MyMedExpert Health Articles

What can you do to decrease your risk for developing cancer of the colon or rectum?

While everyone can benefit from regular screening, if you have a family history of colorectal cancer or another bowel disorder, you should be even more diligent. Ask your doctor how often you should be screened and which colorectal tests you should undergo. In the meantime, there are other things you can do.

DIET: Diet plays a large role in colorectal cancers. Migrants to the United States from Japan and other countries where rates of colorectal cancer are lower than in the U.S. have higher rates of colorectal cancers than do those who remain in their native country. Children of these migrants develop colorectal cancers at rates equal to or even higher than those of the United States white population. Studies have shown that people who eat a lot of well-done, fried, or barbequed meats have an increased risk of developing colorectal cancer. For prevention, NCI encourages people to eat five or more servings of vegetables and fruits each day as part of a low-fat, high-fiber diet and to follow the Dietary Guidelines for Americans.

EXERCISE: Two words: Get moving. Exercise may lower a person’s risk for colorectal cancer, NIDDK experts contend, because it speeds the amount of time it takes for wastes to leave your body.

SMOKING: Do all you can to quit. In addition to smoking’s well-established link to cancers of the lung and head and neck, long-term smoking that begins before age 30 also increases the risk of developing colorectal cancer as well as precancerous polyps.

ALCOHOL: Excessive alcohol consumption — drinking two or more alcoholic drinks a night — has been associated with an increased prevalence of rectal cancer.

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The term “stress” often is used to describe the subjective feeling of pressure or tension. However, when scientists refer to stress, they mean the many objective physiological processes that are initiated in response to a stressor. As this Alcohol Alert explains, the stress response is a complex process; the association between drinking and stress is more complicated still. Because both drinking behavior and an individual’s response to stress are determined by multiple genetic and environmental factors (1-3), studying the link between alcohol consumption and stress may further our understanding of drinking behavior.

The Stress Response

The maintenance of the body’s relatively steady internal state, or homeostasis, is essential for survival. The body’s delicate balance of biochemical and physiological function is constantly challenged by a wide variety of stressors, including illness, injury, and exposure to extreme temperatures; by psychological factors, such as depression and fear; and by sexual activity and some forms of novelty-seeking. In response to stress, or even perceived stress, the body mobilizes an extensive array of physiological and behavioral changes in a process of continual adaptation, with the goal of maintaining homeostasis and coping with the stress (4).

The stress response is a highly complex, integrated network involving the central nervous system, the adrenal system, and the cardiovascular system. When homeostasis is threatened, the hypothalamus gland, at the base of the brain, initiates the stress response by secreting corticotropin releasing factor (CRF). CRF coordinates the stress response by triggering an integrated series of physiological and behavioral reactions. CRF is transported in blood within the brain and in seconds triggers the pituitary gland to release adrenocorticotropin hormone (ACTH), also referred to as corticotropin. ACTH then triggers secretion of glucocorticoid hormones (i.e., “steroids”) by the adrenal glands, located at the top of the kidneys. Glucocorticoid hormones play a key role in the stress response and its termination (4).

Activation of the stress response affects smooth muscle, fat, the gastrointestinal tract, the kidneys, and many other organs and the body functions that they control (4). The stress response affects the body’s regulation of temperature; appetite and satiety; arousal, vigilance, and attention; mood; and more (4). Physical adaptation to stress allows the body to redirect oxygen and nutrients to the stressed body site, where they are needed most (4).

Both the perception of what is stressful and the physiological response to stress vary considerably among individuals. These differences are based on genetic factors and environmental influences that can be traced back to infancy (5).

Stress is usually thought of as harmful; but when the stress response is acute and transient, homeostasis is maintained and no adverse effects result. Under chronic stress, however, when the body either fails to compensate or when it overcompensates, damage can occur (4). Such damage may include suppression of growth, immune system dysfunction, and cell damage resulting in impaired learning and memory (4,6).

Does Stress Influence Drinking?

Human research to clarify the connection between alcohol and stress usually has been conducted using either population surveys based on subject self-reports or experimental studies. In many but not all of these studies, individuals report that they drink in response to stress and do so for a variety of reasons. Studies indicate that people drink as a means of coping with economic stress, job stress, and marital problems, often in the absence of social support, and that the more severe and chronic the stressor, the greater the alcohol consumption (7). However, whether an individual will drink in response to stress appears to depend on many factors, including possible genetic determinants of drinking in response to stress, an individual’s usual drinking behavior, one’s expectations regarding the effect of alcohol on stress, the intensity and type of stressor, the individual’s sense of control over the stressor, the range of one’s responses to cope with the perceived stress, and the availability of social support to buffer the effects of stress (1,2,7,8). Some researchers have found that high levels of stress may influence drinking when alternative resources are lacking, when alcohol is accessible, and when the individual believes that alcohol will help to reduce the stress (1,8).

Numerous studies have found that stress increases alcohol consumption in animals (9) and that individual animals may differ in the amount of alcohol they consume in response to stress (10). Such differences may be related in part to an animal’s experiencing chronic stress early in life: Prolonged stress in infancy may permanently alter the hormonal stress response and subsequent reactions to new stressors, including alcohol consumption (10,11). For example, monkeys who were reared by peers, a circumstance regarded as a stressor compared to mother-rearing, consumed twice as much alcohol as monkeys who were mother-reared (10). According to Viau and colleagues (11), adult rats handled for the first 3 weeks of life demonstrate markedly reduced hormonal responses to a variety of stressors compared with rats not handled during this time (11). In humans, Cloninger reported an association between certain types of alcoholism and adverse early childhood experiences (12).

Animal studies reporting a positive correlation between stress and alcohol consumption suggest that drinking may take place in response to chronic stress perceived as unavoidable (2,13). For instance, rats chronically exposed to unavoidable shock learn to be helpless or passive when faced with any new stressor–including shock that is avoidable–and to demonstrate increased alcohol preference compared with rats that received only avoidable shock (2). The rats exposed to unavoidable shock exhibit the hormonal changes indicative of the stress response, including increased levels of corticosteroid hormones (2).

Whether humans drink in response to uncontrollable stress is less clear, according to Pohorecky (7). In a review investigating the connection between alcohol consumption and stress, Pohorecky notes several studies in which researchers sampled individuals from areas affected by natural disaster. One study found that alcohol consumption increased by 30 percent in the 2 years following a flood at Buffalo Creek, West Virginia. Similarly, there was evidence of increased drinking in the towns surrounding Mount St. Helens following eruption of the volcano (7). Following the nuclear plant accident at Three Mile Island, however, alcohol consumption was infrequently used by those sampled as a means of coping with the resulting stress (14).

In both humans and animals, drinking appears to follow stress (2,3,7,13). Some human research, however, shows that drinking may take place in anticipation of or during times of stress (15).

Does Drinking Reduce or Induce Stress?

Some studies have reported that acute exposure to low doses of alcohol may reduce the response to a stressor in animals and humans. For example, low doses of alcohol reduced the stress response in rats subjected to strenuous activity in a running wheel (3). In humans, a low dose of alcohol improved performance of a complex mental problem-solving task under stressful conditions (3). However , in some individuals, at certain doses, alcohol may induce rather than reduce the body’s stress response (16).

Much research demonstrates that alcohol actually induces the stress response by stimulating hormone release by the hypothalamus, pituitary, and adrenal glands (4,6,17,18). This finding has been demonstrated in animal studies. In one study with rats, the administration of alcohol initiated the physiological stress response, measured by increased levels of corticosterone (19). In addition to stimulating the hormonal stress response, chronic exposure to alcohol also results in an increase in adrenaline (20).

Stress, Alcoholism, and Relapse

Stress may be linked to social drinking, and the physiological response to stress is different in actively drinking alcoholics compared with nonalcoholics (17). Researchers have found that animals preferring alcohol over water have a different physiological response to stress than animals that do not prefer alcohol (21). Nonetheless, a clear association between stress, drinking behavior, and the development of alcoholism in humans has yet to be established.

There may, however, in the already established alcoholic, be a clearer connection between stress and relapse: Among abstinent alcoholics, personally threatening, severe, and chronic life stressors may lead to alcohol relapse (15,22). Brown and colleagues (15) studied a group of men who completed inpatient alcoholism treatment and later experienced severe and prolonged psychosocial stress prior to and independent of any alcohol use. The researchers found that subjects who relapsed experienced twice as much severe and prolonged stress before their return to drinking as those who remained abstinent. In this study, severe psychosocial stress was related to relapse in alcoholic males who expected alcohol to reduce their stress. Those most vulnerable to stress-related relapse scored low on measures of coping skills, self-efficacy, and social support. Stress-related relapse was greatest among those who had less confidence in their ability to resist drinking and among those who relied on drinkers for social support. Although many factors can influence a return to drinking, Brown and colleagues note that stress may exert its greatest influence on the initial consumption of alcohol after a period of abstinence (15).

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People with alcohol use disorders are more likely than the general population to contract HIV (human immunodeficiency virus).¹ Similarly, people with HIV are more likely to abuse alcohol at some time during their lives (1). Alcohol use is associated with high-risk sexual behaviors and injection drug use, two major modes of HIV transmission. Concerns about HIV have increased as recent trends suggest a resurgence of the epidemic among men who have sex with men² (2), as well as dramatic increases in the proportion of cases transmitted heterosexually (3,4). In persons already infected, the combination of heavy drinking and HIV has been associated with increased medical and psychiatric complications, delays in seeking treatment (5), difficulties with HIV medication compliance (6,7), and poorer HIV treatment outcomes (8). Decreasing alcohol use in people who have HIV or who are at risk for becoming infected reduces the spread of HIV and the diseases associated with it.

This Alcohol Alert briefly examines the changing patterns of HIV transmission in the United States; the role of alcohol in the transmission of HIV within, and potentially beyond, high-risk populations; the potential influence of alcohol abuse on the progression and treatment of HIV-related illness; and the benefits of making alcoholism treatment an integral part of HIV prevention programs.

Trends in HIV Transmission in the United States

HIV is most commonly transmitted by sexual contact and the sharing of contaminated needles by injection drug users (9). By the end of 2000, an estimated 900,000 Americans were living with HIV. Approximately 40,000 new cases of active AIDS disease are diagnosed annually (3). Historically, HIV has been most prevalent among men who have sex with men (10) whereas most new HIV infections are reported among men who have sex with men and among injection drug users (3). Recently, however, the proportion of HIV cases acquired through heterosexual contact has increased and almost equals the proportion of cases attributable to injection drug use (3,4). The proportion of all AIDS cases reported among women has tripled since the mid-1980s, primarily as a result of heterosexual exposure and secondarily through injection drug use (4). Minority groups are the most heavily affected by HIV associated with drug injection, and Blacks and Hispanics now account for an estimated 70 percent of all new AIDS cases (3,4).

Alcohol and HIV Transmission

People who abuse alcohol are more likely to engage in behaviors that place them at risk for contracting HIV. For example, rates of injection drug use are high among alcoholics in treatment (11,12), and increasing levels of alcohol ingestion are associated with greater injection drug-related risk behaviors, including needle sharing (13).

A history of heavy alcohol use has been correlated with a lifetime tendency toward high-risk sexual behaviors, including multiple sex partners, unprotected intercourse, sex with high-risk partners (e.g., injection drug users, prostitutes), and the exchange of sex for money or drugs (11,14-16). There may be many reasons for this association. For example, alcohol can act directly on the brain to reduce inhibitions and diminish risk perception (17-19). However, expectations about alcohol’s effects may exert a more powerful influence on alcohol-involved sexual behavior. Studies consistently demonstrate that people who strongly believe that alcohol enhances sexual arousal and performance are more likely to practice risky sex after drinking (19-22).

Some people report deliberately using alcohol during sexual encounters to provide an excuse for socially unacceptable behavior or to reduce their conscious awareness of risk (20). According to McKirnan and colleagues (23), this practice may be especially common among men who have sex with men. This finding is consistent with the observation that men who drink prior to or during homosexual contact are more likely than heterosexuals to engage in high-risk sexual practices (14,24-26).

Finally, the association between drinking levels and high-risk sexual behavior does not imply that alcohol necessarily plays a direct role in such behavior (18) or that it causes high-risk behavior on every occasion (19-22). For example, bars and drinking parties serve as convenient social settings for meeting potential sexual partners (25,27). In addition, alcohol abuse occurs frequently among people whose lifestyle or personality predisposes them to high-risk behaviors in general (14,28,29).

Alcohol and Medical Aspects of AIDS

Alcohol increases susceptibility to some infections that can occur as complications of AIDS. Infections associated with both alcohol and AIDS include tuberculosis; pneumonia caused by the bacterium Streptococcus pneumoniae; and the viral disease hepatitis C, a leading cause of death among people with HIV (9,30). Alcohol may also increase the severity of AIDS-related brain damage, which is characterized in its severest form by profound dementia and a high death rate (9,31).

The progression of HIV and the development of AIDS-associated infections may be controlled by highly active antiretroviral therapy (HAART), a combination of powerful antiviral medications. Despite markedly increased survival rates (9), HAART is associated with several disadvantages, including the emergence of medication-resistant HIV strains and the occurrence of adverse interactions with other medications, some of which are prescribed for AIDS-related infections (32). In addition, many patients fail to comply with the complex medication regimen (2,33). Studies have associated heavy alcohol use with decreased medication compliance (7,8) as well as with poorer response to HIV therapy in general (8). The outcome of HIV therapy improved significantly among alcoholics who stopped drinking (8).

Alcoholism Treatment as HIV Prevention

Studies show that decreasing alcohol use among HIV patients not only reduces the medical and psychiatric consequences associated with alcohol consumption but also decreases other drug use and HIV transmission (8). Thus, alcohol and other drug abuse treatment can be considered primary HIV prevention as well (12). For example, Avins and colleagues (34) found a 58 percent reduction in injection drug use, with similar decreases in high-risk sexual behaviors, among heterosexual patients one year after treatment. Participants who remained abstinent showed substantially greater improvement in both outcomes compared with those who continued to drink (34).

Boscarino and colleagues (15) suggest that for heterosexual alcoholics, the focus of screening and prevention for HIV risk factors should be on people with more severe alcohol dependence. For male alcoholics who have sex with men, the focus should be on those who socialize primarily in bars (15).

Alcoholism prevention among youth is of particular importance. AIDS is a leading cause of death among people ages 15 to 24 (16), and new injection drug users who contract HIV or viral hepatitis often become infected within 2 years after beginning to inject drugs (35). Researchers have found that:

• the prevalence of current, binge, and heavy drinking peaks between the ages of 18 and 24 (36), which is a high-risk period for initiating injection drug use (37);
• drug injection is usually associated with prior use of alcohol in conjunction with non-injection drugs (38), especially among adolescents with alcohol use disorders (37); and
• high rates of risky sexual practices have been reported among adolescents (39) and may be correlated with alcohol consumption (16).

Therefore, it has been suggested that HIV prevention programs for youth should target alcohol consumption in addition to injection drug use and sexual risk reduction (35).

Treatment Access and Integration

Analyses of HIV surveillance data collected by the national Centers for Disease Control and Prevention (3,40), urban and rural health departments (40), and health maintenance organizations (40) revealed that Blacks, Hispanics, women, the chronically mentally ill, and the poor are less likely to obtain appropriate HIV therapy compared with the general population (3). HIV-infected people in rural areas report reduced access to medical and mental health care services relative to their urban counterparts (41).

Timeliness is an essential aspect of effective HIV treatment and prevention. Early detection of HIV infection facilitates the prompt initiation of behavioral changes aimed at reducing transmission and also may enhance treatment effectiveness (42). Unfortunately, many facilities for the treatment of alcohol or other drug use disorders do not routinely or consistently screen their patients for HIV (42). In addition, many people who test positive for HIV fail to seek medical care until the disease has reached an advanced stage (5). Alcohol abuse has been associated with longer delays in seeking treatment (5).

Some evidence suggests that such problems may be ameliorated in part by designing programs that link primary medical care with treatment for abuse of alcohol and other drugs, HIV risk-reduction education, and psychiatric care when appropriate (43,44). In drug treatment programs, for example, both patients and clinicians may focus on what is perceived as the main problem (typically heroin or cocaine use), and neglect or minimize the use of other drugs, including alcohol (45). Yet in one study, a large proportion of patients in a residential drug treatment program reported daily consumption of large quantities of alcohol (45).

In a randomized controlled trial, Samet and colleagues demonstrated the feasibility of incorporating a multidisciplinary medical clinic within a detoxification unit designed to treat alcohol, heroin, and cocaine dependence (46). Because the integration of different services at a single site can be expensive, the researchers recommended that efforts be made to facilitate information transfer or patient transportation among programs based at multiple locations (46).

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Heart attacks and other forms of coronary heart disease (CHD) result in approximately 500,000 deaths annually (1), accounting for 25 percent of the Nation’s total mortality (2). Research has revealed an association between moderate alcohol consumption¹ and lower risk for CHD. This Alcohol Alert reviews epidemiologic evidence for this association, explores lifestyle factors and physiological mechanisms that might suggest ways to explain alcohol’s apparent protective effects, and presents available data on the balance between alcohol’s beneficial and harmful effects on health.

Epidemiologic Evidence

With few exceptions, epidemiologic data from at least 20 countries in North America, Europe, Asia, and Australia demonstrate a 20- to 40-percent lower CHD incidence among drinkers compared with nondrinkers (3,4). Moderate drinkers exhibit lower rates of CHD-related mortality than both heavy drinkers and abstainers (3,4). Such studies range from comparisons of nationwide population data to retrospective analyses of health and drinking patterns within communities.

The most persuasive epidemiologic evidence for alcohol’s possible protective effects on CHD comes from prospective studies, in which participants provide information on their drinking habits and health-related practices before the onset of disease. Participants’ subsequent health histories are evaluated through a series of followup interviews. Large-scale prospective investigations confirm an association between moderate drinking and lower CHD risk. The specific studies described here represent a total population of more than 1 million men and women of different ethnicities. Followup periods average 11 years,² the longest being the 24-year prospective phase of the Framingham CHD mortality study (5). The two largest of these studies were conducted by the American Cancer Society, one including 276,800 men (6) and the other including 490,000 men and women (7).

Other large prospective investigations that associate moderate drinking with lower risk for CHD include a series of studies by Kaiser-Permanente analyzing CHD hospitalization (8,9) and death rates (10,11) in both men and women; studies of CHD incidence (12) and mortality (13) among female nurses; and studies of CHD incidence (14,15) and mortality (16) among male physicians. Results of these American studies are confirmed by data from similar investigations conducted in England (17), Denmark (18), China (19), and other countries (1,4). In addition, a smaller 12-year study found an association between moderate drinking and lower risk of CHD-related death among older persons (average age of 69) with late-onset diabetes, a population at high risk for CHD (20). However, a recent 21-year prospective study from Scotland found no association between moderate drinking and lower risk for CHD among 6,000 working men ages 35 to 64 (21).

Is Alcohol’s Role Causal or Incidental?

An association between moderate drinking and lower risk for CHD does not necessarily mean that alcohol itself is the cause of the lower risk. For example, a review of population studies indicates that the higher mortality risk among abstainers may be attributable to shared traits other than participants’ nonuse of alcohol (22). Substantial evidence (1) has discounted speculation that abstainers include a large proportion of former heavy drinkers with pre-existing health problems (i.e., “sick quitters”). Nevertheless, health-related lifestyle factors that correlate consistently with drinking level could account for some of the association between alcohol and lower risk for CHD (4). Among the most widely studied of these factors are exercise and diet.

Few studies have adjusted for subjects’ levels of physical activity, despite evidence that exercise protects against CHD occurrence and mortality. In a comprehensive review of published studies, Berlin and Colditz (23) concluded that risk for CHD was proportionately lower at higher exercise levels. Measures of activity level vary among studies. Studies evaluate factors such as job-related physical requirements, frequency of participation in unspecified sports, estimated vigorousness of given activities, calculations of energy expended, and tests of cardiovascular fitness (23). Results of a community survey indicated that the prevalence of regular exercise was higher among moderate and heavy drinkers than among nondrinkers (24). Regular exercise was defined as any form of nonoccupational physical activity performed at least three times per week. The role of exercise in the alcohol-CHD association requires additional study.

Diet is one of the strongest influences on CHD-related death among men ages 50 to 70 (25). International comparisons, laboratory data, and prospective studies suggest that diets high in saturated fat and cholesterol increase the risk for CHD (26). Epidemiologic data suggest that moderate drinkers may consume less fat and cholesterol than heavier drinkers (14) and abstainers (27), potentially accounting for a portion of the lower CHD risk associated with alcohol. However, results of other prospective studies indicate that alcohol’s association with lower CHD risk is independent of nutritional factors (12-14).

The Role of Beverage Choice

Some studies report that wine (particularly red wine) affords more CHD protection than beer or liquor at equivalent levels of alcohol consumption (28). This finding suggests that the association between alcohol consumption and CHD risk may result from the effects of beverage ingredients other than alcohol itself. Epidemiologic and laboratory studies investigating this hypothesis have produced conflicting results.

A comparison of data from 21 developed countries concluded that wine consumption was more strongly correlated with lower CHD risk than was consumption of other alcoholic beverages (29). However, large-scale prospective studies have not found any difference in the incidence of CHD associated with beverage type (1,9). Red wine has been shown to contain certain nonalcoholic ingredients that could hypothetically interfere with the progression of CHD (30). However, research has not yet demonstrated a significant role for these chemicals in arresting CHD development in humans (30,31).

Evidence suggests that a preference for wine over other alcoholic beverages is associated with a lifestyle that includes other favorable health-related practices. For example, drinkers who prefer wine tend to smoke less and drink less (10,11,32) and have a more healthful diet (33) than those who prefer beer or liquor.

How Might Alcohol Lower Risk for CHD?

To function normally, the muscle tissue that constitutes the bulk of the heart requires a constant supply of oxygen-containing blood. Blood is delivered to the heart muscle through the coronary arteries. Cholesterol and other fatty substances can accumulate within the coronary arteries, partially impeding the flow of blood. This condition underlies the clinical manifestations of CHD, which may range from episodic chest pain to sudden death. The most common serious manifestation of CHD is the heart attack. Heart attacks are generally triggered by the formation of a blood clot within a constricted coronary artery, obstructing blood flow and depriving a portion of the heart muscle of oxygen. The resulting impairment of the heart’s pumping ability may cause permanent disability or death, either immediately or through the progressive development of medical complications (2).

Researchers have investigated several theories to explain how alcohol itself might lower risk for CHD. For example, alcohol may protect the heart by preventing the constriction of the coronary arteries, inhibiting clot formation, and enhancing recovery following a heart attack. Most of the evidence supporting these potential mechanisms is derived from experiments using animals or cells isolated from artery walls and grown in the laboratory. Controlled clinical experiments are needed to confirm that the effects observed in such studies can alter the development or progression of CHD in humans.

Results of laboratory research indicate that alcohol administration may help prevent arterial narrowing in mice (34). Such an effect could stem from changes in the blood concentrations of certain fatty substances that influence the deposition of cholesterol within the coronary arteries (35). However, human (36) and animal (34,37) studies indicate that less than one-half of the lower risk for CHD associated with alcohol consumption can be explained by altered blood levels of these fatty substances. Therefore, researchers are investigating additional explanations for alcohol’s apparent protective effects.

Alcohol may help prevent clot formation within already narrowed coronary arteries. Clotting occurs partly in response to chemicals released into the blood from the arterial wall. Exposure of these cells to alcohol in the laboratory suppresses the production of substances that promote clotting and stimulates the production and activity of substances that inhibit clotting (38). In addition, analyses of blood samples drawn from human volunteers indicate that alcohol consumption increases blood levels of anticlotting factors (39,40) and decreases the “stickiness” of the specialized blood cells (i.e., platelets) that clump together to form clots (41).

Results of laboratory research suggest that alcohol might help protect against reperfusion injury, a form of damage caused by the sudden restoration of blood flow to heart muscle weakened by previous oxygen deprivation. Alcohol’s effects on reperfusion injury have been studied in guinea pigs (42) and rats (43), but not in humans. Heavy alcohol consumption by humans can cause rapid and irregular heartbeat and can impair the heart’s pumping ability (41), two of the major causes of death following a heart attack (44). Alcohol may also interact harmfully with medications prescribed to treat heart diseases (45). Thus, although alcohol may help protect against CHD, drinking may increase the risk of adverse health effects after a heart attack (46).

Risks and Benefits

The apparent benefits of moderate drinking on CHD mortality are offset at higher drinking levels by increasing risk of death from other types of heart disease (5,16,32); cancer; liver cirrhosis; and trauma, including trauma from traffic crashes (47). Moderate drinking is not risk free. The trade-offs between risks and benefits can be exemplified by the fact that alcohol’s anticlotting ability, potentially protective against heart attack, may increase the risk of hemorrhagic stroke, or bleeding within the brain (12).

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Cancer kills an estimated 526,000 Americans yearly, second only to heart disease (1). Cancers of the lung, large bowel, and breast are the most common in the United States. Considerable evidence suggests a connection between heavy alcohol consumption and increased risk for cancer, with an estimated 2 to 4 percent of all cancer cases thought to be caused either directly or indirectly by alcohol (2).

A strong association exists between alcohol use and cancers of the esophagus, pharynx, and mouth, whereas a more controversial association links alcohol with liver, breast, and colorectal cancers. Together, these cancers kill more than 125,000 people annually in the United States (1). The following sections discuss alcohol’s role in these cancers.

What Is Cancer?

Cancer is a group of diseases characterized by cells that grow out of control; in many cases, they form masses of cells, or tumors, that infiltrate, crowd out, and destroy normal tissue. Although the body strictly regulates normal cells to grow within the confines of tissues, cancer cells reproduce independently, uninhibited by tissue boundaries. Cancer develops in three stages: initiation, promotion, and progression. Cancer-causing agents, known as carcinogens, can contribute to the first two stages.

Cancer initiation occurs when a cell’s DNA (the substance that genes are made of) is irreversibly changed so that, once triggered to divide, the cell will reproduce indefinitely. The “change” involves mutations to the cell’s genes that can occur spontaneously or can be induced by a carcinogen. In some cancers, it has been shown that the mutations occur in oncogenes, genes that normally promote cell division, or in suppressor genes, genes that normally suppress cell division. Thus, it is believed that cancer-causing mutations result in overpromotion or undersuppression of cell reproduction. During cancer promotion, the initiated cell is stimulated to divide. The stimulus can be natural, as when tissue damage requires proliferation of new cells, or it can be caused by a carcinogen. During cancer progression, tumors produced by the replicating mass of cells metastasize, or spread, from the initial or primary tumor to other parts of the body, forming secondary
cancers.

Alcohol’s Link to Cancer

Two types of research link alcohol and cancer. Epidemiologic research has shown a dose-dependent association between alcohol consumption and certain types of cancer; as alcohol consumption increases, so does risk of developing certain cancers. More tenuous results have come from research into the mechanism by which alcohol could contribute to cancer development.

Epidemiologic Research

The strongest link between alcohol and cancer involves cancers of the upper digestive tract, including the esophagus, the mouth, the pharynx, and the larynx (3). Less consistent data link alcohol consumption and cancers of the liver, breast, and colon (3).

Upper digestive tract. Chronic heavy drinkers have a higher incidence of esophageal cancer than does the general population. The risk appears to increase as alcohol consumption increases (4-6). An estimated 75 percent of esophageal cancers in the United States are attributable to chronic, excessive alcohol consumption (7).

Nearly 50 percent of cancers of the mouth, pharynx, and larynx are associated with heavy drinking (7). People who drink large quantities of alcohol over time have an increased risk of these cancers as compared with abstainers (8,9). If they drink and smok e, the increase in risk is even more dramatic (5,6).

Liver. Prolonged, heavy drinking has been associated in many cases with primary liver cancer. However, it is liver cirrhosis, whether caused by alcohol or another factor, that is thought to induce the cancer (10,11). In areas of Africa and Asia, liver cancer afflicts 50 or more people per 100,000 per year, usually associated with cirrhosis caused by hepatitis viruses. In the United States, liver cancer is relatively uncommon, afflicting approximately 2 people per 100,000, but excessive alcohol consumption is linked to as many as 36 percent of these cases by some investigators (2,12).

The association between alcohol use and liver cancer is difficult to interpret, because liver cirrhosis and hepatitis B and C virus infections often confound data (13). Studies of the interactions between alcohol, hepatitis viruses, and cirrhosis will help clarify these associations with liver cancer (see below).

Breast. Chronic alcohol consumption has been associated with a small (averaging 10 percent) increase in a woman’s risk of breast cancer (14-17). According to these studies, the risk appears to increase as the quantity and duration of alcohol consumption increases. Other studies, however, have found no evidence of such a link (18-20).

The inconsistency and weakness of epidemiologic findings suggest that a third confounding factor, such as nutrition, may be responsible for the link between alcohol and breast
cancer (15). However, studies that adjusted for dietary factors such as fat intake found that the association between alcohol and breast cancer remained (14,21,22).

Recent studies suggest that alcohol may play an indirect role in the development of breast cancer. These studies indicate that alcohol increases estrogen levels in premenopausal women, which, in turn, may promote breast cancer (23).

Colon. Epidemiologic studies have found a small but consistent dose-dependent association between alcohol consumption and colorectal cancer (15,24), even when controlling for fiber and other dietary factors (15,25,26). Despite the large number of studies, however, causality cannot be determined from the available data.

Other cancers. A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs (3). However, the association is consistently weak and the majority of studies have found no association (3).

Mechanisms of Alcohol-Related Cancers

The epidemiologic data provide little insight into whether or how alcohol increases the risk for various cancers. For some cancers, such as mouth and esophageal, alcohol is thought to play a direct causal role. For others, such as liver and breast cancers, alcohol is thought to play an indirect role by enhancing mechanisms that may cause cancer. Studies looking at these direct and indirect mechanisms may shed light on alcohol’s role in developing cancers.

Oncogenes. Preliminary studies show that alcohol may affect cancer development at the genetic level by affecting oncogenes at the initiation and promotion stages of cancer. It has been suggested that acetaldehyde, a product of alcohol metabolism, impairs a cell’s natural ability to repair its DNA, resulting in a greater likelihood that mutations causing cancer initiation will occur (27). It has recently been suggested that alcohol exposure may result in overexpression of certain oncogenes in human cells and, thereby, trigger cancer promotion (28).

Alcohol as a cocarcinogen. Although there is no evidence that alcohol itself is a carcinogen, alcohol may act as a cocarcinogen by enhancing the carcinogenic effects of other chemicals. For example, studies indicate that alcohol enhances tobacco’s abil ity to stimulate tumor formation in rats (29). In humans, the risk for mouth, tracheal, and esophageal cancer is 35 times greater for people who both smoke and drink than for people who neither smoke nor drink (30), implying a cocarcinogenic interaction between alcohol and tobacco-related
carcinogens (29).

Alcohol’s cocarcinogenic effect may be explained by its interaction with certain enzymes. Some enzymes that normally help to detoxify substances that enter the body can also increase the toxicity of some carcinogens. One of these enzymes is called cytochrome P-450 (31,32). Dietary alcohol is able to induce cytochrome P-450 in the liver, lungs, esophagus, and intestines (29,33), where alcohol-associated cancers occur. Subsequently, carcinogens such as those from tobacco and diet can become more potent as they, too, pass through the esophagus, lungs, intestines, and liver and encounter the activated enzyme (29,33).

Nutrition. Chronic alcohol abuse may result in abnormalities in the way the body processes nutrients and may subsequently promote certain types of cancer. Reduced levels of iron, zinc, vitamin E, and some of the B vitamins, common in heavy drinkers, have been experimentally associated with some cancers (29). Also, levels of vitamin A, hypothesized to have anticancer properties (34), are severely depressed in the liver and esophagus of rats during chronic alcohol consumption (35-37).

A recent study indicates that as few as two drinks per day negates any beneficial effects of a “correct” diet on decreasing risk of colon cancer (38). Although the study suggests that a diet high in folic acid, a B vitamin found in fresh fruits and vegetables, decreases the risk for colon cancer, it also warns that alcohol consumption may counter this protective action and increase the risk for colon cancer by reducing folic acid levels.

Mechanisms of liver cancer. The possible role of alcohol in the development of liver cancer is incompletely understood. In Asia and Africa, hepatitis B virus infection is thought to cause most liver cancer; the association is less frequent in the United States. Eighty percent of patients with liver cancer also have cirrhosis (39), and between 27 and 80 percent test positive for hepatitis B or C infection (40). The chronic heavy drinking that causes liver cirrhosis might exacerbate cirrhosis caused independently by the hepatitis B or C viruses. Some studies indicate that alcohol consumption hastens the development of liver cancer in patients with hepatitis C infection (41), whereas others indicate that alcohol has no compounding effect in such patients (42).

Suppression of immune response. Alcoholism has been associated with suppression of the human immune system. Immune suppression makes chronic alcohol abusers more susceptible to various infectious diseases and, theoretically, to cancer (43).

Summary

Although epidemiologic studies have found a clear association between alcohol consumption and development of certain types of cancer, study findings are often inconsistent and may vary by country and by type of cancer. The key to understanding the association lies in research designed to decipher how alcohol may promote cancer. Such studies examine
alcohol’s metabolic effects at the cellular and genetic levels. Research examining the ways in which alcohol may induce cancers has found some potential mechanisms, the most promising of which implicates oncogenes.

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Active Drinking and Withdrawal. Sleep disturbances associated with alcoholism include increased time required to fall asleep, frequent awakenings, and a decrease in subjective sleep quality associated with daytime fatigue (3). Abrupt reduction of heavy drinking can trigger alcohol withdrawal syndrome, accompanied by pronounced insomnia with marked sleep fragmentation. Decreased SWS during withdrawal may reduce the amount of restful sleep. It has been suggested that increased REM may be related to the hallucinations that sometimes occur during withdrawal. In patients with severe withdrawal, sleep may consist almost entirely of brief periods of REM interrupted by numerous awakenings (3,20).

Recovery and Relapse. Despite some improvement after withdrawal subsides, sleep patterns may never return to normal in those with alcoholism, even after years of abstinence (3,21). Abstinent alcoholics tend to sleep poorly, with decreased amounts of SWS and increased nighttime wakefulness that could make sleep less restorative and contribute to daytime fatigue (22). Resumption of heavy drinking leads to increased SWS and decreased wakefulness. This apparent improvement in sleep continuity may promote relapse by contributing to the mistaken impression that alcohol consumption improves sleep (23-25). Nevertheless, as drinking continues, sleep patterns again become disrupted (3).

Researchers have attempted to predict relapse potential using measures of sleep disruption. Gillin and colleagues (26) measured REM sleep in patients admitted to a 1-month alcoholism treatment program. Higher levels of REM predicted those who relapsed within 3 months after hospital discharge in 80 percent of the patients. A review of additional research (3) concluded that those who eventually relapsed exhibited a higher proportion of REM and a lower proportion of SWS at the beginning of treatment, compared with those who remained abstinent. Although additional research is needed, these findings may facilitate early identification of patients at risk for relapse and allow clinicians to tailor their treatment programs accordingly.

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How to Recognize a Drinking Problem

Not everyone who drinks regularly has a drinking problem. You might want to get help if you:

* Drink to calm your nerves, forget your worries, or reduce depression

* Lose interest in food

* Gulp your drinks down fast

* Lie or try to hide your drinking habits

* Drink alone more often

* Hurt yourself, or someone else, while drinking

* Were drunk more than three or four times last year

* Need more alcohol to get “high”

* Feel irritable, resentful, or unreasonable when you are not drinking

* Have medical, social, or financial problems caused by drinking

Getting Help

Older problem drinkers have a very good chance for recovery because once they decide to seek help, they usually stay with treatment programs. You can begin getting help by calling your family doctor or clergy member. Your local health department or social services agencies also can help.

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