Quote:
Originally Posted by North Beach Person
Having gone to the link, and read your previous thread, I'd like someone to tell me what it was that totally blocked my right coronary artery a couple weeks ago which necessitated the implantation of four stents.
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I've researched the literature totally independently of anyone else in curing my own coronary heart disease and peripheral artery disease. First I have to agree with the OP that cholesterol has only incidental and not a causative role in atherosclerosis. The best results ever for statins is a 1 to 2% regression of atherosclerosis, whereas high vitamin Ks produced a 100% regression in my leg arteries that were less than 60% occluded.
These are my findings:-
Secondly, the terms atheromatosis, arteriosclerosis and atherosclerosis are used rather loosely
and interchangeably in biomedical literature. I tend to differentiate them in my own mind just for the sake of keeping my thinking clear. The suffix '-sclerosis' means hardening and '-osis' means 'a condition of'. So atheromatosis means a condition or state where swellings called atheromas build up under the lining-cell layer (endothelium) of arteries. There is probably not strictly such a thing as a state of pure atheromatosis unless it applies in the early stages before calcification, or unless the term is restricted to the actual process of formation of atheromas.
The first diagram is a mud map of atherosclerosis of an artery.
Calcification of atheromas seems inevitable to me because atheromas form only in the absence of the vitamin K-dependent Proteins C and S, and calcification occurs only in the absence of osteocalcin or matrix-gla-protein, both of which are also dependent on vitamin K. (There is another ubiquitous liver-produced protein called Fetuin A that prevents calcification, but some speculation exists that it may be too large a molecule to penetrate to the intima and smooth muscle area of blood vessels). The vitamin K-dependent proteins, osteocalcin (aka bone-gla-protein), and matrix-gla-protein, seem to be vital in preventing calcification -- see
https://academic.oup.com/advances/ar.../2/166/4557937.
Many of the following articles talk about calcification of artery walls, without mentioning atheromas. I think this is because, with certain types of non-invasive identification techniques (such as X-rays), it is the only characteristic that can be identified; the atheromas are not visible or measurable. Therefore, the researchers can only objectively talk about the calcification that their methods of detection identify. I could be wrong, but when I think about the collective message from all the research mentioned in this book, I believe it would be unlikely to see a significant degree of atheromatosis without calcification or conversely to have a significant degree of calcification without atheromatosis.
The following article not only suggests that calcium deposition occurs in the general time frame of atheroma development but that the process can begin in human beings at an early age. Stary (2000;
https://academic.oup.com/ajcn/articl.../1297s/4730127) reported cases of the onset of atheromatous lesions in children, and one wonders whether the supply of vitamin K (by injection) at birth, should perhaps be continued orally for life, considering the evidence in this book. Stary found that one-half of infants have small collections of macrophages in artery walls (some containing lipids) and that around puberty, 69% of 12 to 15-year old children, have foam cell accumulations larger than those in infants. He claimed that as soon as lipid cores form, calcium deposits appear in some smooth muscle cells and among the extracellular lipid of the core. This is evidence of course that onsets of atheroma formation and calcification may not be exactly simultaneous in the early stages, but they do occur together from about 15 years of age onwards. The author reported that 15% of 16 to 19-year-olds have pre-atheromas or atheromas in coronary arteries.
If we knew what the macrophages containing lipids were doing in the intima of the arteries of infants, we may have a better understanding of why atheromas form in the first place. But because they do exist, it is plausible to consider that such formations occur in the natural course of events primarily and that substances such as vitamins K are required to control such biological 'mishaps' -- just speculating.
Some further evidence of early onset of thrombosis of coronary arteries was provided by Captain (1943;
https://www.sciencedirect.com/scienc...2870343901024#!) who researched the literature of his time and found reports of five cases of medial coronary sclerosis in infants from birth to 27 months, in which evidence of myocardial damage (presumably infarction) was present, as well as eight cases of coronary thrombosis between the ages of 10 and 20 years; in six of the latter the diagnosis was confirmed by autopsy.
Leeson et al (2000;
https://www.ahajournals.org/doi/full...IR.101.13.1533) in
Cholesterol and Arterial Distensibility in the First Decade of Life used
"A non-invasive ultrasound technique ... to measure arterial distension during the cardiac cycle in the brachial arteries of 361 children from 4 towns in the United Kingdom. This measure was related to their pulse pressure to assess arterial distensibility" and
"There was a significant, inverse relation between (total - mine) cholesterol and distension of the artery across this range P=0.003). Similar relationships were demonstrated with LDL and apolipoprotein (P=0.005 and P=0.01). HDL and triglyceride levels showed no consistent association with distensibility."
Let me present some research on the process of atheroma formation. The first thing to recognise is that it is a process, rather than a passive accumulation of cholesterol and lipids.
As far back as 1981, Gerrity published the results of the experimental reproduction of atheromatosis in pigs here --
https://www.ncbi.nlm.nih.gov/pmc/art...00218-0023.pdf. The author mentioned a previous experiment in which he and his colleagues fed an atherogenic (causing atheromas to form) diet to pigs (lard and cholesterol) and demonstrated that atheroma development was preceded by white blood cells of the type called a monocyte, penetrating the layer of cells that line the aorta. In this experiment, they found these monocytes in various locations of the endothelial lining layer of arteries --1) sticking to the surface of the cells lining the arteries, as well as 2) in the junction between the cells that line arteries, and 3) inside the inner wall of the arteries. In addition, the examination suggested that the monocytes were differentiating (changing) into macrophages (cells that gobble up debris) before becoming foam cells. Ferritin was injected into the arteries and found to be taken up by those monocytes that had penetrated between the cells lining the arteries. This indicates that the monocytes were becoming scavengers of debris even before they had changed into macrophages.
The second diagram shows these STAGES of the PROCESS.
Monocytes are a minor type of white cell. They normally account for between 2 and 8% of leucocytes. This alone suggests that it is a specific rather than a generalised process.
Bobryshev (2006;
https://www.sciencedirect.com/scienc...68432805001642) gave a more up-to-date review. He affirmed that monocytes migrate into the tissue under the cells lining arteries (endothelium), differentiate into macrophages and dendritic cells before differentiating again into foam cells. The author went on to claim that these cells aggregate to form a core that consists of necrotic plaques, lipids, cholesterol crystals and cell debris. Bobryshev also mentioned the presence of chemicals associated with inflammation in these atheromatous lesions. Inflammation accompanies atheroma formation.
Goikuria et al (2018;
https://www.sciencedirect.com/scienc...5961011730196X) provided a good graphic depiction of the formation of atheromas from the fatty streak stage onwards and claimed that inflammatory products, produced by differentiated smooth muscle cells, play a large part in the development of plaque in the late stages. It is these plaques that can suddenly rupture and produce distal thrombus propagation and hence vessel occlusion resulting in ischemic events.
'Fatty streaks' by the way are the earliest signs of atheromas seen with the naked eye by pathologists when they open arteries. They appear as lengthwise yellowish streaks up to several millimetres wide and centimetres long.
I mentioned earlier that signs of atherosclerosis have been recorded in infants and teenagers. This paper by Strong et al (1999;
https://jamanetwork.com/journals/jam...article/188840) reports that in autopsies of 2876 15- to 34-year-old black and white men and women who died of external causes, all of the aortas and more than 50% of right coronary arteries of 15- to 19-year-olds had what they called 'intimal lesions' and these progressively increased in prevalence up to the oldest group of 30- to 34-year old subjects. They concluded that fatty streaks and other early lesions were commencing in youth and progressing up to the 34-year-old span. Naturally, they recommended that the primary prevention of atherosclerosis must begin in childhood or adolescence.
It's easy to say, but the big question of course is how to do this. Could vitamin K supplementation fill the bill?
Others have demonstrated that a whole array of biochemical agents are involved in the initial adhesion of monocytes to the endothelial cells of the arteries, in the attraction of monocytes to migrate through the lining cells into the intima, and then to differentiate into monocytes and foam cells. If we have an adequate vitamin K intake, Proteins C and S are manufactured, and when activated, inhibit all of the above intricate biochemical processes involved in the migration of monocytes into the intima layer of arteries. If this is the case, then atheromatosis and atherosclerosis can be regarded as indications and manifestations of chronic vitamin K deficiency.
My reading of this evidence makes me think that atheroma formation may be something of a status quo, similar to the deposition of calcium into soft tissue, as I will explain later in this chapter. This seems especially so when, as Stary (above) pointed out, fifty percent of infants' arteries already have macrophages, with some containing lipids, under the endothelia of those arteries. I am quite interested to hear if anyone has a theory on that.
A question I ask myself after reading the above information about monocytes migrating through the arterial endothelium into the intima of arteries is whether there is a common stimulus attracting them. Small inhaled particulate matter of less than 2.5 microns just might be involved. Liang et al (2020;
https://particleandfibretoxicology.b...89-020-00391-x) reviewed the literature on small particulate matter and atherosclerosis, summarising
"... the main mechanisms of PM2.5-triggered vascular endothelial injury, mainly involved three aspects, including vascular endothelial permeability, vasomotor function and vascular reparative capacity. Then we reviewed the relationship between PM2.5-induced endothelial injury and atherosclerosis." That relationship sounds plausible to me, particularly because of the established association between particulate matter exposure and cardiovascular disease.
That's enough for one post. It's enough to explain why we get atherosclerosis. My personal experience is that high doses of both vitamin K1 and vitamin K2, caused complete reversal of atherosclerosis, in 14 months, of any arteries in my legs that were less than 60% blocked. My angina attacks have been absent for the last 7.5 years.
I can supply much more evidence if anyone is interested.
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