We've all heard it. Many of us have experienced it. A few of us even swear by it—enough to ceremonially partake in a glass or two of wine before crawling into bed.
In fact, a little booze has been experimentally (and anecdotally) demonstrated to help us fall asleep faster and increase slow-wave, or deep, sleep in the first half of the night.
But its effect on other aspects of sleep—notably, the second half of the night—leaves much to be desired.
What causes alcohol's strange and dichotomous effect on the sleeping brain? And the real question—do you accept the nightcap or not?
Research on alcohol and sleep dates back to—well, almost to the dawn of sleep research as we know it.
Nathaniel Kleitman, in his 1939 book Sleep and Wakefulness (and nearly 20 years before his discovery of REM sleep), first described the effects of alcohol before bed on sleep motility and body temperature in healthy non-drinkers. With the identification of the various sleep stages in the 1950s and 1960s, researchers could begin focusing their attention on alcohol and its effect on sleep disorders.
This yielded an interesting result: despite falling asleep faster, the subjects who consumed more alcohol woke more frequently had experienced lighter sleep during the second half of the night. Williams and Salamy identified this as being a "rebound effect"; that is, after alcohol had been metabolized and eliminated, sleep variables reversed themselves—and, in fact, exceeded those values at baseline.
This manifests as disturbed sleep.
The idea is that the body initially adjusts for alcohol's effects in order to maintain normal sleep during the first half of the night. During the second half of the night, however—even after elimination—the body stubbornly continues to adjust, ultimately overcompensating and resulting in sleep disruption.
But exactly what is adjusting, and what's causing the rebound effect?
The short answer is: nobody really knows the whole story—because nobody fully understands sleep yet. But, neurochemically, we have some theories.
Alcohol mimics gamma-aminobutyric acic (GABA), the major inhibitory neurotransmitter in the brain. When bound to a GABA receptor on a neuron, alcohol allows either the influx of negative (or efflux of positive) ions, giving the cell a more negative charge. Thus, the neuron's attempt to fire an action potential is thwarted.
Similarly, alcohol also inhibits the brain's major excitatory neurotransmitter, glutamate, by blocking function at glutamate's NMDA receptors. (The same is true for acetylcholine and serotonin receptors.)
Since glutamatergic and GABAergic neurons comprise 90% of all brain cells, this is a pretty big deal.
Especially since alcohol also enhances GABA absorption back into the neuron, and even more especially since GABA is recycled into glutamate in a vicious cycle:
|Yes, I know this figure is in French!|
Should you partake in a college night of hard-partying and expect a good night's sleep? No way.
But the real question: is one drink before bed going to affect that much?
Depending on the individual, a person can metabolize 0.25 oz of alcohol each hour—which is quite slow given the speed at which it's absorbed.
So keep the drink small, and keep it early. An evening cap.
Or partake in the alternative to the liquid nightcap, which I prefer (aesthetically, anyway):
|Henry Shaw (1800-1889). Philanthropist, businessman, and fashionista.|
Roehrs, T and Roth, T. (2001). Sleep, sleepiness, sleep disorders and alcohol use and abuse Sleep Med Rev, 5 (4), 287-297 DOI: 10.1053/smrv.2001.0162
Williams, H and Salamy, A. Alcohol and sleep. In: Kissin, B., and Begleiter, H., eds. The Biology of Alcoholism. New York: Plenum Press, 435-483 (1972).
Image credit: Marcus Nisson (NYT); IWS Radio; Jon Sullivan, Pancrat, and Missouri Botanical Gardens (via Wikimedia Commons)