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Alcoholic Liver Disease – Part 1

Alcoholic liver disease is a condition which contributes to the hepatic manifestations of over consumption of alcohol. This includes:
– Fatty liver
– Alcoholic hepatitis
– Chronic hepatitis
– Hepatic fibrosis
– Cirrhosis
• Alcohol is the basic reason for the rise of liver disease especially in Western countries.
• Although steatosis (fatty liver) will build up in a person who consumes a large level of alcohol based drinks spanning a long time, this is transient and reversible.
• Coming from all chronic heavy drinkers, only 15–20% develops hepatitis or cirrhosis, which could occur concomitantly or perhaps succession.
• 80% of alcohol passes over the liver to be detoxified.

Chronic consumption of alcohol results in the secretion of:
– pro-inflammatory cytokines
– oxidative stress
– lipid peroxidation
– acetaldehyde toxicity

These factors cause:
– Inflammation
– Apoptosis
– Eventually fibrosis of liver cells
Why this occurs within a few people remains unclear?

Risk factors for Alcoholic Liver Disease

The chance factors presently known which significantly raises the risk of hepatitis and fibrosis by 7 to 47% are:
Variety of alcohol taken
• Consumption of 60–80g each day (about 75–100 ml/day) for 20 years and up in males.
• 20g/day (about 25 ml/day) for females.

Pattern of drinking
Drinking outside meal times increases the risk of alcoholic liver disease as much as 2.7 times.

• Females are twice as prone to alcohol-related liver disease.
• They may have alcoholic liver disease with small duration and doses of chronic consumption.
• The lesser number of alcohol dehydrogenate secreted from the gut, higher proportion of unwanted fat in women.
• Modifications in fat absorption because of the menstrual period may explains this phenomenon.

Hepatitis C infection
Hepatitis C infection greatly speeds the process of liver injury.

Genetic factors
• Genetics predispose both to alcoholism and also to alcoholic liver disease.
• Monozygotic twins will be alcoholics in order to develop liver cirrhosis than dizygotic twins.
• Polymorphisms within the enzymes mixed up in metabolism of alcohol, for example ADH, ALDH, CYP4502E1.
• Mitochondrial dysfunction
• Cytokine polymorphism
• These may partly explain this genetic component.
• No specific polymorphisms are related to alcoholic liver disease.
• Iron-storage disease (hemochromatosis)

• Fatty change or steatosis may be the accumulation of fatty acids in liver cells.
• To as be viewed as fatty globules under the microscope.
• Alcoholism causes progression of large fatty globules (macro vesicular steatosis) during the entire liver which enables it to start to occur right after times of heavy drinking.
• Alcohol is metabolized by alcohol dehydrogenase (ADH) into acetaldehyde, then further metabolized by aldehyde dehydrogenase (ALDH) into ethanoic acid
• That is finally oxidized into carbon dioxide (CO2) and water ( H2O).
• This process generates NADH, and enhances the NADPH/NADP+ ratio.
• A better NADH concentration processes the synthesis of essential fatty acids.
• A reduced NAD level leads to decreased fatty acid oxidation.
• Subsequently, the higher amounts of EFAS signal the liver cells to compound it to glycerol to create triglycerides.
• These triglycerides accumulate, resulting in fatty liver.

• Malnutrition
• Particularly Vitamin E deficiency
• Can worsen alcohol-induced liver damage by preventing regeneration of hepatocytes.
• Many of the issues as alcoholics are generally malnourished due to a poor diet, anorexia, and encephalopathy.

Alcoholic Liver Disease Dr. Melissa Palmer’s Guide To Hepatitis and Liver Disease The Liver Cleansing Diet

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