Over a decade ago, Antonei Csoka put forward an epigenetic theory of post-SSRI sexual dysfunction (PSSD). His work is referenced in the template letter to epigeneticists.
David Stofkooper, a young man from Holland with PSSD, put great hope in this and went to senior researchers working on gene related problems hoping that something like the proposal below might help him. His questions led him to the conclusion there would be no ‘epigenetic’ cure soon and several years ago he took his own life.
Another person with PSSD has recently offered a similar thought – which is a good question to take to epigeneticists, primarily to find out how plausible and safe an approach like this might be.
SSRIs switch off the gene SLC6a4 so the serotonin transporter cannot be encoded. This inhibits serotonin reuptake in long term not just the immediate term and could cause persistent, long lasting side-effects like PSSD, insomnia, akathisia …
To silence a gene you have to put a methyl group (CH3-Group) on the gene you want to switch off. The chemical structure of SSRIs has lots of CH3-groups.
Perhaps up to 5% of people taking an SSRI have persistent side effects maybe because they cannot break down methyl groups perhaps owing to a loss of something in their body.
CRISPRoff/CRISPRon is a tool that can remove methyl groups (CH3 groups) from genes in an easy, fast and cheap way. This might be able to remove the methyl from the SLC6a4 gene and switch it back on.
Maybe this CRISPRoff/CRISPRon tool would also work for PFS and PAS sufferers. I would be a volunteer in testing this – if it’s possible.
It is definitely worth asking an epigeneticist:
- if this option is remotely possible?
- if possible would it be safe?
- if not possible at present, might it ever be possible?
- are there other ways to achieve this effect?
One of the researchers active on the forum took the question of expression of KISS genes to the team in Baylor who ran an epigenetic study in subjects with PFS, and there seems to be no difference in the expression of the genes for kisspeptin in the scrotal skin of subjects with PFS compared to controls. This is exactly the kind of input that helps move a research forum forward.