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 158 Taubes discusses a paper1 by Pete Ahrens
By 1957, Ahrens was also warning about the dangers of oversimplifying the diet-heart science: maybe fat and cholesterol caused heart disease, or maybe it was the carbohydrates and triglycerides. “We know of no solid evidence on this point,” wrote Ahrens, “and until the question is further explored we question the wisdom of prescribing low-fat diets for the general population.”
However, that quote is taken out of context. Taubes makes you think Ahrens is saying that there is “no solid evidence” regarding whether or not carbohydrates caused heart disease, but Ahrens is really referring to the ambiguity (at the time) of whether HDL or LDL causes heart disease. Actual quote:
[W]e are tempted to ask whether the lower density lipoproteins are less “atherogenic” than the higher-density lipoproteins rich in cholesterol and phospholipids. We know of no solid evidence on this point […]
I don’t think it’s a big deal, but it is misleading. What is even more misleading, though, is the information that is in the Ahrens paper that was purposefully ignored by Taubes because it runs contrary to his argument.
In this chapter (among other chapters) Taubes tries to make the case that cholesterol is not very relevant in discussions of atherosclerosis. The real culprit, according to Taubes, is triglycerides which are raised by those evil carbohydrates. Triglycerides are the only biomarker that matters. But while the Ahrens paper cited by Taubes does indicate that high CHOs can lead to elevated triglycerides it also makes clear a few other things, like vegetarian diets and very low fat diets are best for reducing lipids (triglycerides and cholesterol) and that plant-based fat is preferable to animal fats in the same regard.
Don’t believe me? Here are a few quotes from the paper:
- “Experience to date has shown that two regimens are effective in lowering serum lipid levels of our outpatients. The first is total vegetarianism, in which all dairy products are omitted except for skim milk, washed cottage cheese, skim milk cheeses, and egg whites.”
- “The second regimen consists of a very low fat diet (less than 25 Gm. per day) supplemented by an ounce or more of corn oil at least three times daily.”
- “Serum lipids can be altered by dietary means, and experimental data lead to the presumptive conclusion that unsaturated fats in the diet cause depressions in levels of cholesterol and phospholipids.”
- “[P]atients with existent or threatening arteriosclerosis may be justifiably advised to eat higher proportions of unsaturated fats.”
There is even a nice graph in the paper that Taubes would probably prefer you not see.
I don’t think it needs any editorializing, but in case you can’t tell ALL of the lipid measurements – triglycerides, phospholipids, free cholesterol, and total cholesterol – are higher when fed animal fats at ALL points compared to plant fats.
* * *
On page 159 Taubes discusses a publication by Kuo2 that Taubes uses to support his carbohydrate-leads-to-hypertriglyceridemia-and-therefore-CHD argument. The study in question does show that his study patients with high levels of serum triglycerides were able to lower them when on a low-CHO diet. However, what is made clear in the study is that this is only true for patients with an abnormal condition of carbohydrate sensitivity, and that a diet with moderate carbs does not lead to hypertriglyceridemia in normal patients. In fact, Kuo mentions that one would need to eat an absurd amount of CHOs to induce elevated triglycerides. From the paper (emphasis mine):
A moderately high dietary sugar and other carbohydrate intake, amounting to 35% to 40% of total daily calories, did not appear to exert a significant effect on the blood lipid levels of young normolipemic subjects with negative family history of coronary disease and abnormality in carbohydrate metabolism. It was necessary to raise the carbohydrate intake to 85% to 90% of total calories to induce hyperglyceridemia in patients who were not abnormally sensitive to carbohydrates.
In the same paragraph in which he mentions the Kuo paper, Taubes claims the CHO-triglyceride-CHD hypothesis was confirmed by two other big studies at the time (Goldstein et al. and Carlson and Bottiger).3,4 Except they don’t even mention the pièce de résistance of Taubes’s argument: the carbohydrates. They simply discuss the association between CHD and triglycerides, which has never been disputed as far as I know. No mention of carbs at all in these papers.
* * *
On page 160 Taubes claims that the US government – and, by extension, researchers – ignored triglycerides as a risk factor for CHD in favor of studying cholesterol because everyone had a huge hard-on for Keys, apparently:
The National Institutes of Health, which was effectively the only source of funding for this research in the United States, had already committed its resources to three enormous studies-the Framingham Heart Study, Keys’s Seven Countries Study, and the pilot programs of the National Diet-Heart Study. These studies would measure only cholesterol and so test only Keys’s hypothesis. No consideration was given to any alternative hypothesis.
I’m sure you’ll be shocked to discover that Taubes is not exactly being honest here. Two out of the three studies that he said measured only cholesterol in fact measured both cholesterol and triglycerides (among other things).5-7 In fact, one of the Framingham papers mentions that triglycerides are a risk factor, albeit not as predictive as cholesterol is (emphasis mine):
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. Elevated endogenous triglyceride values appear significant in coronary atherogenesis only when accompanied by high cholesterol values.
* * *
On pg 160 of hardback Taubes states:
By 1961, Keys and his collaborators in the Seven Countries Study had measured cholesterol in over ten thousand men. By 1963, they had completed the exams on another eighteen hundred men. Even had it been technically possible to include triglycerides in the measurements, or to return to the original locales and retest for triglycerides, the cost would have been astronomical. The result, as we’ve seen, was considered a resounding victory for Keys’s fat-cholesterol hypothesis.
His citation for this is page I-7 in the study program and objectives which is a table of causes of death and a table of death rates from US vital statistics.8 There is no reference for cholesterol or triglycerides or exams or cost or really anything that Taubes claims here.
* * *
On page 161 Taubes discusses a series of papers published in the NEJM that report on various disorders of lipoprotein metabolism….. aaaaaaand makes some claims about them that are not backed up by the evidence in the actual papers (emphasis mine):
Four of the five lipoprotein disorders described in this series were characterized by abnormally elevated levels of triglycerides in the very low density lipoproteins. For this reason, Fredrickson, Levy, and Lees also warned against the dangers of advocating low-fat diets for all patients, because these diets increased carbohydrate consumption and so would elevate triglycerides[…]
As evidence for the claim Taubes cites page 219 of Fredrickson et al. 1967.9 That paper neither advocates for or warns against low-fat diets. In fact it’s never mentioned, but here are a few things that are mentioned in the section on dietary management of this disorder:
- “[A] patient with a marginal Type II pattern who has neither of the other components of the triad diagnostic for the familial syndrome and who has a high intake of foods rich in cholesterol and saturated fats warrants dietary advice, for the expectation is good that he will respond.”
- “The 2 components in dietary treatment of the Type II abnormality are limited intake of cholesterol and the substitution of polyunsaturated for saturated fats. Cholesterol and saturated (usually from animal) fats occur together in foods, and many therapists today are more concerned with their elimination […]”
- “Substitution of skim-milk over whole-milk products, severe restriction or even elimination of egg yolks and reduction in meat intake for a daily intake of about 100 mg of cholesterol and 20 to 30 g of fat is one of the most effective dietary regimens.”
- “Most Type II patients (provided they have normal glucose tolerance) can tolerate carbohydrate intakes of approximately 4 or 5 gm. Per kilogram of body weight per day without significant rise in their glyceride concentrations.”
That particular paper he cited dealt with only Type II of the five types of abnormal lipoprotein metabolism. Just FYI. He cites others though. Continuing with Taubes on that same paragraph:
By far the most common of the five lipoprotein disorders was the one designated Type IV, characterized by elevated VLDL triglycerides-“sometimes considered synonymous with ‘carbohydrate-induced hyperlipemia,'” they wrote-and it had to be treated with a low-carbohydrate diet.
Wrong on so many levels. Let’s take a look at the quote first. Taubes excises what follows that quote because the authors go on to say that while some might classify Type IV as “carbohydrate-induced,” it is really not true. Here’s the entire quote on page 273 of the same Fredrickson series, bolding mine:
The Type IV pattern (hereafter called simply “Type IV”) is a valuable indicator of metabolic imbalance; it does not describe a specific disease. It is sometimes considered synonymous with “carbohydrate-induced hyperlipemia.” This is probably too narrow a concept since most patients who have this pattern on a regular diet do not lose it entirely when their diet is changed so that 10 per cent of their calories come from carbohydrate, and an occasional patient does not have an abnormal increase in plasma glycerides when fed 80 per cent of his calories as carbohydrate.
That deals with the blatant quote-mining. What about the claim that the treatment had to be a low-carb diet? The authors also clearly state that carbohydrates should not be assumed to be the cause of the hyperlipemia, at least regarding Type IV, and that weight loss should be considered the primary treatment of such a disorder.
How does Taubes get away with this?
* * *
From page 168 in the hardback:
When they finally were tested in two clinical trials in the 1990s—the Lyon Diet Heart Trial and an Italian study known as GISSI-Prevenzione—both supported the contention that the diet prevented heart attacks, but neither provided evidence that it did so by either raising HDL or lowering LDL, which was how it was now alleged to work
The GISSI study does not measure diet.10 The diets remain the same throughout. The variable of interest in the study is one omega-3 gel capsule with the primary endpoints being death, non-fatal myocardial infarction, and stroke (i.e. not cholesterol). Conclusion: Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit. This study does not prove his claim.
Regarding the Lyon Diet Heart trial, Taubes’s inclusion of HDL and LDL makes his claim technically correct. However, the results of the Lyon Diet Heart trial are actually pretty devastating to Taubes’s overall thesis. What Taubes leaves out is that total cholesterol was very predictive of a second myocardial infarction. From the study: “[E]ach increase of 1 mmol/L of total cholesterol increased the risk of recurrence by 20% to 30%.”11 Not to mention the experimental diet contained – among other things – less saturated fat.
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On pages 168-169:
Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein. Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.
For this paragraph of claims Taubes cites two studies, one by Katan and one by Grundy.12,13 He also cites the USDA National Nutrient Database for the fatty acid profile of his hypothetical steak.
If you actually look at the National Nutrient Database for a porterhouse steak you will note that Taubes is correct when he breaks down the fatty acid composition. However, you’ll notice that he focuses on the stearic acid (18:0) which is only one-third of the SFAs, the other two-thirds that he neglects to mention is palmitic acid (16:0) which according to the Katan study he cites raises LDL cholesterol monumentally compared to stearic acid.
As for the claim that the “remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL,” this is blatantly untrue, even by the studies Taubes himself cites.
Again, does Taubes even bother to read the studies he cites?
“All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly.”
I’m not sure he can make that claim. Based on his own references, carbs seem to decrease both HDL and LDL. That would suggest a more-or-less neutral effect on the HDL/LDL ratio and therefore a neutral effect on CVD.
By the way, does Taubes now accept that cholesterol plays a role in heart disease? It seems that the reason red meat is beneficial for you, according to Taubes, is that is helps lower LDL and raise HDL. The same notion he was arguing against the entire chapter! Moreover, it seems that the source of the cholesterol-mitigating properties is the unsaturated fats that are found more abundantly in vegetable oils. Here’s Taubes again:
The observation that monounsaturated fats both lower LDL cholesterol and raise HDL also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil.
So why not just go for the olive oil? Oh yeah, because vegetable fats cause cancer or some such nonsense. But not meat, of course; it’s perfect.
1. Ahrens, E. H., Jr et al. Dietary control of serum lipids in relation to atherosclerosis. JAMA 164, 1905–1911 (1957).
2. Kuo PT. Hyperglyceridemia in coronary artery disease and its management. JAMA 201, 87–94 (1967).
3. Goldstein, J. L., Hazzard, W. R., Schrott, H. G., Bierman, E. L. & Motulsky, A. G. Hyperlipidemia in Coronary Heart Disease I. Lipid Levels in 500 Survivors of Myocardial Infarction. J. Clin. Invest. 52, 1533–1543 (1973).
4. Carlson, L. & Böttiger, L. E. Ischaemic heart-disease in relation to fasting values of plasma triglycerides and cholesterol. Stockholm prospective study. The Lancet 299, 865–868 (1972).
5. Chapter XIII: Serum Triglyceride Changes. Circulation 37, I–224–I–226 (1968).
6. 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).
7. In fact, Taubes’s citation for Framingham here is actually a newspaper article that doesn’t even mention Framingham. I am assuming it is an innocent citation error.
8. Keys, A. Coronary heart disease in seven countries. I. The study program and objectives. Circulation 41, I1–8 (1970).
9. Fredrickson, D. S., Levy, R. I. & Lees, R. S. Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders. N. Engl. J. Med. 276, 34–44 (1967).
10. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. The Lancet 354, 447–455 (1999).
11. De Lorgeril, M. et al. Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction: Final Report of the Lyon Diet Heart Study. Circulation 99, 779–785 (1999).
12. Katan, M. B., Zock, P. L. & Mensink, R. P. Dietary oils, serum lipoproteins, and coronary heart disease. Am. J. Clin. Nutr. 61, 1368S–1373S (1995).
13. Grundy, S. M. Influence of stearic acid on cholesterol metabolism relative to other long-chain fatty acids. Am. J. Clin. Nutr. 60, 986S–990S (1994).