Scientific reason for why we turn red (Page 3 of 3)

Sensitivity to alcohol— the alcohol flush reaction—depends almost entirely on a person's genotype at two genes, ALDH2 and ADH1B. 23andMe currently reports your genotype at a SNP in ALDH2. It is possible that those with the AG or GG genotypes at the SNP are more sensitive to alcohol due to their genotype at ADH1B (which 23andMe does not report).

Notes from 23AndMe:

Alcohol is a social lubricant for some and an addictive substance for others. But for people with the alcohol flush reaction, alcohol has such an unpleasant, noxious effect that they tend to avoid it altogether. Even a single drink may cause people sensitive to alcohol to become dizzy or nauseous, have headaches, and turn bright red. The alcohol flush reaction is primarily due to variations in two genes that encode proteins responsible for breaking down alcohol in the bloodstream.

The Wrath of Grapes

Alcoholic drinks have been around as long as civilization itself (and possibly longer). Beer and wine have both been described in the written records of ancient Egypt and Mesopotamia. Like many discoveries, the first alcoholic drink was probably an accident, when cereal grains or berries were left out and fermented by yeast in the air. (A similar accident may also have given rise to the other product of the hugely successful human-yeast partnership: leavened bread.)

The first brave soul to try what was essentially spoiled food was a lucky one, as many food-borne microbes, like salmonella or botulism, are very toxic or even fatal. The waste product of brewer's yeast is ethanol—the chemical name for alcohol—moderate amounts of which interact with the brain to produce the pleasant effects of intoxication, like being less shy or more relaxed.

Genetic variation also influences how well you can hold your liquor. Ethanol is poisonous in larger doses, so our bodies have evolved ways to break it down before it has a chance to build up. While your brain is enjoying its temporary loss of inhibition, your liver is doing its best to clear the alcohol out of your system before it kills you.

The liver's ultimate goal is to turn ethanol into harmless acetic acid (i.e. vinegar), which can be easily removed in urine. The problem is that in order to become vinegar, ethanol has to be converted to acetaldehyde, which is as nasty as it sounds. In fact, acetaldehyde is even more toxic than ethanol. Some of the effects of drinking—turning red, increased heart rate—are actually symptoms of acetaldehyde poisoning. Certain versions of genes can cause a logjam in ethanol processing and a buildup of acetaldehyde. If you have these versions, even one drink can result in ill effects, like flushing, dizziness, nausea, and headaches.

The genotypes that result in a buildup of acetaldehyde when drinking alcohol happen to be especially common in Asians compared to Europeans. This is the reason the ill effects are known in some circles as the "Asian flush."

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12 discoveries from 7000 B.C. to 1994.

7000 B.C.
Inhabitants of the neolithic village of Jiahu in Henan province in China make a fermented beverage of rice, honey, and fruit (hawthorn fruit and/or grape). Chemical analyses of ancient organics absorbed into pottery jars reveal their recipe in the 21st century. (sources)

2100 B.C.
The Sumerians use alcohol as a form of medicine and record its use on a cuneiform tablet of pharmacopeia. (sources)

1000 B.C.
Archaeological evidence shows that fermented cacao beverages were being made in Mesoamerica before 1000 B.C. (sources)

800 A.D.
The process of distillation is invented by the Arabian alchemist Jabir (or Geber) ibn Hayyan. He may also have named the distillate alcohol, which derives from the Arabic root, al-kuhul. Al-kuhul originally referred to powdered antimony (kohl) used as an eye cosmetic but with time it came to mean the "essence," and eventually, the essence of wine—its spirit, or alcohol. (sources)

1947
Disulfiram, a drug that inhibits aldehyde dehydrogenase was discovered by accident at the Royal Danish School of Pharmacy in Copenhagen, Denmark, by Danish researchers Eric Jacobsen and Jens Hald. The two were studying compounds to be used for treating parasitic stomach infections. Both men took a small dose of disulfiram to check for possible side effects. At a cocktail party several days later, they both became very ill after having a drink. They concluded that the disulfiram had interacted with the alcohol to trigger the illness. (sources)

1951
Disulfiram is approved by the FDA as a drug to treat alcohol abuse. Its brand name is Antabuse. It discourages a drinker's desire for alcohol by causing extremely unpleasant symptoms (including facial flushing) when a drink is taken. (sources)

1971
Researchers show that disulfiram inhibits the function of aldehyde dehydrogenase. (sources)

1972
To find if the lower incidence of alcoholism in Asians vs. Europeans is due to cultural or biological factors, Wolff conducts an experiment looking at the physiological reactions to alcohol in both adults and infants from both ethnic groups. He finds that many Asians exhibit a pronounced facial flushing when given alcohol. He concludes that since infants showed the same variation in alcohol response as adults, cultural factors and drinking habits could not be at work. The cause must be genetic. (sources)

1979
The absence of the enzyme coded by ALDH2, which is a common occurrence in people of Asian ancestry, is hypothesized to cause alcohol intolerance. (sources)

1980
Experiments show that livers from Japanese autopsies typically show two forms of aldehyde dehydrogenase enzyme. This finding provides evidence for how genetic differences might lead to phenotypic differences in alcohol sensitivity. (sources)

1991
Researchers publish a study of ALDH2 genotypes in Chinese, showing that alcoholics are less likely to have the slow version of acetaldehyde dehydrogenase. This observation lends support to the hypothesis that the same mechanism that leads to the alcohol flush reaction—a buildup of acetaldehyde due to a slow enzyme—protects against alcoholism. (sources)

1994
A group of biochemists show that the two versions of the ALDH2 gene commonly seen in Asians encode two versions of the aldehyde dehydrogenase protein with strikingly different biochemical properties. This evidence connects genetic differences to phenotypic differences by providing a biochemical mechanism. (sources)

Additionally, if you are focusing your efforts on the stomach, how will this new compound address 2nd-pass alcohol metabolism that is done in the liver?

In a way, I'm a little nervous about Alda-1 and being a human beta since it is essentially altering my body to produce a chemical versus just taking the chemical when I need it. I don't think Alda-1 has been used on humans at all...am I missing something?