Hello Owen,
On the 4th page of Rath's and Pauling's paper on A Unified Theory of Human Cardiovascular ...,the following sentence appears:
"In about half of the CVD patients the mechanism of Lp(a) deposition contributes significantly to the development of atherosclerotic plaques."
My question is what about the other half? Lp(a) plays no?role???
Looking forward to your answer.
Richard I.
Good question, I will have to read the paper to remind myself of the context ...
http://www.drrathresearch.org/research/publications/leading-publications/97-unified-theory-of-human-cardiovascular-disease-leading-the-way-to-the-abolition-of-this-disease-as-a-cause-for-human-mortality.html
The statement is in context with "Other Lipoprotein Disorders Associated with CVD" - next section. I do not know where the 50% number comes from, but Levy's book STOP AMERICA'S #1 KILLER (livonbooks.com) explains a multitude of ways the body tries to strengthen and stabilize weak arterial walls - all as a result of collagen deficiency caused by low vitamin C intake. And as the paper points out, although there may be other material in the plaque ( other than Lp(a)) the deposition of these materials frequently follows Lp(a) deposition.