The cause of PSSD has had many theories, but I'm going to skip to the chase.
The REASON we CAN'T treat PSSD *(effectively)* is because we are Obsessing on theories that only "HINT" at one point of the problem.
Where does "the point" originate from, though?
I believe I've found the answer...
It lies in PPARy or "Peroxisome proliferator-activated receptor gamma".
--> Serotonin REDUCES PPARy which normally ACTS to INITIATE Androgen Receptor (AR) activities; that's *WHY* we get DOWNREGULATION of androgen receptors with SSRI - because the "nuclear" receptor of PPARy is being downregulated (persistently) by SSRI's - which causes a continual reduction in Androgen Receptor amounts (densities) and activities. SSRI's like Luvox & Prozac "get in the middle" and cut off the "supply and demand" connection to nNOS from the Androgen Receptor - leading to LESS neuronal nitric oxide synthase and *NO* non-contact erections (erections without touch). STUDY --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5641178/
--> PPAR stimulates Androgen Receptors and activities --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5428145/
5-HT1A & 5-HT1B receptors REDUCE androgen receptors as MESOLIMBO has So Said.
STUDY --> https://www.nature.com/articles/s41598-017-15832-5
5-HT regulates PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA PPAR/PPARy --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2957204/
5-HT1A & 5-HT1B receptors do this via THREE pathways...
PPARy reduction --> study --> https://www.ncbi.nlm.nih.gov/pubmed/25937083
Reduction of cAMP (cyclic adenosine monophosphate) --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121227/ cAMP/PKA and Androgen Receptors --> https://www.ncbi.nlm.nih.gov/pubmed/8702703
Reduction of nNOS --> less blood flow --> less Androgen Receptor "food" or nourishment --> https://gut.bmj.com/content/44/2/143
***FORSKOLIN may also PREVENT FLUTAMIDE and other ANTI-ANDROGENS FROM BINDING/WORKING***
STUDY --> https://www.ncbi.nlm.nih.gov/pubmed/9521705
***MORE EVIDENCE***
PPAR is involved in LEVODOPA induced DYSKINESIAS - a "symbol" of how WELL Dopamine works in the FACE less PPARy (IT DOESN'T!!!)
STUDY --> https://www.ncbi.nlm.nih.gov/pubmed/25486547
***GENETICS***
nNOS contributes to STRESS-induced Depression --> https://www.ncbi.nlm.nih.gov/pubmed/17854383
SOME PEOPLE have GENEs that make them have *MORE* or *LESS* neuronal nitric oxide Synthase --> https://www.ncbi.nlm.nih.gov/pubmed/20888049
nNOS is *LOW* in the LOCUS COERULEUS --> https://www.ncbi.nlm.nih.gov/pubmed/15569249
***EXPLORING SCIENTIFICALLY PROVEN APHRODISIACS***
Exploring scientifically proven herbal aphrodisiacs [STUDY] --> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3731873/
PSYCHOTROPIC DRUGS AND SEXUAL DYSFUNCTION [https://www.ncbi.nlm.nih.gov/pubmed/2645849/]
Format: AbstractSend to
Arch Gen Psychiatry. 1989 Mar;46(3):275-84.
Effects of psychotropic drugs on human erection and ejaculation.
Segraves RT1.
Author information
1
Department of Psychiatry, Case Western Reserve University, Cleveland, OH.
Abstract
Evidence concerning pharmacological effects on human sexuality suggests that dopaminergic receptor activation may be associated with penile erection. Erection also appears to involve inhibition of alpha-adrenergic influences and beta-adrenergic stimulation plus the release of a noncholinergic vasodilator substance, possibly vasoactive intestinal peptide. Ejaculation appears to be mediated primarily by alpha-adrenergic fibers. Serotonergic neurotransmission may inhibit the ejaculatory reflex. An understanding of the neurobiological substrate of human sexuality may assist clinicians in choosing psychotropic agents with minimal adverse effects on sexual behavior and may also contribute to the development of pharmacological interventions for sexual difficulties.
PMID: 2645849 DOI: 10.1001/archpsyc.1989.01810030081011
[Indexed for MEDLINE]