Abstract
Caffeine is the most widely consumed psychoactive substance and is a legal stimulant readily available. Coffee, tea, chocolate, soft energy drinks, cakes, and breakfast bars are the main sources of caffeine, which is consumed in almost all ages, socioeconomic levels, and conditions. Caffeine is also a component in medications—that is, analgesics, anti-histaminics, stimulants, diuretics, diet pills, dietary supplements (Barone and Roberts, Food and Chemical Toxicology 34(1):119–129, 1996). The issue of an eventual potential of abuse is still debated. Undoubtedly, several features contribute to misuse and habituation, when not addiction, to caffeine, can be both physical and psychological.
Abstract
Caffeine is a xanthine alkaloid compound that acts in the central nervous system as a non-selective adenosine receptor antagonist, and its main effects are as a psychostimulant from low to moderate doses, it increases alertness and/or attention and reduces fatigue. It has been reported that caffeine, similar to other psychoactive compounds, when used chronically may induce a clinical dependence syndrome, and may provoke withdrawal symptoms, such as transient cognitive impairment and dysphoria, especially when its discontinuation is abrupt (Strain et al. 1994; Hughes et al. 1998; Thong et al. 2002). Several studies suggest caffeine has an influence on glucose tolerance and insulin sensitivity: ingestion of caffeine by lean persons before an oral-glucose-tolerance test resulted in a greater insulin response and no decrease in the glucose response; furthermore, acute caffeine ingestion significantly dampened whole-body insulin sensitivity in obese, nondiabetic persons (Graham et al. 2001; Thong and Graham 2002a; Petrie et al. 2004). Studies using hyperinsulinemic euglycemic clamps have confirmed that caffeine ingestion reduces whole-body glucose disposal by 15–30 % and glucose uptake in the leg muscle by 50 % (Greer et al. 2001; Keijzers et al. 2002; Thong et al. 2002). Although we know that skeletal muscle is the major tissue that becomes insulin-insensitive after caffeine ingestion, the mechanism of action is uncertain. Although many potential mechanisms exist, considerable evidence indicates that physiologic concentrations of caffeine antagonize adenosine receptors both in skeletal muscle and in the central nervous system, with the latter resulting in an increase in sympathetic activity (Vergauwen et al. 1994; Han et al. 1998; Fredholm 1998; Graham 2001; Thong and Graham 2002a, b).
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Ramacciotti, C.E., Coli, E., Burgalassi, A. (2016). Caffeine Misuse and Weight Loss. In: Hall, M., Grogan, S., Gough, B. (eds) Chemically Modified Bodies. Palgrave Macmillan, London. https://doi.org/10.1057/978-1-137-53535-1_5
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