PSSD Following Ashwagandha/Shilajit usage

Messages
35
Good evening everyone,

I am currently battling what seems to be PSSD symptoms from Ashwagandha KSM-66 usage
My symptoms are:
-Genital Numbness
-Reduced Sensation
-No sexual arousal
-Normal erections
-Morning wood I have every single day.
-No smell
-No good feeling after orgasm. Blunted.

It's literally lasted longer than 2 years now.

About me:
-Low Cortisol
-Low Aldosterone
-High Testosterone, DHT, And E (manageable with calcium d glucarate and nettle root).
-Excellent overall health.

What seems to "cure" me is a drug called Cyproheptadine (Periactin), which is a known serotonin antagonist. But the weird component is this. When I take 1mg of this drug, I will be sleepy (normal response) and wake up feeling tired. The following day I feel the same. BUT it's day 3 and 4 AFTER that first dose, I feel "Cured". I will literally wake up feeling fucking NORMAL again. Its like that vibrational rush is back. My symptoms of Genital numbness, No orgasm, No sexual arousal, no feeling, muscle weakness, all disappear on day 3-4. This stays like this for a week. But slowly slowly, I return back to my numb state.

So the question arises... HOW/WHY? I suspect looking into the 5-HT1a receptor, 5-HT2a receptor and the 5-HT2c receptors.

Is it just a Cortisol rebound following Cypro? Rebound elevation of cortisol following cyproheptadine withdrawal in Cushing's disease from a pituitary macroadenoma. - PubMed - NCBI

Ashwagandha Lowers cortisol and can cause anhedonia/laziness for some people.

So what else makes my symptoms worse:
-High dose Zinc Supplements
-Apigenin rich foods
-Ginger
-Potatoes (nightshades)

If anyone can explain the mechanism as to how Cyproheptadine cures me, that would be greatly appreciated.

I also must add that I got windows of cure with Liquid Zeolite drops, and St Johns Wort Tea.....5-HT1A?!?!?!?
 

barbaar

Well-Known Member
Messages
807
One of the theories here is that GR (glucocorticoid receptor) is upregulated, causing a ton of problems. There's more to it than that but my brain is too fried atm to fully understand it.

If you lower cortisol, it would upregulate GR to compensate for lower levels of cortisol.

Maybe the cortisol rebound temporarily downregulates GR to normal levels again, which could explain the delay before you start feeling better I think.
 
Messages
35
One of the theories here is that GR (glucocorticoid receptor) is upregulated, causing a ton of problems. There's more to it than that but my brain is too fried atm to fully understand it.

If you lower cortisol, it would upregulate GR to compensate for lower levels of cortisol.

Maybe the cortisol rebound temporarily downregulates GR to normal levels again, which could explain the delay before you start feeling better I think.

Thank you for sharing this.
I will look into it. How do I downregulate the glucocorticoid receptors!? How does Licorice work...?
 
Messages
35
You listed shilajit in the title but didn’t list it in your post. Did you use shilajit alongside of ksm66?

HEy man, sorry for delay.

Shilajit I used after KSM66, which also seemed to elicit a negative effect on sensation. It cuases me and my mate ejaculatory anhedonia.
 
Messages
35
Shilajit, a traditional Indian medicine, reduced immobility and increased climbing behavior whilst increasing adrenal weight and corticosterone levels in the forced swim test in rats [72] and Myelophil, based on compounds used for fatigue in Chinese medicine, increased glucocorticoid receptor expression in the hypothalamus and hippocampus , and altered expression of cytokines such as interleukin (IL-10) and tumour necrosis factor-alpha (TNF-í µí»¼) using the chronic cold stress and restraint model in mice [100]. One of the most interesting proposals is the switch to a new steady state from chronic hypocortisolaemia to a healthy, reactive state using the model-based predictive control (MPC) solution originally proposed by Gupta and colleagues [35]. ...
 

5 alpha

Well-Known Member
Messages
226
One of the theories here is that GR (glucocorticoid receptor) is upregulated, causing a ton of problems. There's more to it than that but my brain is too fried atm to fully understand it.

If you lower cortisol, it would upregulate GR to compensate for lower levels of cortisol.

Maybe the cortisol rebound temporarily downregulates GR to normal levels again, which could explain the delay before you start feeling better I think.

Barbaar,

So the cortisol rebound down regulating the unregulated GR receptors. This actually makes sense

I have mentioned on several different threads that I was almost cured of PFS from a three day 50 mg RU cycle back in 2017. My temp recovery was in the form of a bounce back in the weeks following the RU cycle. If what you are suggesting here is correct this is what could of happened in my case:

RU blocked my cortisol receptors causing my already up regulated cortisol receptors to up regulate even more in order to compensate for the fact that they were now blocked. I was only on the RU for three days so did not have the chance to feel worse.

Because the RU was blocking my cortisol receptors I started producing more cortisol to try to compensate for the Cortisol receptors being blocked. (We seen this in jinstewart’e on cycle RU labs)

After I came off the RU and after the RU left my system and my cortisol receptors were no longer blocked. With this being said because I still had high amounts of cortisol in my blood i experienced the rebound effect you mentioned by causing the Down regulation of the up regulated receptors which resulted in my temp 80 percent recovery.

Assuming this theory is correct why did I relapse? Did my cortisol receptors up regulate again in response to stress ? And if so why would they have ?

If this is all correct I should be cycling cortisol.
 

barbaar

Well-Known Member
Messages
807
Barbaar,

So the cortisol rebound down regulating the unregulated GR receptors. This actually makes sense

I have mentioned on several different threads that I was almost cured of PFS from a three day 50 mg RU cycle back in 2017. My temp recovery was in the form of a bounce back in the weeks following the RU cycle. If what you are suggesting here is correct this is what could of happened in my case:

RU blocked my cortisol receptors causing my already up regulated cortisol receptors to up regulate even more in order to compensate for the fact that they were now blocked. I was only on the RU for three days so did not have the chance to feel worse.

Because the RU was blocking my cortisol receptors I started producing more cortisol to try to compensate for the Cortisol receptors being blocked. (We seen this in jinstewart’e on cycle RU labs)

After I came off the RU and after the RU left my system and my cortisol receptors were no longer blocked. With this being said because I still had high amounts of cortisol in my blood i experienced the rebound effect you mentioned by causing the Down regulation of the up regulated receptors which resulted in my temp 80 percent recovery.

Assuming this theory is correct why did I relapse? Did my cortisol receptors up regulate again in response to stress ? And if so why would they have ?

If this is all correct I should be cycling cortisol.

Honestly I couldn't tell you why you would relapse or not. Maybe something else in the HPA axis is screwed too and causes the receptors to get messed up again.

But then on the other hand people have gotten cured or at least significantly better after cycling cortisol, and stay that way.

Maybe you need high cortisol for longer than just the rebound to unfuck whatever else in the system is keeping it out of whack.
 

5 alpha

Well-Known Member
Messages
226
Honestly I couldn't tell you why you would relapse or not. Maybe something else in the HPA axis is screwed too and causes the receptors to get messed up again.

But then on the other hand people have gotten cured or at least significantly better after cycling cortisol, and stay that way.

Maybe you need high cortisol for longer than just the rebound to unfuck whatever else in the system is keeping it out of whack.

Hmmm...

Maybe it’s the CB1 receptor that Helen has mentioned recently in the other thread resulting in the GR receptors being all out of whack

It’s complicated as hell but I have been trying to read this. It’s about the CB1 receptor and a lot of other related complicated shit haha

Neurobiological Interactions Between Stress and the Endocannabinoid System

“Additionally, in almost every brain region examined, exposure to chronic stress reliably causes a downregulation or loss of cannabinoid type 1 (CB1) receptors”

CB1 receptors down regulated causing GR receptors to stay up regulated ?
 
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