National Institute on Alcohol Abuse and Alcoholism No. 39 January 1998
Alcohol and Tobacco
Extensive research supports the popular observation that "smokers drink and
drinkers smoke." Moreover, the heaviest alcohol consumers are also the heaviest
consumers of tobacco. Concurrent use of these drugs poses a significant public
health threat. A survey of persons treated for alcoholism and other drug
addictions revealed that 222 of 845 subjects had died over a 12-year period;
one-third of these deaths were attributed to alcohol-related causes, and
one-half were related to smoking (1). This Alcohol Alert explores the
association between alcohol and tobacco use, possible mechanisms of their
combined health effects, and some implications for alcoholism treatment.
The Co-Occurrence of Alcoholism and Smoking
Between 80 and 95 percent of alcoholics smoke cigarettes (2), a rate that is
three times higher than among the population as a whole. Approximately 70
percent of alcoholics are heavy smokers (i.e., smoke more than one pack
of cigarettes per day), compared with 10 percent of the general population (3).
Drinking influences smoking more than smoking influences drinking. Nevertheless,
smokers are 1.32 times as likely to consume alcohol as are nonsmokers (4).
Most adult users of alcohol or tobacco first tried these drugs during their
early teens (5). Among smoking alcoholics, the initiation of regular cigarette
smoking typically precedes the onset of alcoholism by many years, although data
are inconsistent (6). Adolescents who begin smoking are 3 times more likely to
begin using alcohol (7), and smokers are 10 times more likely to develop
alcoholism than are nonsmokers (6).
Why Are Alcohol and Tobacco Used Together?
Postulated mechanisms for the concurrent use of alcohol and tobacco fall into
two broad, nonexclusive categories: Either drug may increase the desired
(rewarding) effects of the other, or either may decrease the toxic or unpleasant
(aversive) effects of the other. These interactions involve processes of
reinforcement or tolerance, as described below. (A third possibility--that one
drug may alter the metabolism of the other, thereby affecting its absorption,
distribution, or elimination from the body--has not been convincingly
established [8].)
Reinforcement. Reinforcement refers to the physiological
processes by which a behavior--such as consumption of a drug--becomes habitual.
A key process in reinforcement for some drugs occurs when nerve cells release
the chemical messenger dopamine into a small area of the brain called the
nucleus accumbens following consumption of the drug (9). Nicotine is the primary
ingredient of tobacco that triggers reinforcement. After reaching the brain,
nicotine activates a group of proteins called nicotinic receptors. These
proteins, located on the surface of certain brain cells, normally regulate a
host of physiological functions, some of which may contribute to aspects of
reinforcement. Ultimately, nicotine brings about the release of dopamine in the
nucleus accumbens (5). Alcohol consumption also leads to dopamine release,
although the mechanism by which alcohol produces this effect is incompletely
understood (10,11).
Tolerance. Tolerance is decreased sensitivity to a given effect
of a drug such that increased doses are needed to achieve the same effect.
Long-term administration of nicotine in animals can induce tolerance to some of
alcohol's reinforcing effects, and chronic alcohol administration induces
tolerance to some effects of nicotine (8). Such cross-tolerance might lead to
increased consumption of both drugs in an attempt to regain former levels of
reward. In addition, cross-tolerance can develop to the aversive effects of
drugs. For example, smokers may reduce their tobacco intake when they begin to
feel its aversive effects (e.g., increased heart rate, "nervousness"). Alcohol's
sedating effects may mitigate these effects of nicotine, facilitating continued
tobacco use (12). Conversely, nicotine's stimulating effects can mitigate
alcohol-induced loss of mental alertness (8).
Animal studies provide support for these interactions. For example, alcohol
appears to induce loss of physical coordination in mice by inhibiting nicotinic
receptors in the cerebellum, a part of the brain that is active in coordinating
movement and balance. Administration of nicotine appears to remove this
inhibition and restore coordination (13,14). In addition, alcohol interferes
with the normal functioning of the chemical messenger vasopressin, which may
play a role in memory processes. Vasopressin is also associated with the
development of tolerance to alcohol (15). Nicotine helps normalize vasopressin
function in the brain, reducing alcohol-induced impairment of memory and other
intellectual abilities (11).
What Is the Risk of Cancer From Alcohol and Tobacco?
Smoking and excessive alcohol use are risk factors for cardiovascular and
lung diseases and for some forms of cancer. The risks of cancer of the mouth,
throat, or esophagus for the smoking drinker are more than the sum of the risks
posed by these drugs individually (2). For example, compared with the risk for
nonsmoking nondrinkers, the approximate relative risks for developing mouth and
throat cancer are 7 times greater for those who use tobacco, 6 times greater for
those who use alcohol, and 38 times greater for those who use both tobacco and
alcohol (16).
How Do Alcohol and Tobacco Increase Cancer Risk?
Approximately 4,000 chemical substances are generated by the chemical
reactions that occur in the intense heat of a burning cigarette (17). A group of
these chemicals, collectively known as tar, is carried into the lungs on inhaled
smoke. The bloodstream then distributes the components of tar throughout the
body. Certain enzymes found mainly in the liver (i.e., microsomal enzymes)
convert some ingredients of tar into chemicals that can cause cancer. Long-term
alcohol consumption can activate some such microsomal enzymes, greatly
increasing their activity and contributing to smoking-related cancers (18,19).
Microsomal enzymes are found not only in the liver but also in the lungs and
digestive tract, which are major portals of entry for tobacco smoke. The
esophagus may be particularly susceptible, because it lacks an efficient
mechanism for removing toxic substances produced by activated microsomal enzymes
(20). Consistent with these observations, alcohol has been shown to promote
esophageal tumors in laboratory animals exposed simultaneously to specific
components of tar (18,19).
Finally, alcoholics frequently exhibit deficiencies of zinc and vitamin A,
substances that confer some protection against cancer (20).
Addictions Treatment for Smoking Alcoholics
Until recently, alcoholism treatment professionals have generally not
addressed the issue of smoking cessation, largely because of the belief that the
added stress of quitting smoking would jeopardize an alcoholic's recovery (21).
Research has not confirmed this belief. One study evaluated the progress of
residents in an alcoholism treatment facility who were concurrently undergoing a
standard smoking cessation program (i.e., experimental group) (6). A comparison
group of smoking alcoholics participated in the same alcoholism program but
without undergoing the smoking cessation program. One year after treatment,
results indicated that the smoking cessation program had no effect on abstinence
from alcohol or other drugs. In addition, 12 percent of the subjects in the
experimental group, but none of the subjects in the comparison group, had
stopped smoking.
Some data suggest that alcoholism recovery may facilitate nicotine
abstinence. In one study, patients participating in concurrent treatment for
nicotine addiction during residential treatment for alcohol and other drug abuse
achieved at least a temporary reduction in smoking and an increased motivation
to quit smoking (22). Similarly, persons who achieve abstinence from alcohol
without formal treatment often stop smoking at the same time (6,23).
Following the lead of other health facilities, many addictions treatment
facilities are becoming smoke-free, providing a "natural experiment" on the
effectiveness of dual recovery programs. Initial evaluations suggest that
no-smoking policies are feasible in this setting (24). However, no outcome
studies have been performed, and additional research is needed.
Problems encountered in smoke-free alcoholism treatment programs include
surreptitious smoking by patients as well as by staff. Further, researchers have
suggested modifying smoking cessation programs to conform with the structure and
language of concurrent alcoholism programs (e.g., use of a 12-step approach)
(2). Nicotine patch therapy for smoking alcoholics may require higher doses of
nicotine than are usually applied, because of alcohol-induced tolerance to some
of nicotine's effects (25,26).
Smoking alcoholics with a history of depressive disorders are generally less
successful at smoking cessation than are subjects without such a history (27).
Smoking may diminish the chances of recurring depression in some people, and a
major depressive episode may follow smoking cessation in these subjects (28). An
additional clinical consideration is that activation of microsomal enzymes by
alcohol and tobacco tar may reduce the effectiveness of antidepressant
medications (17). Therefore, medication levels should be carefully monitored in
patients undergoing treatment for depression and addiction to alcohol and
tobacco (5).
Alcohol and Tobacco--A Commentary by
NIAAA Director Enoch Gordis, M.D.
Alcohol and tobacco are frequently used together, may share certain brain
pathways underlying dependence, and because of their numerous social and
health-related consequences, are a continuing source of national public policy
debate.
Many alcoholism treatment professionals have not actively pursued smoking
cessation among their patients based on the belief that the stress of quitting
smoking while undergoing alcoholism treatment might cause relapse. As a
physician who has seen the ravages caused by both alcoholism and smoking, I am
pleased that we now have research evidence showing that both can be treated
simultaneously without endangering alcoholism recovery. As basic science learns
more about how alcohol and nicotine act singly and together within the brain,
new treatments for alcohol and nicotine dependence will follow.
Finally, society has attempted to minimize the consequences of using both
alcohol and tobacco through public policy actions, including health warning
labels, restrictions on advertising, and age restrictions on use. Unlike
tobacco, however, moderate use of alcohol has certain health benefits. The
implications of this are discussed in Alcohol Alert No. 16, "Moderate
Drinking," which may be found on NIAAA's Web site at http://www.niaaa.nih.gov.
References
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C.A.; Martin, J.E.; and Owen, N. Can psychiatric and chemical dependency
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Full text of this publication is available on NIAAA's World Wide Web site at http://www.niaaa.nih.gov
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