Amphetamines May Increase Risk of Parkinson's Disease, Study Suggests

You need to burn out about 95% of your dopamine-producing neurons for Parkinson's to set in. That being said, I wouldn't be in a hurry to facilitate the process.
 
This is such bullshit to be called science. Ask somebody a yes or no question and follow them for years based on the answer? No script confirmation? No idea how much, how often, how adulterated?
Hey, lets start a study now?
1) Are you still a queer? Based on answers we can study homosexual morbidity based on whoever will fund us.
2) Interview jr. high school boys. Have you ever masterbated? Have you ever had sexual intercourse? Based on this study I think we all know boys never masterbate, and upwards of 90% have had sex at summer camp or somewhere, despite the fact the representable sample of their available female peers may still contain 75% virgins. Either the boys maybe lying, (you think?) or they also need to be asked question #1.

Many antipsychotic drugs cause down regulation of dopamine as the intended activity. Taken in high doses for extended periods of time and the effects mimic parkinsons remarkably. Remove the drug and remove the effect. Amines do not mimic parkinsons, even at massive doses. A little psychosis maybe, but ... Don't validate PT Barnum fellas.
 
i call bullshit just another media hype up trying to scare people off drugs :\ low loevels of dopamine dont mean yo got parkinson's :S just like smoking off tin foil cause's parkinson's.....cmon what dosen't cause some deadly illness these days :!
 
ehh i herd the foil one, but that has SOME basis in fact
apparently in people with parkinsons the level of aluminum in their body is higher than normal, but ehhh
ill smoke shit off foil, like freebase it or wha-eva but i wouldnt do that often just cause, thats just e
 
on a slightly related matter, I've experienced parkinsonism after working with rusted iron. I inhaled and absorbed so much rust that I tasted it and trembled uncontrollably for hours. Has anyone else felt this?
 
Went to the link referenced here. Affiliated with very good medical center, of whom one of the founding fathers was both a cutting edge, (no pun intended) surgeon and a life long dependent on morphine, in a big way.
The author of this paper tells on himself pretty quickly. Nothing screams I am a dumb ass fishing for federal grant funds more than a dumb ass fishing for federal grant funds. Our esteemed author states his amine mixture mirrors a currently popular ADHD med, and how he received the same formula for his "research". He states as fact, a for some reason somewhat widely held misconception, Adderall is a 25% levo and 75% dextro mix. As I hold in my hand a pharmacy bottle of 100 pills with Shires label stating its a 50% levo, 50% dextro mix. To be more exact, 25% levo aspartare, 25% levo sulfate, 25% dex sulfate, and 25% dex sacchrate. His 75/25 dex sulfate is, like his paper, significantly inaccurate. I would wager he needs a real job. In the private sector, he would have to produce something besides bullshit.
 
This has been known for a very long time, it just hasn't really been widely reported.

Went to the link referenced here. Affiliated with very good medical center, of whom one of the founding fathers was both a cutting edge, (no pun intended) surgeon and a life long dependent on morphine, in a big way.
The author of this paper tells on himself pretty quickly. Nothing screams I am a dumb ass fishing for federal grant funds more than a dumb ass fishing for federal grant funds. Our esteemed author states his amine mixture mirrors a currently popular ADHD med, and how he received the same formula for his "research". He states as fact, a for some reason somewhat widely held misconception, Adderall is a 25% levo and 75% dextro mix. As I hold in my hand a pharmacy bottle of 100 pills with Shires label stating its a 50% levo, 50% dextro mix. To be more exact, 25% levo aspartare, 25% levo sulfate, 25% dex sulfate, and 25% dex sacchrate. His 75/25 dex sulfate is, like his paper, significantly inaccurate. I would wager he needs a real job. In the private sector, he would have to produce something besides bullshit.

This is nitpicking at best. I'm not sure how you've seen all the research as it has not even been published yet. The findings have been reported by previous researchers, so it's not all that surprising.
 
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I seem to be pretty susceptible to little movement disorders... and stimulants do certainly set them off in me for whatever reason. This isn't a surprise to me...
 
Always wondered about high-dose, long-term amp use and Parkinson's, especially after seeing the Hitler documentary that showed his tremor late in life. They questioned whether it was Parkinson's or an effect of his daily meth use but never drew any conclusions (can't remember the show).

I imagine amps can cause similar symptoms, but as for actually causing Parkinson's--a chronic, degenerative disease--I kind of doubt it.
 
Always wondered about high-dose, long-term amp use and Parkinson's, especially after seeing the Hitler documentary that showed his tremor late in life. They questioned whether it was Parkinson's or an effect of his daily meth use but never drew any conclusions (can't remember the show).

I imagine amps can cause similar symptoms, but as for actually causing Parkinson's--a chronic, degenerative disease--I kind of doubt it.

parkinsons is to do with loss of dopamine neurons in the substantia nigra, high dose amphetamines are neurotoxic to dopamine neurons all over the brain. easy connection- no shocks here

parkinsons happens when the levels of neurons reaches a certain %, if amphetamines are killing them off one by one they speed up the process by which you get to the level of having parkinsons
 
Well, the study says there was no increased incidence of parkinson's in patients utilizing stimulants for weight loss...

From this we can form two separate explanations that would circumvent the theory of greater susceptibility to parkinson's in ADHD patients.

First, is it not possible that those predisposed to parkinson's might ALSO be predisposed to ADHD? I'm not up to date with which pathologies present alongside ADHD, but if there were lower concentrations of dopamine then it would make sense that there would be a correlation with ADHD med users and parkinson's disease. The areas of the brain (and types of dopamine receptors contained within them) affected by these two disorders might be completely different, which would invalidate this theory. I'm just not sure.

Secondly, patients utilizing amphetamines for weight loss are obese - you cannot fake obesity. What if some of the ADHD users either falsely obtained their prescription or decided during treatment to abuse their meds? That could certainly explain the discrepancy between the two group types.

Of course, it might also simply be that obese patients have shorter courses with lower dosages.

Anyone mind filling me in? I am prescribed adderall for ADHD and with these recent studies I'm a little concerned about taking the meds. I could always switch over to ritalin, but if adderall is more effective (have not tried it even once yet) and these risks are shown to be overblown, then perhaps it would be better to start and continue with it, as I DO have significant symptoms and difficulty conducting a normal life.
 
Anyone mind filling me in?

you misread:

Researchers found that patients who had taken Benzedrine or Dexedrine developed Parkinson's disease at a higher rate than patients who admitted using weight-loss drugs but did not take the amphetamines.

meaning those who took any weight loss drug other than amphetamine developed less Parkinson's than those who took amp for weight loss. Keep in mind also that this study started enrolling in the early 1970's, when docs were handing out amps to everyone who wanted to drop some weight.

Good point about ADHD possibly being correlated to Parkinson's. The correlation doesn't necessarily have to be positive. From the baboon study:

NSFW:
It is reasonable to wonder why, if clinically relevant doses of amphetamine produce toxic effects on brain dopaminergic neurons in nonhuman primates, evidence of dopaminergic neurotoxicity has not been revealed in clinical or neuroimaging studies of patients with ADHD. With regard to clinical studies, it is important to recognize that parkinsonism may not become manifest until central dopaminergic function is reduced by approximately 80 to 90% (Koller et al., 1991), a degree of dopamine reduction that is approximately 2-fold greater than that observed in the current study. Abnormalities in cognitive function, another potential functional consequence of dopaminergic loss (Robbins, 2003), may be difficult to distinguish from the underlying symptoms of ADHD for which amphetamine is being prescribed. Indeed, given the fact that abnormalities in dopaminergic neural function are believed, in part, to underlie symptoms of ADHD (Fone and Nutt, 2005), any indication of abnormal dopaminergic function in amphetamine-treated patients might be attributed to underlying disease, rather than amphetamine neurotoxicity. With respect to neuroimaging studies, it is important to recognize that most subjects with ADHD who have been included in PET/SPECT studies of the DAT have been medication-naive individuals (Krause et al., 2000, 2003; Jucaite et al., 2005) and that in those isolated instances in which ADHD patients treated with stimulants have been included, those treated with amphetamine (rather than methylphenidate) were either excluded from the analysis (Krause et al., 2003) or were not analyzed separately (Dougherty et al., 1999; Krause et al., 2002). Notably, results of these imaging studies have not been entirely consistent, with both increases (Dougherty et al., 1999; Krause et al., 2000) and no change (van Dyck et al., 2002) in DAT density reported in the striatum of ADHD patients. Thus, for a variety of reasons, the absence of previous clear clinical or PET/SPECT data showing evidence of DAT changes consistent with dopaminergic neurotoxicity in patients with ADHD previously treated with amphetamine should not be construed as evidence that it does not occur.
 
you misread:

I had already read the study on another site before posting here, didn't bother to read the OP. : P

Turns out it was kind of poorly worded; here's the text:

According to the study, those people who reported using Benzedrine or Dexedrine were nearly 60 percent more likely to develop Parkinson's than those people who didn't take the drugs. There was no increased risk found for those people who used drugs for weight loss.

Anyway, so what are the implications of all this, then? Is it believed that amphetamine is neurotoxic even at therapeutic dosages? Some said the deficits could be explained instead by regulatory processes that would reverse, but I'm curious to hear new takes on the matter, or affirmation of one of the existing theories. Obviously there is no certainty to be had, but it's worth discussing I'd say.
 
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