Frodo wrote:pamojja
If atheriosclerosis is indeed a repair mechanism of the body in which the lp(a)-molecule is significantly involved, then the lp(a) value should be increased for all affected persons. If the value is not increased at all, the question remains why not. Are there other biological repair factors, like cholesterol, that cause deposits instead of lp(a)? I have my doubts.
High Lp(a) is only one of many risk-factors. Some others are c-reactive protein, homocysteine, fibriginogen, Lp-PLA2, high blood pressure, insulin resistance, hypothyroid, hormone deficiency, nutrient deficiencies (vitamin C, D, CoQ10, Mg, Omega-3..).
A risk factor is only marker for possibly higher risks. It never means everyone with a risk-marker has the disease. It just becomes much more likely.
But to your question, this one particular repair-mechanism might just be impaired in some individuals. Equally as some 50% of the population aren't able or to a less extent, to metabolize folic acid into active methylfolate. We all have different bio-chemical individuality. And in lack of one repair-mechanism, there are sure a couple of fall-back mechanisms. None seems perfect, otherwise they wouldn't fail so many times.
Frodo wrote:The question remains whether there are people without lp(a). According to Matthias Rath not. And in my experience not either.
Lp(a) is a risk-marker only at higher levels. So I don''t even understand why this question has any relevance.
Frodo wrote:Therefore: Why does lp(a) increase for me if it remains low for other atheriosclerosis patients?
That was the background to my question.
I asked Matthias Rath about it.
Perhaps I only haven‘t understand it.
This question only arises if one believes that Lp(a) is the only possible repair-mechanism, or even the only cause to calcification of arteries. There is sheer stress in magnitudes of different strengths; fungal, bacterial or viral infections again in all possible combinations and strengths, and there are a multitude of repair-mechanism all working like a orchestra. Or a cacophony due to some bio-chemical individuality. Sometime one player - like very high Lp(a) doesn't plays harmoniously out of all these different co-factors in different proportions.
By the way, my Lp(a) is after 10 years still high too. But I'm not concerned because it's only a marker of a possibility. My real verified calcification of my abdominal aorta bifurcation causing a 80% blockage and 60% walking-disability has gone in remission since.
Linus Pauling patent was titled:
So high lp(a) certainly in my case, but probably in yours too, might just have been inhibited from binding. And many other factors employed with Pauling's therapy have to done the clean-up job.