The links I screened didn’t really fit. Therefore will edit this post a few times. Apart from grants some projects may give us valuable contacts to scientists.
GOLIATH: is not for us, but as they what to create tests that detect metabolically disruptive medications (5-ARI change the sugar and fat metabolism), the contact list of the program could hold valuable future cooperation with universities:
ERGO: Looks mainly at the thyroid gland and EDs. But could be extended to other neuroendocrine systems. This project may hold valuable contacts:
Novel Testing Strategies for Endocrine Disruptors in the Context of Developmental NeuroToxicity. Not relevant to us, but may hold contacts to relevant scientists.
Are you aware of the recent german pssd community endeavor to collaborate with university clinics in Germany in order to set up centers for diagnosis of pssd etc.? I can send you some more information if you’re interested however there are probably people within the German pssd community (Verein) that do know effectively more
The first project linked isn’t practically relevant as that is focused on developing a testing methods for the endocrine disrupting potential of substances. However, the relevance of endocrine disruption to human health is enormous, and appropriately it is a growing area of research interest. We believe tapping into funds like the one you list will be an absolute priority for our issue. Awor wrote regarding this and our strategy moving forward here:
We have recently written a large amount on the relevance of our issue to endocrine disruption and the shared endocrine disrupting potential of the substances causing what is currently termed PFS. At the moment we are in the process of reach out to leading centres in Europe to build relationships and research proposals, and if that comes to fruition we can hopefully pursue such applications together with appropriate scientists.
Well, not practically no. That is a pre-development stage collaboration hoping to one day achieve a standardised substance screening system based on prediction. In this case, there is already sufficient published scientific evidence to support these substances being significantly endocrine disruptive; after all, that’s the desired mechanism of action of finasteride. It’s quite literally a textbook example (Patisaul and Belcher, 2017). So we have as much as we need to justify further investigation. What we don’t have is enough clinical evidence of the endpoints. A scientist conducting a literature review on the enduring health problems from accutane and SSRIs will still find relatively little. Given the similar multisystemic symptoms clearly reported by PSSD patients, calling it “post-SSRI sexual dysfunction” is itself a reductive misnomer.
What we also know is that these products appear relatively tolerable in a majority of consumers. The answers we urgently need pertain to the epigenetic pathomechanisms of PFS, how they develop, and what (epi)genetically differentiates patients in the first place. It’s our view that the way we move the fastest is to undertake bioinformatic research using state-of-the-art sequencing and analysis. This is a data based approach that has only in the past couple of years become feasible. However, to do this we need the involvement of a leading genomics center.
The alternative option is hoping the next scientist(s) getting paid have the “right” theory, and given it has proven enormously difficult to illustrate simple epidemiological realities of the condition (partly because of an ongoing and catastrophic failure at the clinical level), I remain unconvinced of that yielding any practically actionable answers in the near future. If that’s how things go, which they may, it will likely retain a purely finasteride focus and we’ll have to just do our best to make sure they take into account the clinical picture, not a partial representation being fit to a theory, and important and novel features such as the “crash” experienced by many patients.
Unfortunately that isn’t safe to say. We obviously don’t dictate research - unless we come into several million dollars. I can only tell you what we would very much like to achieve as an organisation: Collaboration with a leading molecular biologist to undertake genomic research of patients per their design. We would very, very much urge the inclusion of a secondary patient cohort (likely smaller for practical availability reasons) who are suffering an ostensibly similar syndrome after serotonergic antidepressants and isotretinoin.
I also think that the acronym PSSD (post ssri-sexual dysfunction) is improper, it should simply be called Post-SSRI syndrome given the wide range of symptoms, not only on the sexual sphere.
that is too limited as well. This is caused by many types of psych drugs beyond ssri snri. All drugs that cause it should be scoped. Regarding symptoms you are right.
yes exactly. I think maois are the safest, no pssd stories about them. Also benzos are demonized but should be given instead of antidepressants for reasonable period. They do help the symptom that makes you feel pain : anxiety. Depression is more tolerable, and you can find ways to get out of it. Anxiety is what makes people visit the doc in the first place.
This should be followed up on…Already know pfs is epigenetic changes now I wonder if funds would ever become available? To get it classified as an endocrine disruptor I mean
