Further, alcohol may continue to disturb sleep even after the breath alcohol concentration is undetectable. Sleep deprivation due to alcohol consumption can exacerbate performance impairment and daytime sleepiness. People with insomnia may have difficulty falling asleep or keep waking up during the night.

Both acute and chronic alcohol consumption alter the activity of many of these neurotransmitters—such as serotonin, norepinephrine, GABA, glutamate, and noradrenaline—as well as affect other sleep factors. These alterations may contribute to the sleep disturbances observed both in alcoholics and in people undergoing alcohol withdrawal. For the most part, however, the specific mechanisms underlying the relationships between neurotransmitter function, alcohol, and sleep disturbances still require further elucidation. Some studies have estimated that 6 to 19 percent of the general population and 15 to 28 percent of people with insomnia have used alcohol to promote sleep (Brower et al. 2001; Johnson et al. 1998; National Sleep Foundation 2000). To assess the use of alcohol as self-medication for sleep problems more thoroughly, Roehrs and colleagues (1999) studied 20 nonalcoholic adults in the laboratory, 11 of whom had insomnia and 9 of whom were normal sleepers.

The Human Sleep Cycles

However, since the effects of alcohol are different from person to person, even small amounts of alcohol can reduce sleep quality for some people. In fact, between 35% and 70% of individuals who use alcohol have insomnia.3 It may seem surprising, considering that alcohol is a depressant, yet alcohol is known to interfere with fundamental aspects of sleep quality. This article first describes briefly the various sleep stages that researchers have identified and how they are measured. It then reviews alcohol’s effects on the sleep of alcoholics, including effects observed during active drinking, acute alcohol withdrawal, and sustained sobriety. The discussion continues with the potential relationship between sleep problems and the development of alcoholism as well as the possible role of sleep disturbances in predicting relapse to alcoholism. The article concludes by exploring treatment implications of these findings.

In contrast to generalized sleep activity across the brain, “local” sleep involves activities in certain neurons or neuronal assemblies leading to regional sleep-like neuronal activity patterns. These activities are then propagated to other brain regions via signaling systems. Insomnia results from a mismatch involving persistent activity in wake-promoting structures during NREM sleep, leading to simultaneous sleep and wake activity along with psychophysiological arousal (Buysse et al., 2011). From a clinical perspective, insomnia occurs in vulnerable patients with predisposing factors, such as having a family history of AD or certain genetic traits.

Personalized Sleep Profile

Alcohol interrupts this process, causing abnormalities in how circadian hormones are released. Alcohol dependency is rarely the only issue a person in withdrawal is dealing with. This is why a comprehensive approach to treatment is often the key to a successful recovery.

insomnia and alcoholism

Some people may resort to drinking alcohol as a sleep aid or agent that initiates sleep. Consuming two servings of alcohol per day for men and insomnia and alcoholism one serving for women can reduce sleep quality by 9.3%. However, even small amounts of alcohol can have noticeable effects in some people.

Preventing Alcohol Withdrawal Insomnia

They may believe it reduces their anxiety over the day’s events and helps them get to sleep. If this pattern repeats daily, a person is more likely to become dependent upon alcohol to fall asleep. Binge drinking occurs when a man has five drinks, or a woman has four drinks within two hours. This pattern of drinking is linked to insomnia, which can develop after binging. One study on binge drinking and insomnia found that people who binged two days a week had an 84% higher chance of having insomnia.

GABA mediated hyperpolarization of cortical and thalamo-cortical
neurons is thought to underlie the calcium channel mediated burst firing that results in
EEG delta activity (Steriade 1999). While alcohol
does not lead to presynaptic GABA release in the thalamus or cortex the way it does in
some other brain regions (Kelm, Criswell, and Breese
2011), https://ecosoberhouse.com/ it does enhance the function of GABAA receptors. The movement between NREM and REM sleep involves a complex interaction between
REM-on and REM-off neuronal groups in the brainstem. The REM-on groups largely consist of
cholinergic cells in the lateral dorsal tegmentum (LDT) and the pedunculo pontine tegemental
(PPT) nuclei.