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Nutrition Past and Future

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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