Amount of alcohol intake
The amount of alcohol consumption that places an individual at risk of developing AH is not known. However, in practice, most patients with AH drink more than 100 g/d (which corresponds to 6-7 drinks per day where one drink contains 13-15 g of alcohol), with 150-200 g per day being common. The typical patient has consumed alcohol heavily for two or more decades, although in an occasional patient alcohol abuse may be for less than 10 years. However, clinicians should consider anyone drinking more than 30-50 g/d for more than 5-10 years at risk of developing ALD.
Estimates of the amount of alcohol consumed may not be accurate since it is based on interviewing the patient and/or family members. The patient’s history reveals the type of alcohol intake and the amount consumed in volume or number of drinks. One drink is typically defined as 12 ounces (355 mL, 4%-5% weight by volume or w/v) of beer, 5 ounces (125 mL, 10%-12% w/v) of wine or 1.5 ounces (45 mL, 40%-50% w/v) of spirits.
Patterns of alcohol intake around the world are constantly evolving and have a strong bearing on the prevalence and incidence of ALD. In one study reporting data for adult per capita consumption of alcohol in the year 2000, spirits dominated the type of alcohol consumed in most regions of the world. The highest amount of alcohol per adult was reported in Europe, especially in Russia and surrounding countries, and the least was in the mostly Islamic regions of the Eastern Mediterranean and in the less developed region of Southeast Asia, predominantly India. The annual per capita change in alcohol consumption in various countries has a direct correlation to cirrhosis mortality rates. A Canadian study confirmed that per capita alcohol consumption is closely related to mortality rates from alcoholic cirrhosis in both men and women. In another analysis of 22 European countries, the relationship between an increase in liver disease and increase in per capita alcohol intake was shown for both men and women.
Population-based surveys indicate that 68% of adult Americans drink at least one alcoholic beverage per month. Traditionally, drinking is considered harmful if alcohol use impacts the daily functioning and/or social life of the individual such as loss of job, accident, loss of family member, or death. About 10% of the population consumes more than two drinks per day, which is a commonly used definition of “heavy drinking”. However, substantial differences exist in the prevalence of heavy drinking among population subgroups. For example, 18% of men but only 3% of women are classified as heavy drinkers. Further, heavy drinking is reported to be more common in Whites than in African Americans or Hispanics. Heavy alcohol consumption is generally more common in people with low educational level and income, the unemployed, and in those with occupations that are characterized by job alienation, job stress, and low job satisfaction.
Environmental and host factors
A dose-dependent relationship has been observed between self-reported alcohol intake and the risk of developing ALD. Although physicians should consider anyone drinking ≥ 30-50 g/d for more than 5-10 years at risk for developing ALD, the disease does not develop in everyone with this amount of alcohol consumption. About 90% to 100% of heavy drinkers have steatosis, 10% to 35% have AH, and 8% to 20% have alcoholic cirrhosis. The point prevalence of cirrhosis is 1% in persons drinking 30 to 60 g of alcohol a day and up to 5.7% in those consuming 120 g daily. Clearly, other factors related to environment or the host predispose an individual to the development of liver disease. These factors are:
Age: The typical age at presentation of AH is between 40 and 50 years, with the majority occurring before the age of 60 years[17,18].
Gender: The risk of developing alcohol-induced liver disease increases significantly from 7 to 13 beverages per week for women and from 14 to 27 beverages per week for men; the relative risk increases more steeply for women than for men with increasing alcohol intake. This gender difference is due to several factors such as differences in gastric alcohol, dehydrogenase (ADH) levels, and a higher proportion of body fat in women. Although women are at an increased risk of developing liver disease with alcohol intake, the majority of patients with AH are males because men are twice as likely to abuse alcohol compared to women.
Race and ethnicity: The rates of development of cirrhosis and mortality are higher in African Americans and Hispanics compared to Caucasians. This was reflected in an analysis of changes in national drinking patterns between 1984 and 1992, which showed longer and heavier drinking patterns in blacks and Hispanics compared to whites.
Obesity: The presence of long-standing obesity is an independent risk factor for liver disease and cirrhosis in alcoholics. Given the burgeoning problem of obesity in the developed world, it is likely that alcohol-related injury will increase. Obesity potentiates the severity of ALD in all its stages, including fatty liver, AH, and cirrhosis.
Protein Calorie Malnutrition: Most patients with AH are malnourished, and the risk of death is closely correlated with the degree of malnutrition. Mortality increases in direct proportion to the extent of malnutrition, approaching 80% in patients with severe malnutrition (i.e., less than 50% of normal nutritional intake). Micronutrient abnormalities, such as hepatic vitamin A depletion or depressed vitamin E levels, may also potentially aggravate liver disease. Parenteral and enteral feeding improves nutritional status but does not improve short-term survival.
Drinking patterns and type: The type of alcoholic beverage and the pattern of drinking also affect the development of liver disease. In one study from Denmark, the chances of getting liver disease were higher from drinking beer and spirits as compared to drinking wine. Drinking outside of meal times increases the risk of developing liver disease. Binge drinking defined as intake of ≥ 5 drinks at a time, another risk factor for AH, is reported in about 28% of adults with a history of alcohol abuse[31-33].
Hepatitis C virus: Concomitant alcohol abuse and hepatitis C virus (HCV) for various reasons, occur in about 14% of individuals with chronic liver disease. Alcohol and HCV act synergistically to increase the incidence of cirrhosis and HCC, more rapid progression to fibrosis and cirrhosis, and reduced survival compared to when either of these factors is present alone. Drinking more than 50 g/day of alcohol increases the relative risk of liver fibrosis in HCV patients 1.3-fold compared to HCV-infected non-drinkers and is associated with higher viremia. Worse clinical course with a higher mortality is also observed with AH in the presence of hepatitis C. A similar interaction has been postulated between chronic hepatitis B infection and alcohol, but the evidence is unclear.
Genetic factors: There is higher occurrence of alcoholism in adopted children of alcoholic parents and in monozygotic twins compared to dizygotic twins[38,39]. Polymorphisms of genes encoding for ADH and cytochrome P-450enzymes have been associated with higher occurrence of liver disease[40,41].