There are several routes of metabolism of ethyl alcohol in the body. The major pathways involve the liver and in particular the oxidation of ethyl alcohol by alcohol dehydrogenase (ADH).
Playing a role, particularly at higher alcohol concentrations is the oxidation of alcohol by the microsomal (small spherical vesicles) - cytochrome P450 system (MEOS) system. In addition to these routes, there is catalase-dependent oxidation of ethyl alcohol and oxidation of it by the stomach when it is first ingested. These latter two routes of metabolism are minor in comparison to the ADH and MEOS systems.
As mentioned above perhaps the major route of metabolism of ethyl alcohol is its oxidation in the liver catalyzed by the cytosolic enzyme alcohol dehydrogenase (ADH). It catalyzes the following reaction:
CH3CH2OH + NAD+ Û CH3CHO + NADH + H+.
This reaction produces acetaldehyde, a highly toxic substance. ADH has broad specificity, catalyzing various alcohols and steroids and catalyzing the oxidation of fatty acids. It also is not a solitary enzyme in that there are five different ADH genes, two of which ADH2 and ADH3 shown polymorphism (variations). Of importance is the fact that the ability of people to oxidize ethyl alcohol is dependent upon the genetic makeup of the individual. People with alleles (types) of ADH2 and ADH3 may protect those having these genes from developing alcoholism. These genes are common in the Asian population and convert alcohol to acetaldehyde more rapidly than normal. Because of this increased production of acetaldehyde, this toxic compound builds up and makes people who drink too much uncomfortable and ill. Therefore, these carries are discouraged from consuming large amount of alcohol.
A similar situation is found in the second step of ethanol metabolism, which is catalyzed by acetaldehyde dehydrogenase. This enzyme converts acetaldehyde to acetic acid, which is a normal metabolite in humans and hence is non toxic. The past use of Antabuse as a possible deterrent to drinking was based on the ability of Antabuse to inhibit the action of acetaldehyde dehydrogenase, thus slow down or stop the destruction of acetaldehyde. If one drank after taking Antabuse, the person got very ill. It turns out that certain individuals, again common in Asians, have a defective aldehyde dehydrogenase gene, ALDH2, in that it doesn’t not metabolize acetaldehyde as rapidly as normal. Thus, a person who drinks too much builds up acetaldehyde in their system and feels bad or is sick. This manifests in Asians with the defected ALDH gene as a facial flush as they drink. These responses discourage drinking, thus preventing the development of alcohol abuse, dependence, and alcoholism.
OK, Didn't you recently post that you are of Philipino decent? This may be part of what is going on. It's organic chem though and should happen a bit every time you drink if this is the case...
In all fairness I cut & paste the above from :
http://chemcases.com/alcohol/alc-06.htm
I'm a doc but this stuff is largely out of my field. we studied this a bit in Biochem, but I couldn't remember all the details....
Chest, arms, everywhere? WTF is going on? Its not like its the first time this has happend, and I've been drinking Bacardi and Coke for years...
