Good Calories, Bad Calories: A Critical Review; Chapter 9 – Triglycerides and the Complications of Cholesterol

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

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.

ahrens

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.

* * *

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.
Nutrient data for 23002, Beef, short loin, porterhouse steak, trimmed to 0.12 fat, cooked, broiled

fatty acids and cholesterol

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.

fatty acids and cholesterol2

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.
fatty acids and cholesterol3

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.

Refs

 

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).
 

Good Calories, Bad Calories: A Critical Review; Chapter 1 – The Eisenhower Paradox

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

Early in the chapter Taubes claims that most mainstream nutrition authorities were saying that the American diet changed during the 20th century, from a plant-based diet to a diet heavy in meat. On pages 10 and 11 he attempts to refute this notion by saying that the USDA statistics from which this notion is drawn is very flawed, citing a personal interview with David Call and a paper on food disappearance data.1 Specifically he says

  • “The USDA statistics, however, were based on guesses, not reliable evidence.”

  • “The resulting numbers for per-capita consumption are acknowledged to be, at best, rough estimates.”

  • “The reports remained sporadic and limited to specific food groups until 1940 […] Until then, the data were particularly sketchy…”

However, the very next paragraph he makes the argument that the US has always been a meat-eating country, and as evidence he cites data from the USDA! “By one USDA estimate, the typical American was eating 178 pounds of meat annually in the 1830s, forty to sixty pounds more than was reportedly being eaten a century later.” Either the food stats are reliable before 1940 or the are not. Pick a side and be consistent.

He’s really all over the map in this section because he then claims that in fact we did eat less meat in the early 20th century due to a few reasons: the cattle industry could not keep up with population growth, meat rationing during WW1, and Upton Sinclair’s The Jungle. He then makes the argument that Americans started eating more fruits and vegetables and decreased consumption of animal products. Following this change, incidents of heart disease skyrocketed to become an epidemic – an epidemic that earlier in the chapter he claims was completely bogus.

* * *

On pages 14 and 15 Taubes talks a bit about cholesterol and says

Despite myriad attempts, researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream than those who didn’t. “Some works claim a significant elevation in blood cholesterol level for a majority of patients with atherosclerosis,” the medical physicist John Gofman wrote in Science in 1950, “whereas others debate this finding vigorously. Certainly a tremendous number of people who suffer from the consequences of atherosclerosis show blood cholesterols in the accepted normal range.”

It’s interesting to note that immediately after that sentence in the cited text Gofman also wrote2

There does exist a group of disease states (including diabetes mellitus, nephrotic nephritis, severe hypothyroidism, and essential familial hypercholesteremia) in which the blood cholesterol level may be appreciably elevated. Such patients do show, in general, earlier and more severe atherosclerosis than the population at large.

In fact, most of the text makes the case that there are particular cholesterol particles to blame for atherogenesis, specifically those with a density of 10-20 Svedberg units that are currently known as LDL. However, since this paper was published in 1950 they are referred to as the Sf 10-20 class of cholesterol molecules. Gofman also noted – prior to even anything that Keys published on the subject – that dietary lipids affect these Sf 10-20 molecules, stating:

Our preliminary study of a group of 20 patients whose diet we have restricted in cholesterol and fats has demonstrated that the concentration of the Sf 10-20 class of molecules is definitely reduced or even brought down to a level below resolution ultracentrifugally in 17 of the cases studied within two weeks to one month.

I can’t understand why Taubes didn’t mention that, can you?

* * *

Taubes knocks me for a loop on page 15 when he states:

The condition of having very high cholesterol—say, above 300 mg/dl—is known as hypercholesterolemia. If the cholesterol hypothesis is right, then most hypercholesterolemics should get atherosclerosis and die of heart attacks. But that doesn’t seem to be the case.

Actually that seems to be exactly the case… even by the study Taubes cites.

Coronary Artery Disease in 116 Kindred with Familial Type II Hyperlipoproteinemia

click to embiggen

click to embiggen

That study even seems to be in agreement with the other studies on familial hypercholesterolemia at the time3:

Our results are qualitatively similar to analyses on a smaller scale which have established an enhanced risk of premature CAD in affected members of families with familial hypercholesterolemia.

But since certain thyroid and kidney disorders might also cause hypercholesterolemia I suppose Taubes can just ignore all that evidence linking cholesterol to heart disease.

* * *

Pg. 15

Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol. In 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death, and so they autopsied more than a hundred very recently deceased New Yorkers, all of whom had died violently, measuring the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic illness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.”

I was unable to find the cited Landé and Sperry paper. It is so old and obscure that not only was I unable to find it, the databases I used (PubMed, WorldCat, Academic Search Complete) could not find a record of it even existing. But let’s do something we probably should not do and take Taubes at his word here. It is still interesting to note that this is an example of an observational study, specifically a cross-sectional study. Later in the book Taubes will make the case that observational studies are worthless. In fact, you will see throughout the book that Taubes will cite observational studies, usually without caveat, if it fits his meat-is-good narrative. However, if he doesn’t like the conclusion of a study (observational or otherwise) you will find that he impugns the methodology, the authors, or even the entire field of science of which it is a part. Get your popcorn ready.

* * *

Like the above point, this is not a real significant issue, but it shows that Taubes is not above quote mining to try and paint someone in a negative light. On page 16:

Henry Blackburn, his longtime collaborator at Minnesota, described him as “frank to the point of bluntness, and critical to the point of sharpness.” David Kritchevsky, who studied cholesterol metabolism at the Wistar Institute in Philadelphia and was a competitor, described Keys as “pretty ruthless” and not a likely winner of any “Mr. Congeniality” awards.

I imagine the point of these quotes is to paint Keys as kind of an asshole, just in case any reader might find themselves sympathizing with Keys when Taubes takes massive, diarrhea-like shits all over Keys’s research and Keys personally. I cannot verify the Kritchevsky quote above because it was from a personal interview, but adding a bit of context to the Blackburn quote can change the tone entirely4:

Ancel Keys has a quick and brilliant mind, a prodigious energy, and great perseverance. He can also be frank to the point of bluntness, and critical to the point of sharpness. But by the boldness of his concepts, the vigor of his pursuits, and the rigor of his methods, as well as by his personal example, he led several generations of investigators in making powerful contributions to the public health.

The entire article is actually quite praiseworthy.

* * *

Pg. 15:

This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. And even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.

I’m not sure why Taubes names DeBakey as the primary source here, since he was actually the fourth author in the study that was cited, but no matter… It’s interesting to find that if you check the 1964 paper that is cited, it’s a type of observational study called a case series that examines 1,700 surgical patients treated for some sort of atherosclerosis.5 Turns out 1,416 out of the 1,700 (or 83%) have what the Mayo Clinic would describe as “high” cholesterol levels (over 200 mg/dL).

Does Taubes even read the studies he cites? Or does he read them and deliberately misrepresent them?

A second paper he cites in support of that paragraph is not even a study, but a statement by the president of the American Heart Association6 (wait… they’re supposed to be the bad guys, right?). He says many things in that statement, but what is most relevant to this paragraph is he says that

In a nation of over a quarter of a billion people we are a remarkably heterogeneous lot, and in truth there are no two of us alike. Those with low cholesterols as a group seem to have less coronary disease than those with high cholesterols, but this is too often extrapolated to apply directly to one individual.

He goes on to expound that, sure, cholesterol levels are important, but sometimes people get heart disease and don’t have high cholesterol levels so we should individualize our advice. I don’t think it really helps or hurts Taubes’s argument, but evidently he cited it anyway. Probably to pad his references.

* * *

If Taubes’s irrational contempt for Keys was not obvious before, it should be crystal clear after this passage on page 16:

When Keys launched his crusade against heart disease in the late 1940s, most physicians who believed that heart disease was caused by diet implicated dietary cholesterol as the culprit. We ate too much cholesterol-laden food—meat and eggs, mostly—and that, it was said, elevated our blood cholesterol. Keys was the first to discredit this belief publicly, which had required, in any case, ignoring a certain amount of the evidence.

Before Keys came along all of the “evidence” that dietary cholesterol substantially affects serum cholesterol was from animal studies. Studies that, just two pages earlier, Taubes argues have no bearing on human physiology. So Keys decides to conduct some cholesterol research on actual humans, and concludes that dietary cholesterol actually doesn’t have a substantial effect on serum cholesterol.7 If this were anyone else other than Keys Taubes would likely praise them for not following the conventional wisdom of the day and conducting proper scientific research, but instead Keys is accused of “ignoring” evidence. I think that’s fair.

In the same paragraph as above Taubes discusses a cholesterol study:

In 1937, two Columbia University biochemists, David Rittenberg and Rudolph Schoenheimer, demonstrated that the cholesterol we eat has very little effect on the amount of cholesterol in our blood.

Although the statement “the cholesterol we eat has very little effect on the amount of cholesterol in our blood” is true for most people, as we have just discovered, the Rittenberg/Schoenheimer study that Taubes mentions has almost nothing to do with that statement.8 Firstly, the study was conducted on mice, and extrapolating results on people from cholesterol studies on animals are certainly dubious as Taubes himself admits. Moreover, the study itself involves feeding mice water labeled with deuterium then measuring deuterium in their cholesterol and fatty acids in the mice’s tissues to see how much deuterium had been incorporated into those molecules. As far as I can tell it has nothing to do with feeding them cholesterol and seeing if that impacts their blood cholesterol levels. But correct me if I am wrong.

Pg. 16 continued:

As a result, Keys insisted that dietary cholesterol had little relevance to heart disease. In this case, most researchers agreed.

Most researchers agreed… 16 years later.9

* * *

On page 17 Taubes writes:

By 1952, Keys was arguing that Americans should reduce their fat consumption by a third, though simultaneously acknowledging that his hypothesis was based more on speculation than on data: “Direct evidence on the effect of the diet on human arteriosclerosis is very little,” he wrote, “and likely to remain so for some time.”

This is another minor point, but it should be pointed out that THAT IS WHAT A HYPOTHESIS IS. It’s a guess based on little or no evidence, and all scientists have them. Just for context, here’s the quote from Keys that Taubes plucked with a bit more… umm… context10:

[W]e may remark that direct evidence on the effect of the diet on human atherosclerosis is very little and is likely to remain unsatisfactory for a long time. But such evidence as there is, plus valid inferences from indirect evidence, suggests that a substantial measure of control of the development of atherosclerosis in man may be achieved by control of the intake of calories and of all kinds of fats, with no special attention to the cholesterol intake. This means: (1) avoidance of obesity, with restriction of the body weight to about that considered standard for height at age 25; (2) avoidance of periodic gorging and even temporary large calorie excesses; (3) restriction of all fats to the point where the total extractable fats in the diet are not over about 25 to 30 per cent of the total calories; (4) disregard of cholesterol intake except, possibly, for a restriction to an intake less than 1 Gm. per week.

Taubes gets the quotation a smidge wrong, but it still keeps the spirit of the original. The bigger picture here is that Keys is recommending (in an academic journal, by the way) to avoid becoming obese, avoid gorging on food, a diet that’s about 30% fat, and to not worry too much about cholesterol intake. Pretty uncontroversial stuff, if you ask me. Yet Taubes portrays Keys here and elsewhere as some kind of radical crusader, religious zealot, idiot, and kind of an asshole.

* * *

On page 18 Taubes discusses a 1957 paper by Jacob Yerushalmy and Herman Hilleboe, which is something of a response to Ancel Keys’s 1953 paper Atherosclerosis: A Newer Problem in Public Health.11 If you’re not familiar with the Keys paper I will give you a brief synopsis. Keys published some data that suggested a remarkable relationship between fat in the diet and heart disease. Included in the paper was a striking (if oversimplified) figure looking at several countries and their population’s typical fat intake juxtaposed with deaths from heart disease.

YH4

Taubes says:

Many researchers wouldn’t buy it. Jacob Yerushalmy, who ran the biostatistics department at the University of California, Berkeley, and Herman Hilleboe, the New York State commissioner of health, co-authored a critique of Keys’s hypothesis, noting that Keys had chosen only six countries for his comparison though data were available for twenty-two countries. When all twenty-two were included in the analysis, the apparent link between fat and heart disease vanished. Keys had noted associations between heart-disease death rates and fat intake, Yerushalmy and Hilleboe pointed out, but they were just that. Associations do not imply cause and effect or represent (as Stephen Jay Gould later put it) any “magic method for the unambiguous identification of cause.”

I have actually written about this in a previous blog post, but I will revisit this again. Aside from the fact that Keys never claimed a cause-and-effect relationship (much less an unambiguous one) and always identified it as an association, Taubes completely misrepresents the results of the study. It’s true that after Yerushalmy and Hilleboe added more data into the graph the relationship becomes a bit more muddied, but it certainly does not vanish as Taubes claims. There is still a noticeable relationship.12 See for yourself.

YH1

What’s even more interesting is that Y&H actually conclude that consumption of animal fat and/or animal protein is much more strongly associated with heart disease than total fat. Moreover, vegetable fat and/or vegetable protein is actually negatively correlated with heart disease. The resolution is not very sharp, but here are the results. I’ll leave it to you to wonder why Taubes ignores this highly pertinent information.

YH3

YH-2

click to embiggen

See Taubes response #1

* * *

On pages 19-20 Taubes claims that Keys “insisted” that fat elevated cholesterol. I am not sure what Keys was doing that made him so insisting, other than writing a few academic articles concluding that there was an association between dietary fat and serum cholesterol (which there was), while also making sure to point out that there are many details about this association that have yet to be discovered (which there also were). Taubes then goes on to mention some studies that examined those details:

In 1952, however, Laurance Kinsell, director of the Institute for Metabolic Research at the Highland–Alameda County Hospital in Oakland, California, demonstrated that vegetable oil will decrease the amount of cholesterol circulating in our blood, and animal fats will raise it. That same year, J. J. Groen of the Netherlands reported that cholesterol levels were independent of the total amount of fat consumed: cholesterol levels in his experimental subjects were lowest on a vegetarian diet with a high fat content, he noted, and highest on an animal-fat diet that had less total fat. Keys eventually accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.

In other words, Keys did what any good scientist should do: he followed the evidence. Yet the syntax of the last sentence would have you imagine that Keys was some sort of stubborn asshole that refused to accept the truth until the evidence overwhelmed him.

* * *

This may be another nitpicky issue, but the following quote is misleading. Page 20:

This kind of nutritional wisdom is now taught in high school, along with the erroneous idea that all animal fats are “bad” saturated fats, and all “good” unsaturated fats are found in vegetables and maybe fish. As Ahrens suggested in 1957, this accepted wisdom was probably the greatest “handicap to clear thinking” in the understanding of the relationship between diet and heart disease.

First of all, I was never taught that kind of “nutritional wisdom” in high school. Come to think of it I was never taught any nutritional wisdom in high school, but that’s neither here nor there. My issue with this is that in the text that Taubes cites as the source of that quote, Ahrens does not say that the animal fat = bad / vegetable fat = good binarism is the greatest handicap to clear thinking. What he does say is that the good-bad dyad was a greater handicap than the confusion about why experimental diets were designed to be eucaloric.13

* * *

Tabues uses a 1957 review article titled “Atherosclerosis and the Fat Content of the Diet” as a source for three claims in this chapter. One is simply a block quote on page 8. The other two claims are very tenuous, especially the following found on page 20:

In 1957, the American Heart Association opposed Ancel Keys on the diet-heart issue.

The article does mention Keys a few times, as well as a number of other researchers involved with dietary research involving atherosclerosis, but it is very neutral on Keys. In fact, you might even say the author mildly endorses Keys at a couple of points: “Mayer et al. found that high-fat animal or vegetable diets increased and low-fat diets decreased serum cholesterol of normal subjects, confirming earlier data of Keys.” And “Keys, in particular, has placed emphasis on the proportion of total dietary calories contributed by the common food fats […] Certainly there is an abundance of data, both clinical and experimental, that tends to relate excess fat intake to atherosclerosis.”14

After reading the article I certainly didn’t get the idea that the AHA opposed Keys. Even if they did they never explicitly stated this.

* * *

On page 21 Taubes pulls some numbers from thin air:

As Time reported, Keys believed that the ideal heart-healthy diet would increase the percentage of carbohydrates from less than 50 percent of calories to almost 70 percent, and reduce fat consumption from 40 percent to 15 percent.

The Time article actually does report that Keys suggested American reduce their fat intake from 40 to 15 percent. However, there is no mention in the entire article about Keys recommending an increase in carbohydrates.15

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

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Refs

1. Call, D. L. & Sánchez, A. M. Trends in fat disappearance in the United States, 1909-65. J. Nutr. 93, Suppl:1–28 (1967).

2. Gofman, J. W. et al. The Role of Lipids and Lipoproteins in Atherosclerosis. Science 111, 166–186 (1950).

3. Stone, N. J., Levy, R. I., Fredrickson, D. S. & Verter, J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinemia. Circulation 49, 476–488 (1974).

4. Blackburn, H. Ancel Keys. at http://www.mbbnet.umn.edu/firsts/blackburn_h.html

5. Garrett H, Horning EC, Creech BG & De Bakey M. Serum cholesterol values in patients treated surgically for atherosclerosis. JAMA 189, 655–659 (1964).

6. James, T. N. Presidential address. AHA 53rd scientific sessions, Miami Beach, Florida, November 1980. Sure cures, quick fixes and easy answers. A cautionary tale about coronary disease. Circulation 63, 1199A–1202A (1981).

7. Keys, A., Anderson, J. T., Mickelsen, O., Adelson, S. F. & Fidanza, F. Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol. J. Nutr. 59, 39–56 (1956).

8. Rittenberg, D. & Schoenheimer, R. Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation. J. Biol. Chem. 121, 235–253 (1937).

9. Quintão, E., Grundy, S. M. & Ahrens, E. H. Effects of dietary cholesterol on the regulation of total body cholesterol in man. J. Lipid Res. 12, 233–247 (1971).

10. Keys, A. Human Atherosclerosis and the Diet. Circulation 5, 115–118 (1952).

11. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y. 20, 118–139 (1953).

12. Yerushalmy, J. & Hilleboe, H. E. Fat in the diet and mortality from heart disease; a methodologic note. N. Y. State J. Med. 57, 2343–2354 (1957).

13. Ahrens, E. H., Jr. Seminar on atherosclerosis: nutritional factors and serum lipid levels. Am. J. Med. 23, 928–952 (1957).

14. Page, I. H., Stare, F. J., Corcoran, A. C., Pollack, H. & Wilkinson, C. F., Jr. Atherosclerosis and the fat content of the diet. Circulation 16, 163–178 (1957).

15. The Fat of the Land. Time 77, 48 (1961).