Good Calories, Bad Calories: A Critical Review; Chapter 1 – The Eisenhower Paradox



This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Early in the chapter Taubes claims that most mainstream nutrition authorities were saying that the American diet changed during the 20th century, from a plant-based diet to a diet heavy in meat. On pages 10 and 11 he attempts to refute this notion by saying that the USDA statistics from which this notion is drawn is very flawed, citing a personal interview with David Call and a paper on food disappearance data.1 Specifically he says

  • “The USDA statistics, however, were based on guesses, not reliable evidence.”

  • “The resulting numbers for per-capita consumption are acknowledged to be, at best, rough estimates.”

  • “The reports remained sporadic and limited to specific food groups until 1940 […] Until then, the data were particularly sketchy…”

However, the very next paragraph he makes the argument that the US has always been a meat-eating country, and as evidence he cites data from the USDA! “By one USDA estimate, the typical American was eating 178 pounds of meat annually in the 1830s, forty to sixty pounds more than was reportedly being eaten a century later.” Either the food stats are reliable before 1940 or the are not. Pick a side and be consistent.

He’s really all over the map in this section because he then claims that in fact we did eat less meat in the early 20th century due to a few reasons: the cattle industry could not keep up with population growth, meat rationing during WW1, and Upton Sinclair’s The Jungle. He then makes the argument that Americans started eating more fruits and vegetables and decreased consumption of animal products. Following this change, incidents of heart disease skyrocketed to become an epidemic – an epidemic that earlier in the chapter he claims was completely bogus.

* * *

On pages 14 and 15 Taubes talks a bit about cholesterol and says

Despite myriad attempts, researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream than those who didn’t. “Some works claim a significant elevation in blood cholesterol level for a majority of patients with atherosclerosis,” the medical physicist John Gofman wrote in Science in 1950, “whereas others debate this finding vigorously. Certainly a tremendous number of people who suffer from the consequences of atherosclerosis show blood cholesterols in the accepted normal range.”

It’s interesting to note that immediately after that sentence in the cited text Gofman also wrote2

There does exist a group of disease states (including diabetes mellitus, nephrotic nephritis, severe hypothyroidism, and essential familial hypercholesteremia) in which the blood cholesterol level may be appreciably elevated. Such patients do show, in general, earlier and more severe atherosclerosis than the population at large.

In fact, most of the text makes the case that there are particular cholesterol particles to blame for atherogenesis, specifically those with a density of 10-20 Svedberg units that are currently known as LDL. However, since this paper was published in 1950 they are referred to as the Sf 10-20 class of cholesterol molecules. Gofman also noted – prior to even anything that Keys published on the subject – that dietary lipids affect these Sf 10-20 molecules, stating:

Our preliminary study of a group of 20 patients whose diet we have restricted in cholesterol and fats has demonstrated that the concentration of the Sf 10-20 class of molecules is definitely reduced or even brought down to a level below resolution ultracentrifugally in 17 of the cases studied within two weeks to one month.

I can’t understand why Taubes didn’t mention that, can you?

* * *

Taubes knocks me for a loop on page 15 when he states:

The condition of having very high cholesterol—say, above 300 mg/dl—is known as hypercholesterolemia. If the cholesterol hypothesis is right, then most hypercholesterolemics should get atherosclerosis and die of heart attacks. But that doesn’t seem to be the case.

Actually that seems to be exactly the case… even by the study Taubes cites.

Coronary Artery Disease in 116 Kindred with Familial Type II Hyperlipoproteinemia

click to embiggen

click to embiggen

That study even seems to be in agreement with the other studies on familial hypercholesterolemia at the time3:

Our results are qualitatively similar to analyses on a smaller scale which have established an enhanced risk of premature CAD in affected members of families with familial hypercholesterolemia.

But since certain thyroid and kidney disorders might also cause hypercholesterolemia I suppose Taubes can just ignore all that evidence linking cholesterol to heart disease.

* * *

Pg. 15

Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol. In 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death, and so they autopsied more than a hundred very recently deceased New Yorkers, all of whom had died violently, measuring the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic illness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.”

I was unable to find the cited Landé and Sperry paper. It is so old and obscure that not only was I unable to find it, the databases I used (PubMed, WorldCat, Academic Search Complete) could not find a record of it even existing. But let’s do something we probably should not do and take Taubes at his word here. It is still interesting to note that this is an example of an observational study, specifically a cross-sectional study. Later in the book Taubes will make the case that observational studies are worthless. In fact, you will see throughout the book that Taubes will cite observational studies, usually without caveat, if it fits his meat-is-good narrative. However, if he doesn’t like the conclusion of a study (observational or otherwise) you will find that he impugns the methodology, the authors, or even the entire field of science of which it is a part. Get your popcorn ready.

* * *

Like the above point, this is not a real significant issue, but it shows that Taubes is not above quote mining to try and paint someone in a negative light. On page 16:

Henry Blackburn, his longtime collaborator at Minnesota, described him as “frank to the point of bluntness, and critical to the point of sharpness.” David Kritchevsky, who studied cholesterol metabolism at the Wistar Institute in Philadelphia and was a competitor, described Keys as “pretty ruthless” and not a likely winner of any “Mr. Congeniality” awards.

I imagine the point of these quotes is to paint Keys as kind of an asshole, just in case any reader might find themselves sympathizing with Keys when Taubes takes massive, diarrhea-like shits all over Keys’s research and Keys personally. I cannot verify the Kritchevsky quote above because it was from a personal interview, but adding a bit of context to the Blackburn quote can change the tone entirely4:

Ancel Keys has a quick and brilliant mind, a prodigious energy, and great perseverance. He can also be frank to the point of bluntness, and critical to the point of sharpness. But by the boldness of his concepts, the vigor of his pursuits, and the rigor of his methods, as well as by his personal example, he led several generations of investigators in making powerful contributions to the public health.

The entire article is actually quite praiseworthy.

* * *

Pg. 15:

This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. And even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.

I’m not sure why Taubes names DeBakey as the primary source here, since he was actually the fourth author in the study that was cited, but no matter… It’s interesting to find that if you check the 1964 paper that is cited, it’s a type of observational study called a case series that examines 1,700 surgical patients treated for some sort of atherosclerosis.5 Turns out 1,416 out of the 1,700 (or 83%) have what the Mayo Clinic would describe as “high” cholesterol levels (over 200 mg/dL).

Does Taubes even read the studies he cites? Or does he read them and deliberately misrepresent them?

A second paper he cites in support of that paragraph is not even a study, but a statement by the president of the American Heart Association6 (wait… they’re supposed to be the bad guys, right?). He says many things in that statement, but what is most relevant to this paragraph is he says that

In a nation of over a quarter of a billion people we are a remarkably heterogeneous lot, and in truth there are no two of us alike. Those with low cholesterols as a group seem to have less coronary disease than those with high cholesterols, but this is too often extrapolated to apply directly to one individual.

He goes on to expound that, sure, cholesterol levels are important, but sometimes people get heart disease and don’t have high cholesterol levels so we should individualize our advice. I don’t think it really helps or hurts Taubes’s argument, but evidently he cited it anyway. Probably to pad his references.

* * *

If Taubes’s irrational contempt for Keys was not obvious before, it should be crystal clear after this passage on page 16:

When Keys launched his crusade against heart disease in the late 1940s, most physicians who believed that heart disease was caused by diet implicated dietary cholesterol as the culprit. We ate too much cholesterol-laden food—meat and eggs, mostly—and that, it was said, elevated our blood cholesterol. Keys was the first to discredit this belief publicly, which had required, in any case, ignoring a certain amount of the evidence.

Before Keys came along all of the “evidence” that dietary cholesterol substantially affects serum cholesterol was from animal studies. Studies that, just two pages earlier, Taubes argues have no bearing on human physiology. So Keys decides to conduct some cholesterol research on actual humans, and concludes that dietary cholesterol actually doesn’t have a substantial effect on serum cholesterol.7 If this were anyone else other than Keys Taubes would likely praise them for not following the conventional wisdom of the day and conducting proper scientific research, but instead Keys is accused of “ignoring” evidence. I think that’s fair.

In the same paragraph as above Taubes discusses a cholesterol study:

In 1937, two Columbia University biochemists, David Rittenberg and Rudolph Schoenheimer, demonstrated that the cholesterol we eat has very little effect on the amount of cholesterol in our blood.

Although the statement “the cholesterol we eat has very little effect on the amount of cholesterol in our blood” is true for most people, as we have just discovered, the Rittenberg/Schoenheimer study that Taubes mentions has almost nothing to do with that statement.8 Firstly, the study was conducted on mice, and extrapolating results on people from cholesterol studies on animals are certainly dubious as Taubes himself admits. Moreover, the study itself involves feeding mice water labeled with deuterium then measuring deuterium in their cholesterol and fatty acids in the mice’s tissues to see how much deuterium had been incorporated into those molecules. As far as I can tell it has nothing to do with feeding them cholesterol and seeing if that impacts their blood cholesterol levels. But correct me if I am wrong.

Pg. 16 continued:

As a result, Keys insisted that dietary cholesterol had little relevance to heart disease. In this case, most researchers agreed.

Most researchers agreed… 16 years later.9

* * *

On page 17 Taubes writes:

By 1952, Keys was arguing that Americans should reduce their fat consumption by a third, though simultaneously acknowledging that his hypothesis was based more on speculation than on data: “Direct evidence on the effect of the diet on human arteriosclerosis is very little,” he wrote, “and likely to remain so for some time.”

This is another minor point, but it should be pointed out that THAT IS WHAT A HYPOTHESIS IS. It’s a guess based on little or no evidence, and all scientists have them. Just for context, here’s the quote from Keys that Taubes plucked with a bit more… umm… context10:

[W]e may remark that direct evidence on the effect of the diet on human atherosclerosis is very little and is likely to remain unsatisfactory for a long time. But such evidence as there is, plus valid inferences from indirect evidence, suggests that a substantial measure of control of the development of atherosclerosis in man may be achieved by control of the intake of calories and of all kinds of fats, with no special attention to the cholesterol intake. This means: (1) avoidance of obesity, with restriction of the body weight to about that considered standard for height at age 25; (2) avoidance of periodic gorging and even temporary large calorie excesses; (3) restriction of all fats to the point where the total extractable fats in the diet are not over about 25 to 30 per cent of the total calories; (4) disregard of cholesterol intake except, possibly, for a restriction to an intake less than 1 Gm. per week.

Taubes gets the quotation a smidge wrong, but it still keeps the spirit of the original. The bigger picture here is that Keys is recommending (in an academic journal, by the way) to avoid becoming obese, avoid gorging on food, a diet that’s about 30% fat, and to not worry too much about cholesterol intake. Pretty uncontroversial stuff, if you ask me. Yet Taubes portrays Keys here and elsewhere as some kind of radical crusader, religious zealot, idiot, and kind of an asshole.

* * *

On page 18 Taubes discusses a 1957 paper by Jacob Yerushalmy and Herman Hilleboe, which is something of a response to Ancel Keys’s 1953 paper Atherosclerosis: A Newer Problem in Public Health.11 If you’re not familiar with the Keys paper I will give you a brief synopsis. Keys published some data that suggested a remarkable relationship between fat in the diet and heart disease. Included in the paper was a striking (if oversimplified) figure looking at several countries and their population’s typical fat intake juxtaposed with deaths from heart disease.


Taubes says:

Many researchers wouldn’t buy it. Jacob Yerushalmy, who ran the biostatistics department at the University of California, Berkeley, and Herman Hilleboe, the New York State commissioner of health, co-authored a critique of Keys’s hypothesis, noting that Keys had chosen only six countries for his comparison though data were available for twenty-two countries. When all twenty-two were included in the analysis, the apparent link between fat and heart disease vanished. Keys had noted associations between heart-disease death rates and fat intake, Yerushalmy and Hilleboe pointed out, but they were just that. Associations do not imply cause and effect or represent (as Stephen Jay Gould later put it) any “magic method for the unambiguous identification of cause.”

I have actually written about this in a previous blog post, but I will revisit this again. Aside from the fact that Keys never claimed a cause-and-effect relationship (much less an unambiguous one) and always identified it as an association, Taubes completely misrepresents the results of the study. It’s true that after Yerushalmy and Hilleboe added more data into the graph the relationship becomes a bit more muddied, but it certainly does not vanish as Taubes claims. There is still a noticeable relationship.12 See for yourself.


What’s even more interesting is that Y&H actually conclude that consumption of animal fat and/or animal protein is much more strongly associated with heart disease than total fat. Moreover, vegetable fat and/or vegetable protein is actually negatively correlated with heart disease. The resolution is not very sharp, but here are the results. I’ll leave it to you to wonder why Taubes ignores this highly pertinent information.



click to embiggen

See Taubes response #1

* * *

On pages 19-20 Taubes claims that Keys “insisted” that fat elevated cholesterol. I am not sure what Keys was doing that made him so insisting, other than writing a few academic articles concluding that there was an association between dietary fat and serum cholesterol (which there was), while also making sure to point out that there are many details about this association that have yet to be discovered (which there also were). Taubes then goes on to mention some studies that examined those details:

In 1952, however, Laurance Kinsell, director of the Institute for Metabolic Research at the Highland–Alameda County Hospital in Oakland, California, demonstrated that vegetable oil will decrease the amount of cholesterol circulating in our blood, and animal fats will raise it. That same year, J. J. Groen of the Netherlands reported that cholesterol levels were independent of the total amount of fat consumed: cholesterol levels in his experimental subjects were lowest on a vegetarian diet with a high fat content, he noted, and highest on an animal-fat diet that had less total fat. Keys eventually accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.

In other words, Keys did what any good scientist should do: he followed the evidence. Yet the syntax of the last sentence would have you imagine that Keys was some sort of stubborn asshole that refused to accept the truth until the evidence overwhelmed him.

* * *

This may be another nitpicky issue, but the following quote is misleading. Page 20:

This kind of nutritional wisdom is now taught in high school, along with the erroneous idea that all animal fats are “bad” saturated fats, and all “good” unsaturated fats are found in vegetables and maybe fish. As Ahrens suggested in 1957, this accepted wisdom was probably the greatest “handicap to clear thinking” in the understanding of the relationship between diet and heart disease.

First of all, I was never taught that kind of “nutritional wisdom” in high school. Come to think of it I was never taught any nutritional wisdom in high school, but that’s neither here nor there. My issue with this is that in the text that Taubes cites as the source of that quote, Ahrens does not say that the animal fat = bad / vegetable fat = good binarism is the greatest handicap to clear thinking. What he does say is that the good-bad dyad was a greater handicap than the confusion about why experimental diets were designed to be eucaloric.13

* * *

Tabues uses a 1957 review article titled “Atherosclerosis and the Fat Content of the Diet” as a source for three claims in this chapter. One is simply a block quote on page 8. The other two claims are very tenuous, especially the following found on page 20:

In 1957, the American Heart Association opposed Ancel Keys on the diet-heart issue.

The article does mention Keys a few times, as well as a number of other researchers involved with dietary research involving atherosclerosis, but it is very neutral on Keys. In fact, you might even say the author mildly endorses Keys at a couple of points: “Mayer et al. found that high-fat animal or vegetable diets increased and low-fat diets decreased serum cholesterol of normal subjects, confirming earlier data of Keys.” And “Keys, in particular, has placed emphasis on the proportion of total dietary calories contributed by the common food fats […] Certainly there is an abundance of data, both clinical and experimental, that tends to relate excess fat intake to atherosclerosis.”14

After reading the article I certainly didn’t get the idea that the AHA opposed Keys. Even if they did they never explicitly stated this.

* * *

On page 21 Taubes pulls some numbers from thin air:

As Time reported, Keys believed that the ideal heart-healthy diet would increase the percentage of carbohydrates from less than 50 percent of calories to almost 70 percent, and reduce fat consumption from 40 percent to 15 percent.

The Time article actually does report that Keys suggested American reduce their fat intake from 40 to 15 percent. However, there is no mention in the entire article about Keys recommending an increase in carbohydrates.15

Go to Good Calories, Bad Calories: A Critical Review; Chapter 2 – The Inadequacy of Lesser Evidence



1. Call, D. L. & Sánchez, A. M. Trends in fat disappearance in the United States, 1909-65. J. Nutr. 93, Suppl:1–28 (1967).

2. Gofman, J. W. et al. The Role of Lipids and Lipoproteins in Atherosclerosis. Science 111, 166–186 (1950).

3. Stone, N. J., Levy, R. I., Fredrickson, D. S. & Verter, J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinemia. Circulation 49, 476–488 (1974).

4. Blackburn, H. Ancel Keys. at

5. Garrett H, Horning EC, Creech BG & De Bakey M. Serum cholesterol values in patients treated surgically for atherosclerosis. JAMA 189, 655–659 (1964).

6. James, T. N. Presidential address. AHA 53rd scientific sessions, Miami Beach, Florida, November 1980. Sure cures, quick fixes and easy answers. A cautionary tale about coronary disease. Circulation 63, 1199A–1202A (1981).

7. Keys, A., Anderson, J. T., Mickelsen, O., Adelson, S. F. & Fidanza, F. Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol. J. Nutr. 59, 39–56 (1956).

8. Rittenberg, D. & Schoenheimer, R. Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation. J. Biol. Chem. 121, 235–253 (1937).

9. Quintão, E., Grundy, S. M. & Ahrens, E. H. Effects of dietary cholesterol on the regulation of total body cholesterol in man. J. Lipid Res. 12, 233–247 (1971).

10. Keys, A. Human Atherosclerosis and the Diet. Circulation 5, 115–118 (1952).

11. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y. 20, 118–139 (1953).

12. Yerushalmy, J. & Hilleboe, H. E. Fat in the diet and mortality from heart disease; a methodologic note. N. Y. State J. Med. 57, 2343–2354 (1957).

13. Ahrens, E. H., Jr. Seminar on atherosclerosis: nutritional factors and serum lipid levels. Am. J. Med. 23, 928–952 (1957).

14. Page, I. H., Stare, F. J., Corcoran, A. C., Pollack, H. & Wilkinson, C. F., Jr. Atherosclerosis and the fat content of the diet. Circulation 16, 163–178 (1957).

15. The Fat of the Land. Time 77, 48 (1961).

Good Calories, Bad Calories: A Critical Review; Chapter 3 – Creation of Consensus



This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Near the beginning of chapter three Taubes makes some serious unfounded claims. From page 44:

This alliance between the AHA and the makers of vegetable oils and margarines dissolved in the early 1970s, with reports suggesting that polyunsaturated fats can cause cancer in laboratory animals. This was problematic to Keys’s hypothesis […]

Polyunsaturated fats cause cancer?!?!?! That’s a bold claim for which Taubes cites two supporting texts. One is a New York Times article from 1973 titled “Heart Association Strengthens its Advice: Cut Down on Fats,” and it barely has anything to do with Taubes’s claim.1 It mostly deals with atherosclerosis (not cancer), and hardly discusses polyunsaturated fats. The closest thing you will find that even comes close to supporting the claim that “polyunsaturated fats can cause cancer in laboratory animals” is near the end of the article. There is a section titled Challenges and Answers that states the following:

Despite this evidence, doubts and doubters remain. Some of the challenges to the heart disease-fatty diet thesis, and the answers from the heart association, follow: […] Polyunsaturates are dangerous. Dr. Mueller says that there is no evidence that consumption of polyunsaturates is harmful at the recommended levels or even considerably above these levels. While such consumption is known to increase the body’s need for vitamin E, most vegetable oils contain enough vitamin E to satisfy the need.

Hmmm… Is that strong evidence for his claim? Nope. What about the other citation? It not a study involving laboratory animals, but rather a trial of elderly veterans.2 Turns out the data from that trial show a few more people dying from cancer on a diet high in polyunsaturated fat. But the results from the study were something of an outlier. The authors even mention this:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Again you must ask yourself “Is this evidence strong enough to justify the claim that polyunsaturated fats cause cancer in laboratory animals?” It’s up to you to decide. I might even ask myself a few more questions like “Is this an innocent citation error? Certainly a book of this depth and magnitude is bound to have a few simple human errors. If it is an honest mistake, why do all the mistakes happen to be in favor of a low-carb, high-fat diet?”

Taubes also uses this study later in the chapter so we’ll revisit this soon. See Taubes response #2 and #3.

 * * *

In chapter three Taubes devotes much ink to slandering discussing the 1977 publication of Dietary Goals for the United States by a committee led by George McGovern. Now I have no problem criticizing the government. In fact, I think that one of the great things about living in the US is the right to just trash the hell out of the government and politicians either in private or in the public eye. I encourage everyone to exercise that right if they see fit; however, criticisms have a little more bite to them when they are actually legitimate. Much of the cited evidence against the Dietary Goals comes from what were ostensibly personal interviews with a few people involved with its drafting. Of course, no one is privy to this information so we can only go on what is publicly available.

On page 46-47 Taubes claims:

Dietary Goals was couched as a plan for the nation, but these goals obviously pertained to individual diets as well. Goal number one was to raise the consumption of carbohydrates until they constituted 55–60 percent of the calories consumed. Goal number two was to decrease fat consumption from approximately 40 percent, then the national average, to 30 percent of all calories, of which no more than a third should come from saturated fats. The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels, but it justified its recommendation on the basis that, the lower the percentage of dense fat calories in the diet, the less likely people would be to gain weight, and because other health associations—most notably the American Heart Association—were recommending 30 percent fat in diets. To achieve this low-fat goal, according to the Dietary Goals, Americans would have to eat considerably less meat and dairy products.

When Taubes says “The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels…” he is using a straw man that I’m fairly certain is not even discussed in Dietary Goals. By this point total fat was not the issue, but type of fat was and Dietary Goals discusses the evidence that a diet low in saturated fat and high in unsaturated fat will decrease blood-cholesterol levels. Also, I saw no recommendations for eating “considerably less meat and dairy products,” but please correct me if I am wrong.

Taubes’s arguments against Dietary Goals are not even internally consistent at times. For instance on page 45 Taubes writes “McGovern’s staff were virtually unaware of the existence of any scientific controversy” and “They believed that the relevant nutritional and social issues were simple and obvious.” Yet on page 47 Taubes writes “Though the Dietary Goals admitted the existence of a scientific controversy, it also insisted that Americans had nothing to lose by following the advice.” So did the authors know about a controversy or not? I suppose you could imagine a scenario where the authors knew nothing of a controversy yet wrote about one in an official government document anyway, but it seems specious to me.

Let’s go further into Taubes’s Dietary Goals bloodbath shall we? On page 46…

Having held one set of hearings before publishing the Dietary Goals, McGovern responded to the ensuing uproar with eight follow-up hearings. Among those testifying was Robert Levy, director of the National Heart, Lung, and Blood Institute, who said that no one knew whether lowering cholesterol would prevent heart attacks, which was why the NHLBI was spending several hundred million dollars to study the question.

Would Gary Taubes, a New York Times columnist and alumnus of the Ivy Leagues, possibly take someone out of context to misrepresent their position in order to fit his own low-carb narrative? Surely not. But just to be sure let us add a bit more context to Dr. Levy’s statements.3

We have no doubt from the vast amount of epidemiological data available that elevated cholesterol is associated with an increased risk of heart attack, especially some specific types of high cholesterol. We have no doubt that [blood] cholesterol can be lowered by diet and/or medication in most patients. Where the doubt exists is the question of whether lowering [blood] cholesterol will result in a reduced incidence of heart attack; that is still presumptive. It is unproven, but there is a tremendous amount of circumstantial evidence. Not only is there circumstantial epidemiologic data, but there is very exciting animal data. Here is one of many studies that have been done over the last decade with nonhuman primates. It shows that not only can we prevent atherosclerosis from progressing by making dietary changes, but that regression actually occurs. Atherosclerosis will lessen if we lower [blood] cholesterol levels in animals through diet. The problem is we can’t do these kinds of studies in man; it is not ethical. There is no doubt that [blood] cholesterol can be lowered by diet in free-living populations. It can be lowered by 10 to 15 percent.

You have to ask yourself whether Taubes’s characterization of Levy’s testimony is really an accurate representation of Levy’s actual testimony. As a reader are you at all angry that a science journalist like Taubes misrepresents people over and over again? I am genuinely curious. Let me know in the comments section.

 * * *

Taubes makes stuff up again on page 49:

The ASCN committee concluded that saturated-fat consumption was probably related to the formation of atherosclerotic plaques, but the evidence that disease could be prevented by dietary modification was still unconvincing.*

*It also affirmed the suspicion that polyunsaturated fats might be dangerous, and so further diminished the role of margarines and corn oils in dietary recommendations.

As evidence Taubes cites a paper titled The Evidence Relating Six Dietary Factors to the Nation’s Health by Dr. Ahrens.4 The paper gives a score of 0-100 to associations between a given dietary issue and atherosclerosis, where 0 is the weakest evidence for the association and 100 is the most rock-solid evidence. The final score is an aggregation of scores by several experts in the field based on epidemiological evidence, animal studies, human interventions, autopsies, biological plausibility, etc. Cholesterol alone received a score of 62. Saturated fat alone received a 58. Cholesterol and fat together received a 73. For comparison the association between alcohol and liver disease received an 88, and the association between carbohydrate and atherosclerosis got an 11. Carbohydrate and diabetes got a 13.

I don’t want to tell you how you should interpret that data, but it seems pretty clear to me that the evidence that cholesterol and fat play a role in atherosclerosis is quite strong: well above the halfway point and approaching the level of alcohol and liver disease. Taubes, however, tells his readers that the committee found the evidence “unconvincing” for reasons that should be pretty clear by now.

He also tells his readers that the ASCN committee affirmed that polyunsaturated fats might be dangerous, which apparently diminishes the role of margarine and corn oil. However, the committee claims nothing of the sort; there is no implied subtext either. In fact, there is literally no mention of polyunsaturated fats, corn oil, or margarine.

He does cite a separate paper that, as far as I can tell, has nothing to do with the ASCN committee paper other than being published by the same journal.5 There is still no mention of corn oil or margarine or any kind of affirmation that polyunsaturated fats might be dangerous. In fact, the text claims that polyunsaturated fats are generally beneficial, but that the long term effects of specific concerns such as lipid peroxidation of polyunsaturates have yet to be studied.

* * *

On page 54 Taubes strongly implies (like he has done before) that polyunsaturated fats and low levels of cholesterol leads to cancer and death:

The other disconcerting aspect of these studies is that they suggested (with the notable exception of three Chicago studies reported by Jeremiah Stamler and colleagues) low cholesterol levels were associated with a higher risk of cancer. This link had originally been seen in Seymour Dayton’s VA Hospital trial in Los Angeles, and Dayton and others had suggested that polyunsaturated fats used to lower cholesterol might be the culprits.

Dayton actually suggests the opposite in that very study. Pearce and Dayton actually do conduct a trial with elderly veterans where two groups are fed more-or-less the same diet, except one diet has more polyunsaturated fats in it. The results do indicate that in fact the group eating the diet with more polyunsaturates does have a few more cancer deaths in the group. But, as Taubes would say, there were caveats. I’ll let the authors explain:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Indeed, other investigators’ experiences was not the same. A survey of five similar dietary trials published that same year suggested there was no link between low serum cholesterol and cancer.6 There are a handful of studies you can find that will support the link between cancer and low cholesterol, though. You can find them. But perhaps those results are due to the cholesterol-lowering effects of cancer, not the other way around.7

In fact, the authors of the MRFIT study (of which Taubes displays the results in the next chapter) explicitly mention this.8 In case you’re interested:

The increased total mortality at the lowest cholesterol levels has been noted before. It is primarily due to an increased risk of cancer death in those with the lowest cholesterol concentrations and is probably explained by a cholesterol-lowering effect of cancer. The most recent evidence for this explanation is an analysis of the MRFIT screening cohort which showed that the association between low serum cholesterol and cancer incidence does not persist beyond 5 years of follow-up, whereas that between high serum cholesterol and CHD incidence remains after 5 years.

In any case, regardless of whether or not it was evident to Taubes at the time GCBC was published, the results are in: a recent meta-analysis of 27 large-scale human trials confirmed no association between low cholesterol levels and cancer.9 Of course Taubes would probably demand a large, randomized clinical trial where healthy people are randomly assigned to get cancer and then have their cholesterol levels measured before accepting it. Hell, even then he would probably find a way to dismiss it. Dismissing good evidence that contradicts him is one of Taubes’s greatest skills.

* * *

On pages 53-54 Taubes discusses several studies that have found negative correlations between carbohydrate intake and heart disease.10,11 In other words, studies that have found that carbohydrates may be slightly protective against heart disease. Uh, oh! It’s time for Taubes to do some serious spinning. But remember what I said above? This is his specialty. He has a PhD in spinning science. You might even call him a Spin Doctor! Get it? Okay, here’s what he says:

When one is reading this report, it’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations. Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. Now they no longer felt obliged to test any hypothesis, let alone Keys’s. Rather, they seemed to consider their obligation to be that of “reconciling [their] study findings with current programs of prevention,” which meant the now official government recommendations. Moreover, these studies were expensive, and one way to justify the expense was to generate evidence that supported the official advice to avoid fat. If the evidence didn’t support the recommendations, then the task was to interpret it so that it did.

Now scientists can’t even be trusted!! Why? They’re greedy whores, of course; willing to do and say anything to keep those sweet, sugary NSF grants rolling in. Researchers have to maintain their lavish lifestyle, and if that means lying to the public and a few people get diabetes and die because of it, well, so be it. Health scientists didn’t get into the field of research because of a love of science or truth or the public good – they did it for the cold, hard cash.

Not only is that sentiment one of the most cynical things I have ever read, it is completely absurd and without merit. (I wonder if there are issues of psychological projection here; like when a cheating spouse unreasonably accuses their partner of cheating.) And lest you think Taubes took that quote from some secret literature of the Scientist Guild that shares tips and tricks on how to bilk the government out of research funding and promote chronic diseases for shits and giggles, here is a little more context:

Although the findings reported here – particularly those related to starch intake – may eventually be found to have practical implications, it would be premature to propose dietary alterations before the findings are examined more carefully. We consider the inverse relation of CHD incidence to the total daily caloric intake as a prescription for greater physical activity rather than for greater caloric intake.


The apparently protective effect of starch consumption against CHD seems to imply that the proportion of calories coming from starch should be increased. In isocaloric diets, increased intake of starch is a logical way to balance decreased intake of fat. Thus, from a practical point of view there is no difficulty in reconciling our study findings with current programs for prevention of CHD.

Doesn’t really sound so evil, does it? And by the way, there was never any official government “advice to avoid fat.” Never. The Dietary Goals for the United States that Taubes keeps hammering away at recommended a diet consisting of one-third fat. ONE-THIRD. This is not in any way a low-fat diet or advice to avoid fat. What it is is Taubes’s favorite straw man. For the record Dietary Goals recommended Americans cut their sugar intake by nearly 50%, yet no praise was given for that decision. I wonder why.

* * *

On page 57 Taubes discusses a study, the results of which he doesn’t like because they show that lowering cholesterol reduced nonfatal heart attacks, fatal heart attacks, and overall death. Watch the master of spin work his magic:

Nonetheless, these results were taken as sufficient by Rifkind, Steinberg, and their colleagues so they could state unconditionally that Keys had been right and that lowering cholesterol would save lives. Rifkind and his collaborators also concluded that the cholesterol-lowering benefits of a drug applied to diet as well. Although the trial included only middle-aged men with cholesterol levels higher than those of 95 percent of the population, Rifkind and his colleagues concluded that those benefits “could and should be extended to other age groups and women and…other more modest elevations of cholesterol levels.”

Isn’t he good? By the way, the cited source for that Rifkind quote is a National Heart, Lung, and Blood Institute consensus conference, and those words do not appear in it.12

Go to Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good



1. Brody, J. Heart Association Strengthens Its Advice: Cut Down on Fats. N. Y. Times 54 (1973).

2. Pearce, M. L. & Dayton, S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1, 464–467 (1971).

3. United States. Dietary goals for the United States. (U.S. Govt. Print. Off., 1977). at <;

4. Ahrens, E. H. The evidence relating six dietary factors to the Nation’s health. Introduction. Am. J. Clin. Nutr. 32, 2627–2631 (1979).

5. Glueck, C. J. Appraisal of dietary fat as a causative factor in atherogenesis. Am. J. Clin. Nutr. 32, 2637–2643 (1979).

6. Ederer, F., Leren, P., Turpeinen, O. & Frantz, I. Cancer among men on cholesterol-lowering diets: Experience from five clinical trials. The Lancet 298, 203–206 (1971).

7. Rose, G. & Shipley, M. J. Plasma lipids and mortality: a source of error. The Lancet 315, 523–526 (1980).

8. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

9. Cholesterol Treatment Trialists’ (CTT) Collaboration. Lack of Effect of Lowering LDL Cholesterol on Cancer: Meta-Analysis of Individual Data from 175,000 People in 27 Randomised Trials of Statin Therapy. PLoS ONE 7, e29849 (2012).

10. Yano, K., Rhoads, G. G., Kagan, A. & Tillotson, J. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. Am. J. Clin. Nutr. 31, 1270–1279 (1978).

11. Gordon, T. et al. Diet and its relation to coronary heart disease and death in three populations. Circulation 63, 500–515 (1981).

12. Consensus Conference. Lowering blood cholesterol to prevent heart disease. JAMA 253, 2080–2086 (1985).

Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good



This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

On pages 60-62 Taubes discusses a publication by the National Academy of Sciences titled Diet and Health: Implications for Reducing Chronic Disease Risk.

I’m not sure that Taubes actually reads it because he gets a few things wrong about it. First (and this is a minor point) he says the publication is thirteen hundred pages long, when in fact it is not even eight hundred pages long. At least that’s the version I have.

Second — and this is probably a more important point — he says about the publication:

It was no longer about the validity of the underlying science, which was no less ambiguous than ever, but about whether Americans should be eating low-fat diets or very low-fat diets.

Actually, Diet and Health recommends a diet of 30% of total calories from fat.1 I don’t see how this could be seen as a low-fat diet, much less a very low-fat diet. Clearly Taubes wants the committee to have recommended something like a very low-fat diet, but they did no such thing so he just lies and says they did anyway. (See: straw man)

Taubes then says:

One striking fact about this evolution is that the low-fat diets now being recommended for the entire nation had only been tested twice… The results of those trials had been contradictory.

Clearly Taubes didn’t bother to actually read Diet and Health. If he did he would have noticed the literally TWENTY-SEVEN PAGES of references regarding dietary fat alone! In fact, the bulk of the publication was devoted to explaining the evidence behind the recommendations. I don’t really blame Taubes for not reading it, though; it was quite long and it didn’t really fit nicely into the narrative he was attempting to craft. As a matter of fact one of the cited trials, titled Low-fat Diet in Myocardial Infarction in The Lancet, had a group consuming about half the percentage of calories from fat than what the National Academy of Sciences was recommending in Diet and Health so the results aren’t really comparable. Nevertheless, the low-fat group actually had beneficial effects to weight and serum lipids compared to the control group.2

* * *

Taubes does some really excellent minimizing on pages 63 and 64 when he discusses some data from the MRFIT trial:

For every one thousand middle-aged men who had high cholesterol—between, say, 240 and 250 mg/dl—eight could expect to die of heart disease over any six-year period. For every thousand men with cholesterol between 210 and 220, roughly six could expect to die of heart disease. These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand). If we were to stick rigorously to a cholesterol-lowering diet for thirty years—say, from age forty to seventy, at which point high cholesterol is no longer associated with an increased risk of heart disease—we would reduce our risk of dying of a heart attack by 1 percent.

By the way, I find it humorous that in the previous chapter Taubes was talking about what a disaster the MRFIT trial was, but here he’s discussing it as if it were the capital-T truth.

I think his data is actually wrong, too. He publishes a graph on the same page taken from a MRFIT article, and I think he’s simply guesstimating. The actual data from the trial says that a serum cholesterol value of 220 mg/dl would correspond to a CHD death rate of 5.81/1,000 and a cholesterol value of 250 mg/dl would have a death rate of 9.1/1,000.3,4 I suppose it’s a minor point, but I am going to use the real data in a second.

His choice of how to present the results is a great study of how to deceive with statistics. It also reminds of a scene in Pulp Fiction. You’ve probably seen it, but if you haven’t I’m not going to explain the context because I don’t really need to to make my point.

                         What do you think about what happened 
                         to Antwan?

                         He fell out of a window.

                         That's one way to say it. Another 
                         way is, he was thrown out. Another 
                         was is, he was thrown out by 
                         Marsellus. And even another way is, 
                         he was thrown out of a window by 
                         Marsellus because of you.

So Taubes says “These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand).” That’s certainly one way to say it. Another way is that it reduces your risk of dying from a heart attack by 36%. Another way is it reduces your relative risk of CHD death from 2.88 to 1.84 (with 1.0 being optimal). And even another way to say it is that this data suggests that 205,954 lives in the US could be spared by lowering serum cholesterol from 250 to 220, assuming 20% of the population has cholesterol in excess of 250 mg/dl.

* * *

Page 65-66

Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGill University in Montreal addressed the question of how much longer we might expect to live if no more than 30 percent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies. All three assumed that cholesterol levels would drop accordingly, and that this low-fat diet would have no adverse effects, which was still speculation rather than fact.

The Harvard study, led by William Taylor, concluded that men with a high risk of heart disease—such as smokers with high blood pressure—might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months. “Although there are undoubtedly persons who would choose to participate in a lifelong regimen of dietary change to achieve results of this magnitude, we suspect that some might not,” the Harvard investigators noted.

The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay forty-two thousand deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at sixty-five could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be ninety, he could expect an extra four months.* The McGill study, published in 1994, concluded that reducing saturated fat in the diet to 8 percent of all calories would result in an average increase in life expectancy of four days to two months.

Browner reported his results to the Surgeon General’s Office, and only then submitted his article to JAMA. J. Michael McGinnis, the deputy assistant secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why Browner’s analysis should not be considered relevant to the benefits of eating less fat. “They would have liked it to come out the other way,” explained Marion Nestle, who had edited the Surgeon General’s Report on Diet and Health and had recruited Browner to do the analysis. This put Browner in the awkward position of protecting his work from his own funding agents. As he wrote McGinnis at the time, “I am sensitive to the needs of your office to put forward a consistent statement about what Americans should do, and to your dismay when a project that you have sponsored raises some questions about current policy. I am also concerned that the impacts of recommendations that apply to 240 million Americans are clearly understood. This manuscript estimates the effects of one such recommendation—altering dietary fat intake to 30 percent of calories—based on the assumptions that underlie that recommendation. Shooting the messenger—or creating a smoke screen—does not change those estimates.” JAMA published Browner’s article—“What If Americans Ate Less Fat?”—without an accompanying editorial.

*Browner’s analysis also assumed that restricting dietary fat would reduce cancer deaths, which was speculative then and is even more speculative now.

Although the analysis is perhaps more pessimistic about the benefits of reducing saturated fat, it is also a bit more nuanced than Taubes makes it seem.5 The figures of 42,000 saved lives are in there as is the extra four months of life, but there’s also the following:

The analysis indicates that if those assumptions are valid, restricting dietary fat to a maximum of 30% of total energy intake could reduce CHD mortality rates by between 5% and 20%. Mortality due to cancers of the breast, colon, and prostate might be reduced by an even greater proportion. Similar reductions would also occur in the incidence of these diseases.


From the public health point of view, an increase of 3 months in life expectancy multiplied by 240 million Americans results in about 60 million years of additional life […]

Browner also points out that since the 3-4 month estimate is a statistical average, the real effects of lowering saturated fat would probably translate to several extra years in some individuals and possibly no increased lifespan in others.

But that is not the interesting part… The interesting part is where Taubes states that J. Michael McGinnis tried to shut down the publication of the article. This is based on a letter (presumably) that Browner wrote to McGinnis back then. I have contacted both Dr. Browner and Dr. McGinnis to see if they can confirm this. As of this writing I have received no response from Dr. Browner, but I did receive one from Dr. McGinnis that was very interesting. McGinnis claims he was never contacted by Taubes for his side of the story and that what Taubes wrote “certainly doesn’t ring either familiar or true.” In McGinnis’s own words:

Neither Marion nor I worked in the Surgeon General’s office—rather in a parallel office in HHS—but if the paper was done when she worked with me, it would have been nearly 30 years ago. I really have no recollections on any of what is reported in the passage—including the commissioning of the paper. I do recall the general reported finding on the limited impact on heart disease deaths of the lipid intake reduction indicated, although not the individuals or center (or centers) making the reports. Given the fact that the finding of small effects of isolated dimensions was not unusual (recall MRFIT), it would not have been particularly surprising. It is certainly possible that I would have been of a mind that a narrowcast analysis could be misleading if interpreted as reflecting on the impact of broader associated dietary changes. But unless I was a reviewer commenting on methodologic limits, it would be very unlike me—I cannot recall a single instance—to separately suggest that an article not be published. Indeed, to the contrary, I am squarely in the camp that there is great merit in publicly “calling the question” on these issues to prompt further analytic advances.

Dr. McGinnis also said that he will happily recant if someone were to produce the letter in question. I also contacted Dr. Marion Nestle and she claims that, while she can’t remember the specifics, what Taubes wrote about her remarks are generally true.

* * *

On page 72 Taubes discusses the famous Nurses Health Study and states

In 1992, Willett published the results from eight years of observation of the Nurses cohort. Fifteen hundred nurses had developed breast cancer, and, once again, those who ate less fat seemed to have more breast cancer. In 1999, the Harvard researchers published fourteen years of observations. By then almost three thousand nurses had contracted breast cancer, and the data still suggested that eating fatty foods (even those with copious saturated fat) might protect against cancer.

Walter Willett and Meir Stampfer are two of several authors of these obervational studies.6,7 (Interestingly, Taubes says in a blog post that Willett and Stampfer are not real scientists, they don’t do “real” science, and epidemiology is not to be trusted.) The cited studies do not provide evidence for his claim that copious amounts of saturated fats might protect against cancer. The best thing he can say is that consumption of SATURATED fat doesn’t appear to increase one’s risk of BREAST cancer. Of course the same could also be said of MONOUNSATURATED, POLYUNSATURATED, and even TRANS fats, at least according to these studies.

* * *

On page 73 Taubes gets on the polyunsaturated-fats-cause-cancer bandwagon again stating:

This laboratory evidence that dietary fat caused breast cancer began to evaporate as soon as Diet, Nutrition, and Cancer was published, and researchers could get funding to study it. By 1984, David Kritchevsky, one of the authors of Diet, Nutrition, and Cancer, had published an article in Cancer Research reporting on experiments that had been explicitly designed to separate out the effects of fat and calories on cancer, at least in rats. As Kritchevsky reported, low-fat, high-calorie diets led to more tumors than high-fat, low-calorie diets, and tumor production was shut down entirely in underfed rats, regardless of how fatty their diet was.

However, the results from the study itself are different:8

The data from 3 separate studies altering caloric and fat intake support the conclusions that a high-fat diet influences initiation as well as promotion of DMBA-induced mammary tumorigenesis, that high caloric intake increases tumor yield, and that restriction of caloric intake (even concomitant with the provision of twice as much dietary fat) inhibits tumor formation during the promotion period.

At least he got part of the study correct. By the way, I wonder how Taubes squares this circle in his mind when he later advocates eating all the calories you want — as long as it’s all meat, of course.

* * *

Pg 74

Nonetheless, the pervasive belief that eating fat causes breast cancer has persisted, partly because it once seemed undeniable. Purveyors of health advice just can’t seem to let go of the notion. […] By 2006, with the next release of cancer-prevention guidelines by the American Cancer Society, the ACS was acknowledging that “there is little evidence that the total amount of fat consumed increases cancer risk.” But we were still advised to eat less fat and particularly meats (“major contributors of total fat, saturated fat and cholesterol in the American diet”), because “diets high in fat tend to be high in calories and may contribute to obesity, which in turn is associated with increased risks of cancers.” (Saturated fats, in particular, the ACS added, “may have an effect on increasing cancer risk,” a statement that seemed to be based solely on the belief that if saturated fat causes heart disease it probably causes cancer as well.)

Of course, Taubes ignores the reference in the text that immediately follows “may have an effect on increasing cancer risk” and instead tells his readers that the statement is based on some unfounded belief. In case you’re wondering the reference is a review article that pours over several relevant studies on fat and cancer.9 What Taubes also omits is that the main reasons the ACS recommends avoiding red and processed meats have little to do with fat content.10 I’ll let the ACS explain:

Many epidemiologic studies have examined the association between cancer and the consumption of red meats (defined as beef, pork, or lamb) and processed meats (cold cuts, bacon, hot dogs, etc.). Current evidence supports an increased risk of cancers of the colon and/or rectum and prostate. More limited evidence exists for other sites. Studies that have examined red meat and processed meat separately suggest that risks associated with processed meat may be slightly greater than red meat, but the consumption of both should be limited.

Meat contains several constituents that could increase the risk of cancer. Mutagens and carcinogens (heterocyclic amines and polycyclic aromatic hydrocarbons) are produced by cooking meat at high temperatures and/or by charcoal grilling. The iron content (heme) in red meat may generate free radicals in the colon that damage DNA. Substances used to process meat (nitrates/nitrites and salt) contribute to the formation of nitrosamines that can damage DNA. It is also possible that the fat content in meat contributes to risk. For example, foods that are high in fat increase the concentration of secondary bile acids and other compounds in the stool that could be carcinogens or promoters of carcinogenesis.

These cancer properties of red and processed meats have been well-documented over the years. There is a mountain of evidence for them. But of course Taubes has never been one to let evidence ruin a good story about how people that disagree with him are pinheaded schmucks.

* * *

Pg 75, Taubes lies about the results when discussing a study by the Women’s Health Initiative claiming that

The women on the diet also consumed fewer calories—averaging 120 calories a day less than the controls over the eight years of the study.*

*They did not, however, lose any weight because of this, which is paradoxical, and an issue we will discuss later.

Actually, everyone on the diet lost a significant amount of weight.11

See Taubes response #4

* * *

On page 84 Taubes discusses the results of a Cochrane review*:

The review concluded that the diets, whether low-fat or cholesterol-lowering, had no effect on longevity and not even a “significant effect on cardiovascular events.”

The first part of that claim is actually true. The second lies about the results of the systematic review. It actually reduced cardiovascular events by 16%. The same authors published the Cochrane results in BMJ and they concluded then12:

The findings on cardiovascular events are broadly in keeping with benefits that might be expected from modest lowering of cholesterol concentration and certainly provide support, at an individual level, for the central role of dietary fat intake in the causation of cardiovascular disease.

The results also indicated a reduction in mortality by 9%, but that figure was within the 95% CI. In any case, if you’re curious about the updated results they are basically unchanged.13 From the 2012 Cochrane review:

Dietary change to reduce saturated fat and partly replace it with unsaturated fats appears to reduce the incidence of cardiovascular events, but replacing the saturated fat with carbohydrate (creating a low fat diet) was not clearly protective of cardiovascular events (despite small improvements in weight, body mass index, total and LDL cholesterol).The protective effect was seen almost exclusively in those who continue to modify their diet over at least two years, and in studies of men (not those of women). Dietary advice to those at high risk of cardiovascular disease (particularly where lipid lowering medication may not be available), and probably also to lower risk population groups, should continue to include dietary fat modification, possibly as part of a Mediterranean dietary pattern, and it should be stressed that this is a permanent pattern of eating.

*Something Taubes holds in high regard, unless of course a result might contradict his thesis (as is the case with a Cochrane review of salt and hypertension) in which case they are meaningless. But more on that later.

See Taubes response #5


1. National Academy Press. Diet and Health: Implications for Reducing Chronic Disease Risk. (1989). at <;

2. A Research Committee. Low-fat Diet in Myocardial Infarction: A Controlled Trial. The Lancet 286, 501–504 (1965).

3. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

4. Stamler J, Wentworth D & Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded?: Findings in 356 222 primary screenees of the multiple risk factor intervention trial (MRFIT). JAMA 256, 2823–2828 (1986).

5. Holmes, M. D. et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 281, 914–920 (1999).

6. Browner WS, Westenhouse J & Tice JA. What if americans ate less fat?: A quantitative estimate of the effect on mortality. JAMA 265, 3285–3291 (1991).

7. Willett, W. C. et al. Dietary fat and fiber in relation to risk of breast cancer. An 8-year follow-up. JAMA 268, 2037–2044 (1992).

8. Kritchevsky, D., Weber, M. M. & Klurfeld, D. M. Dietary Fat versus Caloric Content in Initiation and Promotion of 7,12-Dimethylbenz(a)anthracene-induced Mammary Tumorigenesis in Rats. Cancer Res. 44, 3174–3177 (1984).

9. Kolonel, L. N. Fat, meat, and prostate cancer. Epidemiol. Rev. 23, 72–81 (2001).

10. Kushi, L. H. et al. American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA. Cancer J. Clin. 56, 254–281; quiz 313–314 (2006).

11. Howard, B. V. et al. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA 295, 39–49 (2006).

12. Hooper, L. et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst. Rev. Online CD002137 (2001). doi:10.1002/14651858.CD002137

13. Hooper, L. et al. in Cochrane Database Syst. Rev. (The Cochrane Collaboration) (John Wiley & Sons, Ltd, 2012). at <;