Once alcohol has been absorbed and distributed, it has many
different effects on the brain and
behavior. To a large extent these effects vary with the pattern of drinking.
Therefore, we discuss the effects of acute, chronic, and prenatal alcohol exposure separately.
ACUTE EXPOSURE
Effects on Behavior and Physical State
Although the effects that a given dose of alcohol
will have on an individual vary considerably, the following table shows the
general effects of a range of alcohol
doses:
Still, there is often
a substantial difference between being impaired and appearing impaired. In one study, trained observers
were asked to rate whether a person
was intoxicated after drinking. At low blood alcohol concentrations (about half the legal limit for
intoxication), only about 10 percent
of the drinkers appeared intoxicated, and at very high concentrations (greater than twice the legal limit), all of the
drinkers appeared intoxicated. However,
only 64 percent of people who had blood alcohol concentrations of 100-150 mg/100 ml (well above the legal limit
in most states) were judged to be
intoxicated. So, in casual social interactions, many people who are significantly impaired—and who would pose a real
threat behind the wheel of a car—may
not appear impaired even to trained observers.
Alcohol and Brain Cells
You've probably heard some variation of the
following statement: "Every time
you take a drink of alcohol you kill ten thousand brain cells." Although it is highly unlikely that anyone would
drink enough alcohol in a given sitting to kill brain cells directly, as with
many such generalizations there is a
grain of truth in the warning.
One way that researchers have tried to determine
which brain regions control which
behaviors in animals is by destroying, or lesioning, a specific brain region and then testing the animal on a
particular behavioral task.
Early
in the use of this lesioning technique, some researchers found that if they injected a very high concentration of alcohol
into the brain (far higher than would
be achieved by a drinking person), the cells in that region would die. There is also another grain of truth in
the warning about alcohol and brain
cells: chronic, repeated drinking damages and sometimes kills the cells in
specific brain areas. And it turns out that it might not take a very long history of heavy drinking to do so. We
will address this in the "Chronic
Exposure" section of this chapter.
There are fundamentally only two types of actions
that a chemical can have on nerve
cells—excitatory or inhibitory. That is, a drug can either increase or decrease the probability that a
given cell will become active and
communicate with the other cells to which it is connected. Alcohol generally depresses this type of
communication, or synaptic activity,
and thus its actions are similar to those of other sedative drugs, like barbiturates (such as phenobarbital)
and benzodiazepines (such as Valium). Despite this general suppression of
neuronal activity, however, many
people report that alcohol activates or stimulates them, particularly soon after drinking, when the
concentration of alcohol in the blood
is increasing. Although we don't know exactly why alcohol produces feelings of stimulation,
there are a couple of possibilities.
First, there is the biphasic action of alcohol. This refers to the fact that at low concentrations alcohol
actually activates some nerve cells. As the alcohol concentration increases,
however, these same cells decrease
their firing rates and their activity becomes suppressed. Or it might be that
some nerve cells send excitatory signals to the other cells with which they communicate, prompting them to send inhibitory messages, actually suppressing the activity
of the next cell in the circuit. So, if alcohol suppresses the activity of one
of these "inhibitory" cells,
the net effect in
the circuit would be one of activation.
Whatever the exact mechanism, it appears that there are several ways in which alcohol can have activating as well
as suppressing effects on neural
circuits.
Effects on Specific Neurotransmitters GABA and Glutamate
For many years it was generally thought that
alcohol treated all nerve cells equally, simply inhibiting their activity by disturbing the structure of the membrane that surrounds each cell. In this
sense the effects of alcohol on the
brain were thought to be very nonspecific. However, it is now clear that alcohol has specific and powerful
effects on the function of at least two particular types of neuronal receptors:
GABA receptors and glutamate
receptors. GABA and glutamate are chemical neurotransmitters that account for much of the inhibitory and excitatory activity in the brain. When the terminals of one
cell release GABA onto GABA receptors
on the next cell, that cell becomes less active. When glutamate lands on a glutamate receptor, that cell
becomes more active. It is in this way that many circuits in the brain maintain
the delicate balance between excitation and inhibition. Small shifts in this
balance can change the activity of
the circuits and, ultimately, the functioning
Alcohol increases the
inhibitory activity of GABA receptors and decreases the excitatory activity of glutamate receptors.
These are the two primary ways
alcohol suppresses brain activity. While the enhancement of GABA activity is probably responsible for
many of the general sedating effects
of alcohol, the suppression of glutamate activity may have a more specific effect: impairment in the
ability to form new memories or
think in complex ways while intoxicated. We know that the activity of a particular subtype of glutamate receptor,
called the NIVIDA receptor, is very
powerfully inhibited by alcohol—even in very low doses. The NMDA receptor is also known to be critical for
the formation of new memory.
Alcohol's powerful suppression of activity at the NMDA receptor may therefore account Mr the memory deficits that
people experience after
drinking. Dopamine
The neurotransmitter dopamine is known to underlie
the rewarding effects of such highly
addictive drugs as cocaine and amphetamine. In fact, dopamine is thought to be the main chemical messenger in the reward centers of the brain, which promote the
experience of pleasure. Alcohol drinking increases the release of dopamine in
these reward centers, probably
through the action of GABA neurons, which connect to the dopamine neurons. Studies in animals show that the
increase in dopamine activity occurs
only while the concentration of alcohol in the blood is rising—not while it is falling. So, during the
first minutes after drinking the
pleasure circuits in the brain are activated, but this "dopamine
rush"
disappears after the alcohol level stops rising.
This may motivate the drinker to
consume more alcohol to start the pleasure sequence again—"chasing the high." The problem is
that although the dopamine rush is
over, there is still plenty of alcohol in the body. Continued drinking in pursuit of the pleasure signals could push
the blood alcohol concentration up to
dangerous levels.
Effects on Memory
One
of the most common experiences people report after drinking is a failure to remember accurately what happened
"the night before." In more
extreme cases, after heavy drinking, people often report that whole chunks of time simply appear to be blank,
with no memory at all having been
recorded. This type of memory impairment is often called a "blackout." (Less extreme versions of
this type of memory loss have been
called "brown outs" or "gray outs," in which the person may
have only very hazy or incomplete memory
for the events that occurred during
the period of intoxication. In these instances, and even in blackouts, the drinker may remember more about events
when reminded of them.) In the past,
blackouts were thought to be relatively rare and were viewed as a strong indicator of alcoholism by many
clinicians. However, it turns out
that blackouts are far more common than previously thought and don't just occur in people with
serious alcohol problems. Researchers are now beginning to look more closely at
how and when blackouts occur, and
there appear to be some disturbing trends. First of all, blackouts appear to be quite frequent among
college students, with as many as 40
percent reporting them. But it's not just the memory loss that's disturbing--it's what happens during the
periods for which no new memories are
made. In one survey, students reported that after a night of heavy drinking
they later learned about sexual activity, fights with friends, and driving, for
which they had no memory at all. So it seems
that blackouts may well be a serious health risk over and above the direct effects that alcohol has on the brain.
Sadly, many people joke about
blackouts as an embarrassingly funny result of heavy drinking. But they are no joke. Think about it this way:
anything that impairs brain function
enough to interrupt memory formation is very dangerous. If it were a blow to the head, exposure to a
toxic chemical, or a buildup of pressure in the brain that caused the blackout,
it would be taken very seriously.
Alcohol-induced blackouts should be taken seriously as well. Short
of blackouts, though, it is also clear that alcohol impairs the ability to form new memories even
after relatively low doses. Therefore,
having a couple of beers while studying for an exam or preparing for a presentation at work is probably not a
good strategy. The alcohol may promote
relaxation, but it will also compromise learning and memory.
Hangover
One of the best-known symptoms of a hangover is a
pounding headache. The cause is not
exactly clear, but it is probably related to the effects of alcohol on blood vessels and fluid balances in the body. In
any case, it is much easier to
prevent the onset of pain than it is to relieve the pain once it has started. Therefore, the sooner a
pain reliever is taken, the better.
Some people take one before going to bed after a night of drinking. This way the chemicals in the pain
reliever can prevent the pain signals
in the brain from getting started as the alcohol is eliminated from the body. However, Tylenol
(acetaminophen) should not be taken to
treat a hangover because it can interact in a very dangerous way with alcohol and its by-products and damage the
liver in some people. Aspirin or
ibuprofen can be used instead, but both of these drugs can irritate the stomach
and small intestine and together with alcohol may cause gastric upset.
The upset stomach and
nausea associated with a hangover are harder to deal with. These may be caused by the toxic by-products of alcohol elimination,
irritation to the stomach, or both. No medicines treat these effects specifically. Rather, the best strategy is to eat foods that are
gentle on the stomach and to drink
plenty of fluids. Morning coffee may help to start the day after a night on the town, but its
irritating effects on the stomach may make it an unpleasant waking. And because
caffeine is a diuretic, it may also
contribute to the dehydration that often accompanies alcohol drinking.
CYNTHİA KUHN
