Although not true for every
tobacco user, the vast majority of users, particularly cigarette smokers, will
develop a dependency relationship with the nicotine contained in tobacco. This state of dependence causes users to
consume greater quantities of nicotine over extended periods of time, further
endangering their health.
Dependence can imply both a
physical and psychological relationship.
Particularly with cigarettes, physical
dependence or addiction, with its
associated tolerance, withdrawal, and
titration, is strongly developed by 40 percent of all smokers. The development of addiction reflects a
strong genetic predisposition to physical dependence. Most of the remaining population of smokers
will experience lesser degrees of physical dependence. Psychological dependence or habituation, with
its accompanying psychological components of compulsion and indulgence, is
almost universally seen.
Compulsion is a strong emotional
desire to continue tobacco use despite restrictions on smoking and the
awareness of health risks. Very likely,
users are “compelled” to engage in continual tobacco use in fear of the
unpleasant physical, emotional, and social effects that result from
discontinuing use. In comparison to
compulsion, indulgence is seen as “rewarding” oneself for aligning with a
particular behavior pattern - in this
case, smoking. Indulgence is made
possible by the existence of various reward system built around the use of
tobacco, including a perceived image, group affiliation, and even appetite
suppression intended to foster weight control.
Much to the benefit of tobacco
industry, dependence on tobacco is easily established. Many experts believe that physical dependence
on tobacco is far more easily established than is physical dependence on
alcohol, cocaine (other than crack), or heroin.
Of all people who experiment with cigarettes, 85% develop various
aspects of a dependence relationship.
A small percentage of smokers,
known as “chippers,” can on occasion without becoming dependent. Most likely, chippers respond differently to
environment cues than do more dependent smokers, thus smoking less
frequently. They may be truly “social smokers”
in that they smoke with only a few selected friends or in a very limited number
of places. Unfortunately, many
inexperienced smokers feel that they too are only social smokers; however, a
few months, or even a few days, of this type of occasional smoking could be a
transitional period into a dependence pattern of tobacco use.
Sandwiched between regular smokers
and chippers is a newly emerging group of smokers – part-time smokers. Today these smokers constitute about 23% of
all smokers. The practice most likely
reflects the reality of the high cost of cigarettes and restrictions in the
workplace. The health effects of this
form of smoking appear to be the same as for regular smokers.
Theories of Nicotine Addiction
The establishment and maintenance
of physical dependence or addiction is less than fully understood. Most experts, however, believe that for a
specific individual, addiction has a multifaceted etiology, or cause, with
increasing attention being directed toward a genetic basis for addiction. Accordingly, several theories have been
proposed to explain the development of dependence. Readers are reminded that many of these
theories are technically sophisticated and only a most basic description can be
provided in a personal health textbook.
Genetic Influences
Although the specific genetic
pathways that influence both the initiation and maintenance of smoking (or
other forms of tobacco use) are less than fully understood, a role for genetic
influence is evident. Applying new
statistical techniques to earlier studies of smoking patterns in families and
between identical twins, it is now believed that initiation and maintenance of
initial smoking is 60% driven by genetic influences. Of course, the smoking of the first few
cigarettes is a choice made by beginning smokers. The remaining influence needed for initiation
and maintenance of initial smoking is 20% environmental and 20% the unique
needs of individuals.
Once the brief period of initial
exposure is passed, the role of genetic influences may be even more powerful –
providing 70% of the stimulus required over decades of smoking. Environmental and personality factors subside
accordingly.
Bolus Theory
In the bolus theory of nicotine
addiction, one of the oldest and most general theories of addiction, each
inhalation of smoke release into the blood a concentrated quantity of nicotine
(a ball or bolus) that reaches the brain and results in a period of
neurohormonal excitement. The smoker
perceives this period of stimulation as pleasurable but, unfortunately, short
lived. Accordingly, the smoker attempts
to reestablish this pleasurable feeling by again inhaling and sending another
serve to condition the novice smoker, resulting in a lifelong pattern of
cigarette dependence. The level needed
for arousal is different for each individual smoker, depending on the length of
addiction, the level of tolerance, genetic predisposition, and environmental
and personal stimuli.
Recognition of two types of
smokers emerges from an understanding of the bolus theory of smoking. Peak
smokers are those smokers who become who become dependent on the arousal of
pleasure centers in the brain that are stimulated by the rapid increase of
nicotine within the CNS. In contrast,
the trough maintenance smokers maintain
an even consistently higher level of nicotine titration in order to avoid the
negative consequences of withdrawal.
These feelings are experienced as unpleasant, and thus to be avoided.
Adrenocorticotropic Hormone (ACTH) Theory
Yet another theory of dependence
suggest that nicotine stimulates the release of adrenocorticotropic hormone
(ACTH) from the anterior pituitary, or “master gland” of the endocrine system
causing the release of beta endorphins (naturally occurring opiate-like
chemicals) that produce mild feelings of euphoria. Perhaps this stresslike response mechanism
involving ACTH accounts for the increased energy expenditure seen in smokers
and thus their tendency to maintain a lower body weight. Others, however, have questioned the ability
of nicotine to stimulate endorphin release.
When these psychological responses
are viewed collectively, nicotine may be seen as biochemically influencing
brain activity by enhancing the extent and strength of various forms of
“communication” between different brain areas and even glands of the endocrine
system. If this is the case, it is
apparent why, once addicted, the functioning of the smoker’s control system is
much altered in comparison with that of nonsmokers.
Self-Medication Theory
Another explanation of addiction
to smoking, called self-medication, suggest that nicotine, through the effects
of mood-enhacing dopamine, may allow smokers to “treat” feelings of tiredness,
lack of motivation, or even depression.
In other words, a smoke lifts the spirit the spirits, if only
briefly. Eventually, however, smokers
become dependent on tobacco as a “medication” to make themselves feel
better. Thus, because tobacco is a legal
drug that is readily available, it becomes preferred to prescription
medications and illegal drugs, such as cocaine and the stimulants, that elevate
mood.
Regardless of the mechanism
involved, as tolerance to nicotine develops, smoking behavior is adjusted to
either maintain arousal or prevent the occurrence of withdrawal symptoms. At some point, however, the desire for
constant arousal is probably superseded by the smoker’s desire not to
experience withdrawal.
The importance of nicotine as the
primary factor in establishing dependence on tobacco is supported by research
that demonstrates that smokers will not select a nontobacco cigarette if a
tobacco cigarette is available. Even
tobacco cigarettes with a very low level of nicotine seem to be unacceptable to
most smokers, as do cigarettes with very low nicotine but with high tar
content. Interestingly, users of
low-nicotine cigarettes tend to inhale more frequently and deeply to obtain as
much nicotine as possible.
Even more impressive (and
alarming) regarding nicotine’s dependency-producing power is seen in conjuction
with the small amount of time needed to become dependent. Using the HONC instruments, it is now established
that beginning smokers (recall that most smokers begin during adolescence)
become dependent on cigarettes within 3 weeks to 3 months of smoking on as
little as two cigarettes per day. Males
are more likely to be a bit more resistant to dependency, taking a month or 2,
while females can become dependent in a matter of a very few days of initial
experimentation.
Acute effects of Nicotine on Nervous System Function
In comparison with the more chronic
effects of nicotine on the central nervous system (CNS) that may eventually
result in physical dependence or addiction, nicotine also produces changes of
short duration. In the CNS, nicotine
activates receptors within the nucleus accumbens (a reward center) and the
locus caeruleus (a cortical activating center) of the brain. Stimulation of the brain is seen by changes
in electroencephalogram (EEG) patterns, reflecting an increase in the frequency
of electrical activity. This is part of
a general arousal pattern signaled by the release of the neurotransmitters
norepinephrine, dopamine, acetylcholine, and serotonin. Heavy use of tobacco products, result in high
levels of nicotine in the bloodstream, eventually produces a blocking effect as
more and more receptor sites for these neurotransmitters are filled. The result is a generalized depression of the
CNS.
The level of plasma nicotine
associated with normal levels of heavy smoking (one to two packs per day) would
not likely produce the depressive effect just described. However, in chain smokers (four to eight
packs per day), plasma nicotine levels would be sufficient to have a depressive
influence on nervous system function. In fact, it has been suggested that chain
smoking is driven by fruitless effort to counter the depressive influence of
chronically excessively high levels of nicotine.
In carefully controlled studies
involving both animals and humans, nicotine increased the ability of subjects
to concentrate on a task. It must be noted, however, that the duration of this
improvement was limited. Most would
agree that this brief is not enough to justify the health risks associated with
chronic tobacco use.
Non-Nervous System Acute Effects of Nicotine
Outside the CNS, nicotine effects
the transmission of nerve signals at the point where nerves innervate muscle
tissue (called the neuromuscular junction) by mimicking the action of the
neurotransmitter acetylcholine. Nicotine
occupies receptor sites at the junction and prevents the transmission of nerve
impulses from nerve cell to muscle cell.
Nicotine also causes the release
of epinephrine from the adrenal medulla, which results in an increase in
respiration rate, heart rate,, blood pressure, and coronary blood flow. These changes are accompanied by the
constriction of the blood vessels beneath the skin, a reduction in the motility
in the bowel, loss of appetite, and changes in sleep patterns.
Although a lethal dose of nicotine
could be obtained through the ingestion of a nicotine-containing insecticide,
to “smoke oneself to death” in a single intense period of cigarette use would
be highly improbable. In humans, 40 to
60 mg (.06- .09 mg/kg) is a lethal dose.
A typical cigarette supplies .05 to 2.5 mg of nicotine, and that
nicotine is relatively quickly broken down for removal from the body.
Psychological Factors Related to Dependence
You will recall that psychological
aspect of dependence (habituation) exists and is important in maintaining the
smoker’s need for nicotine. Both research
and general observation support many of the powerful influence this aspect of
dependence possesses, especially for beginning smokers, prior to the onset of
physical addiction. Consequently, in the
remainder of this section, we will explore factors that may contribute to the
development of this aspect of dependence.
Modelling
Because tobacco use is a learned
behavior, it is reasonable to accept that modelling acts as a stimulus to
experimental smoking. Modelling suggest
that susceptible people smoke to emulate, or model their behavior after,
smokers whom they admire or with whom they share other types of social or
emotional bonds. Particularly for young
adolescents, smoking behavior correlates with the smoking behavior of slightly
older peers and very young adults (ages 18 to 22), older siblings, and, most importantly,
parents.
Negative parental influences on
cigarette smoking by their own children include their own smoking in
combination with their failure to clearly state their disapproval of smoking by
children. Further, for parents who
smoke, it is important that they cease smoking before their children turn 8
years of age if they wish to maximize an anti-smoking message.
Modelling is particularly evident
when smoking is a central factor in peer group formation and peer group
association and can lead to a shared behavioral pattern that differentiates the
group from others and from adults. Further,
when risk-taking behavior and disregard for authority are common to the group,
smoking becomes the behavioral pattern that most consistently identifies who
lack self-directedness or the ability to resist peer pressure, initial
membership in a tobacco-using peer group may become inescapable. The ability to counter peer pressure is a
salient component of successful anti-smoking programs for use with older children
and younger adolescents.
In addition, when adolescent have
lower levels of self-esteem and are searching for an avenue to improve
self-image, a role model who smokes is often seen as tough, sociable, and
sexually attractive. These three traits
have been played up by tobacco industry in their carefully crafted
advertisements. In fact, teens from any
background may see the very young
and attractive models used in tobacco (and beer) advertisements as being more
peer-like in age than they really are.
FCC regulations require that models for both products be 21 years of age
or older, regardless of how youthful they might (and the advertisers hope they
do) appear to older children and young adolescents.
Manipulation
In addition to modelling as a
psychosocial link with tobacco use, cigarette use may meet the beginning smoker’s
need to manipulate something and at the same time provide the manipulative “tool”
necessary to offset the boredom, feelings of depression, or social immaturity. Clearly the availability of affordable
smoking paraphernalia provides smokers with ways to reward themselves. A new cigarette lighter, a status brand of
tobacco, or a beach towel with a cigarette’s logo are all reinforcements to
some smokers. Fortunately, the latter
will become increasingly harder to find as logos can no longer be placed on
items such as beach towels. For others, the
ability to take out a cigarette or fill a pipe adds a measure of structure and
control to situations in which they might otherwise feel somewhat ill at
ease. The cigarette becomes a readily
available and dependable “friend” to turn to with the use of its products. To these users and potential users, the
self-reward of power, liberation, affluence, sophistication, or adult status is
achieved by using the products that they are told are associated with these
desired states. Thus the self-rewarding
use of tobacco products becomes a means of achievement.
With this multiplicity of forces
at work, it is impossible to understand why so many who experiment with tobacco
use find that they quickly become dependent on tobacco. Human needs, both physiological and
psychosocial, are many and complex. Tobacco
use meets the needs on a short-term basis, whereas dependence, once
established, replaces these needs with a different, more immediate set of
needs.
Despite the satisfaction of the
dependency that continued smoking brings, approximately 80% of adult smokers
have, on at least one occasion, expressed a desire to quit, and the majority of
these have actually attempted to become nonsmokers. Today, with the over-the-counter availability
of transdermal nicotine patches, nicotine containing gum, prescription
medications such as antidepressants, and nicotine inhalers, the number of
smokers making concerted and repeated attempts to stop smoking is up
considerably over that seen in the past.
It therefore seems apparent that tobacco use is a source of
dissonance. This dissonance stems from
the need to deal emotionally with a behavior that is both highly enjoyable and
highly dangerous but known to be difficult to stop. The degree to which this dissonance exists
probably varies from user to user.
Preventing Teen Smoking
Even before the 1997 release of
tobacco industry documents confirming the targeting of young adolescents, the
federal government stated its intention to curb these cigarette
advertisements. In August 1995 the FDA
described the specific actions that it hoped it would be given authority to
implement. Collectively, the
restrictions described in the following list were intended to discourage
cigarette smoking among American’s teens, resulting in 50% fewer adolescents
beginning smoking in the year 2002 than in 1995.
- Limit tobacco
advertising in publications that appeal to teens and restrict billboards
with tobacco-related content to no closer than 1,000 feet of schools and
playgrounds. (A August 1995 study
in California found that stores near schools displayed significantly more
tobacco-related advertisements than those far from schools.)
- Restrict
the use of logo and other tobacco-related images on nontobacco-related
products, such as towels, T-shirts, and caps.
- Bar certain
sources of access to tobacco products, such as mail order sales, the
distribution of free samples, and vending machines.
- Halt sponsorship
of high-visibility events, such as auto racing and athletic contents in
which brand names appear on highly televised surfaces, including hoods,
fenders, uniforms, and arena sign boards.
(It is estimated that the Marlboro logo is seen 5,933 times during
the course of a 90-minute televised Winston Cup auto race).)
- Require merchants
to obtain proof of age when selling tobacco products to adolescents. (This particular component of the
initial plan became law in 1997.
Merchants are required to validate the age of people whom they
suspect to be younger than 27 years of age before selling cigarettes to
those 18 years of age and older. If
found in violation, both the salesperson and the store owner will be fined
$500.)
By mid-1998 the federal government’s desire to reduce
youth smoking through implementation of the steps just described was mired in a
larger package of tobacco-related policies being debated in Congress. This undertaking was relating to the class
action suit filed by all 50 (46 as a single large class and 4 as a smaller
class) states against the tobacco industry in an attempt to recoup Medicaid
expenditures for treating tobacco-related illnesses. As Congress attempted to construct a
settlement that would be acceptable to all parties, the impasse fragmented
attempts to reduce youth smoking. Unfortunately,
this outcome diluted some restrictions on tobacco advertisements, as well as
the FDA’S ability to reduce smoking by defining cigarettes as drug delivery
systems. In fact, in 2000 the United
States Supreme Court ruled that the FDA lacked the regulatory authority to
bring tobacco products under its control, unless Congress was willing to
rescind laws that currently define tobacco as an agricultural product that can
be freely marketed to persons18 years of age or older. (If defined as a drug delivery system,
cigarettes would be obtainable only with a physician’s prescription, which
would essentially prevent, or greatly limit, children’s access to them.)
The
Master Settlement Agreement of 1999, that required the tobacco industry to pay
the sates 246 billion dollars was able to restrict some forms of youth-oriented
advertising and funds anti-smoking education, which may accomplish some of the
changes initially proposed. Unfortunately,
during the economic downturn some states have used these funds to meet taxation
shortfalls.
