Alcohol is one of the oldest drugs known and it affects virtually every organ system in the body. The number of physiological systems affected by alcohol is staggering both in the scope of medical consequences and in terms of the economics of medical treatment of alcohol-related disorders. Alcohol damages the heart and can elevate blood pressure. It can increase the risk for heart failure and stroke. Excessive alcohol consumption can injure various tissues, produce diverse physiological changes, and impair and interfere with the hormonal and biochemical regulation of a variety of cellular and metabolic functions. Chronic alcohol exposure increases the risk for certain forms of cancer, and both acute and chronic alcohol use significantly increases the risk for accidental injuries and impairs the recovery from those injuries. However, not all of the medical consequences of alcohol use are deleterious. Substantial research indicates beneficial effects of this drug. Nonetheless, the economic and psychosocial costs of alcohol use in American society alone are estimated at more than $200 billion per year. This chapter will review the most significant and well-known medical consequences of alcohol use and abuse in four basic Read more [...]

Accidental injuries are a direct medical consequence of alcohol intoxication and it is well known that alcohol increases the risk for injuries through impairment of cognitive and psychomotor functioning while performing or engaging in a variety of behavioral activities. Among these, the effects of alcohol on automobile, bicycling, motorcycle, boating, aquatic and pedestrian injuries, as well as homicide, suicide, and death from fire have been examined. Impaired Driving Pedestrian and Fall-Down Injuries Although the relationship between alcohol intoxication and automobile accidents is by far the most well studied of alcohol-caused injuries, investigation of the role of alcohol intoxication in other types of injuries is growing. For example, pedestrian-like behaviors are also impaired by alcohol. Since driving and pedestrian activity rely on divided attention and visual-motor processes, it is reasonable to infer that they share similar alcohol-induced changes in relative risk. Injuries related to falls are the second leading cause of accidents in the United States, and account for about 13,000 deaths per year. Most studies suggest that alcohol increases the risk for injuries due to falls, but one study in particular Read more [...]

Driving while intoxicated is probably the most well-studied injurious consequence of drinking. Whereas the older scientific literature on drinking and driving focused on the effects of high blood alcohol levels on simple reaction time, on the visual system, and on gross impairment, it is now known that the effects of alcohol are much broader and occur at relatively low blood alcohol levels. For example, alcohol use is coupled with increased risk taking and impulsivity, at least among young males, and decreased seat belt use which invariably places drinkers at increased risk for injury. Moreover, whereas high blood alcohol levels (>.15 percent) may produce obvious visible impairment in the absence of any testing, it is now known that very low levels of alcohol (.02 to .03 percent) impair the performance of complex divided attention tasks, at least in laboratory studies. Divided attention is believed to be a critical factor in a variety of tasks outside the laboratory, and divided attention failure is the most likely cause of motor vehicle collisions at blood alcohol levels above .05 percent, for it is at this level that impairment translates into actual highway statistics (in which the intoxicated driver is the cause Read more [...]

Not only does alcohol intoxication produce direct medical consequences as a result of injuries (e.g., fractures, traumatic amputations, etc.) sustained in a motor vehicle crash, for example, it may also affect injury outcome, particularly head injuries. This is highly significant since up to half of traumatic brain-injured patients have blood alcohol concentrations of .10 percent or more at the time of injury. For example, motorcycle riders with head injuries are about twice as likely to have fatal head injuries if they are intoxicated than similarly injured riders who are sober, and contrary to popular misconception, drunk drivers are more likely to be seriously or fatally injured than sober drivers. Alcohol-intoxicated accident victims with central nervous system injuries were more than twice as likely to die sooner than anatomically matched controls. The mechanisms of the exacerbating effects of alcohol on central nervous system injuries are intriguing, but not well understood. Animal studies suggest that the mechanism may be due to the inhibition of free radical scavengers such as dimethyl sulfoxide, alcohol-induced cerebral edema as a result of lipid peroxidation, or increases in plasma osmolality. However, Read more [...]

Although it is not difficult to appreciate the positive and causal relationship between alcohol intoxication and skeletal fractures — one need only look at the large number of motor vehicle and slip-and-fall injuries involving alcohol intoxication — this relationship is more complex and certainly did not start with current epidemiological studies. In fact, the relationship between alcohol abuse and increased risks for skeletal fractures was observed by the ancient Egyptians. This relationship has since been confirmed by research that suggests alcoholics suffer from a generalized skeletal fragility and are prone to fracture. Alcohol-Induced Fractures Alcohol-Induced Osteoporosis In addition to the risk of falls and related injuries previously reviewed, some evidence suggests that alcoholics may also suffer from a generalized skeletal fragility. Bone density is a predictor of fractures and the term osteoporosis is synonymous with low bone density or osteopenia (NIAAA). Saville was the first to demonstrate the association of osteopenia with alcohol abuse. Studying the bone mass of cadavers, Saville found marked reductions in the bone mass of persons with a history of alcoholism and further noted that the bone mass Read more [...]

Current scientific research on the prevalence of fractures in alcoholic subjects is based on epidemiological studies. Those results are generally inconsistent, but there is some evidence of a positive association between alcohol intake and fracture occurrence. For example, men hospitalized for alcohol-related problems are four times more likely to have rib fractures than nondrinking patients and up to 14 times more likely to have spinal-crush fractures. In a prospective study, Tuppurainen et al. (1995) found alcohol intake higher among 3,140 perimenopausal women who experienced fractures than among those without fractures. Women who drank alcohol had a risk of a fracture that was about 50 percent higher than among women who did not drink. In another study, increased weekly alcohol intake was associated with greater risks for osteoporotic fractures in postmenopausal women. In the Paganini-Hill study, osteoporotic fractures in women who consumed more than eight drinks per week were almost twice as likely as in nondrinkers. Similarly, a survey of 84,500 U.S. women (ages 34 to 59) who consumed 25 grams of alcohol per day was associated with a 133 percent increase in risk for hip fractures and a 38 percent increase in Read more [...]

The normal growth of bone cells depends upon a variety of orchestrated factors, including adequate nutrition and the function and interaction of various hormones and intercellular regulating factors. Research in this area suggests that while the exact mechanism through which alcohol affects the integrity of the skeleton is not known, much has been learned. Even so, likely candidates have not been clearly identified. Chronic consumption of relatively low amounts of alcohol (one to two drinks per day for women; three to four drinks per day for men) can interfere with the normal metabolism of nutrients. As a result of poor diets, impaired nutrient absorption, or increased renal excretion, alcoholics often have deficiencies in minerals such as calcium, phosphate, and magnesium, as well as low levels of vitamin D, which is necessary for the absorption of calcium from the intestinal system. However, there is little histomorphometric evidence that nutritional deficiencies related to alcohol use are a major cause of alcohol-induced bone disease. Another candidate that may contribute to alcohol-induced bone disease is calcitonin, a peptide produced by the thyroid gland. Calcitonin inhibits bone resorption, in effect protecting Read more [...]

Gastrointestinal Diseases Not all of the effects of alcohol occur rapidly, as in the cases of motor vehicle crashes, pedestrian falls, and subsequent skeletal injuries. Some medical consequences of alcohol are more insidious, taking years to unfold before any significant medical consequence is detected. Among these are cell damage caused by the direct or indirect toxic effects of alcohol. The first tissue that alcohol comes into contact with is, in most instances, the upper gastrointestinal system. [The author has received anecdotal reports from clinicians and recovering alcoholics about intravenous and rectal administration of alcohol, but it is believed that such experimental drug use is rare] With the exception of minute quantities of alcohol that are directly absorbed through membranes in the buccal cavity and esophagus, when swallowed, alcohol goes directly to the stomach in high concentrations. Since the toxic effects of alcohol are directly related to dose and concentrations, one might reasonably predict that high concentrations of alcohol have potentially deleterious effects throughout the cells of the gastrointestinal system. Alcohol inhibits smooth muscle contractions in the lower esophagus, which may Read more [...]

As the majority of alcohol leaves the gastrointestinal tract, it travels via the hepatic portal vein from the small intestines to the liver, the largest organ in the body and the primary site of alcohol metabolism. Since some alcohol metabolites are toxic, and because the concentration of alcohol reaching the liver is so high and the liver is the primary site of alcohol metabolism, liver damage may be among the most likely and most serious physiological consequences of alcohol abuse. This is particularly significant because of the central role the liver plays in so many physiological activities. Epidemiolog-ical data clearly reveals that alcohol abuse is by far the leading cause of liver-related mortality in the United States. Excessive alcohol consumption leads to three serious types of liver injuries: fatty liver, hepatic inflammation (alcoholic hepatitis), and progressive liver scarring (fibrosis or cirrhosis). Chronic heavy drinking can alter normal metabolism and lead to an accumulation of fat in the liver. As a result, the liver cells become infiltrated and the liver itself becomes enlarged. The bad news is that extensive lipid infiltration may damage cells. The good news is that fatty liver is reversible with Read more [...]

The metabolism of alcohol by hepatocytes requires oxygen, a process that produces free radicals, such as hydroxyl and 1-hydroxyethyl radicals and superoxide anions. These highly reactive compounds can interact with proteins, lipids, and deoxyribonucleic acid to cause damage or death to liver cells. Chronic alcohol consumption also causes white blood cells (neutrophils) to migrate to the liver where they are activated by an inflammatory substance to release large amounts of superoxides which may contribute to liver pathology. Normal liver cells contain antioxidants that can neutralize free radicals. Chronic alcohol consumption decreases antioxidant levels in the liver resulting in a state of oxidative stress that makes liver cells more susceptible to free-radical-induced injury. One such antioxidant is glutathione, which is present at high concentrations in liver cytosol and mitochondria. Alcohol inhibits glutathione transport from the cytosol to the mitochondria of the cell, causing impaired mitochondrial functioning, which is believed to cause necrosis. Acetaldehyde is another highly reactive compound that may promote hepatic injury because high concentrations of this metabolite can become a substrate for aldehyde Read more [...]