The question of why such a large number of people with “desirable cholesterol numbers” have heart attacks requires answers. Averaging various studies and reports, it seems that at least 50% if not more of the patients admitted for myocardial infarction – one study of 65,000 such people -showed a total cholesterol “very desirable” at 170. This shows clearly that lowering LDL cholesterol does not equate to lowering heart attack risk in any meaningful way.
So what does lower heart attack risk, meaningfully? I think that to understand that we must look at what, in fact, causes heart attacks.
It is well accepted by almost all physicians that plaque deposition in the arteries causes blockages which then cause a heart attack. And this is where the explanation has landed, and this is the understanding modern medicine is based off of. There is more to it, but first we have to understand the basics of plaque deposition (atherosclerosis/heart disease).
Plaque deposition is caused by multiple factors, not just “LDL”. Looking beyond, we see that the reason why LDL is important is in fact because the more LDL particles you have, the more likely one is to embed in the artery wall. It is simply a statistical issue, not an issue of how damaging the LDL is in itself.
The potential damage caused by the LDL particle relies on a couple of other potentially more directly important factors. These are: how “buoyant” or “dense” (or oxidized) the LDL particles are themselves, and how much inflammation is present.
These are the puzzle pieces that are generally accepted by progressive physicians, and in general they appear to be not wrong. So, understanding the number of particles and types of particles, as well as inflammation levels, give a much clearer picture on heart disease risk than just “LDL”.
But it’s not the end of the story, as it also appears that although some heart attacks appear to originate from blockage, not all do.
But I’ll get back to that.
Arteries are made, mostly, of collagen. One of the hallmarks of plaque deposition is “hardening” of the arteries – an increase in fibronectin increases binding of collagen, and then an increase in collagen itself causes what is called “collagen remodeling”, a term used to indicate growth in response to damage (such as high blood pressure, or inflammation damage). It was found in 2016 (J of American Heart Association) that sulfur dioxide protects the artery from this abnormal collagen growth.
Now let’s look at taurine. Taurine is a sulfur-containing amino acid that is essential for cardiovascular function. In fact it is used in Japan as a treatment for heart disease complications. It is consistently shown that patients suffering heart attacks have low levels of taurine (and magnesium). In a healthy individual, the highest concentrations of taurine (outside of plasma) are found in the heart. Loss of mechanical function in rat hearts is found to correlate with decreased taurine levels, and cardiomyopathy causing heart failure can be reversed in these rats, with taurine.
Now, to tie it all together, with something that is never considered as part of the heart attack process: the glycocalyx.
This is a gel-like layer that covers the lining of the capillaries, arteries and veins. The slime on the outside of fish is an actual example of glycocalyx. It contains enzymes and proteins that regulate things like dilation of the arteries, but also serves as a protective barrier, shielding the vascular walls from direct exposure to blood and all the potential hazards in it such as dense oxidized LDL particles or bacteria.
The glycocalyx can be disrupted by low oxygen concentration, high blood sugar, high levels of salt, inflammation, and it appears also, low levels of sulfur, read: taurine.
Now, for a minute, let’s consider the heart attack. What is it, actually? Is the body simply overloaded and giving up? This is just not how the body operates. Plaque deposition, for example, is actually the body attempting to fix the problem. The body will always attempt to fix the problem. From this perspective then, what is a heart attack?
We know that a heart attack causes the sudden release of the taurine stored in the heart muscle. Is it possible that a heart attack is the body attempting to provide taurine to the deficient cardiovascular system? During acute coronary events such as heart attacks, oxygen is blocked (most often by atherosclerotic plaque) from an area of the heart. Immediately after, on what is called reperfusion, blood supply full of oxygen returns to the area, causing tissue damage. Taurine however antagonizes the damaging enzymes being activated, thereby protecting the heart. This would make sense then that the heart itself is where taurine is stored. It would also explain why not all heart attacks are caused by blockages – simply too-low levels of taurine and/or sulfur in the cardiovascular system might trigger the sudden release of the taurine stored in the heart as a protective mechanism.
All of this must be considered when looking for the roots of the problem, and when considering treatment and/or prevention.
It appears to me that ensuring a healthy glycocalyx is the first step in preventing and/or treating cardiovascular events such as plaque deposition and heart attacks.