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From: york@mbcrr.dfci.harvard.edu (Ian A. York)
Newsgroups: alt.folklore.urban
Subject: Re: YAWNING CAUSES ORGASMS
Date: 6 Sep 1995 20:40:51 GMT

In article <42kuet$p6c@panix2.panix.com>, Michele Tepper <mtepper@panix.com> wrote:
>
>Now, this sort of range of response always surprises me. Could someone
>with, perhaps, more experience of pharmaceuticals explain it? I
>can understand why different people might have different reactions, but
>completely-contrary-to-the-expected reactions?

Doubt that there's a really solid explanation, but you're dealing with modifiers of the central nervous system, which to me says that any physiological reaction with a nervous system component to it, such as orgasm (which could be considered a central nervous system reaction with a physiological component to it [1], or indeed for some of us practically imaginary altogether [2]), might not be as completely-contrary-to-the-expected as all that. Knowing that opiates can act as stimulants in certain conditions, for example (a condition familar to vets: opiates act as stimulants to cats - there are vet legends about misguided attempts to sedate cats resulting in the cat circling the exam room, at 120 mph, several feet off the floor) gives one a lot more respect for the potential different effects of CNS drugs.

Incidentally, the concept of orgasms being a side-effect of anti-depressives is not exactly new, media frenzy notwithstanding. There was a case report in 1991 of fluoxetine doing this [3], although fluoxetine is more often linked with anorgasmia [4]. I didn't see anything earlier, but I didn't go through all 454 articles on orgasm in any real detail, because there weren't enough NEKKID GIFS, I mean because i didn't have enough time.

>Or is it like aspirin, where the answer is "it happens, but dang if we
>know why"?

Actually, this is the real reason I'm following up. This is the second time recently I've seen this "aspirin works in mysterious ways" concept. My reaction is, "huh?" I mean, acetylsalicylic acid and the other non-steroidal anti-inflammatory drugs are reasonably well understood; they act by inhibition of the arachadoonic acid cascade which generates inflammatory mediators, principally prostaglandins. To be more specific [5],

"Prostaglandins derived from the arachidonic acid cascade are implicated in the production of inflammatory pain, and in sensitising nociceptors to the actions of other mediators. They are synthesised from arachidonic acid via the endoperoxide biosynthesis pathway, the initial step of which is catalysed by the enzyme cyclo-oxygenase. Two forms of the cyclo-oxygenase enzyme (COX-1 and COX-2) have been characterised. COX-1 is important in circumstances where prostaglandins have a protective effect such as gastric mucus production and renal blood flow maintenance. NSAIDs inhibit the synthesis of prostaglandins at 1 or more points in the endoperoxide pathway. Three mechanisms of inhibition of the biosynthetic enzymes have been proposed: (i) rapid, reversible competitive inhibition; (ii) irreversible, time-dependent inhibition; and (iii) rapid, reversible noncompetitive (free radical trapping) inhibition. In addition, there is evidence that NSAIDs have a central antinociceptive mechanism of action that augments the peripheral effect. This may involve inhibition of central nervous system prostaglandins or inhibition of excitatory amino acids or bradykinins. There is considerable variability in the pain relief obtained from NSAIDs. Such variability in drug response may be explained in terms of differences between agents with respect to either pharmacodynamic actions or pharmacokinetic parameters or a combination of both. Stereoisomerism, where preparations exist as racemic mixtures and where only 1 enantiomer is active, may also be important. However, chiral inversion from inactive to active enantiomer may occur and may be rapid or slow."

I personally have memorized this and use it as an introduction at cocktail parties, which may explain [2].

But anyway, there seems to be a proto-UL that the mechanism of action of aspirin is somehow unknown to science. OF course the details are poorly understood, but then the details of *everything* in science is poorly understood. I doubt there are many drugs whose mode of action is understood much better than aspirin.

Ian "Orgasm addict" York

[1] Whipple B. Ogden G. Komisaruk BR. Physiological correlates of imagery-induced orgasm in women. Archives of Sexual Behavior. 21(2):121-33, 1992

"Orgasm from self-induced imagery or genital self-stimulation generated significant increases in systolic blood pressure, heart rate, pupil diameter, pain detection threshold, and pain tolerance threshold over resting control conditions."

[2] If you think I'm providing a reference for that, you're crazier than I am.

[3] Morris PL.
Fluoxetine and orgasmic sexual experiences. International Journal of Psychiatry in Medicine. 21(4):379-82, 1991.

"Fluoxetine was associated temporally with frequent short episodes of sexual excitement described by the patient as feeling like an orgasm."

[4] Zajecka J. Fawcett J. Schaff M. Jeffriess H. Guy C. The role of serotonin in sexual dysfunction: fluoxetine-associated orgasm dysfunction.
Journal of Clinical Psychiatry. 52(2):66-8, 1991

"The authors report 6 cases of orgasm dysfunction associated with the use of fluorxetine in 77 depressed outpatients."

[5] Cashman J. McAnulty G.
Nonsteroidal anti-inflammatory drugs in perisurgical pain management. Mechanisms of action and rationale for optimum use. Drugs. 49(1):51-70, 1995

--
Ian York (york@mbcrr.harvard.edu)
Dana-Farber Cancer Institute, 44 Binney St., Boston MA 02115 Phone (617)-632-3921 Fax (617)-632-2627