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Food such as fructose can increase the rate of alcohol metabolism. The effect can vary significantly from person to person, but a 100 g dose of fructose has been shown to increase alcohol metabolism by an average of 80%. In people with proteinuria and hematuria, fructose can cause falsely high BAC readings, due to kidney-liver metabolism. [106]
The microsomal ethanol oxidizing system (MEOS) is an alternate pathway of ethanol metabolism that occurs in the smooth endoplasmic reticulum in the oxidation of ethanol to acetaldehyde. While playing only a minor role in ethanol metabolism in average individuals, MEOS activity increases after chronic alcohol consumption.
Alcohol flush reaction is a condition in which an individual's face or body experiences flushes (appears red) or blotches as a result of an accumulation of acetaldehyde, a metabolic byproduct of the catabolic metabolism of alcohol. It is best known as a condition that is experienced by people of Asian descent.
Alcohol intolerance is an inherited genetic disorder that impairs alcohol metabolism. [34] The increased accumulation of acetaldehyde in affected individuals due to deficient aldehyde dehydrogenase enzymes often leads to the characteristic symptom of having flushed skin.
Alcohol dehydrogenases are often used for the synthesis of enantiomerically pure stereoisomers of chiral alcohols. Often, high chemo- and enantioselectivity can be achieved. One example is the alcohol dehydrogenase from Lactobacillus brevis (LbADH), which is described to be a versatile biocatalyst. [52]
More recently, ALDH2 has been implicated in a number of pathways beyond alcohol metabolism. ALDH2 dysfunction is supposedly associated with a variety of human diseases including diabetes, neurodegenerative diseases, cardiovascular diseases and stroke, cancer, Fanconi anemia, pain, osteoporosis, and the process of aging. [14]
Some ADH gene variants lead to higher metabolic activity, resulting in the accumulation of acetaldehyde, whereas, a null allele in ALDH2 causes an accumulation of acetaldehyde by preventing its catabolism to acetate. [23] The genetic variants of these enzymes can explain the differences in the alcohol metabolism in different races.
The level of ethanol consumption that minimizes the risk of disease, injury, and death is subject to some controversy. [16] Several studies have found a J-shaped relationship between alcohol consumption and health, [17] [18] [2] [19] meaning that risk is minimized at a certain (non-zero) consumption level, and drinking below or above this level increases risk, with the risk level of drinking a ...