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

cover

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

cloud

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).

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

cover

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

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.

                                     VINCENT
                         What do you think about what happened 
                         to Antwan?

                                     MIA
                         He fell out of a window.

                                     VINCENT
                         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.

AND

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

cloud

1. National Academy Press. Diet and Health: Implications for Reducing Chronic Disease Risk. (1989). at <http://www.nap.edu/openbook.php?record_id=1222&gt;

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 <http://doi.wiley.com/10.1002/14651858.CD002137.pub3&gt;