Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

Hangovers, asians and aldehyde dehydrogenase

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OBJECTIVE: Hangovers are not experienced by all people and whether they contribute to the development of alcoholism is unclear. One population that might provide some insight into the role of hangover in the etiology of alcohol use disorders is that of individuals of Asian heritage. Certain Asians have lower rates of alcohol use and alcoholism, findings associated with a mutation in the aldehyde dehydrogenase (ALDH2) gene. Asians with ALDH2*2 alleles drink less and are less likely to be alcoholic than Asians without this mutation. Following alcohol ingestion, they exhibit more intense reactions to alcohol and generate higher levels of the metabolite acetaldehyde. This study evaluated hangover symptoms in Asian Americans with variations in the ALDH2 gene. METHOD: Men and women of Chinese, Japanese and Korean heritage (N = 140) were asked about their drinking history and a blood sample was collected for genotyping at the ALDH2 locus. Subjects used a Likert-type scale to estimate their severity of hangover and completed a 13-item hangover scale assessing the frequency of hangover symptoms during the previous 6 months. RESULTS: With abstainers (n = 17) excluded and with the effects of gender and recent drinking history controlled, ALDH2 genotype accounted for a significant amount of additional variability in the estimated severity of hangover score with a similar, but nonsignificant, trend for a five-item subscale score derived from the hangover scale. CONCLUSIONS: These results suggest that Asian Americans with ALDH2*2 alleles may experience more severe hangovers that may contribute, in part, to protection against the development of excessive or problematic drinking in this population. Hangover symptoms in Asian Americans with variations in the aldehyde dehydrogenase (ALDH2) gene.

Could a genetic defect like the one described above be of importance to the failsafers who appear to who have inborn food chemical intolerances, particularly those who react to sulphites? This is a brief listing for all three sulphite enzymes. A sulphite oxidase deficiency is an extremely rare, fatal condition. But what about variations in genes that cause only a reduced capacity to detoxify sulphites? Some people may simply be molybdenum deficient, whereas others may have a polymorphism in their sulphite enzymes.

People genetically predisposed to gout make too much xanthine oxidase. If one makes too much of this stuff, perhaps these people might also make too little aldehyde oxidase or sulphite oxidase, due to limited molybdenum resources?

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Written by alienrobotgirl

15 April, 2006 at 4:05 pm

Posted in The Science of FCI

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