Posted by nightlight on November 24, 2001, at 13:31:52
In reply to Re: amphetamine sensitization article, posted by Andy123 on November 23, 2001, at 10:27:34
> This article is very alarming in that it indicates sensitization can occur at the very low therapuetic amphetamine doses used for ADD. I wish I'd read it a long time ago. I'm giving up d-amphetamine (even though I use it at a very low dose of 20mg/day.)
> -AndyHi Andy,
I, too, read the article with great interest, as I have recently been prescibed stimulants and have been trying to find out as much about them as possible.
The article is quite long, as thorough as possible, given certain restrictions on long-term testing of some pertinent groups, but, the overall conclusion, for those *human* patients who take therapeutic doses of amphetamines/ritalin is positive and fairly benign.
But, you have to get to the last section or so, before this is made clear. (There is a great deal of discussion about animal studies and the effects of stimulants on schizophrenics and seasoned meth abusers which can mislead the layman, like me, unless the entire article is studied). Amphetamine psychosis is quite rare among those who take prescribed dosages, and current scientific data suggests that the use of stimulants in childhood and adolescence probably *reduces* substance abuse in the patient who was properly diagnosed and treated for ADHD/ADD.I thought the article was pretty good for allaying some of my fears, although it did remind me that one does not want to consider the taking of any psychotropic med lightly.
I echo Scott in wondering what you found so disturbing about the article. I did simply scan some of it (mostly the stereotypical animal behaviour studies towards the end). So, maybe I missed something???
sincerely~nightlight
>
> > John, did you ever read that web page that I sent you regarding amphetamine tolerance and neurotoxicity?
> >
> > Here's an interesting excerpt from it:
> >
> > http://www.acnp.org/g4/gn401000166/ch162.htm
> > "Methamphetamine toxicity is inhibited by a variety of drug treatments, including: 1) DA synthesis inhibitor alpha-methyl-para-tyrosine; 2) DA receptor antagonists; 3) NMDA receptor antagonists, e.g., MK-801; 4) DA and serotonergic reuptake inhibitors protecting against DA and serotonin toxicity respectively (195). Even though most studies have found that serotonergic and DA reuptake inhibitors specifically protect these two sites, certain reuptake blockers (such as benztropine) do not (195). On the other hand, mazindol, a non-specific blocker, protects against both DA and serotonergic neurotoxicity. Ali et al. (1994) have further demonstrated in mice that a major factor for neurotoxicity is hyperthermia which is highly correlated with the degree of long-term DA depletion (21). Furthermore, haloperidol, diazepam and MK-801, all of which can reduce methamphetamine-induced hyperthermia, protect rats against DA depletion (4). They also demonstrated that reducing the ambient temperature (4°C) reduced neurotoxicity to the same levels found when phenobarbital, diazepam and MK-801 were present to protect the cell. Tolerance to methamphetamine induced by increasing doses also reduces the hyperthermic response and as well protects against neurotoxicity (89, 188).
> > An important caveat is that not all protective mechanisms act by preventing the hyperthermic effect; the monoamine uptake blockers inhibit neurotoxicity in the absence of inhibition of hyperthermia, e.g., fluoxetine blocks methamphetamine serotonin toxicity without reducing temperature (140). The monoamine protection from neurotoxicity by reuptake inhibition is emphasized by the unexpected discovery that even massive and 24-hour continuous dosing of cocaine, e.g., 100 mg/kg/day, does not result in DA system neurotoxicity (119, 182, 183). Hyperthermia has been well documented to increase amphetamine stereotypy (93, 220). Hyperthermia alone is well known to result in neuronal chromatolysis and has been previously proposed as a significant contributor to amphetamine-induced DA depletion and neuronal damage in clinical as well as experimental animal histopathology (52). Hyperthermia may have been one of the factors resulting in deaths among athletes taking moderate doses of amphetamine in the 1960s and 70s (145). Even in mild hyperthermia, increased body temperature induces a linear decrease in the inhibitory feedback of stimulants on somatodendritic autoreceptors (130). Thus, body temperature changes induced by amphetamine should be considered as one of the contributors to toxicity. "
> >
> > I've read on this board ppl saying that Prozac+adderal doesn't poop out much...and this mazindol might even be a better idea. What do you think?
poster:nightlight
thread:84550
URL: http://www.dr-bob.org/babble/20011123/msgs/85044.html