Yes @
Martial, there is lots of conflicting research out there including published papers. The point though is that you would expect to see two groups of abnormal snps, one with snps decreasing enzyme activity, and one with snps increasing enzyme activity, and unless there is strong evolutionary selection at work you would expect to see low function more often than high function, as most mutations decrease functioning of a protein.
If CBS is over-active then homocysteine would be used up, unless there is a second factor such as very poor MTHFR activity which is driving homocysteine accumulation. However even if MTHFR is not working right, you would expect that increasing CBS activity further would result in two things - more glutathione, and lower homocysteine. However it would then pay to monitor ammonia, and probably other consequences.
Homocysteine can form a product that replaces lysine in proteins, destroying their function. It can lead to increased blood coagulation. It often leads to premature death from aggressive vascular disease. One thing I find interesting, and this is completely speculative at this point, is that this may have an impact on herpes viruses.
Let me make one additional comment on herpes viruses - if they incorporate defective lysine then they may have an altered function. It is too hard to say what impact this would have, but it
might lead to latent viruses.
