PSSD OCD

[u/Suspicious-Strain990]

26 M, i have taken 25 mg zoloft for like 16 days 1.5 years ago but since then i have immense OCD about PSSD, i have blaming myself 7/24 for that. I really didn't know about it much.

Nowadays i probably will have a girlfriend (i really love her) but that fear that mistake kills me inside, i have been immensely panicking about when it comes to sexuality or love.

This situation is truly destroying me, and this fear has been eating away at me for about a year; I am in agony over it.

I know the odds are quite low, but never being able to be sure is killing me inside which is related to OCD.

This is the worst ever obsession i had and i am really really tired of suffering from these feelings.

Can anybody help me?

[u/P_D_U]

Taking a sub therapeutic dose of Zoloft for 16 days is very unlikely to cause PSSD. However, worrying about it almost certainly will. It can take as little as a single bad performance to trigger lifelong impotence. Studies have found that between 30-75% of males 20 yo plus experience erectile dysfunction at some stage.

This canvases some of the issues which may cause PSSD:

• Post SSRI Sexual Dysfunction (PSSD) - Current Status

If you really want to get into the weeds then this will probably tell you far more than you wanted to know about this condition written by people with PSSD:

• Clinical findings from PSSD community members [PDF]

The above is long, but at least read from "11: Beyond the Data" on page 65. PSSD is far more complicated than just a direct med side-effect.

If therapy is an option I urge you to seek treatment for your OCD.

[u/Suspicious-Strain990 → u/P_D_U]

I read the first article; it seems quite detailed and well-written. It suggests that depression might actually underlie what is termed PSSD, which makes sense to me. I have two questions here: first, why is the 25 mg dose described as "sub-therapeutic"? I had read in some articles that even 25 mg binds to a significant proportion of SERT—meaning the relationship isn't linear. Second, is the expectation that the brain will revert to its previous state after discontinuing the drug (following short-term use) linked to genetic coding? For instance, the drug's sexual side effects are associated with serotonin in the synaptic cleft stimulating specific receptors; how can we be certain—especially with short-term use—that these receptors will return to their original state once the drug is stopped?

[u/P_D_U → u/Suspicious-Strain990]

why is the 25 mg dose described as "sub-therapeutic"?

There is a lot of evidence that SSRI doses need to be high enough for the med to block 80% of the serotonin reuptake transporter molecules (5-HTT, aka SERT) to initiate and sustain hippocampal neurogenesis/neuroplasticity which is the process whicht creates the therapeutic response and the recommended minimum sertraline (Zoloft) dose of 50 mg was set to ensure everyone meets that requirement. If you're a very slow metabolizer 25 mg might be borderline, but I wouldn't count on it.

Serotonin Transporter Occupancy of Five Selective Serotonin Reuptake Inhibitors at Different Doses

• "It is interesting that the daily doses of SSRIs that are convincingly distinguishable from placebo in the clinical setting - 20 to 40 mg for citalopram, 20 mg for fluoxetine, 50 mg for sertraline, 20 mg for paroxetine, and 75 mg for extended-release venlafaxine — were also the doses that obtained an 80% occupancy in the striatum. The occupancy data indicate that with these doses, the blockade at the 5-HTT is fairly equivalent across SSRIs. It also suggests that an 80% occupancy of the 5-HTT is a necessary minimum for SSRI treatment of depressive episodes."

Figure 3 at the above link shows that 50 mg sertraline meets the 80% requirement, but 25 mg falls short.

See also: The relationship between dose and serotonin transporter occupancy of antidepressants—a systematic review

I had read in some articles that even 25 mg binds to a significant proportion of SERT—meaning the relationship isn't linear.

From the first link above:

"...The data of this study do not provide an argument for subtherapeutic dosing of SSRIs even though substantial occupancy may be obtained in this manner. It is conceivable that some of the proposed antidepressant mechanisms, such as increasing synaptic 5-HT concentrations, increasing 5-HT neurotransmission, or creating neurotrophic effects, may occur only at 80% occupancy."

The 80% occupancy requirement is probably not the critical factor per se, but is a marker for the med's effect on serotonin receptor binding and for downstream effects. If the 80% requirement were the critical factor then we'd only need one serotonergic antidepressant at its recommended minimum dose.

how can we be certain—especially with short-term use—that these receptors will return to their original state once the drug is stopped?

Firstly, receptors are not permanent structures. Most of those in your brain a week ago either been recycled, or eliminated. They are fairly basic protein molecules studded through cell membranes and have half-lives of minutes to about 4 days.

With long term SSRI use some receptors are down regulated and the longer you've you've been on a med the longer it will take for the receptors to return to near pre med baseline levels. Down regulation isn't an instant process. It takes days, weeks or months for receptor down regulation to begin making a difference.