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).

Nutrition, Pregnancy, and Omega-3s



FYI: My co-host Carrie Dennett has written a series of great posts on nutrition and pregnancy on You should definitely check them out. Now on to the post…

The thing about proper nutrition when you’re pregnant is the following: It’s DAMN IMPORTANT. For instance, not getting enough folate/folic acid during pregnancy can result in major neural tube defects.1–3 Think about it: You’re literally building a human from scratch. You’re going to need all the necessary components for doing that, plus some extra.

Really, the topic of nutrition and pregnancy is far too large to cover in one blog post, which is why Carrie had to break it up into several posts. So I am going to briefly touch on a few things that were discussed in the show.

Nutrition and Fertility

I mentioned Dr. Walter Willett appearing on The Diane Rehm Show some years ago to plug his book The Fertility Diet. I have not read The Fertility Diet, but Dr. Willett is chair of the department of nutrition at the Harvard School of Public Health. He is a bit of a rockstar in the field of nutrition because he has written many hard-hitting papers on the subject, and he’s a principal investigator on the Nurses’ Health Study.

I will let the science speak for itself, but one thing that struck me during the interview was that whole milk was associated with greater fertility than skim milk. So if you are a milk drinker, choose whole milk while trying to get pregnant or have a small dish of ice cream or full-fat yogurt every day.* For the other main takeaways from the fertility diet visit the HSPH website.

Prenatal Nutrition

I’m not going to go into a big long post on everything you need to know about nutrition and pregnancy. If you want something a bit more comprehensive visit Carrie’s posts linked above or check out the Mayo Clinic’s pages on what to eat and what not to eat during pregnancy. Or download this very informative review.4 Or buy a textbook on the subject.

What I would like to do is explore the topic of Omega-3 intake during pregnancy and IQ.

Omega-3s During Pregnancy and IQ

This is a very thorny issue indeed, but one that I think warrants further investigation. In that spirit I did some digging after we recorded our podcast and found the following…

A paper was published in 2005 in the American Journal of Preventive Medicine that you might call something of a meta-analysis.5 The author took all the relevant studies regarding n-3 fatty acids and cognitive development, aggregated them, and summarized their findings. This was the conclusion:

This analysis finds that an increase in maternal intake of DHA during pregnancy of 1 g/day will increase child IQ by 0.8 to 1.8 points (central estimate of 1.3 points). Because typical DHA intake associated with fish consumption is well under 1 g/day, changes in fish consumption will result in IQ effects amounting to a fraction of a point.

In other words, the evidence suggests that large amounts of DHA n-3 will have possibly the only the mildest effects on IQ. The analysis included 7 randomized controlled trials (RCTs) on formula feeding and one RCT on maternal supplementation during pregnancy. The author also points out that that there are large differences in the relevant studies so direct comparison is difficult, and that different tests were used to estimate IQ.

But what has been published since that analysis??

No Link

In 2008 a RCT published in the journal Pediatrics found nothing. From the conclusion:

Our study did not reveal any difference in overall IQ scores at 7 years of age between children whose mothers had taken n-3 very-long-chain PUFAs or n-6 long-chain PUFAs during pregnancy and lactation.

Positive Link

In 2007 an observational study was published in the Lancet where pregnant women completed a food frequency questionnaire (FFQ), and later their child was measured for pro-social behavior, fine motor skills, communication skills, and social development.6 From the paper:

[M]aternal consumption of more than 340 g seafood a week was beneficial for the child’s neurodevelopment.

American Journal of Epidemiology in 2008 published results of a cohort study that measured maternal fish intake and child cognition. Another mild association was found.

[M]aternal fish intake more than twice a week was associated with improved performance on tests of language and visual motor skills.

But what about n-3s? Some fish are sources of a ton of n-3s while others not so much. The authors accounted for n-3s. For each 100 mg of maternal daily DHA & EPA intake from fish, children had Peabody Picture Vocabulary Test (PPVT) scores that were 0.5 points higher and Wide Range Assessment of Visual Motor Abilities (WRAVMA) total scores that were 1.1 points higher – another mild endorsement of the link between n-3s and cognition. However, the authors noted that higher prenatal mercury exposure was associated with lower developmental test scores. Unfortunately, often times fish and mercury go hand in hand. Ugh… what now?

Fish and Mercury

Pregnant women are often cautioned to avoid eating too much fish because of the mercury levels. This is important, and like alluded to earlier can have impacts on the child’s cognitive development. The thing is that mercury levels can vary greatly by the type of fish, whether it was farmed or wild-caught, and where it was sourced. For more information visit the NRDC website or check out this handy chart from the University of Maine.

Nutrition and the Epigenome

We touched on nutrition, epigenetics, and the pop science book Survival of the Sickest (If you’ve read it, tell me what you think in the comments section). I’d like to discuss that area of research, but it’s so meaty7 that it requires its own post.


* However, to be clear most of the evidence presented in the book comes from the Nurses’ Health Study, which is an epidemiological study. An important fact about epidemiological studies is that they measure associations (or links) not necessarily causes. So it may be true that there is something about whole milk that produces greater fertility over skim milk, but it is also possible that more fertile women prefer whole milk over skim milk and that the milk really doesn’t affect fertility. It’s difficult to determine, and won’t be determined unless/until some sort of randomized controlled trial takes place. This is important to clarify, especially since I made the mistake of saying in the podcast that milk influences fertility. It would be more accurate to say that skim milk is associated with infertility or whole milk is linked to fertility or something like that.


  1. Honein MA, Paulozzi LJ, Mathews TJ, Erickson JD, Wong LY. Impact of folic acid fortification of the US food supply on the occurrence of neural tube defects. JAMA 2001; 285: 2981–6.
  2. Berry RJ, Li Z, Erickson JD, et al. Prevention of neural-tube defects with folic acid in China. China-U.S. Collaborative Project for Neural Tube Defect Prevention. N Engl J Med 1999; 341: 1485–90.
  3. Laurence KM, James N, Miller MH, Tennant GB, Campbell H. Double-blind randomised controlled trial of folate treatment before conception to prevent recurrence of neural-tube defects. Br Med J 1981; 282: 1509–11.
  4. Williamson CS. Nutrition in pregnancy. BNF Nutr Bull 2006; 31: 28–59.
  5. Cohen JT, Bellinger DC, Connor WE, Shaywitz BA. A quantitative analysis of prenatal intake of n-3 polyunsaturated fatty acids and cognitive development. Am J Prev Med 2005; 29: 366–74.
  6. Hibbeln JR, Davis JM, Steer C, et al. Maternal seafood consumption in pregnancy and neurodevelopmental outcomes in childhood (ALSPAC study): an observational cohort study. Lancet 2007; 369: 578–85.
  7. Pardon the pun.

Gary Taubes is a Blowhard

Imagine if you will that you make a living by selling an idea. You are a merchant in the marketplace of ideas, and you sell an idea that we will call Idea X. You sell books that promote Idea X, you give lectures across the country extolling the virtues and benefits of Idea X, etc. Turns out that Idea X is somewhat controversial but quite lucrative. You tried selling other stories and ideas in the past, but none have been nearly as profitable to you as Idea X. Espousing this idea has afforded you the ability to provide your spouse and children a comfortable living in these tough economic times. Imagine also that a scientific study was recently conducted by prominent researchers and the results are published in a prestigious scientific journal. As it happens the results of the study are pretty devastating to Idea X and contradict some of its main points. In the following days the study results are much-discussed in various media outlets, and some people begin to doubt the idea that you’re selling. The study results have left the more loyal adopters of your idea confused as to what to believe, and they beg you to respond to the study.

What do you do?

There are probably a few different choices you could make in this case.

  1. You could ignore the study and hope this bad news blows over soon. Then after the media gets bored of discussing the study results and moves on, you can try to resume preaching your idea to the people still adhering to your idea. As time goes on you can try to re-convert those who left Idea X.
  2. You could follow where the evidence leads and come out and say “I don’t want to mislead anybody. It looks like Idea X is not supported by the evidence. I was wrong, and I’m sorry.” Then you face the very tough challenge of trying to find another idea that is both as profitable as your last idea with the caveat that it is also evidence-based and grounded in reality. If you don’t find another profitable idea then you’ll have to move your family out of your nice neighborhood and into a lousier one while you work unappealing jobs to put food on the table.
  3. You could denounce the study and the scientists who conducted it. You could try and poke holes in the evidence and muster your greatest argument for why no one should believe the results. It may not be intellectually honest, but the truth must be an unfortunate casualty when you and your family’s quality of life is at stake.

Gary Taubes has chosen #3, except he takes it even further and denounces not only the specific study and the researchers that conducted it, but the field of epidemiology as a whole. This is actually pretty shrewd since most epidemiological evidence is against him anyway. Taubes’s Idea X in this analogy is the assertion that, contrary to popular belief, foodstuffs like red meat, saturated fat, and cholesterol are actually healthy and pose no threat of disease while just about any and all carbohydrates are unhealthy.

Mr. Taubes recently wrote a blog post responding to a recent study titled Red Meat Consumption and Mortality published in Archives of Internal Medicine. The study concludes “red meat consumption is associated with an increased risk of total, CVD, and cancer mortality.”1 If I had to summarize Mr. Taubes entire blog post it would be something like: Epidemiology is a pseudoscience. Well, not all epidemiological research, just any research suggesting that eating red meat for every meal might not be healthy. Any scientist or nutrition researcher claiming that is practicing a junk science. Those that come to other conclusions are the real scientists, the good scientists. Also, I will never accept any scientific claim unless there are randomized, placebo-controlled clinical trials to back it up. Except for the claim that smoking causes lung cancer. I will accept that one without RCTs.

Let’s Break it Down

To start things off Taubes does not refute any specific thing in the actual paper. He leaves that job to someone else.

Zoe Harcombe has done a wonderful job dissecting the paper at her site.

Taubes prefers instead to respond to the paper’s general tone and the tone of some of the researchers involved with the paper, notably Dr. Walter Willett and Dr. Meir Stampfer.

Who is this Zoe Harcombe and why should I trust her judgment? The biography on her webpage does not tell me much about her credentials other than she is a

[Q]ualified nutritionist with a Diploma in Diet & Nutrition and a Diploma in Clinical Weight Management, but she is first and foremost an obesity researcher.

A “qualified nutritionist”? What does that even mean? Who “qualified” her and gave her “Diplomas”? Were these actual universities or did she just pay 30 bucks (or pounds perhaps, since she’s from the UK) for some shady online certification that means nothing? We are not told, and I suspect for good reason.

She is also an obesity researcher, huh? A quick Google Scholar search of her name came up with no publications. Is she actually a researcher or does she just call herself one? I suspect the latter. I love how Taubes apparently thinks she is some sort of authority on the matter but the Harvard School of Public Health is full of incompetent boobs.

Here is one of her “key problems with this study”

1) This study can at best suggest an observed relationship, or association. To make allegations about causation and risk is ignorant and erroneous.

Nowhere in the study did the authors claim to have a causal relationship. It is always stated as an association. Harcombe misrepresents the results.

Eventually her “key problems” devolve into irrelevant and unverifiable ad hominem

[O]ne of the authors (if not more) is known to be vegetarian and speaks at vegetarian conferences

It is like the author is a communist or something!  As if being a vegetarian would have any bearing on the results of the study. Are vegetarians not supposed to conduct nutrition research now, only omnivores? What about Jews or Muslims? If they do research involving meat should their results not be published? What’s more is this claim isn’t even verified. She has a citation but it takes me to this page that tells me nothing. I also went to the page with the 2013 speakers but none of them authored the study in question.

Okay, back to Taubes now.

The problem with observational studies like those run by Willett and his colleagues is that they do none of this [testing hypotheses]. That’s why it’s so frustrating. The hard part of science is left out and they skip straight to the endpoint, insisting that their interpretation of the association is the correct one and we should all change our diets accordingly.

You mean like how you do, Taubes, with your books and lectures? Except that you are not a scientist and have no medical training or research experience like Willett et al. I don’t want to engage too much in tu quoque, but pointing out hypocrisy is so much fun. Let me get in one more jab, and then I’ll move on.

I’m no expert in Taubesian hermeneutics, but I think he meant to say The problem with observational studies like those run by Willett and his colleagues is that they are so devastating to my position that everyone should eat truckloads of meat. Okay now I’ll get to the substance of his point.

Mr. Taubes seems to be accusing Willett et al. of laziness despite the fact that they churn out hundreds of studies that take decades to complete and are peer-reviewed and published in top-tier journals.2 The reason for this is because, according to Mr. Taubes, epidemiology is not a true science, and if Willett and his colleagues really wanted to study certain dietary aspects and their link to colon cancer mortality or cardiovascular disease mortality they have to conduct randomized, double-blind, placebo-controlled human clinical trials (I will abbreviate as RCTs). Anything less is not “good science.”

I’m not about to give you a lecture on what epidemiology is and why it is important. It may be a good subject for a future post, but for now I will say that it is a useful field when studying large populations, incidence and prevalence of disease, or when RCTs would be unethical or impossible.

Here is a visual reference to help understand the hierarchy of evidence a little better. At the top of the triangle you have the most rock-solid evidence that we have on a given subject and the bottom is the least valuable evidence.

As you can see, the cohort studies in question are not quite as good as RCTs, but they are as close as you can get. They are not meant to replace RCTs in evidence-based medicine, but they can be a good proxy when conducting a RCT would be impossible. Here’s another visual that explains each method.

Mr. Taubes asserts that the experts are wrong and red meat does not lead to any kind of mortality. He asserts this with barely any evidence and zero RCTs to back up his assertion, yet if anyone would disagree he demands they provide RCTs because Taubes will not accept cohort studies. Conveniently for him the RCTs he demands will  almost certainly never take place. Let me explain.

Mr. Taubes seems to think that RCTs examining specific dietary constituents and their roles in disease mortality are low-hanging fruit. I’d like to see Taubes design one for, say, red meat and colon cancer. It would be worth a read just to see how he deals with the problem of blinding alone. Furthermore, what would be a good placebo? I get that one group would be assigned red meat every meal, but how do you get the control group to eat placebo meat without the subjects really knowing if they are in the meat-eating group? Surely people can tell the difference between a tofu steak and a genuine ribeye. Plus cancer is not something that you get only a few weeks into a feeding study. It takes decades to arise, so it would mean that a RCT would also have to take as much time. There are many more difficult study design issues Mr. Taubes would need to tackle before he could begin.

This is all assuming of course that the study would be funded (it almost certainly wouldn’t because it would be the single most costly RCT in history) and that it would pass IRB approval (it wouldn’t because the study itself would be unethical considering there is a fair amount of evidence that red meat does in fact lead to colon cancer3, Red Meat Consumption and Mortality notwithstanding).


Throw it Against the Wall and See if it Sticks

If you don’t buy into his Epidemiology Sucks theory Taubes also hurls some other arguments against the study hoping at least one of them will stick. One is that the increase in mortality from red meat eaters is only an increase of 0.2 so it’s basically nothing and you should just forget about it. Of course another way to present that increase is 20%. An increase of only 0.2 seems like such a small number compared to 20%, doesn’t it? What if I told you that drinking Generic Beverage That You Sort Of Enjoy everyday increases your risk of developing esophageal cancer by twenty percent? My guess is you would cut down on Generic Beverage That You Sort Of Enjoy, even if you enjoyed it.

Another argument Taubes uses is admitting the following:

[T]he people who avoided red meat and processed meats were the ones who fundamentally cared about their health

If I may paraphrase: Okay, sure, vegetarians are healthier than meat-eaters. But is it because of the meat? I say it’s because vegetarians are just generally healthier than meat-eaters. They are more health-conscious and they smoke less. It has nothing to do with meat! It’s simply the “healthy cohort effect”!

Are you sitting down? I hope so because I’m about to rock your world: I agree with Taubes here. This is a legitimate concern with epidemiological studies. If you are not careful with your study design and statistical analysis these kinds of things can bias your results. However, there are many ways you can adjust for things like this, and I think it goes without saying that if you have a poor study design or no adjustments then you don’t get published in the top tier journals in which Willett and Stampfer get published. Furthermore, sampling biases like the healthy cohort effect are stronger in smaller cohorts of 10 or 20, but when you increase sample size to 100 or 1,000 the effect becomes negligible. In the case of Red Meat Consumption and Mortality the authors use cohorts of 37,698 men and 83,644 women, so if they did their due diligence with the statistical analysis (and I’m not about to check their math, that’s what the peer-review process is for) if the effect is even present it should be so weak as to be nonexistent.

As it stands the authors of the paper in question did in fact adjust for smoking status as well as a host of other lifestyle factors.4

Watch now as Taubes removes any possible hope you might have about his scientific literacy.

So do an experiment to see which is right. How do we do it? Well you can do it with an N of 1. Switch your diet, see what happens.

The ol’ do-it-yourself randomized controlled trial. The very pinnacle of oncological research. Have you switched to a high-beef, low-carb diet? Check. Have you died from colon cancer and/or cardiovascular disease? No? Well then the experts were wrong! Help yourself to some more mutton. Take note future lawyers: this is special pleading at its finest.

Credit Where Credit is Due

Although completely irrelevant to a discussion of Red Meat Consumption and Mortality Taubes does cite one randomized trial (not placebo-controlled) that kind of shows some benefits in a low-carb Atkins diet over other somewhat popular diets such as Zone or Ornish. It is totally a red herring, but let’s touch on it anyway. The study takes premenopausal women that are either overweight or obese and assigns them to one of several diets. They all receive instructions on how to follow their assigned diets and are followed-up on after one year. Turns out the Atkins people lost more weight than the other people. They also had a slightly more favorable lipid profile (i.e. higher HDL levels lower triglyceride levels) but elevated LDL levels compared to the other diets.5

A few things to note:

  • I think it is hilarious that earlier in his post Taubes criticizes the Red Meat Consumption and Mortality study because he claims “they use questionnaires that are notoriously fallible” to collect dietary information.6 Meanwhile he praises this “A to Z” study for its design without mentioning that the authors use telephone-administered dietary recalls, which are not bad per se but chosen mainly for their efficiency rather than robustness.
  • One could make an argument that simply giving people some instruction on the diets in the beginning and then coming back in a year to measure outcomes is not the best study design. For example, many nutrition labs in the Fred Hutch (including mine) will actually provide all of the meals to be eaten during the study free of charge. This accomplishes a couple things: 1) It increases compliance with the diet7 and 2) It allows the researchers to strictly control the calories, vitamins, fat content, etc. I don’t think the above study was a poor design, but there are stronger (albeit more costly and time-consuming) feeding designs one could use when studying diet.
  • I was not surprised that the Atkins group lost more weight. There are actually good and interesting reasons for why low-carb diets are very effective in that area, but I won’t get into that now. What did surprise me at first was that the Atkins group had lower triglyceride levels. But then I remembered that weight loss in general will produce that effect, especially if subjects are overweight at baseline. If the other diets produced as much weight loss as Atkins I would expect a similar reduction of triglycerides.8
  • This study uses exclusively disease-free, non-diabetic, non-pregnant or lactating (etc…9) overweight and obese premenopausal women, so to extrapolate these results and suggest that the general population would be healthier if they adopted this diet is certainly dubious.
  • This is a diet study that examines carbohydrates and weight loss and lipid profiles after 12 months. The Red Meat Consumption and Mortality study in question deals with red meat and cancer, CVD, and other mortalities after 28 years. The former does not and cannot refute the latter. They are almost unrelated. You can eat meat three times a day and have the bulk of your calories come from carbohydrates. You can be a vegan that eats a ton of fat and protein but very few carbs. They are not mutually exclusive.

Stunning Hypocrisy

Now you may be thinking that this is a guy who simply demands the highest levels of evidence. Sure Taubes may miss out on a ton of great knowledge obtained from epi studies but the man takes a hard line on evidence. He will only accept findings from human randomized controlled trials and you can’t fault him for that.

Except that he doesn’t.

If you take a look at some of Taubes’s other posts you will see he makes other controversial claims that run contrary to mainstream science.10 In other posts he conveniently uses epi studies to bolster his narrative while impugning the RCTs that run contrary to his point.

Some examples of this are his posts on sodium. He cherry-picks cohort studies and case-control studies as evidence that the sodium-hypertension link is one big hoax. He even cites ecological and cross-sectional studies which are among the least substantial types of studies not just in epidemiology but in all of science (they would be blue or green-ish on the above pyramid), and he misrepresents their results to claim that sodium does not cause hypertension. Cross-sectional and ecological studies literally cannot show causation; they are not designed to do so.

Meanwhile, Taubes tries to downplay one of the strongest and most-lauded RCTs on the subject (The DASH trials) saying that blood pressure change was only “modestly lower.” If you call nearly a ten-point decrease in blood pressure by only manipulating sodium intake11 “modest” then sure. I suppose I can’t argue with such vague wording.*  He also says that while the researchers measured blood pressure, they failed to measure other things such as lifespan. Big deal, right? Let’s just forget about that stupid study that completely contradicts me. He says basically the same thing about the Cochrane reviews that do not support his position on the subject. Sure the reviews state that cutting back on salt will lower blood pressure, but it doesn’t prove that cutting back will make you live longer so who cares, amiright? By the way, Cochrane reviews are at the very tip of the aforementioned evidence pyramid.

At least he doesn’t sink to the level of anecdotal evidence and personal testimony to prove a point. I take that back; he does:

All I knew was that I had played high school football in suburban Maryland, sweating profusely through double sessions in the swamplike 90-degree days of August. Without salt pills, I couldn’t make it through a two-hour practice; I couldn’t walk across the parking lot afterward without cramping.

You know what? Of all the evidence on the subject that story of Taubes in high school is the smoking gun we have all been waiting for, so I take it all back. You were right all along Taubes. Go collect your Nobel Prize. You have earned it, my friend.


In Conclusion

Mr. Taubes takes the position that red meat does not contribute to cancer or CVD mortality.  He took this position without any evidence from RCTs since, as he said, they have never been done.12 Moreover, he claims that any epidemiological evidence against his position is meaningless because the epidemiology field itself is meaningless.13 The only evidence Mr. Taubes is willing to accept are those of RCTs which are nearly impossible when it comes to things like diet and cancer mortality. So Mr. Taubes has set things up to where he cannot be proven wrong even if he is wrong.

You know what? I can do that, too! I contend that parachutes are not beneficial and life-saving when it comes to falling out of the sky. Prove me wrong. Oh and you can’t point to instances where groups of people have jumped out of an airplane and the parachute has slowed their velocity toward earth allowing a safe landing while those who had a malfunctioning parachute or no parachute at all suffered major trauma or death. Those would have to be either cohort or case-control studies and therefore meaningless. There have been zero RCTs studying the effect of parachutes and gravitational challenge.14 The basis for parachute use is purely observational, and its apparent efficacy could potentially be explained by a “healthy cohort” effect. My contention stands!

If Mr. Taubes had any intellectual consistency he would have to agree with that point. At best he would have to remain neutral on parachutes, since there are no RCTs to prove they do anything.

Some Additional Nit-Picky Stuff

Nutritionists and public health authorities have gone off the rails in their advice about what constitutes a healthy diet.

Wow, that’s painting with a pretty broad brush now isn’t it? It’s like saying “Government bureaucrats are wrong.” Much like government bureaucrats there are quite a few “nutritionists and public health authorities” in the world and they hold a variety of positions on a variety of topics. You mind picking one, telling me what it is, and why it is wrong? Or do you just want to construct a straw man that grossly misrepresents what a few people may or may not be saying so you can more easily refute it?

Are you talking about the advice of dietitians? What specific piece of advice do you object to? Do you have a problem with the following statement that I took off the AND website: “A well-balanced diet filled with whole grains, fruits, vegetables, healthy fats, low-fat dairy and lean protein is important for health and wellness.” Is that advice “off the rails”? Here’s a statement I copy-pasted from “Limit the amount of foods and beverages with added sugars your kids eat and drink.” Is this bad advice? If so, why?

I first wrote about the pseudoscience of epidemiology in Science back in 1995, “Epidemiology Faces It’s Limits”[sic]… my Science article has since been cited by over 400 articles in the peer-reviewed medical literature…

Over 400 citations? Wow! Congratulations Mr. Taubes. You should be proud of yourself. Although I’m confused as to why you put that bit of self-aggrandizement in your post. Is it to imply that because your article has so many citations your thesis (Epidemiology is a bogus science) is correct? If citations = truth then I’m afraid that Willett (the villain in your narrative) is right and you are wrong. Why? Because Willett has actually published far more papers than you have, many of which have well over 1500 citations each. Furthermore, Willett’s papers are actual peer-reviewed scientific studies as opposed to simply lay commentary.

One last (petty) thing.

I’m writing this post with a little more haste than is my wont.

What are you doing Taubes? How about you quit pretending to be an 18th century British aristocrat and start acting like a 21st century American, you pretentious windbag. You are not Christopher Hitchens. Knock it off.

Way down at the bottom of the blog post Taubes admits a correction to an earlier version of the post. Evidently he instructed Dr. Willett to go read a chapter in a textbook titled Modern Epidemiology and learn how the “best epidemiologists” conduct real research. As it turns out Dr. Willett actually wrote the chapter in question. I won’t add any commentary here. Just let that bit of delicious schadenfreude wash over you like a warm bath.

*EDIT: This sentence originally said “more than ten-point decrease.” As it was pointed out to me by a commenter the more than 10 point decrease in blood pressure was between a low-sodium DASH diet compared to a typical high sodium diet. The data where ONLY sodium is manipulated resulted in decreases of 6-7 points.

  1. Pan A, PhD, Sun Q, MD, ScD, Bernstein AM, MD, ScD, et al. (2012) Red Meat Consumption and Mortality Results from 2 Prospective Cohort Studies. Arch Intern Med. 172(7):555-563.
  2. The number of studies published by Willett is currently at 1279 according to Pub Med
  3. WCRF/AICR (2007) Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global perspective. Second Expert Report. London, UK: World Cancer Research Fund; 280-288
  4. From the article: “The results were adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; and intakes of total energy, whole grains, fruits, and vegetables, all in quintiles.)”
  5. Gardner CD, Kiazand A, Alhassan S, et al. (2007) Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women the A to Z Weight Loss Study: a Randomized Trial. JAMA. 297(9):969-977.
  6. By the way the food frequency questionnaires used in Red Meat Consumption and Mortality as well as many other studies certainly have their limitations. No one disputes that. But they have been repeatedly verified for validity and reproducibility in many other studies, especially when looking at overall dietary patterns.
  7. something that the authors of this study were concerned with by stating: “limitations included the lack of a valid and comparable assessment of individual adherence to the 4 different diets”
  8. In fact the authors mentioned exactly that: “[T]he trajectories of weight change between 6 and 12 months suggest that longer follow-up would likely have resulted in progressively diminished group differences.”
  9. “Women were excluded if they self-reported hypertension (except for those whose blood pressure was stable using antihypertension medications); type 1 or 2 diabetes mellitus; heart, renal, or liver disease; cancer or active neoplasms; hyperthyroidism unless treated and under control; any medication use known to affect weight/energy expenditure; alcohol intake of at least 3 drinks/d; or pregnancy, lactation, no menstrual period in the previous 12 months, or plans to become pregnant within the next year”
  10. Omigosh! I did not see that coming (/sarcasm)
  11. Sacks FM, Svetkey LP, Vollmer WM, et al. (2001) Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med. 344:3-10.
  12. and in this author’s estimation won’t be done in our lifetimes, if at all
  13. unless we’re talking about smoking, of course
  14. Smith GC, Pell JP. (2003) Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials. BMJ. 20;327(7429):1459-61.