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Last weekend I was invited to speak at the Freedom Law School's 2009 Health and Freedom Conference, which was an interesting mix of nutrition and politics, the latter portion largely devoted to opposition to the income tax, opposition to the Federal Reserve, and alternative theories about what happened on September 11, 2001. I don't agree with all of the political views expressed, but I found the political talks enjoyable and thought-provoking. They asked me to speak about the health benefits of eating animal fat, which of course I was happy to do.

Knowing very little about the organization, I did not expect an award. But the head of the organization, Peymon Mottahedeh, is an extremely generous and warm-hearted person who obviously loves to give awards since he gave out about twelve of them. He gave one to me. The plaque reads, “Freedom Law School, In Recognition of Your Tenacious Efforts to Find Health Solutions And Expose the Truth About Cholesterol, Recognizes You, Chris Masterjohn, As A Health Freedom Fighter.”

While Richard Gage, the founder of Architects and Engineers for 9/11 Truth, gave the talk that provided the most compelling evidence-based alternative to a mainstream dogma, it wasn't the most radical talk when one considers that over a third of Americans believe there was some government complicity or direct involvement in the attacks. (Of course, A&EFor9/11Truth does not promote this idea directly, but rather analyzes the physical evidence demonstrating explosives were used in the WTC building collapses and demands an investigation of this matter, without placing blame on any particular group).

The most radical talk was Dr. Tom Cowan's. He argued that blockages in coronary arteries do not cause heart attacks. Heart attacks, according to his view, cause blockages in coronary arteries. The real cause of heart attacks is a buildup of lactic acid in the cells of the heart muscle. (He has also written an article on this here.)

Well, everyone agrees that a buildup of lactic acid in the heart muscle is what causes heart attacks. The difference is what is believed to happen before this. The mainstream view is that, in most cases, direct rupture of an atherosclerotic plaque in the coronary artery leads to a blood clot, which then blocks the artery and deprives the heart muscle of oxygen. In a large minority of cases, the endothelial lining above the plaque erodes, leading to a clot. In a smaller minority of cases, the plaque itself becomes so severe that it occludes the artery. Cowan's view, shared by other scientists mostly based out of Brazil, is that capillary dysfunction, not artery blockage, deprives the heart muscle of oxygen.

At some point in the future, I will thoroughly research this issue and present my conclusions.

For the time being, I could like to present one important argument that should leave a quiet unease in anyone who believes that atherosclerotic plaque is not at least one major cause of heart attacks: the genetic evidence that the activity of the LDL receptor can almost completely control the risk for heart attacks.

Goldstein and Brown won a Nobel Prize in 1985 for their discovery of the LDL receptor in the 1970s. They have written a new review of the LDL receptor that provides a historical overview.

Goldstein and Brown are remarkable scientists, but they have made some unscientific public statements. On the homepage of this site, I quote them describing researchers and physicians as militant warriors against cholesterol rather than inquisitive and helpful people searching for truth. Nevertheless, as some say, God gave us two ears and only one mouth for a reason, so rather than looking for an excuse not to listen to them, we should gratefully learn from their expertise. We should also nevertheless critically evaluate the evidence they provide, because God gave us a mind too.

The LDL receptor brings LDL into cells. Familial hypercholesterolemia is a genetic defect in the LDL receptor. One in 500 people are heterozygous for this condition, meaning they have one copy of the defective gene, resulting in half the quantity of active LDL receptors and twice the concentration of LDL in the plasma. One in a million people are homozygotes, people with two copies of the defective gene. They have 6-fold to 10-fold elevations in plasma LDL levels.

Heterozygotes develop atherosclerosis early and begin having heart attacks as early as age 30. Although they only constitute 0.2% of the population, they constitute 5% of people who have heart attacks before the age of 60.

Homozygotes develop atherosclerosis much, much earlier, and can have heart attacks in childhood. Homozygotes have cholesterol deposition in many other places besides arteries, like the extreme versions of the cholesterol-fed rabbit model. As in arterial plaques, this cholesterol comes from the accumulation of oxidized LDL into macrophages (immune cells), which is a phenomenon mediated not by the cholesterol but by the oxidation of the polyunsaturated fatty acids (PUFAs) in the LDL membrane, which in turn damages the protein in the membrane, leading the immune system to mop it up before it wreaks havoc on every cell it encounters.

Homozygotes, according to case reports I have found, have died of heart attacks as early as age 3. I have read reviews claiming death even in two-year-olds.

As I pointed out in Issue #14 of my free newsletter, a genetic mutation in the enzyme that degrades the LDL receptor has the opposite effect, increasing the expression of the LDL receptor and reducing the risk of heart disease by 88 percent, nearly abolishing it.

This suggests that LDL receptor activity has almost complete control over the risk of heart disease: when it is low, one gets heart attacks earlier; when it is absent, heart attacks can occur in young children; when it is high, one is almost guaranteed freedom from a heart attack.

Now, what exactly does the LDL receptor do that can affect the risk of heart disease?

As Goldstein and Brown recount in their review, they found that cells tightly regulate their cholesterol synthesis in response to the cholesterol provided them from LDL. In a normal cell, LDL will suppress cholesterol synthesis by delivering cholesterol to it. In a cell from someone homozygous for famililal hypercholesterolemia, however, the cell cannot take in LDL, so its cholesterol synthesis remains very high at all times. Thus these cells are not suffering from cholesterol deficiency. They are making plenty of their own cholesterol, as much as a normal cell makes in the total absence of LDL.

The only thing changing is the LDL in plasma. Golstein and Brown thus conclude that this defect provides “formal genetic proof that elevated LDL alone can produce atherosclerosis in humans.”

But is this true?

Consider an analogy to a traffic jam. Two things happen:

  • The concentration of cars in the road increases.
  • The time it takes you to get home increases.

It is the same for LDL. The concentration increases, but so does the time it spends in the blood. Which determines the risk of heart disease?

In the late 1970s and early 1980s, it was discovered that LDL incubated with endothelial cells, the cells that line the inside of the artery, would over time become oxidized, due to the interaction between the PUFAs in its membranes and free radicals produced by the endothelial cells. Normal LDL would be taken up in small amounts by macrophages, but as soon as the macrophage obtained a little bit of cholesterol, it would shut off its LDL receptors and stop taking any more in. The “endothelial cell-modified LDL,” however, would accumulate in macrophages unregulated. For a five-fold increase in the concentration of normal LDL, there would be absolutely no increase in the absolute amount of LDL taken up into the macrophage. For the same concentration, however, oxidized LDL would be taken up at five-fold the rate of normal LDL. Moreover, as higher and higher concentrations were reached, oxidized LDL would be taken up at higher and higher amounts, but normal LDL would not.

Obviously, these experiments showed that the concentration of normal (called “native”) LDL could not affect the amount of LDL that macrophages would take up.

Later experiments, as described in my article linked to above, showed that it was oxidized derivatives of linoleic acid, mainly derived from dietary vegetable oils, that were the key constituents of the LDL particle that could turn on the genes in the macrophage that would cause it to turn into a foam cell.

It is these macrophages and foam cells that populate atherosclerotic plaques, initiating the inflammatory process, eventually degrading the fibrous cap and increasing the chances of rupture, and committing suicide, leaving cellular debris and large pools of oxidized lipid — that is, a giant mess of toxic waste — in the center of the plaque.

This evidence not only presents a problem for Goldstein and Brown, who argue that the concentration of LDL is the main determinant of heart disease risk, but also presents a problem for those who would argue that atherosclerotic plaque does not cause heart disease.

The “myogenic” theory promoted by Dr. Cowan is not necessarily at odds with the atherosclerotic-thrombotic theory promoted by the mainstream. Atherosclerotic plaque not only impedes oxygen delivery to heart tissue by occluding arteries, it also contains a mass of oxidized toxic waste. If it ruptures, and a clot doesn't form right away, then all that toxic waste would be free to wreak havoc on the oxygen-based metabolism of heart cells.

The obstacle to the myogenic theorists is this: if the LDL receptor activity exerts almost complete control over the risk of heart attacks, then any theory of how heart attacks happen must give a central role to the lipoproteins that interact with that receptor (this actually includes most lipoproteins, not just LDL).

So the question the myogenic theorists must answer is, what is the role of LDL or oxidized LDL in promoting capillary dysfunction or otherwise compromising the oxygen status of heart tissue, if not in promoting atherosclerosis, plaque rupture, and thrombosis?

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  1. 9/11 was an inside job committed by the US National Security State Apparatus. There were NO TERRORISTS! Flight 93 never crashed in PA and a missile hit the Pentagon. It is the State which protects free-market capitalism that committed this crime. Long live Communism!!!! Death to Imperialism!!!!

  2. Since when does the immune system come to the aid of oxidized cells, tissue and blood? Even if the "immune system" and macrophages existed, which they don't it would be hard for you to explain. I think you have a very elaborate and unsupported theory of heart diesease that doesn't take into account the contraction and relaxation of the heart muscle.

  3. Sorry for being a "bit" late, but I'd like to comment on this you said:

    "Well, everyone agrees that a buildup of lactic acid in the heart muscle is what causes heart attacks."

    Actually, in muscles the rapid drop in pH causes exhaustion and lactic acid is mostly just a marker of it.

    Which brings up the possible role of pH buffers like carnosine, beta-alanine, anserine and bicarbonate in heart muscle failure. What's more, carnosine & BA are NO-boosters too, so they dilate vessels.

    You have written previously on carnosine (I think) so I thought I'd just mention this.

    – Neonomide

  4. Chris,

    A little late to the game here…

    I found this paper suggesting that families with FH didn't have increased mortality risk in the 19th and 20th centuries. The authors speculate that some environmental trigger that became prevalent in the later 20th century explains the difference. My guess is industrial seed oils, refined flour and HFCS.

    Could it be that FH is only problematic in the presence of these environmental/dietary triggers?

  5. Chris, perhaps the response for your question may be given in the acidity theory of atherosclerosis (1). Please see the chapter “Acidic environment and atherosclerosis”
    We support the myogenic theory of myocardial infarction at htt://
    Carlos Monteiro
    1. Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at

  6. Dave,

    Good idea. I don’t know if WGA binds the LDL receptor, but the LDL receptor has critical mannose and N-acetyl-glucosamine components. WGA is an N-acetyl-glucasmine-binding lectin, and gliadin, the protein blamed for celiac present in the white flour portion, is a mannose-binding lectin. So, insofar as they make it into the bloodstream, it seems very plausible that they could interfere with LDL receptor function.


  7. Hi Stephan,

    Sorry it took me so long to respond.

    I do not think they are suggesting the finding is an artefact in this paper. Rather, they suggest that heterozygous FH is not in and of itself a guarantee of excess mortality, and that there are other factors that can protect against or aggravate the risk conferred upon the person by their heterozygous FH.

    You cannot try to tease out the effect of CAD-based ascertainment of FH status by looking at non-CAD FH alone. That is introducing a new level of bias, selecting for the non-CAD subpopulation of the FH population. They way you tease out the effect of CAD-based ascertainment is to combine both CAD-based and non-CAD-based ascertainment so you are looking at the FH population as a whole.

    The FH relatives as a whole population had an SMR of 1.34, which was statistically significantly higher than the general population. This is because they have a higher rate of premature CHD.

    When you separate the population into two subpopulations, one with premature CHD and one without premature CHD, you find the excess mortality in the former subpopulation.

    Is that a surprise? Of course not! All that means is that the excess mortality found in the FH population is due to the higher rate of CHD.

    This is consistent with the cholesterol-fed rabbit model and everything discovered about CHD after that model. Suppression of LDL receptor activity through genetics, feeding massive amounts of cholesterol, or other means, is necessary to produce atherosclerotic plaque, but oxidation of the lipoprotein PUFAs is also necessary, and many other factors modulate the risk of occlusion, plaque rupture, thrombosis, and the other aspects of myocardial infarction that ultimately produce mortality.


  8. Here’s a thought: suppose there was something in your food that blocked the LDL receptor or effectively decreased its activity. If I’m not mistaken, that was the original idea of how saturated fat increased cholesterol and thus CHD risk (since shown not to be the case).

    But what about lectins? Does WGA bind to the LDL receptor?

  9. Chris,

    The relevant part is this:

    “The SMR of 62 families referred with premature CAD was 1.62
    (95% CI 1.32–1.93, PB0.001) and the SMR was 1.10 (95% CI 0.86–1.34, P0.4) in 51 families without premature CAD.”

    If I understand this correctly, what it’s saying is that FH families identified by their propensity for CAD had more CAD, while FH families identified by routine screening didn’t.

    In the paper, they compared the risk ratio of FH vs non-FH families who had both been identified because of CAD risk factors, and they were also the same. I’ll send you the full text.

  10. Stephan,

    Are you sure that’s the right study? They don’t seem to have an online version of the full text, and the abstract says that excess mortality is observed especially at ages 40-54, and declines thereafter. They don’t say anything in the abstract about testing the difference between FH identified by cholesterol level screening and FH identified by relatives of CHD patients.


  11. Chris,

    Good post. I came across a study a while back that I wanted to ask your opinion about. It’s from the Netherlands and it looked at mortality in FH heterozygotes. They determined that when taken from the general population by routine cholesterol screening, FH patients don’t have increased mortality. Only when selected from a pool of patients previously identified for CVD risk factors did hets have an increased risk. But the risk was the same as for relatives of CVD cases without FH.

    They suggest in the paper that decreased survival of FH hets is because of an ascertainment bias in other studies, i.e. the people they studied who had FH were identified because they were related to cardiovascular patients, hence the increased risk may have been an artifact. Here’s the paper, I’m curious to know what you think.

    Additional risk factors influence excess mortality in heterozygous familial hypercholesterolaemia

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