This delays the onset of drowsiness and releases dopamine.Studies have demonstrated that people who take in a minimum of 100 mg of caffeine per day (about the amount in one cup of coffee) can acquire a physical dependence that would trigger withdrawal symptoms that include headaches, muscle pain and stiffness, lethargy, nausea, vomiting, depressed mood, and marked irritability. Professor Roland R. Griffiths, a professor of neurology at Johns Hopkins in Baltimore strongly believes that caffeine withdrawal should be classified as a psychological disorder. His research suggested that withdrawal affects 50% of habitual coffee drinkers,  beginning within  12–24 hours after cessation of caffeine intake, and peaking in 20–48 hours, lasting as long as 9 days.Continued exposure to caffeine leads the body to create more adenosine-receptors in the central nervous system, which makes it more sensitive to the effects of adenosine. It reduces the stimulatory effects of caffeine by increasing tolerance, and it increases the withdrawal symptoms of caffeine as the body becomes more sensitive to the effects of adenosine once caffeine intake decreases. Caffeine tolerance develops very quickly. Tolerance to the sleep disruption effects of caffeine were seen after consumption of 400 mg of caffeine 3 times a day for 7 days, whereas complete tolerance was observed after consumption of 300 mg taken 3 times a day for 18 days. Physiological effects
When a person becomes caffeine dependent, it can cause a person to suffer different physiological effects which could lead to withdrawal.
Infantile cerebral and cerebellar atrophy with postnatal progressive microcephaly is a rare hereditary autosomal recessive malformation syndrome of the central nervous system characterized by profound motor delays and intellectual disabilities, progressive microcephaly, hypertonia, spasticity, clonus and epilepsy. MRI findings include severe cerebellar and cerebral deterioration (atrophy) and impaired myelination. This condition is an example of consequences from the Founder effect, especially that of Jewish populations.It has been described in 5 infants from 4 Israeli families of ethnic Caucasus Jewish descent. The genetic cause was found to be a homozygous mutation of the MED17 gene, located in chromosome 11, this mutation is called L371P.In vitro functional expression assays of the L371P mutation showed that it results in a functionally inactive MED17 protein. == References ==