ALCOHOL DEPENDENCE:
DIAGNOSIS, CLINICAL ASPECTS, AND
BIOPSYCHOSOCIAL CAUSES.
By Joseph R. Volpicelli, M.D., Ph.D.
Alcohol drinking has decreased in recent
years. Still,
two- thirds of all adults drink alcohol and one-third of all high
school
seniors report that they drink alcohol. The average alcohol consumption
for Americans over the age of 14 is 3 gallons of pure alcohol per
person
per year. The lifetime prevalence of alcoholism is about thirteen
percent
in the United States. There are significant sex differences: about five
times as many men as women are alcohol-dependent . About one in five of
the people who use alcohol for recreational purposes become
alcohol-dependent
for some part of their lives. Later, we will discuss why certain people
may be at special risk to become dependent on alcohol.
Alcohol-related deaths account for about
five percent
of all deaths in the U.S.--this ranks alcohol-related death between the
3rd (cerebrovascular diseases) and 4th (injuries) major causes of death
(Stinson, 1992). It is impossible to calculate the high cost of human
suffering,
but we can calculate the cost of alcohol dependence with medical
complications,
lost work productivity and legal costs. On this basis alone, it is
estimated
that alcohol dependence costs society about 116 billion dollars per
year
(National Council on Alcoholism, 1986). About 40 percent of all
hospital
admissions are alcohol-related. Alcohol-dependent people use health
services
at twice the rate of the general population. Alcohol dependence is the
leading cause of lost productivity resulting from missed work days, as
well as, home and industrial accidents. Legal costs from drunk driving
and the prosecution of rapes and homicides also contributes to the high
cost of alcohol dependence.
DEFINITION OF ALCOHOL DEPENDENCE
When does someone cross that boundary
between recreational
alcohol use and dependence? Three main symptom clusters have been used
to help draw this distinction.
Loss of Control. Some people have defined
addiction
by focusing on the degree of control over alcohol. In the past,
addiction
experts called this psychological dependence. For example, a business
executive
may plan to have 1 or 2 beers after work, but he ends up having 5 or 6.
Loss of control also becomes evident when a person makes repeated, but
unsuccessful, attempts to cut down or stop drug use. Finally, loss of
control
is marked by compulsive thoughts and actions. Much of the day is spent
either thinking about getting high again or recovering from a previous
high.
Maladaptive Consequence. A second measure
of alcohol
dependence is the presence of negative psychological, social, and
medical
consequences. As discussed above alcohol dependence is the leading
cause
of missed days at work. Alcohol dependence is also associated with
severe
medical problems which we will discuss in more detail below. People who
continue to use alcohol despite adverse effects on their health,
occupational
or social functioning show symptoms of alcohol dependence.
Biological Adaptation. Finally, some
substance abuse
experts define dependence solely with physiological adaptation to
alcohol.
In the past this has been referred to as physical dependence. Physical
dependence is shown by either tolerance or withdrawal. Tolerance is
defined
as a decrease in the response to alcohol as use continues over time.
Thus,
it takes a progressively larger amounts of alcohol to produce the same
effect. Chronic alcohol users may also experience withdrawal symptoms
such
as rapid heart rates or excessive sweating when they stop or decrease
alcohol
drinking. People who show either physical tolerance or symptoms of
withdrawal
are said to be physically adapted to the drug.
CLINICAL COMPLICATIONS OF ALCOHOL
Intoxication
The behavioral effects of alcohol
intoxication depend
on two factors: one's beliefs and expectations about alcohol and the
amount
of alcohol consumed. These factors interact in complex ways to
influence
behavior.
For example, many people think that
alcohol can increase
sexual arousal. Contrary to these expectations, sexual arousal
decreases
as blood alcohol level increases. However, sexual arousal increases for
people who believe they have consumed alcohol, but have really been
given
a non-alcohol substitute.
The dose of alcohol also interacts with
alcohol's psychological
effects. Alcohol is a CNS depressant. At low doses, however, it
selectively
depresses inhibitory centers. This means that alcohol may decrease
behavioral
inhibitions at low doses, and paradoxically increase aggressive or
social
behaviors. For example, some people will have a drink or two before a
social
function to decrease their social inhibitions. Other people are more
likely
to express their feelings including anger when intoxicated. About one
half
of all suicides and homicides occur during alcohol intoxication. Also,
thirty-five percent of all rapes are related to alcohol drinking,
particularly
date rapes.
At higher concentrations (BAC > 100 mg
%), alcohol
depresses both the excitatory and inhibitory centers. That is it
suppresses
everything, from rational thinking to motor coordination. Alcohol
drinking
is responsible for about 50 percent of fatal car accidents and accounts
for 25,000 traffic fatalities each year. At still higher concentrations
(BAC > 500 mg %), alcohol suppresses consciousness leading to
blackouts.
Finally, alcohol can suppress respiratory centers and, particularly
when
combined with other sedatives (e.g.Valium), can lead to death.
Chronic Alcohol Dependence
There are several medical and psychiatric
complications
from alcohol dependence. Clinical effects of alcohol dependence are
summarized
below.
Gastrointestinal. Alcohol dependence is
the most common
cause of cirrhosis of the liver, the eighth leading cause of death in
the
United States. Alcohol is also associated with other gastrointestinal
disorders
such as ulcers, gastritis, and pancreatic cancer.
Cardiovascular. Alcohol causes several
cardiovascular
complications and is responsible for about 15% of all cases of
hypertension
and most of the cases of cardiomyopathy.
Neurological. Chronic alcohol dependence
can produce
severe damage to the peripheral and central nervous system. Peripheral
neuropathy is often responsible for the ataxia seen in chronic
alcoholics.
Other neurological complictions caused by chronic alcohol abuse include
the following: Weinicke's disease (ocular disturbance, ataxia and
confusion)
associated with thiamine dificiency, Korsakoff's psychosis, a permanent
inability to learn new information and finally, structural changes in
the
brain associated with severe cognitive impairment (dementia).
Immunologic. Alcohol drinking suppresses
neutrophil
function and cell-mediated immunity. This predisposes alcoholics to
serious
infections including fatal cases of pneumonia and tuberculosis.
Suppression
of cell-mediated immunity may be responsible for the higher incidence
of
several types of cancers seen in alcoholics.
Endocrine. Male alcoholics have increased
estrogen
and decreased testosterone. This leads to impotence, testicular atrophy
and gynecomastia.
Obstetric. An often overlooked
complication of alcohol
drinking is the adverse effects of alcohol during pregnancy that can
cause
mental retardation, facial deformity, other neurological problems
(fetal
alcohol syndrome).
Psychiatric. Chronic alcohol dependence
is often associated
with emotional problems. Many alcoholics have co-existing anxiety
disorders
(about 25%), depression (20%-40%), and occasionally hallucinations
(alcohol
hallucinosis). It is not clear if psychiatric disorders predispose to
alcohol
dependence (self- medication hypothesis) or result from chronic abuse
of
alcohol. Alcohol-dependent patients are often suicidal, and about
one-quarter
of all suicides are committed by alcoholics, generally white males over
35 years old.
Withdrawal
Just as alcohol intake depresses the
nervous system,
alcohol withdrawal produces overexcitation of the nervous system. Many
alcoholics begin to experience tremors called "the shakes" about 24
hours
after their last drink. Without a drink, they begin to experience rapid
heart rates, sweating, decreased appetite, and difficulty sleeping. For
some individuals, symptoms of withdrawal can become quite severe. One
to
three days after their last drink, alcoholics can have a generalized
seizure
(rum fits). About three to five days after their last drink, these
patients
can suffer from disorientation, high fevers, and visual hallucinations.
This syndrome is call delirium tremens (DTs). During the DTs people are
very susceptible to suggestion. For example, one patient became
convinced
that a pink elephant was dancing on an imaginary string between his
therapist's
fingers. Individuals in DTs can also be paranoid. The DTs are a serious
medical emergency. Before aggressive modern medical treatment, fifteen
percent of patients with DTs died. Now with adequate medication and
nutritional
support, fatalities from DT's are rare.
Following this initial withdrawal phase,
many people
go through protracted alcohol withdrawal. This can last anywhere from
one
to four weeks. People in the protracted withdrawal phase remain anxious
and have difficulty eating and sleeping. In serious cases, alcohol
hallucinosis
occurs.
CAUSES OF ALCOHOL DEPENDENCE
PSYCHOSICIAL THEORIES
All the psychological theories of drug
dependence assume
that alcohol satisfies some important need. Psychoanalytic theories
focus
on unconscious needs while behavioral theories focus on the role of
tension
reduction to account for alcohol abuse.
Psychoanalytic. One early psychoanalytic
theory suggested
that children who are fixated at the oral stage are more prone to abuse
alcohol later in life. Psychoanalysts theorize that oral fixation
results
when children are either frustrated in their oral dependent needs
(unloving
mother) or too easily satisfied by oral stimulation (overprotective
mother).
When stressed as adults, oral-dependent people are more likely to turn
to alcohol to cope.
Adams (1978) suggests that it is not
deprived infants
who develop oral traits but rather children (particularly boys) with
overprotective
mothers. Later in life such men will have a strong need to remain
dependent
on either their mother or another woman. When their needs become
frustrated,
they become angry. Unable to deal with anger assertively, these people
find that alcohol provides an effective way to reduce aggressive
impulses.
It has the additional advantage of hurting those people around
them.
Psychoanalytic theories make some
intuitive sense since
many alcoholics have immature social skills. They often turn to alcohol
to help cope with life stresses. Despite this intuitive appeal, there
are
little prospective data to support these theories. An alcohol dependent
person may exhibit dependent traits, however, these traits are just as
likely to result from chronic alcohol use as they are to lead to it.
Even
if correlations exist between alcohol abuse and dependent
personalities,
it is not clear which is the cause and which is the effect. In summary,
there is little evidence to support the oral fixation theory.
Tension Reduction. Another important
theory for alcohol
abuse is that alcohol drinking is reinforced because alcohol reduces
tension.
Conger (1951) proposed the Tension Reduction Hypothesis as a model for
alcohol drinking. The model assumes that alcohol can reduce tension and
people learn to drink alcohol to avoid or reduce unpleasant stress.
Clinical
observations and studies appear to support this theory.
First, alcohol dependence and anxiety
symptoms often
coexist. Many anxious patients say that drinking alcohol helps them
reduce
anxiety. This is especially true of phobic patients who often use
alcohol
to help face their fears. One patient could only travel over bridges
after
drinking five or more beers. Another patient needed to drink before
attending
any social function. She would have one or two drinks while getting
dressed
and another two or three at the social function to help her feel more
relaxed.
One can easily see how using alcohol in this way can quickly lead to
the
sorts of problems we have outlined.
Alcohol relapse often occurs following a
negative life
event such as loss of a job or death of a spouse (Marlatt and Gordon,
1980).
For example, one patient had a very severe relapse following the
breakup
with his girlfriend. Stress from the breakup may have increased the
patient's
desire to use alcohol to relieve this stress. Epidemiological studies
also
support the Tension Reduction Hypothesis, since alcohol drinking is
associated
with cultural stress. States with high rates of divorce, births,
unemployment
and other stressful life events also have high rates of alcohol abuse
(Linksky,
Straus, and Colby, 1985).
While clinical and epidemiological
studies support
the Tension Reduction Hypothesis, experimental studies fail to show
that
increased tension leads to increased drinking. If people drink alcohol
to reduce tension, we would expect that alcohol drinking would increase
during tension-arousing situations. This prediction led to many
conflicting
results. For example, in laboratory studies, subjects who are
threatened
with an electric shock or who receive feedback that they have done
poorly
on a test do not increase drinking.
How can we account for these conflicting
results? The
tension reducing properties of alcohol may be specific to certain
situations.
Alcohol may reduce tension only for social stress but not for other
sorts
of stresses. Also, alcohol may reduce tension only in particular doses
(low doses but not high doses) and under certain conditions (in
naturalistic
but not experimental situations). In addition, alcohol may reduce
tension
only for some individuals who carry a gene for alcoholism. Finally,
alcohol
may not reduce tension but may dampen the impact of a stressful
situation.
The results of several studies support this hypothesis. Experienced
male
drinkers who are threatened with electric shock or social evaluation
show
less subjective and physiological signs of anxiety when intoxicated
than
when sober (Levenson, et al., 1980).
Recent reviews suggest yet another view
of the relationship
between stress and alcohol drinking. According to this analysis people
do not drink alcohol to reduce tension. Rather, they drink once tension
has stopped and a sense of relief has set in. This is known as the
"happy
hour" effect. It accounts for the frequent observation that anxiety and
alcohol drinking often go together. However, it is the sudden removal
of
stress that sets the occasion for drinking, rather than the situation
causing
stress . For example, Volpicelli et al. (1990) found that rats
increased
their alcohol drinking following, but not during, uncontrollable
stress.
In another study, rats living in a fearful environment tended to drink
less alcohol than rats removed from the fearful environment and placed
in a safe, home cage (Volpicelli, et al., 1982). One study of college
students
showed similar results. After completing a difficult (stressful) test,
half the students were told they did poorly, scoring in the lower 15th
percentile of their peers. The other half were told they did well,
scoring
in the upper l5th percentile. The relieved subjects--who thought they
did
well on the test -- drank more alcohol than subjects who believed they
did poorly (Lisman, 1986).
Biological
Genetics. Researchers have discovered
that alcohol
dependence runs in families. A classic study by Goodwin (1974),
compared
the adopted children of alcohol-dependent parents to the adopted
children
of non-alcohol-dependent parents. In the children of alcohol-dependent
biological parents, the risk of becoming alcohol dependent increased.
In
contrast, if the adoptive parents were alcohol-dependent, there was no
increased risk of alcoholism. In general, if one biological parent is
alcoholic,
the likelihood of a child becoming dependent increases nearly three
times.
If both parents are alcoholic, the likelihood of alcohol dependence
increases
about five times. However, the likelihood of alcohol dependence does
not
increase in children whose nonbiological parent is dependent on
alcohol.
This work shows that genetic factors affect the risk of alcohol
dependence
more than the family environment.
In an attempt to determine what specific
inherited
factor(s) increase their risk of alcohol abuse, researchers have
conducted
a series of studies comparing the biological children of alcohol
dependent
parents to the biological children of non-alcoholic parents. Several
differences
emerge between these two groups.
One source of biological vulnerability
suggests that
high risk subjects have some instability in their nervous system that
can
be counteracted by drinking alcohol. For example, sons of alcohol
dependent
fathers are less able to hold their body still when asked to stand at
attention,
compared to sons of nonalcoholic fathers (Hegedus et al., 1984).
Typically,
people without alcoholic fathers sway more when intoxicated. However,
when
sons of alcoholic fathers drink alcohol, there is less body sway
(Schuckit,
1985). Also, patients who have an inherited disorder in which their
hand
shakes, familial essential tremor, are more likely to abuse alcohol.
When
they drink alcohol, the tremor vanishes.
Another biological mechanism that may put
people at
risk for alcohol dependence is increased sensitivity to the pleasure
producing
effects of alcohol. Alcohol dependent patients will often report that
they
noticed a wonderful calm high the very first time they drank alcohol.
Alcohol
dependent patients also show pain relief, analgesia, following a small
dose of alcohol. These studies suggest that alcoholics receive more
pleasure
or obtain more pain relief compared to non-alcohol abusing people.
Similarly people who are not abusing
alcohol, but have
alcohol dependent parents, are more sensitive to the pleasure producing
effects from alcohol. They report more pleasure associated with their
first
drink (Negoshi and Wilson,1987). Also, high risk people show increased
alpha waves (a measure of relaxation) after a small dose of alcohol.
Finally,
studies show that in subjects with alcoholic parents, small doses of
alcohol
increase peripheral levels of beta-endorphin by 170 percent. In
contrast,
subjects without alcoholic parents do not have this large increase in
beta-endorphin
(Gianoulakis, 1990).
