“Alcohol makes you sleepy.”
We’ve all heard about it. Many of us have experienced it. A few of us even swear by it — enough to 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 effects on other aspects of sleep — notably, the second half of the night — leave little 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.
Nathaniel Kleitman, in his book “Sleep and Wakefulness” (published in 1939, 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 nondrinkers. 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.
Perhaps the best replications of, er, college life, anyway, came with studies by Williams and Salamy in the early 1970s. Thirty to 60 minutes before bedtime — which yields the peak blood-alcohol concentration at lights-out — participants were assigned to consume anywhere one to six drinks. (A standard drink is 12 ounces of beer, five ounces of wine or 1.5 ounces of 80-proof distilled spirits.)
This yielded an interesting result: Despite falling asleep faster, the subjects who consumed more alcohol woke more frequently and experienced lighter sleep during the second half of the night. Williams and Salamy identified this as being a “rebound effect.” After alcohol had been metabolized and eliminated, sleep variables reversed themselves.
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, 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.
When you take a swig of alcohol, it goes right into the bloodstream, and it’s in your brain within minutes.
Alcohol mimics gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the brain. When bound to a GABA receptor on a neuron, alcohol allows 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.
Alcohol also inhibits the brain’s major excitatory neurotransmitter, glutamate, by blocking function at glutamate’s NMDA receptors.
Since glutamatergic and GABAergic neurons comprise 90 percent 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: After an evening of drinking, the theory is that GABA dominates the first half of the night, allowing us to fall asleep (and deeply!). But once GABA is metabolized, much of it becomes the excitatory glutamate. And it’s in glutamate-releasing brain regions (such as the reticular activating system which partially modulates sleep/wake and arousal) that the midnight disruptions kick in.
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?
A typical person can metabolize something like a quarter of an ounce 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.
This was excerpted from the Gainesonbrains blog.