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Nutrition Past and Future

6 The Journalist Gary Taubes 6: Lessons from the Dead

The cholesterol confusionists have worn out what I call the “atherosclerosis at autopsy” argument over the years. Perhaps this issue was legitimately confusing thirty or forty years ago, but this line of attack should have been long dead and buried by now. Let’s lay this nonsense to rest once and for all. I’m going to show you how this old bugger has broken down over the years. Low carbers, I know you have a strong stomach, so let’s get started.

At the top of this excerpt from Good Calories, Bad Calories, you see Gary Taubes informs us of a study from all the way back in 1936 conducted by two investigators named Lande and Sperry. Taubes tells us that their conclusion after studying a series of bodies at autopsies was unambiguous. The extent of atherosclerosis in those bodies bore no relation to the cholesterol levels measured in the blood of those bodies. The subjects had died suddenly, he says, so their cholesterol levels could not have been influenced by the cause of death. This line of reasoning requires us to accept a rather strange premise. For this finding to matter at all, we must believe that the cholesterol levels in these people had been stable throughout the many decades it took for them to develop arterial plaque. Stable since their youth. Stable since last week. Stable even after they died. That’s a lot to ask of us. Taubes offers us no reason we should believe these things. Or maybe he is suggesting an even more unlikely premise: that the amount of plaque in your arteries comes and goes along with periodic rises and falls of the amount of cholesterol in your blood. Can you imagine that? If your cholesterol is high today, you have severe hardening of the arteries. If you take a bunch of drugs so that you have low cholesterol next year, you will have arteries as clean as a child’s. Which premise is believable to you? Because if neither sounds good to you, then you shouldn’t be falling for this one.

Here is that old paper. If we look it over, we can understand how they arrived at such suspect conclusions. As you see, they were aware that infections could affect cholesterol levels in sick patients. They didn’t know much more than that. Other conditions such as cancer can alter lipids as well, but they just didn’t know that in 1936.

Here you see the fatal flaw in their reasoning. They stated that “it is probable that each person maintains a particular level of cholesterol in the serum over long periods, perhaps throughout adult life.” This is not even true throughout the month, much less throughout life. Gary Taubes knows this very well and that’s why he shouldn’t have tried to slip this into his book. I’ll prove that to you in my Cholesterol Confusion video about measurement error. He just threw this study in here hoping no one would think about it any further. I won’t let him get away with that.

Cholesterol levels can vary in the same person even when the composition of the diet is held constant. This variability is a bigger problem when the sample size is small. In this case we’re talking about only 147 bodies.

These doctors did not refer to records collected from these subjects when they were alive, much less through the course of their lives. They simply collected blood from bodies as they showed up at the morgue. They had absolutely no way of knowing what their cholesterol levels had been over the long term.

Here you see their collection technique. They acknowledged that in their day they didn’t know if cholesterol levels changed after death. They said the success of their investigation was contingent on cholesterol remaining stable after death. It doesn’t.

Here you see a study which looked at the accuracy of cholesterol measurements taken post-mortem. After death, cholesterol levels dropped 13% on average. This paper was from 1997. Let’s give those guys back in 1936 a break. They didn’t know much then. Gary Taubes wrote his book, however, in 2007. I don’t think he deserves a break on this one.

You see in their conclusion that they were overly eager to make a hasty generalization about the role of cholesterol in developing atherosclerosis. Gary Taubes chose this line to put in his book. I wonder how I could explain to Taubes why this line shouldn’t have been in his book. I wonder who might explain it in a way that is unambiguous.

TAUBES: You do not over-interpret your data. You do not say your studies say something they do not say. And to do that is bad science.

That’s exactly right, younger Gary Taubes. Does Taubes actually believe that cholesterol in the blood has no effect on atherosclerosis, too? If he does, he should say so and explain himself. If he doesn’t, he should explain why he brought up this distraction.

Let’s look at this type of argument further. There was one doctor, J.C. Paterson, who was especially invested in this “atherosclerosis at autopsy” argument. Here is one of his papers. This one appears to hold promise. He says that in this study of dead bodies, he had the opportunity to measure cholesterol in subjects while they were alive over long periods of time. How did he manage this?

He was working in an institution which treated the mentally ill – patients with psychosis, as he put it – and the elderly.

This paper by Paterson was just one autopsy study that was referenced by these researchers in 2000, so we should be able to get a contemporary take on this issue here. You can see I highlighted it for you and provided the footnote. The Lande and Sperry paper that Mr Taubes liked is in there, too. You can read here how the methods of quantifying the extent of disease at autopsy have gotten better over the years. Who knows how consistent they were back then in judging plaque thickness, for example? Studies like Paterson’s used sickly patients who were institutionalized. That meant their sampling was bad.

Paterson and company’s final paper which reported the results of their autopsy studies included some strained logic. See if you can follow this. They were aware that a criticism could be made that their study only included older patients who probably had health problems. Their defense on this point was to cite the Lande and Sperry paper, which they said didn’t suffer those faults. Now think about this. They knew their study could be challenged because they used old people with comorbidities. They attempted to brush off this major flaw by saying that they arrived at the “right” answer anyway because they were saying what Lande and Sperry had said. “Don’t mind our methods; just know we got the right answer.” You won’t often see an excuse that weak in a paper today. Paterson just wants you to know that they were right even if their methods were wrong and that’s what counts! Paterson goes on to say that the criticism one might make of the Lande and Sperry paper– that the blood in the dead bodies had undergone changes – couldn’t be made of their study, so that made their study good. In other words, put together two studies with different flaws, and the problems just cancel each other out and you are left with two good studies. Paterson also said they couldn’t stand behind the accuracy of their measurements of plaque. Wow, what a mess this one was!

This doctor named Pomerantz pulled an Ancel Keys on Dr Paterson. He wrote a devastating critique of his methods and reasoning. Paterson had only compared pre- and post-mortem cholesterol in six subjects, he said. No accounting had been made of high blood pressure or diabetes. No information was given about changes in body weight or other markers of illness.

Realize that Paterson’s paper was published in 1960. You can see here that even back in 1947, it was known that postmortem examinations of atherosclerosis could not be reliably related to nutrition because when alive the subjects were likely in declining health. Sigmund Wilens here stated that one must at least try to factor in this issue before attempting to relate nutrition to atherosclerosis at autopsy. Paterson did not do that.

Here is the gist of Paterson’s defense against Pomerantz. I won’t read it aloud because it doesn’t make much sense. He seems to be saying that in a young person, if there is no blockage, there is no heart disease. That’s not how it works.  As you will see in the Cholesterol Confusion videos, his assumption that heart disease doesn’t have different characteristics in different age groups is just wrong.

Note the last line. For him, cholesterol below 400 was nothing to worry about. This guy was way out there.

The atherosclerosis at autopsy approach has been employed in many studies over the years. If you read the propaganda from the confusionists, you’d think these studies stopped appearing sometime in the 1960s. They didn’t. Here is one from 1976. You can see this references the International Atherosclerosis Project. Please notice the quote on the right, the fourth line from the top. “Using data of the International Atherosclerosis Project, Scrimshaw and Guzman reported a significant correlation between population ranks for mean involvement with advanced atherosclerotic lesions and population ranks, either for percentage calories derived from fat or for mean serum cholesterol levels. These studies indicate that, on a group or a population basis, there is a relation between atherosclerotic lesions and the diet.” That’s pretty clear, right? The International Atherosclerosis Project found that both dietary fat and blood cholesterol were linked to the severity of the hardening of arteries.

We are told that this study found that diets based on starch and vegetable protein were associated with less atherosclerosis in autopsies. Animal fat and protein, regardless of source, were associated with more atherosclerosis. This should be rather devastating research for the animal food pushers. Let’s look more closely at this project now.

Here is a description of how it got started. In 1959, pathologists from around the world met to standardize their procedures for studying this very issue. They went on to examine 23,000 cases over the next five years. Contrast this with the other autopsy studies the confusionists like which involved only dozens of bodies.

Here is another description of the IAP. It ended in 1964.

Here are the rankings of heart disease by country that the project produced. At the very top for the most and worst heart disease you see the white folks of New Orleans, LA. This is a place known the world over for their fatty cuisine. Follow the list downward and you will see there is a general trend away from cultures eating a lot of meat and fat and toward cultures that were poor and relied on starches. Now take a look at that author’s name at the top. Henry McGill. The year is 1968.

Look at the bottom here. McGill. 1968. This is Mary Enig, co-founder of the Weston Price Foundation saying, “Investigators found the same degree of atheroma (artery clogs) in all parts of the world—in populations that consumed large amounts of animal products rich in saturated fats and in those that were largely vegetarian.” What is she talking about? Didn’t she see that list?

Here is the other founder of the Weston Price Foundation, Sally Fallon Morell, saying the same thing. “…Vegetarians had just as much atherosclerosis as meat eaters.” Where is she getting this?

If everyone had the same level of atherosclerosis, why did they rank them? Why did they put the white New Orlenians on top and the South African Bantu on bottom?

The Bantu had already been studied and shown to have less atherosclerosis than Americans. They were said to eat a low-fat diet.

In this table we can look at the results of the International Atherosclerosis Project and compare rankings by serum cholesterol with rankings by raised arterial lesions. It’s not an exact match, but the correlation is unmistakable. At the top of both lists were whites in New Orleans. I’ve been to the French Quarter and I’ve seen what they eat there. This makes perfect sense to me. No one ever said Cajun and Creole cuisine, or the traditional foods of the Deep South, are low in fat.

In this table we can see components of the diets of people just in New Orleans and compare that to atherosclerosis at autopsy. This was a separate study from 1976. Diets that emphasized animal protein were compared with diets that emphasized vegetable protein. You can see that they had very different effects upon the frequency of raised lesions. Pause the video to look closely. If you really believe the results of autopsies are a good way to determine the effects of diet on heart disease, it’s pretty hard to make a case against starches, isn’t it? But the effects of saturated fats are obvious. More animal protein, more lesions. More saturated fat, more lesions. More starch, many fewer lesions. The Weston Price founders say something different but that is why I do videos like this. Who are you going to believe, them or your lying eyes?

Given all that, you may be wondering what Mary Enig and Sally Fallon could possibly have latched onto to make their statement that the same degree of atherosclerosis was found in big saturated fat eaters and in vegetarians. I wondered, too. Let’s give them the benefit of the doubt and say they are not just  flagrantly lying, although I don’t think they deserve that slack. You may have noticed that we didn’t look at their specific reference yet. Maybe that has a line that supports their claim. Maybe they just didn’t do any other research on the International Atherosclerosis Project. Low carbers do seem to lack the energy to do thorough research. Well, I looked up this study and I scoured it for support for their claim. Notice that study is titled “General Findings…” and it was published in Laboratory Investigations in 1968.

There it is. “General Findings.” 1968. The first author is Henry McGill.

And here you see is every word in the paper about diet. The word “vegetarian” does not appear in this paper anywhere. Unequivocally, I can say that they made that up. This report states, “These findings are consistent with the large body of experimental and epidemiologic evidence relating atherosclerosis to fat consumption and serum cholesterol.” Did Enig and Fallon miss that part? The authors did say at the bottom that, “The estimated percentage of total dietary fat consisting of animal fat does not appear to be associated with severity of atherosclerosis.” But notice before that they said “available data regarding dietary consumption were not sufficiently precise to determine whether the type of fat and amount of cholesterol in the diet are important in relation to atherosclerosis.” You should be able to see the rank order they produced, that list we just saw with white New Orlenians on top, and understand that the effects of animal foods were operative. If you disagree, you will have to explain why serum cholesterol tracked with disease severity so well if saturated fat wasn’t what raised cholesterol in these populations. I don’t think we can find here any support for Fallon and Enig. Maybe they saw something else in this paper.

I think it’s likely that this is what they misinterpreted. Durban is a city in South Africa that had a high concentration of Indian immigrants. This paper tells us that they tended to have more atherosclerosis there. I am guessing the Weston Price ladies read the word “Indian” and thought “vegetarian” and decided that vegetarians had heart disease problems, too.

That would be an incorrect assumption. South African Indians are culturally diverse. Many were Muslim, not Hindu, so they certainly were not vegetarian. Most if not all Hindus ate animal foods back then, especially ghee. Their fiber intake was low.

As a result, many of them had high cholesterol and diabetes. That study did say that cholesterol related well to atherosclerosis.

The Weston Price ladies are totally wrong about this, but just as you saw in my Vegan Propaganda video, they are responsible for propagating untruths all over the internet based on non-existent evidence. The Weston Price Foundation site is heavily reliant on imaginary evidence so they often are totally wrong on the science.

If you’ve seen my Futility of Cholesterol Denialism videos, you know that I think we can learn a lot about the effects of diet on heart disease from cross-cultural studies. High-animal-fat cultures demonstrated dramatically worse arterial lesions than did low-fat cultures in autopsy studies. New Orlenians were three times worse off than Guatemalans.

Look at those small numbers for the Guatemalans, with their diet of rice, beans, corn, and fruit. Pause this and compare their numbers to those from Olso, Norway.

Here is a nice scatter plot to give you another visual. This came from a separate study from Oslo. This matches serum cholesterol for the x-value and the degree of disease for the y-value.

Here is a reference to an autopsy study that was run in Bangkok, Thailand. Very little atherosclerosis was found there. The authors said the Thai consumed substantially less animal fat than did Americans at that time.

A very good study comparing cholesterol and atherosclerosis in the dead was a part of the Framingham Study and it was published in 1979. These investigators were able to compare the degree of atherosclerosis with cholesterol measurements taken 1, 5, and 9 years before death. In men the relationship was clear. If you read this, I have talked in past videos about the 10-year advantage women have on men in the area of heart disease. That explains why they needed 9-year measurements to see this relationship in women.

The Framingham authors stated that “biochemistry can be drastically changed in the terminal illness.” They explained that this is why they used measurements going back nine years. They also pointed out an advantage to their work that Paterson could not claim. “The findings are not confined to those observations which happen to be available in the hospital record.” They had much better data at their disposal.

Because terminal disease can affect cholesterol levels, they said that “it appeared that cardiovascular risk factor measurements made about one year before death were somewhat poorer predictors of what is to be found at autopsy than measurements obtained earlier in life.” With all his research, do you think Gary Taubes missed this big paper from the Framingham Study?

We’re up to 1995 with this paper. This was conducted in Bogalusa, LA and it focused on younger subjects. Now we don’t have to worry about what was happening to cholesterol levels in sickly old people. It was stated here that coronary artery fatty streaks were associated with elevated total cholesterol and LDL cholesterol, among other things.

Lastly, here is a paper from 2005 and this looked at young people, too. These authors measured Non-HDL cholesterol rather than total or LDL cholesterol. They examined the bodies of more than 1100 15- to 34-year-olds who died of trauma. They concluded that the traditional heart disease risk factors did predict the severity of plaques. You can see how strongly they weighted high cholesterol by comparing it to the weighting they used for smoking. Yes, high cholesterol is just that bad. You don't see many autopsy studies looking at atherosclerosis nowadays because modern medicine can take advantage of advanced imaging technologies applied to living patients.

Gary Taubes slipped in many quick little references to various studies in his book. They are sometimes closely packed together, even within the same sentence. He seems to have tried to give his readers the impression that there were a whole lot of good studies floating around out there that the bad guys like Ancel Keys decided should be ignored because they didn’t support diet-heart. Well they weren’t ignored, and they will not be ignored by me. These old papers get dusted off and shared with you starting with the next video.