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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following inpatient addictions treatment: Role of tobacco use in a community-based
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J.E.; and Owen, N. Can psychiatric and chemical dependency treatment units
be smoke free? J Subst Abuse Treat 13(2):107-118, 1996. (3) Collins,
A.C., and Marks, M.J. Animal models of alcohol-nicotine interactions.
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J.E.; Calfas, K.J.; Patten, C.A.; et al. Prospective evaluation of
three smoking interventions in 205 recovering alcoholics: One-year results
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F.; et al. Effect of history of alcoholism or major depression on smoking
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Source: National Institute on Alcohol Abuse and Alcoholism - January 1998
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