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While excessive alcohol consumption has been linked to a number of serious health and social problems, moderate alcohol consumption has been associated with some important health benefits. The relationship between alcohol consumption and mortality is often described as J-shaped, meaning that when graphed from alcohol abstinence on the left to heavy drinking on the right, light to moderate consumption is associated with lower rates of mortality—mostly from cardiovascular disease—than abstention, while heavy alcohol consumption is associated with higher rates of mortality from a number of causes (3). Because the consumption of alcohol can be viewed as a “double-edged sword,” individual decisions regarding alcohol use should take into consideration scientific evidence regarding potential health benefits and risks as well as personal and family histories of health problems and addictions.
Standard alcoholic drink
A standard alcoholic drink contains approximately 14 grams of alcohol, which is equivalent to 12 fluid ounces of beer, 5 fluid ounces of wine, 3.5 fluid ounces of fortified wine (e.g., sherry or port), or 1.5 fluid ounces of liquor (distilled spirits).
Moderate Alcohol Consumption (as defined by the U.S. Department of Agriculture (5))
Heavy Alcohol Consumption
*In addition to weighing less, on average, women absorb and metabolize alcohol differently than men. In general, women have less body water than men of similar body weight, so women achieve higher blood alcohol concentrations after drinking equivalent amounts of alcohol (6). Women also appear to be more vulnerable to adverse health effects of heavy drinking than men. Thus, some definitions of "moderate" or “heavy” drinking offer a lower threshold for women.
#Age-associated decreases in lean body mass may result in decreased total body water and higher blood alcohol concentrations in older adults compared to younger adults after drinking equivalent amounts of alcohol (7).
Over the past three decades, the most consistent evidence of a health benefit associated with moderate alcohol consumption has been a significant reduction in the risk of coronary heart disease (CHD)—a finding confirmed by more than 60 epidemiological studies (8). When the results of 28 prospective cohort studies were combined in a meta-analysis, adults who consumed an average of 25 grams/day of alcohol (the amount in two standard alcoholic drinks) had a risk of CHD that was 20% lower than adults who did not consume alcohol (9). Recent data from two large prospective cohort studies conducted in the U.S. suggest that the magnitude of CHD risk reduction associated with moderate alcohol consumption may be closer to 30%. In a 12-year study of more than 38,000 male health professionals, those who consumed alcohol at least 3-4 times weekly had a risk of myocardial infarction (heart attack) that was 32% lower than men who drank alcohol less than once weekly (10). Similarly, in a 20-year study of more than 120,000 men and women, those who reported consuming 1-2 alcoholic drinks daily had a risk of death from CHD that was 30% lower than those who did not drink alcohol (11). Coronary heart disease is a major cause of heart failure. A prospective study in a cohort of 21,601 men and another in a cohort of 126,236 men and women found that moderate alcohol intake was inversely associated with heart failure, especially heart disease related to CHD (12, 13).
How does alcohol consumption reduce CHD risk? The development of CHD is characterized by the formation of cholesterol laden plaque in the arteries (atherosclerosis), vascular inflammation, and clot formation (14). Numerous small randomized trials have examined the effect of daily alcohol consumption on markers of CHD risk. One of the actions of high density lipoproteins (HDL) is to transport cholesterol from tissues, including arterial walls, back to the liver for elimination or recycling. Not surprisingly, higher levels of HDL-cholesterol are associated with reductions in CHD risk (15). Randomized trials have consistently demonstrated that moderate daily alcohol intake significantly increases HDL-cholesterol levels (16). Clot formation is the result of complex interactions between factors that promote coagulation and factors that inhibit coagulation or promote the dissolution of clots. Several randomized trials have found that moderate alcohol consumption decreases serum levels of a protein that promotes clot formation (fibrinogen) and increases levels of an enzyme that helps dissolve clots (tissue type plasminogen activator) (16). Moderate alcohol consumption may also have an anti-inflammatory effect since serum levels of C-reactive protein (CRP), a marker of systemic inflammation and sensitive predictor of CHD risk, are lower in people who drink moderately than those who abstain from alcohol (17-20). Further, moderate alcohol consumption has been associated with improved insulin sensitivity, lower serum triglycerides, and reductions in abdominal obesity (21).
Does the consumption of red wine reduce CHD risk more than other alcoholic beverages? Significant reductions in CHD risk have been associated with moderate consumption of wine, beer, and liquor. However, the “French Paradox”—the observation that mortality from CHD is relatively low in France despite relatively high levels of dietary saturated fat and cigarette smoking—led to the idea that regular consumption of red wine might provide additional protection from CHD (22, 23). Wine is rich in phenolic compounds like resveratrol that have been found to have antioxidant, anti-inflammatory, and other potentially anti-atherogenic properties in the test tube and in some animal models of atherosclerosis (24). However, it is not yet known whether increased consumption of the nonalcoholic compounds in red wine provides any additional protection from CHD beyond that associated with its alcohol content. The results of epidemiological studies addressing this question have been inconsistent. While some large prospective studies found that wine drinkers were at lower risk of CHD than beer or liquor drinkers (11, 25, 26), others found no difference (9, 27, 28). Socioeconomic and lifestyle differences between people who prefer wine and those who prefer beer or liquor may explain part of the additional benefit observed in some studies. Several studies have found that people who prefer wine tend to have higher incomes, have more formal education, smoke less, and eat more fruits and vegetables and less saturated fat than people who prefer other alcoholic beverages (29-31). Although moderate alcohol consumption has been consistently associated with 20-30% reductions in CHD risk, it is not yet clear whether nonalcoholic compounds abundant in red wine confer any additional CHD risk reduction. See articles on flavonoids and resveratrol for more information on polyphenolic compounds in red wine.
Ischemic strokes are the result of insufficient blood flow to an area of the brain, which may occur when an artery supplying the brain becomes blocked by a blood clot. Hemorrhagic strokes occur when a blood vessel ruptures and bleeds into the brain. Eighty-three percent of strokes are classified as ischemic strokes (32). Moderate alcohol consumption has been associated with a reduced risk of ischemic stroke but not hemorrhagic stroke in a number of observational studies (33-36). When the results of 19 prospective cohort studies and 16 case-control studies of alcohol consumption and the risk of stroke were combined in a meta-analysis, moderate alcohol consumption was associated with a significant reduction in the risk of ischemic stroke (37). Overall, those who consumed one or two drinks daily had a 28% lower risk of ischemic stroke than those who did not consume alcohol. Thus, moderate alcohol consumption decreases risk of ischemic stroke, but not hemorrhagic stroke, because alcohol consumption appears to inhibit clot formation.
Just as atherosclerosis of the arteries supplying the heart muscle leads to coronary heart disease, atherosclerosis of the arteries of the extremities leads to peripheral arterial disease. When atherosclerosis is severe enough to diminish blood flow to the legs, even walking may result in leg or hip pain known as intermittent claudication (38). Although much less consistent than the evidence for heart disease and stroke, there is limited evidence that moderate alcohol consumption is associated with decreased risk of peripheral arterial disease. Three large prospective studies have found moderate alcohol consumption to be associated with significant decreases in several different indicators of peripheral arterial disease (39-41). The most recent prospective study found that the inverse association between alcohol intake and peripheral arterial disease risk was significant in nonsmokers but not smokers, suggesting that the adverse effects of cigarette smoking on peripheral arterial disease risk may outweigh any protective effects of alcohol consumption (39).
A number of prospective cohort studies have found that adults with moderate alcohol intakes are at significantly lower risk of developing type 2 diabetes than adults who do not consume alcohol (42-50). In contrast, several prospective studies found heavy alcohol consumption to be associated with an increased risk of type 2 diabetes (42, 46-49, 51-53). A recent meta-analysis of 15 prospective cohort studies concluded that moderate alcohol consumption reduces risk of type 2 diabetes by about 30%, but heavy alcohol consumption does not offer protection against the disease (54). Increased insulin secretion by the pancreas and decreased insulin sensitivity are important factors leading to the development of type 2 diabetes. Recent research suggests that moderate alcohol intake may be associated with decreased serum insulin levels and improved insulin sensitivity (55-57). On the other hand, heavy alcohol consumption may increase the risk of type 2 diabetes by contributing to obesity, especially abdominal obesity, disturbing carbohydrate metabolism, and/or impairing pancreatic or liver function (52).
Although alcoholism is known to increase the risk of cognitive impairment and dementia, the effects of moderate alcohol consumption on cognitive function and the risk of dementia are less clear. While previous studies of alcohol intake and the risk of dementia have reported conflicting results (58, 59), two prospective studies that followed older adults without dementia for six years found that those who reported moderate alcohol intakes were significantly less likely to develop dementia than those who abstained from alcohol (60, 61). Compared to nondrinkers, a recent prospective study in 11,102 women participating in the Nurses' Health Study reported that moderate alcohol consumption was associated with improved cognitive function and less cognitive decline over a two-year period (62). Alzheimer’s disease is the most common cause of dementia in the U.S. and Europe, but vascular dementia (dementia due to insufficient cerebral blood flow) is also an important cause. Two epidemiological studies have used magnetic resonance imaging (MRI) to examine relationships between alcohol intake and subclinical abnormalities in the brains of older adults. Although one study found that infarctions (areas of dead tissue) were less frequent in the brains of those reporting moderate alcohol intakes compared to those who abstained from alcohol (63), another study found no relationship between alcohol intake and the presence of infarction (64). In contrast, measures of brain atrophy, a characteristic of Alzheimer’s disease and alcoholic dementia, were lowest in those who abstained from alcohol and increased with alcohol consumption in both studies (63, 64). Because of the complex nature of alcohol’s effects on the brain, further research is needed to determine the risks and benefits of moderate alcohol consumption with respect to cognitive function and dementia.
The majority of prospective cohort studies (65-69) and case-control studies (70, 71) have found that men and women with moderate alcohol intakes are at a significantly lower risk of gallstones or gallbladder surgery (cholecystectomy) than those who do not consume alcohol. Although the reasons for the consistent inverse association between alcohol consumption and gallstone risk are not entirely clear, regular alcohol intake may result in bile that is less likely to crystallize into gallstones or stimulate gallbladder emptying (68).
The majority of epidemiological studies have found that breast cancer risk increases with alcohol consumption (72). Regular alcohol consumption as low as one or two drinks/day has been associated with modest but significant increases in breast cancer risk. This dose-dependent relationship between alcohol consumption and breast cancer risk has been observed for premenopausal and postmenopausal breast cancer regardless of the type of alcoholic beverage consumed. An analysis that pooled the results of six prospective cohort studies found a linear relationship between alcohol consumption and breast cancer risk, such that each 10 gram (slightly less than one drink) increase in daily alcohol consumption was associated with a 9% increase in the risk of breast cancer (73). A more recent analysis of ten prospective cohort studies and 43 case-control studies concluded that each 10 gram increase in daily alcohol consumption was associated with a 7% increase in a woman’s risk of breast cancer (74). The most recently published meta-analysis found that each 10 gram increment of alcohol intake was associated with a 10% increase in breast cancer risk (75). Although the mechanisms for the consistent association between alcohol intake and breast cancer risk have not been clearly identified, increased circulating estrogen levels in women who consume even moderate amounts of alcohol are likely to play an important role (72, 76). Current estimates are that about one in eight women (13.3%) in the U.S. will develop breast cancer at some point in their lifetime (77). Although there are many risk factors for breast cancer, alcohol consumption is one of only a few modifiable risk factors.
Folate and breast cancer: Alcohol interferes with the absorption, transport, and metabolism of folate, which is required for DNA methylation and DNA repair (see Folic Acid). Alterations in these processes may result in mutations or altered gene expression, which increase the risk of cancer (72). Several studies have provided evidence that sufficient folate intake may modify the association between alcohol intake and breast cancer risk (78-81). A prospective study that followed more than 88,000 women for 16 years found that those who regularly consumed at least 15 grams/day of alcohol (slightly more than one drink/day) and also consumed at least 300 micrograms (mcg)/day of folate had a significantly lower risk of breast cancer than those who consumed the same amount of alcohol but consumed less than 300 mcg/day of folate (81). However, in a prospective cohort study of more than 66,000 postmenopausal women, folate intake was not associated with breast cancer risk across levels of alcohol consumption, but alcohol intake of at least 15 grams/day was associated with an increased risk of breast cancer (82). Although the interactions between folate, alcohol, and breast cancer risk remain to be clarified, the available evidence suggests that women who drink alcohol should take a daily multivitamin containing 400 mcg of folic acid.
Each year in the United States, an estimated 40,000 infants are born with problems related to fetal alcohol exposure (83). Fetal alcohol syndrome is a cluster of physical and mental birth defects associated with heavy alcohol consumption during pregnancy. Some of the problems associated with fetal alcohol syndrome include facial abnormalities, mental retardation, and poor growth. More moderate alcohol consumption during pregnancy (7-14 drinks/week) has been associated with more subtle effects on cognitive and behavioral development (84). Children of mothers who drank moderately during pregnancy have been found to have problems with memory, attention and learning, and behavior (85). Since no safe level of alcohol consumption has been established at any stage of pregnancy, pregnant women and women who are planning a pregnancy should abstain from alcohol (83).
Some people, such as recovering alcoholics and those with family histories of alcohol abuse or alcoholism, may not be able to maintain moderate drinking habits. Susceptibility to alcoholism is affected by genetic, psychosocial, and environmental factors. Children of an alcoholic parent have been found to be at significantly higher risk of developing alcoholism than those without an alcoholic parent (86). This increase in risk is likely related to interactions between genetic factors and factors related to the family environment. The National Institute on Alcohol Abuse and Alcoholism recommends that people with a family history of alcoholism, especially in a parent, approach moderate drinking carefully (87).
In the liver, alcohol is metabolized by the same enzymes as many medications. Therefore, alcohol consumption can affect the activation or breakdown of a number of medications. The consumption of alcohol may also increase sedation or drowsiness caused by numerous prescription and over-the-counter medications. Although serious interactions between alcohol and medications are more common in the presence of heavy alcohol consumption, even moderate alcohol consumption may hypothetically increase the risk of some adverse reactions in susceptible people (88). Women and older adults are particularly at risk for interactions between alcohol and medications (89). Many different classes of prescription medication may interact adversely with alcohol, including antibiotics, anticonvulsants, anticoagulants (Coumadin), antidepressants, antidiabetic agents, antihypertensive agents, barbiturates, benzodiazepines (sedatives), histamine H2-receptor blockers, muscle relaxants, and narcotic and non-narcotic pain relievers. Over-the-counter medications and herbal preparations may also interact with alcohol, including pain medications like aspirin, acetaminophen (Tylenol), ibuprofen (Advil, Motrin), and naproxen sodium (Aleve), cold and allergy medications like diphenhydramine (Benadryl) and chlorpheniramine, heartburn medications like cimetidine (Tagamet) and ranitidine (Zantac), and herbal preparations like chamomile, valerian, and kava. To help avoid potentially serious interactions between alcohol and medications, make sure your health care provider is aware of your alcohol intake. Before taking prescription or over-the-counter medications, read the product warning labels or consult a pharmacist or health care provider to determine whether alcohol consumption increases the risk of adverse effects. It may, in general, be advisable to separate taking any medication and drinking alcohol by 2-3 hours. For more information on potentially serious interactions between alcohol and medications, see the National Institute on Alcohol Abuse and Alcoholism Web site.
Heavy alcohol consumption has been consistently associated with an increased risk of high blood pressure (hypertension) in prospective and case-control studies (90, 91). The results of numerous clinical trials also indicate that reducing alcohol intake lowers blood pressure in hypertensive and normotensive individuals. A meta-analysis that combined the results of 15 randomized controlled trials found that reducing alcohol consumption resulted in significant decreases in systolic and diastolic blood pressure (92).
Ischemic strokes are the result of insufficient blood flow to an area of the brain, which may occur when an artery supplying the brain becomes blocked by a blood clot. Hemorrhagic strokes occur when a blood vessel ruptures and bleeds into the brain. Although moderate alcohol consumption has been associated with decreased risk of ischemic stroke, heavy alcohol consumption has been associated with increased risk of ischemic stroke and hemorrhagic stroke. A meta-analysis that combined the results of 19 prospective cohort studies and 16 case-control studies found that heavy drinking more than doubled the risk of hemorrhagic stroke and increased the risk of ischemic stroke by 70% (37). Heavy alcohol consumption may increase the risk of stroke by contributing to hypertension, cardiomyopathy (heart muscle damage), cardiac rhythm disturbances, and coagulation (clotting) disorders. The anti-thrombotic effects of alcohol might simultaneously decrease the risk of ischemic stroke while increasing the risk of hemorrhagic stroke.
The long-recognized association between bouts of heavy alcohol consumption and cardiac rhythm disturbances (arrhythmias) was called “holiday heart syndrome” because it was first described in people who were admitted to hospitals after holidays or weekends (93). Atrial fibrillation is the cardiac arrhythmia most commonly associated with heavy alcohol use (94, 95). Several studies have found heavy alcohol consumption (more than five drinks/day) increases the risk of sudden cardiac death (96, 97).
Alcoholic cardiomyopathy is a heart muscle disease caused by long-term heavy alcohol consumption (98). The disease occurs in two stages: an early asymptomatic stage, when the damage to the heart muscle has no obvious symptoms, and a symptomatic stage, when the heart muscle is too weak to pump effectively. Although the level of alcohol consumption resulting in alcoholic cardiomyopathy has not been clearly established, people consuming at least seven alcoholic drinks/day for more than five years are thought to be at risk of developing asymptomatic alcoholic cardiomyopathy. Those who continue to drink heavily ultimately develop heart failure. Research suggests that women may be more susceptible to alcohol’s toxic effects on the heart muscle than men (99, 100).
Chronic excessive alcohol use is a major cause of illness and death from liver disease in the United States (101). Heavy alcohol consumption is known to increase the risk of alcoholic hepatitis, a potentially fatal inflammation of the liver, as well as alcoholic cirrhosis, the most advanced form of alcoholic liver disease. In cirrhosis, the formation of fibrotic scar tissue results in progressive deterioration of liver function. Complications of advanced liver disease include severe bleeding from distended veins in the esophagus (esophageal varices), brain damage (hepatic encephalopathy), fluid accumulation in the abdomen (ascites), and kidney failure. A population-based study in Italy found that the risk of alcoholic liver disease began to rise in those who reported consuming more than 30 grams/day of alcohol (about 2.5 drinks/day) (102). Serious liver disease has been found to develop in approximately 10% of those who consume more than 60 grams/day of alcohol (5 drinks/day). However, women are more susceptible to serious alcoholic liver disease than men (103), as are individuals with hepatitis C infection (104).
Heavy alcohol consumption has been found to increase the risk of cancer at a number of sites (105). Heavy alcohol consumption is consistently and dose-dependently associated with increases in risk of cancers of the mouth, throat, larynx, esophagus, and breast. Moreover, the combination of smoking and alcohol results in even more dramatic increases in cancer risks (106). Long-term heavy alcohol consumption is associated with an increased risk of liver cancer, which may be related to alcoholic cirrhosis of the liver or increased susceptibility to cancer caused by viral hepatitis. Although less consistent, there is evidence that the risk of colorectal cancer is increased with heavy alcohol consumption, especially in the presence of inadequate folate intake (107-110).
Chronic heavy alcohol use and alcohol-dependence are associated with
detrimental effects on the brain and its function. Alcoholics have been
observed to suffer from cerebral atrophy (shrinkage of brain tissue),
which likely contributes to alcohol-associated dementia
and cognitive impairment (111).
In contrast to the progressive cerebral atrophy observed in Alzheimer’s
disease, alcohol-related cerebral atrophy may decrease after a period
of abstinence. Alcohol-related brain disorders may be associated with nutritional deficiencies, including thiamin (112)
or niacin (113).
Pancreatitis is a painful inflammation of the pancreas. Acute pancreatitis is characterized by the sudden onset of severe upper abdominal pain, often accompanied by nausea and vomiting (114). Although most attacks of acute pancreatitis require only supportive care, a small percentage of people may experience serious or life-threatening complications. About 30% of acute pancreatitis cases in the U.S. are alcohol-induced (115). Chronic pancreatitis results in progressive destruction of the pancreas leading to loss of pancreatic function (116). Approximately 70-90% of chronic pancreatitis cases in the U.S. and other developed countries are alcohol induced. The risk of developing chronic pancreatitis increases with the quantity and duration of alcohol consumption, although it is uncommon at alcohol intakes less than 80 g/day (seven drinks/day) for more than five years (115). Only a small percentage of heavy drinkers develop alcoholic pancreatitis; thus, hereditary and environmental factors are also thought to play a role. The disease is more common in men than in women, in blacks compared to whites, and in smokers versus nonsmokers (117).
Alcohol use is associated with an increased risk of injury in a number of circumstances, including motor vehicle accidents, falls, and fires (118). Data from hospital emergency departments indicate that consuming as little as one or two alcoholic drinks in the previous six hours significantly increases the risk of injury (119). Forty-one percent of all traffic fatalities in the U.S. are alcohol-related (120). Although the legal blood alcohol concentration (BAC) limit for drivers ranges from 0.08-0.10 in the U.S., most scientific studies found significant impairment of driving-related skills at a BAC of 0.05 (121). For reference, a BAC of 0.05 might be achieved by a 175-pound male consuming three standard alcoholic drinks in one hour or a 120-pound female consuming two drinks in one hour (122). Excessive alcohol use is associated with all forms of violence, including suicide, homicide, domestic violence, sexual assault, and gang violence. Although the reasons for alcohol-associated violence are complex, alcohol use appears to increase the risk of violent behavior in some populations (123).
Written in January 2004 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in December 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in December 2007 by:
Arthur L. Klatsky, M.D.
Senior Consultant in Cardiology
Adjunct Investigator, Division of Research
Kaiser Permanente Medical Care Program
Copyright 2004-2014 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, foods, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
The information on dietary factors and supplements, foods, and beverages contained on this Web site does not cover all possible uses, actions, precautions, side effects, and interactions. It is not intended as nutritional or medical advice for individual problems. Liability for individual actions or omissions based upon the contents of this site is expressly disclaimed.
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