Ward et al  examined nutrigenetic interactions between the alcohol dehydrogenase 1C (ADH1C
) single nucleotide polymorphism (ADH1C
c.-64T>C) and vitamin A levels and the impact on IMF deposition in Angus-cross steers.
Around 80 percent of Asian people (less common in Thailand and India) have a variant of the gene coding for the enzyme alcohol dehydrogenase called ADH1B, whereas almost all Japanese, Chinese, and Korean people have a variant of the gene called ADH1C
, both resulting in an alcohol dehydrogenase enzyme that converts alcohol to toxic acetaldehyde at a much higher efficiency than other gene variants from Caucasians.
Genetic variation in alcohol dehydrogenase (ADH1A, ADH1B, ADH1C
, ADH7) and aldehyde dehydrogenase (ALDH2), alcohol consumption and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.
Osier et al., "Allelic variation at alcohol metabolism genes (ADH1B, ADH1C
, ALDH2) and alcohol dependence in an American Indian population," Human Genetics, vol.
Agundez, "Variability in ethanol biodisposition in whites is modulated by polymorphisms in the ADH1B and ADH1C
genes," Hepatology, vol.
Genome-wide association studies have identified numerous genes that contribute to drug abuse including CHRNA3-5 for nicotine dependence and ADH1B and ADH1C
genes for alcohol dependence.
The variation in alcohol elimination and the oxidation of acetaldehyde, genetically determined alcohol dehydrogenase 1-3 (before named ADH1A, ADH1B and ADH1C
) and aldehyde dehydrogenase (ALDH2) plays a major role in the pathogenesis of the clinical syndrome.
The rates of metabolic pathways responsible for converting alcohol to acetaldehyde and acetaldehyde to acetate are mostly influenced by functional polymorphisms on ADH1B (previously called ADH2), ADH1C
(previously called ADH3),andALDH2 [5-7].
The human ADH genes, ADH1B and ADH1C
were found to have alleles that produce enzymes that catalyze the oxidation of ethanol to acetaldehyde.
** P = 4 x [10.sup.-33] With alcoholism and alcohol-induce medical diseases.
The study identified several SNPs in a region on chromosome 2 that previously had been linked to alcohol dependence, as well as SNPs in a gene called CDH13 that is located on chromosome 16 and the ADH gene ADH1C
on chromosome 4.
The researchers have found that individuals with a polymorphism of the alcohol dehydrogenase 1C (ADH1C
) gene produce more acetaldehyde when they drink, which creates a higher risk for colorectal cancer.