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Re: Pstims for OCD?? Really? Not!

Posted by Larry Hoover on April 25, 2003, at 12:12:38

In reply to Re: Pstims for OCD?? Really? McPac and » Caleb462, posted by Ron Hill on April 25, 2003, at 11:55:59

> > I've never heard of amphetamines helping OCD until I read that, so I wanna check out that study. Large doses of amphetamines can CAUSE obsessive-compulsive behavior, so it is somewhat suprising.
>
> Caleb and McPac,
>
> Yeah, that's the same reaction I had when I read it. However, if the study is correct and pstims do in fact help OCD, and if one wants to use a natural supplement treatment approach (as previously indicated by McPac), then Enada NADH might be worth a trial. As I understand it, the primary neurochemical action of both Enada NADH and the pstims is along dopaminergic pathways.

Lots of if's there, Ron. Here's the study abstract:

J Clin Psychopharmacol 1991 Aug;11(4):237-41

Acute psychostimulant challenge in primary obsessive-compulsive disorder.

Joffe RT, Swinson RP, Levitt AJ.

Department of Psychiatry, Toronto General Hospital, Ontario, Canada.

The effects of acute oral administration of methylphenidate 40 mg versus dextroamphetamine 30 mg versus matched placebo were compared in 11 patients with primary obsessive-compulsive disorder. Dextroamphetamine but not methylphenidate had a significantly greater antiobsessive-compulsive effect as measured by the Comprehensive Psychiatric Rating Scale--Obsessive-Compulsive Subscale, as compared with placebo. This effect appeared unrelated to their effect on depression although a differential effect of the two psychostimulants on anxiety was observed. Although both these stimulants affect serotonin, the differences noted between dextroamphetamine and methylphenidate suggest that catecholamines may be implicated in the pathophysiology of obsessive-compulsive disorder.

The following abstract shows dopamine agonism is indeed a potential *cause* of OCD-like behaviour in laboratory animals.

Pol J Pharmacol 1999 Jan-Feb;51(1):55-61

Role of dopamine systems in obsessive-compulsive disorder (OCD): implications from a novel psychostimulant-induced animal model.

Szechtman H, Culver K, Eilam D.

Department of Psychiatry and Behavioral Neurosciences, McMaster University, Ontario, Canada.

OCD was once considered a rare psychiatric disorder, but recent studies estimate that, in the general population, the lifetime prevalence of OCD is 1 to 2%, twice that of schizophrenia or panic disorder. The most common form of OCD is compulsive checking. Our studies show that the behavior of rats treated chronically with the dopamine agonist, quinpirole, meets the ethological criteria of compulsive checking in OCD; may have a similar motivational basis as compulsive checking in the human; and is partially attenuated by the anti-OCD drug, clomipramine. Thus, the behavioral changes induced by chronic treatment with quinpirole may constitute an animal model of OCD checking. Since behavioral sensitization is an associated effect of quinpirole treatment, the induction of compulsive checking by quinpirole may involve the same mechanisms as the induction of drug-induced sensitization. In this respect, we demonstrated that the MAO inhibitor clorgyline, not only prevented the development of locomotor sensitization to quinpirole, but also reversed it in sensitized rats. To the extent that the quinpirole treatment is an animal model of OCD with strong face validity, it strengthens the hypothesis that dopamine systems play a role in OCD and raises the possibility that MAO inhibitors, which are used clinically for OCD, may exert their effects by acting at the MAO inhibitor displaceable quinpirole binding site.

> I take several supplements, but (as it stands right now) Enada NADH is at the core of my "natural-Rx" for the treatment of the atypical depressive side of my bipolar II disorder.
>
> -- Ron

So, is your pattern still the same, with respect to the NADH?

My response has kind of settled into the following pattern. The day I take it, I feel somewhat unwell, though I'd have trouble defining that. I just don't feel motivated. After maybe 12 hours, that wears off, and I feel enhanced cognitive clarity and motivation.

By and large, and notwithstanding the serious illness I've recently endured, I would say that I did not have my fatigue/crash last month. That breaks a pattern that has existed for 18 months. I go back on the road next week, so it will be extremely interesting to me to see how I do in June. I *love* doing experiments, particularly when they seem to go well. <grinnage>

Lar

 

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poster:Larry Hoover thread:221657
URL: http://www.dr-bob.org/babble/20030423/msgs/222313.html