The beginning of the end of ischemic vascular diseases in humans

It is simply absurd to claim that any one human being today hatched their idea out of thin air.  There is a chain of education and events to a moment in time that is supported by the generations of humanity previous.  There is an unspoken etiquette in the field of science that you cite the person you got the idea from if it isn't totally original.  There can be some heated disagreements as to chronology such as the whole DNA structure thing.  To all that human misery, I say: "whatever..."  Such mundane trifles are the stuff of little men, and little women in the intellectual sense, not the physical sense.

I went for 20 years or so before running into the idea of Vitamin C as a preventive cure for atherosclerosis.  At the time it had to do with preventing cholesterol oxidation and blowing bile cholesterol out your rear end.  There wasn't a whole lot of sophistry behind what I knew other than the fact that the last time I measured my LDL, it was below normal.  Youth had a lot to do with it, maybe even youthful malnutrition, but I knew that the bogus prescription medicines story couldn't be true.  At the time, all doctors knew that oat, apple, vegetable, grain, and fruit fibers were enough to sequester colonic cholesterol enough to lower LDL.  So why bother with all this toxic fibrate crap and all the rest?  Statins are a fungal poison originally designed with cancer in mind. In fact, the first statins are so toxic, they cause cell cycle arrest by poisoning the mevalonate pathway, the one doctors poison now with statins!  Does it make sense?  Of course it doesn't.  Neither did doctors recommending tobacco smoking on national TV and ashing out on the floor of hospitals as they treated their heart patients.

Eventually, I ran across Matthias Rath/Linus Pauling's ideas which were logically satisfying rather than totally illogical like the chemotherapy concept - "Kill the tumor before the chemicals kill you."  OF COURSE Dr. Rath and Dr. Pauling are whom I got the idea from to design the animal.  Any resistance offered to me at various times by other people are from a simple but somewhat pitiful reason - human jealousy.  To this I just remark - it WASN'T these jealous detractors who risked everything to try it.  They did not, and they would not now have tried it either.  Certainly, had this not all matched up as a theory, I would have been ruined.  It's my whole credibility at stake too. 

The Ice Age – Cardiovascular Disease Connection

"These effects are achieved by nutritional supplements reversing impaired blood flow to the heart muscle as well as improving metabolism of millions of heart cells. The most important among these nutrients are vitamin C, vitamin E, niacin, lysine, proline, coenzyme Q10, carnitine as well as certain minerals. Particular emphasis in the book is given to my earlier discoveries of the therapeutic effect of ascorbate, lysine and related compounds in neutralizing the risk from lipoproten(a).5 Moreover, a new therapeutic mechanism is described by which lysine and proline, together with other essential nutrients, decrease the "atherosclerotic tumor" in the vascular wall caused by smooth muscle cells." //

Okay, sure.  Foam cells - don't forget about them.  They are not as irritating as they appear because....Foam cells do not happen in the ears, the nose, the knees, the veins; they simply never occur there.  We know now that foam cells locate at the hemodynamically prone areas just where the atherosclerotic SMC tumor may arise too.  They can overlap.  Lp(a) is always found in a plaque, whatever kind it is, if there is Lp(a) in the blood.  I have yet to see one without Lp(a) in it.   What are they?  Intra-arterial fat cells.  Just as specialized adipose can expand and get rid of lipids, so can foam cell lesions expand, shrink, and vanish.  The fact that foam cells are present in arteries of people of all ages indicates their normal function beyond their pathological one, which does exist.  The debate about the immune system in the artery in health and atherosclerosis is too long to address in one page but do not contradict the findings of Matthias Rath.  One group says that macrophages do not respond to vitamin C...in an ApoE KO system.  The ApoE KO mouse is like a one-way train.  It may leave the home station, but it cannot return.  No such thing in people except in cases of sporadic familial hereditary mutations.  HDL is the vehicle to which ApoE hands off its cargo among other ways, but LDL can also assume the function of reverse transport to the liver too.  HDL can also assume the function of forward cargo carrier too, and does in wild mice!  So it is very much not so simple as it is made to appear.

What is straightforward is that a lack of Vitamin C creates the damage that triggers the repair in an artery.  However the repair occurs, if it keeps going for decades without stop, it is like building a pile of stuff over the same spot over and over which is exactly what an advanced plaque looks like - an old tree with many rings of stuff.  It may be rings of the same stuff or a variegated mixed composition plaque.  The lipid core plaque, the obsession of many human cardiologist/statin salesmen for its cholesterol composition, the foam cell lesion the obsession for its chemokine triggered quality thereby justifying ox-LDL, the fibrous lesion obsessed on for being evocative of simplistic old school "arteriosclerosis," and "arterial stiffening" which is true but hardly so simple, calcium the love of the fast CT people and EDTA chelator people, the smooth muscle tumor may or may not be there, or they may all be piled one on top of one another in one portmanteau lump.  All these various events are goaded along by a lack of ascorbate ion above a critical efficacy threshold.  If 500mg were all anybody needed in a day, why would we bother?  We would just close shop and declare, "That's it everybody, all you need is this mediocre fruit juice gamish and that is the end of the story."  Unfortunately, the drought of vitamin C is caused by a genetic defect.  Genetic defects require the gene product to be rescued in the amount that was once there, not less.

"My earlier publications in the Journal of Orthomolecular Medicine triggered repeated interest in the history of these discoveries. Thus, a brief personal chronology may be in order: In 1987, after having discovered the lipoprotein(a)-vitamin C connection I recommended vitamin C supplementation to an individual with high lipoprotein(a) levels. This marks the first therapeutic attempt to lower elevated blood concentrations of this risk factor by using vitamin C.8,9 During my research project at Hamburg University I used L-lysine and synthetic lysine analogs to isolate lipoprotein(a) from blood and from arterial walls. This suggested the therapeutic use of lysine and synthetic lysine analogs5, a therapeutic technology for which I recieved patents in the meantime.. In early 1990, after the prominent role of lipoprotein(a) in human atherosclerosis was established 10, I came to the United States to work on the physiologic role of lipoprotein(a) as well as to pursue my earlier therapeutic discoveries."

So there you have it.  The crossing of the animal did not occur to anyone but me, but the application of vitamin C, L-Lysine, and nutrients to prevent atherosclerosis was not my idea but a Dr. Matthias Rath and a Dr. Linus Pauling.  There were others afterwards who helped the stage for the ultimate test of the concept which is incredibly important, but saying they were responsible for the idea is like saying I am the discoverer of the DNA structure.  (I am not.) I am also not responsible for many amazing ideas in this world, but I don't go insane and try to become responsible for each and every great idea in the world.  There would be something wrong with my brain if I were to do that.  I hope that all the great scientists of this world achieve their wish of personal discovery and get to see it...before the day they die.