Should we be concerned about medications?Although I've spent most of my life enjoying the role of the boy who pointed out the emperor wasn't wearing any clothes, this is one time I hope I'm wrong. Because if I'm right, it means we're doing some serious and irreversible damage to millions of children and adults. As you know, I've never been an opponent of medication for ADHD – my own son briefly took Ritalin. I have for years, however, said that if we were to change our schools to become more stimulating environments, then the need for stimulant medications could be either eliminated or greatly reduced. But now there's research out that has me concerned. My curiosity on this started with the "ADHD is a disease" gang citing a study done a few years ago (Nasrallah HA, Loney J, Olson SC, McCalley-Whitters M, Kramer J, Jacoby CG. Cortical atrophy in young adults with a history of hyperactivity in childhood. Psychiatry Res 1986 Mar;17/3:241-6) that showed that the frontal lobes of children and young adults with ADHD were atrophied or less functional when compared to "normal" people. In pointing this out, they were, of course, trying to prove the recently discredited theory that ADHD is a genetic disease with absolutely no redeeming virtues and no value in the human genome.
When I tracked down the study that showed ADDers with atrophied frontal lobes, I found that 100 percent of the ADHD people whose brains were scanned with PET scanners had been long-term users of Ritalin or other stimulant drugs. Which raised in my mind the question: "Did the brain atrophy occur as a result of the ADHD, or did the stimulant drugs cause it?" Interestingly, just over the past decade a number of researchers have been asking similar questions, although few have been noticed by the ADHD community because the results have had to do with other areas of science or not been promoted by the pharmaceutical industry.

For example, it's well documented that users of the recreational drug ecstasy (MDMA) suffer a long-term and probably permanent loss of brain cells (neurones) that leads to long-term problems with short-term memory. But why and how? A study published in 2000 in the Proceedings of the National Academy of Sciences of the USA found that it was the contamination of ecstasy by amphetamine that was causing the brain damage, not the ecstasy itself. To quote the study, "These initial observations suggest that the sole use of ecstasy is not related to dopaminergic neurotoxicity in humans. In contrast, the reported use of amphetamine by regular users of ecstasy seems to be associated with a reduction in nigrostiatal DA neurones." A study published in the Spring, 2001 issue of the Journal of Child and Adolescent Psychopharmacology ("Early methylphenidate administration to young rats causes a persistent reduction in the density of striatal dopamine transporters") looked at how the brains of rats changed when, as youngsters, they were given methylphenidate (the generic name for Ritalin). The researchers pointed out that nobody had ever looked into the long-term brain effects of giving Ritalin to any mammal (including humans), saying,"…until now possible effects of this treatment [using Ritalin for ADHD] on brain development and the maturation of monoaminergic systems have not been investigated systematically."
The study found that doses of methylphenidate (Ritalin) given during rat childhood led to a permanent loss of up to half of the neurotransmitter transporters in some parts of the rats' brainsin adulthood. The language was explicit: "…the density ofdopamine transporters (Bmax values of [3H]-GBR binding in the striatum but not in the midbrain) was significantly reduced after early methylphenidate administration (by 25% at day 45), and this decline reached almost 50% at adulthood (day 70), that is, long after termination of treatment."                                                                
A dozen or more other studies – most funded by anti-drugabuse agencies within the federal government – have connected use of amphetamine (an ingredient of the second-most popular ADHD medication) with long-term loss of brain cells. Examples from the literature include: "Amphetamine-induced loss of human dopamine transporter activity," "A single exposure to amphetamine is sufficient to induce long-term behavioral, neuroendocrine, and neurochemicals sensitization in rats," and "Changes in striatal D sub(2)-receptor density following chronic treatment with amphetamine as assessed with PET in nonhuman primates."
The National Institute on Drug Abuse even promoted stem cell research in the hope that it could.

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