10. FINAL WORRIES AND QUESTIONS UNANSWERED
In technical language:
1. Kman made some particularly good points about the fact that H2-blockers may not actually be slowing the metabolism of alcohol (thereby allowing acetaldehyde metabolism to keep up) but instead simply targeting the histamines that are produced as a result of elevated acetaldehyde levels.
2. This suggestion was made in light of the fact that ethanol levels in subjects were not elevated despite taking famotidine. However, these studies are from some time ago – Kman if you are still around, could you possibly look up some recent ones perhaps circa 2005-2008?
3. If this is indeed the way the famotidine is operating, perhaps it is a dangerous drug as drinkers will still have elevated acetaldehyde level but simply not realize.
4. A side note that was worth noting is that according to Kman’s research, it is likely ranitidine is ‘better’ for you as alcohol levels were increased in subjects when taking ranitidine suggesting it inhibits the enzyme alcohol dehydrogenase.
Lovely summary. And as requested, I have crawled out of my hole to give you some updates....
There are 2 recent reports which confirm my earlier position. Both by the same author.
http://www.ncbi.nlm.nih.gov/pubmed/1920 … d_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/1920 … d_RVDocSum
Essentially, I think he summarises old info.
Firstly he confirms that some H2 Blockers have an effect on ADH (the enzyme that breaks down acetaldehyde). And again Ranitidine is named. But this is nothing new. Old studies as far back as 1991 confirm "at therapeutic doses in vivo, the degree of inhibition by cimetidine and ranitidine should be significant and comparable, that by nizatidine should be smaller, and that by famotidine should be negligible." So we know for a fact that Ranitidine has SOME inhibitory effect on ADH but not famotidine (Pepcid). The second report states:
"Increased blood acetaldehyde resulting from abnormalities of alcohol dehydrogenase genotype in the Orientals population can release histamine from mast cells and basophiles, which induces the hypersensitivity reactions (flushing). These reactions may be blocked by antihistamine drugs. H2-receptor antagonists influence on the ethanol metabolism by the inhibition of the activity of alcohol metabolizing enzymes in the stomach and liver."
So essentially, this author surmises that the H2 blockers work by inhibiting ADH. Now, I don't think he has the whole picture, or at least the whole picture relating to famotidine. Since he himself and other studies have found that famotidine has no or negligible effect on ADH, there must be some other mechanism by which famotidine works. Whatever it is, as far as the studies show, there is nothing to show that famotidine stops the production of acetaldehyde. It may stop the symptoms (the histamine release), but not the production of acetaldehyde, which is the killer carcinogen.
Another poster, nohxtk1, seems to have come on board recently, and he is a med student. He seems to share my view, and would probably be in a better position, with his training, to find more studies, or explain things.
So let me continue my nagging crusade of warning all of you not to get carried away. Even ranitidine doesn't completely inhibit ADH, and if anything just lowers levels of acetaldehyde (not sure to what extent).
Alcohol is dangerous to asian flushers. The link to cancer is very very clearly established.
Conviva sounds promising though!