Sleep disorders and substance abuse disorders are widespread across
the United States, researchers have found. According to the National
Commission on Sleep Disorders Research, more than 80 million Americans
complain of sleep difficulties, while Schuckit and Irwin reported
the lifetime prevalence of alcohol abuse or dependence to be 13
percent and nonalcohol drug abuse, 5.9 percent.
People with substance-related disorders consume psychoactive substances
such as alcohol, caffeine, stimulants, sedative-hypnotic agents
and nicotine routinely in an effort to achieve the desired effect
upon alertness. Obtaining information from patients regarding
their sleep habits, as well as their use of psychoactive substances
to manipulate sleep and alertness, is an important part of a complete
Alcohol has known effects upon sleep physiology in both intoxication
and withdrawal. In moderate dosages (3 to 8 ounces), alcohol will
initially shorten sleep latency and decrease REM (dream) sleep
in the first half of the night. However, later in the night, REM
sleep will rebound and the patient will experience more frequent
arousals with fragmentation of sleep. While individuals develop
tolerance to the sedating effects of alcohol over time, they can
learn to override that tolerance by increasing the amount of alcohol
consumed near bedtime. As the blood alcohol level falls throughout
the night, the known somatic effects of this falling blood alcohol
level also contribute to the fragmentation of sleep. And for the
recovering alcoholic, the effects upon sleep, with a decrease
in slow wave sleep and more frequent arousals, may persist for
Alcohol also clearly increases the frequency of upper airway obstruction.
With the prevalence of obstructive sleep apnea estimated to be
approximately 4 percent of those aged 40 to 59, it is important
to advise patients of the effects of alcohol upon sleep and breathing.
Twenty-four percent of patients age 65 and older have more than
five apneic events per hour of sleep. Alcohol appears to selectively
decrease the motor activity of the upper airway muscle dilators,
thus increasing the risk of upper airway collapse. In addition,
alcohol alters the arousal threshold response to hypoxemia and
hypercapnia, elongating the apneic events. Alcohol can induce
apneic events not only in snorers, but in healthy asymptomatic
males as well.
A clinical correlation exists between sleep disorder diagnoses
and alcohol dependency or abuse, with higher frequency of alcoholism
seen in patients with disorders of hypersomnolence (such as sleep
apnea syndrome) as well as in those patients with complaints of
insomnia or poor sleep maintenance.
This correlation is also present in patients with narcolepsy,
a disorder defined by its extreme effects on daytime alertness.
As many of these patients will need to be treated with psychoactive
substances, a thorough history of drug and alcohol use, along
with patient education regarding the effects of alcohol upon sleep
and sleepiness, is essential.
It is important to note that the sleepiness that is induced by
alcohol is potentiated by sleep deprivation, Zwyghuiz-en-Doorenbos
and others reported. This enhancement of alcohol's sedating effect
by sleep deprivation raises significant concerns regarding safety
while driving. Since sleep deprivation may be significant among
patients with insomnia and other sleep disorders, physicians should
advise them of this potentiating effect. The National Transportation
Safety Board has found that lethal accidents are in large part
accounted for by the effects of alcohol coupled with sleepiness.
Given the obvious public health risks that sleepiness induces,
it is extremely important that the public be made aware of both
the hazards of sleepiness and the availability of risk management
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