Method of away from the alcohol liver disease
Normal 24-hour vivo metabolism of alcohol 120g. The long-term drinking over the body’s metabolism, can cause alcoholic liver disease. Intake of alcohol, mainly in liver cells under the action of alcohol dehydrogenase into acetaldehyde. The occurrence of alcoholic liver disease is mainly the toxic effects of ethanol and acetaldehyde caused.
The long-term excessive drinking by alcohol itself, acetaldehyde and its derivatives can recurring fatty degeneration of liver cells, necrosis and regeneration, which led to alcohol-induced liver disease (alcoholic liver disease), including alcoholic fatty liver (alcoholic fatty liver ), alcoholic hepatitis (alcoholic hepatitis), liver fibrosis (alcoholic fibrosis) and cirrhosis (alcoholic cirrhosis). In the United States and Europe, alcohol-induced liver disease is the leading cause of death of young and middle aged. It is estimated that in 1993 approximately 1530 million people in the United States alcoholism, alcoholic liver disease who suffer from more than 200 million people; each year 2.6 million people die of cirrhosis of the liver, of which at least 40% may be as high as 90% of the patients had history of heavy drinking . In China, with the improvement of living conditions, alcoholism, there is a growing trend, although the incidence of alcoholic liver disease there is no precise figures, but it is not uncommon. As domestic liver disease caused mainly by hepatitis B virus, hepatitis virus, the number of carriers more likely to conceal the fact of alcohol as a cause of liver disease. Therefore, a correct understanding of alcohol-induced liver damage, timely diagnosis and prevention of great significance.
Normal 24-hour vivo metabolism of alcohol 120g. The long-term drinking over the body’s metabolism, can cause alcoholic liver disease. Intake of alcohol, mainly in liver cells under the action of alcohol dehydrogenase into acetaldehyde. The occurrence of alcoholic liver disease is mainly the toxic effects of ethanol and acetaldehyde caused. Acetaldehyde for high-active compounds, can interfere with liver cells perform many functions, such as the effect on mitochondrial ATP generation, protein biosynthesis and excretion, damages microtubules, so that protein and fat excretion barriers to accumulation in liver cells. At the same time ethanol, acetaldehyde is oxidized, the resulting large number of reduced coenzyme Ⅰ, on the one hand the promotion of fat synthesis, on the other hand inhibit the oxidation of fatty acids in mitochondria, leading to the formation of fatty liver. Has proved to be the pathogenesis of alcoholic liver disease with immune factors are involved, such as self-antigens and separation of liver alcohol and transparent body, it can stimulate lymphocyte transformation and walk migration inhibitory factor activity; some cytokines such as tumor necrosis factor (TNF), Interleukin (IL) etc. and the occurrence of alcoholic hepatitis. Alcohol-induced lactic acidosis, by stimulating the proline hydroxylase activity and inhibit the oxidation of proline, proline can increase, thereby increasing the formation of hepatic collagen to speed up the process of cirrhosis of the liver. A number of inflammatory cytokines and ethanol, the toxic effects of acetaldehyde can hepatic stellate cells, liver cells, Kupffer cell activation, secretion of some extracellular matrix, promoting alcoholic cirrhosis. Affect the occurrence and development of alcoholic liver disease there are other factors that acetaldehyde metabolism in genetic variation, such as alcohol dehydrogenase, cytochrome P450 2E1 and aldehyde dehydrogenase polymorphisms. Sex (for the same amount of alcohol, more women than men is more susceptible to alcohol-induced liver disease), diet and nutrition also affect the occurrence of alcoholic liver disease.