The World of Caffeine (54 page)

Nevertheless, millions of students use caffeine to fuel “all-nighters.” Based on the available scientific evidence, how does this use of caffeine affect studying and test taking? Caffeine helps people to feel less drowsy and less fatigued, be better able to perform some manual or perfunctory tasks, such as typing or calculating, and, under certain circumstances, to be more capable of sustaining rapid thought and to remember more. However, some studies have found that caffeine does not significantly alter numerical reasoning, short-term memory of complex data, or verbal fluency. In other words, caffeine may help you to stay awake, but it won’t necessarily improve your intellectual skills.

Students depending on caffeine to extend their study time should also be aware of its possible adverse effects when taken in large quantities and be prepared for the crash after its stimulating powers subside. As Socrates suggested, the best guide for students is to know themselves: From a couple of Vivarin tablets, the sensitive may experience restlessness, anxiety, nausea, headache, tense muscles, and sleep disturbances, or a subsequent letdown, while others, from a much higher dose, might feel fine.

A recent startling discovery by Menachem Segal, professor of neurosciences at the Weizmann Institute in Rehovot, Israel, and an expert on neuromodulators in the brain, suggests that caffeine causes changes to brain cells that are likely to have profoundly beneficial effects on
long-term memory
.
¹¹
In earlier research, Segal discovered that increasing the amount of calcium absorbed by brain cells is one way of improving longterm memory. Because caffeine augments the ability of these cells to metabolize calcium, Segal studied the effects of adding caffeine directly to the hippocampus, an area of the brain that is critical to learning and long-term memory, to test the hypothesis that the calcium levels inside the cells would rise as a result. The outcome of his experiment confirmed this conjecture, proving that caffeine increased the calcium levels in brain cells. But Segal also observed a more astonishing phenomenon:
Caffeine caused existing dendritic spines, the branching extensions
at the ends of nerve cells that allow them to make synaptic connections with each other, to grow longer and even caused new
spines and branches to develop as well
. Although no direct experimental data are available on the actual effects, if any, of caffeine on long-term memory,
¹²
neuroscientists have long believed that an improvement in “wiring” does in fact improve both long-term memory and learning. If this connection is demonstrated in future studies, caffeine would be confirmed as
the
only known substance that can augment brain functions by altering the physical structure of the brain
.

Few people would ever question that caffeine helps to keep you awake and alert during the day. In 1990 this phenomenon was first systematically investigated under laboratory conditions and quantified using sophisticated measuring techniques: Researcher Zwyghuizen-Doorenbos led a group of scientists who orally administered 250 mg of caffeine at 9 A.M. and 1 P.M. on two successive days. Checking repeatedly for objective parameters of wakefulness and alertness, they determined that caffeine does in fact help keep people awake and alert. More surprisingly, the subjects who had been previously given caffeine continued to demonstrate increased alertness over the placebo group, even on the third day of the experiment, on which a placebo containing no caffeine was administered to all participants. In discussing this study, researcher Jack James concludes that this extended effect is psychological rather than pharmacological, asserting the “development of conditioned alerting responses to certain contextual stimuli that had been associated with caffeine (e.g., the coffee beverage vehicle used to administer the drug) during the previous two days.”
¹³
In ordinary parlance, this means that if you think you are drinking a caffeinated beverage, you may wake up just as if you had actually drunk it simply because you expect that you will.

A broad range of studies from the 1930s through the 1990s have produced conflicting findings about caffeine’s effect on reaction time.
¹⁴
Some of the apparently contradictory results may be explained in terms of the 1987 findings of researcher J.D. Roache and R.R.Griffiths, who found that reaction times were improved more by a dose of 400 mg of caffeine than by doses of 200 mg or 600 mg.
^15
,
16
Inother words, there is no simple, linear relationship between dosage and improvement in reaction time of which we could state, “If some is good, more is better.” Other studies have confirmed that varying amounts of caffeine produced similarly differing effects on reaction time, finding, for example, that in young adults 300 mg of caffeine significantly improved scores, while doses of 600 mg left them unaffected.

As in the debate over the nature and extent of improvements in
cognitive performance,
there has been some controversy over whether caffeine can improve
psychomotor performance
only if you are fatigued to begin with or whether it improves such performance even in a well-rested person. Most researchers agree that it is now well established that the beneficial effects of caffeine are found both before and after decrements in performance owing to fatigue. For example, it has been demonstrated that real-life and simulated automobile driving performance levels are improved by caffeine, irrespective of whether the person was tired or well rested to start.
¹⁷

Alertness, the complex of mental capacities that suffer during sleep loss, was studied by Michael H.Bonnet and colleagues in 1994 when he compared the value of caffeine and naps in helping to sustain performance during two days and nights of sleep loss.
¹⁸
Previous studies had shown that performance during sleep loss is, not surprisingly, “improved by prophylactic naps as a function of varying nap length.” Bonnet compared the improvement conferred by naps with that realizable with either repeated or single-dose administration of caffeine. As would be expected, the results showed that an eight-hour “nap,” which is to say, a good night’s sleep, did more to improve performance, mood, and alertness than any sort of caffeine regimen and that the benefits lasted longer than the effects of caffeine, which peak and lose effect within six hours. The study also found that naps could be combined effectively with small repetitive doses of caffeine to maintain alertness. Nothing lasts forever, though. Bonnet concludes that neither a nap nor repeated doses of caffeine could preserve performance, mood, and alertness past twenty-four hours. Beyond that, caffeine’s effects in these respects approached those of a placebo.

One of the definitions of drugs that produce a physical dependence is that the abrupt cessation of their use will cause people to perform tests poorly and feel listless and generally “blue.” Leading caffeine researcher Jack James advances a theory that
a
nearly universal yet unacknowledged physical dependence on caffeine may have confounded the results of many studies that
purported to show the psychomotor advantages conferred by the drug
.
¹⁹
His argument is plausible: If nearly everyone uses caffeine nearly every day, then when a scientist takes a pool of subjects and administers caffeine to one part of the group and withholds it from the others, those not receiving caffeine will enter varying stages of caffeine withdrawal and therefore will perform more poorly than those who are not suffering from withdrawal. In effect, James is asserting that most people have what among heroin users is called a “chippie,” a lowgrade habit, of which the habituated person is sometimes unaware, that renders them mildly dysphoric and uncomfortable when deprived of the drug. Such heroin users would probably demonstrate better performance if given a small amount of heroin, simply because the heroin would restore them to a normal metabolic balance and remove the impediment of the mild withdrawal syndrome. If James is correct, all the “improvements” worked by caffeine in psychomotor or cognitive performance may simply be artifacts of an unknown caffeine chippie or a hidden need
for caffeine that impairs the habitué when he stops using it. The only way to determine if a nearly universal addiction is distorting experimental findings is to make sure that all the subjects in a given study have been weaned off of caffeine for at least a week or two, so that they begin without any taint of addiction.

It may be nothing to worry about, but anxiety, including such symptoms as unwarranted trepidation, apprehension, agitation, turmoil, and uneasiness, is the most common psychological disorder in the United States. In severe cases, it erupts into recurring panic attacks, the symptoms of which include increased heart rate, palpitations, jitters, irritability, perspiration, and rapid breathing. Caffeine is generally recognized by researchers as an anxiogenic substance—that is, one that is productive of anxiety. The pharmacological basis of this effect remains uncertain. One possible contributory mechanism is the process by which caffeine binds to adenosine receptors, interfering with the systems that would otherwise have reduced anxiety. (Binding to benzodiazepine and endorphin receptors have been cited as well, but at ordinary levels of consumption this activity appears too small to be of significance.) Another is that caffeine interferes with the noradrenergic system so as to increase the release of adrenaline.
²⁰
Adrenaline, the hormone the adrenal glands excrete in response to excitement, stress, or fear, produces a more rapid and stronger heartbeat and more rapid and deeper breathing, and it can also produce anxiety. Some claim that caffeine in combination with emotional distress causes the release of more adrenaline than emotional distress alone, suggesting that even if it cannot cause anxiety, caffeine may exacerbate it.

In 1971 R.Lynn, a leading British researcher, conducted a monumental study of personal traits and practices and physical and psychological disorders, including psychiatric disorders, cigarette smoking, suicide, coronary heart disease, and anxiety. Observing that the peoples of different nations suffered from different levels of anxiety, Lynn hypothesized that, in those countries in which anxiety levels were high, people would tend to consume less caffeine in order to avoid exacerbating their problems with it. His theory was confirmed by the data. In those countries in which caffeine consumption is low, anxiety is relatively higher, and in those in which it is high, anxiety is lower. Several studies have supported Lynn’s conclusion.
²¹
It has been shown that patients with panic disorder have lower caffeine consumption and that panic attacks can be induced even in normal people challenged with high doses of caffeine.
²²

People with high caffeine consumption have higher usage rates of anxiety-reducing drugs such as benzodiazepine or meprobamate, when compared to those with moderate to low caffeine use. No one is sure if they consume higher levels of caffeine in order to shake off the sedative effects of the minor tranquilizers, or if they take minor tranquilizers to counteract the anxiety resulting from high doses of caffeine, or even if there is simply a certain population that enjoys using mild psychoactive substances of both the stimulating and sedating varieties.

In any case, the studies dispel one illusion: the image of the nervous, edgy caffeine user. Only excessive caffeine use is correlated with anxiety. If a correlation with normal use can be stated, it is that the people who do not consume caffeine are more likely to have problems with their nerves than those who do. The members of the population who consume caffeine are dispositionally more relaxed than the general population, and, conversely, those who do not consume caffeine are more jittery than most.

As reflected in a new specific and separate diagnosis category in the American Psychiatric Association’s
Diagnostic and
Statistical Manual IV (DSM-IV)
, psychiatrists now believe that caffeine can produce a distinct anxiety disorder, over and above the symptom of anxiety that appears as a component of caffeine intoxication and caffeine withdrawal. The
DSM-IV
states that, as with the anxiety induced by other psychoactive substances such as cocaine, caffeine-induced anxiety disorder can resemble panic disorder, generalized anxiety disorder, social phobia, or even obsessive-compulsive disorder. There have been no studies on the prevalence or incidence of caffeine intoxication anxiety or applying the
DSM-IV
set of diagnostic criteria.

Just as it is conjectured that Nervous Nellies spontaneously adjust their caffeine intake downward to avoid its anxiolytic effects,
²³
it is also supposed that some depressives increase their consumption in order to multiply the benefit from caffeine’s euphoric and stimulating powers.
²⁴
In other words, they effectively self-medicate with caffeine to dissipate the dark clouds of lassitude, lethargy, and despair that hover around them. The studies remain inconclusive. An example of the ambiguity that still lingers is found in the Tromsø Heart Study, conducted in 1983, of almost 150,000 people, which found significant correlations between high coffee consumption and depression in women (but not in men). However, because this correlation disappears when the results are adjusted for cigarette smoking, it is difficult to draw any conclusions.

A number of studies have found that people who drink at least two portions of caffeinated beverages a day report improved moods, a better social disposition, and more self-confidence and energy. Two large-scale studies, apparently demonstrating lower rates of suicide among coffee drinkers, strongly suggest that caffeine can significantly ameliorate long-term depression
and even make life worth living for some people. A 1993 Kaiser Permanente Medical Care Program study of more than one hundred thousand men and women, reported in the
Annals of Epidemiology,
examined the effects of coffee and tea on mortality and found a lower risk of suicide among people who ingested more caffeine. Under the direction of Arthur Klatsky, M.D., a cardiologist, the study tracked nearly 130,000 Northern California residents, including the records of 4,500 who died during the research, and demonstrated a statistically significant lower rate of suicide among coffee drinkers than coffee abstainers. Klatsky asserted that this was not a fluke finding, because the study was very large, involved a multiracial population of men and women, and examined closely many factors related to mortality such as alcohol consumption and smoking. Another large-scale study, of more than 85,000 female nurses, conducted by Dr. Ichiro Kawachi of Harvard Medical School and Brigham and Women’s Hospital in Boston, funded by the National Institutes of Health and published by the
Archives of Internal Medicine
in 1996, concluded that women who drink coffee are less likely to commit suicide than those who do not. Even though coffee drinkers appear to engage in the sort of behavior that would increase their risk of depression and suicide (for example, they tend to smoke more and drink more alcohol than non-coffee drinkers and have higher levels of perceived stress), they seem to be highly protected. This study also found that only 100 mg of caffeine a day, about one cup of coffee, could produce increased feelings of well-being, energy, and motivation for work. However, specialists in depression argue that Kawachi failed to control for several factors, including the effects of antidepressants, high-blood-pressure medication, and whether depressed subjects had been told not to drink coffee by their doctors.