PSSD anhedonia vs. PFS anhedonia

Just curious if people with PFS also suffer from such severe anhedonia/ loss of motivation/drive, unable to feel absolutely any joy, unable to connect with people, no endorphins when exercising, etc?

For me it’s absolutely the worst symptom.
It’s torture.

I have PSSD, so for me, it makes sense that the (hypothetical) cause of this anhedonia is too much serotonin which then causes very low dopamine. Or something along the lines of damage to serotonin/ dopamine system.

I wonder what theory is there for PFS anhedonia? Does it also involve dopamine?

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I have all of these, there is a belief that there is a connection between these drugs . Ie ssris, finasteride, accutane, antibiotics as the symptoms are very similar.

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For PFS the Androgen Rezeptor seems to be silenced (by over expression).The Androgen Rezeptor molecule DHT complex docks to the DNA of the androgen driven target tissues and promotes the expression of the androgen Gen clusters. Androgen driven is everything in a male body and brain: The Drive, fun for life, sexuality, muscles, Neurosteroides everything and 3800 genes are altered in their expression in a PFS patient.

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Without delving too much into specifics or speculations, there is a significant overlap in symptom reports from PSSD/PAS/PFS patients, including reports of anhedonia and what people have dubbed ‘exercise intolerance’.

It has been suggested before that these conditions might actually be one and the same condition caused by the same underlying mechanism and causing the same end result, despite originating from different drugs. The commonality between all these drugs is that they have anti-androgenic or otherwise endocrine disruptive properties.

In other words, there is a possibility that PSSD is not necessarily related to dopamine problems.

There is a reason why our patient surveys, and member story templates, and patient profiles allow specifically for mentioning the substance they took that caused their post-drug experiences. If you can find the time and energy @kathy, it would be great if you could introduce yourself via a Member Story topic in our Member Stories section as well and perhaps contribute to our ongoing patient survey.

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I have PFS and my anhedonia is so severe that I cannot feel even the slightest feeling of joy or pleasure. It’s just been replaced by irritability and pain of not being able to enjoy the many things that I used to be so interested and passionate about. It’s absolutely inhumane and one of my worst symptoms as well. This extends to not being able to feel love, empathy, connection, well being, comfort, motivation/reward, libido etc. After trying to get a spark so many times I have just started to avoid anything that I used to enjoy as it is just worse suffering than doing nothing at all. I have no idea how else to address this and none of my friends or family understand why I can’t even do simple things like watch TV or read a book, listen to music or exercise (I also have muscle wastage/exercise intolerance). It’s been over a year now and I was hoping these symptoms would improve but unfortunately no luck.

The worst is when people think I am just depressed, unhappy or lazy. Obviously it’s nothing close to these things. This is the disease state yet it’s impossible to prove or make anybody understand.

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@kathy, Post-Accutane here. The level of torment I have experienced from anhedonia/blunting is equal to, if not worse, than the sexual symptoms. Emotional range went from typical happy-sad to a narrow band of rage-malaise. Often, just nothingness, which I rarely experienced before the drug. I became like a sick old dog that growls at everything at 18 years-old and have been stuck that way.

It does “feel” like there is a problem somewhere down the line where I don’t produce or respond to endorphins.

It’s confusing why there are some people still focusing on the differences among PFS/PSSD/PAS, rather than the similarities. Why isn’t it “what mechanism explains why these different drug classes are causing an ostensibly similar, almost identical, syndrome among a rare minority of patients on each drug?”

SSRIs were/are marketed under a false assumption that serotonin is some sort of catch-all “happy hormone” or that serotonin reuptake inhibition is the mainline mechanism of action of SSRIs, while strong evidence to the contrary was/is completely ignored.

This is the best summary of the problem I have found so far:

Lacasse, Jeffrey R., and Jonathan Leo. “Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature.” PLOS Medicine , vol. 2, no. 12, Nov. 2005, p. e392.

This article unfortunately omits evidence that SSRIs and serotonergic herbal supplements barely work better than placebo at treating depression.

Sticking with the notion that increased intersynaptic serotonin equals happiness, while ignoring the plethora of other paracrine/endocrine effects of SSRIs, sells pills and that’s about it.

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