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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 ...
Auto-brewery syndrome (ABS) (also known as gut fermentation syndrome, endogenous ethanol fermentation or drunkenness disease) is a condition characterized by the fermentation of ingested carbohydrates in the gastrointestinal tract of the body caused by bacteria or fungi. [1]
Drinking alcohol in addition to consuming calcium cyanamide can cause permanent or long-lasting intolerance (nitrolime disease), [11] [12] contributing (in conjunction with other substances) to the accumulation of harmful acetaldehyde in the body by inhibiting the acetaldehyde dehydrogenase enzyme.
Long-term effects of alcohol include changes in the metabolism of the liver and brain, with increased risk of several types of cancer and alcohol use disorder. [1] Alcohol intoxication affects the brain, causing slurred speech, clumsiness, and delayed reflexes. There is an increased risk of developing an alcohol use disorder for teenagers while ...
Chronic consumption of alcohol results in the secretion of pro-inflammatory cytokines (TNF-alpha, interleukin 6 and interleukin 8), oxidative stress, lipid peroxidation, and acetaldehyde toxicity. These factors cause inflammation, apoptosis and eventually fibrosis of liver cells. Why this occurs in only a few individuals is still unclear.
Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis.
The reaction is the result of an accumulation of acetaldehyde, a metabolic byproduct of the catabolic metabolism of alcohol, and is caused by an aldehyde dehydrogenase 2 deficiency. [ 4 ] This syndrome has been associated with lower than average rates of alcoholism, possibly due to its association with adverse effects after drinking alcohol. [ 5 ]
Excessive alcohol use causes neuroinflammation and leads to myelin disruptions and white matter loss. The developing adolescent brain is at increased risk of brain damage and other long-lasting alterations to the brain. [60] Adolescents with an alcohol use disorder damage the hippocampal, prefrontal cortex, and temporal lobes. [46]