研究表明酒精可以使人昏昏欲睡同时也能将人在半夜唤醒

研究表明酒精可以使人昏昏欲睡同时也能将人在半夜唤醒

A night cap may get you to sleep, but studies show it may also wake you up during the night

“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.

A nightcap.

In fact, a little booze has been experimentally (and anecdotally) demonstrated to help us fall asleep fasterand 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.

我们都听说过“酒精能使人昏昏欲睡”。很多人有过这样的经历。有些人甚至对此深信不疑，乃至在爬上床之前一定要喝上一两杯。

睡前酒

实验证明（也如传闻所说），喝一杯小酒有助于我们快速入眠，对于上半夜进入深眠也大有益处。

但它对睡眠其他方面的影响，尤其是下半夜的睡眠，就不尽如人意了。

是什么导致了酒精对熟睡中的大脑产生这种奇怪而且在不同时间段截然不同的影响呢？真正的问题在于，你能否在睡前喝酒呢？

关于酒精和睡眠的研究几乎要追溯到睡眠研究产生之初。

纳撒尼尔·克莱特曼（Nathaniel Kleitman）在他的书《睡和醒》（“Sleep and Wakefulness”）（这本书出版于1939年，20年后他发现异相睡眠）中首次描述了睡前喝酒对健康的非酒徒睡眠运动和体温的影响。随着20世纪五十至六十年代睡眠各阶段的划分，研究者开始关注酒精及其对睡眠障碍的影响。

对大学生活影响最深可能要数20世纪70年代威廉姆斯（Williams）和萨拉米（Salamy）所做的调查。

睡前30-60分钟实验参与者被分配到各处饮用了1-6杯酒，熄灯之后血液中的酒精浓度达到了峰值。（这里一杯酒的标准相当于12盎司啤酒，5盎司葡萄酒或者1.5盎司80度的蒸馏酒）

这个调查产生了一个有趣的结果：尽管实验对象很快入睡，但是他们摄入的酒精越多，醒来得越频繁，并且他们在下半夜睡得越浅。威廉姆斯和萨拉米认为这是“反弹效应”。在酒精新陈代谢后，睡眠的波动就与之前颠倒了。

这表现为干扰睡眠。

这个观点是，人体开始因酒精影响而不断调整适应，从而在上半夜得以维持正常的睡眠。但在下半夜，机体仍然惯性地调整适应，最终由于过度补偿导致了睡眠紊乱。

但准确的说是什么在调整，又是什么引起了“反弹效应呢”？

简单来说：我们无从知晓。因为迄今为止，还没有人能参透睡眠的奥秘。但从神经化学的角度去考虑，我们有一些理论可以说明。

当你喝酒的时候，酒精会很快进入血液循环，并很快流经大脑。

γ-氨基丁酸（GABA）是大脑中重要的抑制性神经递质。当酒精与GABA受体结合，负离子流入（或正离子流出），使得

细胞中有更多的负电荷。因此神经元不能触发动作电位。

酒精能阻断NMDA受体功能，抑制大脑中重要的兴奋性神经递质—谷氨酸。*

大脑的90%由谷氨酸能神经元和GABAergic神经元构成，数目相当庞大。特别的是，酒精也可以加强神经元对GABA的重吸收，甚至，GABA再循环生成谷氨酸盐，进入恶性循环：这个理论说明了，在一整晚的豪饮之后，上半夜，GABA在大脑中起着主导作用，允许我们入睡（并且进入深眠）。不过，一旦GABA被代谢，大部分GABA转化成了兴奋性的谷氨酸盐。正是谷氨酸盐释放的大脑区域（如部分调节睡/醒和唤起的网状激活系统）这破坏了午夜的睡眠。

你还想在一个狂欢豪饮的大学之夜后睡个好觉吗？没门儿！

但问题在于，睡前喝一杯真有那么大的影响吗？

研究表明一个特定的人可以每小时代谢四分之一盎司的酒精，这远远慢于酒精的吸收速度

因此，如果一定要喝酒，那么就少喝点，早喝点。傍晚喝也未尝不可。

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