In a detailed, carefully controlled study in 1986, Roland Griffiths provided a more detailed schedule of caffeine withdrawal symptoms than had been available previously. He found that caffeine withdrawal generally begins within twelve to twenty-four hours after discontinuing caffeine use. It generally peaks within twenty-four to fortyeight hours, and it lasts from about two days to a week.2 As with many of the manifestations of caffeine use, there is considerable variability both between people and within the same person in the effects, duration, and severity of caffeine withdrawal.
The single best estimate of the incidence of caffeine withdrawal symptoms in a clinical setting was provided in a 1992 study3 of more than sixty normal adults with low to moderate daily caffeine consumption, an average of 235 mg a day, or the equivalent of about two cups of coffee. This was a double-blind study, that is, one in which neither the researcher nor the subject knows who is receiving caffeine and, if so, in what quantities. More than 50 percent of the participants who did not receive caffeine had moderate to severe headaches, about 10 percent had symptoms associated with anxiety and depression, and about another 10 percent had significantly high ratings of fatigue. Nearly 15 percent used analgesics for aches and pains occasioned by withdrawal.
What is it about the cessation or relative decrease in the intake of caffeine that generates the range of physical and psychological problems listed above? Caffeine withdrawal is probably caused by the cessation of adenosine antagonism, which is caffeine’s chief pharmacological mechanism of action. When caffeine use ceases, caffeine’s supression of adenosine ceases, and it is natural that the abstainer should experience sluggishness, torpor, difficulty in concentrating, and depression. In addition, the prior use of caffeine may have resulted in a compensatory increase in the number of adenosine receptor sites, intended by the body to help restore the level of adenosine to that which existed before regular caffeine use.4 Specifically, caffeine withdrawal symptoms may be partially explained by the decrease in central nervous system activity and the increase in cerebral blood flow associated with increased adenosine activity. The results of an EEG study which demonstrated increased alpha and beta voltage in the frontal-central cortex during caffeine withdrawal has been interpreted as being consistent with the hypothesis that caffeine withdrawal may be due to cerebral blood flow changes.5
The most common and notorious feature of caffeine withdrawal is the headache, which, consistently with the above analysis, has been described as a feeling of cerebral fullness. Typically it is a generalized throbbing headache that can, in extreme cases, be accompanied by flulike symptoms such as nausea and vomiting. The caffeine withdrawal headache is worsened with physical exercise and, not surprisingly, is relieved by caffeine. The withdrawal headaches usually abate within two to four days, although some subjects continue reporting sporadic headaches for ten days or more after cessation of caffeine use. It should be noted that several reports have concluded that sudden extreme increases in caffeine or coffee consumption can also produce headaches.
The caffeine withdrawal headache has frequently been observed in a hospital setting. One registered nurse at a hospital reports what turns out a common pre- and post-operative observation of caffeine withdrawal: “When I worked in an ambulatory surgery setting, many patients who were NPO [not to eat or drink anything] and therefore [had gone] without their usual cup of caffeine since the night before would experience quite severe headaches if they were still NPO by 11 A.M. or so. For most routine caffeine users, the first thing they said in the recovery area was ‘Can I get some coffee?! I have a headache!’ The phenomenon occurred often enough that even nurses new to the area caught on pretty quickly, and widespread enough for it to be a topic of informal conversation during nationwide nurses’ conventions!”6 Recently some surgical teams have given patients caffeine intravenously to avoid headaches and other withdrawal symptoms during the operation and recovery periods.
This complex of caffeine withdrawal symptoms is compellingly reminiscent of what might be termed the “addict’s flu,” the generalized withdrawal symptoms common to many addictive drugs, notably including heroin and other opiates and barbiturates. The symptoms of withdrawal from these drugs are typically much more severe than those exhibited in the flulike symptoms of caffeine withdrawal, but the pattern of symptoms, including fatigue, aches and pains, irritability, running nose, perspiration, and cravings for the drug, are otherwise identical.
Several studies have found that both the likelihood of caffeine withdrawal and its severity increase as the daily dose attained before cessation is increased. However, it has been shown that caffeine withdrawal can occur after discontinuation of surprisingly low regular doses of caffeine, as little as 100 mg per day, which is the equivalent of about one cup of coffee or two cans of cola.
There is one report of eight infants with suspected caffeine withdrawal born to mothers who had moderate to heavy caffeine consumption during their pregnancies (200–1,800 mg a day). The infants’ symptoms, including irritability, jitteriness, and vomiting, began an average of about twenty hours after birth and then abated completely.7
The possible onset of caffeine withdrawal makes it advantageous for caffeine users to plan ahead as they approach circumstances where it may be necessary or desirable to eliminate caffeine. Because many general medical conditions can have signs and symptoms that are similar to caffeine withdrawal, it is necessary to systematically exclude other explanations for the symptoms. An adequate differential diagnosis should encompass conditions as diverse as viral illnesses, sinus conditions, migraine or tension headaches, other drug withdrawal states, such as amphetamine or cocaine withdrawal, and idiopathic drug reactions.
Clinical Dependence Syndrome
Opinions vary among psychologists and psychiatrists about whether caffeine should be branded, along with heroin, cocaine, and nicotine, as a drug of abuse, that is, as an agent supporting a clinical dependence syndrome. The majority opinion, supported in studies by Strain, Griffiths, and others at the Department of Psychiatry and Behavioral Sciences, the Johns Hopkins University School of Medicine, and reported in JAMA in 1994,8 provides clinical evidence supporting a caffeine clinical dependence syndrome similar to the dependence syndromes of heroin and cocaine but milder.9 A minority of professionals, citing the modest and transient discomforts of caffeine withdrawal, assert that caffeine has little in common with dangerous psychoactive drugs of abuse and should not be described as supporting a clinical dependence syndrome.10
The best opinion seems to be an amalgam of the two. On the one hand, there is no doubt that caffeine, like cocaine, has all the hallmarks of a drug that supports a clinical dependence syndrome: It produces the subjective effects of euphoria, energy, and self-confidence; it demonstrates a “reinforcing effect,” that is, the capacity of a pharmacological agent to encourage sustained use; and, finally, as we have noted, it supports a physical dependence, including a developed tolerance and withdrawal symptoms on cessation.11 On the other hand, it is clear that caffeine’s subjective effects, reinforcing effects, and withdrawal symptoms are far less pronounced than the recognized drugs of abuse, such as cocaine, dextroamphetamine, or pentobarbital, and therefore, caffeine’s clinical dependence syndrome, if it indeed exists, cannot be uncritically equated with the clinical dependence syndromes of these other drugs.12
Extrapolating from a telephone survey of two hundred Vermont residents conducted by a group of researchers in 199213 (the only study using standardized psychiatric criteria to evaluate the prevalence of caffeine clinical dependence), and applying the estimate that more than 80 percent of all American adults consume caffeine daily, with an average consumption among users of nearly 300 mg a day, we could venture that, in the United States alone, 75 million people would fit the criteria for moderate caffeine clinical dependence syndrome. The average daily consumption and, therefore, the estimate of the levels of this dependence syndrome in other countries may be considerably higher.
So the question r
emains: Does caffeine, like cocaine, support compulsive use, that is, an habitual pattern of self-administration persisting despite untoward personal, health, economic, or social consequences and repeated attempts to discontinue taking it? It is very difficult to determine the extent to which the nearly universal use of caffeine, in some surveys reaching 92 to 98 percent of North American adults, is, in one researcher’s words, “due to its centrally mediated stimulus functions, rather than liking the taste of hot coffee, or the fact that drinking coffee is such a socially acceptable behavior.”14 Although anecdotal reports of the regular patterns of consumption engaged in by most caffeine users satisfy the criterion of habitual use, there is little evidence to help us decide whether the strength of the desire to persist in these patterns would satisfy the definition of compulsive behavior. Nevertheless, it remains a credible speculation that a minority of caffeine users consume caffeine compulsively, to the extent that they would find it difficult to reduce or eliminate it from their diet. Whatever the outcome of current studies, it is safe to assert that caffeine dependence, like other drug dependence syndromes, in all likelihood represents the interaction of social and cultural forces, of individual histories and predispositions operating at the same time as a psychoactive substance that produces pleasant mood-altering and reinforcing effects.
Is Caffeine a Drug of Abuse?
If asked to explain the nature of a drug of abuse, many people might answer, “I may not be able to define a drug of abuse, but I know one when I see one.” Consideration of patterns of drug use in other societies, however, may disturb such comforting smugness. As we saw in the Yemen, for example, the plant khat, which contains a very powerful stimulating, habituating, and intoxicating drug, is brewed into tea, much in the way we use caffeine, and is used by the great majority of both children and adults. Outside observers have frequently assumed that khat is a drug of abuse and that the Yemeni population suffers from an addiction problem, similar to Western problems with heroin and cocaine, that should be addressed by every available educational, social, and legal countermeasure. Most people who live in the Yemen, however, do not share this opinion. The same question arises for us in relation to caffeine: If an entire society accepts a pattern of drug use, is that use, by definition, a normal one?
Researchers attempting to determine whether caffeine should be branded a drug of abuse have suggested that the word “addiction” be restricted to those conditions in which physical dependence and clinical dependence syndrome both obtain. Hirsh asserted that an addictive drug was one that engenders a “compulsion” or “an over-whelming involvement that pervades the total life activity…to the exclusion of all other interests,”15 and concluded that caffeine, like other methylxanthines, was not addictive. R.R.Griffiths and colleagues have argued that to qualify as a drug of abuse a substance must have both reinforcing effects and produce harmful effects on the user and the society. Caffeine’s reinforcing effects make it a candidate to be considered as a drug of abuse, but, Griffiths cautions, its classification as such must await a fuller appraisal of its possible deleterious effects.16
Photograph of Russian brick tea money. (Courtesy of Chase Manhattan Archives)
Photograph of Russian brick tea money. (Courtesy of Chase Manhattan Archives)
Looking at the question from a different angle, we note that the remorseless metabolic and psychical demand for certain intoxicants combines with their portability to enable them to function as money in a black market. In fact, one hallmark of a psychoactive drug of abuse, therefore, is a history of its use as a medium of exchange. Opium, for example, is as good as money among black-market traders in Southeast Asia. Cocaine is like gold bullion to the cartel managers of South America. Similarly, caffeine-rich seeds, beans, and processed leaves have frequently served as mediums of exchange throughout the world. In some African countries, cola nuts are still used as money, the way the Maya, and other South Americans until the eighteenth century, used cacao beans. In China and Russia, dried tea leaves were pressed into bricks and used as currency. In Egypt and elsewhere among the Moslems, coffee was used as tender in the marketplace from the beginning of the sixteenth century.
Caffeine Intoxication: Too Much of a Good Thing
Many consumers of coffee, tea, and cola, never having entertained an association between caffeine and drug use, may be surprised to learn that the massive modern catalogue of psychiatric problems, the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), includes an entry for “Caffeine Intoxication,” which it describes either as an acute drug overdose condition, occurring after the ingestion of a large amount of caffeine, or as a chronic condition, otherwise known as “caffeinism” or “caffeism,” associated with the regular consumption of large amounts of caffeine.
There is nothing new about the awareness of caffeine intoxication, for it has been well described as a psychiatric disorder for more than a hundred years. Yet despite long-standing recognition, which perhaps began with the coining of the Arabic word “marqaha” or “caffeine high,” in the sixteenth century, there is, even today, little information available about its prevalence or incidence.
In 1896 J.T.Rugh17 reported the case of a traveling salesman who had resorted to excessive coffee consumption to maintain an intense pace of work and was troubled by nervousness, involuntary contractions in the arms and legs, a sense of impending danger, and sleep disturbance. Similar reports of caffeine intoxication first appear in medical literature from the middle of the 1800s, and the profile of common symptoms remains unchanged today. The most common are anxiety or nervousness, insomnia, gastrointestinal disturbances, irregular heartbeat, tremors, and psychomotor agitation. Other reported symptoms include excessive urination, headaches, diarrhea, and irregular breathing.
An interesting and unusual case was reported to JAMA early in 1914 by Otis Orendorff, M.D., of Canon City, Colorado. “A young miss, 18, an office clerk, of a slight, frail physique, had ordinary symptoms of asthenopia [eyestrain] for four years,” Orendorff wrote. She grew worse over a period of several months. Although tests were administered and full correction for her vision was provided, she experienced no relief. The patient was alternately exhilarated and depressed. She had memory lapses and maintained a “deportment with an indifference to the usual conventionalities and proprieties.” She had intermittent headaches, apparently not caused by work, but that increased when she attempted to read. She had insomnia at night but fell asleep at work. Her condition was getting serious. The physician was at his wits’ end, when the patient asked him “if there could be any danger in an overindulgence of Coca-Cola? stating that she drank from three to six glasses a day. In addition, she had two or three cups of strong coffee at mealtime, sometimes taking but little other nourishment.” He reports prompt improvement on curtailing her daily caffeine ingestion, concluding, “I feel that such a case is of interest from an ophthalmologic point of view and also because it indicates that the profession should be more alive to the pernicious influence in habit formation of some of the popular beverages served to young persons at public ‘slop’ fountains.”18
Unknown to the typical coffee or tea drinker, there exists a subterranean culture of undetermined extent in which caffeine is consumed with the fixed intention of inducing intoxication. That is, many people across the country and around the world regularly use large doses of caffeine to get high. In doing so, they frequently encounter many of the symptoms of toxicity, somatic and psychological, that we discuss in this
chapter. (See Appendix B, table 5, for the diagnostic criteria for caffeine intoxication from the Diagnostic and Statistical Manual of Mental Disorders.)
Internet news groups are electronic confraternities in which people who have generally never met each other post public messages, photographs, and even sound files pertaining to a common interest. If you access such newsgroups as “alt.drugs.caffeine” or “alt.coffee” on any given day, you are certain to find questions, comments, confessions, misgivings, and boasts r
egarding the use of large amounts of caffeine. Here are quotations from Internet postings, which are rife with misinformation and misspellings:
Q: What are some of the affects you’ve experienced when you suck down too much caffeine?
A: I actually seem to get less alert. Well, actually the only effect I get from overdosing on caffeine is severe nausea and vomiting. Man, I just go numb in my hands and feet and start shaking all over, as my mind and body go hyper. I can’t focus, can’t think straight. I go through oscillating emotional states, and I experience cold sweats, shaking, and sometimes tachycardia. I usually have oscillations from paranoid to psychotically calm and back again, along with racing thoughts, while getting slight muscle cramps.
A friend of mine snorted pharmaceutical grade caffeine once; he said it was extremely harsh on the nasal lining and not worth the buzz.
Q: I know a guy who once smoked a teabag and he claims that it gave him a buzz. Does anybody know if what he said is true?
A: Yes it works, i did it in england with the cheap tea they give you in a generic (low end) hotel, you just unfold the tea bag, you roll it up into something resembling a joint, and you light it, it is next to impossible to keep it lit though. oh it is the caffiene in it that gets you buzzed, the problem is that it goes away after about an hour and it leaves you with a bitch of a headache and some really bad cotton mouth.
• • •
I have used both caffeine and ephedrine together. It was related to one of my experiments, how to stay awake and keep going one whole week. I had to use quite a lot. I would say round 1500–2000 mg caffeine per day and around 200–300 mg ephedrine. Finally me and my head were quite mixed up. I was sleeping two hours a day and I kept this up for 19 days. I didn’t just think that I saw God, I thought I was God I only drink coffee now. Be careful.
The World of Caffeine Page 46