Thom Hartmann's ADD/ADHD Newsletter

May, 2002
Subject: [ADD News] 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.
http://www.thomhartmann.com/websites.shtml

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' brains in adulthood. The language
was explicit: "?the density of dopamine 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-drug- abuse 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 provide cells to replace those burned out by
stimulant drugs. In a National Institutes of Health website, they note:
"Pluripotent stem cells offer a potential means of replacing neurons
destroyed by drug abuse. This will be especially useful for individuals who
have abused drugs such as methamphetamine, MDMA (ecstacy) and inhalants
which have been shown in animal and some human studies to cause long-term,
possibly permanent damage to selected areas of the brain.

"For example, recent research has shown that methamphetamine can have
significant toxic effects on dopaminergic and serotonergic neurons in the
brain. This is of particular concern because of the spreading use of this
drug and may be related to the dramatic behavioral effects, including the
development of psychotic-like behavior patterns that methamphetamine can
have in some people. Pluripotent stem cells stimulated to develop into
dopaminergic, serotonergic or other types of neurons, could offer a
potential means of replacing neurons destroyed by drug abuse. In this way,
we may be able to eventually reverse some of the debilitating behavioral
effects of drugs such as methamphetamine."
www.nih.gov/news/stemcell/achieve.htm

In the past few years, a startling number of adults who've used stimulating
medications for ADHD for years have reported to me that their short-term
memory seems shot. All attributed it to aging, often making jokes about it.


Perhaps it's no joke. It's time for a dialogue on these studies and the
troubling questions they raise, and for us to again revisit the issue of
how we can improve our schools so that fewer children need medication to
succeed.

-- Thom

Here are a few websites relating to this newsletter (thanks to Vaudree
Lavallee and Bonnie Dennedy for much of this info):
some of the links are broken in this e-mail you can find them intact at:
www.thomhartmann.com/newsletter-2.shtml

www.ucsf.edu/cnba/Center/ JournalClub/Articles/9780.pdf
ethesis.helsinki.fi/ julkaisut/mat/farma/vk/mikkola/roleofbr.pdf
www.amphetamines.com/methylphenidate/longtermdop.html
www.erowid.org/chemicals/mdma /articles/texts/2002_whitworth_1.pdf
www.unifr.ch/biochem/DREYER/drug sensitization.htm
www.psychiatry.wustl.edu/Resources/LiteratureList/ 2001/April/Volkow.pdf
yahoogroups.com


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Rob Kall
Futurehealth, Inc.
211 N. Sycamore St., Newtown, PA 18940  215-504-1700, fax 215-860-5374

11th annual  Winter Brain Meeting  www.futurehealth.org/2003.htm

"Stories serve the purpose of consolidating whatever gains people or their
leaders have made or imagine they have made in their existing journey
thorough the world."
Chinua Achebe  Nigerian novelist

www.storycon.org
Storycon World's First Conference on the Science Art and Application of
Story, Sept 26-29, 2002, Palm Springs


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