. I approach the subject with the words of one of my mentors, Dr. Suhas Kshirsagar M.D., BAMS, in mind, “There is no right way to do a wrong thing.”

  36. In theory, adding the ‘right’ amount of chromium would be OK. But only if you add the right amount of everything else that’s been removed. Otherwise, the chromium can’t be utilised, and of course nor can the sugar, which will end up as fat and free radicals.

    1. I finally was able to put aside some time and give this a thorough read. Congratulations Denise on once again bringing the truth to light! A very enjoyable and scientifc take-down on what the USDA tells us what’s good for us.

  37. I find it strange that people accuse the farm industry of rigging the USDA toward more whole grains when the farm industry also comprises a highly-profitable meat & dairy (which this website seems to promote heavily). I question why the author of this blog, speaking with alleged neutrality, almost universally writes in defense of meat & dairy.

    1. If you read her blog and personal history, you’ll see that her diet contains no dairy, only some raw fish and raw eggs (that she gets from a neighbor with 13 free ranging hens) and mostly raw fruits and vegetables. She does not promote eating meat or dairy. By critiquing studies as she’s been doing, the only thing she is promoting is that we, her readers, have a more critical eye about we read.

    2. Hi Ian,

      I write a lot about meat and dairy on this blog because they’re so often blamed as the source of disease, even when the science doesn’t back it up (especially with the saturated fat and cholesterol connection). Dairy hasn’t been a part of my own diet in years and I eat very modest amounts of meat, but I don’t think these foods are unhealthy in their pastured/organic form — quite the opposite, humans can thrive on them.

      The new USDA guidelines sing the praises of vegetable oils and grains while telling us to slash intake of foods with “solid fats” like meat and dairy. I have some strong opinions about factory-farmed meat and dairy (I would put some forms of dairy in an even worse category than grains), but the USDA is definitely not pushing these foods as heavily as the grains and industrial oils, as profitable as their industries may be. The 2010 guidelines make that abundantly clear. The message is to eat more unsaturated fat and plant foods while cutting down on animal products.

      1. Eat the liquid fats, but not the solid fats? Hmm, coconut oil is solid in the winter by liquid in the summer, so eat it seasonally? Shades of macrobiotics. If it’s partially liquid, I can pour off the liquid parts?

        Do these guidelines make any sense?

    3. Maybe because meat and dairy have been shown to be much healthier for you than grain-based foods? Believe me, I`m a doctor and only learned about all this about a year ago. but when you look at the science and know something about physiology and biochemistry, eating foods which constantly raise our Insulin levels (as carbohydrates do) can only do harm and promote fat-gain. Read up on it.

  38. There is a misuse of the studies you mention here:


    As you say,

    “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.”

    The data in [1] show that low fat diets slow the rate of tumor growth. The data in [2] show that, with saturated fats, the amount does not influence tumor growth. It does not, as you imply, compare saturated fats to vegetable fats, it only compares whether amount in a pure diet of one or the other matters. For you to make your argument, you would need (which you do not have) a study that shows that saturated fats slow tumor growth more than unsaturated fats.

    1. Hi Ian,

      Not sure I agree. The first study shows that a low-fat diet slows tumor growth in comparison to a high-fat diet when the fat is corn oil. The second study shows that a low-fat diet and high-fat diet don’t produce any differences in tumor growth when the fat is saturated. The studies are by the same researchers and have a similar design, so it’s not a stretch to place those findings side-by-side and observe that the corn oil was promoting more rapid tumor growth than saturated fat.

      Even the researchers note this:

      “Previous mouse studies suggesting that low fat diets slow prostate cancer growth often used corn oil (omega-6), which enhances prostate cancer growth, as the primary fat. Using a saturated fat based diet we previously found no significant difference in tumor growth between low and high fat fed SCID mice…”

      “In this xenograft model we found no difference in tumor growth or survival between low fat vs Western fed mice when the fat source was saturated fat. These results conflict with those of other studies in which corn oil was used to show that low fat diets delay prostate cancer growth, suggesting that fat type may be as important as fat amount in the prostate cancer setting.”

  39. You’re fake. You’re a pretty face put in front of a PR campaign to support the dairy/beef industries.

    All you say is “everyone who criticizes dairy is wrong.” You’re so transparently fake it’s as if you didn’t even try to be real.

    Try harder!

    1. Andrew, how can anything Ms. Minger has said about the current state of the meat and dairy industry be seen as advocative? She has been very outspoken about the SAD state of our current system of rasing animals on CAFOs, feeding them the same toxic GMO, govt grown grains they push on us year after year. She is simply bringing to light that trading the sick animals for the grains fed to them doesn’t make much sense. That’s basically what the USDA is telling us to do. I don’t mean to speak for her but that is the basic message I have gleaned from this blog post.

      1. A PR campaign for Ugly Product X doesn’t need to prove that Ugly Product X is good. All it has to do is suggest that the work that went in to demonstrating flaws with Ugly Product X was itself flawed. Muddy the waters.

        Minger could be a scientist and her writing could be published in peer-reviewed journals; that’s the level of her criticisms. The fact that it isn’t being published there indicates her criticisms don’t stand up to peer review. If not from Ms. Minger (maybe she doesn’t feel like publishing in peer reviewed journals?), then from any other scientist willing to steal her ideas and put their names on them. There’s motive aplenty to do that. But it hasn’t happened doesn’t speak to the integrity of scientists, rather to the fact that they don’t stand up to peer review.

        1. “The fact that it isn’t being published there indicates her criticisms don’t stand up to peer review.”

          Dude, I’m in the process of getting the China Study reanalysis peer-reviewed with a researcher right now. Hold your horses! It’s not an overnight event. 😉

    2. Psst — I don’t eat dairy. I think some forms of it are darn near toxic, depending on how the milked animal was raised. I do think those who criticize full-fat dairy and push low-fat forms are wrong, though.

      1. I missed these two responses of yours as I was catching up on the thread this morning.

        I’ll be patiently waiting to read your article when it comes out. I do hope you will comment on its publication when it does.

  40. Andrew, I know the basic tactics of PR and I know the powerful impact of a lie. You can’t accuse Ms. Minger of doing anything of the sort. She herself eats very little meat. Her work here is simply to discredit the “rock” of evidence upon which we base all of our public food and health policy. Are we not allowed to investigate the literature and the peer-review process itself with respect to the modern agricultural conglomerate between those who feed us and those who govern us? A responsible reader would come away with the sense that our USDA is either lying to us or only looking at half the story. I personally believe the latter as I am not a huge conspiracy theorist. Our food supply has changed more in the last 10 years than it has in the last 10,000. Our food science is only in it’s infancy and responsible criticisms like this are more important to us than ever. It doesn’t do any of us any good to call people fakes because they seem to indirectly advocate a particular food. Besides, the type of meat/dairy consumption Ms. Minger advocates is not profitable to any entity save for the people. Nobody can make millions from growing your own food and getting meat and dairy from a local (real) farm. You know…the kind with grass and sunlight.

    1. You didn’t respond to either of my criticisms. Why not?

      I say: muddying the waters is an end in itself.
      You say: she hasn’t proven beef/dairy is good for you.
      I say again: she has muddied the waters saying beef/dairy is bad for you. She needn’t prove it’s good for you.

      I say: if Minger’s claims held water, they would be published by her or others in peer-reviewed journals; they haven’t been.
      You say: she’s playing a vital role making criticisms of peer-reviewed research
      I say again: if her arguments held water, they would appear in peer-reviewed journals.

      This is a bluff, people. Minger is a carefully (yet imperfectly) constructed puppet. The purpose of this puppet is to “teach the controversy;” to pretend as if there is a debate on whether or not beef/dairy is bad for you. The puppeteers don’t need to win the debate, they only need you to believe there is one.

      … This is the danger of the internet. No one knows who you really are, so large interests can masquerade as actual people: puppets.

      What’s a reasonable person to do when they encounter a possible puppet? That’s a hard question. Certainly the onus is on the reader to look for and find and demand responses to pieces of evidence that the blogger is real instead of just accepting everything on face value.

        1. Bobby, with all due respect, I’m starting to have doubts about your existence as well. Your blog has nearly an identical template and ideology to this one, and, not coincidentally, are actively promoting it on your own! Your blog and twitter account were started within 10 days of each other, and your twitter feed (no offense) basically reads like a spam feed. You don’t seem to have any actual human contacts on it, and you even laughably speak against bill s510, which increases the FDA’s ability to regulate the food industry over food-borne illness and contamination??? And you’re an alleged health nut? LOL, you are making this too easy for us. Whatever company/PR firm you are working for needs to beef up a little on the filling-in-on-the-background-stories.

          Hilariously, despite you both being prolific advisors on how people should become healthy and dispute academia, neither of you seems to exist outside of the blog! Tell you what Bobby, if you’re such an expert on how to live healthily, why don’t you share some of your credentials, or a sliver of evidence that you are a real person?

          1. Ok, not that it counts for much but am I the only one who realizes that Ms. Minger and I are the only two in this conversation with our full names, pictures, websites, etc available for all to see? Personally, I take it as a great compliment that anyone would ever suspect me or my humble blog to be funded or run by some Big Dairy interest. Thanks guys.

            Ian, I’m not about to invite you over to prove my existence however, if this is a fake, call the American Council on Exercise and the American Heart Association and let them know they certified a phony.
            If this doesn’t satisfy you, I’ll have my mom call you 😛

            As far as s510 goes, I oppose it on two fronts. One, granting the FDA more power would mean the end of real, whole foods for the consumers. They would have us all eating out of neatly packaged rations with the perfect, clinically proven macro-nutrient profile. The law was not about food-borne illness. Fact is, those outbreaks come largely from the CAFO type operations they would have us subsidize more and more as we all took up the call to get our energy from grains and soy. You have just shown your true ignorance of how our food-politics works in this country.

            As I said before, I’m all for peer-review but you must maintain common sense. The belief that we can engineer the perfect diet for everybody, or at least a majority is a utilitarian dream. No one thing works for all people and if we sacrifice our true nature at the altar of the lab, we will grow evermore sick as time goes by.

      1. I give up. You figured me out, Andrew. I’m a puppet. A marionette, specifically. I can’t even tell you how hard it is to type with these stupid strings yanking my hands off the keyboard all the time. But your harsh words are hurtful to my fragile puppet ears. Do you not understand how empty my life is? I have no innards. I have no brain. I have no heart. I have no seeing eyes. No one will love me, because I have no soul. No one will talk to me, because my mouth is just a dollop of paint. No one will hold me tenderly, because my body is just a lump of cold, hard wood. I wait in darkness for my puppeteer to lift me up and grant me with momentary motion, with the semblance of life.

        If I had tear ducts, I would weep. Please be gentle with me. I’m antique.

        1. “I’ve got no strings to hold me down, to make me fret, to make me frown…”

          Thank you for that entertainment. Care to respond to my challenges, now? Why you no publish in peer-reviewed journal?

      2. Andrew, I agree wholeheartedly. Peer-review is the standard by which scientific findings become fact. This is especially important in health domains, where people’s reactions to facts can mean the difference between life and death. I believe the purpose of this blog is only to provide plausible deniability to the meat and dairy industry. Ostensibly, Minger might claim to not eat much meat, or oppose factory farms, but these details are meant to obscure the greater purpose of exonerating meat and dairy. Until Minger is able to make an actual “human” appearance and push her work through the normal channels of scientific progress, this blog will remain a shill for snake oil.

      3. Ok Andrew. Thank you for your patience. I have a 9-5 and can’t spend too much time with the back and forth nor can devote too much thought to my arguments. Here is where we left off:

        Andrew says: muddying the waters is an end in itself.
        Bobby says: she hasn’t proven beef/dairy is good for you.
        Andrew says again: she has muddied the waters saying beef/dairy is bad for you. She needn’t prove it’s good for you.

        Bobby says: Sure, if she were a puppet, that would be an effective tactic. It leads people to re-think their assumptions and learnings on diet and health. I fully agree with you on this however, since I have no way of saying for sure if she is who she is, I’ll simply defend her criticisms with my own knowledge of how research gets bought and paid for mixed in with a little common sense. I don’t think you could deny that most of our health troubles today are a result of sacrificing common sense for the sake of the research of the day. If you have enough money, you can fund the research, control the model, hire professional writers to draft the reports and come up with an incomplete study that gets put in to legislation by some tunnel visioned law maker or committee.

        Andrew says: if Minger’s claims held water, they would be published by her or others in peer-reviewed journals; they haven’t been.
        Bobby says: she’s playing a vital role making criticisms of peer-reviewed research
        Andrew says again: if her arguments held water, they would appear in peer-reviewed journals.

        Bobby says: Despite my cynical tone towards research in my last response, I have a deep love of the peer-review process. I feel as you do that societies and science need standards and criteria. You can not get very far on conjecture alone. That said, the system is only as good as the men who run it. If you are the sceptic you have demonstrated on this thread, you will look very closely on the revolving door between the government bureaus, universities and food producers. Research is heavy work with a lot of schooling with little monetary reward unless you align yourself and your work with the dogma of the day. That is why literature like hers is not yet as ubiquitous and the SAD, low-fat, heavy grain literature.

        I may alienate myself a bit here but I’ll use the “climategate” e-mails to show how the peer-review process can be perverted to serve an agenda. Science is no longer sacred my friend. It’s been used for decades for political and fiscal ends.

        1. Bobby: “I don’t think you could deny that most of our health troubles today are a result of sacrificing common sense for the sake of the research of the day. If you have enough money, you can fund the research, control the model, hire professional writers to draft the reports and come up with an incomplete study that gets put in to legislation by some tunnel visioned law maker or committee.”

          This can happen, but if done through normal channels, the source of funding is transparent, and if the results are flawed, they are likely to get discovered by the peer committee. This is an important contract to this rawfoods blog, where such details can be hidden (as in any publication not going through accepted channels).

          Bobby: “Research is heavy work with a lot of schooling with little monetary reward unless you align yourself and your work with the dogma of the day.”

          This is true of the rawfoods blog! Remind me where her money is coming from? Why is “hard work and no money” better when done via a blog than via the peer review process? In addition, you should try familiarizing yourself with actual researchers before making broad claims about the expectation they align with dogma.

          Bobby: “I may alienate myself a bit here but I’ll use the “climategate” e-mails to show how the peer-review process can be perverted to serve an agenda. Science is no longer sacred my friend. It’s been used for decades for political and fiscal ends.”

          Showing a flaw in a system does not prove the system is corrupt. The scientific process remains the best way to vet and disseminate information, and it involves experts with years to decades of training. A blogger can say anything. What if another blogger “debunked” decades of scientific research on the link between lead toys and child poisoning, by identifying and exaggerating flaws in previous studies? Are you going to let your kids play with lead? Experts help the public sort out the explosion of noise and misinformation on the web, and I fear your belief that the science community is broken means everyone simply draws their information from whatever blog that espouses their preexisting viewpoint (e.g., “I don’t want to reduce my consumption meat like my doctor recommends, so I’ll only take my information from rawfoodsos, who says my doctor is an idiot!”)

          I don’t doubt your healthy skepticism about the relationship between big business and government. It needs emphasis that much of the “take-home” message of this rawfoods blog is in support of an immensely profitable meat & dairy industry. In addition, you should be aware that the university system does not enable scientists to pocket money from any funding source. That’s why you don’t see many rich scientists.

          1. How much of the general public actually sees the source of funding? Nobody bothers to look because everybody lies supine when they hear the words, “studies show….”. Sure the peer-review process is a good thing; and the only way we have of establishing truth based on evidence however it only takes one peer-reviewed study that offers no real conclusion save for “a moderately positive association between X and Y” to make policy. It just needs to fall on the right, scientifically illiterate ears of a politician to launch a whole PR campaign for X or Y. We’re just asking people to hear what they learn at school and in the doctors office and hold it up against common sense and their life experience. What we do is empowering to the reader. We’re not telling them how dumb and dependent they are. You’ll never see me advocating any one diet or food group to the masses because that goes against one conclusion I have come to through my healthy criticism and study. People like you, (I used to be one by the way, while I was doing my pre-med studies and just started my job in a pharmacy) look at those who presume to know their bodies better than the Surgeon General with contempt. You counter arguments read like someone defending a certain theology. There is plenty of research to support both of our positions, I’m simply asking the reader to take everything with a grain of salt and educate themselves as the by whom and why our food guidelines are created.

            The academy is paid for by the government or private funding that sets less limits on salary. They do alright without bribes from funding sources. Besides, the people in academia are in it for the immortality anyway. Lobbyists and politicians know this.

            1. I never said people should ignore their life experience. If doctors say wheat is good for you, but you get sick when you eat it, then you shouldn’t eat it (obviously you have an allergy). But a large portion of health effects aren’t measurable by “life experience” until it’s too late. For example, your life experience cannot detect carcinogens in cigarettes, nor cholesterol in beef, nor lead in paint. The medical and scientific communities work hard to learn about these effects and provide them to the public.

              As you mention, I also advocate more information for the public as well. But health information should reach the public through the proper peer-reviewed channels (none of which exclude Minger). Unfortunately, difficult matters involving the synthesis of a large body of research, complex statistics, etc, are beyond the scope of most of our capabilities (i.e., we are not trained to do these kinds of analysis). This is a role that the scientific process fills. That’s why it is important for experts to be involved in the oversight and dissemination of health-based information. For example, do you really think people want to or should learn that lead paint is bad for children based on trial-and-error or their own analysis of both scientific and blog related data?

              1. But your main argument throughout has been, “trust the peer-review process and throw out the rest”. I guess our main point of contention is that I find fault with the process. Your refrain of, “muddy the waters” is a little backwards unless you assume that the “waters” are clear to begin with. If our recent 50 year health history is reflexive of the calrity of “the waters”, I’ll have my drink somewhere else. That somewhere else being blogs like this, traditional medicine, life experience (body awareness specifically I hold the intuitive wisdom of the body above what scientists tell me about long term lifestyle reccomendations. The scientific model just isn’t suited to fully explain the complete span of an individuals life yet, IMHO. I know it sounds a little “fluffy” of an idea but it’s served our species for hundreds of thousands of years and I’m not prepared to chuck it all for the sake of the lateset installment in this UDSA set of dieatary guidelines.

            2. “Nobody bothers to look” is wrong. Peer reviewers look.

              And the incentive is there for people to look; if you’re in academia, and you find a flaw in someone else’s study, or find a conflict of interest, you publish that finding. Your name gets on that finding, it draws the attention of your peers. People cite your paper. You get articles in the NYTimes. Increased exposure makes you more valuable to your university. It also draws job offers from other universities, which you can leverage for a pay raise.

              Nothing is juicier (to scientists) than a retracted paper. Look at the press over the Autism/Vaccine fraud! Peer review is the BEST way to overturn flawed conclusions. It doesn’t perfectly prevent bad ideas from getting out there, but the system does incentivize their correction.

              Don’t suggest that everyone in every university across the world has been bought out by “the government” or “lobbyists.” That’s a dynamically unstable system, like a cartel: there’s so much incentive to break out of the conspiracy (fame for uncovering it) that it couldn’t possibly remain in tact.

              The “fad” accusation is especially ridiculous. How long have people been saying “don’t eat too much saturated fat?” or “Fiber seems to be good for you.” It’s been my whole lifetime. How long did you see people walking around in MC Hammer pants?

              (In fact, most fads come in the form of rapid weight-loss diets — South Beach, Atkins — not the FDA’s recommendations)

              But this is all secondary to my main point, which I’ve stated before and which you’ve still avoided confronting:

              Anyone or any entity can publish something on a blog, but for an idea or an analysis to pass the peer-review process takes a lot more rigor. The criticisms of this blog, if they hold water, are significant enough to be published in dozens of top-notch journals. Why haven’t they been published there?

              I’ll try to guess at your responses to this question:

              a) grand conspiracy to keep this research under wraps.

              Doubtful: Journals have just as much motivation as academians to publish paradigm-shifting analyses. Big Fiber can’t buy out every journal, every editorial staff, every peer-reviewer…

              b) Minger doesn’t feel like putting in the effort to write an article and submit it to a peer-reviewed journal.

              Really? Why has she put so much time into this blog, then? Certainly she already has done the hard part of gathering and analyzing the data.

              c) Minger thinks the peer review process is for losers.

              But then, why hasn’t anyone else stolen her ideas and published them? There are other people who respect peer-review; what has held them up?

              1. So you are saying when she does get her work published in a peer-reviewed journal (if you read her comments you would see this is in the works), it will all be kosher, right? Her peer-reviewed paper would absolutely trump and completely demolish The China Study, a non peer-reviewed diet book, right? A diet book vs a peer-reviewed journal paper would be absolutely laughable, right? I mean ROTFL laughable, right? Open and shut – to anybody concerned about science, The China Study would be toilet paper, right? And then you would go to all the vegan websites, right, and anytime someone mentioned The China Study, you would say ‘OMFG! You are just muddying the waters’, right? And you would spread the word to all the vegans that The China Study was absolutely demolished by real peer-reviewed science, right? And you would tell them to stop muddying the waters on behalf of the PETA lobby, right? And you would tell them if Campbell’s woo-woo holistic science was worth a shit, he would have published his “meat is bad” arguments in peer-reviewed journals instead of a diet book, right? His China Study data peer-reviewed articles would not be about aflatoxin, right? I mean aspergillus is not even a chordate, let alone has a face, right? And you would do all this in the name of good science, right? It would be important to prevent the vegans from muddying the waters with their non peer-reviewed woo-woo science, right? And you would do this, right?

                1. By the time Minger’s article makes it through peer review, my opinion won’t amount to a whole lot, will it?

                  My wager is that it doesn’t make it through peer review, but if it does, then the controversy of Minger’s analysis will get a lot more press than a few comments I could make on her blog.

                  My beef (oh, I kill me!) with Minger is that she’s promoting anti-science. She’s using science sounding analyses to make her readers — and journalists, to boot — to come to the conclusion that nothing can be trusted and that all conclusions are equally valid.

                  “Yeah, well. That’s just your opinion, man.” — The Dude.

                  I say “cheese burgers every day would, on average decrease your longevity”, you say “nuh uh”, and we just have to agree to disagree? We have to conclude that, even if there is a fact to the matter, there’s no way to arrive at it, because studies are just hot air.

                  I say “jump of a bridge, you’ll fall” and you say “nuh uh”, and we just have to agree to disagree?

                  I say “HIV causes AIDS” and you say “nuh uh,” and we just have to agree to disagree?

                  I say “Carbon dioxide causes global warming” and you say “nuh uh.” and we just have to agree to disagree?

                  I say “Dinosaurs used to roam the earth”, and you say “nuh uh,” and we just have to agree to disagree?

                  I say “Microwaves are tuned to the bond-vibration frequency of the O-H bond in water and that’s why they make you’re food warm”, and you say “nuh uh,” and we just have to agree to disagree?

                  Without science, we’re still sacrificing virgins to prevent floods. Minger promotes anti-science.

                  1. I don’t see exactly where you get “anti-science.” Most of her blog posts have argued for better science. Campbell, who Minger spent several blog posts critiquing, is the guy claiming that the whole “correlation is not causation” thing does not apply to his new woo-woo holistic science.

                    The main thrust of Minger’s argument on the USDA is that there is not really much scientific evidence behind many of the recommendations and that there should be better evidence when setting policy and making recommendations. That way you don’t get every restaurant in the country adopting transfat cooking oil. Oops.

                    1. The anti-science happens when health advice is provided in the absence of vetting and debate. I don’t mean debate like you and me arguing on blog comments. I mean debate by experts who have training in biology, nutrition, statistics, etc., not hobbyist bloggers. I welcome Minger to step up her game and elevate this debate to the proper forums.

                    2. The anti-science happens when health advice is provided in the absence of vetting and debate. I don’t mean debate like you and me arguing on blog comments. I mean debate by experts who have training in biology, nutrition, statistics, etc., not hobbyist bloggers. I welcome Minger to step up her game and elevate this debate to the proper forums.

                  2. “””She’s using science sounding analyses to make her readers — and journalists, to boot — to come to the conclusion that nothing can be trusted and that all conclusions are equally valid.

                    “Yeah, well. That’s just your opinion, man.” — The Dude.

                    I say “cheese burgers every day would, on average decrease your longevity”, you say “nuh uh”, and we just have to agree to disagree? We have to conclude that, even if there is a fact to the matter, there’s no way to arrive at it, because studies are just hot air.””” – Incredible shot, Andrew. Was glad someone could finally fucking say this.

              2. No, nice try at the guesses though. The reason this vein of thought is not embraced in the peer-review real is that those reviewers are not exactly the peers of any of the young, up-and-coming academics who share our ideas. I have seen it everyday at my day-job at a national HMO. The review boards are filled with gray haired and bearded PhDs who got to their position on a certain ideology. Anytime they see a paper that is powerfull enough to shake that foundation and challenge their own cirriculum vitae, they are more inclined to find fault where there is none. Science can be spun just like politics. It’s not a rock solid institution. As I said before, either to you or Ian, our main point of contention is that the system works or the “waters are clear”. This stuff is underground because it is in its infancy. Modern medicine has brought about so many unimaginable wonders in recent centuries that we have all become drunk with it’s infallability. We are only starting to see that the recipe does not work. Our epidemic of obesity is not just a matter of will power. I don’t want to see science politicized.

                Oh and to your Autism/vaccine statement. That doesn’t prove your point (that detractors are usually seen as heros and get the fame and NY Times write-ups.) Dr. Wakefeild stood alone and his work was not originally reported with nearly the vigor that the recent “debunking” has been.

  41. I’d like to see evidence that Ian and Andrew are real people. I think they’ve been sent here by the grain industries to try and muddy the waters.

      1. Since the grain industries are the puppeteers of the USDA, and the USDA continually downplays the need for meat and fat it shouldn’t be that hard to imagine. Unless, of course, it’s all meant to be contradictory and therefore cancel each other out, so Americans will just ignore all of it and continue to eat whatever is in their faces! Ah Ha! Thank you for clarifying, Andrew.

        Oh and I almost forgot…

        One more thing….your not even close to wrinkling the image here much less sabotaging it. Better luck next time. There are some excellent propaganda guides out there. I suggest you do your homework and read one so next time your attempt won’t come across so “junior high”-ish.

          1. If they didn’t use it to fatten up livestock they would be trying to sell more to humans. It doesn’t matter if humans or livestock eat it they still make their profit.

            1. The food industry makes money on grains AND meat AND dairy. They sell less than 50% of the grain they produce, but they sell 100% of the meat they produce. The margins of meat sales are also higher than grain sales. Why on earth would they rig the USDA in favor of the less profitable product? Your argument is not only unproven, but it is the less rational explanation.

              1. The margins of meat sales are also higher than grain sales.

                Please stop pulling garbage out of your ass.

                Wheat+industrial seed oils+HFCS+salt+brand name = machine-grown & processed product that never spoils, ships cheap, costs pennies, sells for dollars, and is addictive, spiking blood sugar making people HUNGRIER the more they eat. Grain-based products are pseudo-food made by cynical multinationals for the lower classes (which it is destroying with diabetes.) INSANELY profitable.

                Meat = expensive, labor-intensive, slow to grow, raised by hand, slaughtered by hand, packed by hand, hard to ship, expensive to store, spoils quickly, costs dollars, sells for dollars, NOT brandable, NOT addictive, rapidly QUENCHES hunger UNLESS eaten with carbs. LOW margins.

                1. “Wheat+industrial seed oils+HFCS+salt+brand name = machine-grown & processed product ”

                  You left out the sugar and HFCS, not to mention added flavorings.

          2. lol. Someone is taking themselves way too seriously. Either that or you need to up your calcium intake. Loss of the Funny Bone is one of the first signs of Osteoporosis.

  42. I for one am so incredibly thankful to people like Denise and all the other (nutritional truth seekers) bloggers and writers who are doing the hard work of wading through endless dreary scientific studies. Once they point out the incompatibilities I can see them too. I know in my heart that they are on the right path to truth. Our health is too important to leave it’s fate to fads and fashion. Give me honest solid facts and some common sense. It’s been very hard to know who to trust for a long time when it comes to health. You folks have been a godsend and may you not be thwarted by ignorance….

    1. “Our health is too important to put in the hands of the peer review process. Why should science tell me what to eat when I don’t want to hear it? I’ll just read one blog, assume everything on it is accurate, ’cause I don’t know the statistics to tell if it is or not, and conclude that no one has ever used statistical analysis on these peer reviewed studies. Then I’ll go back to eating my cheese burgers without having to listen to that little angel on my shoulder, thank you very much.”

      1. way to resort to a straw-man Andrew. This tone is more in line with your original comment calling Ms. Minger a fake. Since you are the one who first brought up the issue of puppets and posers, maybe you are just some reactive dude who got himself in to a serious discussion and paid the smart girl down the hall to fight his battles. If not, stick with the serious tone. It suits you better.

        1. Skepticism suits you well, Bobby; it suits humans well. We shouldn’t buy everything we read, and we should leave no stones unturned.

          I don’t have proof I didn’t post Helen’s comment, but I’ll tell you I didn’t.

          For the sake of argument, I’ll go ahead and pretend I did and that she was a strawman I constructed so I could mock it thuroughly.

          So you agree with me, then, that if there were people who just casually read a critique of a scientific study and came to the conclusion that all science is wrong or maybe more specifically, that the science being criticized is wrong, that such a person would be behaving foolishly? Let’s take it a step further: what if a whole society just started doubting science when it suited their purposes? Would they also be behaving foolishly?

          Is there science you trust?

          Helen, do you want to defend yourself?

          1. I do trust science when it confirms common sense. If it is counter intuitive, I ask for furthur explanation. That is all blogs like this do. We hold science to the standard it is designed to satisfy. This argument is not new by any means. Dr. Ignaz Semmelweis died of a beating he sustained at the insane assylum he had landed in due to his hair-brained idea that hand washing was a good medical practice. Read his story if you haven’t already. I’m not saying people like me are modern day Semmelweises; I’m just saying all of your arguments thus far are very simmilar to those of the myopic medical community in 19th Century Hungary.

            1. Common sense is subjective. For example, my common sense would say that milk is an unnatural product. Some caveman, tens of thousands of years ago, saw this fat cow with an engorged teet and thought, “damn that looks TASTY!”. Humans have not evolved to drink another animal’s milk; animal husbandry is a relatively recent innovation for humans. So common sense dictates that a relationship between casein and bad health has evolutionary support.

              1. What you described is conjecture. Common sense is something the majority of the people would agree upon. As applied to the milk issue, you would have to show that there is a clear link between disease and casein relevant enough to overpower our entire human history of consuming it. Once a powerfull enough argument is established and accepted, it becomes common sense. I draw my common sense from both a keen sense of self and an awareness of how those before me approached a particular issue. The statement in this blog post is that the arguments for a low-fat, high grain diet are not yet strong enough to reverse an entire human history of consuming animal products as available. Now, you see, that is not a defense of factory farming. It’s simply a statement that you will not win me over just yet until you satisfy the requirements necessary to prove that God put animals here to make us sick.

                1. Bobby: “Common sense is something the majority of the people would agree upon.”

                  I’m not sure this is an argument you really want to make. By this definition, the world used to be flat (1000 years ago, most people thought it was).

                  Bobby: “As applied to the milk issue, you would have to show that there is a clear link between disease and casein relevant enough to overpower our entire human history of consuming it.”

                  Doesn’t this go against your original point of arguing for common sense? Who has common sense in terms of the relationship between casein and disease? It’s a scientific issue! My point was that, in terms of common sense, milk is not natural. You might pick an apple off a tree and eat it, but I guarantee you would not suckle a cow’s teet. This isn’t rocket science.

                  1. You are missing the point Ian. Common sense holds true only as long as it can be defended. When people thought the Earth was flat 500 years ago, they had no reason to believe otherwise and that belief had no real implications upon their world. When Copernicus came up with valid arguments, he was ridiculed and prosecuted much like Dr. Semmelweiz, Ms. Minger and myself. Don’t you see? You hold the dogmatic “Earth is flat” paradigm to closely to heart for there to be any room for someone to come along and question the only thing you know to be true.

                    To drink the milk of an animal is actually far more common sensical than to pluck the ripened ovary from an apple tree and eat it. I’m ambivalent on the casein issue thus far because I haven’t looked in to it enough. All I know is that milk, butter and ghee have been used to promote health and sustain humans for thousands of years.

                    If real research is what you seek, keep an eye on this guy. His name is Chris Masterjohn and he is a PhD candidate for Bio Chem sciences at UConn. Here’s a snippet from his website:

                    “Other questions, such as what effect different types of processing have on casein’s capacity to promote tumor growth, remain unanswered. Pasteurization, low-temperature dehydration, high-temperature spray-drying (which creates carcinogens), and fermentation all affect the structure of casein differently and thereby would affect its physiological behavior.

                    What powdered, isolated casein does to rats tells us little about what traditionally consumed forms of milk will do to humans and tells us nothing that we can generalize to all “animal nutrients.” Furthermore, Campbell fails to address the problems of vitamin A depletion from excess isolated protein, unsupported by the nutrient-dense fats which accompany protein foods in nature.”

                    View the rest of the article here:


                    1. Not missing any point. You used common sense as a defense of your belief. I argue that common sense is subjective and therefore not usually a reasonable alternative to established, reproducible, scientific results.

                      You countered by limiting your use of common sense to cases in which it reflected majority sentiment. This point is undermined by many historical examples of majority belief being incorrect.

                      Your latest point about common sense being defendable is circular. It is defendable by evidence, than it is actually science. If it is only defendable by subjective reasoning, it isn’t really defendable, it is personal.

                      I believe in common sense in many areas, but I do not consider it to be a very good replacement for scientific evidence, especially on health matters.

                      Also final comment: it is an unfair characterization of Minger and yourself as being “persecuted”. We are disagreeing with you. There’s a difference.

                    2. you are an ass dude. you like to argue with everyone plain and simple. whatever response you give to this is just you being a faggot and nothing more; if no response is given, you are still a faggot.

  43. I will defend myself. I am a scientist myself so am not a total idiot when it comes to the scientific method. I read The China Study two years ago on the advice of my doctor. It sounded valid even though it was in complete contrast to ‘Good Calories Bad Calories’ which I had read 6 months earlier. This plunged me into a dilemma. Two completely contrasting views. Both making sense in their own ways. Since then I’ve read a few dozen books, read thousands of blog postings and listened to countless podcasts. The Gary Taubes, Denise Mingers of the world and all of the members of that community have won me over with their logic and ability to put a very complex concept into perspective. I imagine there’s a lot more to uncover but I’m betting on them to find the truth. Besides, a lot of it is common sense. I don’t want to wait for the “definitive” studies to be done before I start eating healthier. Weston Price witnessed the “truth” decades ago. That truth may be impossible to duplicate through studies that could take the rest of my life to play out.
    In general, I rely heavily on science. Unfortunately science (or the lack thereof) has failed us on this issue….

  44. Since I can’t comment on Ians response to me (a couple comments up) I’ll respond here.

    Ian, nothing I have written here, or ever, calls for the spplantation of science with common sense. My purpose is to remind you that science alone is not useful. Ghandi’s quote comes to mind, “Use truth as your anvil and non-violence as you hammer. Anything that does not stand the test when hammered with non-violence against the anvil of truth-reject it.”

    Replace “non-violence” with common sense and you’ve got my own personal recipe for sifting through scientific literature. Of course you can not just reject a peer-reviewed study because it is proven truth, however, the manner in which it is applied is up to you. This is not “scientific relativism” so much as responsible interpretation and application of the proven revelations of ultimate truth. Most people get so excited when they arrive at a bonafide conclusion that they seek to explain all of reality through that spectrum.

    1. This is silly, Bobby.

      Common sense says the world is flat. Common sense says the shortest distance between two points is a straight line. Columbus disproved the first, Einstein disproved the second.

      Saturated fat is bad for you. This is something Minger wants you to stop believing, and so she tries to appeal to your common sense, and to cherry pick results from a large body of literature. Neither you or I are qualified to tell if she’s misleading us. TW seems to be qualified. Have a look at his/her posts, would you?

      Peer review works because experts evaluate other expert’s work. The system works because there’s huge incentive to discredit faulty results.

      So stop with this “don’t trust science when you don’t want to” rhetoric. It comes off as silly.

      1. Common sense does not confirm the two examples you offered. Once you know about centripital force, gravity and space-time, common sense re-aligns with ultimate truth. It is only through the closing of the mind that allowed for the rejection of a round Earth and the persecution of anybody who refuted a Geo-centric system of planets. If you close your mind the minute you think you know truth, you end up rejecting wisdom for the sake of the latests study. I’ll let the reader decide which approach to science and truth is more silly.

        BTW, it’s not, “don’t trust science when you don’t want to”. Nothing I have said implies that the truth seeker should bring his or her own will in to the evaluation of facts. I would say, “question science when it doesn’t add up against what others have shown and what you experience in real life.” To have such an etherial mind, so as to lie supine to the letters PhD, is foolish. Just because I have no such title does not mean I should be silenced in this debate and leave it to the experts to peer-review, as you have suggested.

  45. () = PubMed reference, ie. (20130097) can be accessed via:

    There are many serious omissions and inaccuracies in Ms. Minger’s review of the recent USDA guidelines, perhaps the most serious are her claims in regards to the two meta-analyses showing the association between saturated fatty acids [SFA] and coronary heart disease [CHD]. The participant size did not significantly differ between studies [n=344,696 and n=347,747], and not only did the results of the more recent (2010) meta-analysis not show the effect on risk of replacing SFA with PUFA [polyunsaturated fatty acids], the authors actually failed to state what calories SFA was compared with. Perhaps if Ms. Minger had kept her ‘eyes peeled’ on major publications, she may have come across a paper from the 26 year follow-up to the Nurses’ Health Study which was co-authored by two of the authors [Hu FB and Sun Q] from the 2010 meta-analysis, that explained that there is an association between SFA and coronary heart disease [CHD], but that the meta-analysis failed to find a significant association because “saturated fat was compared with other calorie sources, primarily refined carbohydrates”.(20713902)
    The other two authors of the 2010 meta-analysis had strong conflicts of interests. Siri-Tarino PW was supported by the National Dairy Council, and the senior researcher Krauss RM reported receiving grants from the National Dairy Council, the National Cattleman’s Beef Association, and the Robert C. and Veronica Atkins Foundation.

    It seems unlikely that the obscured results from the 2010 meta-analysis would play a role in the dietary recommendations for any health authority, and seems more likely that Ms. Minger and her peers have intentionally ignored the editorial by Jeremiah Stamler pointing out the serious flaws and omissions in the meta-analysis, which only a few are listed below:(20130097)

    ‘In univariate analyses of population-based observational data, are there direct relations of dietary SFAs to CHD?
    “…the issue of whether SFA [saturated fatty acids] relates to CHD [coronary heart disease] in univariate analyses is relevant. If findings on this subject are positive but the association is markedly reduced or ceases in multivariate analyses, this may be due to confounding (eg, by dietary cholesterol) and/or overadjustment (eg, by inclusion in analyses of serum total or LDL cholesterol, a major CHD risk factor influenced by SFA intake)… Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, >1.07, which was the estimated CHD RR in the meta-analysis. Do these larger RRs reflect freedom from confounding and overadjustment?”

    ‘Do limitations in quality of dietary data in epidemiologic studies on SFA-CHD influence results?’
    “…the meta-analysis reported its findings as independent of a quality score including diet assessment. Of the 16 CHD studies, 4 relied on one 24-h dietary recall; the SFA-CHD RR was >1.00 for only one of these studies. Seven used a food-frequency questionnaire (FFQ); the RR was >1.00 in 3 of these studies. Five used dietary history or multiday food record; the RR was >1.00 in all 5 studies, even though 3 were adjusted for serum or dietary lipids. These facts, which were unnoted in the meta-analysis, prompt the question: Did low-level reliability (reproducibility) of dietary SFA data drive RR values toward 1.00 (the regression-dilution bias problem)?… The ability to evaluate the validity of dietary data on free-living people is limited; validity was not assessed in the meta-analysis. Also, the meta-analysis says nothing about the problem for the 16 studies of possible bias in SFA-CHD findings due to dietary change (eg, reduced SFA intake) in people with higher serum total cholesterol seeking to lower total cholesterol/CHD risk (as occurred for the earliest of the 16 studies).”

    1. Hi TW,

      Thanks for the comments! I don’t have time (at the moment) for a lengthy back-and-forth, but I’ll try to address some of your points today:

      “not only did the results of the more recent (2010) meta-analysis not show the effect on risk of replacing SFA with PUFA [polyunsaturated fatty acids], the authors actually failed to state what calories SFA was compared with.”

      Absolutely, but the take-home message is that there was no clear connection between saturated fat consumption and cardiovascular disease. If saturated fat is truly a unique and undeniable contributor to heart disease, as the USDA repeatedly claims, then we would expect to find some sort of significant association in an analysis this large. Even if you take a theoretical (and highly unlikely) stance and say that 100% of the saturated fat reduction could have been matched calorie-for-calorie by Wonder Bread, it’s still a slam to the USDA’s guidelines — because their stance on refined grains is far more lax than their stance on saturated fat (“up to half your total grain intake can be from refined grains; you should eat some fortified refined grains for the added nutrients”).

      I’d also point out that the Jakobsen study did not report which forms of PUFAs were replacing saturated fat. If there was any tendency to choose foods that created a better (n-3):(n-6) ratio or even resulted in a net lowering of n-6 (similar to what happened with the Lyon Diet-Heart Study), then the perceived benefit of replacing SFA with PUFA could really be attributed to a simple lowering of omega 6. Both meta-analyses have a lot of question marks. I’m not in some sort of “any amount of dietary PUFA is terrible” camp (though I do believe they’re inherently problematic in large doses) — my main concern is the USDA’s use of studies like this to promote high omega-6 vegetable oils. Google “Israeli paradox” if you want to know what happens when a population reduces saturated fat and loads up on high-omega-6 foods. The result ain’t pretty.

      “Perhaps if Ms. Minger had kept her ‘eyes peeled’ on major publications, she may have come across a paper from the 26 year follow-up to the Nurses’ Health Study which was co-authored by two of the authors [Hu FB and Sun Q] from the 2010 meta-analysis, that explained that there is an association between SFA and coronary heart disease [CHD], but that the meta-analysis failed to find a significant association because “saturated fat was compared with other calorie sources, primarily refined carbohydrates”.”

      Actually, the authors never state that the nonassociation was “because” saturated fat was compared with other calorie sources; they only include that fact as a potential caveat (which I agree is important to consider):

      “A recent meta-analysis reported that saturated fat consumption was not significantly associated with CHD risk; however, in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates, and high intake of refined carbohydrates has been associated with a high risk of CHD.”

      Regardless, there’s a common tendency for researchers to rationalize or dismiss their findings when they don’t jibe with prevailing beliefs.

      “The other two authors of the 2010 meta-analysis had strong conflicts of interests. Siri-Tarino PW was supported by the National Dairy Council, and the senior researcher Krauss RM reported receiving grants from the National Dairy Council, the National Cattleman’s Beef Association, and the Robert C. and Veronica Atkins Foundation.”

      Do you believe the above invalidates the study’s findings? Quite a few of the USDA’s Evidence Library studies were funded by companies with vested interest in the outcome (e.g., from their page on “How are non-caloric sweeteners related to energy intake and body weight?”, the very first study is about the effects of aspartame and was funded by the Ajinomoto Company, the world’s largest producer of aspartame). If you believe studies can automatically be discredited on the basis of their funding, then the USDA’s evidence library just shrunk considerably.

      “It seems unlikely that the obscured results from the 2010 meta-analysis would play a role in the dietary recommendations for any health authority, and seems more likely that Ms. Minger and her peers have intentionally ignored the editorial by Jeremiah Stamler pointing out the serious flaws and omissions in the meta-analysis, which only a few are listed below”

      Not ignored; just disagreed on many points and didn’t find it logical to discuss the many commentaries and replies that the meta-analysis generated. (That could be an entirely new entry in itself.) The focus of this post is on the studies the USDA cited, not an elaborate discussion of the others I threw in as references.

      1. You have ignored many of my points I made about the industrial funded 2010 meta-analysis by claiming that “the take-home message is that there was no clear connection between saturated fat consumption and cardiovascular disease”.
        As Katan MK correctly pointed out that “First, the notion that there exists such a thing as ‘‘the effect of saturated fat’’ is flawed. A lower intake of saturated fat implies an increased intake of some other source of calories to maintain caloric balance. Different substitutions for saturated fat have different effects on risk of coronary heart disease (CHD) and need to be discussed separately.”

        In populations where the majority of energy is consumed from disease promoting foods, it is absolutely essential to clearly state what sources of energy are being displaced, as not doing so may considerably attenuate the relationship between disease promoting nutrients and disease. Unlike the 2009 pooled analysis, the authors from the industry funded 2010 meta-analysis failed to disclose what the calories were displaced, however two of the authors Hu FB and Sun Q who recently co-authored a paper from the Nurses’ Health Study stated that “in this meta-analysis saturated fat was compared with other calorie sources, primarily refined carbohydrates.”

        The researchers do not use to word “because”, but are implying of something more than a “caveat”, as the meta-analysis found a association between SFA and CHD similar to other caloric sources that are associated with a higher risk of CHD. The sentence before this, the authors stated that “Compared with polyunsaturated fat, high intakes of saturated fat and cholesterol have been linked with increased CHD risk.”, implying that if SFA had been compared to polyunsaturated fat which was largely adjusted for in this study, the association between SFA and CHD would have been stronger, similar to that found in the 2009 pooled analysis.

        You seem to have ignored my point that the meta-analysis included results adjusted for confounding and intermediate variables between the SFA-CVD/CHD relationship such as serum cholesterol and dietary cholesterol.
        “Of 15 studies that unequivocally concern the SFA-CHD relation, 4 did not include other dietary lipids or serum lipids among covariates. Their CHD relative risks (RRs) ranged from 1.22 to 2.77—ie, .1.07, which was the estimated CHD RR in the meta-analysis”
        Also the meta-analysis included invalidated studies that are well known to fail to find a relationship between diet and serum cholesterol, and therefore would not be expected to find a relationship between diet and CHD.

      2. Industrial ties does not necessarily mean that the results are automatically invalid, however it is important that these details are disclosed, and it is known that at least Krauss RM failed to originally disclose his conflicts of interest in the meta-analysis, as he has done so in numerous other studies. It is convincing that the conflicts of interests in this meta-analysis were the reason why the authors intentionally ignored well established evidence.
        The authors failed to disclose that SFA was mainly compared to refined carbohydrates and instead attempted to claim that there such a thing as ‘‘the effect of saturated fat’’, and included adjustments for confounding and intermediate variables between the SFA-CHD/CVD relationship, included of invalidated studies, ignored evidence for confounding variables between the SFA CHD/CVD relationship such as dietary cholesterol, ignored possible bias findings due to dietary changes, inaccurately described and downplayed unfavourable studies, excluded some unfavourable studies, and likely used mathematical errors.

        The fact that cholesterol sceptics have posted thousands of posts on the internet citing the 2010 meta-analysis while completely ignoring the editorial makes it fairly convincing that it is intentionally being ignored because of strong unfavourable evidence. Despite the author’s strong efforts to attenuate the SFA-CHD relationship, the fact that there was still a 32% increased risk of fatal CHD completely slams down the cholesterol sceptics who claim that the study is of high quality.
        It should be concluded that the relationship between saturated fat and CVD largely relies upon multiple simultaneous changes in nutrient intake as well as intermediate and confounding variables such as serum and dietary cholesterol and other covariates, whereas the increase risk of fatal CHD may not be explained by serum and dietary cholesterol alone, but also by other factors unadjusted for such as increased inflammation.

        You have a very good point about USDA being too lax about refined grains, but this does not automatically make recommendation to replace SFA with unsaturated fat flawed. Two wrongs do not make a right.

        The quality of the 2009 meta-analysis (Jakobsen et. al) is considered of higher quality as it focused on the effects of displacing nutrients, and being a pooled analysis this allowed for consistent adjustments across multiple studies, although adjustments for dietary cholesterol and fiber would have attenuated the results for displacing SFA with certain macronutrients such as carbohydrates. Also in this study the main source of MUFA was animal fat and therefore greater supports evidence of a relationship between animal fat and CHD, not olive oil as you appear to be claiming.

        This meta-analysis did not report which forms of PUFAs were replacing SFA, but we know that the populations studied have a high n-6:n-3 ratio and therefore can assume that increased PUFA intake were rich in n-6. Studies on non-human primates show that replacing SFA with n-6 rich PUFA protects against atherosclerosis, and randomized control studies [RCT] on humans have found that replacing SFA with PUFA decreases CHD, but have yet to demonstrate the most optimal ratio of n-6:n-3.

      3. The Lyon Heart Study RCT supports evidence that a high n-6:n-3 ratio of 20:1 is may not be optimal, and that SFA should probably be replaced by n-3 rich PUFA and complex carbohydrates, not your belief that SFA intake can be high as long as the n-3:n-6 ratio is maintained. In the large Women’s Health Initiative RCT where saturated fat was displaced mostly by carbohydrates, the researchers found that “Trends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat or higher intakes of vegetables/fruits.”

        I do share your concern about the recommendation of consumed refined oils, and believe more studies need to focus on the effects of n-6:n-3 ratio especially when consumed as whole foods.

        In regards to the paradox of Jews in Israel, both animal and vegetable fat have been associated with significant increases of cardiovascular disease mortality, whereas complex carbohydrates, particularly fruits and vegetables were associated with lower diabetes mortality.

        One of the best cross-culture studies on the Jews dates back all the way to the 1950s comparing Italian and Jewish works in New York where both groups were similar in age, sex, occupation, socioeconomic status, body weight and blood pressure. The Jews had two fold prevalence of heart disease mortality, and while total fat intake of the Jews and Italians were both similar, the Jews consumed a greater amount of animal fat and had higher serum cholesterol levels than the Italians, explaining some of this difference.

        CHD has dropped dramatically in North America and Europe since the 1960’s when animal fat was displaced in favour of vegetable fat even despite a significant increase in obesity and increased intake of sweeteners. Imagine what the decrease could have been if people replaced animal fat, refined oils and sweeteners with fresh produce and continued to exercise.
        A few paradoxes should not be favoured over the preponderance of evidence, and results have not been pretty when SFA has been increased in favour of other nutrients in numerous other populations.

  46. ‘Is the SFA-CHD relation similar for ‘‘hard’’ fatal CHD and ‘‘soft’’ total CHD?’
    “…the meta-analysis did not compare SFA–fatal CHD and SFA–total CHD outcomes (total CHD is undefined). This merits exploration. My calculations, from data for 16 CHD studies (meta-analysis tables), with RRs weighted by person-years of exposure, yielded contrasting CHD risks: for ‘‘hard’’ fatal CHD (11 studies), the RR was 1.32; for ‘‘soft’’ total CHD (5 studies), the RR was 0.99; and for all 16 studies, the RR was 1.09 (compared with the meta-analysis RR estimate of 1.07)”

    In a reply to the 2010 meta-analysis, Katan et al. pointed out that in regards to the use of invalidated dietary measurement assessments, that “Such methods cannot reliably rank individuals by their long term intake, especially within populations with a uniformly high saturated fat intake… Observational studies that used such dietary assessment methods failed to show an association between diet and serum cholesterol concentrations. This shows the shortcomings of such dietary methods, because the effect of diet on serum cholesterol concentrations has been well established in randomized controlled trials. Thus, the lack of a significant association between saturated fat intake and CHD may well reflect the consequences of regression dilution bias.”(20534745) Needless to say with Ms. Minger’s apparent vast knowledge of statistics, she would be aware that such observational studies are subject to the ‘regression-dilution bias’, and that the association of determinants with the disease are likely to be driven down towards a null RR due to lack of control, high quality dietary assessment and adequate dietary assessment follow-ups. The results of the meta-analysis actually suggest that the majority of the CHD studies found a null result because of overadjustment and the regression-dilution bias problem, and that studies with a significant RR reflected freedom from confounding and overadjustment, not publication bias.

    Despite the fact SFA was mainly compared to refined carbohydrates, and the inclusion of adjustments for serum cholesterol and dietary cholesterol, a 32% increased risk of fatal CHD is certainly a cause for concern. In the 2009 meta-analysis it was found that replacing 5% energy from SFA with [mostly refined] carbohydrates decreased CHD mortality by 4% even though adjustments included dietary fiber and cholesterol [which would bias the results in favor of SFA], and for PUFA there was 24% decrease.
    Agreement with the conclusions of the 2010 meta-analysis also requires agreeing that dietary cholesterol intake and serum cholesterol is positively associated with coronary heart disease, and that PUFA, fiber, fruit and vegetable intake is inversely associated with coronary heart disease, as these factors were largely adjusted for in this meta-analysis.

    Although Ms. Minger failed to mention the existence of the editorial by Jeremiah Stamler and the reply by Katan MB et al. to the 2010 meta-analysis, she did cite the editorial to the 2009 meta-analysis also authored Katan MB, but took the author’s statements completely out of context by handpicking a few sentences from the editorial that made it sound as if the author disagrees with the diet-heart hypothesis. Katan MB actually concluded that the real decrease risk of coronary events from replacing 5% of SFA with PUFA is probably closer to what was found in a meta-analysis of randomized controlled trials of 8%,(20351774) rather than the 13% decrease risk that was found in the 2009 meta-analysis.

    1. TW said: “Although Ms. Minger failed to mention the existence of the editorial by Jeremiah Stamler and the reply by Katan MB et al. to the 2010 meta-analysis, she did cite the editorial to the 2009 meta-analysis also authored Katan MB, but took the author’s statements completely out of context by handpicking a few sentences from the editorial that made it sound as if the author disagrees with the diet-heart hypothesis. Katan MB actually concluded that the real decrease risk of coronary events from replacing 5% of SFA with PUFA is probably closer to what was found in a meta-analysis of randomized controlled trials of 8%,(20351774) rather than the 13% decrease risk that was found in the 2009 meta-analysis.”

      I think TW’s critical remark is off the mark here. Denise’s point was that the risk may not be 33%, as stated in the cited study, but rather something possibly more statistically contentious, like 8% or 13%. Whether or not Katan MB agrees with the diet-heart hypothesis doesn’t matter at all. Handpicking is not an issue.

      1. Clearly the take home message from Ms. Mingers article is that replacing SFA with PUFA is not protective.

        Given how she points out numerous times that SFA is related to unhealthy lifestyle habits, the average reader would likely come to the conclusion that Katan MB is indicating that there was no association (not even 8%) when reading the lines “Is this 13% due to residual confounding by imperfectly measured aspects of a healthy lifestyle, or is it real?”.However reading the entire paper would give a completely different message to the one given by Ms. Minger.
        I believe that this was intentional just as the other misinformation througout her article were probably intentional.

        1. The take home message is actually that the USDA’s promotion of industrial/vegetable oils is unfounded and most likely dangerous.

          I don’t believe we *need* high amounts of saturated fat in our diets, but I also don’t believe that exceeding the USDA’s recommended limit is going to do any harm, assuming it doesn’t also go hand-in-hand with worsening the omega 3/6 ratio (such as by saturated fat replacing omega 3 but not omega 6).

          As for saturated fat being uniquely harmful to cardiovascular health, we have enough counter-examples of populations who’ve thrived with ample saturated fat to make this idea either erroneous or incomplete. (For instance — TW, do you have any thoughts on the Kitavans with their extremely high SFA intake and nearly nonexistent rates of cardiovascular disease or diabetes?)

          1. The Kitvans consume 95% of their calories from whole plant foods, and the majority of their saturated fat is derived from intact coconuts, not refined oil or animal fats. Their intake of ruminant and industrial trans fats are next to none, and the intake of dietary cholesterol and salt is very low, whereas dietary fiber and phytochemical intake is very high. They also consume a relatively low calorie diet, and although approximately 17% of energy intake is derived from SFA, the actual amount of energy derived from SFA is probably similar to that of many developed nations, which is probably not considered as being “extremely high”.

            It is not surprising that some populations may avoid cardiovascular with a healthy diet including modest amounts of unrefined coconut, and is consistent with animal studies which show that saturated fat have a less effect on the progression of atherosclerosis in the absence of dietary cholesterol. Nevertheless it would be interesting to see a large scale autopsy study on the Kitvans as well as validated age-related CVD rates in Kitava.
            Populations in and around Papua New Guinea and Fiji have high rates of smoking yet low rates of cardiovascular disease and tobacco related cancers. This does not automatically mean that smoking does not increase the risk of developing these diseases. The low rates of these diseases in these populations can in part be explained in part by their high intake of vegetables.
            A few studies should not be favored over the preponderance of evidence, as tobacco skeptics also point out numerous paradoxes to claim that tobacco is actually health promoting rather than disease promoting, such as numerous frauds among the board of the Weston A. Price Foundation including Barry Groves and William Campbell Douglaass.

            Here is a paper reviewing numerous autopsies of well preserved ancient Eskimo’s, showing that they had severe atherosclerosis and osteoporosis even when they were consuming their traditional diet high in animal protein and fat and free of all the foods that you claim to be disease promoting.

            It is important to note that the author confused the diets of the ancient Egyptians mummies with atherosclerosis who were the elites in Egypt with plant based diets of the lower class. Several years after this study was published, another study found that trace elements in the hair of the Egyptian mummies confirmed that the Egyptian elites actually consumed diets relatively high in animal protein and fat, which is consistent with estimates based on hieroglyphic inscriptions. Furthermore there is a lack of atherosclerosis found in less well-preserved remains of the lower class Egyptians.

        2. TW said: “However reading the entire paper would give a completely different message to the one given by Ms. Minger. I believe that this was intentional just as the other misinformation througout her article were probably intentional.”

          I think it’s too much to read sinister intent into the way a few sentences in a lengthy blog post were written. I also would not assume Denise is being intentionally misinformative without giving her a chance to participate in the conversation. I find Denise is remarkably courteous and fairminded in her exchanges with respondents, whether they agree with her or not. Would that all interlocutors were to extend the courtesy in kind.

  47. In regards to the USDA’s strong body of evidence linking SFA and CHD, Ms. Minger quoted that “The answer may lie in their evidence summary page, which recaps the 12 studies they looked at to assess saturated fat”. The USDA clearly cited 24 studies in the ‘evidence summary page’ link that she provided, including 12 studies linking saturated fat and type 2 diabetes risk that she failed to mention, which the USDA made clear in their conclusion as part of the reasoning for the recommendations.
    On the “fatty acid page”, that she also provided a link for, the USDA stated that “the conclusions expressed in the 2010 DGAC report are informed by evidence compiled for the 2005 DGAC report, but are based primarily on Nutrition Evidence Library (NEL) evidence gathered and reviewed since 2004.”. There is a large body of evidence published prior to 2004 associating SFA with CHD that has refined the dietary recommendations over the decades, including well controlled metabolic ward studies. A meta-analysis of metabolic ward studies including 395 dietary experiments showed that SFA does significantly elevate cholesterol, and that SFA decreases the HDL:LDL ratio when replaced by PUFA and MUFA and to a degree complex-carbohydrates, and that dietary cholesterol also decreases the HDL:LDL ratio.(9006469) Another review found that both industrial and ruminant sources of trans fats also decrease the HDL:LDL ratio.(20209147) Numerous controlled studies have also linked SFA with other markers of cardiovascular disease, such as the down-regulation of LDL-C receptor activity, and impairment of endothelial and HDL-C functionality,( 9478045, 19328268, 18195164, 15774905, 16904539) suggesting that a high HDL-C achieved in the presence of a high intake SFA is not protective. Ms. Minger’s statement that “the lipid hypothesis in all its unproven, scientifically-feeble glory” is unfounded without taking these studies into account, especially considering that she ignored the large body of evidence linking dietary cholesterol with heart disease and excess mortality.(21076725, 20130097, 9094885, 21135028)

    Ms. Minger describes a pie chart on page 28 of the guidelines that show the “Sources of Solid Fats” claiming that it represented sources of SFA, where it actually included industrial trans fat. “Sources of Saturated Fats” was on page 26 of the report, which showed that cheese is the second-largest contributor to America’s saturated fat intake, whereas grain-based desserts were in fourth place.
    She seems to be claiming that studies tend to find a association between SFA and disease because the major sources of SFA are derived from junk foods, but failed to mention that this is also true for PUFA and MUFA,* which are often associated with better health outcomes in studies when used to replace SFA.

    Ms. Minger also pointed out studies that show that corn oil promotes prostate tumor growth in mice. Refined oils are poor sources of nutrients, and should be replaced with nutrient dense nuts and seeds, of which walnuts have been shown slow prostate tumor growth in mice.** In humans elevated IGF-I is constantly associated with prostate cancer,(19142965) and various other cancers,(15110491) and diets high in essential amino acids, especially dairy protein are strongly associated with IGF-I.(18843793, 12433724, 10883675, 19746296) She failed to mention that human studies have linked SFA with various cancers, neurological disorders, and increased bone loss and hip fractures.(14583769, 8230280, 10528026, 19010900, 19336640, 12580703, 9392577, 10661654, 20980487, 9932142, 16365076)

    1. I am enjoying this debate. I can only offer non-technical comments.

      TW said: “The USDA clearly cited 24 studies in the ‘evidence summary page’ link that she provided, including 12 studies linking saturated fat and type 2 diabetes risk that she failed to mention, which the USDA made clear in their conclusion as part of the reasoning for the recommendations.” While the USDA is making general dietary recommendations concerning saturated fat, part of their case is its relation to heart disease. And they list their supporting studies under two headings – “Cardiovascular Disease (CVD)” and “Type 2 Diabetes.” It appears that the focus of Denise’s post is sfa’s connection with CVD. To that extent, it seems reasonable that her focus was on the 12 studies under the CVD heading. Time and space limitations may have precluded an examination of the other 12 studies. But even if Denise had/has no plans/time to conduct one, it seems worthwhile to review the studies that the USDA points to as supportive of the CVD claims.

      1. It does seem that her focus was under the CVD heading but did not make this clear in her post stating that “As best I can tell, these [12] studies are the main pieces of research the USDA used to back up their “replace saturated fat with unsaturated fat” recommendation”. This statement is misleading and simply is not true.
        Remember that she also omitted the T2D study on the PUFA page and stated “Of the 10 polyunsaturated fat studies in the Evidence Library, not all were relevant to heart disease. Here are the ones worth looking at: “. Considering T2D significantly increases the risk of CVD and judging by her post, it would seem that she may have intentionally ignored the studies as they may have been more difficult to downplay, rather than the fact that her post was already long. Most readers are already aware of the lipid hypothesis, but however are still unaware about the relationship between SFA and T2D, making these studies easy to ignore.

        1. Covering the single T2D study in the PUFA summary would not have made a big difference in the size of the post, and she simply ignored this study just like she ignored the 12 T2D studies in the SFA summary.

          1. It wouldn’t have made a difference in length, but it would have made a difference in the direction of this blog post. I chose not to include any fat/diabetes studies rather than put only one in and omit the rest for saturated fat.

            1. The single study in the PUFA summary should have been covered under the Polyunsaturated Fat section of your post, but instead you claimed that it was not relevant to heart disease and was not worth looking at.

              1. Stop being a fuckin dick, TW. “TW” stands for “Tiny Wiener” in your case. And stop calling her “Ms. Minger”; that shit is annoying as fuck – you aren’t her dad, just call her Denise, Neisy, or whatever goofy ass nickname she wants to be called. And HEY…just because she doesnt know what she is doing, doesnt mean she did anything wrong on purpose! So go give your tranny mom head (again), and eat shit (like usual). Rant over.

        2. Again, the context of what you quoted:

          “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.”

          Does that not make it clear enough that the focus is going to be on the heart disease link?

          1. Type 2 diabetes is a well established risk of heart disease, and cannot be ignored when assessing the risk of heart disease.

            You also state “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.”

            The USDA stated:
            “Strong evidence indicates that dietary saturated fatty acids (SFA) are positively associated with intermediate markers and end-point health outcomes for two distinct metabolic pathways: 1) increased serum total cholesterol (TC) and LDL cholesterol (LDL-C) and increased risk of cardiovascular disease (CVD) and 2) increased markers of insulin resistance and increased risk of type 2 diabetes (T2D). Conversely, decreased SFA intake improves measures of both CVD and T2D risk. The evidence shows that a five percent energy decrease in SFA, replaced by monounsaturated fatty acids (MUFA) or polyunsaturated fatty acids (PUFA), decreases risk of CVD and T2D in healthy adults and improves insulin responsiveness in insulin resistant and T2D subjects.”
            Does this not make it perfectly clear that the USDA recommendations to “replace saturated fat with unsaturated fat” are due to both the adverse effects on serum cholesterol and markers of type 2 diabetes risk?

            It is painfully obvious that you are intentionally pushing a preconceived bias favoring saturated fat and animal foods, as can be easily seen in your fraudulent claims in regards to the pie graph showing ‘Sources of Solid Fats’. It seems possible that you found it more difficult to downplay the studies in regards to risk markers of T2D and therefore decided not to cover them.

            1. TW — I enjoy your comments and am glad to have you around. But the accusations of me being intentionally fraudulent aren’t really pushing the discussion forward. If you read my back-history or current diet on this blog, you’ll see that I eat zero dairy and only small amounts of animal products, and don’t promote a single diet (much less one high in animal products). If you’re a produce-loving vegan, my diet is probably not all that far off from yours.

              The pie graph, as I noted below, was a blooper on my part, but even using the correct chart doesn’t alter the figures considerably. The main source of saturated fats in the diet of Americans are what would be considered “junk” foods. The point stands. 🙂

    2. TW said: “On the “fatty acid page”, that she also provided a link for, the USDA stated that “the conclusions expressed in the 2010 DGAC report are informed by evidence compiled for the 2005 DGAC report, but are based primarily on Nutrition Evidence Library (NEL) evidence gathered and reviewed since 2004.”. There is a large body of evidence published prior to 2004 associating SFA with CHD that has refined the dietary recommendations over the decades, including well controlled metabolic ward studies.” [discussion of some of those studies follows]

      Denise’s post is largely a critique of the USDA’s claimed support for the connection between SFA and heart disease. And if they say that their conclusions are based primarily on evidence gathered and reviewed since 2004, then what else can such a critique do but take them at their word? If the USDA had cited other studies, I imagine Denise would have looked at those, too.

      Of course, there are further questions that can be explored. We can ask: is there support for a connection between SFA and heart disease, whether that support is cited by the USDA’s 2010 guidelines or not? TW’s pre-2004 citations show that he/she is going in that direction. I would guess that Denise is just as interested in that as TW. Perhaps that will be the focus of her next 30 posts. 😉

      In connection with the question above, we might also want to ask: is the USDA a competent defender of its own claims? Maybe not. But looking at what the USDA actually says is quite blogworthy.

      Frankly, if the case presented by the USDA in their own guidelines falls apart – and I am not claiming that it does – that looks pretty bad. From the standpoint of an observer, a failed case is worse than no case at all: it suggests that the hypothesis may not be defensible.

    3. “In regards to the USDA’s strong body of evidence linking SFA and CHD, Ms. Minger quoted that “The answer may lie in their evidence summary page, which recaps the 12 studies they looked at to assess saturated fat”. The USDA clearly cited 24 studies in the ‘evidence summary page’ link that she provided, including 12 studies linking saturated fat and type 2 diabetes risk that she failed to mention, which the USDA made clear in their conclusion as part of the reasoning for the recommendations.”

      If you read the full paragraph you grabbed that quote from, the sentence right before it says “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?” Hopefully that indicated clearly enough that the saturated fat studies I wanted to look at in this blog post were the ones focused on heart disease. Examining the 12 diabetes studies would be interesting, and will be the subject of a future blog post, but including them in this one would mean adding another 3,600 words and many hours of research and typing (unfortunately, blogging is my spare-time pursuit and not my day job).

      “There is a large body of evidence published prior to 2004 associating SFA with CHD that has refined the dietary recommendations over the decades, including well controlled metabolic ward studies.”

      My focus in this article was on the specific studies the USDA cited as evidence — not research they didn’t use.

      “A meta-analysis of metabolic ward studies including 395 dietary experiments showed that SFA does significantly elevate cholesterol, and that SFA decreases the HDL:LDL ratio when replaced by PUFA and MUFA and to a degree complex-carbohydrates, and that dietary cholesterol also decreases the HDL:LDL ratio.(9006469) Another review found that both industrial and ruminant sources of trans fats also decrease the HDL:LDL ratio.(20209147)”

      These don’t suffice as evidence that saturated fat is actually unhealthy to cardiovascular health (see comment on lipid hypothesis below).

      “Ms. Minger’s statement that “the lipid hypothesis in all its unproven, scientifically-feeble glory” is unfounded without taking these studies into account, especially considering that she ignored the large body of evidence linking dietary cholesterol with heart disease and excess mortality.(21076725, 20130097, 9094885, 21135028)”

      TW — the lipid hypothesis IS unproven (and isn’t about dietary cholesterol, so I’m not sure why you cited those studies — although it’s interesting that the third one found that saturated fat significantly protected against intima-media thickness progression). I know some anti-lipid-hypothesis folks argue that blood lipids are completely irrelevant; I don’t agree with that and I think there are elements of it that are valid (and that are part of the reason cholesterol profiles have any association with heart disease risk). But the bulk of the evidence points to oxidized LDL and small, dense LDL rather than LDL concentration being the culprit, and this is why PUFAs seem so suspect. Oxidized LDL forms when LDL particle lipids (more specifically, the unsaturated fats — saturated fats are structurally resistant to oxidative damage) degrade after reacting with oxygen. The main PUFA in LDL is linoleic acid, the one that’s super high in most vegetable oils. (This is all stuff the USDA ignores!)

      Oxidized LDL alone has been shown to be a better indicator of heart disease than the traditional combo of total cholesterol, HDL, blood pressure, age, diabetes, and smoking status ( and is a hugely better predictor of heart disease than the typical lipoprotein profile and common heart-disease risk factors ( The evidence for oxidized LDL is much much much greater than simple LDL concentration or ratios with HDL/LDL/total cholesterol, both on a research level and “biological plausibility” level. (If you’re at all interested in the mechanism, I can send you some references when I have a bit more time). Bottom line — I’ve never seen any sort of plausible link between saturated fat and oxidized LDL, but the link with PUFAs is clear. LDL can’t just randomly attach itself to artery walls and cause heart disease because of its excess; but oxidized LDL puts all the elements in place (it damages arterial walls, promotes inflammation, turns macrophages into foam cells, and triggers a host of responses involved in all stages of atherosclerosis).

      LDL density is also an issue, since small, dense particles seem to be more prone to oxidation and is also more likely to get stuck in the subendothelial space. Incidentally, saturated fat tends to promote *larger* LDL particle size ( Dr. William Davis (Heart Scan Blog) notes that the effect of saturated fat may be dependent on your dominant or genetically-determined form of LDL, which is something I haven’t studied enough to comment on myself — but it seems possible that the folks disposed to LDL-subclass pattern B (who are a population minority) may respond differently to saturated fat than pattern A people.

      Regardless — there is definitely research out there contradicting the idea that replacing saturated fat with polyunsaturated fat is healthier (e.g. — postmenopausal women saw an increase of atherosclerotic progression when PUFAs replaced other fats), and the lipid hypothesis has far too many holes to be accepted as gospel.

      “Ms. Minger describes a pie chart on page 28 of the guidelines that show the “Sources of Solid Fats” claiming that it represented sources of SFA, where it actually included industrial trans fat. “Sources of Saturated Fats” was on page 26 of the report, which showed that cheese is the second-largest contributor to America’s saturated fat intake, whereas grain-based desserts were in fourth place.”

This was my error, and I appreciate you pointing it out. I used the wrong chart. I’ll fix it on the blog post tomorrow. Looks like 39.5% of saturated fat comes from non-animal, sugary-animal, or processed meat sources, 18.7% comes from dairy, and 17.2% comes from other animal sources that are either eaten alone or “mixed” with undetermined ingredients (and then the mysterious 24.5% encompassing “all other food categories”). The ratios are a bit different, but there are still more saturated fat calories coming from “junk” than coming from animal foods.

      “Ms. Minger also pointed out studies that show that corn oil promotes prostate tumor growth in mice. Refined oils are poor sources of nutrients, and should be replaced with nutrient dense nuts and seeds, of which walnuts have been shown slow prostate tumor growth in mice.**”

      The point of the comparison was that refined polyunsaturated fat (corn oil) promoted tumor growth, while refined saturated fat did not. I agree with you that most refined oils are poor sources of nutrients and personally advocate whole foods.

      1. P.S. Thanks again for the discussion. Quick request — if you could post links (when possible) to the full-text of studies instead of the Pubmed IDs, it would save me a lot of time and I’ll hopefully be able to reply to your comments in greater depth. I haven’t had time yet to look up the all of studies you’ve referenced, and probably won’t until I get back to Oregon, but I want to thank you for your detailed comments and citations. Debate like this is incredibly useful, and I think having ideas ‘challenged’ is one of the most important things to happen in the nutrition community.

        1. There is strong evidence that endothelial dysfunction is associated with increased risk of cardiovascular events, atherosclerosis progression and erectile dysfunction, and saturated fat has constantly been linked in controlled studies to endothelial dysfunction when consumed in a variety of diets including very low carbohydrates diets during both weight loss and weight maintenance.

      2. Dietary cholesterol is considered part of the lipid hypothesis which dates back approximately one hundred years when Anitschkow induced atherosclerosis in rabbits by the ingestion of cholesterol. Dietary cholesterol is an important confounding variable for SFA intake, and there is convincing evidence from animal experiments including non-human primates that dietary cholesterol in the presence of SFA induces atherosclerosis. A higher intake of saturated fat is also likely to be associated with higher intakes of disease promoters such ruminant trans-fats, heme and sodium, and lower intakes of health promoting nutrients such as dietary fiber and phytochemicals.

        The third study you referred to, the authors stated that “increased intakes of stearic acid and monounsaturated fat relative to saturated fat consumption were significant predictors of a reduction in the annual rate of carotid artery IMT progression.” The study found that stearic acid which does not elevate serum cholesterol is less harmful than other chains of SFA, and clearly does not show that SFA as a whole is protective especially considering the fact that dietary cholesterol was found to be a strong promoter of intima-media thickness progression. The main dietary related recommendations that can be concluded from this study is that dietary cholesterol should be significantly restricted and that SFA should be replaced with MUFA, which is why cholesterol sceptics do not cite this study.

        In regards to your theories on LDL, it is important to recognize the there is a strong dose-relationship between, total cholesterol, LDL, and especially the total cholesterol:HDL ratio and cardiovascular disease that would not exist if oxidized and small LDL particles were the only major predictors of disease.
        It is also important to recognize that virtually all free-ranging mammals, including carnivores, omnivores, herbivores and non-human primates have very low serum cholesterol levels, suggesting that the low serum cholesterol would also be optimal for human health.
        Regarding LDL particle size, a systematic review of studies from 1950 to 2009 found that the LDL number not LDL size was a strong predictor of heart disease. There is insufficient evidence that LDL density should be a major focus of disease prevention, and this theory tends to be focused more on by industry paid researchers such as Krauss RM.

        Initial findings do provide some evidence for an independent relationship between oxidised LDL and heart disease, but have yet to provide sufficient evidence to be favoured over other established risk factors of heart disease. It is however important to consider that numerous micronutrients in whole foods including nuts have been shown to protect against PUFA oxidation while also having a favourable effect on the total cholesterol:HDL ratio.

        Nevertheless saturated fat still has a negative effect on the serum lipids and type 2 diabetes risk factors, which are established risks of cardiovascular disease.

        As I previously stated, SFA and dietary cholesterol have also been associated the down-regulation of LDL receptor activity as well as impairing the anti-inflammatory properties of HDL, which provides evidence that SFA increases risk the of cardiovascular disease independently of the negative effect it already has on serum lipids levels.

      3. Saturated fat and dietary cholesterol intake have also been related to worsening of numerous other cardiovascular risk factors such as increased blood pressure, increased risk of microalbuminuria, increased body weight, increased arterial stiffness, and accelerated thrombus formation.

        I will accept your mistake as I may have made a few in my posts as well. However the intake oleic acids, n-6 and ALA are also mostly from disease promoting foods, and it appears that less than 10% of energy are probably derived from whole plant foods.

      4. In regards to the last study you cited about atherosclerosis progression in post menopausal women, there are significant limitations in this study due to the fact that the selection process of participants are limited to those with preexisting coronary artery disease. When studies measures base line dietary and lifestyle habits of people with preexisting heart disease, the participants with greater risk factors of fatal heart disease are likely to be underrepresented in the study and tend to be limited to those with favorable genetics as they have avoided fatal disease up to the base line of the study despite being at high risk. These people are then compared with people who have heart disease despite having lower risk factors and therefore are likely to have unfavorable genetics. There are numerous large studies, including one with nearly 50,000 participants with a similar selection process which have found that smokers have better survival rates than non-smokers, known as the “smoker’s paradox”. One large angiography study found that smokers had less disease than non-smokers, and that greater number of pack-years, duration of smoking and peak daily cigarette consumption were all related to less disease. It is well established that smoking increases the risk of heart disease, and perhaps the best explanations for this paradox is that smokers are underrepresented due to higher rates of fatal CHD prior to base line of the study, limiting smokers in the study to people with favorable genetics.

        This would question as to how this study should have adjusted for habits that are associated with fatal CHD such as smoking, as adjusting under the assumption that smoking promotes disease could attenuate results and make a disease promoter appear health promoting. It is important to look at the unadjusted results, as the participants in second to forth quartiles of SFA intake all had the same amount of progression, but after adjustment for covariates the progression of disease in the groups who consumed more SFA attenuated as SFA correlated with other habits normally associated with disease progression.
        The fact that LDL cholesterol was actually lower in the group with the highest smoking rates and the highest intake of saturated fat, trans-fat and dietary cholesterol, and lowest dietary fiber intake despite insignificant differences in BMI indicates the likelihood that either that the dietary measurement methods used were very inaccurate or that the people in the quartiles of higher SFA intake had favorable genetics.
        It should be noted that the groups that consumed the most SFA had a two fold increase of diabetes compared to the group that consumed the least despite similar average BMI, but the authors adjusted for this even though it is considered an intermediate variable between the SFA-CHD relationship.
        It is therefore very likely that in studies where the participants have heart disease at base-line without using a dietary intervention, that such paradoxical results are to be expect, and in this study increased intake of trans fat, having diabetes and being a current smoker were all associated with less progression of disease.

        Here are other studies showing a relationship between saturated fat and increased progression of atherosclerosis in humans, including studies with larger participant numbers, better validated dietary measurement methods, and dietary intervention studies.

      5. Saturated fat also promotes diseases through other various means, for example SFA is decreases IGFBP-3, while animal protein increases IGF-1 which are strong predictors of cancer risk in humans.
        Also as I previously mentioned a lot of commonly consumed food rich in [but not limited to] saturated fat tend to be high in Advanced Glycation End Products, which is why Dr. Davis agrees that butter is disease promoting.

  48. In regards to the studies on PUFA cited by the USDA, Ms. Minger omitted one study relating to diabetes risk and one study on inflammatory and cardiovascular risk factors. Is she claiming that such risk factors are not “relevant to heart disease”?

    In regards to the first paper on polyunsaturated fat Ms. Minger cited, although the study may not justify replacing seeds with seed oils, it did show between a near significant and significant inversed association between PUFA and mortality, with one interesting point she omitted was that “Men with energy-adjusted dietary PUFA intake in the upper third had less than half the risk of premature CVD mortality as men with intake in the lower third, even after multivariate adjustment”
    Serum fatty acids indeed “showed more robust associations”, and the researchers found that “Serum esterified PUFA proportions were even more strongly associated with CVD mortality than dietary PUFA intake”, and found similar results for the PUFA/SFA ratio. The researchers stated and backed-up with references that “Serum esterified fatty acid proportions are thus a good measure of habitual dietary fat composition”. It is quite likely that serum fatty acids may more accurately reflect long term fat intake than the single 4-day food record used in this study, and therefore may have more accurately reflected “the effect of actual fat intake on heart health”.

    In regards to Ms. Minger comment on the 20 year follow-up to the Nurses Health Study, she quoted that “saturated fat and monounsaturated fat were not statistically significant predictors of CHD when adjusted for nondietary and dietary risk factors.“ The results actually showed that SFA was not significantly associated with CHD compared to carbohydrates [mostly refined] after adjustment for multivariate analysis which included dietary cholesterol. PUFA however was associated with a significantly lower rate of CHD compared with other sources of energy including SFA despite adjustments for dietary cholesterol. In the 26 year follow-up of the Nurses’ Health Study study, it was found that red meat and high fat dairy showed the strongest association with CHD compared to other protein rich foods, whereas nuts and beans showed the strongest inverse association.(20713902)
    Also in the 18 year follow-up of the Nurses Health Study among women with type 2 diabetes, dietary cholesterol and SFA significantly increased the risk of cardiovascular disease compared to virtually all other macronutrients.(15159229)

    Fruits and vegetables contain tens of thousands of phytonutrients, many still undiscovered that work together in an extremely complex manor to combat disease. The complexities of these foods are so great that scientists are not yet sure of the exact mechanism that combats disease. Fruits and vegetables have consistently shown in meta-analyses to show a reduction in cardiovascular disease and cancer, that clearly show that optimal intake is above 5 servings a day.(17443205, 16443039, ***) Suggesting that any less may be optimal is to ignore a large body of research.

    1. TW said: “Fruits and vegetables contain tens of thousands of phytonutrients, many still undiscovered that work together in an extremely complex manor to combat disease. The complexities of these foods are so great that scientists are not yet sure of the exact mechanism that combats disease. Fruits and vegetables have consistently shown in meta-analyses to show a reduction in cardiovascular disease and cancer, that clearly show that optimal intake is above 5 servings a day.(17443205, 16443039, ***) Suggesting that any less may be optimal is to ignore a large body of research.”

      I didn’t see that Denise said people should eat less or even suggested the possibility. Having read some of Denise’s other posts, I take her to be quite a fan of fruits and veggies. Denise merely pointed out that the USDA said that they are unsure of the mechanism by which fruits and veggies promote health, and that fruits and veggies may – speaking with methodological scruples – promote health by displacing other foods.

      Knowing the Denise has no problem with f and v, she is most likely making the broader point that the USDA (admittedly) makes dietary recommendations without knowing exactly why.

  49. Although the scientific literature does not support the recommendation for whole grains to play a more dominant role in the food pyramid than fruits, vegetables, nuts and probably legumes, the literature clearly show that they are more health promoting than foods rich in saturated fat and dietary cholesterol.
    In a recent paper from the NIH-AARP study containing over 300,000 participants it was found that intake of cereal fiber significantly decreased all cause mortality after adjusting for confounding variable.(21321288) The same was found in another recent paper from the Nurses’ Health Study containing over 50,000 women, which showed that cereal fiber significantly decreased all cause mortality independent of numerous factors including the glycemic load, and therefore independent of refined carbohydrate intake. It was also found that dietary cholesterol was associated with increased all cause mortality, whereas PUFA also decreased all cause mortality independent of all other factors, but not to the extent found when replaced by an equivalent calories from nuts.(21135028) The recommendation therefore should not be to increase seed oils, but to increase the intake of nuts and seeds.
    Ms. Minger makes some remarks about studies showing that Paleo and low-carbohydrate diets improving disease risk factors. Studies on Paleolithic diets often show in improve risk factors during weight loss and while consuming a reduced calorie diet lower in SFA intake and higher in fruit and vegetable intake.(19604407) Low carbohydrate diet studies that find improved risk markers of disease, the participants are either consuming relatively low amounts of SFA, or the lowered risk factors are directly related to the amount of weight loss rather than the health properties of the diet.(19506174, 1386186, 12975389) High SFA low carbohydrate diets clearly show increased risk markers of disease in the absence of weight loss, although some studies find increased risk even in the presence of significant weight loss.(19328268, 15774905, 12091753)
    Autopsies on persevered ancient Eskimos bodies including pre-European Eskimos clearly showed that they had severe atherosclerosis and osteoporosis, which can mostly be related to their traditional high cholesterol low carbohydrate diet.(8298320)
    Jeremiah Stamler pointed out that “Serum total cholesterol, LDL cholesterol, triglycerides, glycated hemoglobin, uric acid, and fibrinogen were lower in Japanese in Japan than in Japanese Americans in Hawaii [who’s carbohydrate intake is significantly lower], and HDL cholesterol was higher (in men) or as high (in women)—ie, with no evidence of carbohydrate-induced dyslipidemia/metabolic syndrome.”(20130097)

  50. Ms. Minger’s description of dairy studies contains numerous omissions, including the 2009 review of dairy studies authored by individuals related to the dairy industry such as Kruass RM. It is well established that not all chains of SFA elevate LDL-C but that all forms of high fat dairy contain significant amounts of the LDL-C elevating chains of SFA, and the authors of the review did cite metabolic studies that backed this up. However the authors then went on to cite some observational that are known to fail to show the relationship between diet and cholesterol levels, perhaps to intentionally downplay the effect of dairy fat on LDL.
    The researchers cite three cross country studies showing a favorable association with cheese and CHD.
    The first study compared cholesterol and saturated fat intake in 40 countries, and found that milk and butterfat were associated with increased CHD mortality, and that there was a small inverse association for cheese, which became positive after excluding France and Finland from the analysis. In regards to the SFA paradox between France and Finland, the authors explained that “This paradox may be explained as follows. Given a high intake of cholesterol and saturated fat, the country in which people also consume more plant foods, including small amounts of liquid vegetable oils, and more vegetables (more antioxidants) had lower rates of CHD mortality.”(8252690)
    The second study was similar to the first one, and the authors stated that “From the Seven Countries Study and recent statistics from WHO and the OECD, it is clear that saturated fats, mainly dairy fats, are closely associated with the mortality rate from ischaemic heart disease (IHD).”(2650697)
    The third study found the researchers stated that “cheese was negatively correlated, though not strongly”, and go on to conclude “We suggest that non-fat aspects of milk, particularly the Ca/Mg ratio, lactose and MFGM antigens, have specific coronary atherogenic effects, both biochemical and immunological, and the simultaneous attack from these three directions may explain why this foodstuff has such a strong effect. Wine appears to be an antidote for the harmful effects of milk.”(12559541)

    Low fat dairy and calcium have been shown to reduce the risk colorectal cancer, which is probably in part due to its effect on inhibiting the absorption of heme in red meat which has been linked to cancer in both observational and experimental studies.(21209396) There is conflicting evidence between the association between high fat dairy and colon cancer as numerous studies have linked it with higher risk.(12548291) Also, a 65 year follow-up found that the participants who consumed the largest quantity of dairy as a child had a nearly 3 fold risk of developing colorectal cancer as an adult, which is consistent with the fact that adult attained height is an established risk factor for colorectal cancer.(18065592) Agreement with the conclusions of the study on colorectal cancer she cited requires agreeing that red meat increases risk and fiber decreases risk as these factors were adjusted for in the study.
    Of course she failed to mention that other meta-analyses and numerous large studies have found an association between dairy and an increased risk of prostate cancer,(20843485) ovarian cancer, (16492930) and parkinson’s disease,(17272289) and that it elevates IGF-I, which is known to promote cancer.(19746296, 15110491) She also failed to mention that dairy fats are high in advanced glycation end products (AGEs) which have been shown to promote chronic diseases and aging in animal and human models.(20497781)

  51. In regards to the ‘large study of Australians’ Ms. Minger cited showing an inverse associated between high-fat dairy and CHD, the study contained only 1529 participants who were followed for 16 years and only administrated food frequency questioners during the first 4 years of the study.
    She ignored a recent paper from the Nurses’ Health Study of 84,136 women who were followed for 26 years and administrated numerous food frequency questioners over a period of 22 years, which found a significant positive association between high fat dairy, processed and fresh red meat and CHD. After adjustment for confounding variables, replacing just one serving of unprocessed red meat with low fat dairy, poultry, fish, nuts, and beans reduced CHD risk by 13%, 19%, 24%, 30% and 35% respectively.(20130097) Macronutrient displacement could not predict the difference in CHD in this study, and therefore studies should concentrate more on replacing different types of food rather than just concentrating entirely on macronutrient ratios, as non-caloric factors such as micronutrients play a very important role in the risk of disease.(15585762)
    For example a meta-analysis of randomized controlled trials found that legume intake significantly lowers total cholesterol and also increases the HDL:LDL ratio despite being rich in carbohydrates.(19939654) Also a controlled study that put participants on a diet high in leafy and green vegetables, fruits and nuts decreased LDL by 33% and the total cholesterol:HDL ratio by 21%, apolipoprotein by 23% and lipoprotein by 24% compared to the control group in a period of only 2 weeks. The decrease in total cholesterol was 34% to 49% greater than would be predicted by differences in dietary fat and cholesterol.(11288049)

    One major problem with the new guidelines, was the USDA’s attempt to downplay the association between fresh red meat and colorectal cancer. For example the USDA stated that the near significant association observed in the EPIC study (15956652) as finding “no association”, and failed to cite a meta-analysis containing over one million participants which found a significant association for both fresh and processed red meat with colorectal cancer.(16991129)

    There have been numerous well controlled studies carried out on humans living in a metabolic suite which show that the concentration of N-nitroso compounds (NOCs) [which most are cancerous] formed in the digestive system as a direct result of a high red meat diet intake are similar to the concentration found in cigarette smoke,(8631138) and that the NOC concentration in red meat directly correlates to the heme content of the meat, demonstrating that meat from both industrial grain-fed and organic grass-fed livestock would have a similar effects on NOC formation as the heme content does not significantly differ.(12750250) The researchers were able to extract NOC-induced damaged DNA from the lining of the colon, and showed that dietary heme increases and dietary fiber decreases the formation of DNA adducts which are an established risk of genotoxity and cancer risk.(16452248, 16926174) A recent meta-analysis of observational studies, and controlled human and animal experiments strongly support that there is a causal relationship between dietary heme and colorectal cancer.(21209396)
    The largest systematic review on lifestyle and diet and cancer risk to date, carried out by the World Cancer Research Fund and the American Institute for Cancer Research came to the following conclusion:
    “A substantial amount of data from cohort and case-control studies showed a dose-response relationship, supported by evidence for plausible mechanisms operating in humans. Red meat is a convincing cause of colorectal cancer.” –

    1. TW: It’s funny how you cast aspersions on associative data you don’t like while applauding associative data you do like.

      It’s even funnier how you’re citing food frequency data from the Nurses’ Health Study, which has been proven to be complete trash:

      “Focusing on the second questionnaire, we found that butter, whole milk, eggs, processed meat, and cold breakfast cereal were underestimated by 10 to 30% on the questionnaire. In contrast, a number of fruits and vegetables, yoghurt and fish were overestimated by at least 50%.”

      And the data for red meat was even worse: reported intake of hamburgers explained 1.4% of the actual variance in hamburger consumption.


      In other words, the NHS doesn’t tell us red meat is unhealthy: it tells us that healthy people lie about how much red meat they eat.

      Hat tip to Chris Masterjohn, here:

      But please do continue cutting and pasting huge bricks of unattributed text. Ctrl-V really shows your erudition and expertise.

      Also, please continue to never include links to your citations, or even titles and authors…because that way people can’t verify for themselves that the study says what your cut-and-paste claims it does. (I’ve found, through experience, that people who don’t link their citations are often misrepresenting them, sometimes dramatically.)


  52. TW. I appreciate the effort you’ve gone to here. I’m surprised your posts haven’t generated any responses from Minger herself or Bobby.

    1. Minger herself is currently out of town and juggling a billion projects, but I’ll certainly respond in depth when I get a chance. 🙂

        1. I almost never delete non-spam comments, but that one didn’t even add anything substantial. Folks, you can hate me and call me whatever slices of profanity suit your fancy, but at least offer something to the discussion if you’re going to do that! This is a blog, not a high school’s bathroom wall.

          1. Consider the following two cases:

            Local news blog:

            High school bathroom wall:

            I think… that, perhaps, the set of blogs does not necessarily reserve any greater amount of reverence than the set of bathroom walls. of course, by resorting to ‘high school bathroom walls,’ you greatly increase the veracity of your claim. But as any blog or any surface can be used for writing (or excreting on, for that matter 0_o), then it’s important not to diminish the value of bathroom walls; even if they are those of a high school and presumably contain material of a nature more foul. Perhaps, though, that the foulest high school bathroom wall writing is much less foul than the foulest of blogs. Of which I will point to no example, but am certain one’s imagination can glean the truthfulness nonetheless.

            Oh- yea… Food rocks! Or is this still spam?

            1. Marco – she was referring to my comments under a different username. In short, you are an ass, and your post was queer and useless. Stop trying to get laid and at least say something amusing. Oh-yea…You’re an ass! Or is this still spam?

          2. There is no point keeping comments that just go around name-calling and should just be deleted. Or just keep them to show the animosity that exists. These comments and all comments not in agreeance wouldn’t survive at that banana place.

            1. Sue – you are worried about “comments” surviving at a place where people attempt (pretend) to “survive” on bananas…by the way, there is no point in posting fabricated “words” Glad we are all in “agreeance” with that. Back to deepthroatin’ the ol’ banana, eh, Sue?

          3. No one is being mean. Don’t pout. Some bathroom walls are fairly educational and, perhaps even, worldly. When I was in the 3rd grade, I came upon a stall whose wall read: “Once upon a toilet I started, came to shit, but merely farted.” Tell me this doesn’t tickle your literary fance (among tickling other things – YOWZA!)

      1. Can’t wait to read it in 2014! The suspense is killing me! Joking aside, everyone (including me) is grateful for what you have done; you ought to consider enlisting a personal assistant/secretary/etc though. By the way, you would LOVE to read the email exchange I had with Campbell a month (or so) back. Very…interesting.

    2. Same goes for me. In the middle of a move and took a break to attend the Healthy People 2011 conference out at Loma Linda Adventists University. Keynote was by Dr. Caldwell Esselstyn and all the meals were vegan so I need a couple days to re-center myself due to the starvation I subjected myself to. Lol. I will say this however, I am becoming more and more convinced that because most of the research and anecdotal evidence in support of a plant based diet is relatively short term, I, at this point in my investigation, regard such a diet to be highly beneficial as a remedy to the SAD diet. I think of plant-based more like a cleanse than a viable way of life. I have not read TW’s responses yet but I have yet to see a study yeild results in favor of a plant-based diet that could control for the quality of SFA and/or the quality and state of the subjects diet for any number of years prior to the study.

      The angiograms Dr. Esselstyn showed were jaw dropping however, every one of his subjects were in terrible shape, living off of terrible diets to begin with. It is my opinion that the plant-based diet served more as a reprieve/fast/cleanse than it did as a medicinal therapy. As the refutation to the Atkins diet goes, of course you’ll lose weight if you go from eating big macs everyday to just the patty; the same can be said of Dr. Esselstyn’s research. Of course your coronary arteries will recover if you swich your carbs from ho-hos to swiss chard.

      1. I suggest that you read the posts, or at least just the studies I have cited. I am not sure if you are aware of a large percentage of the studies I cited, and feel that you may have limited your reading to posts by individuals with very strong preconceived bias such as Chris Masterjohn, and Denise Minger.

        I am curious as to whether you are classing a plant-based diet as 100% plant based or as consuming the majority of energy from plants. There are probably few examples of very long term studies on people consuming 100% plant based diets, but there is long-term evidence of people consuming mostly plant based diets such as the population studies that Dr. Esselstyn cites in his papers. I have yet to see the details of the 25 year follow-up of his study, as well as the results from the additional 250 patients. From the information I have gathered, it sounds that 99.5% of the committed patients were successful in either arresting or reversing their disease.
        Although I am very interested in Dr. Esselstyn’s research, I do not agree with everything that he says, as you can probably tell with my posts about nuts.
        With the billions of dollars owned by the industries who promote animal food heavy diets, the fact that they have not been able to produce such results, it is likely because it cannot be achieved, and is even possible that the industries are preventing negative results from be published. It would not be difficult to fund a study measuring the the actual underlying disease rather than the risk factors. This maybe why such industries only focus on disease risk factors and only during weight loss. As I pointed out, an increase HDL may not be protective if the anti-inflammatory effects of HDL are inhibited.

        My purpose here is not to change the opinion of some of the people who post in numerous blogs, but rather to challenge their statements and provide additional information to the readers who are subject to misinformation. I do not believe the minds of many posters would be changed by any significant amount of proof, especially of those who intentionally push misinformation. I also do not believe that I will be able to change the minds of those readers who still believe that Ms. Minger does not have a preconceived bias after reading all of my comments.

        1. I love the posts, TW. I don’t have a settled viewpoint and very much appreciate reading the contrary case. I’ll reserve judgment on the alleged preconceived bias and intentional pushing of misinformation, though.

        2. Actually, after seeing your posts here and your posts on the FatHead blog (it is you as I see a pattern), your purpose is to confuse people with long rambling posts that have absolutely no substance. You follow the same MO, and that is flood the forum with contradictory evidence. I seem to be coming across the same thing when a blog or forum seems to promote animal or dairy products.

          In fact, the above post is the first time I have seen anything close to be coherent from you, instead of just rambling rubbish. And why is this? Because you are actually answering someone who posted something that happens to be pro-vegetarian/vegan. And this post alone gives so much away about you and your intentions, in that you are pro-vegetarian/vegan and heavily anti-meat/dairy, and you will try your best to ruin the blogs/forum that your elevangelical nature disagrees with.

          You are nothing but a troll. Your rambling also causes people to skim through your posts!

      2. Am in agreement with what you have said, but would have been nicer to end it with “Of course your coronary arteries will recover if you switch your carbs from Swiss Rolls (ho-ho’s) to Swiss Chard.

  53. I’m a pastry chef, and a nutritionist friend passed this along. We both say: AMEN. There’s so much info out there about what one should/n’t eat–much of it flawed or just lies–that I can understand how the average person could have a hard time sorting fact from fiction.
    But what about throwing away the data and the charts, start eating like the thinking, moving omnivores we are? Eating like our ancestors ate. Plant-based diets. Foods that are real foods and not food-like substances.
    And for Chrissakes, America, just eat LESS! 🙂

  54. Shame how decency is lost as accountability and face is removed from discourse. That’s why I post my full name and picture; to keep myself honest. The cowards use initials and funny nick-names to represent their ideas. As a result, they only mean as much in the end.

  55. I’ve decided to test eating paleo on my whole family – particularly on my mother who has a pre-existing heart condition, so heart healthy foods are important for her. For years, she was told that vegetable oils, margarines, whole grains, eliminating satured fat, eating less meat and wolfing down more plants will make her heart healthier. But her condition didn’t get any better on that kind of diet so she tried paleo.

    She gave up wheat, sugar, grains (except rice) and began eating more tuber starches, meat (red, white and organs), eggs, butter, cholesterol-rich seafood, coconut oil, lard used in cooking and whole fruits/vegies (although she normally eats loads of plant food anyway). She did eat some processed food though but nothing with wheat/grains or sugar in it. Her lifestyle remains the same so she didn’t embark on more exercise or yoga or anything.

    She just got her blood test back and lo behold: triglycerides went down, LDL went down, HDL remained stable, her iron levels have improved (it was too low last year), her blood glucose has normalized (also went down from last year’s test), and her cholesterol has gone down!!

    I’m still reeling from that because after she told her doctor what diet she was on, he told her it’s not healthy and that the lard would make her cholesterol worse – which ironically it did the opposite 🙂

    After consuming more protein from meat along with saturated fat from many sources, her cholesterol went down. The doctor didn’t know what to say when the results came back. The test came back BETTER than her last year’s one (at the time she was eating more plant foods, grains, sugar and small amounts of meat and hardly any saturated fat)

    I’ll be doing my blood test soon too. I’ve been eating traditional diet for longer than my mother, so the results should be interesting.

  56. Denise, I want to thank you for all your efforts in shining a light into the USDA Dietary Guidelines and maintaining this blog. You’ve also demonstrated amazing class and respect for other’s ideas. I tell my wife, I want to be like you when I grow up (I’m 54).

    When I read all the responses on your blog, I’m encouraged by the time and effort people put into discussing these issues, whether or not I agree with them. Most importantly, I’m become very aware of the limitations of any study, and the conclusions that can rightfully be drawn from them.

    As a young man in pharmacy school, I accepted everything that was in my textbooks as absolute truth. After all, everything was based upon “good science”. I tried to minimize the feeliing that there were many grey areas where science seemed to fall short. I felt very uncomfortable with that idea. Years later, after I became bored counting to 30, I earned a degree in chemical engineering. The most valuable skill I obtained from that degree was “critical analysis” or to put it simply “what do I really know versus what do I think I know”. I realized that most of my knowledge is built upon a collection of shaky “proofs” and biases with a small smattering of actual truths.

    I’ve also been in the Federal government for 20 years and the bottom line for regulatory agencies is that their primary customers are the industries they regulate, not the public. Key decision leaders in departments and agencies often come from the regulated agencies. Federal agencies also fund a major portion of scientific research and federally-funded researchers can quickly find their funds gone if they publish results contrary to established research.

    I’n extremely grateful for blogs like yours who take the time and effort to pour over data and point out inconsistentcies in research results. Blogs who ignore the proclamation to “pay no oattention to the man behind the curtain.” The scienitifc method requires that we contantly examine the “facts” and to question any that have inconsistentcies. That we always question “what we think we know” versus “what we really know”. The fleld of nutrition is complex and there are no simple answers.

    There are sufficient studies available that would allow me to take any stance I chose and to cite research to support that stance, if being “right” is the most important goal I have. Or, I can choose to examine research, acknowledge its limitations, and carefully draw conclusions that may be correct. I am also occassionally guilty of the mindset “don’t try to confuse me with the facts, my mind’s already made up.” Being sure about something is emotionally comforting, but ultimately futile. I appreciate your efforts to be fair about your opinions and findings and to point out the obvious, and above all, your ability to communicate with clarity of though and the gentle manner you display.

    Keep up the good work.

  57. Brillant, Denise. Simply brilliant. 🙂

    I’m thankful for these articles.
    I can’t wait for the wheat one.

    Don’t pay attention to the petty naysayers polluting your blog, you’ve got countless admirers out there, who really understand what you’re doing. And who hope you’ll keep on doing it!

    Go Denise! 🙂

  58. Denise what do you think of this news: French vegans in court over baby’s death

    Two vegans who fed their 11-month-old daughter only mother’s milk went on trial in northern France on Tuesday charged with neglect after their baby died suffering from vitamin deficiency.

    Sergine and Joel Le Moaligou, whose vegan diet forbids consuming any animal product including eggs and cow’s milk, called the emergency services in March 2008 after becoming worried about their baby Louise’s listlessness.

    When the ambulance arrived at their home in Saint-Maulvis, a small village 150km north of Paris, the baby was already dead.

    The ambulance workers called the police because the child was pale and thin, weighing 5.7kg compared to an average 8kg for her age.

    The baby had only been fed on the milk of her mother, who was aged 37 at the time and a vegan.

    An autopsy showed that Louise was suffering from a vitamin A and B12 deficiency which experts say increases a child’s sensitivity to infection and can be due to an unbalanced diet.

    “The problem of vitamin B12 deficiency could be linked to the mother’s diet,” said Anne-Laure Sandretto, deputy prosecutor in the city of Amiens where the trial is taking place.

    1. @Zoe

      Mostly gossip.

      When you know the whole story, it’s very likely that it has very little to do with food. It’s about basic care.

      The baby died of bronchitis because the parents refused to take her to a hospital, refused to give her any kind of medical treatment, and lived in a house without proper heating. Any baby with acute bronchitis put in these conditions is in jeopardy.

      Talk about blowing something (the parent’s vegan diet) out of all proportions by gutter press.

      This said, I’m against vegan diets nonetheless. I understand and totally respect a vegetarian’s point of view, but vegan, well, just seems to me to make absolutely zero sense.

  59. TW, while it’s delightful that you like Minger’s blog enough to participate in the comment section — and research references are great — you have surpassed “commenter” here and have reached “spammer” on this post’s comments thread.

    I like to read comments but when one person just goes on at such repeat posts length, at some point one has to say “Dude, get your OWN blog, and post a few notes and a pointer!” There is a difference between participating in comments vs. using someone else’s media for your own billboard.


  60. Which are the clotting saturated fats if not stearic (also what about lauric in coconut oil)?

    Transcend says Typically solid at room or body temperature, saturated fats are sticky and can cause red blood cells to clump together, inhibiting their ability to carry oxygen to the cells. Saturated fats can also cause blood platelets to stick together and form blood clots that can cause a heart attack or stroke. Reducing consumption of saturated fat improves the health of most people. They provide support to your cell membranes and serve as precursors to a variety of hormones and hormonelike substances. A middle of the road approach to saturated fat consumption is to consume about 3 to 7 percent of your daily calories as saturated fat.

    1. There is a huge difference between room temp and body temp and not all saturated fats are equal in their qualities. To lump them altogether is silly.

      Coconut oil is liquid in the lower 70 degrees F.

      And dietary saturated fats do not cause platelets to stick together.

  61. According to Weston A Price’s studies, the world’s healthiest populations ate butter as a main staple of their diet. Coconut has many health benefits as well. Raw organic butter and coconut oil are my go-to fats.

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