CHAPTER 3

Not Guilty as Charged

Vegetable oils, and indeed all plant foods, contain little saturated fat^* and never any cholesterol, while animal fats contain both. This is a fact. Also a fact: the demonization of saturated fat and cholesterol is an obvious marketing strategy.

The attack on animal fats began with the accusation that they caused heart disease, especially myocardial infarction or heart attack. But accusers soon added other ailments to the list: stroke, high blood pressure, cancer, diabetes, obesity, autoimmune disease, kidney disease and impotence. The 1973 McGovern committee report went so far as to claim that America’s ten greatest disease killers would give way with a dietary change from butter to margarine, and from lard to vegetable oils for cooking.

The accusations against cholesterol and saturated fat rely upon the following logic: In 1900, heart disease and cancer were rare; by 1970, these and other chronic diseases had reached epidemic proportions. In 1900, Americans ate very little cholesterol and saturated fat; they followed a virtuous, abstemious, low-fat diet. By 1970, Americans had become rich, spoiled, and indulgent, gorging themselves on fatty meats, bacon, sausage, butter, eggs and cream—foods new to the American diet.

But what were Americans eating in 1900? The 1895 Baptist Ladies’ Cook Book: Choice and Tested Recipes Contributed by the Ladies of Monmouth, Ill gives us a good idea.¹ This collection of recipes from the turn of the century contradicts what the establishment is telling us—that the reason we have so much cancer and heart disease today compared to a century ago is because we are eating much greater levels of saturated fats from animal foods. Yet there’s hardly a recipe in this little book that does not contain butter, eggs, cream or lard—beginning with the soup chapter and ending with the large collection of the desserts.

Did Americans eat lean meat in 1900? The inhabitants of Monmouth, Illinois enjoyed steaks and rib roasts—one recipe suggests cooking the roast in beef drippings. Lean roasts were “larded” to make them tender—that is injected with bits of pig fat. Most meat and chicken recipes call for gravy made with drippings and occasionally with added cream. The good Baptist ladies cooked the whole chicken, not skinless chicken breasts.

In 1895, nobody had heard of al dente steamed vegetables. All the vegetable recipes in the book are cooked a long time and many call for a cream sauce. They include asparagus dressed in cream, four versions of cabbage with cream sauce, corn and eggplant fritters fried in lard, potato balls fried in “good drippings” and parsnips fried in bacon fat. Indeed, it seems that vegetables in those days were just an excuse for a sauce.

Seafood recipes include fish à la crème, scalloped fish, creamed salmon and creamed fish. The sauce for broiled fish calls for one large spoonful of butter and one-and-one-half cups of cream. A whole chapter devoted to oysters includes recipes for deviled oysters made with egg yolks, creamed oyster patties made with eggs and butter, oysters wrapped in bacon, scalloped oysters, oyster pie made with one quart of cream, oyster fritters fried in drippings, oysters fried in hot lard and scalloped oysters made with butter and whole milk.*

A chapter on organ meats includes fried veal liver and sweet breads—both creamed and fried. A scrapple recipe calls for hog’s head, heart, tongue and part of the liver. This rich mixture was stored in a crock and covered with melted lard. Midwestern families consumed scrapple for breakfast, sliced and fried in lard.

There are separate full chapters for eggs and cheese.

What about salads? Only one salad recipe in the book calls for lettuce, “when available.” Lettuce is a modern luxury—in the past we ate lettuce only during the growing season.^† The other salad recipes feature apples, cabbage, ham, tongue, chicken, oysters, fruit, potatoes, veal, lobster, sweet breads, shrimp and nasturtium flowers.

The recipes for salad dressing are of great interest to our argument. The dressing for coleslaw features sweet cream. Three recipes for salad dressing contain egg yolk, mustard and vinegar. One recipe calls for olive oil or melted butter. If they didn’t have olive oil in Illinois in 1895, which they probably didn’t, they used melted butter instead. Another recipe includes one cup of whipped cream. Just one salad dressing recipe in the book calls for “oil.” Americans at the turn of the century nourished themselves with butter, cream, egg yolks and lard, not with vegetable oil. Some Italian communities may have used olive oil—and cottonseed oil was just beginning to appear in the food supply—but Americans generally used animal fats, even on salads.

The Baptists were fond of rich desserts. Half of the book is devoted to cakes, pies, ice creams, puddings and donuts. The donuts were fried in lard, of course, and the cakes were made with butter. Two advertisements for dentists at the back of the book testify to the known negative effects of sugar and white flour on the teeth, but cancer and heart disease were rare before the turn of the century. While people were sturdy and strong, true obesity was uncommon.

The argument that Americans today eat more animal fats than they did a century ago does not hold up to the facts. Quite the opposite. Today’s typical American diet of lean meat, skinless chicken breasts, reduced-fat milk, margarine and vegetable oil contain little animal fat. Based on The Baptist Ladies’ Cook Book and many other cookbooks of the period, the American diet in 1900 was far richer and more “indulgent” than it is today.

EVEN IN THE 1960s, SOME communities cooked everything in lard. In 1961, scientists studied the residents of Roseto, Pennsylvania, and the findings baffled researchers. The citizens of Roseto had exceptionally low rates of heart disease. In Roseto, men over sixty-five enjoyed a death rate of 1 percent while the national average was 2 percent. Widowers outnumbered widows, too. In his bestselling book Outliers: The Story of Success, author Malcolm Gladwell notes that in Roseto men and women under fifty-five years old had almost no heart disease whatsoever, and those over sixty-five suffered roughly only 50 percent as much heart disease as did average Americans. The men worked in the slate quarries where they did contract illnesses from gases and dust, but Roseto also had no crime, and very few applications for public assistance.2

The experts looked at genetics, geography and other factors, yet nothing explained why the inhabitants of Roseto were “outliers,” that is, statistical anomalies, when it came to the rate of heart disease within the community. They did not tend to slimness, and in fact were often obese. They didn’t exercise much either, and the men enjoyed their cigars.

Then the investigators looked at their diet. People in Roseto did not use olive oil; instead they cooked in lard. They preferred wine to soft drinks and milk. They piled pepperoni, sausage, salami and sometimes eggs on their pizzas. They ate hard and soft cheese. Over 40 percent of their caloric intake was from saturated fat, a large portion of it from lard. Of course, today’s dietitians can’t even say the word “lard” without clutching their chests in pain. So they concluded with perfect political correctness that diet was not a factor either.

Instead, scientists concluded that the close-knit community experienced a reduced rate of heart disease because of lower stress levels. They called it the “Roseto Effect.” According to Dr. Stewart Wolf, one of the original study authors, “The community [of Roseto] was very cohesive. There was no keeping up with the Joneses. Houses were very close together, and everyone lived more or less alike. Elderly were revered and incorporated into community life. Housewives were respected, and fathers ran the families.”³ Many studies followed, including a fifty-year study comparing nearby towns Bangor and Nazareth. As the original authors had predicted, when the Bangor cohort shed their Italian social structure and became more Americanized in the years following the initial study, heart disease rose.⁴

The town of Roseto should hold no mysteries for the scientific community. As we discussed in Chapter 1, anyone with some scientific background in the subject of fats and oils would know that in the United States, from 1920 to 1960, heart disease skyrocketed while animal fat consumption (especially lard consumption) dropped equally drastically. They would also be familiar with the many other studies that contradict the notion that animal fats cause heart disease. Instead the politically correct pundits reached into their barrel of lame explanations and pulled out the familiar “strong family and social ties.” While obesity in the Roseto folks was probably due to their lack of exercise and the sweet desserts they liked, their hearts were strong because they consumed plenty of the ideal fuel for the heart—saturated fat.

Shortly after the Roseto study, the British Medical Journal published a study where patients who had already suffered one heart attack were assigned to one of three groups and given polyunsaturated corn oil, monounsaturated olive oil or saturated animal fats respectively. The endpoints were further heart attack or death. Those in the corn oil group saw their blood cholesterol levels come down by an average of 30 percent, while there was no change in the other two groups. However, at the end of the two-year trial only 52 percent of the corn oil group were still alive and had avoided a second heart attack. Those on the monounsaturated olive oil fared a little better: 57 percent survived and had no further heart attacks. But those eating saturated animal fats fared the best with 75 percent surviving and without further attack.5 Perhaps this third group had strong family ties as well?

CONTRADICTORY EVIDENCE CONTINUES TO ACCUMULATE, but the diet-heart and lipid-theory dogma persists—just changed slightly after the bad news about trans fats became public. The American Heart Association (AHA) and almost every other conventional medical group and government agency just tacked trans fats on to saturated fats, creating the bad fats brothers—Sat and Trans—both of whom raise the villainous LDL-cholesterol and therefore cause heart disease.

Source: The American Heart Association

In 2014, the AHA proclaimed the evidence “irrefutable that saturated fat should be decreased to 5 to 6% of calories by replacement with polyunsaturated fat to lower LDL-cholesterol and reduce CVD risk.”6 Polyunsaturated oils became the “good” replacement for both trans and saturated fats—anything to prevent the population from embracing delicious foods like chicken wings, butter and cheese.^*

The Harvard Health website parrots the AHA, advising readers to “Choose foods with healthy unsaturated fat (fish, nuts, and most plant oils), limit foods high in saturated fat (butter, whole milk, cheese, coconut and palm oil, and red meats), and try to avoid foods with trans fat.”⁷

Seven years earlier, in 2006, the results of the Women’s Health Initiative (WHI) Dietary Modification Trial appeared in the Journal of the American Medical Association. The study involved more than forty-eight thousand postmenopausal women, who were randomly assigned to either a regular unrestricted diet or to a “healthy” diet that was low in fat (20 percent fat) and high in fiber, with at least five servings of fruits and vegetables and six servings of grains per day—in other words, they followed the dietary guidelines to a T.⁸ The “healthy” eaters attended group sessions led by dietitians who administered “intense behavioral modification” to keep them on their diets. And the “healthy” diet women did surprisingly well, maintaining their fat intake at 24 percent of total calories and the dreaded saturated fat at 8 percent. By contrast, the control group consumed 38 percent of total calories as fat with about 12 percent as saturated fat—still low in fat compared to the traditional American diet, but way more than the amount the AHA considers safe. The “healthy” diet group also consumed more fruits and vegetables, grains and fiber. Researchers followed the women closely for more than eight years while recording cases of clinically confirmed breast cancer, colon cancer, heart disease, heart attacks and strokes, confidently predicting, for example, a 14 percent decrease in breast cancer incidence. When the results came, the benefit from years of restrictive eating was… nothing! The two groups showed no difference in the incidence of cancer, stroke and heart disease, and no difference in weight gain either.9

More recently, a 2010 mega-analysis published in the American Journal of Clinical Nutrition combined the relative risk rates from twenty-one studies representing almost three hundred fifty thousand people whose diets and health outcomes were followed for five to twenty-three years. The conclusion: “There is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD (coronary heart disease) or CVD (cardiovascular disease).”¹⁰ Not one word about this study appeared in the mainstream press. An accompanying editorial voiced outrage at the findings and repeated the same advice—avoid red meat, whole milk, egg yolks and cheese, and eat more egg whites, grains, fat-free dairy foods and seed oils. Only James H. Hodges of the American Meat Institute Foundation spoke out: “This study is critically important because of its size and statistical power. No doubt, it will be viewed with skepticism by some researchers who believe strongly in a link between heart disease and saturated fat. But when it comes to science, we must view new findings with an open mind and critical thought. Without an open mind, we risk enacting misguided public policies. While this study may not reflect prevailing nutrition advice, it is a very substantial body of work… The magnitude of this study and its findings merit both respect and thoughtful consideration.”¹¹

On the heels of the meta-analysis exonerating saturated fat is a prospective 2010 study from Australia which looked at adults over a period of fifteen years. People who ate the most full-fat dairy products had a 69 percent lower risk of cardiovascular death than those who ate the least; or to put it another way, people who mostly avoided dairy foods or consumed low-fat dairy had more than three times the risk of dying of coronary heart disease or stroke compared to people who ate the most full-fat dairy.¹² A 2004 study from Sweden got similar results. The researchers measured blood levels of two biomarkers for milk fat in over four hundred heart attack patients and over five hundred healthy controls. The markers, pentadecanoic acid and heptadecanoic acid,^* provide a good indication of how much dairy fat a person has been eating. The researchers found that people with the highest levels of these milk fat biomarkers—that means they were consuming butter and full-fat dairy foods—were at lower risk of heart attack; for women the risk was reduced by 26 percent and for men the risk was 9 percent lower.¹³ The study has particular relevance because the researchers did not rely on dietary questionnaires, which are notoriously inaccurate, but on blood markers of fatty acid consumption.

Also in 2004, researchers found that in postmenopausal women with relatively low total fat intake, a greater saturated fat intake was associated with less progression of coronary atherosclerosis, whereas carbohydrate intake was associated with a greater progression.¹⁴

The 2013 Sydney Diet Heart Study not only further exonerated saturated fat, but also found problems with polyunsaturated oils—the kind we are supposed to use in place of saturates. It involved four hundred fifty-eight men ages thirty to fifty-nine. One group was advised to replace dietary saturated fats with omega-6 oils, while the other received no specific dietary advice. The result: all-cause mortality and mortality from coronary heart disease were higher in the intervention group than in controls. These findings are the more remarkable because the researchers lumped “common margarines and shortenings” with saturated fat, so the intervention group avoided not only saturated fat but trans fats as well. The researchers concluded, “These findings could have important implications for worldwide dietary advice to substitute omega-6 linoleic acid, or polyunsaturated fats in general, for saturated fats.”15 Not a peep about this study appeared in the major media.

Another exhaustive analysis, published in 2014, looked at nearly eighty studies and found no evidence that eating saturated fat increases the incidence of heart attacks and other cardiac events. The study did not find that people who ate higher levels of saturated fat had more heart disease than those who ate less, nor did the study find less heart disease in those dutifully eating higher amounts of polyunsaturated and monounsaturated fat.¹⁶ “My take on this would be that it’s not saturated fat that we should worry about” in our diets, said Dr. Rajiv Chowdhury, the study’s lead author and a cardiovascular epidemiologist in the department of public health and primary care at Cambridge University.

Here in the United States, health officials will make sure we keep worrying. Dr. Frank Hu, professor of nutrition and epidemiology at the Harvard School of Public Health, said that the findings “should not be taken as a green light to eat more steak, butter and other foods rich in saturated fat.” Prominent food Puritan Alice H. Lichtenstein, a nutritional biochemist at Tufts University, chided, “It would be unfortunate if these results were interpreted to suggest that people can go back to eating butter and cheese with abandon.”¹⁷

A large review of existing research published in 2015 found that saturated fats were not associated with all-cause mortality, heart disease, ischemic stroke or type 2 diabetes while trans fats were associated with higher all-cause mortality, total CHD and CHD mortality. The authors noted wryly, “Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats.” The researchers included data from forty-one studies covering more than three hundred thousand people, and twenty studies of trans fat intake and health outcomes that covered more than two hundred thousand individuals.

But researchers in this field still cannot bring themselves to give the green light to butter and meat fats. “This study shows that focusing on reducing saturated fats as the primary goal in eating well is not quite right,” said Patty W. Siri-Tarino, of Children’s Hospital Oakland Research Institute. “Eating well means replacing those saturated fats with polyunsaturated fats rather than carbohydrates, particularly refined and processed carbohydrates, which is what usually happens,” she added.¹⁸ In other words, there is nothing wrong with saturated fats but you still shouldn’t eat them!

While Americans may remain fat-phobic, the anti–saturated fat mantra is crumbling in other parts of the world. In the UK, the British Medical Journal published an article by cardiologist Aseem Malhotra, who blasted the notion that saturated fats cause heart disease, noting that when you take satisfying fats out of the diet, the food tastes worse and you compensate by replacing saturated fat with sugar.19 Following Malhotra’s article, Joanna Blythman, writing for The Guardian, staunchly defended butter. “The anti-sat-fat message has been used effectively by food manufacturers to woo us away from whole, natural foods such as butter, which is only minimally processed, on to their products, which are entirely the opposite, such as margarine,” she said,²⁰ noting the 2010 review, which found no convincing evidence that saturated fat causes heart disease.²¹

In Australia, ABC’s Catalyst TV program, Heart of the Matter, sent the Internet abuzz with its critique of the low-fat agenda²²: Part II, Cholesterol Drug War,²³ challenged the notion that we should be taking cholesterol-lowering drugs.^*

And finally, Sweden has become the first Western nation to reject the low-fat diet dogma in favor of low-carb, high-fat nutrition. The switch in dietary advice followed the publication of a two-year study by the independent Swedish Council on Health Technology Assessment, which reviewed sixteen thousand studies. The conclusion: butter, olive oil, heavy cream and bacon are not harmful foods.²⁴

STILL, THE FORCES ALLIED WITH the vegetable oil industry have plenty of research they can point to in support of their agenda.

During the late 1990s, when news about the dangers of trans fats emerged, conventional dietary gurus pointed to a study published in 1997 in the American Journal of Cardiology²⁵ to justify avoidance of red meat and butterfat, the two main sources of saturated fat in the Western diet.

Arthur Agatston, author of the best-selling South Beach Diet, refers to this research when he states: “The major problem I have with the Atkins Diet is the liberal intake of saturated fats. There is evidence now that immediately following a meal of saturated fats, there is dysfunction in the arteries, including those that supply the heart muscle with blood. As a result, the lining of the arteries (the endothelium) is predisposed to constriction and clotting. Imagine: Under the right (or rather, wrong) circumstances, eating a meal that’s high in saturated fat can trigger a heart attack! In addition, after a high-fat meal certain elements in the blood called remnant particles, persist for longer than is healthy. These particles contribute to the buildup of plaque in the vessel wall.”²⁶

Agatston recommends consuming polyunsaturated and monounsaturated vegetable oils, including tub spreads, rather than animal fats like butter.

In the study Agatston describes, carried out by Robert A. Vogel and his team, ten volunteers were tested for “endothelial function” using ultrasound to measure the diameter change in the brachial artery after a high-fat and a low-fat meal, each of nine hundred calories. The high-fat meal contained 50 grams of fat and the low-fat meal contained, according to the authors, no fat at all.^†

“Flow-mediated vascularity” did decrease more in the high-fat group compared to the low-fat group. Interestingly, LDL-cholesterol declined slightly for both groups, but in the low-fat group, the so-called good HDL-cholesterol also declined, whereas it remained stable in the high-fat group. Blood pressure declined in the high-fat group, but rose in the low-fat group. Most significantly, blood glucose rose in the low-fat group, but declined slightly and then returned to baseline in the high-fat group.

For years the conventional view held that high-fat foods raise so-called bad LDL-cholesterol and blood pressure and therefore contribute to heart disease. But since that didn’t happen in this study, the authors declared that an inherently subjective measurement of “endothelial function” would serve as a better marker for heart disease.

But was it saturated fat that caused the decline in endothelial function? The high-fat meal consisted of an Egg McMuffin, a Sausage McMuffin, two hash brown patties and a noncaffeinated beverage. The low-fat meal consisted of Frosted Flakes, skim milk and orange juice. According to the authors, the high-fat meal contained 50 grams of fat, of which 14 were saturated fat—so only 28 percent of the fat in the high-fat meal was saturated. The rest was a combination of trans fats, monounsaturated fat and polyunsaturated fat, any one of which, or all together, could contribute to the decline in endothelial function. But Agatston (along with the study authors) blames the adverse effects on saturated fats!

The low-fat meal that won the endothelial-function contest was obviously a terrible dietary choice—extremely high in sugar and devoid of nutrients. Yet it did have one thing going for it—it is unlikely that Frosted Flakes, skim milk or orange juice contained MSG, an inflammatory additive, whereas the high-fat meal certainly contained MSG in the sausage and hash browns. If the bread contained soy, which it probably did, this would be another source of MSG. The presence of MSG in the high-fat meal provides a likely explanation for the decline in endothelial function.

The subjects in this study ate junk food, and the research itself can only be described as junk. The study was designed so poorly that no conclusions should be drawn from it. In order to test the effects of saturated fat on endothelial function, the researchers should have provided two identical meals of simple whole foods, except for the addition of a mostly saturated fat such as suet or coconut oil to one of the meals. Then, to compare the effects of the various fats with saturated fat, the researchers should have repeated the experiment adding a mostly monounsaturated fat, such as olive oil, to one of the meals, a high-trans fat such as vegetable shortening, and finally a polyunsaturated fat such as corn oil.

To correlate their findings—a temporary decline in endothelial function—with long-term effects such as heart disease, the authors should have bolstered their argument with reference to numerous studies; but they cite only one, which postulates a chronic decline in endothelial function with atherosclerosis. They provide no evidence that the temporary decline in endothelial function observed in this study is associated with atherosclerosis in the long term or that such a decline can “trigger a heart attack.”

As it becomes more and more obvious that cholesterol levels have little predictive value for heart disease—and that saturated fats in fact have little or no effect on cholesterol levels anyway—researchers who know where their bread is buttered—or rather, spread with margarine—are searching for other ways to demonize saturated fats. The study carried out by Vogel and his team can only be characterized as “garbage in, garbage out”—a grasping-at-straws attempt to stem the change in consumer eating habits toward real, whole foods.

Endothelial function returned to the news in 2006 with the publication of a study entitled, “Consumption of Saturated Fat Impairs the Anti-Inflammatory Properties of High-Density Lipoproteins and Endothelial Function.”27 The findings indicated that a single meal rich in saturated fats disrupts arterial function and contributes to the inflammation of the blood vessels. An Associated Press story by Joe Milicia quoted Kansas City cardiologist Dr. James O’Keefe, who claimed the study showed that “when you eat [saturated fat], inflammation and damage to the vessels happens immediately afterward.” Dr. Nicholls, principal author of the study, insisted that his research showed the “need to aggressively reduce the amount of saturated fat consumed in the diet.” According to the article, that meant reducing our intake of beef, pork, lard, poultry fat, butter, milk, cheese, coconut oil, palm oil and cocoa butter, and replacing them with safflower oil, sesame oil, sunflower seeds, corn oil and soybean oil.²⁸ The study design? The researchers fed fourteen adults a meal of carrot cake and a milk shake on two separate occasions one month apart, one made with highly saturated coconut oil and one made with highly polyunsaturated safflower oil. Both oils were nonhydrogenated, organic, unrefined and virgin.

Despite the newspaper reports and Nicholls’s attention-grabbing claims, the researchers found no clearly discernible effect of any type of fat on arterial function, and those consuming saturated fat had the best arterial function at all time points measured. In fact, the researchers did not even study the inflammation occurring in the blood vessels of the people eating the meals. Instead, they looked at isolated cells in which they found high-density lipoprotein (HDL) taken from people eating safflower oil to have greater anti-inflammatory power than HDL taken from people eating coconut oil. Without a shred of evidence, the newspaper reports attributed this observation to the saturated fat that the study subjects consumed. In fact, in the published study the authors actually made no such claim, noting that these effects might be due to the large difference in vitamin E content of the two diets. In any event, the carrot-cake-and-milkshake study has no relevance in the real world.

Along with cholesterol, a compound called homocysteine is thought to be a marker for proneness to heart disease. Researchers in the Netherlands studied the effects of different fatty acids, including saturated fatty acids and very-long-chain omega-3 fatty acids, on homocysteine levels in two age groups, forty-seven to forty-nine years old and seventy-one to seventy-four years old. The results were published in the American Journal of Clinical Nutrition with the following conclusion: “High intakes of SFAs [saturated fatty acids] are associated with high plasma concentrations of tHcy [homocysteine].”²⁹

Here was another study that the food industry could use to bash saturated fats, but if you look closely at the tables, you find no tenable or consistent relationships between consumption of various fatty acids and homocysteine levels. By contrast, the difference in homocysteine levels was significantly associated with age, with levels ten times higher in the seventy-year-olds compared to the forty-year-olds, but the study abstract contains no mention of this important fact.

The current Cinderella study—used as damage control to counter the increasing attention on butter—is a 2014 meta-analysis of thirteen studies involving more than three hundred thousand participants. The findings: individuals who traded 5 percent of the calories they consumed from saturated fat for sources of omega-6 polyunsaturated oil lowered their risk of CHD by 9 percent and lowered their risk of death from CHD by 13 percent.30 Every single study reviewed in the meta-analysis dates from the 1990s to the present, after decades of recommendations to consume polyunsaturated fatty acids to prevent heart disease—so the potential for bias (not to mention influence) is very great. Obtaining precise figures of 5 percent and 13 percent from a meta-analysis defies logic.

RED MEAT, AS A SOURCE of saturated fatty acids, gets repeated bashings in the media. In fact, in a recent report, the World Health Organization (WHO) ranked bacon, sausage and other cured and processed meats as “group 1 carcinogens,” which puts them in the same category as tobacco, asbestos, alcohol and arsenic. It also placed fresh red meat in the “group 2A” category, which suggests that it is “probably carcinogenic” to humans.

Such accusations are becoming more common. An example is a 2009 study published in the Archives of Internal Medicine.³¹ “Eating red meat increases the chances of dying prematurely,” said the newspaper reports. “Americans who consumed about four ounces of red meat a day were more than 30 percent more likely to die during the 10 years they were followed, mostly from heart disease and cancer.”³² The report itself describes the increases in total mortality as “modest,” and a careful reading of the text reveals some important details. Participants in the highest quintile of meat consumption, when compared to those in the lowest quintile, were three times more likely to smoke, 50 percent less likely to engage in vigorous exercise, were less well educated, had lower fiber consumption and ate fewer fruits and vegetables. The authors did not explore the possibility that frequent meat eaters were more likely to eat processed vegetable oils and processed food in general.

Commenters noted that the study was not designed to determine cause and effect, and its ability to determine or verify the participants’ true meat intake was almost nonexistent. According to researcher Chris Masterjohn, PhD, the flawed study “emphasizes the most basic principle of science that they want us all to forget: that correlation does not prove causation. There are thus two important points we need to understand about this study to realize just how little it does to increase our knowledge: the study found a correlation between increased mortality and a population’s propensity to report eating meat, not a correlation between mortality and true meat intake… these may be two completely different things; and correlation does not show causation. There is absolutely no scientific basis to conclude from this study that eating meat increases mortality.”³³

HIGH BLOOD PRESSURE IS SAID to be a risk factor for heart disease. During the 1960s, Fleischmann’s Margarine ran advertisements in the Journal of the American Medical Association touting 100 percent corn oil unsalted margarine for “hypertensive patients.” The copy ran: “The substitution of Fleischmann’s Unsalted Corn Oil Margarine for butter or ordinary margarines in your hypertensive patients’ dietary regimen, has the added advantage of increasing their intake of high polyunsaturates… important because of their association with hypertension and atherosclerosis.” At that time, not a single study linked consumption of polyunsaturated fatty acids with protection against high blood pressure.

To lower blood pressure, doctors today recommend the DASH (Dietary Approaches to Stop Hypertention) Diet, endorsed by the American Heart Association and the 2010 Dietary Guidelines for America. The diet calls for reducing salt, reducing processed foods containing salt, reducing meat products “high in saturated fat,” and eating more whole grains, legumes, fruits and vegetables. However, studies on the diet showed that it only worked, and worked only a little bit, in people whose blood pressure was only moderately high.³⁴ Any one of these strategies—including the avoidance of processed foods—could take credit for the slight reduction in blood pressure.

Today, even conventional medical websites admit that intake of dietary fats has no relationship to blood pressure. For example, we read at medtv.com: “People often wonder if fats in the diet affect blood pressure. The answer is no. Fats in a person’s diet do not directly affect blood pressure.”35

Physicians operate under the assumption that high blood pressure predisposes an individual to heart attack (as well as stroke and kidney disease). Surprisingly, no randomized clinical trial has ever proven that lowering high blood pressure reduces the risk for death from heart disease. For example, one of the goals of the Multiple Risk Factor Trial (MRFIT) was to reduce participants’ blood pressure below 140/90, along with lowering cholesterol and quitting smoking, but the conscientious patients fared no differently from controls. In fact, those who took diuretics to lower their blood pressure had the highest mortality rates,36 possibly due to potassium depletion.

The truth is, there are many causes of hypertension, including kidney disease, hormone imbalance, diabetes, atherosclerosis and a range of nutrient deficiencies—such as CoQ₁₀, potassium and protein. Trans fats inhibit biochemical processes in the cell membranes and high blood pressure is a probable outcome of this biochemical chaos.

STROKE IS THE THIRD LEADING cause of death in the United States and a leading cause of disability. The American Heart Association claims that high cholesterol levels contribute to stroke and are another reason to avoid cholesterol-rich foods such as butter, egg yolks and organ meats.³⁷

The fact is, researchers have not found much correlation between cholesterol levels and risk of stroke. For example, a 1995 report in which researchers pooled together the results of forty-five prospective cohort studies involving over four hundred thousand people found “a weaker relationship between cholesterol levels and the risk of stroke than with coronary artery disease.”³⁸ The 2010 Japan Collaborative Cohort Study for Evaluation of Cancer Risk found that saturated fat intake was inversely associated with mortality from stroke.³⁹

The association of stroke with cholesterol levels becomes clearer when we distinguish between ischemic and hemorrhagic stroke. Ischemic stroke, where a blockage closes the flow of blood, is the more common type, but the hemorrhagic stroke, where a blood vessel ruptures, is more deadly—hemorrhagic stroke patients end up with greater neurological problems and are four times more likely to die within thirty days than victims of ischemic strokes.

It turns out that as cholesterol levels go up, the risk of ischemic stroke goes up while the risk of deadly hemorrhagic stroke goes down. So cholesterol-rich foods that might raise cholesterol levels should protect against hemorrhagic stroke; the logic is that avoiding these foods will protect against the more common ischemic stroke, but the research shows otherwise. In the Honolulu Heart Study, the risk of ischemic stroke decreased as the intake of total and saturated fat went up.⁴⁰ And the Framingham Heart Study, which followed eight hundred men over the course of nineteen years, found that “intakes of fat, saturated fat, and monounsaturated fat were associated with reduced risk of ischemic stroke in men [emphasis added].”⁴¹

In an analysis of all the studies on stroke and cholesterol, Chris Masterjohn, PhD, argues that the likely cause of stroke is oxidized cholesterol in the blood. This means that the best protection against stroke is avoiding polyunsaturated oils, full of oxidizing free radicals, and choosing tasty and nutritious foods containing stable saturated fat—like butter, eggs and organ meats.⁴²

DIABETES IS ON THE INCREASE and represents a huge burden on families and the medical system. The dietary advice from the American Diabetes Association is cloned from the American Heart Association: avoid trans fats found in processed foods like snacks (crackers and chips) and baked goods (muffins, cookies and cakes) made with hydrogenated oil or partially hydrogenated oil, stick margarines, shortening and some fast-food items such as French fries—but also avoid saturated fats found in lard, fatback and salt pork; high-fat meats like regular ground beef, bologna, hot dogs, sausage, bacon and spareribs; high-fat dairy products such as full-fat cheese, cream, ice cream, whole milk, 2 percent milk and sour cream; butter; cream sauces, gravy made with meat drippings; chocolate; palm oil and palm kernel oil; coconut and coconut oil; and poultry (chicken and turkey) skin. In addition, they recommend keeping your cholesterol consumption below 300 milligrams per day by avoiding high-fat dairy products (whole or 2 percent milk, cream, ice cream, full-fat cheese), egg yolks, liver and other organ meats, high-fat meat and poultry skin.*⁴³

Modern advice to diabetics assures them that they do not need to worry too much about carbohydrates—their daily insulin can take care of that. But for many years, scientists and physicians recognized the fact that diabetes was a consequence of a diet rich in carbohydrates, especially simple sugars. Before the discovery of insulin, the only treatment for diabetes was a very high-fat, low-carb diet, because the body does not need insulin to process fats. In those days, the medical community recognized only one type of diabetes: type 1 or juvenile diabetes resulting from a malfunction of the pancreas. If the pancreas—worn out by a constant onslaught of sugar in the diet or simply not functioning properly due to nutrient deficiencies—cannot produce enough insulin to transfer the sugar from the bloodstream to the cells, glucose levels in the bloodstream remain abnormally high, with serious consequences.

Today, we recognize a second type of diabetes, type 2 diabetes, which is the inability of the insulin receptors on the cell membrane to efficiently uptake the glucose from the blood. The result is high levels of both sugar and insulin in the bloodstream, again with serious consequences.

Researchers and physicians are adamant that saturated fat causes insulin resistance leading to type 2 diabetes. They cite several studies, from the years 2002–2003. One was published in the British Journal of Nutrition entitled, “Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women.”⁴⁴ In the study, four groups of subjects consumed a breakfast of Rice Krispies, banana, skim milk, “Nesquik” (a chocolate drink) and something called “Marvel,” along with 40 grams of fat. The first group got mostly saturated fat from palm oil, the second group got mostly monounsaturated fat from olive oil, the third group got mostly omega-6 fatty acids from safflower oil, and the fourth group got high levels of omega-3 fatty acids from a combination of safflower oil and fish oil.

The researchers measured levels of insulin and glucose in the blood at intervals after breakfast and also after a so-called low-fat lunch consisting of cheese pizza (said to contain only 5.4 grams of fat), lettuce, cucumber and tomatoes. Those given the mostly saturated palm oil had higher insulin levels an hour after breakfast and lunch compared to the other three groups. However, insulin levels were the same for all groups two hours after each meal. Blood glucose levels followed a similar curve for all four groups.

The study provides a poor justification for recommending against saturated fat. All four groups consumed a very unnatural diet high in processed foods, and the fats used do not reflect the type of fatty acid profiles found in normal diets. Furthermore, the levels of insulin in the subjects were not chronically high, as one finds in a person with type 2 diabetes, and the glucose curves were normal for all groups. The study tells us nothing about what happens in real life with people eating real food.

Another 2002 study, this one published in Diabetologia, was titled “Substituting dietary saturated fat with polyunsaturated fat changes abdominal fat distribution and improves insulin sensitivity.”45 It looked at a small group of subjects—a total of seventeen—who received instructions to follow a diet rich in saturated fatty acids (by using more dairy products) or polyunsaturated fatty acids (by using more oils and spreads) for five weeks. The subjects on the saturated fat diet had a slightly lower measure of insulin sensitivity, but their glucose levels and body mass indices were virtually identical with those in the polyunsaturated group. Again, this study has little to do with real life. The researchers did not measure the actual amount of saturated or polyunsaturated fat (or trans fat) in each diet, and the number of subjects was too small to be meaningful.

Neither of these studies tells us what happens to people with or without diabetes who eat a diet high in natural saturated fats compared to those whose diets contain a lot of vegetable oils. The fact that the researchers so soundly condemn saturated fats after such trivial findings constitutes strong evidence of bias.

Another study, this one from the University of Minnesota,⁴⁶ and reported in the December 2003 issue of Prevention magazine, reported that “among three thousand people tested, those with the highest blood levels of saturated fats were twice as likely to develop diabetes as those with the lowest.” According to Aaron Folsom, MD, one author of the study, “Saturated fats in the blood appear to affect your body’s ability to effectively use insulin, the hallmark of type-2 diabetes.” Naturally this report was followed by warnings not to eat saturated fats like butter, cream and the fat on meat. But Dr. Folsom makes an error common to those not trained in fatty acid metabolism. A high level of saturated fatty acids in the blood is reflective of high-carbohydrate intake and subsequent synthesis of fatty acids from excess carbohydrates. Saturated fatty acids in the blood are not an appropriate marker of dietary fat intake, but are rather a marker of carbohydrate intake. What the researchers at the University of Minnesota actually discovered (or rather, reaffirmed) was that people who eat a lot of carbohydrates are more likely to develop diabetes.

Telling people to avoid saturated fats almost invariably results in their consuming more trans fats or omega-6 vegetable oils, both of which have many adverse effects. Trans fats, for example, interfere with the insulin receptors in the cell membranes, thereby contributing to type 2 diabetes. The saturated fats, on the other hand, have no effect when appropriate comparisons are made.47

Regarding dairy fats, new evidence indicates that they actually have protective properties. Swedish research from 2014, presented at the annual meeting of the European Association for the Study of Diabetes (EASD), shows that people who consumed eight or more portions of high-fat dairy products per day had a 23 percent lower risk of getting type 2 diabetes than those who had fewer portions per day. The study included almost twenty-seven thousand individuals (60 percent women), ages forty-five to seventy-four.^*

In spite of these interesting findings, Dr. Richard Elliott, Diabetes UK research communications manager, warned: “This study adds to research which suggests that different sources of fat in the diet affect the risk of type 2 diabetes in different ways. However, this does not mean that adding high-fat dairy products to your diet will actively help to protect against type 2 diabetes, and we would not recommend this. Consumption of dairy products can form part of a healthy diet, but it’s important to be aware of the amount you consume, as they can be high in calories, which can contribute to becoming overweight, and therefore increase your risk of type 2 diabetes. More research will be needed before we change our advice that the best way to reduce your risk of type 2 diabetes is by maintaining a healthy weight through increased physical activity and a balanced diet that is low in salt, saturated fat and sugar and rich in fruit and vegetables.”⁴⁸

In summary, the results of studies into dietary fats and diabetes do not justify the advice to limit saturated fat. Type 2 diabetes is a new disease, one that has now reached epidemic proportions. Type 2 diabetes did not exist one hundred years ago when our diets were very rich in saturated fats, but appeared when trans fats came into the diet and became an epidemic with the consumption of more and more foods containing trans fats and processed food in general. And since we know that trans fats interfere with insulin receptors in the cells, it is clear that the blame lies with new industrial fats, not traditional saturated fats.

THE ANTI–ANIMAL FAT CAMPAIGN BEGAN with a focus on heart disease, not cancer, and relied upon a kind of logic that appealed to both physicians and laymen. Animal fat contains cholesterol, and cholesterol clogs arteries, and clogged arteries lead to heart disease. But the logic that fingers saturated fat as the culprit in other diseases, especially in cancer, is more difficult to trace. Since saturated fats are stable, protect against oxidation and play essential roles in cell membrane integrity and hormone production, scientists find it difficult to articulate just how and why saturated fats could cause cancer.

Nevertheless, the scientific literature—followed by the popular press—takes it as a given that saturated fat causes cancer, and that we can protect ourselves by eating lean meat and substituting polyunsaturated vegetable oil for saturated fats like cream and butter. These are shocking recommendations given the fact that modern polyunsaturated oils predispose both animals and humans to cancer in study after study.

The American Cancer Society (ACS) advises us to choose fish, poultry or beans instead of red meat (beef, pork and lamb). If you eat red meat, advises the ACS, choose lean cuts and eat smaller portions. These strictures are mixed with advice that is sensible. We should avoid fried foods (since they are invariably fried in vegetable oils) and charbroiled meats (since charbroiling creates carcinogens). The ACS guidelines advise limiting the use of creamy sauces, dressings and dips with fruits and vegetables. This is good advice also, since “creamy sauces, dressings and dips” are usually concocted with vegetable oils and not real cream. But since the guidelines do not explain this fact, the reader comes away with the erroneous impression that cream is bad.

“High-fat diets are associated with increased cancer risk, so good health relies on fat-conscious eating decisions,” admonishes the ACS.*⁴⁹ But what kind of fats? The kind we can see, like the butter on our bread, the fat on our meat or the yolks in our eggs, or the fats that we don’t see, like the vegetable oils in fried and processed foods, in “healthy” spreads, or emulsified to make cream-like substances?

Women worried about breast cancer have become a major target of the saturated fat guilt trip. When guilt doesn’t work, the food industry turns to the other potent weapon in their arsenal: fear. Take this headline, for example: “Women Who Eat High-Fat Foods Could Be Doubling Their Risk of Breast Cancer, Scientists Say.” This and similar pronouncements heralded a study published in 2003 in the International Journal of Cancer: “Eating high-fat red meats and dairy products such as cream may increase the risk of breast cancer in premenopausal women.” Nutrition researcher Eunyoung Cho said of the study: “I would not recommend that [Atkins] diet for premenopausal women unless they replace red meat with poultry and fish… Breast cancer risk increases 58 percent by eating animal fat.”⁵⁰

But a close look at the study does not raise any real alarms. The researchers found that if your diet contains 14 percent of calories as animal fat, your chances of getting breast cancer are 0.68 percent; if your diet contains 18–21 percent of calories as animal fat, your chances of getting breast cancer are 0.88 percent; and if your diet contains more than 21 percent animal fat, your chances of getting breast cancer actually go down to 0.73 percent.

Spokespersons for the study used every trick in the book to make these trivial results seem scary. In addition to the incredible hype over minor differences, they divided the subjects into unequal quintiles (the highest quintile of 21–46 percent had the greatest range); determined fat percentages by self-assessed dietary recall that was surveyed only twice during the study; and neglected to indicate the important fact that there were twice as many smokers in the group with highest animal fat consumption compared to lowest.⁵¹

The study authors also fail to mention a survey showing that women on low-fat diets have just as much breast cancer as those on high-fat diets.52 Two subsequent reviews have found weak or insignificant associations of saturated fat intake and breast cancer risk, and note the prevalence of confounding factors.⁵³

The Women’s Health Initiative Dietary Modification Trial, specifically designed to examine the effect of a low-fat diet on the development of breast cancer, showed similar rates of breast cancer in women eating a low-fat diet and in those eating a “regular” diet.⁵⁴ One recent study from the National Institutes of Health—the AARP Diet and Health Study—found a very weak positive association between fat and postmenopausal breast cancer,⁵⁵ but when other studies are considered, the overall evidence does not support a relationship between saturated fat intake and breast cancer.

WHAT ABOUT THE ACCUSATION THAT beef causes cancer, in particular cancer of the colon? The genesis of this myth involves more than just muddied thinking, but actual skullduggery. In 1965, an influential physician, Ernst Wynder, took worldwide consumption data for industrial vegetable oils, called them animal fat (which they were not) and compared them with worldwide colon cancer mortality.⁵⁶ The table he produced showed high rates of colon cancer in European countries and low rates of colon cancer in Japan, and concluded that there was a positive effect, in other words, that saturated fat, the kind found in beef, caused colon cancer. What the data actually showed was that consumption of polyunsaturated vegetable oils, not saturated animal fats, was associated with a higher incidence of colon cancer. And Wynder forgot to mention that Asians have much higher rates than Americans of other types of cancers, particularly harder-to-treat cancers of the liver, pancreas, stomach, esophagus and lungs.

Then in 1973, William Haenszel and his colleagues from the National Cancer Institute reported the findings from a study that relied on notoriously unreliable dietary recall and lacked matched controls—in other words, a very poorly designed study.⁵⁷ The researchers stated that they found a relationship between beef and colon cancer that fit the earlier work of Wynder. Actually, what they really found was that among Westernized Japanese Americans, those who said they consumed lots of macaroni, green beans and peas, as well as beef, had the highest rates of colon cancer; while among traditional Japanese Americans, those who said they consumed lots of dried cuttlefish, Chinese peas, bamboo shoots, rice and fermented soy products had the highest rates of colon cancer. Thus, the researchers singled out beef as the culprit from a choice of several foods associated with cancer in Westerners and ignored politically correct foods like soy products, fish and vegetables as a potential cause of cancer in Japanese Americans. Unfortunately, this second-rate and inconclusive study has become firmly fixed in the consciousness of the scientific community as providing evidence for the assertion that beef causes colon cancer.

Two American studies conducted in the 1990s did find a higher risk of colon cancer among those who eat red meat.⁵⁸ However, no study conducted in Europe has ever shown an association between meat consumption and cancer.⁵⁹ These findings suggest that European sausage and luncheon meat, included in the rubric of “meat consumption,” are prepared by traditional methods that require few additives, while similar products in the United States contain many carcinogenic preservatives and flavorings. Unfortunately, the American Cancer Society’s 1996 recommendation that Americans cut down on their consumption of meat—particularly fatty meat—in order to avoid cancer makes no distinction between fresh meats and those embalmed with modern chemicals.

While two U.S. studies have implicated meat consumption as a cause of colon cancer, several others contradict these findings. In 1975, researchers compared Seventh-Day Adventist physicians, who do not eat meat, with non-Seventh-Day Adventist physicians, and found that the vegetarian doctors had higher rates of gastrointestinal and colorectal cancer deaths.60 National Cancer Institute data show that Argentina, with very high levels of beef consumption, has significantly lower rates of colon cancer than other Western countries where beef consumption is considerably lower.⁶¹ A 1997 study published in the International Journal of Cancer found that increased risk of colon and rectal cancer was positively associated with consumption of bread, cereal dishes, potatoes, cakes, desserts and refined sugars, but not with eggs or meat.⁶² And a 1978 study published in the Journal of the National Cancer Institute found no greater risk of colon cancer, regardless of the amounts of beef or other meats ingested.⁶³ The study also found that those who ate plenty of cruciferous vegetables, such as cabbage, Brussels sprouts and broccoli, had lower rates of colon cancer.

Actually, we do know one of the mechanisms that initiates colon cancer, and it does not involve meat, per se. Colon cancer occurs when high levels of industrial fats and oils, along with certain carcinogens, are acted on by certain enzymes in the cells lining the colon, leading to tumor formation.⁶⁴ This explains the fact that in industrialized countries, where there are many carcinogens in the diet and where consumption of vegetable oils and carcinogens, in addition to meat, is high, some studies have correlated meat eating with colon cancer; but in traditional societies, where vegetable oils are absent and the food is free of additives, meat eating is not associated with cancer.

Riding piggyback on the alleged link between beef and colon cancer are supposed associations with other cancers. Here the evidence shows a similarly inconsistent pattern. Cancer is a disease of rich countries where numerous factors can be fingered—altered fats, fabricated foods, low levels of protective nutrients, high levels of carcinogens—and rich countries consume lots of beef. But association is not the same as cause. Countries with more telephones have more cancer, but that does not mean that telephones cause cancer. As for prostate cancer, a 2010 meta-analysis found little correlation with red meat and even processed meat.⁶⁵ It also showed little protection from fruits and vegetables.⁶⁶

The fats most associated with cancer are trans fats. In a 1999 analysis of the Nurses’ Health Study, Harvard researchers found that a high intake of trans fats was associated with risk for non-Hodgkin’s lymphoma.⁶⁷ A 2013 study found that a pooled analysis of twelve cohort studies observed no association between total fat intake and ovarian cancer risk; but further analysis revealed that omega-3 fatty acids were protective against ovarian cancer and that trans fats were a risk factor.⁶⁸

In summary, beef became the fall guy for vegetable oils and other ingredients in processed foods, which flooded the marketplace, especially after the Second World War, and ushered in the epidemic of cancer—now estimated to occur in one person out of three.

DO SATURATED FATS MAKE US FAT? Do animal fats lead to lard ass and butter belly? The most cursory look at modern trends should be enough to convince us that the answer is no. The USDA dietary guidelines, implemented in the 1980s, demonized animal fats and gave Americans the green light to eat all the carbohydrates from the base of the food pyramid they wanted. Obesity rates have since doubled, from 15 percent to 30 percent of the population. Many of these high-carb foods are also high in vegetable oils, hidden fats deemed better for weight loss than animal fats. But why would animal fats cause weight gain more than vegetable oils? They are equally caloric. In fact, per weight and volume, animal fats contain slightly lower levels of calories than vegetable oils.

By analyzing menus from turn-of-the-century cookbooks, we can estimate that most diets at that time contained about 35–40 percent of calories as fat. Fats contain about twice as many calories per gram as protein or carbohydrate foods. In a diet of 2,500 calories, 35 percent of calories as fat translates to 97 grams of fat (slightly less than ½ cup) per day, as added fat or distributed in food. Pictures of the general populace at the time do not show large numbers of obese individuals, and in fact, they showed mostly healthy-looking people unless the scene was one of poverty.

A diet low in carbs and high in protein and fat for weight loss is not a new idea. First popularized by William Banting in 1863 in a booklet called Letter on Corpulence, Addressed to the Public, Banting’s diet included meat, vegetables and fruit, and left out bread, potatoes and sweets. Many low-carb versions have followed, including Robert Cameron’s Drinking Man’s Diet (1964) and the immensely popular low-carb diet of Dr. Robert Atkins. But conventional weight loss advice still calls for replacing fats with carbs because—so the logic goes—fats by volume contain more than double the calories of carbohydrate foods (one tablespoon of butter contains about 100 calories, while one tablespoon of sugar contains 50).

And the high-carb school is sticking to its story. Vigorous debate broke out with the publication of science writer Gary Taubes’s 2002 exposé in the New York Times Magazine, “What If It’s All Been a Big Fat Lie?” In it, Taubes explains why the USDA-endorsed high-carb diet is more likely to make us fat (and diabetic) than a diet containing higher levels of fat, including saturated fat. Many dieters wrote to the newspapers confirming their experience that only the Atkins-type diet helped them lose weight and keep it off.

In response, low-fat guru Dean Ornish got plenty of column space to sputter about the dire consequences of a high-fat diet and prime-time exposure on Oprah Winfrey’s show to warn dieters about the Atkins regime. Oprah was polite but noncommittal. According to the tabloid Globe, by 2002, Oprah’s days of yo-yo dieting were over. She had come down to a reasonable weight of 174 pounds and was “filled with joy.” Her successful dieting approach? Eliminate the “white stuff”—potatoes, white rice, pasta, refined sugar, bread and salt. Eliminating salt is probably not necessary, but the TV star seems to have found the winning combination—reasonable expectations and an elimination of all those high-carb foods that we’ve been told will keep us healthy and slim.

A study by Dr. Eric Westman of Duke University, presented at the annual scientific meeting of the American Heart Association, looked at one hundred twenty overweight volunteers, who were randomly assigned to the Atkins diet or the AHA’s Step 1 Diet, a widely used low-fat approach. On the Atkins diet, people limited their carbs to less than 20 grams per day, and consumed 60 percent of their calories from fat. After six months, the people on the Atkins diet had lost an average of 31 pounds, compared with 20 pounds on the AHA diet, and more people stuck with the Atkins regimen. Total cholesterol fell slightly in both groups, but only those in the Atkins group saw an increase in HDL.69 The results were relegated to a side column in the Washington Post.⁷⁰ Sally Squires, author of “Lean Plate Club,” a weekly column, reported the good news in a few sentences, followed by paragraphs of backpedaling—the Atkins diet could cause heart disease, constipation and nutritional deficiencies. “We were surprised that women could adhere to it [the Atkins diet] as well as they did,” said dietician Bonnie Brehm. “I’m not sure that there is a take-home message from this study, except that there is more research needed… We by no means are recommending the Atkins diet from this one study.” But there was more than one study confirming these results.

A 2003 study conducted by Harvard School of Public Health (presented to the Association for the Study of Obesity, but not published) followed twenty-one overweight volunteers, divided into three groups. All food was prepared for the volunteers so the researchers knew exactly what they were eating. Those eating a high-fat diet (65 percent of calories as fat) lost more weight than those eating high-carb diets (23 versus 17 pounds lost), even though their calorie intake was the same. In fact, those eating a high-fat diet containing 300 more calories per day still lost more weight than the lower-calorie, high-carb group (20 versus 17 pounds lost). This interesting research received no media attention whatsoever, and all descriptions of it and its findings have disappeared from the Internet.⁷¹

Diets high in fat are more satisfying and can lead to voluntary calorie restriction, as shown by a 2007 study conducted by Temple University School of Medicine. The study took place in a clinical research center where every calorie eaten and spent was measured. After a week of typical eating, ten obese patients with type 2 diabetes followed a diet that limited their carbohydrate intake to 20 grams per day, but allowed unlimited protein and fat. With carbs out of the diet, the patients spontaneously reduced their daily energy consumption by 1,000 calories per day. “When carbohydrates were restricted,” said lead researcher Guenther Boden, MD, “the subjects spontaneously reduced their caloric intake to a level appropriate for their height, did not compensate by eating more protein or fat, and lost weight. We concluded that excessive overeating had been fueled by carbohydrates.” In addition to calorie reduction and weight loss, the subjects experienced markedly improved glucose levels and insulin sensitivity, as well as lower triglycerides and cholesterol.⁷² The interesting thing about this study was the fact that the subjects did not consciously try to restrict calories or lose weight, showing that restricting carbs and increasing fat in the diet works better than will power.

Also in 2007, other researchers found that a high-fat diet is just as effective as a high-carb diet for long-term weight loss, with better HDL-cholesterol (the so-called “good” cholesterol) levels among high-fat dieters.73 And in the same year, researchers at Louisiana State University found that participants who ate eggs for breakfast had greater weight loss results and better energy levels than those who ate two bagels, even though the number of calories in both diets was about the same.⁷⁴

Another study that year compared popular diets and found that overweight women trying the Atkins low-carbohydrate diet plan lost more weight (ten pounds versus about six) than women following the LEARN low-fat diet, which was patterned after the government dietary guidelines, and the Ornish diet, a very low-fat, mostly vegetarian plan, and much more (ten pounds versus three) than women following the Zone diet, a high-protein, restricted-carbohydrate plan. The weight loss occurred in spite of the fact that the Atkins dieters did not follow the guidelines very well, consuming far more carbs than allowed on the plan.⁷⁵ According to Christopher D. Gardner, assistant professor at the Stanford University School of Medicine and the study’s lead author, “There’s something to the low-carb thing that’s intriguing. Cutting back drastically on simple carbohydrates is clearly a step in the right direction to helping people lose weight.” Other markers, such as blood pressure and cholesterol levels, were similar or better among Atkins dieters, in spite of the fact that these diets contained about 30 percent of calories as saturated fat—triple the recommended amount.

The results did not please proponents of low-fat diets. “Once the weight-loss stops, the effect of saturated fat would be negative,” said James O. Hill, director of the Center for Human Nutrition at the University of Colorado at Denver. “There is no magic combination of fat versus carbs versus protein,” said Alice Lichtenstein of Tufts University. “It doesn’t matter in the long run. The bottom line is calories, calories, calories.”⁷⁶ And finally, from Dean Ornish himself: “It’s a lot easier to follow a diet that tells you to eat bacon and brie than to eat predominantly fruits and vegetables… I’m concerned that this study may cause people to forgo eating a healthy diet for one that’s actually harmful for them.”⁷⁷

That same year, researchers in Sweden published an interesting study involving almost twenty thousand perimenopausal Swedish women over nine years. Some weight gain is a normal occurrence at menopause, in part because midriff fat produces a type of estrogen to compensate for the estrogen produced by the ovaries, which at menopause are winding down. The researchers found that participants eating cheese and full-fat dairy had a lower rate of weight gain as they grew older.⁷⁸ Like the Harvard study a few years earlier, these findings received no coverage in the press.

In a 2008 trial carried out in Israel, described by Gary Taubes as “arguably the best such trial ever done and the most rigorous,” researchers found that a low-carbohydrate diet high in saturated fat resulted in the greatest weight loss and the most desirable lipid profiles. The trial compared three diets: a calorie-restricted American Heart Association (AHA) diet with about 30 percent of calories from fat, with less than 10 percent of calories as saturated fat; a calorie-restricted Mediterranean diet, high in dietary fiber and monounsaturated fat; and a low-carbohydrate diet, described as “high in saturated fat,” containing about 40 percent of calories as fat, with 12.5 percent as saturated fat. Calories were not restricted on the low-carbohydrate diet, yet after two years, this group had lost the most weight—ten pounds versus six in the low-fat diet. LDL-cholesterol reduction was best with the Mediterranean diet, while those on the supposedly heart-healthy AHA-recommended diet saw no reduction in LDL-cholesterol. Those on the low-carbohydrate diet had a moderate reduction of LDL-cholesterol, but the best results for the ratio of total cholesterol to HDL-cholesterol, with increased HDL-cholesterol, the so-called “good” cholesterol, whereas the other two groups did not. Furthermore, the low-carb dieters saw the biggest reduction in C-reactive protein, a marker for inflammation, and the nondiabetic low-carb dieters had the lowest fasting insulin levels. (Diabetics on the Mediterranean diet had the best markers for fasting glucose and insulin levels.)79

The two primary press sources, HealthDay and Reuters, both reported this study incorrectly. The Reuters headline: “Similar weight loss on 3 different, popular diets.”⁸⁰ According to HealthDay: “Diet Plans Produce Similar Results: Study finds Mediterranean and low-carb diets work just as well as low-fat ones.”⁸¹ Tara Parker Pope of the New York Times minimized the results by reporting, “The results highlight the difficulty of weight loss and the fact that most diets do not work well.”⁸²

Still, low-fat diets do work for some people. The explanation is that when a person changes his diet from the typical American diet of processed foods to the recommended low-fat diet containing lots of whole grains and vegetables, the body is no longer taking in all the excess omega-6 and trans fats found in industrial foods. And he is replacing foods loaded with sugar and additives with more natural foods containing more vitamins and minerals. But most importantly, the body turns the excess carbohydrates into saturated fat. This saturated fat can replace omega-6 and trans fatty acids in the tissues, which is advantageous and helps the patient feel better. A high-carbohydrate diet is really a high-saturated-fat diet, and as we shall see in Chapter 4, various processes on the cellular level work better when ample saturated fatty acids are available.^*

Under experimental conditions of overfeeding simple sugars (sucrose and glucose) in a diet that provided 40 percent of energy as fat, the researchers found that the carbohydrate was oxidized and turned into fat in such a manner to prevent weight loss.⁸³ In other words, a diet high in both fats and carbohydrates may cause weight gain, especially when these are processed vegetable oils and refined carbohydrates.

AUTOIMMUNE DISEASE IS ANOTHER CRIME laid at the feet of saturated animal fats—conditions such as MS, asthma, inflammatory bowel disease and rheumatoid arthritis. The logic goes like this: saturated animal fats contain a fatty acid called arachidonic acid (AA), and arachidonic acid causes inflammation. Thus, saturated fats cause inflammation. Indeed, animal fats are our only source of this critical fatty acid—it is involved in the life-saving process that leads to inflammation, and without inflammation, we cannot heal. But AA also helps resolve inflammation. As we shall see in Chapter 5, AA is also critical to gut health and plays many important roles in the body.

The chief culprit in causing inflammation is trans fatty acids. In a 2002 study, human subjects who consumed stick margarine saw an increase in the production of inflammatory prostaglandins associated with atherosclerosis, while neither liquid soy oil nor butter had the same inflammatory effect.^*84

Regarding asthma, several studies have shown that full-fat dairy products such as whole milk and butter protect against asthma, especially in children.⁸⁵ (More on this in Chapter 8.)

Most popular books on multiple sclerosis (MS), a chronic and debilitating wasting of the nervous system, warn against the consumption of saturated fatty acids. Saturated fats are said to interfere with anti-inflammatory prostaglandins, a statement that is not supported by research. In fact, analysis of almost two hundred thousand women involved in the Nurses’ Health Studies found that saturated fat, animal fat and cholesterol were protective against MS.⁸⁶ A high intake of omega-6 and trans fatty acids—in other words, industrial fats and oils—was associated with increased risk of MS. Even consumption of monounsaturated fat, the kind found in olive oil, carried a slight increase in risk.

As for rheumatoid arthritis, just about all the “experts” say that saturated fat contributes to painful joints because it causes inflammation. This advice constitutes mere speculation; in fact, very few studies have looked at the effects of saturated versus polyunsaturated fatty acids on the symptoms of rheumatoid arthritis, and those that have cannot be used to claim that saturated fats are bad for arthritis sufferers. In one study, a group of patients consumed a diet high in polyunsaturated fatty acids supplemented with omega-3 fatty acids called EPA and DHA (more about these in Chapter 5), while the other group consumed a diet high in saturated fatty acids. The researchers found no statistical difference between the two groups in markers for inflammation and arthritis.⁸⁷

In another study, a diet high in polyunsaturated fatty acids and low in saturated fats reduced morning stiffness and tender joints in the short term, but the control group on a diet higher in saturated fat fared better on follow-up, one to two months later.⁸⁸

IN 2009, JUST IN TIME for Valentine’s Day, an ad alerting men and their partners to the supposed link between fatty, meat-heavy diets and erectile dysfunction aired on CNN, ESPN and Lifetime, thanks to the Physicians Committee for Responsible Medicine (PCRM). The ad, titled “Room 103,” depicts a romantic hotel room and a steamy sexual encounter that comes to a crashing halt because of failure to perform. The camera then pans to the remains of the couple’s dinner: a meat-heavy, high-fat dinner on the room service tray. The ad ends with the tag line, “Eating meat contributes to artery blockages—and that can make you impotent.” The press release specifically targets the Atkins diet, high in meat and saturated fats, as a cause of erectile dysfunction, claiming that high cholesterol levels contribute to impotence.*⁸⁹

Impotence appears to be a huge problem these days, given the sales of performance-enhancing drugs like Viagra, but saturated fats should not get the blame for the vast inadequacies of the standard American diet. San Diego nutritionist Kim Schuette is seeing erectile dysfunction in men as young as twenty. She treats it—very successfully—by advising them to eat a half pound of butter and six egg yolks per day. They usually return to her office a month later with grins on their faces. Egg yolks are considered a fertility food in many parts of the world.

Impotence is a commonly reported side effect of cholesterol-lowering regimes because the body makes testosterone out of cholesterol. Vitamin A is key to this conversion—and cholesterol-lowering drugs block the uptake of vitamin A. Cardiovascular disease alone is associated with erectile dysfunction, but treatment with statins seems to worsen this condition.^†90

Saturated fats are often blamed for lowered sperm count as well. “Eating a fatty diet could reduce a man’s sperm count by 40 percent,” declared the Daily Mail, “enough to put every man off his bacon and egg.”⁹¹ This dire warning referred to a 1999 study published in the American Journal of Clinical Nutrition⁹² which claimed that saturated fat was associated with reduced semen quality among seven hundred Danish men. Zoë Harcombe, PhD, of the UK produced a brilliant analysis of the document,⁹³ which noted that the researchers jumped to sweeping conclusions based on differences in fat consumption that were actually very small; they could have equally concluded from the data that monounsaturated fat and polyunsaturated fat lowered sperm count. The study did reveal that the period of abstinence for those consuming more saturated fat was less, which could explain the lower sperm count. A much more interesting—and more accurate—headline would declare: “Men who eat more saturated fat have sex more frequently!”

“SATURATED FAT CAN MAKE YOU STUPID.” That was the headline in a 2006 Swedish newspaper report linking saturated fat with a decline in cognitive performance.

The newspapers were referring to a study published in the European Journal of Neurology. Male and female rats were divided into two groups, one fed a diet of 42 percent fat from a mixture of coconut oil and corn oil; the other was fed a diet of 10 percent fat. The high-fat diet had a negative effect on “hippocampal neurogenesis,” that is, the generation of nerve cells in an area of the brain called the hippocampus, but only in the male rats. The authors concluded, “Our study provides the first compelling evidence that a high intake of dietary fat per se has a negative influence on hippocampal neurogenesis.”94

But the authors did not single out saturated fats in their conclusion—these accusations appeared only in the media. In fact, the authors did not provide any information in the study about the percentage of fatty acids in the dietary mix. The mix could have been mostly polyunsaturated corn oil—and several studies have shown that polyunsaturated oil inhibits neurological development and function. Nor did the researchers indicate what kind of coconut oil they were using. Most of the coconut oil used in scientific experiments is fully hydrogenated, a process that gets rid of all the essential fatty acids. Thus, a diet of corn oil and coconut oil may have induced a deficiency in omega-3 fatty acids, another likely explanation for cognitive decline. But the interesting thing about these findings is that they occurred only in male rats, not in the females, an indication that the lack of neurogenesis was related to hormonal factors. Most rat chow is based on soy, rich in estrogenic compounds shown to have deleterious effects on male rats.

There is no way to tell from this study which factors inhibited hippocampal neurogenesis, but the least likely one to be the culprit—the normal brain contains very high levels of saturated fat—was singled out as the whipping boy for the others.

The following year in Britain, a similar article appeared in The Daily Mail. The article, titled, “Diet High in Cholesterol Can Trigger Onset of Alzheimer’s,” warned readers about studies showing that “eating lots of foods containing saturated fats, such as butter and red meat, can boost levels of proteins in the brain linked to dementia,” and that “large amounts of harmful cholesterol are found in foods high in saturated fats such as red meat, butter, cheese and offal such as liver and kidneys.”⁹⁵ These dire warnings are not based on studies of humans eating red meat and butter—an online search for red meat or butter plus Alzheimer’s yields nothing—but are based on research in which rats are given large amounts of purified cholesterol. The article cites “growing evidence that taking cholesterol-lowering statins makes people less likely to develop Alzheimer’s later in life.” No reference is provided for this remarkable statement, remarkable given the many published reports of statin-induced cognitive decline.

More sobering news comes from the Honolulu-Asia Aging Study. Researchers followed more than one thousand Japanese-American men over a forty-year period, starting in 1965. They found that cholesterol levels in men with dementia and, in particular those with Alzheimer’s, had declined at least fifteen years before the diagnosis and remained lower than cholesterol levels in men without dementia throughout that period. Their conclusion: “A decline in serum total cholesterol levels may be associated with early stages in the development of dementia.”⁹⁶

Another headline, this one from 2009: “High Fat Diet May Make You Stupid and Lazy.” According to the article, “A new study on rats finds that ten days of eating a high-fat diet caused short-term memory loss and made exercise difficult.”⁹⁷ There’s just one problem with the press release: the rats in the experiment were not fed fat, they were fed oil. The fatty acid composition of the “high-fat” diet that caused memory loss and muscle weakness was 27 percent saturated, 48 percent monounsaturated, and 25 percent polyunsaturated—an oil that would be liquid at room temperature.98 The predominant fatty acid in the mix was monounsaturated, the kind of fatty acid in olive oil, peanut oil, canola oil and high-oleic safflower oil, the kind that is supposed to be so good for us. The rats in this study encountered problems typical of those on diets high in industrially processed vegetable oils. So while the media is urging you to avoid meat, sausage and cheese, the foods you really need to avoid are cooking oils, commercial salad dressings, fried foods, chips, snack foods and bakery products like donuts and cookies. If anything will make you stupid and lazy, it is foods like these.

THE NATIONAL KIDNEY FOUNDATION WEBSITE predictably warns kidney patients to avoid “cholesterol-raising” saturated fats. The tragic epidemic of kidney failure, so common in diabetics, taxes our health care system, by some estimates accounting for half of all medical costs. What if saturated fats were the very food that could reverse kidney failure? A recent study on mice indicates the possibility. Researchers at the Mount Sinai School of Medicine in New York used mice with both type 1 and type 2 diabetes. Once kidney damage had developed, half the mice were put on a ketogenic diet, low in carbohydrates and very high in fat. After eight weeks, the researchers noted that kidney damage was reversed in those on the high-fat diet.

Such exciting results should be shouted to the skies, but health officials are administering a large dose of cold water. “This research was carried out in mice so it is difficult to see how these results would translate into any real benefits for people with diabetes at this stage,” said Dr. Iain Frame, director of research at Diabetes UK. “It is too simple to say that kidney failure could be prevented by diet alone and it is also questionable whether the diet used in this model would be sustainable for humans, even in the short term.”⁹⁹ Of course, Diabetes UK and its counterparts in the United States have been pushing a low-fat, high-carb diet for diabetics for decades; this study suggests that this disastrous advice may hasten kidney failure in these patients.

THE PATTERN IS CLEAR. At every turn, saturated fats get the blame for everything that ails us—from kidney disease to cancer to stupidity. What the public doesn’t realize is the fact that the research simply does not support these conclusions; if anything, the science vindicates saturated fat as a cause in all of these diseases, even heart disease.

But what if saturated fats are not merely harmless, but absolutely essential for biochemical processes? That is the premise we will explore in Chapter 4.