Neuropsychiatric Effects of Caffeine: Exacerbation of Anxiety and Sleep Disorders

Pages: 6 (2094 words) Published: July 25, 2013
Neuropsychiatric effects of caffeine
Psychiatrists rarely enquire about caffeine intake when assessing patients. This may lead to a failure to identify caffeine-related problems and offer appropriate interventions. Excessive caffeine ingestion leads to symptoms that overlap with those of many psychiatric disorders. Caffeine is implicated in the exacerbation of anxiety and sleep disorders, and people with eating disorders often misuse it. It antagonises adenosine receptors, which may potentiate dopaminergic activity and exacerbate psychosis. In psychiatric in-patients, caffeine has been found to increase anxiety, hostility and psychotic symptoms. Assessment of caffeine intake should form part of routine psychiatric assessment and should be carried out before prescribing hypnotics. Gradual reduction in intake or gradual substitution with caffeine-free alternatives is probably preferable to abrupt cessation. Decaffeinated beverages should be provided on psychiatric wards. ‘. . . coffee sets the blood in motion and stimulates the muscles; it accelerates the digestive processes, chases away sleep, and gives us the capacity to engage a little longer in the exercise of our intellects.’Honoré de Balzac (paraphrasing Brillat-Savarin)Traité des Excitants Modernes(1838), (translated from the French by Robert Onopa) Caffeine is the most widely used psychoactive drug in the world. It is found in more than 60 known species of plants, and dietary sources include coffee, tea, cocoa beverages, chocolate and soft drinks. Coffee was consumed in Arabia in the 13th century and was introduced into Europe in the early 17th century. Tea was probably drunk in China before the birth of Christ and was brought to Europe in the 16th century. Most dietary caffeine is still consumed as tea and coffee, and the latter accounts for 55% of per capita intake in the UK (Scott et al, 1989). Despite (or perhaps because of) its ubiquity, caffeine is rarely thought of as a problematic drug. Doctors do not often ask patients about its use and enquiry into caffeine consumption is not usually included in psychiatric assessment. On average, a cup of brewed coffee contains 100 mg of caffeine, compared with 75 mg for instant coffee and 50 mg for tea (Food Standards Agency, 2001); a can of Coca Cola contains 30 mg. Increasingly, stimulant drinks such as Red Bull (80 mg of caffeine per can) are being marketed to the public, and sales have increased dramatically since they first became available in 1987 (Finnegan, 2003). Pharmaceutical caffeine may be bought over the counter (for example as ProPlus tablets) and is also contained in numerous proprietary analgesics, cold and ’flu remedies, diet pills and diuretics; Anadin Extra, for example, contains 90 mg of caffeine per dose. In the UK, mean caffeine consumption is estimated at 359 mg/day (Scott et al, 1989). Previous SectionNext Section

Effects and diagnostic classification
The primary effect of caffeine is to relieve fatigue and enhance mental performance. Excessive ingestion leads to a state of intoxication known as caffeinism, which is characterised by restlessness, agitation, excitement, rambling thought and speech, and insomnia. These symptoms clearly overlap with those of many psychiatric disorders. The potential harmful effects of caffeine have long been recognised. As long ago as 1900, the Journal of the American Medical Association reported a conference on ‘Coffee as a beverage: its deleterious effects on the nervous system’, at which a contributor complained that ‘most physicians had given the subject little if any attention’. Another contributor asserted that coffee could cause a variety of symptoms, including depression, irritability, insomnia, tremulousness, loss of appetite and ‘frequent eructations of gas’ (JAMA, 2001). Four caffeine-related syndromes are recognised in DSM–IV (American Psychiatric Association, 1994): caffeine intoxication; caffeine-induced anxiety disorder; caffeine-induced...
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