Caffeine - Nursing Research (Chapter 2 of 5)

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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. 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 improvement 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.

Reichard and Elder (1977) 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 normal. 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.

A restless leg 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 effect on striated muscle. This is reflected in anxiety, depression, and insomnia: and the heightened proprioceptive awareness may result in restless legs. This manifestation consists of 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 disturbances, e.g. a restless leg 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 over dosage 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. This is a known effect of caffeine and all medications including caffeine have a potential for abuse and many individuals clearly ingest symptom-producing doses daily”.

Based on study conducted by Niolde in 1975 supports the relationship indicated above. For example, a prisoner with severe anxiety symptoms admitted to drinking 50 cups of coffee per day. 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 clear if the caffeine intake intensifies the psychiatric disorder or whether those with more severe problems tend to drink more coffee. In any event, in another study by Dr. Greden in 1978 and associates 83 hospitalized psychiatric patients were internee and showed an association of symptoms with high caffeine intake provides an explanation of some problems which have been experienced in diagnosing out-patient disorders. Eighteen of the 83 patients (22 percent) were high caffeine consumers (70 mg or more). They scored significant higher on the State-Trait anxiety 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.

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