HOW CAFFEINE MOVES THROUGH THE BODY

HOW CAFFEINE MOVES THROUGH THE BODY

Caffeine is almost always taken by mouth, and so it is absorbed into the blood primarily through the linings of the stomach, small intestine, and large intestine. It is only slowly absorbed through the stomach, and so most absorption occurs at the next step along the gastrointestinal tract, the small intestine. However, once it reaches the intestines, virtually all of the caffeine that was ingested is absorbed. A given oral dose of caffeine takes full effect within thirty to sixty minutes, depending upon how much food is in the stomach and intestines and how concentrated the caf­feine is in the substance that contains it.

Caffeine is evenly distributed throughout the body, metabolized by the liver, and its breakdown products are excreted through the kidneys. The body eliminates it rather slowly, with the half-life of a given dose of caf­feine being approximately three hours. Thus, some of the caffeine that one consumes in the morning is still around well into the afternoon. A person who drinks several cups of coffee or caffeinated sodas across a morning or afternoon is adding on to an existing load of caffeine with each subse­quent drink and may end up feeling rather jittery by the end of the day.

HOW CAFFEINE WORKS

Caffeine is the best known of a class of compounds called xanthines (pro­nounced "zan-theenez"). Theophylline, another xanthine found in tea, is prescribed for breathing problems because it relaxes and opens breathing passages. However, there is so little of it in brewed tea that it exerts no significant stimulant effects in that form. In addition to a small amount of caffeine, chocolate contains theobromine, another xanthine, but one with far less potency than caffeine.

All the xanthines, including caffeine, have multiple actions. The major action is to block the action of a neurotransmitter/neuromodulator called adenosine, which is in the brain (more on this in the following). There are also adenosine receptors throughout the body, including those in blood vessels, fat cells, the heart, the kidneys, and many types of smooth mus­cle. These multiple actions create a confusing picture because the direct effects of caffeine on a system can be enhanced or suppressed by indirect effects on other systems.

EFFECTS ON THE BRAIN

Adenosine receptors, the main site of caffeine action, cause sedation when adenosine binds to them. Adenosine, a by-product of cellular metabolism, leaks out of cells. So, as neurons become more active, they produce more adenosine, and this provides a "brake" on all the neural activity—an ingenious self-regulation by the brain. Caffeine thus produces activation of brain activity by reducing the ability of adenosine to do As job. This is a good example of how a drug can produce an effect (in this case, central nervous system iCNSI stimulation) by inhibiting the action of a neu­rotransmitter that produces an inhibiting effect (a positive coming from two negatives). At moderate doses of around 200 milligrams (about what you get from one to two cups of strong coffee), electroencephalograph (EEG) studies indicate that the brain is aroused. Higher doses, in the range of 500 milligrams, increase heart rate and breathing. Activation of these centers also causes a constriction, or narrowing, of blood vessels in the brain (though outside the brain caffeine has a direct effect on blood vessels that does just the opposite—dilating, or widening, them).

Caffeine also lowers the amount of blood flow within the brain. It seems strange at first that a drug with such strong stimulant effects in the brain would actually decrease blood flow within the brain. But studies have shown that a dose of 250 milligrams (about what you get from two to three cups of coffee) reduces blood flow by nearly one-fourth in the gray matter of the brain (made up mostly of nerve cells) and by about one-fifth in the white matter through which fibers connect groups of nerve cells

into functioning circuits. The fact that caffeine has such powerful stimulant effects despite its decrease of cerebral blood flow underscores how powerful its stimulant effects really are. Further, the effects of a single dose of caffeine on cerebral blood flow were the same in heavy caffeine users and in light users, indicating that the blood flow effect is not one to

which people become tolerant.

People may develop a mild tolerance to some of the effects of caffeine, but most tolerant people can achieve an arousing effect by increasing the dose. The tolerance that develops to the brain-arousing effects of caffeine is less severe than the tolerance that develops to some of its effects on other parts of the body (see the following).

Dependence on caffeine can develop as well, as indicated by the occur­rence of withdrawal symptoms when caffeine intake is abruptly stopped. Between twelve and twenty-four hours after the last dose of caffeine, users generally experience headaches and fatigue that may persist for several days to a week but that are usually strongest during the first two days after quitting. Nonprescription pain relievers such as acetaminophen (Tylenol) or ibuprofen relieve the headaches, and moderate doses can be taken throughout the withdrawal period—just be careful to avoid taking pain medications that include caffeine Many people have found that they enjoy, and indeed rely on, the psy­chological effects of caffeine. While this wouldn't meet our definition of addiction, most caffeine users find the effects pleasant enough to continue using this drug. Therefore, those who decide to quit should also be pre­pared to give up those caffeine-aided feelings of alertness and mild eupho­ria, which may have become a very regular and important part of each day. A related issue is that people who drink caffeinated beverages often do so at the same or similar times of day. In that way the drinking itself may become a part of important daily rituals. It is important to anticipate that changing those rituals may be difficult as well.

Children Of Alcoholic Parents

            CHILDREN AND ADOLESCENTS

By far, alcohol is the drug used most often by high school students. Although most seniors cannot buy alcohol legally, 80 percent of them have tried alcohol and about one in five report that they have drunk heav­ily (more than five drinks in a row) in the past two weeks. This is actually good news, because the number of teens drinking heavily has declined somewhat in recent years. But that's not the end of the story. Recent stud­ies show that among students who engaged in heavy drinking, half had consumed ten or more drinks in one episode and a quarter had consumed fifteen. So, while heavy drinking at the "low" end of the scale (about five drinks in an episode) has declined recently, the rates of extreme heavy drinking have remained high.

The story among college students is not as simple as the media sometimes portray. Reports of "binge drinking" among college students can be mis­leading. First, the term hinge drinking is a bad one. Many people think of an alcohol binge as a period of several days during which a person stays drunk nearly all the time. This, of course, is a very dangerous pattern of drinking but is not what is meant by the media when they report on binge drinking among college students. In that context, binge drinking refers to a man haying five or more drinks in one sitting or a woman having four or more—clearly enough to put a person at risk for trouble, but hardly a binge in the traditional sense. We prefer to think of the four- or five-drink level as "high-risk drinking"—a more descriptive term. About 40 percent of college stu­dents report this level of high-risk drinking in the past two weeks, but there are also a significant number of college students who don't drink at all—about 20 to 25 percent depending upon the college. So it's important for students to know that, while a lot of students drink, not everybody on campus gets drunk every weekend, and a solid number of students don't drink at all. Still, there are often negative consequences for those who do. Nearly 600,000 college students suffer unintentional alcohol-related inju­ries each year, and more than 1,800 die from those injuries. In addition, 25 percent of college students report negative academic consequences related to their drinking each year, and more than 150,000 develop a health prob­lem related to alcohol use. Clearly, college drinking remains highly preva­lent and continues to take a toll on students' lives.

The problems associated with underage drinking are well known, and in recent years research has continued to show that alcohol affects the brain of younger people very differently from the way it affects that of adults. Part of this may be related to brain development. For example, we know that the brain does not finish developing until a person is in his midtwenties and that one of the last regions to mature is the frontal lobe area, which is intimately involved with the ability to plan and make com­plex judgments. Young brains also have rich resources for acquiring new memories and seem to be "built to learn." It is no accident that people in our society are educated during their early years, when they have more capacity for memory and learning. However, with this greater memory capacity come additional risks associated with the use of alcohol. Studies using animals have shown that when the brain is young, it is more sus­ceptible to some of the dangerous effects of alcohol, especially on learn­ing and memory function. And one study in humans showed that people in their early twenties were more vulnerable to the effects of alcohol on learning than were people just a few years older, in their late twenties. So it appears that children and adolescents who drink are powerfully impairing the brain functions on which they rely so heavily for learning. This is already indicated by very detailed cellular studies on learning-re­lated brain regions. In these studies (which, of course, can only be done using brain tissue from animals), it is clear that alcohol decreases the ability of brain circuits to change in the ways they must for learning to  basic cellular functioning occur far more strongly when the alcohol expo‑sure occurs during adolescence, compared to adulthood. In other words,it appears that adolescence is not only a time when single doses of alcohol affect the brain differently but also a time of enhanced vulnerability to the long-term effects of repeated alcohol exposure—even down to the level of individual brain cells. This adds to a strong and growing scientific literature that tells us that adolescents should hold off on drinking.

Another very good reason for teens to hold off on drinking is that there is a very strong relationship between the age at which one starts to drink and the likelihood of developing dependence on alcohol. People who start

drinking in their early to midteens are far more likely to develop alcohol

dependency, and to experience recurring episodes of dependency, than

are people who start drinking at age twenty-one or older. There are cer­tainly a number of reasons for this increased risk, and not all of them are biological, but it is clear from animal studies that adolescents develop tol­erance to some of alcohol's effects more rapidly than adults. In humans this could lead to a greater motivation to drink repeatedly. So, although it has always been controversial, our current state laws requiring a person to be twenty-one to drink make good sense from this perspective.

Most parents tend to be clueless when it comes to their children's drinking. For example, while 52 percent of tenth graders report having drunk alcohol in the past year, only 10 percent of parents of tenth graders believe that their child has consumed alcohol in that period. Interestingly, parents report believing that about 60 percent of tenth graders have con­sumed alcohol within the past year. So parents actually tend to overesti­mate the proportion of kids who drink—they just don't think it's their kids who are drinking! There are similar gaps between older teens' reported drinking and parents' beliefs about their drinking. Parents of twelfth graders are starting to see the light, but they still underestimate their kids' drinking significantly. The important message for parents is that alcohol is out there and its use is getting thrust at their children from many angles. Talk to your children about them.

WİLKİE WİLSON

Acohol Dependence

It is important to distinguish between alcohol dependence and alcohol abuse. Generally, alcohol abuse refers to patterns of drinking that give rise to health problems, social problems, or both. Alcohol dependence (often called alcoholism) refers to a disease that is characterized by abnormal seeking and consumption of alcohol that leads to a lack of control over drinking. Dependent individuals often appear to crave alcohol. They seem driven to drink even though they know that their drinking is causing problems for them. The signs of physical depen­dence begin within hours after an individual stops drinking. They include anxiety, tremors (shaking), sleep disturbances, and, in more extreme cases, hallucinations and seizures. Until a chronic drinker actually stops drinking, it is quite difficult to make a definitive assess­ment of alcohol dependence. But for most practical purposes, this for­mal diagnosis is unnecessary, because the social and medical problems that most alcoholics experience should be recognizable to health profes­sionals. See the section "How to Spot a Problem Drinker" on page 55 for some general guidelines.

PRENATAL EXPOSURE

The dangers of prenatal alcohol exposure have been noted since the time of Aristotle in ancient Greece. However, it was not until 1968 that formal reports began to emerge. The early studies of fetal alcohol syndrome (FAS) described gross physical deformities and profound mental retarda­tion among children of heavy-drinking alcoholic mothers. Although this was a very important set of findings, at first there was no evidence that women who drank more moderately were placing their children at risk. In fact, for many years, pregnant women were often encouraged to have a glass of wine with dinner or take a drink now and then during pregnancy to help them fall asleep or just to relax.

It took a while for the effects of moderate prenatal drinking to be noticed, because the children have none of the very obvious defects asso­ciated with the full-blown fetal alcohol syndrome. However, it is now clear that there is a less severe, but very well documented, pattern of defi­cits associated with more moderate prenatal drinking—a pattern described as fetal alcohol effects (FAE). School-age children with FAS or FAE are frequently described as hyperactive, distractible, and impulsive, with short attention spans—behaviors similar to those observed in chil­dren with attention deficit disorder (ADD). However, the FAS and FAR children differ from ADD children in that they are more intellectually

impaired. In recent years the term fetal alcohol spectrum disorders (FASD) has emerged as an umbrella term to include the full range of neurological, cognitive, behavioral, and learning disabilities associated with prenatal alcohol exposure.

The impairments of intelligence and behavior in people with FASD appear to persist into adulthood and are probably lifelong, resulting in IQ scores markedly below average, often well into the moderately retarded range. Those with PAS scored worse than those with RAE, but both were significantly below normal, hampered in reading and spell­ing and most profoundly deficient in mathematical skills. More import­ant, the FAE patients did not perform any better than the FAS patients on academic achievement tests, though their IQs were somewhat higher. What all this means is that even moderate drinking during pregnancy can create permanent intellectual disabilities. Some studies using animal models of FAE even suggest that just one drink per day impairs the function of brain areas related to learning in the adult offspring.

The bottom line is that there is no identified safe level of drinking during pregnancy. The smart decision for a woman is simply not to drink if she is pregnant or thinks that she might be.

Chronic Alcohol Abuse

Effects on Mental Functioning

Five areas of mental ability are consistently compromised by chronic alcohol abuse: memory formation, abstract thinking, problem solving,attention and concentration, and perception of emotion. As many as 70 percent of people who seek treatment for alcohol-related problems suffer significant impairment of these abilities.

Memory Formation

By memory formation we mean the ability to form new memories, not the ability to recall information that was learned in the past. That is, an individual with a chronic drinking habit might vividly and accurately recall what he learned early in life but not be able to tell what he ate for lunch four hours ago. And the richness and detail of his memories during the past few years of drinking might be significantly less than in those earlier memories. On some tests of mental ability that assess differ­ent kinds of brain functions, chronic drinkers often perform lust fine on most of the categories but perform poorly on the memory sections. This selective and profound memory deficit may be a result of damage to spe­cific brain areas, such as the hippocampus, the mammillary bodies, or the frontal lobes.

Abstract Thinking

By abstract thinking we mean being able to think in ways that are not directly tied to concrete things. We think abstractly when we interpret the meaning of stories, work on word puzzles, or solve geometry or alge­bra problems. Chronic drinkers often find these abilities compromised. One way to measure abstract thinking is to show someone a group of objects and ask her to group the objects according to the characteristics they share. Chronic drinkers will consistently group things based on their concrete characteristics (such as size, shape, and color) rather than on the basis of their abstract characteristics (such as what they are used for, or what kinds of things they are). It is as if abstract thoughts do not come to mind as easily for the chronic drinker.

Problem Solving

We all have to solve problems each day. Some are simple ones, like deter­mining whether to do the laundry or the grocery shopping first. Some are more complicated, like setting up a new personal computer or deciding on what inventory to order for the next month's needs in a business. In either case, one of the required abilities is mental flexibility. We need to be

able to switch strategies and approaches to problems (particularly the complicated ones) to solve them efficiently. People with a history of chronic drinking often have a lot of difficulty with this. Under testing conditions, it often appears that they get stuck in a particular mode of problem solving and take a lot longer to get to a solution than someone who is better able to switch strategies and try new approaches. This diffi­culty could relate to the effects of chronic drinking on the "executive functions" of the frontal lobes.

Attention and Concentration

Chronic drinkers also develop difficulty in focusing their attention and maintaining concentration. This appears to be particularly difficult when related to tasks that require visual attention and concentration. Again, the deficits may not appear until the person is challenged. In casual conversa­tion, the sober chronic drinker may be able to concentrate perfectly well, but placed in a more challenging situation (like reading an instruction manual, driving a car, or operating a piece of equipment), she may be quite impaired.

Perception of Emotion

One of the most important elements of our social behavior is the ability to recognize and interpret the emotions of other people. Alcoholics have a deficit in the ability to perceive emotion in people's language. There is a specific brain function that normally gives us the ability to detect attitude and emotion in conversation. It turns out that chronic, heavy drinking markedly reduces this ability. It is important to realize that this deficit is one of perception and does not reflect the alcoholic's own emotional state. It's as if the subtle things like the tone and cadences of the other person's language that convey attitude and emotion are simply not perceived by the alcoholic. This is particularly interesting because we know that chronic heavy drinkers often have difficulty in social relationships. Per­haps this perceptual deficit causes some of these problems.

Do These Deficits Go Away?

Chronic heavy drinkers who quit recover these functions partially during the first month or two after the last drink. However, once this

time passes, they have gotten back all that they will recover. It is difficult to identify precisely how much recovery occurs, but clear deficits do appear to persist permanently in these individuals. In one study, people who had quit drinking completely after many years of alcohol abuse were examined for seven years. Even after this time they had significant memory deficits. This persistent pattern of memory deficits in previous alcoholics is common enough to have a specific diagnosis. It is generally

called either alcohol amnestic disorder or dementia associated with alcoholism.

SCOTT SWARTZWELDER

Short Term Effects Of Alcohol On The Brain

Brain-imaging techniques create a window into the effects of alcohol on the brain. Using these techniques, researchers have observed shrinkage of brain tissue in people after long-term use of alcohol. But there is also recovery of brain tissue volume in people who stop drinking and remain abstinent, so this "shrinking" effect appears not to be due exclusively to the loss of brain cells. Interestingly, some studies indicate that certain parts of the brain may be more vulnerable to damage by alcohol than others, such as the cortex—the folded, lumpy surface of the brain (it gets its name because of its resemblance to the bark of a tree), which endows us with consciousness and controls most of our mental functions. One region of the cortex that appears to be particularly vulnerable is the frontal lobe. The frontal lobes are unique in that they act like a kind of executive manager for the rest of the brain. They monitor and help to coordinate the actions of the other cortical lobes—much like an execu­tive does in a corporation. The analogy is so apt that the functions of the frontal lobes are often called "executive functions." They endow us with the ability to bring together our mental abilities to solve complex prob­lems, to make and execute plans of action, and to use judgment in ser­vice of those plans. Even in people who have never been diagnosed with an alcohol use disorder, chronic drinking can contribute to frontal lobe damage. Another vulnerable region is the mammillary bodies, which are very important for memory. (These small, round structures near the base of the brain got their name from the neuroanatomists who first noticed them and thought that they looked like breasts. Actually, their resemblance to breasts is quite remote, but neuroanatomists do have good imaginations!)

Although many of the studies of brain shrinkage have been done with alcoholics, some of the more recent ones have assessed social drinkers and found similar effects, though less severe. The shrinkage occurs while the person is still using alcohol. If she stops drinking for a prolonged period, her brain will recover somewhat—not because new nerve cells grow but because support cells, or parts of the remaining nerve cells, grow. Therefore, the regrowth of brain size does not mean that the deficits in mental functioning that many alcoholics experience will be erased simply by abstaining from alcohol.

It is not known if there is a safe level of chronic drinking. Clearly many people who drink do not appear to suffer any damage to their mental functioning. Still, as with acute intoxication, the lack of any obvi­ous impairment does not mean that there is none. Studies using animals instead of humans can look more closely at nerve-cell damage. Such studies have shown that more moderate alcohol exposure can damage and kill brain cells. A number of these studies have shown large areas of nerve-cell loss in a region of the brain called the hippocampus, which is known to be critical for the formation of new memories. This could be one reason why people who drink chronically can end up with relatively poor memory function, though of course this will vary with the person's drinking history.

Another study in animals has shown that in the case of very heavy drinking, brain damage may occur much sooner than previously thought. Using a model in which animals are exposed to a heavy "binge" of alcohol around the clock for four days, it was discovered that cells in some of these same regions started to die off after the first two days of the binge. If this holds true for humans, it will show that even one very heavy episode of binging across a couple of days could damage the brain. These effects were

          particularly pronounced in adolescent animals, raising some concern that teenage binge drinking may have more serious long-term consequences than we once thought.

                                                                                                                                                 
                           Wilke Wilsion

BRAIN AND BEHAVIOR

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

of the brain.

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