Neuropsychiatric effects of caffeine

‘… 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 (Reference Scott, Chakraborty and MarksScott 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 (Reference FinneganFinnegan, 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 (Reference Scott, Chakraborty and MarksScott et al, 1989).

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 sleep disorder; and caffeine-related disorder not otherwise specified. Caffeine withdrawal is included in the Appendix to DSM–IV under ‘Criteria sets and axes provided for further study’. The ICD–10 (World Health Organization, 1992) is less specific. It recognises ‘Mental and behavioural disorders due to use of other stimulants, including caffeine’ (F15), which are then sub-classified in the same way as other substance use disorders (acute intoxication, harmful use, dependence syndrome, withdrawal state, etc.). However, there is no specific guidance on diagnosing problems due to caffeine misuse, and the diagnostic criteria are the same as for other substance use disorders. The prevalence of the various caffeine-related syndromes is uncertain. Despite this formal recognition, caffeine generally receives little attention from psychiatrists. For example, the New Oxford Textbook of Psychiatry (Reference Gelder, Lopez-Ibor and AndreasenGelder et al, 2003) does not discuss caffeine misuse, although caffeine is mentioned briefly as a cause of insomnia. Consequently, psychiatrists rarely enquire about caffeine intake when assessing patients. This may lead to a failure to identify caffeine-related problems and offer appropriate interventions. This article describes the clinical effects of caffeine consumption in a variety of psychiatric disorders and offers some guidance on assessing and managing caffeine-related problems.

Assessment and treatment of caffeine-related problems In summary, although there is little evidence that caffeine produces clinically significant dependence, it may play a contributory role in a variety of psychiatric disorders. Assessment of caffeine intake should therefore form part of routine psychiatric assessment. This is particularly important in people with anxiety and sleep disorders, eating disorders and substance misuse. Assessment can easily be incorporated into the assessment of alcohol and drug use. In people who misuse drugs or have an eating disorder, it is appropriate to ask about use of over-the-counter products that contain caffeine. Intake should be quantified roughly in terms of the number of cups/mugs of tea or coffee and cans of carbonated drinks consumed in an average day. This can be converted into daily caffeine intake (Box 1). Intake may be classified as low (<250 mg/day), moderate (250–750 mg/day) or high (>750 mg/day). • Average cup of instant coffee 75 mg • Average mug of instant coffee 100 mg • Average cup of brewed coffee 100 mg • Average cup of tea 50 mg • Regular can of cola drink up to 40 mg • Regular can of energy drink up to 80 mg • Plain 50 g bar of chocolate up to 50 mg • Milk 50 g bar of chocolate up to 25 mg (Data from Food Standards Agency, 2001, with permission) Psychiatrists should always enquire about use of caffeine before prescribing hypnotics. Other situations where caffeine intake may be relevant include poor response to hypnotics, recurrent headaches and palpitations (Reference GredenGreden, 1974). General practitioners, who see large numbers of patients with anxiety and sleep disorders, should also be made aware of the importance of caffeine and encouraged to ask about its use. Those who consume large amounts of caffeine should be given information about is effects and encouraged to reduce their intake. If overuse of caffeine is established, gradual reduction in intake or gradual substitution with caffeine-free alternatives is probably preferable to abrupt cessation. Decaffeinated coffee and tea are now readily available. Although there have been concerns about potential carcinogenic effects when beverages are decaffeinated chemically, processes that use water and carbon dioxide seem to be safe. Caffeine-free cola is also becoming more available. Those responsible for in-patient psychiatric units should be aware of the potential role of excessive caffeine consumption in exacerbating sleep problems and behavioural disturbance and should encourage patients to reduce their consumption. Decaffeinated beverages should be provided on psychiatric wards. Box 2 gives useful website addresses for further information on caffeine. For the general public http://www.eatwell.gov.uk/healthydiet/nutritionessentials/drinks/waterandsoftdrinks For professionals Health effects: http://www.jr2.ox.ac.uk/bandolier/band58/b58-4.html Psychiatric effects: http://www.emedicine.com/med/topic3115.htm