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Anxiety induced sexual arousal responsible for stimulant’s aphrodisiac qualities

Burn it up

Bluelighter
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Anxiety induced sexual arousal and stimulant’s aphrodisiac qualities share similar mechanisms. Is increased libido from stimulant use produced by a stress response?

It is well known that anxiety triggers an increase in libido and sexual arousal. You might have experienced it personally on many occasions (exam period, extra work, etc…) Many studies have been conducted that demonstrate the relationship between an increase in sexual arousal and anxiety [Anxiety increases sexual arousal. Barlow, David H.; Sakheim, David K.; Beck, J. Gayle ; Some evidence for heightened sexual attraction under conditions of high anxiety. Dutton, Donald G.; Aron, Arthur P.].

This makes a lot of sense, as stress increases vassopresin levels and activates many processes which in turn can also increase sexual arousal [ENDOCRINOLOGY OF THE STRESS RESPONSE, Evangelia Charmandari, Constantine Tsigos, and George Chrousos]. The evolutionary reason for this is not completely understood [The evolution of human sexuality revisited, Donald Symons; Stress and the evolution of condition-dependent signals, Katherine L. Buchanan ] because it doesn’t make too much sense that in stress circumstances individuals start to procreate, as it will decrease their fitness by forcing pregnant females and their offspring to survive in adverse conditions. However, there is the possibility that stress generated by weather changes (the beginning of the cold season) could be beneficial, as procreation at that time would produce an offspring in the warm months.

Well, anyway, many stimulant drugs also produce an activation of some anxiety induced responses (increase in vasopressin, etc, etc…) amongst many other effects. Heck, they even directly produce anxiety.

I was thinking the other day that we tend to oversimplify when we state that stimulants increase libido and sexual arousal just by the direct psychological effects of the drug. I believe that stimulants produce sexual arousal mainly in a physiological way by activating the stress mechanisms in the body, which in turn produce an increase in libido. It is not the direct action on of the drug in our libido, but more it’s action on the stress mediated responses.

I have really not researched too much about this, so I would love to hear your ideas on this issue. Is increased libido from stimulant use produced by a stress response?
 
I'd be more inclined to think it's a pavlov's dog scenario with the mind remembering and wanting that 10-15minute euphoric relaxation that occurs after orgasm, to act as a powerful anxiolytic.
 
Are there any ΔFosB inhibitors?

ΔFosB is just a shortened variant (there are more splice variants than just this one) of FosB, which is a pretty basic transcription factor involved in many processes, for instance:

transcription from RNA polymerase II promoter; response to drug; response to cAMP; response to mechanical stimulus; multicellular organismal development; behavior; response to morphine; negative regulation of transcription from RNA polymerase II promoter; female pregnancy; response to progesterone stimulus; response to corticosterone stimulus; cellular response to hormone stimulus

you likely won't find something that only inhibits ΔFosB and probably don't want to mess too much with FosB at all. but inhibition is likely better than overexpression, the Fos transcription factors are involved in cell proliferation and therefore cancer.
 
^ well the pharmacological approaches to addiction treatment aren't all that great as is, but thank you for the Frank answer.

ΔFosB seems to be a(/the?) central protein in addiction and surely a good starting point for research. but i think we'd need to know what causes this variant to be expressed therefore find an upstream protein that can be targeted by drugs. hopefully there will one enzyme/receptor that's largely responsible for this and that doesn't do a whole lot of other things. but these things take a long time and almost always turn out to be much more complicated with many factors involved...

well, ΔJunD is a (mutant) protein that inhibits ΔFosB and does what we want of it, but it's a protein and therefore not really accessible to therapeutic applications, even if it were specific for ΔFosB, which i doubt. it's a very promosing direction, but i wouldn't expect something anytime soon.
 
Interesting post, and I'd certainly agree that DA/NE-based stimulants do cause an increase in libido (I'm actually rather horny right now on adderall... haha). However, what about MDMA which often causes the opposite? I know most guys, at least, really don't feel horny on MDMA. I'm also in that category. Surely if it was the basic peripheral mechanisms of stimulants causing the libido increase, we'd see increased libido in MDMA-users also? Or any serotonergic stimulant for that matter.

Thoughts?
 
Based entirely on preclinical research (mainly animal studies, some human studies, and 1 study on rats in particular that I don't have handy - too lazy to look up the PMIDs), I think D3 receptor activation in the NAcc in the presence of sufficient levels of testosterone is responsible for the libido-enhancing effect of amphetamine and methamphetamine (or any other DRD3-activating dopaminergics) in humans.

I'll look for the studies in the event anyone is legitimately curious and can't find what I'm talking about on pubmed.
 
However, what about MDMA which often causes the opposite?

I think it could be that serotonergic transmission tends to attenuate many downstream dopaminergic effects, particularly pathways involved in reward seeking. Eg, the more serotonergic a stimulant is, the more infrequently rats will press a lever to repeatedly dose.

ebola
 
I think it could be that serotonergic transmission tends to attenuate many downstream dopaminergic effects, particularly pathways involved in reward seeking. Eg, the more serotonergic a stimulant is, the more infrequently rats will press a lever to repeatedly dose.

ebola

Right, but why would this change sexual arousal induced by the stimulant? Unless you mean that reward-related DA is the main driving cause of stimulant-induced libido.
 
Yeah...I guess there isn't a simple model for this considering that D3 activation is inversely related to delta FosB level in the NAcc...

D3 agonists can definitely cause hypersexuality in humans (aside: like this one and another one that apparently can even make a 75 year old man pleasure himself while out cold... o.O - must've had some pretty stimulating dreams. lol)...
and, delta FosB plays a key role in sex addictions...

Kind of weird since this basically means the two hypersexuality-inducing factors in the NAcc oppose each other. There's likely a fair bit of interplay with that transcription factor and other DA receptor types too though.
 
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