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October 25, 2018 by

Skin and Drugs and Sex


( – During a recent hot spell one of our regular contributors asked if atmospheric pressure could change mood or cause pain and other problems and if so how might it do it. This led her to investigate Keratinocytes – the outer layer of the skin. It turns out there is an extensive literature about atmospheric effects on keratinocytes and knock-on effects elsewhere in the body.

She then found a group in the Netherlands working on phenytoin, an old anti-convulsant with multiple effects on a range of different ion channels and autocoids – hormones within the body, who were also interested in keratinocytes and in investigating the effects of phenytoin on pain and peripheral neuropathy.

The end result has been that two of our regular contributors who have PGAD are now trying phenytoin cream to see if it might make any difference to their symptoms. We will update you if we get any useful results.

See AutocoidsVulvodynia and Keratinocytes for more.

Flibanserin – Addyi

Three different people have been in touch about Flibanserin, a last millenium drug that is very like buspirone – Buspar – a drug lots of people with PSSD have tried with no clear benefit.

Buspirone and related drugs like flesinoxan have the opposite effects on sex to the SSRIs. Where SSRIs inhibit orgasm, buspirone and flibanserin can advance it and this underpinned company interest in this group of drugs as possible treatments to stimulate female desire and the interest of PSSDers to see if they could help.

The Flibanserin trials produced only hints of meagre benefits but despite this, FDA were willing to let it be pushed at women. It came on the market for female hypoactive sexual desire disorder under the brand name Addyi.

Trials often underestimate a drug’s effects. Whether Addyi can do more than these trials suggest, if it offers a benefit in PSSD or PRSD or PFS, this almost has to come from some difference between it and buspirone, as they are otherwise very similar drugs.

So is there a difference between Flibanserin and Buspirone on something like Sodium Channels or keratinocytes or other effects?  We need you to start the search.


Alex from Russia pinpoints the kind of observations that can help.  He took trazodone which is different to flibanserin but is also sex enhancing.

I had PSSD symptoms: loss of libido, emotions, loss of sensations in ejaculation and premature ejaculation, as well as insomnia, dilated pupils and red eyes.

After 3 weeks of taking trazodone, sleep became almost normal and the time of ejaculation also normalized. and this result so far has been holding for several months after stopping trazodone.

But my emotions and sexual sensitivity did not return, the pupils also did not come back to normal.

So I conclude that premature ejaculation and insensitivity depends on two different things. The dilated pupils, as far as I know, are a consequence of the blockade of the cholinergic receptors, and from this blockade there may also be problems with the genital sphere.

Maybe this information will help you somehow to establish the causes of PSSD symptoms. If trazodone improves libido in normals, but this does not happen in PSSD, the problems cannot just come from stimulation of 5НТ2, and 5НТ1 receptors”.

Entamoeba Histolytica

Another colleague sent the following:

“I’ve been suffering PSSD for two years now. I recently got diagnosed with a parasite called Entamoeba Histolytica.  I stumbled upon a story from the Post Finasteride forums, about another guy who had been diagnosed with this parasite, and after clearing it out he found himself cured of his PFS. I’ve pasted it below.

“I’m writing this because I was one of the several people who experienced dramatically compromising side effects after taking finasteride in the form of Propecia. Said side effects included an essential collapse of my sexual system (no libido, impotence), brain fog, anxiety issues, depression, ‘emotional blunting,’ and fatigue.

It took me 11 years and several doctors, but I finally got a diagnosis and–lo and behold–I’m cured. I’m cured!

It turns out I had a parasitic protozoa called e. histolytica. It’s been mentioned on this website before and it seems exceedingly common globally. An estimated 10% of the population has it, but apparently it’s asymptomatic in most people.

I did eventually come to suspect I had a parasite when I tried an elimination diet. Wheat was fine, dairy was fine, eggs were fine, but Sugar (sucrose) triggered my symptoms to a terrible degree. The Sugar connection is what eventually led me to question parasites.

I did try a few at-home remedies, and some of them were genuinely effective in abating symptoms but none of them cured the infection. It must be treated with antibiotics.

Alternative treatments that offered release were avoiding sugar, Humaworm, and ParaGone.

I’d personally recommend ParaGone over Humaworm, but I think they’re both effective.

I also experienced relief from Lactoferrin (Jarrow’s brand), and found they made the other treatments (including antibiotics) much more effective.

The antibiotics that cured me were metronidazole (500mg 3x a day for 10 days) and paromomycin (1,000mg 3x a day for 5 days). Relief came pretty quickly–I felt 90% on top of the world by day three.

I have no idea where I caught e. histolytica. I assume it was in my body for a while, and then the Propecia made it rage out of control.

If you or anyone you know is having problems with Propecia, please see a doctor about e. histolytica! I had a stool test come back negative initially, but it showed up on a retest. I’d recommend finding an infectious/tropical disease specialist in your area, or a gastroenterologist familiar with e.h”.

After doing some further reading I then found this:

“The gastrointestinal parasite Entamoeba histolytica secretes serotonin, causing a sustained secretory diarrhea in some people.[17][92] Patients infected with E. histolytica have been found to have highly elevated serum serotonin levels, which returned to normal following resolution of the infection.[93] E. histolytica also responds to the presence of serotonin by becoming more virulent.[94] This means serotonin secretion not only serves to increase the spread of entamoebas by giving the host diarrhea but also serves to coordinate their behaviour according to their population density, a phenomenon known as quorum sensing. Outside the gut of a host, there is nothing that the entamoebas provoke to release serotonin, hence the serotonin concentration is very low. Low serotonin signals to the entamoebas they are outside a host and they become less virulent to conserve energy. When they enter a new host, they multiply in the gut, and become more virulent as the enterochromaffin cells get provoked by them and the serotonin concentration increases.”


Antonei Csoka and colleagues who have been chasing genetic and epigenetic aspects of PSSD for years have just published a Paper on their work in the International Journal of Genomics.

This is Open Access and comes with a large number of supplements on the journal website. We (and they) need someone who knows something about genetics to explore and try to pick out key leads.

It also looks worth exploring the following Genes linked papers.

Pharmacogenetics of glutamate system genes and SSRI-associated sexual dysfunction – 2012

“We examined whether polymorphisms in the GRIK2, GRIA3 and GRIA1 genes were associated with selective serotonin reuptake inhibitor (SSRI)-associated sexual dysfunction in 114 participants treated for depression. One polymorphism in GRIA1 (rs1994862) was associated with arousal dysfunction, providing further evidence for the role of GRIA1 in mechanisms underlying SSRI-associated sexual side effects.”

And linking back to Entamoeba Histolytica, there is this paper.  Fluoxetine and some other SSRIs are antibiotics that can alter your gut flora – and lead to thrush and other problems as a result.  There are people who have reported benefits in withdrawal and for PSSD from fecal transplants which might have some link.

Antidepressant fluoxetine induces multiple antibiotics resistance in Escherichia coli via ROS-mediated mutagenesis – 2018

Nicotinamide Riboside

Another regular contributor has been trying Nicotinamide Riboside for the last two months and has reported slow but steady improvements in cognitive abilities as well as emotional state and physical sensations through the body.

Niacin is Vitamin B3. Googling Nicotinamide which is part of B3, there are claims this is the active form of the vitamin and that Niacin does not produce the same benefits. Nicotinamide Riboside (Niagen) can now be bought in its own right but it is pretty expensive.

Again we’d be interested in any reports anyone has of benefits or problems that this might produce.

Report your experience in the comment section at


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