Caffeine: Psychological Effects, Use And Abuse
- From: rpautrey2 <rpautrey2@xxxxxxxxx>
- Date: Mon, 11 Aug 2008 08:05:20 -0700 (PDT)
Orthomolecular Psychiatry, Volume 10, Number 3, 1981, Pp. 202-211
Caffeine: Psychological Effects, Use and Abuse
Sanford Bolton, Ph.D. and Gary Null, M.S.
Note: The information on this website is not a substitute for
diagnosis and treatment by a qualified, licensed professional.
ABSTRACT
Caffeine, probably the most widely used drug, affects the
psychological state of those who consume it. Abuse results in symptoms
of caffeinism which include agitation, disorientation and a syndrome
which may be mistaken for anxiety/neurosis. It is a habit-forming drug
in which tolerance develops. It affects sleep in a dose related manner
which is dependent on the daily caffeine intake, i.e., high users have
less effect. Its central nervous system stimulation can cause pleasant
effects with improved attention and concentration at lower doses. At
high doses, the reverse may occur. Used judiciously, it may be a
useful therapy in the treatment of hyperkinetic children. These and
other effects of caffeine are discussed in this review article.
INTRODUCTION
Caffeine is among the most widely used drugs because of its ubiquitous
occurrence in commonly consumed beverages such as coffee, tea and
cola. Many drugs contain caffeine and are readily accessible to the
public in the form of OTC stimulants and combination analgesics.
Clearly caffeine is an important drug-food substance in our society
which deserves attention.
To begin to have a new consciousness about caffeine so that we can
become aware of how this drug can affect our physiology and psychology
is a problem. The reasons for this are certainly complicated, but we
can start by considering a factor dominating all of our lives, our
"habits." When we become aware of and take responsibility to change
habits, we are taking a first step in the process of awakening. The
result must be not only an improvement in the quality of our lives but
the world itself will be changed for the better.
The use and abuse of caffeine is a major public "habit' and may be as
important a factor as heredity and environment in the etiology 6f
physiological and psychological disorders. To recognize this, we must
know that we are creatures of habit. Most people are caffeine
consumers because from birth this food-drug is set before us, if not
offered directly, along with orange juice, cereal, dessert and
cigarettes.
This paper reviews the literature relating to the psychological
effects of caffeine. Caffeine is a potent central nervous system
stimulant and much of its "psychological" activity may be related to
this action of the drug. its effects on the nervous system are
obviously adverse at high doses. it may not be obvious that at lower
doses when used in moderation, it may have beneficial effects. For
example, its possible therapeutic use in hyperkinetic children
certainly would seem advantageous when compared to the current
treatment with more powerful stimulants which have concomitant adverse
reactions. Also, with the intense day to day pressures imposed on and
accepted by many of us, is there any harm in "relaxing" with a hot cup
of coffee? On the other hand, caffeine is a drug which is subject to
abuse. The fact that it is a drug with a potentially powerful
physiological effect escapes most of us who think of coffee as a
relatively harmless beverage. Recently published studies and reports
of personal observations have shown without doubt that caffeine abuse
(caffeinism) may result in a syndrome which resembles and may be
confused or confounded with true psychotic states. This may lead to
misdiagnosis and mistreatment. A question arises from the varied
reports of caffeine consumption in psychiatric populations: Does
caffeine stimulate psychosis or does psychosis stimulate caffeine
consumption?
These are not trivial findings because of the ready availability of
caffeine and the epidemic of psychological problems which we are
experiencing in this era. This report reviews some of the knowledge of
caffeine's effects with the hope that we will all be more educated and
more careful in the use of this commonly ingested drug.
The physiological action of caffeine is briefly reviewed, as
psychological and physiological effects must go hand-in-hand. In
addition to its central nervous system effects, caffeine has
significant effects on the cardiovascular system, gastric acid
secretion and catecholamine (adrenaline) release. In large doses, it
has been shown to be a mutagen in animals, plants and bacteria, and
has been shown to exhibit teratogenic properties in various animal
species.
PHYSIOLOGICAL AND PHARMACOLOGICAL EFFECTS
J. Murdoch Ritchie, in Goodman and Gilman's Pharmacology Text
(Ritchie, 1975) described the pharmacological effects of caffeine. The
largest sources of caffeine are from the plants used to make coffee,
tea, cocoa and kola (the basis of cola beverages), although it is also
found in Latin America as mate' and guarana. Caffeine particularly has
a profound effect on the central nervous system, but it also affects,
to a lesser degree the heart muscle, gastric secretion and diuresis.
Interestingly, caffeine is ingested daily by a vast number of people
and is unique in that it is a potent drug, considered to be part of
our normal diet.
Caffeine stimulates the central nervous system first at the higher
levels, the cortex and medulla, and finally the spinal cord at higher
doses. Mild cortex stimulation appears to be beneficial resulting in
more clear thinking and less fatigue. Caffeine has been shown to
improve attention in a study which simulated night driving (Leinart,
1966). The onset of the effect of caffeine occurs within one hour and
lasts for three to four hours (Baker, 1972).
The equivalent of one or two cups of coffee (150 to 250 mg of
caffeine) is sufficient to induce adverse effects. The occurrence of
hyperesthesia, an unpleasant sensory sensation, can be stimulated by
large doses of caffeine.
The medullary, respiratory, vasomotor and vagal centers are stimulated
by caffeine. This effect is due to an increased sensitization to
carbon dioxide but needs large doses to elicit this effect, 150 to 250
mg, parenterally. The spinal cord is stimulated at higher doses and
convulsions and death may result. More than 10 g are needed for such
toxicity to occur in man (Ritchie, 1975).
Stimulation of the CNS is followed by depression (Klein and Salzman,
1975), although the effect is small at low doses e.g. a single cup of
coffee. After two hours, Klein reported that males (but not females)
showed a lower CNS stimulation compared to placebo. The post
stimulation "let down" with caffeine results in fatigue and lethargy
and the constant stimulation caused by chronic caffeine dosing could
be disastrous (Abrams, 1977; Dowell, 1965).
Children, because of their smaller size, are more susceptible to
caffeine. One report noted that hyperactivity and ir~somnia observed
in children could be attributed to excess caffeine intake from cola
drinks (Consumer Research, 1973). According to Dr. Page, "There is no
doubt that children should be kept from using coffee and the popular
caffeine containing soft drinks." (Abrams, 1977).
Caffeine's effect on the cardiovascular system is less profound than
its central nervous system action. Its direct stimulatory effect on
the heart may be neutralized by its central vagus stimulation. The
direct effect predominates at very large doses with tachycardia and,
eventually, arrythmias resulting. Caffeine's ability to potentiate
cyclic AMP can explain its ability to potentiate ionotropic responses
to B-adrenergic agonists and glucogon (Ritchie et al, 1975).
Although caffeine dilates blood vessels by a direct action, its
central effect is one of constriction. At higher doses, the dilating
effect is apparent (Peach, 1972; Poisner, 1973).
Similarly, because its direct and central effects are antagonistic,
the resultant effect of caffeine on blood pressure is unpredictable.
The net effect is usually of less than 10 mm of Hg in blood pressure
(Ritchie et al., 1975). Caffeine's purported efficacy in hypertensive
headaches may be due to a decrease in blood flow as a result of the
increased cerebral resistance (Ritchie et al., 1975).
Caffeine also stimulates releases of catecholamines from the adrenal
medulla and norepinephrine is released from nerve endings in the
isolatA heart (Bellett et al., 1971). .
It has been shown that prolonged augmentation of gastric 'secretion
results from caffeine administration and that ulcer patients have
sustained elevation of acid as opposed to normals (Ritchie et al.,
1975).
Although a dose of approximately 10 g or more taken orally can be
fatal, an oral (3.2 g IV) one gram dose will cause adverse effects
(Gleason et al., 1969). The toxic effects are due to CNS and
circulatory system stimulation and include some well recognized
prominent symptoms in addition to those which can result at high doses
or in hypersensitive persons: insomnia, restlessness, excitement,
tinnitus, flashes of light, quivering muscles, tachycardia,
extrasystoles, and even low grade fever and mild delirium have been
observed.
Harrie (1970) described a patient whose constant headaches were due to
excessive caffeine consumption. He states, "I suspect that the
condition is much more common than supposed and could well be one of
the more frequent causes of chronic recurrent headache." Headaches can
also be precipitated by caffeine withdrawal especially by those who
have the "habit".
Although caffeine is well absorbed when taken orally, its absorption
may be erratic because of its low solubility and because it may cause
gastric irritation. Caffeine is principally metabolized with only 10
percent excreted in the urine unchanged (Ritchie et al., 1975).
Caffeine has a physiological half-life of three and a half hours
(Parsons anjd Neims, 1978) to six hours (Aranda et al., 1979). Its
physiological effects are observed in less than one hour (Parsons and
Neims, 1978). Infants do not metabolize caffeine as well as adults and
thus have a half-life of about four days (Aranda et al., 1975).
Certainly, continuous ingestion of caffeine by infants can be
dangerous. If a cup of coffee is consumed by an adult six or seven
times a day it would result in a high steady concentration of caffeine
in the blood. As little as four cups a day can result in appreciable
omnipresent amounts of caffeine in the body.
Caffeine can accumulate in severe liver disease (Stratland, 1976) when
its half-life can increase to 96 hours. If these patients drink
coffe(~ they should be closely monitored.
Caffeine is known to interact with other drugs resulting in a modified
effect. For example, caffeine administered with nardil (an MAO
inhibitor) caused headaches and high blood pressure (Pakes, 1979).
This potentially dangerous interaction was first noted by Berkowitz et
al., (1971) and implicated serotonin in the mechanism.
Caffeine and barbitol are antagonistic, with caffeine (in coffee)
reducing the sleeping time induced by barbitol. Decaffeinated coffee
had no effect (Aeschbacher et al., 1975). In another study, caffeine
resulted in reduced sleeping time which was counteracted by
pentobarbitol in hospitalized patients (Forrest et al., 1972).
PSYCHOLOGICAL EFFECTS OF CAFFEINE
Because of the wide spread use of caffeine and its known potent
physiological effects, caffeine has been the subject of research in
psychological related studies. This work has been stimulated by
personal experiences and observations as well as by efforts to
understand its action and mechanism.
Habituation and Tolerance: Caffeine ingestion and coffee drinking have
been investigated with regard to the degree that this habit results in
tolerance and withdrawal effects. These studies look beyond the
obvious social implications and psychic dependence (Ritchie et al.,
1975) of coffee consumption which may be related to the "first cup of
coffee to wake me up" or "the coffee break" or to its association with
smoking. In the latter case, it is of interest that coffee drinkers
were shown to take more nicotine when deprived of coffee (Kozlowski,
1976).
Caffeine has not only been considered habit forming, but also
addicting. Crothers considered morphinism and caffeinism to be
similar, with caffeine causing loss of self-control, spells of
agitation and depression as well as psychotic behavior (Stephenson,
1977). Ritchie mentions a report by Colton that tolerance can develop
for the diuretic, salivary stimulation and sleep disturbance effects
of caffeine.
Cola consumed in amounts of 48 to 111 ounces per day (144 to 333 mg of
caffeine per day) was reported to have caused physical effects on
withdrawal (Diamond and Pfifferling, 1974). The resultant effects
we'Pe depression, nervousness, decreased alertness,, sleeping
difficulty, frequent mood changes, and various other behavioral
difficulties which were attributed to caffeine withdrawal.
The dependence of coffee drinkers on caffeine was illustrated in a
study by Kozlowski (1976) in which coffee drinkers drank more coffee
if the caffeine content was lowered.
Abrams (1977) says "There is no doubt that a certain degree of psychic
dependence, that is habituation, develops from the use of xanthine
beverages".
A questionnaire completed by more than 200 young housewives showed
that the perceived effects of caffeine depended on previous use
(Goldstein et al., 1969). The heavy coffee drinkers had few sleep
disturbances and less evidence of nervousness after their morning
coffee as compared to nondrinkers. if the morning coffee was stopped,
the habitual coffee drinkers experienced nervousness, headache and
irritation. The non-coffee drinkers reacted negatively to coffee,
experiencing effects opposite to the coffee drinkers. An experiment
was devised to verify the results of the questionnaire involving 18
housewives, non-coffee drinkers, and 38 who drank five or more cups
per day. The results confirmed those obtained from the questionnaire
previously administered (Goldstein et al., 1969). This experiment was
double-blind and placebo controlled and caffeine was administered in
coffee at 0, 150 and 300 mg. Coffee drinkers showed a dose-response
effect whereas non-coffee drinkers showed signs such as nervousness,
jitters and upset stomachs at all doses of caffeine but not on
placebo.
Ritchie (1975) says that tolerance and psychological dependence to
caffeine beverages does occur to some extent but he feels that this
does-not present a problem. He says that coffee or tea drinking are
socially acceptable and are apparently not harmful when practiced in
moderation.
However, it does appear that at least in some persons excess
consumption of caffeine can result in severe phychological dependence
and withdrawal effects and is a problem to be reckoned with.
Behavioral Effects: Caffeine's stimulating activity on the central
nervous system as well as other body organs results in certain
physiological effects which may be considered to be behavior oriented.
Caffeine produces more rapid, clearer flow of thought, allays
drowsiness and fatigue, increases the capability of a greater
sustained intellectual effort and more perfect association of ideas.
It also causes a keener appreciation of sensory stimuli, and reaction
time is diminished. Motor activity is increased; typists, for example,
work faster with fewer errors. Tasks requiring delicate muscular
cobrdination and accurate timing may, however, be adversely affected.
All of this occurs at doses of 150 to 250 mg of caffeine
(approximately two cups of coffee) according to Ritchie (1975).
In 1912, Hollingsworth who was a psychologist reported caffeine's
effect on mental and ~notor efficiency in a study sponsored by Coca-
Cola. In nine double-blind tests, he found beneficial effects for both
mental and motor performance at doses of 65 to 130 mg of caffeine. At
a dose of 300 mg, caffeine caused tremors, poor motor performance and
insomnia. These results have withstood the test of time (Stephenson,
1977).
Goldstein (1965) showed no effect of caffeine on objective measures of
performance although most subjects "felt" more alert and physically
active. However, some subjects felt nervous.
Mitchell, Ross and Hurst showed caffeine to prevent attention lapses
in a visual monitoring test which simulated night driving. The effect
persisted for the two to three hour experiment (Stephenson, 1977).
A 200 mg dose of caffeine resulted in decreased decision time scores
and improved motor time scores in volunteers (Smith et al., 1977).
Hand steadiness, however, was impaired. After a caffeine intake of 200
mg, introverts performed less well on a verbal ability test as
compared to extroverts when time pressure was applied (Ritchie et al.,
1975).
Wayner et al. (1976) reported on the effects of caffeine on schedule
dependent'and schedule induced behavior in mice. Caffeine, (3.125,
6.25, 12.5, 25, 50 and 100 mg/kg) was tested on lever pressing,
schedule induced licking and water consumption of mice. The effect on
mice at 80 percent of body weight was different than when mice were
allowed to recover the lost weight. At the lower weight, caffeine had
little effect except at the highest dose (equivalent to 100 cups of
coffee given at once). At their ordinary weight, the mice were more
sensitive to caffeine, with all measures enhanced, even at the lowest
dose (equivalent to approximately three cups of coffee). At high
doses, all measures decreased; the mice became tolerant.
Castellano (1976) studied mice behavior under two sets of conditions.
One involved a natural preference (swimming towards a light-"L" ) and
the other involved an acquired behavior pattern (swimming toward the
dark-"D"). A facilitation of learning and consolidation after caffeine
dosing was noted in naive mice after the -D" procedure. Natural
tendencies were also enhanced by caffeine as noted by improved
performance in the "L" procedure. Animals pretrained in the "D"
procedure exhibited behavioral disruption after treatment. Animals
pretrained in the natural -U procedure needed very high doses to cause
disruption. Caffeine decreases five HT turnover in rat brain.
Amphetamines do not show the results as demonstrated in this paper,
whereas other drugs such as hallucinogens show a similar effect. The
implication is that the mechanism of caffeine's action may be similar
to hallucinogenic drugs.
Effect on Sleep: Caffeine is known to cause insomnia because of its
central nervous system stimulating activity. In fact, its major
therapeutic use is to allay sleep and drowsiness, being the only OTC
stimulant approved by the FDA. Several studies investigating this
action in some detail have been published.
Karacan (1976) found that caffeine given half an hour before sleep
adversely affected the sleeping process in normal sublects. The effect
is dose related. Caffeine's effect simulates clinical insomnia and
gave the same response as coffee containing an equivalent amount of
caffeine. Decaffeinated coffee showed no effect on sleep.
Dorfman and Jarvick (1970) showed a dose-response effect of caffeine
on the self estimation of sleep latency (which was increased) and
quality (which was decreased). This was a double-blind study in which
0, 60, 120, and 250 mg of caffeine was administered one hour before
bedtime.
Mikkelsen (1978) notes that caffeine seems to inhibit deeper stages of
sleep as opposed to disturbances of the REM stage. Other studies show
contradictory evidence, REM being affected by caffeine, leaving the
situation to be resolved.
The tolerance developed to caffeine's effect on sleep by coffee
drinkers has been documented by Colton (Stephenson, 1977). Non-coffee
drinkers were more sensitive to coffee's insomnic effect whereas
coffee drinkers were relatively insensitive in this regard. Non-coffee
drinkers experienced disturbed sleep patterns and delayed onset of
sleep.
Mueller-Limmroth (Stephenson, 1977) showed that the quality of the
first three hours of sleep was impaired by the ingestion of coffee
before retiring. This is approximately equal to the half-life of
caffeine in the body.
Goldstein did extensive work on the effect of coffee and showed that
coffee drinkers slept more soundly when they took placebo as opposed
to caffeine in coffee. If 150 to 200 mg of caffeine was taken before
bedtime, there was an increased sleep latency which was less
pronounced in persons who were heavy ingestors of caffeine (Goldstein
et al., 1965).
These studies show that caffeine has a profound effect on sleep. Heavy
and continued use of caffeine results in tolerance so that heavy users
have less sleep disturbance or need more to obtain its stimulating
effect.
Treatment of Hyperkinetic Children: Hyperkinetic children have been
shown to respond to central nervous system stimulants, resulting in
improved attention, concentration, -and decreased activity. Side
effects are usually disturbing with the more powerful drugs and
include insomnia, anorexia, nervousness, weight loss and abdominal
pain.
A study by Schnackenberg (1975) showed that 200 to 300 mg of caffeine
was similar in effect to methylpheniclate in treating hyperkinetic
impulse disorder secondary to minimal brain dysfunction syndrome. Some
hyperkinetic children, he observed, drank coffee to calm down. Sixteen
children who had shown improvement on methylphenidate but who had
annoying side effects were given one cup of coffee at breakfast and
lunch. Test scores showed a similar im-
provement with coffee as compared to methylpheniclate and the annoying
side effects disappeared when the children were on caffeine.
Schnackenberg recommends 200 to 300 mg of caffeine in a time-release
form.
In 1977, Reichard and Elder published an article on caffeine's effect
on reaction time in hyperkinetic children. They tested the effect on a
choice reaction time task and simple reaction time as compared to
normal children. Caffeine increased the accuracy of stimulus
identification and processing and decreased lapse of attention in the
hyperkinetic group. This is what might be expected based on caffeine's
known effects on such tasks in normals. Hyperkinetic children have a
slower reaction time, are less able to maintain attention and have a
lower rate of correct responses on a vigilance performance task as
compared to normal children. In this study, six normal and six
hyperkinetic children were compared in a double-blind design. Caffeine
significantly raised the rate of correct responses on simple reaction
time in the hyperkinetic group. The reaction time was reduced with
caffeine but was not significantly less than the control period or
placebo. Similar results were found with choice reaction time. The
response is a function of the initial state of the children, i.e., the
more severely afflicted had a larger response. The authors note that
other studies have shown methylpheniclate was more effective than
caffeine in controlling certain aspects of clinical behavior
(impulsivity and hyperactivity). This result does not contradict those
obtained in this study; they are compatible.
Garfinkel was unable to confirm the results of caffeine's
effectiveness in controlling the behavior of children with minimal
brain damage (Stephenson, 1977). Children responding to
methylpheniclate did not necessarily respond to caffeine.
Firestone and associates in a study funded by the Ontario Mental
Health Foundation (1978) showed a significant improvement with
methylphenidate as rated by mothers and teachers on tests of
impulsivity and motor control. No significant improvement was noted
with caffeine although some children showed a slight improvement. Side
effects with both drugs were minimal. Each of 21 hyperactive children
received 500 mg of caffeine, 300 mg of caffeine, and 20 mg
methylpheniclate. This was' a carefully controlled study consisting of
17 boys and four girls. In 1978, Firestone did a study comparing 300
mg of caffeine with placebo in a double-blind crossover design. In
this study, subjective ratings by teachers and parents as well as a
reaction time task showed caffeine to be better than placebo although
the difference was not statistically significant. Firestone concludes
on the basis of the most recent study that caffeine is not a
meaningful alternative as a treatment for hyperkinetic children.
The use of caffeine in the treatment of hyperkinetic children remains
unresolved at this time. Further work seems warranted to ensure that
if caffeine is useful in this prevalent condition that it be available
as a viable alternate treatment in lieu of more powerful CNS
stimulants.
"Restless Legs, Anxiety and Caffeinism" (Lutz, 1978)
Restless legs is a syndrome %vh1ch may be associated with anxious -
depressed as well as other clinical states. Dr. Lutz, in an article
titled as above, suggest that this syndrome is primarily caused by
caffeine. Anxiety is not a causative factor. Caffeine stimulates the
nervous system and has a direct contractile ef. fect on striated
muscle. This is reflected in anxiety, depression, insomnia: and the
heightened proprioceptive awareness may result in restless legs. This
manifestation consists.iof nervousness and movement of legs as a
result of a distressing creeping sensation. Its symptoms are most
obvious at night when the patient is trying to be still, and results
in insomnia. Dr. Lutz describes cases of this disorder in detail and
cites examples, all of which were alleviated when caffeine was removed
from the diet. This condition has been attributed to many causes
including psychiatric disturbinces, e.g. restless legs is a frequent
symptom of hysteria, anxiety, depression. In periods of stress,
"normal" persons are also afflicted. All of these states are
associated with high central nervous system arousal. Also, rest. less
legs syndrome, was first described in England at the time when coffee
and tea first were introduced in the country. Thus, diagnosis of the
restless legs syndrome, as has also been observed in certain
psychological disorders, may simply be the result of overdosage of
ubiquitous caffeine.
Psychological Disorders: Dr. John Greden, a professor of psychiatry at
the University of Michigan, says . caffeinism can be found among those
who have psychiatric problems". Symptoms of excessive caffeine
consumption are similar to anxiety neurosis (Avery, 1980) and include
nervousness, irritability, recurrent headache. twitching, and
gastrointestinal disturbance among other symptoms (Greden, 1974). This
is a known effect of caffeine and Greden adds "...all medications
including caffeine have a potential for abuse and many individuals
clearly ingest symptom-producing doses daily".
Other studies support the relationship indicated above. For example, a
prisoner v6th severe anxiety symptoms admitted to drinking 50 cups of
coffee per day (Niolde, 1975). The symptoms remitted after the coffee
drinking stopped. Excess drinking of coffee by prisoners is not
uncommon and may initiate a vicious cycle: a bored person drinking
more coffee resulting in caffeinism which may result in more
consumption.
The intake of caffeine (coffee, etc.) has been correlated with the
degree of mental illness in psychiatric patients. it is riot clear if
the caffeine intake intensifies the psvchiatric disorder or v,-hether
those v, ith more se\ ere problems tend to drink more coffee. In any
event, in another studv bv Dr. Greden and associates (Greden, 1978) 83
hospitalized psychiatric patients were_inter~oe\\ed and showed an
association ot symptoms ~\ith high caffeine intake. This ma~ pro\ ide
an explanation of some problems \\hich have been experienced in
diagnosing out-patient disorders. Eighteen of the 83 patients (22
percent) were high caffeine consumers (7~0 mg or more). They scored
significantIv higher on the State-Trait anxietv index and the Beck
Depression Scale than lower caffeine consumers. The high consumers had
more clinical symptoms: their physical health was worse; they used
more sedatives, hypnotics, and minor tranquilizers. These patients
showed a tolerance to sleep effects which could be due to a change in
body kinetics or metabolism. Catecholamines contribute to the anxiety
profile and patients may drink more coffee in response to stress,
accentuating a neuro-transmitter response cycle. Since caffeine
affects catecholamine levels and inhibits phosphodiesterase breakdown
of C-AMP, sensitizing receptor sites, the association of caffeine with
anxiety and depressive symptoms is indeed a possibility.
Dr. Greden considers caffeine to be a psychotropic drug and 25 percent
of the population may take more than 500 mg per day, a large
physiologically active dose. He describes three cases in which
caffeinism may be misdiagnosed as an anxiety syndrome.
Dr. Greden concludes that caffeine is found among a fairly large
percentage of hospitalized patients with psychiatric symptoms.
Caffeine should not be used as part of psychiatric treatment routines,
e.g., to reduce drowsiness from psychotropic medications as has been
occasionally suggested.
Dr. John Neil and associates (1978) reported on the possible
complication of caffeinism in diagnosing psychiatric patients. He
suggests that self-medication may confound behaviors of patients.
Caffeine has been considered the most popular "psychotropic" drug in
North America and coffee and tea drinking are not usually in the
records of psychiatric patients. In this experiment, hypersomnic
patients with various diagnoses and caffeine consumption participated,
The authors conclude that "self medication with large doses of
caffeine is a likely response to the anergia and hypersomnia
experienced during certain types of depression". This may lqad to
diagnostic confusion and a complicated course of therapy. Mixed
depressive states may be caused by excess caffeine consumption and
they suggest, also, that unipolar 11 depressives may use more caffeine
as they become depressed.
Caffeine, in these patients, provides only transitory relief as it is
not a true antidepressant. Caffeine also may render anxiolytic and
antipsychotic medications less effective.
Mikkelsen (1978) noted caffeine's involvement in schizophrenic-like
states similar to that observed by Greden in anxiety/neurosis symptoms
of patients who consumed large quantities of caffeine (coffee). One
case cited was of a white male in a catatonic state who threatened his
mother after having gone on a coffee jag over injustices caused to him
by his mother. He developed paranoid delusions which he felt were, at
least in part, due to the coffee. A 30 year old white single female
exhibited paranoid and auditory hallucinations. An anxiety state had
resulted in increased coffee consumption. in the hospital she noted
the correlation of these strange feelings with coffee consumption.
Other examples of psychotic behavior as noted in the literature are
described in this paper. Forty years ago a case of psychosis was
reported in which a 24 year old female took 60 gr (about four g) of
caffeine. Manic symptoms developed. He theorizes that adenyl cyclase
which is increased by caffeine may be a receptor for dopamine. If this
system is abnormal in schizophrenics, caffeine may further sensitize
the patient. Certainly, coffee should be considered as a factor in
this disease.
Reimann (1967) noted that symptoms of a psychoneurotic woman
disappeared when coffee was reduced. She presented with an irregular
fever, insomnia, anorexia and irritability, having consumed large
amounts of coffee.
Clearly, as recommended by Drs. Greden, Mikkelsen and Neil, caffeine
intake should be considered as a factor in diagnosing and treating
psychiatric patients.
SUMMARY
A review of the literature reveals that caffeine is an important
factor in modifying the psychological state of its consumers under the
present condition of usage. Caffeine is probably the most widely used
drug and those who drink coffee, tea, cola or take OTC caffeine
containing drugs are all potential and susceptible candidates. Those
of us who are "normal" can expect manifestations which may be subtle
at low doses, overt at high doses, with the possibility of being the
victims of a habit which results in tolerance and possible severe
withdrawal symptoms. The pleasant stimulant feeling which often occurs
at low doses may be replaced by psychological symptoms which resemble
anxiety and depressive neuroses at high doses. Those with more severe
psychological problems may have their symptoms exaggerated with
excessive caffeine usage, or such symptoms can actually be caused by
excess. Diagnosis of such conditions must take caffeine usage into
account.
As a result of its potent physiological activity, caffeine can alter
our behavior. it affects our sleeping habits generally resulting in
insomnia and hyperactivity. Task oriented performance, attention, and
concentrations may be modified by caffeine. At lower doses, these
effects appear to be beneficial. At higher doses, we can expect the
reverse, including toxic and rebound effects.
The common "Restless Legs Syndrome" which has often been related to
psychological disturbances may, in fact, be primarily a symptom of
caffeinism according to Lutz.
Caffeine has been investigated as a possible treatment for
hyperkinetic children since central nervous system stimulants have
been shown to be effective in this condition. Results of caffeine
treatment are controversial, some studies showing a beneficial effect
with little adverse reactions and other studies showing little or no
benefit.
Caffeine's effect on our body, our nervous system, our mind, our
psychology is no illusion. It is a potent drug. That it may cause
symptoms of mental illness as recently published is no small concern.
With these findings we see that caffeine abuse is more prevalent than
we may imagine. These facts should be brought to the attention of the
medical community as well as the public in order that we may have the
opportunity of being aware of the possible interactions between
ourselves and our environment.
References
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