By Mary S. Esther, M.D.

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 history.

Alcohol's Effects

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 years.

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 programs.

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