Animal experiments have shown caffeine-mediated effects at the neuroendocrine level, such as increased serum corticosterone and ^-endorphin and decreased serum growth hormone and thyrotropin, but it is expected that habitual human consumption has only marginal or inconsistent neuroendocrine effects. Caffeine is described as a central nervous system (CNS) stimulant, and the increased formation and release of neurotransmitters such as catecholamines, serotonin, 7-aminobutyric acid, norepinephrine, and acetyl-choline have been reported.
Behavioral effects can be observed in humans after acute and moderate doses of 1-5 mgkg-1 of caffeine. In these studies, the subjects felt more alert and active with improved cognitive function, including vigilance, learning, memory, and mood state. It was claimed that they would be better able to cope with their jobs when bored or fatigued and after night work and sleep deprivation. Population-based studies of the effect of caffeine intake on cognition showed a positive trend, especially among elderly women. Comparative studies on regular and deprived caffeine consumers suggest that reversal of caffeine withdrawal is a major component of the effects of caffeine on mood and performance.
A dose-dependent delay in sleep onset is found as well as a decrease in total sleep time and an impairment of sleep quality characterized by an increased number of spontaneous awakenings and body movements. In premature infants, sleep organization appears to be unaffected by treatment with 5mg/ kg/day caffeine to prevent apnoea.
The observation that sensitive subjects are more likely to have trembling hands is considered to be a CNS effect and not a direct effect on muscle. Caffeine doses higher than 15mgkg_1 induce headaches, jitteriness, nervousness, restlessness, irritability, tinnitus, muscle twitchings, and palpitations. These symptoms of chronic excessive caffeine intake are part of the criteria used to make the diagnosis of caffeinism. The same symptoms have been reported in adults on abrupt cessation of caffeine use.
With 100-200 mgkg-1 doses, mild delirium appears, followed by seizures and death. Although tolerance with low doses led to a pleasant stimulation, alertness, and performance benefits, on withdrawal, headache, drowsiness, fatigue, and anxiety were reported.
Epidemiology and laboratory studies suggest beneficial effects of caffeine consumption in the development of Parkinson's disease and the mechanisms involved may be mediated through adenosine A2A receptors. The role of these receptors in neuronal injury and degeneration, as well as in other diseases such as Alzheimer's disease, has important therapeutic potential but needs further investigation.
Was this article helpful?