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 <;

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



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

Page 24:

The press also played a critical role in shaping the evolution of the dietary-fat controversy by consistently siding with proponents of those who saw dietary fat as an unneccessary evil. These were the researchers who were offering specific, positive advice for the health-conscious reader—eat less fat, live longer. The more zealously stated, the better the copy. All the skeptics could say was that more research was necessary, which wasn’t particularly quotable. A positive feedback loop was created. The press’s favoring of articles that implied Keys’s hypothesis was right helped convince the public; their belief in turn would be used to argue that the time had come to advise cholesterol-lowering diets for everyone, thus further reinforcing the belief that this advice must be scientifically defensible.

There is no proof for this entire paragraph. None. This is just hyper-biased conjecture.

* * *

On page 24 Taubes misquotes an American Heart Association official

 In 1964, when the study still hadn’t taken place, a director of the AHA described its purpose as the equivalent of merely “dotting the final i” on the confirmation of Keys’s hypothesis.

The Wall Street Journal article, from which this is taken, quotes the AHA director as saying something similar, but a different statement with a different meaning.1 There is also no mention of Keys. From the article:

A director of the heart group explained yesterday the association decided to make the recommendation because heart disease is becoming such “a pressing public health problem.” Efforts to stem heart disease “just can’t be left until the last i is dotted and the last t is crossed,” he explained.

* * *

On page 25:

In 1957, Keys insisted that “each new research adds detail, reduces areas of uncertainty, and, so far, provides further reason to believe” his hypothesis. This is known technically as selection bias or confirmation bias; it would be applied often in the dietary-fat controversy. The fact, for instance, that Japanese men who lived in Japan had low blood-cholesterol levels and low levels of heart disease was taken as a confirmation of Keys’s hypothesis, as was the fact that Japanese men in California had higher cholesterol levels and higher rates of heart disease. That Japanese men in California who had very low cholesterol levels still had more heart disease than their counterparts living in Japan with similarly low cholesterol was considered largely irrelevant.

Damn this Keys fellow is so insistent! Does he have to insist literally everything? All kidding aside, the Japanese men in California study he cites was published in 1975. Yet Keys was apparently ignoring that evidence in 1957. Was Keys a person from the future who traveled back in time to the 50s to ignore research that had yet to be published?

Going back to the study that Taubes cites here you will find that it is an observational, cross-sectional study. (Keep that in mind because peppered throughout the book and in a recent blog post he essentially claims that all observational studies are meaningless.) Not only that but the researchers also measured other risk factors beside cholesterol, namely hypertension. Turns out that Japanese Californians also had more hypertension than their Japanese brethren, and hypertension is another major risk factor for coronary heart disease.

I can hear people screaming right now “SEE? This only proves the point that heart disease is caused by other things!” 1) No one is claiming that cholesterol is the sole cause of heart disease. Many things are considered risk factors: smoking, hypertension, cholesterol, diabetes, obesity, etc. Of course that doesn’t prove that cholesterol is not a risk factor. 2) This study is a cross-sectional study so it can’t measure causes, only associations. Taubes beats this drum later.

* * *

Pg 25-26:

The Masai nomads of Kenya in 1962 had blood-cholesterol levels among the lowest ever measured, despite living exclusively on milk, blood, and occasionally meat from the cattle they herded. Their high-cholesterol diets supplied nearly three thousand calories a day of mostly saturated fat. George Mann, an early director of the Framingham Heart Study, examined the Masai and concluded that these observations refuted Keys’s hypothesis. […] To explain away Mann’s research on the Masai, Keys then evoked more recent research suggesting that the Masai, living in nomadic isolation for thousands of years, must have somehow evolved a unique “feedback mechanism to suppress endogenous cholesterol synthesis.” This mechanism, Keys suggested, would bestow immunity on the Masai to the cholesterol-raising effects of fat.

HA HA!! Keys is such an idiot! Does he actually think that humans are capable of developing traits over time that help them adapt and survive in their environment?? A unique “feedback mechanism to suppress endogenous cholesterol synthesis. Is he serious? That’s almost as absurd as some Europeans developing a gene to digest lactose! That’s about as ridiculous as saying that some people have a gene that produces normal alcohol dehydrogenase, while other people of mainly Asian descent have a variant of the gene that codes for an enzyme that metabolizes alcohol differently. Could you imagine? Keys, don’t you understand that you sound like a jackass when saying these things? That’s almost as foolish as saying one could inherit genes that produce more melanin in the skin to protect from the sun’s UV radiation. How preposterous would that be! Oh… wait…

All sarcasm aside, the Masai do seem to be a unique bunch. Evidently much of their diet is raw, unrefrigerated milk, some sort of tea/stew made from the bark of a local tree, and some blood for good measure. I read the study Taubes cited and it’s a strange one. Take note that it is also an observational, cross-sectional study.2 First of all, Mann claims he had trouble recording the diet:

The accurate measurement of dietary intake of these people proved extraordinarily difficult. We were able to make only limited measurements. This difficulty is because of the erratic intake of food, there being no fixed meal patterns in the families, because there are no uniform units of measurement or utensils and because of the disruption of usual behavior in the presence of an observer.

It seems he mainly relies on urine samples to estimate the protein intake of the Masai. Moreover, atherosclerosis was estimated by looking at ECG graphs. That’s odd, right? How accurate is that? In any case, Mann estimated very little atherosclerosis in the Masai. Cholesterol levels were made using the usual method, and they were indeed low.

So the Masai had low cholesterol levels and low atherosclerosis. Makes sense. The only thing that doesn’t really fit is thinking about a diet ostensibly high in saturated fat and cholesterol, but one that doesn’t lead to high serum cholesterol. As Mann put it, there can be one of two explanations: “Either such a diet does not in fact contribute to those consequences or the Masai have some other protecting mechanism which allows them to eat these foods with immunity.”

As it turns out the Masai do have such a protective mechanism as was demonstrated by a controlled feeding study published in the New England Journal of Medicine.3,4 I’ll quote from the abstract:

The Masai of East Africa exhibit some unique biologic characteristics. Despite their customary diet comprised of 66 per cent calories as fat, they have persistent low serum cholesterol and beta-lipoprotein levels. Post-mortem examinations provided direct proof of a paucity of atherosclerosis. Metabolic studies revealed that the Masai absorbed large amounts of dietary cholesterol, but also possessed a highly efficient negative feedback control of endogenous cholesterol biosynthesis to compensate for the influx of dietary cholesterol. Two unusual serum-protein patterns were observed: the presence of a double alpha2 band; and a high level of serum IgA that is apparent at an early age (four years). The high ratios of phospholipid to cholesterol in their gallbladder bile explain the extreme rarity of cholesterol gallstones. All these characteristics may reflect a long-term biologic adaptation of the tribe.

Hm. I guess both Darwin and Keys were right. Natural selection exists after all. However, Mann published another study some years after his ’64 study on the Masai. This one actually examined the hearts and aortae of recently deceased Masai (average age: 38). This newer study now claimed that the Masai actually had “extensive atherosclerosis” but for some reason the Masai’s blood vessels enlarge as they age to compensate for the blockage.5 Now I don’t know what to think about these people, except that they are indeed unique.

* * *

On page 27 Taubes discusses some early data from the Framingham Heart Study, noting that according to some results high serum cholesterol levels did indeed confer about a 5X greater risk of coronary heart disease.6 “But,” he says “there were caveats.”

As the men aged, those who succumbed to heart disease were ever more likely to have low cholesterol (as had Eisenhower) rather than high cholesterol. The cholesterol/heart-disease association was tenuous for women under fifty, and nonexistent for women older. Cholesterol has “no predictive value,” the Framingham investigators noted in 1971. This means women over fifty would have no reason to avoid fatty foods, because lowering their cholesterol by doing so would not lower their risk of heart disease. None of this was deemed relevant to the question of whether Keys’s hypothesis was true.

Talk about selection bias! This has to be one of the most selective readings of that study. The actual text says that serum cholesterol was highly predictive of heart disease.7 Lemme give you a few more quotes from that study that Taubes missed:

  • An increased risk proportional to antecedent serum cholesterol was found whether or not it was associated with elevated Sf20-400 prebeta lipoprotein.
  • When adjustment was made for the concomitant prebeta lipoprotein concentration and other factors related both to coronary heart disease risk and to blood lipids, a residual gradient of coronary heart disease risk proportional to the serum cholesterol was still evident.
  • Risk of coronary heart disease in men can be estimated using any of the lipids evaluated; however, none proved more useful than an accurate total serum cholesterol.
  • Cholesterol, as indicated by the size of the coefficient in Table 2, carries most of the weight as a contributor to coronary heart disease in men, whether manifested as angina or some more serious form of the disease.
  • Risk of each particular clinical manifestation of coronary heart disease (including angina, myocardial infarction, and sudden death) proved proportional to the antecedent serum cholesterol level in men of all ages studied.
  • In men and younger women the risk simply rose in proportion to the antecedent serum cholesterol concentration from the lowest to highest values recorded in this population sample (Figure 3). There was nothing to suggest that some particular level was “critical.” Hence, it does not appear logical to examine the relation of cholesterol to risk of coronary heart disease in terms of “hypercholesterolemia” but rather in terms of the actual concentration of cholesterol in the plasma.
  • Examination of the risk of developing coronary heart disease according to the actual serum cholesterol concentration of each subject grouped into quartiles showed an increase in risk proportional to the antecedent cholesterol concentration, not only in the general population but in persons free of factors believed associated both with hypercholesterolemia and with coronary heart disease
  • Even after excluding persons with hypertension, diabetes. ECG abnormalities, and the cigarette habit, a distinct gradient of risk proportional to the cholesterol concentration can be demonstrated. This tends to brand the lipid, not associated variables, as the culprit. As shown in an earlier analysis, a net effect of cholesterol is clearly apparent in men of all ages
  • According to this analysis the dominant effect was assigned to serum cholesterol, with an insignificant contribution of the other lipids It is apparent that in men cholesterol accounts for more of the total distance between those who developed and those who remained free of the disease than does Sf20-400 prebeta lipoprotein in all but the oldest subjects.
  • For cholesterol in men a strong residual effect remains after accounting for the level of Sf20-400 lipoprotein and the other factors In younger, but not older, women distinctly higher cholesterol values may also contribute independently to risk
  • Of all the identified host factors associated with increased susceptibility to coronary heart disease, the blood lipids are among the strongest.
  • If there is in fact a single common denominator through which the multiple interrelated predisposing factors in coronary heart disease operate, an abnormal accumulation or handling of blood lipids would appear the most likely candidate.
  • These investigators have found significant differences in the blood content of a variety of lipids and have implicated the total fasting triglyceride, beta and prebeta lipoprotein, alpha to beta cholesterol ratio, cholesterol to phospholipid ratio, and fatty acids
  • There were 6 xanthomatous individuals in the Framingham population sample of 5,127 men and women. All had serum cholesterol values exceeding 400 mg/100 ml and a strong family history of coronary heart disease, and within the follow-up period all six died of coronary heart disease before their fiftieth birthdays.
  • Any one of the lipids or lipoproteins examined, and, by inference, a triglyceride as well, can be used effectively for assessing vulnerability to coronary heart disease. None, however, would appear superior to the more convenient serum cholesterol determination for this purpose.
  • In women, however, the picture appears to be somewhat different. In women under the age of 50, as in men, high cholesterol values and not Sf20-400 prebeta lipoprotein appear to be associated with an increased risk. In older women, on the other hand, cholesterol appears to have no predictive value, and Sf20-400 prebeta lipoprotein actually appears to be superior to cholesterol for estimating risk.
  • The data presented suggest that in men the moderately elevated cholesterol values commonly encountered in the general population, regardless of the metabolic aberration responsible or how it is transported or partitioned among the lipoproteins, are associated with increased risk of coronary heart disease.

In case you were wondering, pre-beta lipoprotein is now called very low density lipoprotein (VLDL) which is similar to LDL and HDL in that it transports triglycerides and cholesterol through the blood. How anyone can read that study and only come away with cholesterol values in women over 50 doesn’t make much difference is really missing the point of the whole damn study. Especially when you consider what is very predictive of heart disease in women over 50 is a protein that transports lipids through the blood.

Here’s a simple chart from the article that shows the risk of heart disease on those with high serum cholesterol. FYI: Anything above a 1.0 means an increased risk. A 1.0 means no risk. Less than 1.0 means reduced risk. So a 2.0 would indicate a two-fold risk increase, 3.0 would be three times the risk, etc.

Serum Cholesterol, Lipoproteins, and the Risk of Coronary

* * *

On page 27 Taubes mentions the Western Electric study but again leaves out important data that runs contrary to his thesis.

Two decades later, Jeremiah Stamler and his colleague Richard Shekelle from Rush–Presbyterian–St. Luke’s Medical Center in Chicago revisited Western Electric to see how these men had fared. They assessed the health of the employees, or the cause of death of those who had died, and then considered the diets each subject had reportedly consumed in the late 1950s. Those who had reportedly eaten large amounts of polyunsaturated fats, according to this new analysis, had slightly lower rates of coronary heart disease, but “the amount of saturated fatty acids in the diet was not significantly associated with the risk of death from [coronary heart disease],” they reported.

Immediately prior to the quoted phrase is a sentence that Taubes probably doesn’t want in his narrative so it is left out. I have reproduced it below.8 Bolding is mine.

When the risk of death from CHD was analyzed in terms of the component dietary variables, it was inversely related to intake of polyunsaturated fatty acids and positively related to intake of dietary cholesterol.

* * *

Taubes spills some ink on discussing a major dietary trial called the Anti-Coronary Club Trial on page 36:

The first and most highly publicized was the Anti-Coronary Club Trial, launched in the late 1950s by New York City Health Department Director Norman Jolliffe. The eleven hundred middle-aged members of Jolliffe’s Anti-Coronary Club were prescribed what he called the “prudent diet,” which included at least one ounce of polyunsaturated vegetable oil every day. The participants could eat poultry or fish anytime, but were limited to four meals a week containing beef, lamb, or pork. This made Jolliffe’s prudent diet a model for future health-conscious Americans. Corn-oil margarines, with a high ratio of polyunsaturated to saturated fat, replaced butter and hydrogenated margarines, which were high in saturated fats. In total, the prudent diet was barely 30 percent fat calories, and the proportion of polyunsaturated to saturated fat was four times greater than that of typical American diets. Overweight Anti-Coronary Club members were prescribed a sixteen-hundred-calorie diet that consisted of less than 20 percent fat. Jolliffe then recruited a control group to use as a comparison.

I’m gonna talk about what some might consider a minor point, but to me is significant. It is about rhetoric and word choice, so if you think this is petty and boring please skip ahead. What struck me was this: “In total, the prudent diet was barely 30 percent fat calories…” Barely? 30% of total calories as fat is smack dab in the middle of normal for most people. It’s nowhere near what anyone would consider a low fat diet. Yet Taubes uses the word “barely” to modify the 30% figure. Webster defines “barely” as “in a meager manner,” yet there is really nothing meager about eating a diet of 30-33% fat as it was stated in the actual study.9

As I have stated before and will no doubt state again, this is an example of when, if Taubes doesn’t blatantly misrepresent the results of a study, he will editorialize the figures in misleading rhetoric.

Let’s keep going with the Anti-Coronary Club Trial.

Jolliffe died in 1961, before the results were in. His colleagues, led by George Christakis, began reporting interim results a year later. “Diet Linked to Cut in Heart Attacks,” reported the New York Times in May 1962. “Special Diet Cuts Heart Cases Here,” the Times reported two years later. Christakis was so confident of the prudent-diet benefits, reported Newsweek, that he “urged the government to heed the club results and launch an educational and food-labeling campaign to change U.S. diet habits.”

The actual data, however, were considerably less encouraging. Christakis and his colleagues reported in February 1966 that the diet protected against heart disease. Anti-Coronary Club members who remained on the prudent diet had only one-third the heart disease of the controls. The longer you stayed on the diet, the more you benefited, it was said. But in November 1966, just nine months later, the Anti-Coronary Club investigators published a second article, revealing that twenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent. Eight members of the club died from heart attacks, but none of the controls. This appeared “somewhat unusual,” Christakis and his colleagues acknowledged. They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.

The “somewhat unusual” quote occurs in the first report, and not the second report as Taubes implies. What’s more is that the figures Taubes gives are not correct. The second report discusses deaths not related to heart disease:

Out of the 814 experimental group subjects, there have been 18 known deaths from causes other than coronary heart disease among individuals who had not experienced a new coronary event. This is in comparison to six such deaths out of the 463 individuals in the control group.10

The first report details deaths specifically due to heart disease, which was three in the experimental and zero in the control.9 This is not unusual considering the experimental group began with more risk factors for heart disease compared to the controls, namely greater rates of obesity, hypertension, hypercholesterolemia, etc. The results of the other endpoints (which Taubes surprisingly states, but also kind of minimizes) was that by the end of the trial the non-prudent dieters had significantly higher cholesterol, significantly higher blood pressure, significantly more obesity, and about triple the incidence of heart disease. All of this despite having less risk factors than the prudent group at the beginning of the trial. But I suppose these things aren’t important; what is important, according to Taubes, is the made-up death numbers.

Taubes states that further discussion of mortality was omitted which is clearly false because both reports obviously discuss the deaths in the trial. How do you pull numbers on mortality from the reports and then turn around and claim no discussion on mortality? Moreover, I don’t know what would make the data “less encouraging.” Considerably less encouraging for Taubes’s meat-heavy narrative, perhaps. The results are pretty consistent with the other similar dietary trials that Taubes tries to spin.

* * *

Pg 37 Taubes discusses another dietary study:

In July 1969, Seymour Dayton, a professor of medicine at the University of California, Los Angeles, reported the results of the largest diet-heart trial to that date. Dayton gave half of nearly 850 veterans residing at a local Veterans Administration hospital a diet in which corn, soybean, safflower, and cottonseed oils replaced the saturated fats in butter, milk, ice cream, and cheeses. The other half, the controls, were served a placebo diet in which the fat quantity and type hadn’t been changed. The first group saw their cholesterol drop 13 percent lower than the controls; only sixty-six died from heart disease during the study, compared with ninety-six of the vets on the placebo diet.

Only 66 died on the unsaturated fat diet while 96 died on the saturated fat diet? That’s only a difference of 30 lives! It’s 31% fewer deaths. Practically nothing, right? Barely a difference at all. By the way, in case you’re interested there are a few pertinent facts that Taubes left out (yet again). I have reproduced it below. Remember the control group was high in saturated animal fat, and the experimental group was high in unsaturated fats from plants.11

The number of men sustaining events in major categories, in the control and experimental groups, respectively, was: definite silent myocardial infarction, 4 and 9; definite overt myocardial infarction, 40 and 27; sudden death due to coronary heart disease, 27 and 18; definite cerebral infarction, 22 and 13. The difference in the primary end point of the study-sudden death or myocardial infarction was not statistically significant. However, when these data were pooled with those for cerebral infarction and other secondary end points, the totals were 96 in the control group and 66 in the experimental group; P = 0.01. Fatal atherosclerotic events numbered 70 in the control group and 48 in the experimental group; P < 0.05. Life-table analysis in general confirmed these conclusions. For all primary and secondary end points combined, eight year incidence rates were 47.7% and 31.3% for the control and experimental groups, respectively; P value for the difference between the two incidence curves was 0.02.

If you don’t want to read the above block quote, I’ll summarize it for you: in all but one endpoint that was measured the experimental diet of unsaturated fats had less overt myocardial infarction, sudden death, cerebral infarction, fatal atherosclerotic events, etc. And not by a tiny margin – a significant margin.

The next paragraph Taubes states:

Thirty-one of the men eating Dayton’s experimental cholesterol-lowering diet, however, died of cancer, compared with only seventeen of the controls. The risk of death was effectively equal on the two diets. “Was it not possible,” Dayton asked, “that a diet high in unsaturated fat…might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities among the self-selected diets of human population groups.” Because the cholesterol-lowering diet failed to increase longevity, he added, it could not provide a “final answer concerning dietary prevention of heart disease.”

What’s interesting is the the authors’ statement Taubes quotes from the paper. I want to make something clear: Taubes introduces the author and gives a brief background of the trial. Then he relates the conditions and methods of the study, then he cherry-picks one of the myriad results. In the next paragraph Taubes then gives his interpretation of the results, and tells you why he thinks the results were pretty much a wash. ONLY AFTER ALL THAT Taubes then reproduces a couple sentences from the journal article questioning whether a diet of unsaturated fat might have “noxious effects” presumably because of the study results. What Taubes likely wants the reader of GCBC to think is that after the results of the study are in and the numbers have been crunched and the data has been analyzed, Dr. Seymour Dayton is sitting at his desk and ruminating on what could have produced these results. As if he is asking a rhetorical question or providing a hypothesis for a future dietary trial.

What the reader of GCBC does not know is that Dayton asks this question in the introduction of the text, then later will explicitly answer this very question with his own data. Do you want to know if the experimental diet has noxious effects? Well there’s a section in the results portion of the study titled “Does the Experimental Diet Have Noxious Effects?” where Dr. Dayton states:

As indicated in table 29 and discussed in some detail above, the excess mortality in nonatherosclerotic categories was not sufficiently impressive to justify the conclusion that harmful effects had been demonstrated.


One may also wonder whether the experimental diet may have exerted its effect on mortality data primarily by accelerating nonatherosclerotic deaths (see table 28), decreasing the atherosclerotic mortality by inducing early death due to other cause. Such a mode of action would be associated with higher numbers of deaths in the experimental group compared with the controls, whereas the reverse was true in this trial (fig. 13).


The other observation which raised some question of a possible toxic effect was the low arachidonic acid concentrations in atheromata of long-term, high-adherence subjects on the experimental diet (tables 37 to 40). For reasons already cited, this may be more appropriately viewed as evidence of a salutary rather than a toxic effect.

I’d like to take this opportunity to mention that this is one of the many examples that shows that Taubes is not merely mistaken, but he is working very hard to quite literally deceive his readers. The numbers he cites as deaths from cancer is likely an honest citation error – no one could possibly know. But when you think about the information he presents it is evident that he read this text very carefully and thoroughly, yet only included the bits that he could spin to fit his narrative. With this text and many, many others he explicitly does not mention the very relevant information that runs contra to his nutritional ideology. He is essentially in the marketing business; marketing the low-carb religion rather than informing readers. It’s as if a movie critic were to review a film and write “Whoever was involved in making this film should be put in a gas chamber,” and the film’s marketer took the review and wrote “A gas!” on the movie poster.

Okay, I think I’ve made my point. Moving on…

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



1. Heart Association Stirs Up a Controversy By Urging Public to Alter Intake of Fats. Wall Str. J. 1923 – Curr. File 6 (1964).

2. Mann, G. V. et al. Cardiovascular disease in the masai. J. Atheroscler. Res. 4, 289–312 (1964).

3. Ho, K. J., Biss, K., Mikkelson, B., Lewis, L. A. & Taylor, C. B. The Masai of East Africa: some unique biological characteristics. Arch. Pathol. 91, 387–410 (1971).

4. Taylor, C. B. & Ho, K.-J. Studies on the Masai. Am. J. Clin. Nutr. 24, 1291–1293 (1971).

5. Mann, G. V., Spoerry, A., Gray, M. & Jarashow, D. Atherosclerosis in the Masai. Am. J. Epidemiol. 95, 26–37 (1972).

6. Dawber, T. R., Kannel, W. B., Revotskie, N. & Kagan, A. The Epidemiology of Coronary Heart Disease–The Framingham Enquiry. Proc. R. Soc. Med. 55, 265–271 (1962).

7. Kannel, W. B., Castelli, W. P., Gordon, T. & McNamara, P. M. Serum Cholesterol, Lipoproteins, and the Risk of Coronary Heart Disease: The Framingham Study. Ann. Intern. Med. 74, 1–12 (1971).

8. Shekelle, R. B. et al. Diet, Serum Cholesterol, and Death from Coronary Heart Disease. N. Engl. J. Med. 304, 65–70 (1981).

9. Christakis G, Rinzler SH, Archer M & Kraus A. Effect of the anti-coronary club program on coronary heart disease risk-factor status. JAMA 198, 597–604 (1966).

10. Christakis, G. et al. The anti-coronary club. A dietary approach to the prevention of coronary heart disease–a seven-year report. Am. J. Public Health Nations Health 56, 299–314 (1966).

11. Dayton, S., Pearce, M. L., Hashimoto, S., Dixon, W. J. & Tomiyasu, U. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation 40, II–1 (1969).

Good Calories, Bad Calories: A Critical Review (part 1)

I have a special place in my heart for pop science books. They can be a great way for accomplished scientists to take a complex field of study and distill it down to its essentials. They can also be a great way for excellent science communicators to take what might seemingly be a dry and boring field and make it exciting. Several years ago I stoked my interest in nutrition with a pantheon of pop science books. I devoured these books as quickly and pleasurably as I would a delicious meal. However, now looking back with many advanced science and nutrition classes under my belt I view these texts as overly simplistic and usually presented with a heavy bias. I still think popular nutrition books are fine if you want a good yarn with some nutrition science thrown in or maybe you’re waiting in an airport somewhere for your plane to arrive, but I wouldn’t take any of them too seriously. Their claims will not be vetted well, if at all. The first amendment of the US constitution allows for virtually anything to be published. Textbooks and scholarly journal articles on the other hand are different animals because they experience more rigorous evaluations prior to publishing. Although they can be quite dry and contain more scientific jargon, textbooks and journal articles are the way to go if you are looking for cold hard facts.

With that out of the way let me introduce Good Calories, Bad Calories by Gary Taubes. I had heard the name of Gary Taubes some time ago, but I did not directly engage any of his writing until recently when he wrote a blog post that I found to be extraordinarily ideological.

I decided to read Taubes’s Good Calories, Bad Calories because it was apparent to me that, much like Ayn Rand’s Atlas Shrugged, it was hugely influential to a pocket of its readers. Also like Atlas Shrugged it is an awful, awful book.1


The Essentials

The title of this post includes the words “Part One” because GCBC is a seven-course meal. There is no way I would be able to address the entirety of the book in a single blog post; however, I do not plan to write a part two. I just don’t feel like it would be worth my time. Just know that a single post on GCBC is incomplete.

GCBC is truly one of the most researched and meticulously-referenced nutrition books out there. Unfortunately it’s also heavily biased as well, but I’ll get to that in a moment. Here are the main ideas presented in the book:

  • A Harvard epidemiologist named Ancel Keys fabricated some data linking heart disease to saturated fat intake. Taubes refers to this as the “Lipid Hypothesis”2 and was able to convince many scientists, the media, the public, non-governmental organizations (such as the AMA & AHA), and ultimately policy-makers at the highest levels of government to accept his flawed ideas.
  • Contrary to mainstream thinking saturated fats, especially those coming from animal sources are actually quite good for you.
  • Most diseases of modern civilization including obesity and cancer can be attributed to carbohydrates.
  • Consuming excess calories does not make one fat, nor do burning excess calories make one thin.

The Actual Science

Let’s tackle that last claim first: excess calories does not make one fat, nor do burning excess calories make one thin. Instead of citing the studies in the footnotes where they will probably be ignored I will plaster them right here.

  1. Metabolic effects of isoenergetic nutrient exchange over 24 hours in relation to obesity in women. Conclusion: “There were no large differences in energy expenditure between the two diets or between the groups…”
  2. Energy-intake restriction and diet-composition effects on energy expenditure in men. Conclusion: “There was no significant difference in 24-hour energy expenditure between the diet groups.”
  3. Nutrient balance in humans: effects of diet composition. Conclusion: “Total daily energy expenditure was not affected by the composition of the diet when caloric intake was fixed. Similarly, the different diet compositions did not alter SMR [sleeping metabolic rate], RMR [resting metabolic rate], or MRACT [energy expenditure due to activity or movement] of the subject.”
  4. Nutrient balance and energy expenditure during ad libitum feeding of high-fat and high-carbohydrate diets in humans. Conclusion: “Individual body weights fluctuated (by < 0.25 kg) throughout the study, but we did not observe any systematic increase or decrease in the body weight of any subject. Additionally, there was not a significant change in the average body weight of the group as a whole over the course of the study.”
  5. Substrate oxidation and energy expenditure in athletes and nonathletes consuming isoenergetic high- and low-fat diets. Conclusion: “The amount of energy expended in all activities … during the day was not significantly different among groups for either unadjusted … or adjusted data… The proportion of energy expended in activity did not differ among groups or among days… There were also no significant differences in sleep EE [energy expenditure] among groups…”
  6. Regulation of macronutrient balance in healthy young and older men. Conclusion: “Body mass, percentage fat, and fat-free mass were similar in the two groups. Twenty-four-hour energy expenditure (EE) and energy balance did not differ across diets or between groups…”
  7. The effect of protein intake on 24-h energy expenditure during energy restriction. Conclusion: “24-h EE [energy expenditure] and SMR [sleeping metabolic rate] declined on all three diets… Weight loss was similar on all three diets [high protein, high carbohydrate, and high fat].”
  8. Effects of dietary fat and carbohydrate exchange on human energy metabolism. Conclusion: ”Twenty-four-hour RQ [respiratory quotient] and 24-h EE [energy expenditure] were not significantly different between restrained and unrestrained eating subjects on the LF, M and HF [low-fat, medium-fat, and high-fat] diet…”
  9. Energy expenditure in humans: effects of dietary fat and carbohydrate. Conclusion: “In the nondiabetic group there was no decrease in 24-h energy expenditure or in any component of 24-h energy expenditure on the high-fat compared with the high-carbohydrate diet… In the diabetic group the high-fat diet did not result in a decrease in either 24-h energy expenditure or in any of the components of 24-h energy expenditure…”
  10. Failure to increase lipid oxidation in response to increasing dietary fat content in formerly obese women.Conclusion: “Although the study was carried out over a period of a year the subjects succeeded in maintaining a constant body weight so that no differences were present during the different diets. Twenty-four-hour EE was influenced by diet composition in postobese women but not in control women, but the group x diet effect was not significant.”
  11. Energy intake required to maintain body weight is not affected by wide variation in diet composition. Conclusion: “Even with extreme changes in the fat-carbohydrate ratio (fat energy varied from 0% to 70% of total intake), there was no detectable evidence of significant variation in energy need as a function of percentage fat intake.”
  12. Weight-loss with low or high carbohydrate diet? Conclusion: “Neither diet offered a significant advantage when comparing weight loss or other metabolic parameters over a 12 w period.”
  13. Effect of high protein vs high carbohydrate intake on insulin sensitivity, body weight, hemoglobin A1c, and blood pressure in patients with type 2 diabetes mellitus. Conclusion: “Patients in both the high-carbohydrate and the high-protein groups lost weight… The difference between groups was not significant…Initial REEs were similar in the two groups… and did not change during the study.”
  14. Is a calorie a calorie? Conclusion: “We conclude that a calorie is a calorie. From a purely thermodynamic point of view, this is clear because the human body or, indeed, any living organism cannot create or destroy energy but can only convert energy from one form to another.”
  15. Energy intake required to maintain body weight is not affected by wide variation in diet composition. Conclusion: “Even with extreme changes in the fat-carbohydrate ratio (fat energy varied from 0% to 70% of total intake), there was no detectable evidence of significant variation in energy need as a function of percentage fat intake.”

That should take care of the ridiculous claim that excess calories do not make you fat. What about the carbohydrates v. fat issue at the heart of the book? Below are a few studies showing that high carbohydrate, moderate carbohydrate, and low carbohydrate diets are more-or-less the same when it comes to weight loss.3

  1. Long Term Effects of Energy-Restricted Diets Differing in Glycemic Load on Metabolic Adaptation and Body Composition Conclusion: “There was no statistically significant difference in metabolic adaptation to the HG [high-glycemic] and LG [low-glycemic] diets but adherence to the LG regimen apparently caused greater loss of body fat and less loss of FFM [fat-free mass] for the same amount of overall weight loss.”
  2. Long-term effects of 2 energy-restricted diets differing in glycemic load on dietary adherence, body composition, and metabolism in CALERIE: a 1-y randomized controlled trial. Conclusion: “There was a statistically significant decrease in mean percentage fat over time (P < 0.0001) consistent with body weight change; however, the difference between diet groups was not statistically significant over time.” And “[C]hanges in energy intake, body weight, body fat, and resting metabolic rate did not differ significantly between groups.”
  3. Efficacy and safety of low-carbohydrate diets: a systematic review. Conclusion: “At the end of both lower- and higher-carbohydrate diets, participants’ weight, BMI, and percentage of body fat decreased. In general, for both lower- and higher-carbohydrate diets, we found the greatest weight loss occurred among those participants receiving diets with the lowest caloric content and for those participants with the highest baseline weights.”
  4. Popular Diets: A Scientific Review Conclusion: “Data support the contention that those consuming low-fat, low-calorie diets are most successful in maintaining weight loss.”
  5. Effects of 4 weight-loss diets differing in fat, protein, and carbohydrate on fat mass, lean mass, visceral adipose tissue, and hepatic fat: results from the POUNDS LOST trial. Conclusion: “Fat loss or lean mass loss did not differ between diet assignments of high (25%) and average (15%) protein… high (40%) and low (20%) fat… or highest (65%) and lowest (35%) carbohydrate… at 6 mo. Between-diet differences remained nonsignificant at 2 y…”
  6. In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Conclusion: “There was no difference in weight reduction between the groups at 6 months … There were also no statistically significant differences in weight reduction between groups after adjustment for baseline carbohydrate or fat intake…”
  7. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. Conclusion: “Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize.”
  8. Similar weight loss with low- or high-carbohydrate diets. Conclusion: “The results of this study showed that it was energy intake, not nutrient composition, that determined weight loss in response to low-energy diets over a short time period.”
  9. Effect of energy restriction, weight loss, and diet composition on plasma lipids and glucose in patients with type 2 diabetes. Conclusion: “Despite differences in dietary composition, weight loss was not significantly different between groups.”
  10. Effects of moderate variations in macronutrient composition on weight loss and reduction in cardiovascular disease risk in obese, insulin-resistant adults. Conclusion: “[P]atients lost weight in response to both the 60% carbohydrate (5.7 ± 0.7 kg) and 40% carbohydrate (6.9 ± 0.7 kg) dietary interventions… [T]he difference in the amount of weight loss was not significant when the 2 diet programs were directly compared.”
  11. Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss? Conclusion: “There is no clear evidence that Atkins-style diets are better than any others for helping people stay slim, and despite the popularity and apparent success of the Atkins diet, evidence in support of its use lags behind.”
  12. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Conclusion: “At the end of the 6-wk trial, the total weight loss did not differ significantly between diet groups.”
  13. Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. Conclusion: “Within both diet groups, patients lost weight… There was no significant difference in weight loss between the 2 diet groups…”
  14. Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial. Conclusion: “The results in Table 5 indicate that the mean weight loss from baseline was similar between the two diet groups … There was no significant difference in the change in either waist circumference (reflecting central adiposity) or percentage body fat (determined by DEXA) between the diet groups…”
  15. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. Conclusion: “[A]ll 4 diets resulted in modest statistically significant weight loss at 1 year, with no statistically significant differences between diets…”
  16. Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo. Conclusion: “[T]here was a significant reduction in weight (P < 0.001), but no significant difference between diets…”
  17. Weight and metabolic outcomes after 2 years on a low-carbohydrate versus low-fat diet: a randomized trial. Conclusion: “We found no statistically significant differences in weight loss at any time point between the low-carbohydrate and low-fat diet groups…”
  18. The effect of a plant-based low-carbohydrate (“Eco-Atkins”) diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Conclusion: “No significant differences were found in any of the variables between the 2 groups.”
  19. Fat and carbohydrate overfeeding in humans: different effects on energy storage.Conclusion: “Excess dietary fat leads to greater fat accumulation than does excess dietary carbohydrate, and the difference was greatest early in the overfeeding period.”
  1. Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose, or fat in lean and obese women. Conclusion: “There was no significant difference in fat balance during controlled overfeeding with fat, fructose, glucose, or sucrose.”
  2. Effects of isoenergetic overfeeding of either carbohydrate or fat in young men. Conclusion: “No significant differences between the C[carbohydrate-rich]- and F[fat-rich]-group were observed.”

The above studies are focused on weight loss. Of course diets may be different when looking at other markers of health such as triglycerides, cholesterol, inflammation, C-reactive protein, insulin, glycosylated hemoglobin, blood pressure, etc. We can have a spirited debate about what diets might be best for overall health (and I’m sure we will in the comments section), but at least in terms of weight loss or weight gain calories matter far more than the macronutrient composition.


Not in Good faith?

GCBC was published in 2007. Knowing what I do about the publishing industry4 I imagine Mr. Taubes would have had to submit a final manuscript to his publisher in either 2006 or very early in 2007. In his epilogue on page 453, Taubes claims he spent five years researching and writing the book which would put the start date of his research at roughly 2001 or 2002. On page xxv of the prologue he mentions conducting over 600 interviews with different people as part of his research, which is an impressive number of people. However, there is one person featured prominently in the book that Taubes does not interview: Ancel Keys. If you have read the book you will notice that much ink is devoted smearing Dr. Keys and his work yet, according to Taubes’s references, not one interview was conducted with Keys. If one was interested in fair, objective reporting you would think that you would try to speak with a man that essentially invented and popularized the “lipid hypothesis.” Right?

Let’s try to think of reasons why Taubes did not interview Keys… Maybe Taubes repeatedly tried to obtain an interview with Keys, but was turned down or simply ignored. This is certainly possible, but I saw no mention of it in the book. I think Taubes would want to mention something like that, because that’s what good reporters do, plus it could add to the narrative that Keys’s work is indefensible.

Other reasons? Dr. Ancel Keys died in late 2004 at the age of 100, so perhaps he was too old and infirm to conduct any interviews. Maybe he had Alzheimer’s or dementia and could not speak intelligently about his past. It’s possible. Of course Taubes could speak to Keys’s surviving wife, Margaret, about her husband’s life and work. Taubes even writes a bit about her anyway because they did quite a bit of research together and even co-wrote How to Eat Well and Stay Well the Mediterranean Way that Taubes cites in GCBC. She would be a great interview! She’s probably full of interesting stories. But no, he did not interview Margaret Keys either. They also had a son that is now a doctor residing in New York state –Taubes also lives in New York state, it’s perfect! I’ll bet junior Keys has some great insight into his dear old dad. Welp, if he does Taubes was not interested in hearing them. It’s a shame. I bet any one of them could have provided some great information.

My theory? Taubes knew he was going to vilify Keys before he even began writing; after all the book would lose much of the spicy narrative about a mad scientist tricking the world into believing dietary nonsense. If Taubes is beholden to an ideology over evidence then any interview with a member of the Keys family is wholly unnecessary.

You Are Being Manipulated

Taubes uses subtle manipulation techniques to persuade his audience. Consider the following list of words.

These are the words Taubes uses to describe proponents of what he calls the “lipid hypothesis.” Even if you have never read the book or even know anything about its subject matter, a negative impression begins to form in your mind of the idea and its advocates. For instance you might feel that it’s nothing but speculation at best and at worst it’s a downright dangerous falsehood that is being shoved down our throats by religious zealots. I don’t blame you. That is some strong rhetoric Taubes is using. Now contrast this with the word choice used to describe those who espouse low-carb diets:

These people seem to be calmly and coolly presenting the facts. Instead of bombarding and crusading with a ridiculous dogma like the other guys, these people are merely skeptics suggesting an alternative hypothesis. Hell, you barely need to think for yourself or fact-check the author. Choosing the right side of this argument should be a no-brainer.

In rhetoric this is known as Framing or sometimes as Priming. It’s a subtle manipulation technique leading you to implicitly associate two unrelated ideas with one another. In this case Taubes wants you to associate “lipid hypothesis” with “myth” and those who do not advocate low-carb diets, such as Ancel Keys, with religious zealotry. By the way, these words are from only the prologue & first chapter; the verbiage gets piled higher and deeper as you get further into the book.

Lies, Damned Lies, and Gary Taubes

I honestly did not expect to find near as many misleading quotes, misrepresentation of studies, or outright fabrication as I did in Good Calories, Bad Calories. I mean Taubes writes for The New York Times for Christ’s sake – arguably the most prestigious and most influential newspaper in the history of the world.

Nearly every single time I bothered to check a reference made in Good Calories, Bad Calories I found that Taubes had at best taken something out of context or at worst completely misrepresented a study. Not kidding. Here are a few examples beginning with the more anodyne.

  • Taubes takes Steven Jay Gould out of context.

On page 18 of the hardcover edition of GCBC, Taubes discusses Ancel Keys and the relationship between diet and heart disease and writes “Associations do not imply cause and effect or represent (as Stephen Jay Gould would later put it) ‘any magic method for the unambiguous identification of cause.’” While reading that paragraph, you might get the impression that SJG was responding to Keys’s work or perhaps making a more general critique of nutrition science, but you would be wrong. In fact that quote by SJG come from a book titled The Mismeasure of Man5 which is about racism, IQ, and evolutionary biology and had absolutely nothing to do with diet, fat intake, heart disease, Ancel Keys, or essentially anything discussed in GCBC. It’s a really strange and out-of-place quote, and I’m not sure why Taubes would use it. The only reason I can imagine would be in the hopes that some of SJG’s gravitas would be associated with Taubes’s own ideas in the reader’s mind. Although there is nothing technically dishonest here Taubes does take Gould out of context, and as Albert Einstein said “I agree with your remark.”6

  • Taubes completely lies about the results of a study

This is actually one of the juicier lies in GCBC and occurs on the very same paragraph as the above Gould remark. For a bit of context, Taubes is discussing a cross-sectional study by one Ancel Keys that demonstrates a relationship between a population’s fat intake and its rates of heart disease. Taubes writes “Many researchers wouldn’t buy it. [Yerushalmy and Hilleboe] 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.” This is not true.7 Let’s look at the actual Yerushalmy and Hilleboe study, shall we? (I apologize for the poor definition of these pictures. I did not scan them in. Long story.)

The top graph shows Keys’s data as presented by Yerushalmy and Hilleboe. It’s a very strong correlation, but Y&H are skeptical and decide to take similar data from the Food and Agriculture Organization of the United Nations that includes more countries than the measly six that Keys had. However, contrary to Taubes’s claim the correlation does not vanish. If I were to run a R2 coefficient analysis I may not get 1.0, but I would certainly get above 0.0. In other words, sure the association is not as strong as with Keys’s data, but there is a definitive relationship.

But Y&H don’t stop there. Just for kicks let’s read on and see what else Y&H have in store for us… What’s this? It appears that Y&H have separated out some dietary components for us and have done some statistical analyses. Let’s take a look at what they found.

It’s difficult to see because of the cheap scanner, but those are negative signs in front of the vegetable fat and vegetable protein numbers.

As you can see in the table if you separate animal fat from vegetable fat and do an individual analysis on each then vegetable fat ends up being negatively correlated with heart disease while animal fat has a strongly positive correlation with heart disease. This correlation is also true of animal protein and vegetable protein and even remains if you calculate total fat/protein intake or fat/protein intake as a percentage of calories.  Remarkable.

In the second picture you can see an association with mortality that becomes even tighter when examined with animal protein. I’ll leave it to you to imagine why Taubes might leave such highly relevant data so conspicuously absent from his book.

  • Taubes wildly exaggerates the results of a study

Page after page and chapter after chapter Taubes hammers away at the “lipid hypothesis” and on page 44 even goes so far as to claim that “polyunsaturated fats can cause cancer in laboratory animals.” This is supposed to be a devastating blow to anyone who might espouse a Mediterranean-style diet that advocates a limited consumption of fats from beef and lard in favor of fats from fish, seeds, and nuts. It probably would be a devastating blow if it were true. Considering I had never heard or read anything in all my graduate and undergraduate nutrition courses that would even approach authenticating this statement I decided to check his references for this bold claim.

He cites two references to support his claim. One is not even a study, but a 1973 New York Times article that is behind a paywall so I cannot read it in its entirety.8 The NYT website does provide a summary of the article that does not mention polyunsaturated fats, cancer, or laboratory animals.

Let’s give Taubes the benefit of the doubt here; let us assume that the article does go into detail about some studies that have been done on laboratory animals examining the potential link between polyunsaturated fats and cancer. Why not simply cite those studies? Why make your readers go through the trouble of unearthing an ancient NYT article, only to have them sleuth further to find the actual data? I have my own theory, but moving on…

The second reference he cites in support of his bold polyunsaturated-fats-cause-cancer-in-laboratory-animals claim is actually an original dietary study! It’s older even than the NYT article mentioned above, and it does not involve laboratory animals but rather elderly men.9 Ready for some details? Briefly, men were randomly assigned to a control diet or an experimental diet. The control diet consisted of 10% polyunsaturated fatty acids (PUFAs) and ~650 mg/day of cholesterol. The experimental diet consisted of 40% PUFAs and ~365 mg/day of cholesterol. Both groups, however, had the same total fat intake as a percentage of calories. Subjects were followed for eight years. So what were the results? Unsurprisingly to most the control group had the most “fatal atherosclerotic events” as the authors put it. But what about cancer? Turns out the experimental group did experience more cancer deaths than the control. This is certainly incongruous with most of the current evidence on the subject as well as the available evidence at the time when the study was published. The authors even mention this, stating, “The experience of other investigators using similar diets has not been the same” and “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.” I’ll let you decide whether or not this singular study provides sufficient backing for the claim that polyunsaturated fats can cause cancer.

Cognitive Dissonance

One major arc presented in Good Calories, Bad Calories is essentially a conspiracy theory. Taubes makes the argument that politicians, the press, and scientists are all in collusion to deceive the general public. The problem with this (aside from simply being absurd) is that Taubes tries to use scientific studies to make a positive case for why everyone should be eating low-carb diets and debunk any healthfulness of non-low-carb diets.  Yet almost in the same breath he will decry scientists and their studies for being mindless government minions bent on pushing nutrition propaganda. Is this rational?

For instance, on page 53 Taubes brings up four studies that show no significant association between dietary fat consumption and heart disease.10 This is done to bolster the narrative that the public has been sold a bill of goods when it comes to fat and heart disease. Then on the very same page he implies that they are corrupt by saying “[I]t’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… Now they no longer felt obliged to test any hypothesis.” I don’t know why Taubes would do this; the studies kind of helped him make a case, but then he shot himself in the foot by questioning the researchers’ ethics.

Funky References

Gary Taubes has a strange way he cites references – well strange to me anyway. If Taubes makes a factual claim or quotes someone and you want to get the juice for the claim or the context for the quote then you have to read-over the sentence in question remember either the first few words the sentence starts with (like “The amazing thing about…”) or the subject of the paragraph (e.g. “Fiber and colon cancer”) and note the page you’re on. Then you flip to a series of pages titled “References” near the end of the book. Look for the page number and then the subject matter in question. Hopefully you can find it easily. So let’s say you find the beginning of your sentence then you’ll get one or more references, like “Keys 1975.” Then you hop over to another section of the book titled “Bibliography” and look for Keys. Once found look for a source published in 1975 since there are quite a bit of Keys references cited in the book. If you find more than one Keys 1975 reference (there are multiple) then you’ll just have to go with your gut (no pun intended) on which reference is actually the one you are looking for.

Another thing to note is that many (if not most) of Taubes’s sources are not available to the average Joe. You might be able to get the abstracts through NCBI, but with all of the studies that I decided to look up I had to go through my university’s library system to access the actual paper. Even then I had to order a couple of things via an interlibrary loan from Canada and Oregon to get the actual source because it was not available online or even in physical form in University of Washington’s vast physical archives. After a while I simply gave up on any source that was not available at UW. I’m not getting paid to fact-check this guy, after all. This, of course, does not even include things like personal one-on-one interviews that Taubes conducted which are only available to Taubes.

I was also interested in two books that Taubes cited, neither of which contained a page number in the reference.

If I was a more cynical man I would say Taubes is making it difficult for the reader to fact-check him.  You can trust this face. Would this face lie to you?

  1. To be fair, after my previous encounter with Taubes’s work I was predisposed to not like the book, but I approached it as impartially as could.
  2. despite the fact that I have never heard that term used by actual scientists, nutritionists, dietitians, professors, etc.
  3. I have to give credit where it is due. I did not do the leg-work when it comes to aggregating these studies. That goes to eric_twinge.
  4. Which is admittedly very little.
  5. Taubes cites the book as the source of the quote, but does not give a page number on where to find it in the book’s 352 pages. Incidentally the passage can be found on page 272 in the paperback version.
  6. On the Christian maxim “Love thy enemy”, in a letter to Michele Besso (6 January 1948)
  7. Yerushalmy J. and H. E. Hilleboe. 1957. Fat in the diet and mortality from heart disease. A methodologic note. New York State Med. Jour. 57:2343-2354.
  8. I’m not about to pay for the privilege of reading it nor do I want to wade through my university’s microfilm collection to look at it.
  9. Pearce ML and Dayton S. (1971) Incidence of Cancer in Men on a Diet High in Polyunsaturated Fat. The Lancet Vol. 297, Issue 7697, Pages 464-467.
  10. In actuality only three of the four studies show no association between dietary fat and heart disease, but at this point I am no longer surprised when Taubes exaggerates the science. Interestingly some of the studies do show carbohydrates providing a mild protective effect against heart disease. One wonders if Taubes even bothers to read the stuff he cites.