Substance Use Disorders 407
confusion, and, in some cases, seizures (NIDA, 2005c). People who have become
dependent on a barbiturate and want to discontinue or decrease their intake of
the drug should do so only after medical consultation to determine an appropriate
schedule for tapering off without inducing dangerous withdrawal symptoms; other-
wise, abrupt discontinuation of the drug can lead to convulsions and death.
Benzodiapines
Benzodiazepines are usually prescribed to alleviate muscle pain, to aid sleep, or as
a short-term treatment for anxiety (see Chapter 7); however, long-term use leads
to tolerance and withdrawal. Examples of benzodiazepines include lorazepam
(Ativan), triazolam (Halcion), chlordiazepoxide (Librium), diazapam (Valium), and
alprazolam (Xanax). As with barbiturate dependence, a person with benzodiazepine
dependence should gradually taper off of the drug, in consultation with a physician.
For people who are dependent on these drugs, abruptly stopping use can lead to
seizures and psychosis.
Understanding Depressants
In what follows, we will fi rst discuss how brain systems and neural communication
are affected by depressants in general and then turn to the effects of alcohol in par-
ticular. A considerable amount is known about the genetics of alcoholism, and we’ll
look closely at these fi ndings before considering psychological and social factors.
Neurological Factors
In this section, we consider a set of closely related topics: the effects of depressants
on the GABAnergic system, the neural bases of alcohol abuse and dependence, and
the genetics of alcoholism.
Brain Systems and Neural Communication
Benzodiazepines (such as Valium), barbiturates, and alcohol directly affect the
GABAnergic system, which is widespread in the brain and primarily activates in-
hibitory neurons. The resulting inhibition affects neurons in brain structures that
are involved in anxiety, such as the amygdala. As we’ve noted before, the amygdala
plays a key role in fear, and hence inhibiting it dulls the sense of fear and the related
feeling of anxiety. Thus, it is not surprising that people who experience anxiety,
for whatever reasons, fi nd the use of depressants particularly reinforcing. In fact,
those who suffer from phobias or panic disorders are at high risk to abuse alcohol
and other depressants (Pihl, 1999). Depressants also indirectly affect the dopamine
reward system.
Like other depressants, alcohol inhibits neurons, which has the net effect ofdampening—or depressing—the nervous system so that it is less responsive. How-
ever, some of the brain systems that are most affected by alcohol normally inhibit
other brain systems, which thereby become disinhibited—which is why people may
seem “looser” after a couple of drinks, perhaps by talking more than usual or act-
ing impulsively. Alcohol has a number of distinctive effects, which we consider in
the remainder of this section: the nature of withdrawal, hangovers, and indirect ef-
fects on nutrition.
Chronic Alcohol Drinking and Withdrawal Although alcohol consumption induces the
production of dopamine, which is rewarding, chronic use of alcohol stimulates
the production of a type of neurotransmitter called endogenous opioids, sometimes
referred to as “pleasure chemicals.” (There is a class of drugs referred to as opioidsor
opiates, which we’ll discuss later in the chapter. The word endogenous—meansorigi-
nates within the body—is used to distinguish the neurotransmitter opioids from the
drugs of the same name.) Endogenous opioids are responsible for “runner’s high,”
the feeling that occurs when someone has pushed herself or himself to a physical
limit and experiences a sense of deep pleasure. In chronic drinkers, the activity of
endogenous opioids occurs only in response to alcohol; when they stop drinking,
their bodies no longer produce endogenous opioids. Thus, when a chronic drinker