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

Introduction

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

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

Not the Introduction

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

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

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

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

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

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

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

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

 * * *

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

On page 46-47 Taubes claims:

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

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

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

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

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

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

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

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

 * * *

Taubes makes stuff up again on page 49:

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

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

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

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

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

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

* * *

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

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

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

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

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

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

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

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

* * *

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

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

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

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

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

[…]

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

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

* * *

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

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

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

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

Refs

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

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

3. United States. Dietary goals for the United States. (U.S. Govt. Print. Off., 1977). at <http://catalog.hathitrust.org/Record/011389409&gt;

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

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

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

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

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

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

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

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

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

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