Caffeine and dependence

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Brain mapping technology
The issue of possible dependence on caffeine has been debated for many years. In humans, the widely recognized behavioral stimulant, and mildly reinforcing, properties of caffeine are likely to be responsible for the maintenance of caffeine consumption66.

People may also drink coffee from habit: the possible reinforcing effects of coffee may not be due to the caffeine per se, but linked to the pleasurable aroma and taste of coffee, as well as the social environment that usually accompanies coffee consumption67.

Learn more about caffeine’s effect on the brain by watching a video here.

Drugs of abuse such as cocaine, morphine and nicotine specifically activate the dopaminergic mesolimbic brain circuit of dependence and reward at low doses.

  • Pre-clinical studies have reported that caffeine given to rats, in doses corresponding to human consumption levels (1-5mg/kg body weight, i.e. 1-5 large cups of coffee in one sitting), fails to increase energy metabolism68 and dopamine release69,70 in this circuit.

This research has also been extended to humans.

  • Subjects in one study received 3 mg/kg body weight of caffeine, or the equivalent of about 2 large cups of coffee. Cerebral blood flow measurements showed that, as in rats, caffeine did not activate the brain circuit of dependence in humans, but activated regions involved in attention, vigilance and anxiety (the internal parietal zone), as well as regions controlling vegetative functions (the hypothalamus and anterior insular cortex)71.

These results represent the first ‘brain mapping’ approach to the study of dependence in humans, and confirm the pre-clinical data reporting no involvement of the circuit of dependence in the physiological effects of caffeine69,70. In other words, based on brain mapping technology, caffeine does not fulfil the criteria to be described as a drug of dependence.

Among the symptoms linked to drug dependence is withdrawal. In 2013, the American Psychiatric Association released an updated edition of its Diagnostic and Statistical Manual of Mental Disorders, the DSM-5, which provides standardized criteria for the classification of mental disorders. For the first time since its launch in 1952 it addresses ‘caffeine withdrawal’. In the manual, caffeine withdrawal is defined as a syndrome resulting from abrupt cessation or reduction in caffeine, following prolonged daily use72.

Only a subset of the population of coffee/caffeine consumers suffer withdrawal symptoms (headache, reduced alertness, and drowsiness). These symptoms generally begin about 12-24 hours after sudden cessation of caffeine consumption and reach a peak after 20-48 hours. Importantly, these symptoms can be avoided altogether if caffeine intake is decreased progressively66.

  • A study measuring cerebral blood velocity, after the exposure of subjects to either 400mg caffeine or placebo for two weeks, reported that acute caffeine abstinence produced significant increases in blood flow velocity that, consistent with earlier studies, highlight the link between vascular changes and the caffeine withdrawal symptoms of headache, increased drowsiness and decreased alertness73.
  • Likewise, the ingestion of 250mg caffeine, by caffeine consumers (mean intake of 375mg caffeine per day), after 30 hours of abstinence, had a greater effect than placebo on mood and choice reaction time (i.e. the reaction time for a task in which an individual has to make one of two or more choices). Caffeine also improved selective attention and memory in both those who had abstained from caffeine and those who had maintained their habitual intake levels, suggesting no evidence of withdrawal on these markers of mental performance74.
  • A 2012 review on the role of caffeine as a performance enhancer also concluded that caffeine’s beneficial effects on both simple and complex attention tasks could not be attributed to withdrawal reversal6.
  • Another study, using quantitative perfusion magnetic resonance imaging, reported that cerebral blood flow increased during the abstinence period and reduced after caffeine ingestion, in both those who abstained or did not abstain from caffeine before the test. This study also showed that in high consumers (950mg/day), the cerebrovascular adenosine system has a limited capacity to compensate for the high amount of daily caffeine used. However, this study is limited by several factors, including the arbitrary classification of daily caffeine intake and possible under-reporting of withdrawal symptoms75.

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