The Pharmacology of Caffeine
Like alcoholics and cocaine addicts, people with an impressive tolerance for coffee and tea may find themselves chasing a caffeine high in a losing battle against fluctuating neuroreceptor growth patterns.
The typical caffeine dose in a cup of coffee–between 50 and 200 milligrams, with an average of about 115 milligrams–is enough to produce a measurable metabolic effect. Supermarket coffee in a can has considerably more caffeine per brewed cup than gourmet blends. Robusta beans have more caffeine than Arabica varieties. Instant coffee is the most potent coffee of all. The side effects of overdose–excessive sweating, jittery feelings, and rapid speech–tend to be transient and benign. Withdrawal is another matter: Caffeine causes a surge in limbic dopamine and norepinephrine levels–but not solely at the nucleus accumbens. The prefrontal cortex gets involved as well.
Caffeine’s psychoactive power and addictive potential are easily underestimated. The primary receptor site for caffeine is adenosine, which, like GABA, is an inhibitory neurotransmitter. Adenosine normally slows down neural firing. Caffeine blocks out adenosine at its receptors, and higher dopamine and norepinephrine levels are among the results. Taken as a whole, these neurotransmitter alterations result in the bracing lift, the coffee “buzz” that coffee drinkers experience as pleasurable.
Scientists at the National Institute of Mental Health (NIMH) have demonstrated that high doses of caffeine result in the growth of additional adenosine receptors in the brains of rats. In order to feel normal, the rats must continue to have caffeine. Take away the caffeine, and the brain, now excessively sensitized to adenosine, becomes sluggish without the artificial stimulation of the newly grown adenosine receptors. Like alcoholics and cocaine addicts, people with an impressive tolerance for coffee and tea may find themselves chasing a caffeine high in a losing battle against fluctuating neuroreceptor growth patterns.
Increased tolerance and verifiable withdrawal symptoms, the primary determinants of addiction, are easily demonstrated in victims of caffeinism. Even casual coffee drinkers are susceptible to the familiar caffeine withdrawal headache, which is the result of caffeine’s ability to restrict blood vessels and reduce the flow of blood to the head. When caffeine is withdrawn, the arteries in the head dilate, causing a headache. Caffeine’s demonstrated talent for reducing headaches is one of the reasons pharmaceutical companies routinely include it in over-the-counter cold and flu remedies. The common habit of drinking coffee in the morning is not only a quick route to wakefulness, but also a means of avoiding the headaches associated with withdrawal from the caffeine of the day before.