Caffeine is very commonly consumed the World over. Caffeine is present in many plants that are part of the Western diet, but most commonly it is found in tea and coffee. Intakes of caffeine are estimated at around 300 mg per person per day in the Western nations. Caffeine is part of the methylxanthine group of drugs, and its stimulatory activity on the central nervous system is thought to come from interaction with the adenosine receptor, for which it is an antagonist. Blocking the adenosine receptor leads to increases in the release of catecholamine hormones, particularly adrenaline. This mechanism is what provides the stimulatory effects of caffeine that are experienced by not habitual consumers. One of the effects of the catecholamine hormone adrenaline is to initiate the mobilisation of fuels, and in this regard adrenaline causes the lipolysis of triglycerides to fatty acids. This can increase plasma levels of free fatty acids in the blood, something that is also induced by adrenaline release following exercise.
Free fatty acids in the blood have been shown to decrease insulin sensitivity. Therefore it is possible that caffeine may have insulin desensitising effects based on its ability to raise plasma levels of free fatty acids. Researchers have used caffeine intravenously to assess its effects on insulin sensitivity1. Administration of caffeine at 3 mg per kg of body weight proceeded prior to assessment of insulin sensitivity, and the results were compared to a control group who received no caffeine, but instead an inert placebo was infused. The results of the study showed that the infusion of caffeine caused plasma adrenaline levels to increase for around 15 minute following the infusion, compared to the placebo. In addition the caffeine cause the levels of free fatty acids in the plasma to increase for around 15 minutes in comparison to the placebo. Following this initial 15 minute increase, there were no differences between the placebo and caffeine treatment for adrenaline or free fatty acid levels.
The increase in plasma adrenaline and free fatty acids was accompanied by a 15 % reduction in insulin sensitivity in the caffeine treated subjects. From this it could be theorised that it was the elevated levels of free fatty acids and adrenaline that may have been the cause of the reduced insulin sensitivity. As caffeine is an adenosine antagonist, the researchers gave an adenosine agonist (dipyridamole) to the subjects to assess the effect of the adenosine receptor on the change in insulin sensitivity. However, administration of the drug had no effect on the change in insulin sensitivity, precluding adenosine receptor antagonism as directly contributing to the effects seen. Although these results are interesting, it should not be inferred that regular consumption of tea or coffee or other caffeine containing drinks and foods are able to cause insulin insensitivity. Evidence supports weight loss effects from caffeine consumption, and the changes to insulin sensitivity seen in this study were transient in nature, lasting a few minutes at most.
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