I am going to drop a major bomb soon

[MindChanger]

5HT1A alters serotonin levels. Serotonin levels interefer with other serotonin receptors. These receptors lead to immune dysfunction, including your hyperresponsiveness to mycoplasma pneumoniae, and low cd57 number, similarly to low th2 number in me.

[cdraham]

5HT1A alters serotonin levels. Serotonin levels interefer with other serotonin receptors. These receptors lead to immune dysfunction, including your hyperresponsiveness to mycoplasma pneumoniae, and low cd57 number, similarly to low th2 number in me.

Could make sense. So the actual treatment is focused on 5ht1a. I wonder how much infections contribute to my symptoms. And if treating m pneumoniae will lead to any degree of recovery from symptoms.

Probably the fatigue, cognitive dysfunction could be helped by treating the immune dysfunction induced infections

[MindChanger]

5HT1A alters serotonin levels. Serotonin levels interefer with other serotonin receptors. These receptors lead to immune dysfunction, including your hyperresponsiveness to mycoplasma pneumoniae, and low cd57 number, similarly to low th2 number in me.

Could make sense. So the actual treatment is focused on 5ht1a. I wonder how much infections contribute to my symptoms. And if treating m pneumoniae will lead to any degree of recovery from symptoms.

Probably the fatigue, cognitive dysfunction could be helped by treating the immune dysfunction induced infections

The answer is simple here. How could SSRIs bring those infections? They could not. Do people with those infections have PSSD? No.

The only thing SSRIs could actually do is change your response to those infections through serotonin (downregulation of presynaptic 5HT1A), which would result in a significant change in cytokine levels, thus in the number of CD+ cells (including Cd4+ and CD57+).


Your pneumonie either does not have any relation to your PSSD or was caused by hyperresponsive reaction because of the changes in immune system.

[cdraham]

5HT1A alters serotonin levels. Serotonin levels interefer with other serotonin receptors. These receptors lead to immune dysfunction, including your hyperresponsiveness to mycoplasma pneumoniae, and low cd57 number, similarly to low th2 number in me.

Could make sense. So the actual treatment is focused on 5ht1a. I wonder how much infections contribute to my symptoms. And if treating m pneumoniae will lead to any degree of recovery from symptoms.

Probably the fatigue, cognitive dysfunction could be helped by treating the immune dysfunction induced infections

The answer is simple here. How could SSRIs bring those infections? They could not. Do people with those infections have PSSD? No.

The only thing SSRIs could actually do is change your response to those infections through serotonin (downregulation of presynaptic 5HT1A), which would result in a significant change in cytokine levels, thus in the number of CD+ cells (including Cd4+ and CD57+).


Your pneumonie either does not have any relation to your PSSD or was caused by hyperresponsive reaction because of the changes in immune system.

The thing is I tested those infections for active. I have no infection tests from before but I highly doubt that they were active before. What I think is what happened, is a combination of altered immune response by serotonin and additional immunosurpression, which allowed the pathogen to reactivate.

Some PFS cases test low in cd57 too and pfs has nothing to do with serotonin.

Ssri withdrawal raises cortisol. When i got pssd I was stressed and overtrained, in a state of much cortisol, I think ssris worked as corticosteroids in my case.

[cdraham]

https://www.prunderground.com/antidepre ... y/0040770/

[climb]

https://www.prunderground.com/antidepre ... y/0040770/

It's interesting but if increased susceptibility to latent viruses was a cause, I don't understand why the onset of extra symptoms on withdrawal for many people, or were you referring to the impact on cortisol that was also mentioned?

[cdraham]

https://www.prunderground.com/antidepre ... y/0040770/

It's interesting but if increased susceptibility to latent viruses was a cause, I don't understand why the onset of extra symptoms on withdrawal for many people, or were you referring to the impact on cortisol that was also mentioned?

"However, dendritic cells, (types of immune cells) that find microbes and foreign material entering the body and educate the immune system on how to fight them, also use serotonin to quickly excite a T-cell (another type of immune cell) response. “Drugs that block serotonin reuptake likely change some of the parameters of T-cell activation.” (2) In other words, antidepressants can change how immune cells work, which makes it more likely that a latent virus will increase in number and cause disease."

Here a more detailed article https://www.sciencedaily.com/releases/2 ... 230939.htm

" He said that while it may be possible that SSRI drugs may restore a healthy immune function in people who are depressed and prone to infections, it is possible that they might also bolster immunity to the point that they trigger autoimmune disease. "At this point we just don't know how these drugs might affect immunity, so we really need to clarify the normal role of serotonin in immune cell functioning," Ahern said."

Cortisol raises in withdrawal. This should explain some things.

Plus the ssris alter some parameters of immune response, which makes it even more likely for pathogens to reactivate

For me symptom onset was with one trazo pill or a few, then after venla withdrawal everything worsened to the point I couldn't leave my bed, imo it's the same as giving corticosteroids for lyme, they get alot worse etc.

[Jaxx]

Thanks for posting the theory, it is good to see it triggers a further discussion instantly. The community needs this.
I am a bit surprised with some points however, for instance sjw was mentioned to be a (post?)5ht1a agonist. The research on sjw is quite messy, but one of its main effects is post 5ht1a upregulation, and afaik limited impact on the autoreceptor.
I am also not entirely clear how some of the crashes seen here, that occur from post 5ht1a activation/agonism (and i assume downregulation soon after) fit your theory?
Finally, how do you see buspirone in this? (Autoreceptor agonist, doesnt do much for most but did give some people relief, sometimes in combination with prozac)

[arahant]

Jaxx.

Buspirone is pre synaptic agonist at low doses, and post synaptic at higher doses. I only saw relief and still experience it on higher doses (greater than 30 mg).
The thing that most misinterpreted here is that 5HT1a works via negative feedback, the agonizing it doesn't down regulate it, as it happens when agonizing other receptors that works via positive feedback. As for the crashing business seen around, I have seen people claiming crashes due to the most weird things, also followed by panic and reassurance seeking. It's difficult to use those exceptional claims to base any theory.

[Jaxx]

Jaxx.

Buspirone is pre synaptic agonist at low doses, and post synaptic at higher doses. I only saw relief and still experience it on higher doses (greater than 30 mg).
The thing that most misinterpreted here is that 5HT1a works via negative feedback, the agonizing it doesn't down regulate it, as it happens when agonizing other receptors that works via positive feedback. As for the crashing business seen around, I have seen people claiming crashes due to the most weird things, also followed by panic and reassurance seeking. It's difficult to use those exceptional claims to base any theory.

And thats an important part of the puzzle. I assume most people also tried buspirone at lower/medium dose so who knows what the potential could be. Afaik it is a partial agonist for post synaptic 5ht1a however, but i dont know if that is dose dependent tbh.
As crashes can be a more complex story for sure, continuous activating the post 5ht1a receptors seem to be responsible according to several people (eg vortioxetine, flibanserin, although these also have other effects ofc)