Clomid experience

Hello!
Just wanted to share my brief clomid experience with you. So, i took 25 mg for 7 days only because of the reason that after the first dose, my symptoms became 10x worse. It was even worse than when I first dropped saw palmetto. I decided to run it further for quite some time to make sure that it is not related to my ups and downs, but they just remained very bad.

Before I took it, my testosterone values were ranging between 18-20 nmol/l and after I took it my testosterone was 26 nmol/l. Had I taken 50mgs I guess it would be in the 30’s. I don’t know if these symptoms are from increased androgens or from the pharmacology of clomiphene as it is an E2 receptor antagonist(primarily in the hypothalamus). The only way to check if this is true is by injecting test itself, which I don’t plan at the moment nor the near future.

As of now, I recovered to my previous PFS baseline, so it didn’t have any long-term effects fortunately.

I don’t question the quality of the clomid that I bought as I bought it directly from the pharmacy and not from the shady markets.

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Thanks for sharing

clomid is not the cure

No shit sherlock.

I’m saw p-PFS.

I got worse while on Clomid as well

There is a theory that “Saw p-PFS” cases involve the estrogen and the estrogen receptors more so then regular PFS.

I recently achieved noticeable favorable results in some of the sexual sides by taking Hops extract which is an estrogen receptor alpha agonist. There are two estrogen receptors. Estrogen receptor alpha and estrogen receptor beta. I was taking the hops extract with tons of supplements to increase neurotransmitters. I ended up crashing into PFS type insomnia

I’m making a thread soon outlining everything that happened to me recently. There is no way I can know for sure which supplement crashed me but I don’t believe it was the hops extract. If your looking for something to try and this sparks your interest it’s an option.

It would be very interesting to see what happened’s to another Saw P-PFS person on the hops extract.

I got better erections while on it. Did not help with any of the other sexual sides. But my ability to achieve and maintain erections while on it was improved enough to point where I could function. Not optimally but if it stayed at that level it would have been just enough to get by if that makes any sense.

I was believer in ERα theory, but haven’t found any solid proof of its impact on sexual function. But on the other hand i had very positive results with licorice root which also messes with ERa. Also Aromasin is mild ERa agonist.

ERα or aromatase knockout male mice displayed decreased intromissions and ejaculations compared with wild-type controls9,10. In contrast to these findings, several case reports indicated that sexual behavior did not change in men lacking ERα or aromatase11,12. Therefore, the influence of ERα or aromatase in males remains controversial.

These data show that the ERα is not essential during development or adulthood for the expression of masculine sexual behavior in mice. Moreover, dopamine can activate sexual behavior via a mechanism that either acts on an ER other than ERα or via an estrogen-independent pathwa


https://www.nature.com/articles/s41598-020-69712-6

Interesting studies

Things that caught my eye from this study:

“Moreover, this male-typical copulatory performance is not dependent on the ERα in mice of either sex”

“In addition dopamine was elevated in male brains relative to females in four of these six regions, including the MPOA, MA, nucleus accumbens, and the substantia nigra (p < 0.05 at least)”

“In the MA and AOB significant sex differences were noted in epinephrine (E), homovanillic acid (HVA), and 5-HT content (p < 0.05 at least). Finally in the substantia nigra males had significantly more norepinephrine (NE) than females (p < 0.05)”

“In the MA and AOB significant sex differences were noted in epinephrine (E), homovanillic acid (HVA), and 5-HT content (p < 0.05 at least). Finally in the substantia nigra males had significantly more norepinephrine (NE) than females (p < 0.05)”

“In male rats, extracellular dopamine increased in the striatum after copulation (Damsma et al., 1992). Thus, it is possible that ERαKO males, like castrated rats (Hull et al., 1995) accumulate, but do not release DA in the brain. This inability to release DA may contribute to the failure of ERαKOs to display masculine sexual behaviors”

“Many lines of evidence show that dopamine is involved in male sexual behavior. Sexually experienced, long-term castrated rats can display copulatory behavior, including ejaculation in some cases, after treatment with APO”

“More reliable sexual behavior is seen when castrated male rats are treated with subthreshold doses of T and APO is provided”

“These data suggest that T regulates NOS via actions on ERα. Data collected on endothelial NO production supports this hypothesis”

From this study it’s clearly saying that as it pertains to male sexual disfunction :

https://www.nature.com/articles/s41598-020-69712-6

“The estradiol value was significantly elevated in the ED group than the control group (109.44 ± 47.14 pmol/L vs. 91.88 ± 27.68 pmol/L; P < 0.001)”

But the thing is the sexual disfunction we see in PFS is probable not regular sexual disfunction. Which is probably why we can’t just simply increase our T and decrease our estrogen and get better. Or why we can’t simply increase blood flow with cilias and get better. We also get much wider range sexual disfunction type symptoms. This probable means something else is going on in PFS that causes sexual disfunction. Also our imbalances in PFS are probable not the same even though our symptoms are the same. For example you get better on licorice. I get worse on licorice. I get worse when I inhibit estrogen while others get better. In my opinion the only way out of this mess is to classify different cases and try to find patterns that could provide hints towards the underlying mechanism or mechanisms involved specific to each case

This is why I’m saying to “the saw P-PFS guy in this thread that he could consider trying hops extract which appeared to have helped me and I am a Saw P-PFS case myself” furthermore there is already a pattern we have seen in a handful of Saw P-PFS guys where we get worse when we inhibit estrogen and better when we either increase estrogen or agonize the estrogen receptors. hops extract does agonize estrogen receptor alpha and I do get improvements when I take hops extract. Obviously the conclusions that I can make from this experiment are speculative. However if more Saw p-PFS people decide on their own to try hops extract and see improvements now we are probably starting to get somewhere…

Lastly in response to this point:

“ERα or aromatase knockout male mice displayed decreased intromissions and ejaculations compared with wild-type controls9,10. In contrast to these findings, several case reports indicated that sexual behavior did not change in men lacking ERα or aromatase11,12. Therefore, the influence of ERα or aromatase in males remains controversial”

This is pretty straight forward as to what this study on mice is telling us here. But that does not change the facts. And the facts are that several PFS victims get worse when they inhibit the aromatase enzyme including myself. And 4 other saw P-PFS people that I know not including myself get worse when we inhibit the aromatase enzyme and or estrogen. Therefore in my opinion it’s important to not try to put all PFS people in the same boat. Because all available evidence we have so far shows we are probably not in the same boat. In fact in our exchange alone we just distinguished a key difference between our cases. You get improvements when you take licorice extract and I get worse. We are probably different cases