THIS is a follow-up to last week’s article on the lipid-cholesterol heart disease debate that has spanned over the last half-century.

Coronary heart disease (CHD) remains the No. 1 killer worldwide. The prevailing belief underlying conventional approaches to CHD treatment is that a diet high in cholesterol and saturated fats is the main contributory factor leading to heart attacks. Others think cholesterol and saturated fats are not the key factors. This contention is known as the “cholesterol war”.

The previous piece mentions the Malaysian Lipid Study by Karupaiah et al (2019), which observed that a high-fat diet might not be a cause of heart disease. The blame has shifted from fats (1950s) to saturated fats (1960s), low-density lipoprotein cholesterol (LDL-C) (1970s) and oxidised LDL (1980s).

Currently, the focus is on the particle size of LDL-C. It is believed that these small, dense particles can easily penetrate the intima of the arterial walls, and over time, cause atherosclerotic cardiovascular disease (ASCVD). The actual mechanism, and why they enter the arterial walls, have not been clearly explained.

There is another hypothesis on the cause of CHD, that it stems from a deficiency in dietary nutrients, particularly Vitamin C. Rath & Pauling’s “A unified theory of human cardiovascular disease leading the way to the abolition of this disease as a cause for human mortality” (1992) postulated that cholesterol is not the cause, but rather, CHD is the direct result of the prolonged weakening of the coronary arterial walls due to the body’s inadequate production of collagen molecules. Cholesterol appears as a repair factor to compensate for this, but only after the arterial walls have ruptured. More specifically, lipoprotein (a), or Lp(a), cholesterol, which is synthesised in the liver.

LDL-C, irrespective of its particle size, is also synthesised in the liver for a myriad of physiological functions. Its main role, however, is to transport cholesterol to various parts of the body. There is nothing “bad”, as commonly perceived, about LDL-C.

Two studies that support the Rath & Pauling hypothesis have largely been ignored. O’Neal et al (1996) observed similarities between small, dense Lp(a) and small, dense LDL particles. They observed that these Lp(a) particles could increase cardiovascular risk in a manner corresponding to that of the LDL particles – something that prior publications had missed.

Moon et al (2007) saw studies conducted on 490 patients to investigate the relationship between the serum Lp(a) level and LDL particle size in coronary artery disease (CAD) patients, and the relationship between small, dense LDL and Lp(a), and the extent and severity of CAD. The conclusion was that “both increased Lp(a) and small-density LDL fraction were correlated with the severity of CAD”.

Scientific knowledge was already available in 2007 on the particle size of Lp(a) analogous to small, dense LDL, including the causative factor for ASCVD. Furthermore, Rath & Pauling’s study showed that Lp(a) is a key causative factor in CHD. The mechanism has been explained. High pressure and weaknesses in the arterial walls, most prominently of the coronary arteries, cause ruptures. When the arterial walls rupture, receptor sites for apo(a), a sticky protein and component of Lp(a), appear. Apo(a) functions as an adhesive for the damaged artery. For those currently in the ASCVD field to ignore these earlier publications, especially those of Linus Pauling, who got two Nobel Prizes, is a travesty.

Such misgivings have two reasons. First, no drug is able to dislodge apo(a) from the arterial walls, and statin has no effect in reducing the Lp(a) level. Second, Rath & Pauling postulated that the problem with ASCVD could be solved by strengthening the arterial walls and uprooting Lp(a) using Vitamin C, lysine and proline amino acids, as well as niacin. These are natural nutrients and not patentable. And, it is not in the corporate interest to promote non-patentable natural therapies.

The three questions worth repeating are:

* Why do cholesterol deposits form in the arteries and not veins, while the same cholesterol level circulates in the arteries and veins?

* Why is coronary sclerosis the most frequent form of atherosclerosis? In the 98km-long human vascular system, cholesterol deposits are predominantly found in the coronary arteries.

* Why is atherosclerosis characteristic of humans, while being practically unknown in the animal world except for a few species that are not able to produce Vitamin C internally (e.g. primates and guinea pigs)?

In the meantime, the “cholesterol war” between sceptics and the so-called “preponderance” of evidence continues. – October 10, 2019.

* Captain Dr Wong Ang Peng is a researcher with an interest in economics, politics, and health issues. He has a burning desire to do anything within his means to promote national harmony. Captain Wong is also a member of the National Patriots Association.

* This is the opinion of the writer or publication and does not necessarily represent the views of The Malaysian Insight. Article may be edited for brevity and clarity.