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Nutrition Past and Future

Response to Denise Minger 2: Not Benefiting from Hindsight

Response to Denise Minger, Part 2:
Not Benefiting from Hindsight

Minger thinks Yerushalmy and Hilleboe were awesome.  She says by going over their paper, she and her readers looked at these issues more deeply than Keys did. The cholesterol deniers are in perpetual admiration of their own cleverness.

Here are excerpts from a presentation given by Yerushalmy in which he recounts their supposed correction of Keys. You can see in the text that he was basing his skepticism on isolated populations he didn’t fully understand like the Eskimos and the Masai and similar tribes.  I have, of course, examined these outliers already in the Primitive Nutrition Series.  You can also see on the right he presented a graph with Mexico even though he should have known there was a problem with their record keeping. Why would she think these guys knew what they were doing any better than Keys did? Why do low carbers care about that paper so much? It has to be because of their agenda. I see no other explanation.

These excerpts are from the same presentation when he turns his attention to the epidemiology of smoking.  He states, “The evidence appears, therefore, to support the proposition that the incidence of low birth weight infants is due the smoker and not the smoking.” He is saying that the sort of people who tend to be smokers would be more likely to have babies with low birth weight regardless of whether or not they smoked.  He is suggesting that smoking does not affect the development of the fetus.  Pretty awesome, right Ms Minger?

Here’s some more evidence of his amazing skepticism at work. Just like his finger wagging at Keys, his defense of smoking while pregnant hasn’t faired so well over time.

Smoking during pregnancy can cause low birth weight.

Dr Yerushalmy died at the age of 69.

To be fair, he did important work in other areas and is remembered with respect. Here’s a good line from his essay.  He said other modes of investigation beside epidemiology were needed to understand which correlations in the diet indicated real causations.  He was quite right, and this is exactly what Ancel Keys did.  Minger fails to mention this, as she is not trying to provide a service to readers who want to make healthier choices.  She prefers to leave them instead stuck in a fifty-year-old blind alley.

What about Yerushalmy’s co-author for that paper, Herman Hilleboe?  He agreed, further studies were needed to study the connection between diet and atherosclerosis.  He mentions a pilot study in Minnesota looking into the topic, calling it “excellent.”

Who do you think was running this study, Ms Minger?  The only Minnesotan actively investigating diet and heart disease was Ancel Keys.

He was the leader of his day in this sort of research.

If you think Hilleboe is so awesome, maybe you should have mentioned his observation in 1963 that cholesterol was the most important risk factor for ischemic heart disease.

Denise Minger says her only purpose in this blog is to present history and data as objectively as possible. 

In her supposed correction of the record she also doesn’t give any ground in blaming Keys for, as she puts it, demonizing saturated fats, and this made him far from perfect in her estimation.  She says he glorified polyunsaturated fats.

Keys was on an anti-saturated fat crusade in his later career, says Minger.  “Crusade” is a word with religious overtones, but I ask you, if we compare Minger and Keys, who is looking at diet through the inflexibility of semi-religious belief and who is dispassionately following the scientific method? 

If you look at the paragraph on the right, in 1953 – a time when Key’s had not yet figured the unique dangers of saturated fats - he did not glorify polyunsaturated fats and demonize saturated fats.  To the contrary, he said fats used in cooking should be reduced, including polyunsaturated oils such as corn oil and cottonseed oil, along with vegetable shortening and lard.  He also offered a rationale for the continued use of butter.  It only contributed 5% of fat calories, he said. He didn’t seem to think it was important. He thought fats other than butter should be reduced and provided a quote from the USDA with the phrase, “excluding butter”. Does this look like the writing of a crusader who was hell-bent on promoting oils and opposing animal foods like butter? I don’t see it. But Ms Minger says she is just laying out the truth.

He said it was not reasonable to expect people to consume more than 7% of total calories from polyunsaturated oils.  This is glorification?

For Minger, Keys’ belief that dietary cholesterol was not a significant factor in blood cholesterol levels was one thing he got right, implying she is in a position to say he got a lot of other things wrong.  I wonder why she likes these quotes. They say that dietary cholesterol doesn’t raise blood cholesterol. So does she believe high blood cholesterol does cause atherosclerosis? She says, “good for him”. Is she endorsing the lipid hypothesis?  I can’t figure out her perspective, but I can say that the one thing she says Keys got right is in fact something he got wrong.

As I pointed out in my Primitive Nutrition Series video number 39, once you have elevated blood cholesterol levels, additional dietary cholesterol doesn’t have much of an effect.  But if you eat a healthy diet low in saturated fat and cholesterol, with your body making all the cholesterol it needs, then consuming dietary cholesterol will have an appreciable effect. So Keys was clearly wrong on this point. This meta-analysis from 1992 should have resolved this.

This should have been apparent all the way back in 1965, but Minger still hasn’t caught up with this fact. Do you see the author of this one? His name is Hegsted. Hegsted says, “Dietary cholesterol is obviously an important variable in determining the serum cholesterol level.” Do you see the title of this study?

There you see it is reference number 10 in this editorial by Ancel Keys. It looks like he agreed with Hegsted. By 1995, Keys seemed to be warming up to the idea that dietary cholesterol wasn’t desirable.

We have yet to look into the basic charge being made against Keys by Minger and others. They say he cherry picked his data. We’ll see if that’s fair in Part 3.


Response to Denise Minger 1: Scrupulous

Response to Denise Minger,
Part 1: Scrupulous

It may seem odd that I made four videos attempting to defend Ancel Keys. After all, he died in 2004. I have no personal connection to him at all. He wasn’t a vegan or a vegetarian.

He was certainly fine with milk, eggs, and meat in 1952, provided the overall diet was not high in fat.

Even after he figured out that saturated fat raised cholesterol, he still gave a green light to plenty of meat in the diet. No, he definitely wasn’t a vegan, so that’s not why I defended him.

I’m interested in Keys because he was an incredibly productive scientist who made important contributions on a hugely important subject. I also admire him for his willingness to adjust his views as he learned more. Even though he wasn’t a vegetarian himself, by the end of his career he seemed to be receptive to the idea of it. For someone who had once recommended people eat calf livers and Canadian bacon, this is a pretty fair-minded quote. He wanted the Mediterranean diet he introduced to America to be understood as a nearly vegetarian diet. Now that’s progress.

This is the man who has been portrayed as a fraud by the low carb fringe. Even when one of their apologists, Denise Minger, represents herself as the one who will finally give the man his due, she still suggests he was less than scrupulous as he pursued an agenda. She really shouldn’t go there.

Ms Minger has expressed her intent to go to graduate school.

Before she goes, she should familiarize herself with the concept of academic dishonesty.  George Washington University says it is dishonest to represent another’s work as one’s own.

Stanford has a similar policy. says that if a source for your research is central to your work, you should summarize its importance and main ideas. This is because an honest person would not want anyone to think he or she was pretending to have thought of those ideas independently.

For this blog post about Ancel Keys, Minger says she was only “inspired” by my videos.  Rather than give me credit for my research, she simply says I somehow glossed over something in my look at Ancel Keys.  She is not in any way saying she is basing almost all the content of her blog on my work.  Rather, she implies she is actually correcting my work.  This takes some chutzpah.

After all, my video was date stamped December 1, 2011.

Her comment proving she learned about the lies the low carbers tell about Ancel Keys is stamped December 17 for the whole world to see.

And her blog post about Ancel Keys is stamped December 22, only five days later.

Maybe she thought she could get away with this because not many people watched my video at the time. Knowing that few people had seen it, Minger could have chosen to demonstrate her honesty by citing my properly. She did not.

The fact that she didn’t speaks volumes. Instead, she received the praise of her commenters without any indication of reservation. They think her analysis was brilliant, incredible, and awesome.

Many have criticized my videos as ad hominem critiques of individuals, including Minger. I was criticized in this manner for simply quoting Minger’s own words recounting her biography. Some seem to think it is ad hominem to say someone lacks appropriate training in a field. Pointing out Minger’s failure to cite me properly here could be called ad hominem by her fans, too, I suppose, but credibility matters. I can’t devote all the time it would take to fact check every faulty argument appearing on a blog somewhere. It is actually a more efficient use of my limited time to explain why the opinions of some should be taken with a grain of salt.

Eventually, she did give me some form of credit in her comments section for what she had represented as her own discoveries. She says she really appreciates me pointing out frequent misunderstandings about Keys. I think it is more accurate to call them frequent libels rather than misunderstandings, as she says. Yet she still doesn’t say to which content of mine she is referring. Ms Minger, I would really appreciate you giving me due credit and representing my work fairly if you use it for your blog. Your personal appreciation alone is not worth anything to me.

Someone I really appreciate is this commenter, who pointed out how bad all this looks. Thanks, Richard.

I am not going so far as to say I was plagiarized by Minger. After all, I pointed out how easy it was to find out that Yerushalmy and Hilleboe found animal protein to be more problematic than fat based on this data. But I am not aware of anyone calling out the cholesterol denialists on this matter before me, and Minger clearly took advantage of my work without citing me properly. She pretended she was the one busting a myth perpetuated by the low carbers, and this was clearly not so. She says we all got it wrong about Ancel Keys in her title. The degree to which she is demonstrating that is the degree to which she is using my work. I think that is plain.

Maybe Minger will say she has contributed fresh content about this affair. Let’s look for that. She says she is busting a myth and revealing the truth. Here she summarizes the truth as she sees it. In the first paragraph she distinguishes the Seven Countries Study from earlier work of Keys. This is in my videos. She mentions a 1955 WHO conference at which some were dubious of his findings. Read her link and you’ll see this is at best a footnote to history of little consequence. There is no myth out there among low carbers about a meeting in 1955.  Next she points out that that paper actually found a stronger correlation with animal protein, something the low carbers fail to mention.  This, of course, was central to my videos. This isn’t new from her, either.

This was the slide I showed to make that point, along with textbook references.

I don’t see what she has come up with that busts a myth. All that is interesting here was already in my videos.

That paper about the 22 countries was written by two men named Yerushalmy and Hilleboe, and here she summarizes her main points about it. First, she says Keys cherry-picked. I’ll show you why this probably isn’t true, and even if it is, it’s beside the point. Next, she says animal food consumption correlated to income. I made this point repeatedly in the Primitive Nutrition Series. This is the food ladder concept and it is common knowledge. Next, she says that many countries referenced in the Yerushalmy and Hilleboe paper failed to keep accurate records of the cause of death back then. Not only did I demonstrate this, even Uffe Ravnskov, the author whom I was criticizing, said as much. Next, she says the food consumption data used at the time was inaccurate. It’s true that I didn’t mention this one. I didn’t because I didn’t think it was a serious point.

She thinks she has identified an issue that should render Keys’ observations useless.  Keys was using data indicating the available fats in the food supply, not the fats that were directly consumed by people.  He didn’t factor in food waste.  Therefore his estimates of fat consumption were exaggerated.  I’ve seen this same criticism of Keys from others as well.

For example, Uffe Ravnskov raised this very point in The Cholesterol Myths. He said some fat was wasted or eaten by rats or mice. Apparently rats like fats more than carbs or protein. Keys was comparing different nations to each other, so unless Ravnskov could demonstrate that there were important differences in food waste among the six countries, this shouldn’t affect the comparison. Is he saying that in the US no one was recording how much fat was actually consumed, but in post-war Japan they were carefully monitoring this somehow? Is he saying that the US had more mice, rats, and dogs eating up all the extra fat than in other countries? Is this not absurd? I didn’t include this because it seemed so ridiculous.

Moreover, Keys himself was aware of the inaccuracy of this data due to waste back in 1953. That’s what the paragraph to the left is all about. Minger didn’t correct Keys or bust a myth here, either.

Keys reasonably concluded that the amount of fat in the food supply would bear some correlation to the amount fat consumed. Remember, Keys was making a comparison between countries. As long as fat was measured with the same methodology in each country, their consumption relative to one another should track closely with their usage.

That raises the next issue. What shall we make of the criticism from Yerushalmy and Hilleboe that this wastage would be less in countries less rich than the United States? People with less wealth would be less wasteful.

It seems to me this complaint is negated by a later argument of theirs.  Here they say, and Minger concurs, that the amount of animal fat and protein consumed increases as countries become wealthier. Again, this is the food ladder. I talked about this. As countries become richer they eat more animal food. I think this argument creates a contradiction for Minger and for Yerushalmy and Hilleboe.

1.) One should not compare the fat use in these countries because wealthier nations waste more fat. Fat in the food

supply does not reflect fat consumed.

“… it does mean the fat intake (as well as total calories)

for wealthier nations may be overestimated.”

                - Denise Minger

2.) As per capita income increases, so does the

consumption of animal foods and fat.

“Intake of fat and protein—particularly from animal

sources—is usually a proxy for a country’s development.”

                - Denise Minger

They have established two opposing ideas.  Wealthier countries waste more fat because they can afford to.  But wealthier countries eat more animal fat because that’s what wealthy people do.  So which is it and what exactly is the point that is being made here? 

And if fats were being wasted, which fats were more likely to be wasted?  Would vegetable oils have been conserved more than animal fats?  I would guess that wealthier nations would have been more likely to waste vegetable oils, not animal fats, so they would have been wasting those fats that lower cholesterol and reduce the risk of heart disease and they would have been conserving the ones that raise cholesterol and cause heart disease. Animal fats were more expensive, in lower supply and consequently less likely to be wasted. Do you see the problem here?  To the degree that food waste was an issue, this factor probably adds further support to the link between saturated fat and heart disease.

Additionally, instead of cherry-picking, as Minger claims, it is more likely Keys was doing his best to compare apples to apples when he chose his countries.  I’ll come back to this weak claim of cherry-picking later.

Lastly, she repeats “correlation isn’t causation” as if she is writing on a blackboard during detention. This is as cliché as it gets, so again, nothing new here.

So what is the original content she has dug up that I missed? She later says I didn’t discuss what she thinks were the important points in the Yerushalmy and Hilleboe paper. The first is the food waste issue, already discussed. Next, she says I left out the fact that the consumption of animal foods is higher in wealthy nations. This is the issue of the food ladder and its affect on so-called diseases of civilization, something I discussed in video 40 …

Here we can see what Hilleboe thought in his  own words.  The association between cardiac death and diet is stronger for animal protein.  Now he does go on to say that non-cardiac death is inversely related to animal protein, but this is explained by the difference between diseases of poverty and diseases of affluence.  I’ll  talk about this in Playing Games with your Heart.  Hilleboe’s overall point here was simply that the definition and causes of heart disease were hard to nail down, which may have been true in 1957 but is far less true now.

As well as in video 37.  This is my script.  I did mention this.  I said, “Now he goes on to say that non-cardiac death is inversely related to animal protein, but this is explained by the difference between diseases of poverty and diseases of affluence.” I raised this point while discussing another paper.  I just didn’t think the Yerushalmy and Hilleboe paper was worth more discussion.

Here's another problem with using that data for 22 countries to argue against the Seven Countries Study, if that’s really what the confusionists insist on doing.  As I said, that data came from a statistical compilation by the FAO.  That was not data used in the Seven Countries Study.  The Seven Countries Study was a prospective cohort study. Researchers were dispatched within the seven countries to collect their own data using uniform standards.  Individuals were studied prospectively, or over time, so they were considered cohorts.  This study was not created by merely crunching someone else’s data, which is what Yerushalmy and Hilleboe did.  Keys was working with far better and more useful data than those two.  I'll give you an example of a problem with their data...

- Plant Positive

She is ignoring one of my main points in my Keys videos.  Here is my script at the beginning of video 38.  Some of the data for the 22 countries was too poor to be usable. Think about this. She thinks I should have spent more time on the Yerushalmy and Hilleboe paper because she thinks it’s so great…

Even as she says the data was poor herself.  For example, she says Mexico lacked a death certificate system in the ’50s.  Maybe this is the fresh and original observation in Minger’s blog!

Moreover, when they were recorded, the accuracy of the cause of death was notoriously unreliable there.

In 1958, it was known that these factors made the determination of rates of mortality from heart disease very difficult there.  Keys didn’t have such enormous problems with his data, but Yerushalmy and Hilleboe did.

- Plant Positive

Here’s my script from video 38 talking about this very issue.

Here’s a slide I displayed.  It’s about Mexico and their death data. It’s amazing to me she would criticize me for missing this even as she takes the idea from me. Put yourself in my place. How would you react to this? Do you see why I am concerned with her credibility?

Ms Minger wants to portray Yerushalmy and Hilleboe as the good guys here, and Keys as the sloppy, agenda-driven crusader. With the benefit of hindsight, we can see that this is an overly simplified – you might say glossed-over – portrayal. That’s next.


The Futility of Cholesterol Denialism 3: A Process of Elimination

The Futility of Cholesterol Denialism, Part 3: A Process of Elimination

I called a chapter of The Primitive Nutrition Series “Anything but LDL” because the cholesterol confusionists would be happier to focus on any possible biomarker that might indicate heart disease risk other than LDL. LDL is the one biomarker that high-saturated-fat diets cannot bring into a healthy range without calorie restriction, and it just happens to be the biomarker that has the most direct role in the pathogenesis of atherosclerosis. They are in a similar state of denial about nutritional factors that are linked to heart disease. Dietary saturated fat and cholesterol are the best understood and most widely accepted contributors to heart disease, but in the minds of the low carbers the blame should go anywhere but there. It must be the wheat. It must be the carbs. It must be the sugar. It must be the polyunsaturated oils. But there is no way fatty animal foods are to blame. There must be a conspiracy against such foods, or medical science must be captive to a shared delusion. Why else would they blame the greasy, fatty, mutagenic, high-calorie, cholesterol-laden foods of animal origin? They seem so innocent.

To illustrate the absurdity of this belief it might be useful to take a historical view of another category of research into heart disease and diet beside cross-cultural comparisons, animal research, and basic cholesterol science.

It is true that animal foods were early suspects in heart disease. Of course, as you have seen in my Cholesterol Denialism videos, a century ago atheromas were observed to be engorged with free cholesterol.

And Anitschkow induced atherosclerosis in rabbits by feeding them cholesterol. Only animal foods contain cholesterol.

Therefore it should only seem reasonable that dietary cholesterol was investigated as a contributor to heart disease. In 1951 a researcher not named Ancel Keys treated individuals with high cholesterol through a low animal fat diet and found that the cholesterol levels of most could be lowered. This investigator also observed that high blood cholesterol was associated with heart disease.

Also in 1951 another researcher not named Ancel Keys conducted a study that indicated that mortality from atherosclerosis could be reduced on a low-cholesterol, low-fat diet.

As for Ancel Keys himself, in 1957 he was conducting experiments on patients in a metabolic research unit, feeding them different types of fat. Among the fats he studied were olive oil, cottonseed oil, and sardine oil. Butterfat caused cholesterol to increase the most.

Later, he narrowed his focus to specific fatty acids, finding lauric and myristic acid to be of particular concern.

Other researchers did the same. Dietary fat in general did not appear to affect serum cholesterol levels, but specific saturated fatty acids did. Did these researchers harbor an anti-myristic acid bias back in 1963? Or did they arrive at their conclusions through honest scientific inquiry? Read the literature and the answer is obvious.

In this 1991 study different sources of saturated fatty acids were examined for their effects on cholesterol. Beef fat, cocoa butter, and butter fat were compared to olive oil. Butter fat raised LDL the most. LDL was lower with the consumption of beef fat, and LDL after cocoa butter was lower still. The lowest LDL numbers were attained with olive oil. Therefore, all those saturated fats are worse for heart health than olive oil.

Here is a table from a 2010 paper relating the effects of different sources of dairy fat on cholesterol. It appears butter is worse for cholesterol than cheese. Butter even fares poorly in comparison to other dairy products.

This study examined 420 dietary observations from 141 different groups of subjects. That’s a lot of experimental data. The authors concluded that Keys was right about saturated fat. It raises cholesterol. However, he was wrong about dietary cholesterol. Dietary cholesterol raises blood cholesterol.

Here’s an interesting cross-cultural comparison demonstrating the effects of saturated fats. Cholesterol levels in boys and men living in 20 countries were measured. Total cholesterol rose with increasing saturated fat intake, and this was most evident in comparisons of boys, who would have had lower cholesterol levels on average than the men. This is one more study showing us that unhealthy food has less of an effect on your cholesterol if you already have high cholesterol. Those living in developing countries and vegetarians ate more carbs and consequently had lower cholesterol.

I am not aware of either Brown or Goldstein ever going vegan, but they asserted that animal fats and cholesterol raised LDL levels.

This textbook states that the molecular basis for the effects of saturated fats on LDL is well understood. Essentially, saturated fat causes LDL to be removed from the blood by the liver at a lesser rate.

One might think that saturated fat’s effect on LDL by itself would be enough to explain how it causes atherosclerosis. After all, if there is more LDL in the blood, there is more opportunity for it to penetrate the artery wall. That’s true, but it’s not the whole story. In this important experiment on mice, dietary saturated fat was shown to increase selective uptake of LDL into the artery wall, even in mice that were resistant to atherosclerosis. Saturated fat caused disease to take root.

Saturated fats have been connected to adverse health outcomes in innumerable studies, some of which fly by in The Primitive Nutrition Series. Diabetes is a major risk factor for heart disease, and saturated fat is linked to that as well. In this study of men with heart disease, saturated fat intake correlated to more body fat and worse insulin sensitivity, unlike carbohydrate.

I have not found any evidence that researchers into the connection between diet and heart disease ever excluded any nutritional factors from consideration. Forty years ago , a scientist at the World Health Organization said that one cannot help but conclude that saturated fats play a role in heart disease, but he said there was no proof they are the only or even the main culprit.

The saturated fat apologists would love for you to believe an important scientist like Ancel Keys had a vegan agenda, or that nutrition science has made an overly simple distinction between animal and plant fats. We should be clear that neither of these were the case. Distinctions have been made not between animal and plant fats, but rather between saturated and unsaturated fats. Furthermore, all saturated fats have not been the subject of concern, but rather a few specific fatty acids, primarily lauric, myristic, and palmitic acids. I just don’t see evidence of any sort of bias at work in the research that implicated these.

Ancel Keys did not set out to raise alarms about animal foods, no matter how much the anti-vegan spin doctors try to make it seem that way. In this excerpt, he did note the correlation between low animal protein intake and low cholesterol, but he resisted blaming the protein itself, reasoning that those low animal protein diets were also low in fat, which he considered to be the real problem in 1957.

Many proteins were studied for their effects on cholesterol. Here, you can see what various proteins did to blood cholesterol in rabbits. Animal proteins were found to raise cholesterol much more than plant proteins.

It does seem that vegetable proteins promote healthier cholesterol levels, yet how often do you hear about this from nutrition authorities?

I’ll mention here that Keys also investigated a range of other non-dietary factors for their influence on heart disease as well, including excess body fat. He did not find a reason to suspect it in 1954.

Nor did he in 1972 after correcting for age, blood pressure, smoking habits, and yes, blood cholesterol.

Speaking of blood pressure, I’ll side track for a moment to respond to one of the more bizarre confusionist arguments. Sometimes the deniers will say that cholesterol can’t be the cause of heart disease since atherosclerosis forms in arteries but not in veins. Since the blood in both types of vessels carries cholesterol, the cholesterol can’t be the cause of disease. The portions of arteries that are subjected to the greatest stress from the force of the movement of the blood inside them are where plaques form. Where the blood is less agitated, plaques don’t form. Therefore, it is the stress from the movement of blood that causes the heart disease, not cholesterol.

The location of disease is an interesting subject. It’s just not an argument against the lipid hypothesis. Yes, it is true that the fluid dynamics of the blood within the coronary arteries seem to be a necessary condition for plaque to form. But tell me, how would a cholesterol denier propose he go on living without this rough blood flow in his arteries? Perhaps ways to eliminate this stress on your coronary arteries would be either to have the heart stop pumping or to drain them of blood. I’m pretty sure if either of those conditions are met, arterial plaque won’t be your biggest problem. It’s a little like saying you need a heart to have heart disease. Yes, you need a heart, and arteries, and you need excess cholesterol. I’m pretty sure only one of those is considered a modifiable risk factor, unless you get a fancy mechanical heart pump like the one former Vice President Cheney has, which does not beat like a heart.

It is true, high blood pressure is an important risk factor for heart disease. Higher blood pressure increases the damage done by high LDL levels. At lower blood pressure, (excess) LDL is less of a problem.

Let’s go back to looking at the process of elimination researchers undertook with other dietary factors. Here’s an excerpt from Gary Taubes’ Good Calories, Bad Calories. Taubes seems to think a promoter of the idea that sugar caused heart disease, John Yudkin, was treated unfairly somehow. He was replaced at the school where he worked by Stewart Truswell, who accepted Ancel Keys’ research on saturated fat. Taubes spins away here, saying that Truswell thought it was more important to encourage the public to eat more onions to avoid thrombosis rather than eat less sugar. It seems clear to me that Taubes is just fabricating a narrative that suits his preconceptions here.

It does seem that onions are anti-thrombotic, so Truswell might have been right about this. However, I haven’t seen evidence that he wanted a publicity campaign for onions, as Taubes suggests.

And Truswell himself makes a strong case against the direct guilt of sugar. It does not raise cholesterol. No one has even considered sugar to be a plausible enough suspect to subject it to a controlled trial. I don’t know, Mr Taubes. It seems your sugar hypothesis is weaker than the lipid hypthesis.

It’s hard to read Taubes’ writing and fail to notice signs of bias. In the quote at the left he seems to believe researchers were caught up in a false choice between saturated fat and sugar as the cause of heart disease. He says it is just assumed that if one hypothesis was right, the other was wrong, and I guess he is saying that is a bad assumption. He says the evidence from epidemiology suggested either sugar or saturated fat could be at fault. But then he switches the focus to what he calls “the potentially deleterious effects of sugar in the diet”. Wait, what about heart disease? Wasn’t that the topic? Does he really think it is in doubt today which is the bigger factor in heart disease? And if he can see that it should not be assumed that this was an either/or choice between sugar and fat, is he willing to entertain the notion that perhaps both might cause heart disease? No, he won’t. Taubes will not concede that saturated fat is at least a part of the problem. He’s the one bogged down in the either/or fallacy.

He tells his readers they should doubt that saturated fat might harm their cardiovascular health, despite all the evidence saying it does. I think Taubes is the one captive to dogma.

As if expressly for the purpose of breaking Gary Taubes free of his false choice between sugar and animal foods as contributors to heart disease, the results of two major epidemiological studies were announced on the same day. Whether or not they cause heart disease, sugary soft drinks were associated with it in men in the study on the left. Red meat, both processed and unprocessed, was associated with increased mortality in the study on the right. Both of these can be true at the same time.

Regarding sugary drinks, individuals who consumed them had elevated triglycerides. Whether or not this is explanatory, it is smart to keep your triglycerides down, and I can offer a good suggestion for that.

In this study, vegans had much lower LDL and triglycerides than omnivores. Mr Taubes, skip the sugar AND skip the meat if you are really interested in avoiding heart disease.

Diets high in sugar did cause atherosclerosis in monkeys in this study, but their diets were also high in saturated fat. This doesn’t contradict the lipid hypothesis.

Now fructose has been investigated as a contributor to heart disease, but again, a study such as this one does not contradict the lipid hypothesis, as the fructose caused an elevation in LDL. Note the subjects here obtained most of their fructose from refined junk food, not from whole food sources.

A more recent review of the effects of fructose put that study in some context. The effects of fructose on LDL seem to be weak. This doesn’t mean refined sugar is healthy. It just doesn’t replace saturated fat as a likely cause of heart disease, regardless of what Gary Taubes says.

Yes, Ancel Keys investigated sugar as a potential cause for heart disease and found the evidence lacking. Yet I don’t see evidence of his refusal to consider the effects of carbs.

Here he set out to determine the effects of various carbohydrates on cholesterol. Even though these did not raise cholesterol, he did not eliminate the possibility that some carbs would. Again, no bias is apparent. This man was a good scientist.

You’ll notice that wheat is one of the foods Ancel Keys investigated for its affect on cholesterol. This one should be understood by all the low carb apologists who want to blame heart disease on wheat. Keys did not have an agenda in his study of the effects of food on cholesterol. He simply tested a variety of foods for their effects on cholesterol and reported the results. It just so happens that saturated fats raise cholesterol and wheat doesn’t. This is the reality, folks. You may as well accept it.

There are so many people online today trying to cobble together a case for wheat’s role in heart disease. The same individuals pushing the myth that Ancel Keys was on a crusade against saturated fat are themselves guilty of stringing together the weakest evidence in their own crusade against wheat. Here, wheat gluten’s ability to bind bile acids is put forth as a way in which it might reduce cancer risk. This should also help to lower cholesterol. This study is based on in vitro experiments.

Here, a diet high in wheat gluten was shown to lower cholesterol in human bodies as well. Wheat gluten is looking good.

Also in humans, this study showed that wheat gluten reduced oxidized LDL and triglycerides, which are the preferred heart disease risk factors of many saturated fat apologists who want you to believe your cholesterol levels are not of concern. Low carbers, shouldn’t you like wheat gluten as a result of this study?

Here, an examination of twenty years-worth of studies showed whole grains and whole wheat bread to have a strong inverse association with heart disease. This is not what you would expect from a food that causes heart disease. The fact that low carbers insist on blaming wheat for heart disease indicates to me that they have never taken an objective look at the evidence out there.

Another dietary factor to receive some attention in the search for the causes of heart disease is lactose. As you know, I’m a vegan. I would have no problem telling you that lactose causes heart disease if it were true. Here, a doctor named Segall sounded alarms over lactose. Yet I have not suggested lactose causes heart disease in my videos. Why not? Am I just a subpar advocate for veganism?

Well, maybe, but that’s not the issue here. I haven’t made this argument because it is not a strong one. The saturated fat in dairy certainly contributes to heart disease, but the lactose probably does not. Segall’s idea has not been supported by the evidence over time. Only a real propagandist would make an argument this weak to serve his agenda.

Someone like Loren Cordain, who continued to cite Segall in his efforts to talk you into quitting dairy. This is how Cordain operates. He has a fad diet to sell. Do you see he references a publication by Segall from 2002?

There it is. It’s about lactose. Lactose probably doesn’t cause heart disease. Dr Cordain, there are plenty of good reasons to cut out the dairy. This is not one of them

Now that I’ve set you up with a solid understanding of the case against saturated fat for it’s contribution to heart disease, I can begin to address my critics. I’ll start with Denise Minger in the next video.


The Futility of Cholesterol Denialism 2: Cholesterol in Populations

The Futility of Cholesterol Denialism, Part 2: Cholesterol in Populations

Some of the most important research to establish the connection between diet and heart disease has come from comparisons of contrasting cultures. Epidemiology has enabled connections to be made between lifestyle factors and heart disease prevalence within populations.

If you’ve seen The Primitive Nutrition Series, you know I give Loren Cordain credit for at least paying lip service to the appropriateness of low cholesterol targets. He noted that many hunter gatherer cultures had much lower cholesterol levels than is typical in contemporary societies consuming large amounts of animal foods. They also had lower apparent rates of heart disease. Hunter gatherers give us nice opportunities for cross-cultural comparisons, but as I noted in my other videos, an important explanation for their low cholesterol seems to be consistently overlooked by the paleo community.

Without hygienic food preparation and clean water, parasitic infections are common in primitive populations. Parasites gobble up cholesterol in the blood. I found this study by reading the excellent PaleoVeganology blog. Parasites metabolize cholesterol, affecting the lipid profiles of their hosts. The cultures Cordain likes to hold up as models for his diet ideas ate a lot of animal foods, but they didn’t need statins to maintain their cholesterol in a healthy range. They had parasites for that job.

This understanding of the effects of parasites has inspired yet more compelling support for the lipid hypothesis. In this noteworthy experiment on mice, schistosomiasis actually caused the regression of arterial lesions. These scientists recognized the implications of this. Schistosoma parasites can counteract effects of an otherwise atherogenic diet. Any time you see a primitive culture held up by the cholesterol confusionsts as a model of healthy living on a high-fat, high-animal food diet, ask yourself if that culture somehow managed to avoid parasitic infections. I’d say that would be unlikely. Parasites are pretty unpleasant to contemplate. Who wants to imagine themselves hosting tapeworms or toxoplasma. But I think parasites deserve a little more respect as marvels of evolution. Low carbers in sanitized environments tapping on computers don’t seem to understand their pervasiveness throughout human history.

Even today one third of humanity suffers from helminthic infections.

Unfortunately, the malaria parasite is also still quite common, and it lowers blood lipids as well.

Parasites have coevolved with us and all our ancestral species. This is an important aspect of our history. Let’s not pretend otherwise. The low cholesterol of hunter gatherers might also be explained in other ways, including food scarcity and genetic adaptations.

The ATP III panel stated that only in populations with very low serum cholesterol is there a near absence of coronary heart disease.

As you know, the relationship between cholesterol and heart disease was observed in less isolated populations as well. In early heart disease epidemiology, the Japanese were documented to have much lower rates of coronary heart disease than Americans despite their more widespread cigarette smoking and similar rates of high blood pressure. While smoking and hypertension are serious risk factors, without accompanying high cholesterol, they are less dangerous. Their lower serum cholesterol resulted from their lower consumption of saturated fat and dietary cholesterol.

Various African populations were also found to have very low rates of heart disease. Some were described as being “virtually free of hypertension and CHD”.

Their diets were based on cereals, legumes, and greens. Their consumption of animal-sourced foods was minimal.

T Colin Campbell and Chen Junshi reported that low rates of heart disease accompanied low cholesterol and low animal food consumption in China as well. Read The China Study for more on this.

You can hate on T Colin Campbell all you want but there is no reason to doubt his conclusions. Here is a study from 1991 of urban Chinese relating cholesterol concentrations to heart disease deaths. Look as hard as you want at the list of authors. Campbell’s name is nowhere to be found. Yet the study authors wrote that even in this population with relatively low mean cholesterol, there was still a strongly positive association between blood cholesterol and death from coronary heart disease. Only 43 deaths among over 9000 men were attributable to heart disease after 8 to 13 years of follow up. This is a very similar finding to that reported by Campbell. Did all these researchers also have a vegan ideology to push?

What about these researchers who compared ethnic Chinese in Hong Kong and Singapore? They explained the dramatically higher rates of all-cause and cardiovascular mortality in Singapore on their greater saturated fat consumption. The diets of the Singaporeans drove up their total cholesterol and their LDL. The authors didn’t blame animal fat, but rather coconut and palm oils. If they had a vegan agenda, it’s hard to tell from what they wrote. Coconut and palm oils are vegan.

Of course, Ancel Keys’ Seven Countries Study showed clear relationships between serum cholesterol, saturated fat consumption, and deaths from coronary heart disease in this most famous of cross-cultural comparisons.

The relationship between blood cholesterol and coronary heart disease death was also apparent in a 40-year follow-up with the cohorts in those seven countries.

This 1994 cross-cultural comparison reached similar conclusions. Rural Chinese had the lowest cholesterol levels while the Finnish had the highest, and their rates of ischemic heart disease corresponded as we might expect. The researchers said that variations in serum cholesterol accounted for four-fifths of the regional variations they observed in death rates.

Saturated fat apologists try to taint these observations by trying to link the researchers who made them with random vegans. Ancel Keys wasn’t a vegan and vegan fitness enthusiast Noel Polanco hasn’t conducted any research into heart disease, but Denise Minger chose to associate them anyway. This is pure spin. Actually, there is a bit of irony in trying to connect an animal rights activist to a heart disease researcher.

The first chairman of the ATP, which set cholesterol guidelines in the US for the first time, called animal rights activists a problem due to their antiscientific thinking. Ms Minger, have you not noticed how much of the research into heart disease was conducted on experimental animals? You know they usually kill the animals in the experiments, don’t you? These recommendations were not created by vegans or vegan-sympathizers, I assure you.

This is an interesting excerpt from that ATP chairman’s lecture. In The Primitive Nutrition Series, I showed you that the medical community was slow to accept the lipid hypothesis, but they did come around eventually. The public was initially less resistant to the lipid hypothesis than the doctors, however.

We see in this lecture the frustratingly conservative mindset of past cholesterol experts. Diet and drugs were considered treatments to be reserved for at-risk individuals. Why exactly should anyone consume a diet that raises cholesterol? A clear message about nutritional excellence was apparently not considered.

LDL cholesterol was to be the basis for treatment when deemed appropriate. Diet was considered a therapy.

Even the author of this tepid approach, who held animal rights activists in low regard, could see that high protein and high fat diets were dangerous and unscientific.

The science community did not approach the diet-heart question with an agenda to promote animal rights or polyunsaturated oils. Mortality data made their engagement with this question inevitable. The middle of the twentieth century saw a dramatic decline in infectious disease deaths in America as our nation took on the characteristics of a wealthy, modern nation.

Taking the place of infectious disease as our top killer was heart disease. Trend lines like these focused the attention of all public health officials.

This rise in heart disease was accompanied by changes in diet. Carbohydrate consumption measured as a percentage of total calories fell in these years. Carbs were displaced by protein and especially fat, which rose markedly.

Both saturated and unsaturated fats were consumed more.

Those who wish to blame grains for heart disease should know that through this period of rising mortality carbohydrate consumption fell by a quarter, and in comparison to other sources of carbohydrate, grain consumption fell especially fast.

I have highlighted food categories that might be of interest to you. Those in green along the right were eaten less, including potatoes and cereals. Even sugar was eaten a little less during this time. In red to the left you can see that meat and dairy were eaten more. This alone was not the basis for the acceptance of the link between saturated fat with heart disease. I’ll show you a bit of that history in Part 3.



The Futility of Cholesterol Denialism 1: How Much LDL?

The Futility of Cholesterol Denialism, Part 1: How Much LDL?

In my Primitive Nutrition Series, I tried to offer enough of an overview of the science and history of cholesterol for a reasonable person to recognize that the lipid hypothesis is probably correct.  I just wanted to present enough information  to help people realize that they need not bother with the foolishness they might see online. For any rational individual not intimately familiar with the science of cholesterol, the starting presumption should be to accept the lipid hypothesis, not out of bias, not because they are mindless drones, but because they recognize that the relationship of cholesterol to heart disease is a matter best addressed by science, and the top specialists in the relevant fields have come to a virtually unanimous conclusion: yes, high blood cholesterol is a major and preventable risk factor for heart disease. But online, anything goes.

Anyone gullible enough to believe a random blogger rather than the thousands upon thousands of talented and highly trained people whose business it is to understand and prevent heart disease…

… shouldn’t complain when that bill finally comes due for all the unhealthy food they ate.

The confusionists appeal to their own vanity as well as their audience’s.  They never let slip a hint of uncertainty. Anyone can set up a blog and declare himself or herself enlightened. I won’t be able to convince the personally and professionally invested cholesterol deniers. But in reading the responses to my work, I have come to feel I left out a lot of important points that address the confusionist deceptions. I’ll try to pick up some spares in these videos, called The Futility of Cholesterol Denialism. There will be some overlap between this material and my videos in the Primitive Nutrition Series, but I’ve tried to keep this as fresh as possible.

As you watch this set of videos, ask yourself if Anthony Colpo is right when he says that the connection between saturated fat and heart disease has never been made. He thinks all those smart people in the biomedical research community have a fundamentally flawed understanding of our number one killer. I doubt you’ll agree with him by the end of this set of videos. Before we connect saturated fat with heart disease, we need to connect cholesterol with heart disease. There’s a very basic reason cholesterol is associated with heart disease by practically everyone in medicine.

You’re looking at a cross section of an artery with a severe atheroma. This is what atherosclerosis is all about. The artery wall is infiltrated by cholesterol and that cholesterol gets there from the blood. The confusionists will turn over every stone for an excuse to explain how it got there, but the bottom line is cholesterol that was in the blood forms the bulk of the atherosclerotic lesion. That nasty yellow stuff is not sugar or lectins or a carbohydrate. It’s mostly cholesterol and cholesterol gets there via the LDL particle in the blood after it attaches to the artery wall.

Have a look at this table showing how the lipid content of the walls of arteries compare over different life stages and among different stages of disease. Triglycerides actually decrease as a percentage of the lipid-filled core as the disease progresses. The same is true of phospholipids. But in the diseased, swollen sack of fat that is an atheroma, it is the cholesterol and cholesterol esters that make up the bulk of the lipids.

This is why LDL is not just a mere risk factor, like any other biomarker. It is the actual delivery mechanism of the very substance that forms most of the lesion. Therefore, unlike the other risk factors, it alone is sufficient to drive the disease process.

This is made obvious by the unlucky one-in-a-million indivdual who is a homozygote for familial hypercholesterolemia, meaning he or she has genes for inherited high cholesterol in both chromosomes. With no other risk factors beside high LDL, they can die of heart disease in their twenties. This shows us how dangerous high LDL can be. The deniers don’t talk about this condition very much.

I’ve shown you already how heterozygotes for inherited high cholesterol, who only have this gene in one chromosome, also are likely to die young from heart disease, although their situation is not quite as dire as that of the homozygotes.

It is common knowledge that some people have a genetic tendency to have high cholesterol, but there are also some who have one of a few possible defects in their cholesterol regulation in the other direction. They actually have inherited low cholesterol, and they tend to live longer than their peers because this defect protects them from heart disease. They naturally have low LDL, so they are less likely to have cholesterol infiltrate their artery walls.

One genetic condition that lowers LDL is called familial hypobeta lipoproteinemia and those who have it were found to have an average lifespan 9 to 12 years longer than what would otherwise be expected.

A specialist in cardiovascular disease may disagree with my focus on LDL. One might counter that there are other atherogenic particles and that non-HDL-C or ApoB provide a better measurement of them. My response is that this may be so but this distinction is too subtle to be explored in my videos.

For the moment, LDL suits my purposes fine. I hope you can understand why I’ve made this decision.

Of course, high cholesterol is known to associate with heart disease in the general population without the influence of genetic abnormalities. This study all the way back in 1950 showed that cholesterol levels were higher among those suffering from heart disease.

This association between high cholesterol and heart disease has been observed many times. This study even showed higher all-cause mortality for those with higher cholesterol. These authors found a continuous, graded relationship of serum cholesterol to all-cause mortality. Younger men with favorable lipid profiles had higher life expectancy. The confusionists don’t want you to know about this study.

One difficulty I have with the arguments of the cholesterol confusionists is that they try to argue that the high LDL levels that result from eating fatty animal foods are not a problem while completely ignoring the basic question of how much LDL is needed in the first place. They always remind us that cholesterol is good and performs very important functions. Do they every stop to wonder how much LDL is really needed for those functions? What would be the benefit to having excess cholesterol? In their Nobel lecture, Brown and Goldstein argued that the physiologic need for LDL is quite low. Other mammals have LDL around 80 mg per dL. Human babies have LDL at around 30. Humans on low fat diets are healthy at a range between 50 and 80.

And yet low LDL, or what I would call LDL at the level the body needs and no more, is only recommended for people with a very high risk of heart disease. In the United States, a rich country that loves its fatty animal foods, we are told that normal is twice the level that is physiologically necessary.

Others beside Brown and Goldstein have explained why very low levels of LDL make sense and are completely healthy. Richard Kones of the Cardiometabolic Research Institute echoed their arguments. He also mentioned the low LDL levels observed in hunter gatherer cultures. I’ll come back to that in the next video.

Kones is one of many to conclude that having very low LDL would virtually eliminate the possibility of heart attack.

Daniel Steinberg, one of the foremost experts on cholesterol, has pointed out that when plasma cholesterol drops, cholesterol in the cell does not. He thinks LDL of only 10 mg per dL would be adequate. He notes that those individuals with genetically low LDL are perfectly healthy with LDL as low as 15 mg per dL.

John LaRosa, of the State University of New York Health Science Center in Brooklyn has had patients do fine with LDL of only 20.

This is one reason why high risk patients are recommended by some to be put on statins regardless of their LDL level. There is no upside to having more LDL than is absolutely necessary for these people.

The Mayo Clinic’s targets for LDL come from a revision to the government recommendations made by the Adult Treatment Panel III. That revision lowered the targets for LDL originally made by ATP III in 2002.

But here’s what I find so strange. Read the original report from ATP III and you’ll see that LDL under 100 was considered optimal because low levels are associated with very low risk of coronary heart disease.

It also said any LDL above 100 appears to be atherogenic.

Yet even the revised ATP targets call LDL from 100 to 129 near ideal. Why didn’t they give a lower number in 2002? They wouldn’t have had to do a revision two years later. Why did the revision call LDL above 100 “ideal”…

If they had known years earlier those levels were atherogenic? I’ll let you answer that question for yourself. In my opinion, atherogenic levels of LDL are not ideal.

The very low levels of LDL that are actually physiologically necessary make an argument like this from the Weston Price Foundation seem completely absurd. They want you to think of cholesterol as police officers that show up to a high crime neighborhood. The police are there to prevent any problems, just the same way that cholesterol is. They are actually suggesting that cholesterol prevents heart disease here!

Are they saying low cholesterol can cause this? How would that work? This is nonsense.

And what about their police analogy? How many police officers does a neighborhood need to be safe? If a thousand armed police officers swarmed a city block, would that make it safer? Would life function as normal or would adverse consequences result at some point? It’s a poor analogy, of course, but I didn’t choose it. It seems completely mindless to me. It ignores entirely the question of how much is the right amount. I start off assuming that the body is evolved to properly regulate itself, and that its every metabolic process has a purpose. There is a “just right” and a “too much” amount for every molecule I can think of. Why would cholesterol be any different?

I thought this was a really interesting paper. Here you see the cholesterol levels of infants and mothers from different ethnic and cultural backgrounds. African and European babies came into the world with total cholesterol mostly between 50 and 90. In the right two columns you can compare the cholesterol levels of their mothers. The African mothers were mostly below 200. The European mothers were mostly above 200, with some over 300. Why would humans so similar as babies need to be so different as adults?

The explanation for these numbers is simple, of course. The Africans ate diets that were low in animal foods and high in carbs and fiber. Therefore, their blood cholesterol wasn’t jacked up by unhealthy food.

Those who argue for the false choice between cholesterol and inflammation as a cause of heart disease seem to think someone can get away with high LDL if they consume a lot of antioxidants. I’ll come back to this, but why do they want high LDL in the first place? It’s hard to understand their logic. Have a look at this paper to see what I mean. The author, Peter Libby, is the chief of the cardiovascular medicine division at Harvard’s Brigham and Women’s Hospital. He says the traditional view of atherosclerosis as a lipid storage disease crumbles in the face of evidence of the central role of inflammation in all aspects of the disease. The narrowing of arteries does not necessarily lead to heart attacks. This seems like a strong statement in favor of the confusionist argument that the problem is inflammation, not cholesterol.

But he goes on to say that lipid lowering is in itself anti-inflammatory. He says that a low cholesterol diet in rabbits stabilized arterial plaques. He argues for low cholesterol. In the mind of this expert, there is no false dilemma. He is not a confusionist.

Daniel Steinberg explains why inflammation is considered secondary to high cholesterol in heart disease. In primate studies, heart disease was regressed by switching from an atherogenic diet to a healthier diet. As cholesterol in the blood went down, inflammation went away. As Steinberg puts it, in the absence of high cholesterol, the inflammatory process is not self-sustaining. Inflammation appears to be secondary to high cholesterol.

Steinberg references this amazing study. These scientists transplanted a portion of a diseased artery from a mouse with high cholesterol into a mouse with low cholesterol. In its new environment, that chunk of artery had its atherosclerosis healed almost completely in only nine weeks. This demonstrates very clearly that inflammation is not a separate and independent phenomenon from high cholesterol. We see that inflammation in heart disease apparently requires high cholesterol.

There are those who say the reason the class of drugs called statins are effective in preventing cardiac deaths is because of their other effects beside cholesterol lowering. This is a typical argument from confusionists like Anthony Colpo. The problem with this argument is that all of the other proposed effects are not as well supported by evidence as cholesterol lowering. As of 2009, there existed no randomized controlled trial evidence for any of these effects.

People who make this argument don’t remind you that the benefits of lowered LDL have been proven through other methods beside statins, including bile acid sequestrants, diet, and surgery.

I’ll briefly remind you of the amazing work of Henry Buchwald, who proved that LDL lowering through surgery led to fewer cardiac events and greater life expectancy. I think this is devastating to confusionist claims.

Here is a really good journal article about atherosclerosis. The authors relate it to tuberculosis, which might be said to share similar characteristics. Tuberculosis has a root cause, a bacterial infection. Yes, there is an important inflammatory element to it, but it is secondary to this root cause. Atherosclerosis also has a root cause, which is excess LDL, and it too has inflammation as a secondary feature.

Here is another excerpt from this excellent article. I think it’s worth pausing the video to read this. It is an interesting thought that the inflammation in atherosclerosis is maladaptive, meaning the inflammation itself worsens the condition. This causes me to wonder if atherogenic levels of LDL were ever common in our history as a species. Perhaps our widespread high fat, low parasite, high calorie condition has no precedent in our history. How about this, you paleo believers? If you find evolution to be so instructive to your diet choices, and if it is so clear that our immune systems don’t know how to respond to heart disease, then shouldn’t you conclude that our history as a species didn’t include much atherosclerosis? And if hunter gatherers have such low cholesterol levels, why don’t you accept that you should, too?

This study came out after Steinberg wrote his article. Here, mice had their genes altered to compare low LDL or “bad cholesterol” with high HDL or “good cholesterol”. As is standard practice, advanced atherosclerosis was induced in the mice by not wheat or sugar or lectins but by a diet high in cholesterol and saturated fat.

A sustained low LDL condition induced dramatic healing of their arteries. Low LDL also resulted in a decreased expression of inflammatory genes. Elevated HDL, on the other hand, did not induce regression. In the absence of low LDL, I doubt raised HDL can actually heal heart disease.

Low carbers often take false comfort in their high HDL numbers. Unfortunately for them, it turns out that HDL can sometimes actually be pro-inflammatory. The researcher named here says that HDL might be responsible for some of the inflammation associated with cardiovascular risk. He said, “Lowering the LDL level is therefore still even more important than raising the HDL level.”

If you want your HDL to be anti-inflammatory, it looks like that can be accomplished with a high-fiber, low-fat diet.

When you exclude the HDL number from your total cholesterol score, you are left with what is called non-HDL cholesterol. This includes LDL or “bad cholesterol”. I hope you remember what fatty streaks are. Those are the early anomalies in our arteries that are the beginnings of atherosclerosis. In post-mortem examinations of more than 2800 young people, fatty streak development was correlated to levels of non-HDL cholesterol. So cholesterol deniers, how do you explain this? Coincidence? Were the examiners a bunch of dishonest vegans?

It seems for dramatic healing of atherosclerosis to be possible, low levels of LDL are necessary. These researchers are looking to drugs to accomplish this. The cholesterol denialists and saturated fat apologists can make no claims that their ideas can actually heal and rejuvenate the cardiovascular system. If they really cared about your heart health, they would clearly acknowledge this. They should at least say to those with heart disease that there is absolutely no reason to believe their approach can offer them anything unless they are willing to severely restrict their calories.

Of course, the results of drug trials proved to be the most convincing evidence of the connection between LDL and cardiovascular disease to the medical community. While the effects of drugs do provide an important line of support to the lipid hypothesis, they are only one piece of the puzzle. I’ll explain at the end of the current batch of videos why arguments for or against the lipid hypothesis based on the effects of drugs are the least interesting to me.

Observations in populations provide more evidence of the role of cholesterol in heart disease. I’ll look at that in part 2.


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