Replies to post #142745 on Biotech Values

[genisi]

Urche, when I wrote

the question raised by urche in #msg-75751678

I referred to this question:

However, I find it odd that the study apparently did not study the famous group of people with the Apo A-1 Milano variant who I thought clearly had a demonstrated profile with higher than normal HDL and lower than normal cardiovascular risk.

Regarding your other question on HDL subtypes, it is not a question addressed in the Lancet genetic study as they tested SNPs that are associated with elevated HDL-C plasma level and not a spesific HDL subtype. Their data implies that raising HDL-C plasma level alone is not going to be clinically useful. Perhaps targeting a specific subtype or changing HDL molecule from pro-inflammatory HDL to anti-inflammatory HDL instead of raising HDL-C is the way to go, but this is far beyond my knowledge.

[biomaven0]

This brief article discusses the difference between a SNP and a mutation:

http://learn.genetics.utah.edu/content/health/pharma/snips/

(about half way down the page, under the heading SNPs and disease-causing mutations: Not the same!

Originally the hope was that some combination of SNP's in each person would determine propensity for most diseases and traits; the growing belief is that uncommon mutations are the actual drivers.

Peter

[kamehameha]

"if a particular beneficial or harmful HDL subtype could be identified, then it might be possible to design therapeutic approaches involving genetic regulation."

be aware that there is no causal relationship between choelsterol (HDL, LDL) and heart disease, about 50% of patients with heart attack have no signs of arteriosclerosis, as well many people with severe arteriosclerosis have no heart problems:

Baroldi G, Silver MD :THE ETIOPATHOGENESIS OF CORONARY HEART DISEASE:A HERETICAL THEORY BASED ON MORPHOLOGY. Medical intelligence unit, 2nd ed. Eurekah com, Landes Bioscience, Georgetown, Texas, USA, 2004; http//www.eurekah com