Amphetamine is a drug that stimulates the brain by acting via the brain-stimulating natural “amine neurotransmitter” chemicals, dopamine and norepinephrine. The drug causes release of both of these from the neurons that make them. Amphetamine also slows the activity of the protein enzyme monoamine oxidase that normally breaks them down. It also stimulates the receptors for dopamine and norepinephrine on other neurons, mimicking the actions these chemicals themselves. The result is a profound increase in neural activity in many brain areas and with higher doses, an intense euphoric sensation. This is the basis for the extreme addiction potential to forms of the drug that rapidly enter the blood in large doses, as when smoked as in “crystal meth”, “shabu”, “yaba”, etc., or when directly injected into a vein. These large illegal “recreational” doses have been traditionally blamed for killing off neurons via a process called “excitotoxicity” in which brain neurons that get over-stimulated are prone to dying. It has been generally assumed that by taking the drug via the oral route and using a limited prescribed dose that is too low to produce the euphoria, you would avoid the higher dose excitotoxicity issues.
Amphetamine comes in many forms and under many trade names. Some common ones are Adderall and Ritalin for ADD (attention deficit disorder) and Dexedrine (for weight loss). The chemical difference in the actual drug preparations is beyond the scope here but all forms eventually yield a single compound, amphetamine, in the bloodstream. This is important because a study on let’s say the harmful effects of Dexedrine can in most cases be pretty accurately generalized to the other amphetamine preparations as is the case here.
In fact a recent study looking at Dexedrine use has sparked concern over the safety of Adderall and Ritalin. For roughly half a century, different forms of amphetamine have been given to children who were originally deemed “hyperactive,” now referred to as suffering from ADD (attention deficit disorder) or ADHD (attention deficit hyperactivity disorder). The number of adults being diagnosed and medicated for ADD has also skyrocketed. The recommended dosages of these drugs has been deemed safe by both the FDA and the prescribing medical community.
Amphetamine in prescribed doses for ADD/ADHD measurably improves cognitive ability by acting rather paradoxically in the “hyperactive.” Even though it’s a stimulant, it seems to have a calming effect on the pathologically restless. There has always been the allegation by many, that these “hyperactive” kids were being drugged to conveniently placate frustrated parents and teachers even though they were haplessly exposing the children to a potentially addictive and dangerous drug. The objective data regarding school performance, reversal of dyslexic symptoms, and general cognitive ability has argued against those allegations. However the possibility of potential harm even at prescribed regulated doses could be very real.
In laboratory animals (rats and monkeys) amphetamine raises levels of the stimulant neurotransmitters discussed above but with extended use, the levels of the brain chemicals dopamine and serotonin both drop. Rats given a prolonged dosing lose cells un the upper brainstem: near the very neighborhood where dopamine neurons originate (substantia nigra). These academic results were always dismissed because of a lack of clinical proof that this occurs in humans who were not abusing the drug, but rather taking it in a lower controlled prescribed dosing.
This was until now when 64,000 HMO patients in California were recently polled regarding the use of prescribed amphetamines for weight loss. A study on such a large group makes results more solidly convincing from a statistical viewpoint. Over 1000 polled had Parkinson’s. Volunteers who said they had taken amphetamines were 60 percent more likely to be part of the Parkinson’s group. The authors warned not do draw any sudden conclusions from their results, but to rather, wait until further studies are done to confirm or deny a causal link between amphetamine use and Parkinson’s.
However considering the theoretical risks discussed above, I might worry. One needs to wait and see. However this author would hope that the results produce a sense of caution in the ADD/ADHD stimulant-prescriber community and among educational professionals who have taken a rather routine view in referring children with ADD/ADHD suggestive profiles to such prescribing professionals.