Originally posted by: Xylitol
Originally posted by: krnxpride83
i weigh about 165lb... and even if i take a sip of beer.. i just get all red... perhaps im allergic?
Are you asian?
Cuase most asians cant take strong liquor/alcohol and turn red really easily
ENZYME DEFICIENCIES AND ASIAN FLUSHING
An interesting phenomenon that occurs in some people is the familiar flushing of the face after low to moderate amounts of alcoholic beverage consumption (Luu et al., 1995). This alcohol-flush reaction occurs in some Caucasians, but is particularly common among Asians. Degrees of flushing can range from slightly pink, to bright red. The reaction has been found to be caused by a mutation in the structural gene for the mitochondrial aldehyde dehydrogenase (Takeshita et al., 1994). Approximately 500f Asians have a deficiency in low Km aldehyde dehydrogenase (ALDH2), which is the result of inheritance of a mutant ALDH2*2 allele (Wall et al., 1997). The mutation has the effect of both reducing enzyme activity and increasing the turnover of this activity (WWW3).
ALDH2, located mainly in mitochondria, is responsible for the oxidation of most of the acetaldehyde generated in alcohol metabolism (Takeshita et al., 1994). Acetaldehyde normally is removed by ALDH, but a deficiency of the mitochondrial form
means prevalence of the cystolic version. Cystolic ALDH2 has a
high Km, which causes a lower affinity for acetaldehyde. This leads to slower conversion of acetaldehyde to acetate, giving a steady-state level of acetaldehyde (WWW3). Acetaldehyde therefore accumulates in the blood of individuals deficient in ALDH2 activity, even after small doses of alcohol. The build
up of acetaldehyde results in vasodilation, causing facial flushing.
In addition to flushing of the face, other unpleasant effects also can occur. These include tachycardia or increased heart rate, low blood pressure, headache, hyperventilation, and nausea (WWW3). The presence of these unpleasant and uncomfortable symptoms therefore tends to reduce the frequency and amount of alcohol consumption by the person affected. It has been proposed that these effects combine to deter drinking among many Asians, and may effectively act as a protective mechanism to prevent them from reaching consumption levels indicative of alcohol dependence and abuse (Takeshita et al., 1994). Carriers of the inactive allele do not drink as often, and have consumption levels of alcohol that are significantly lower than non-carriers which include Caucasians and other Asians (WWW4). This genetic trait seems to be one of the strongest factors that influence drinking behavior and risk of alcoholism (Xiao et al., 1996). Studies have found that alcohol use and alcoholism are indeed lower in people of Asian
descent than rates in other ethnic groups (WWW4).
The exact connection between ALDH2*2 and its protective role in alcoholism is not yet thoroughly understood. Other factors may also regulate the mechanism. These include regulation by histamine, prostaglandins, and stimulation of bradykinin (WWW3). What is certain, however, is that elevated levels of acetaldehyde in the blood, rather than blood alcohol concentration, are required to induce flushing. Acetaldehyde is therefore the originator of the physiological effects of flushing (WWW3). Future studies and research would be required to completely determine the role in alcohol consumption and alcoholism.
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