My Long PFS Journey

Yes I also have a feeling E2 receptors may be involved because being on Clomid (SERM) last summer gave me very undesirable sides since it’s known to block E2 receptors. My E2 has been very low for far too long. I too read research about E2 involved in brain Serotonin transmission. Figuring this part, however, may prove impossible so I try to focus more on balancing hormones, minerals & vitamins. Hopefully that should sort out most of the processes on cellular levels.

Yesterday I over did it at the gym and I woke up today very sore and feeling extremely burnt out. I think I taxed out my adrenals with high intensity workout. I tried to load on sea salt and get more restful sleep.

There were times when even pde5 inhibitor Cialis did not produce any erections for me. Ever tried low dose Ginko Biloba? I’m on 30mg a day these days and it seems to help with erections and brain activity.

Ginko did nothing.
I am testing forskolin at the moment. It kicks libido but at the same time elevates anxiety incredibly.
Only things really works for me until today are methylphenidate and Aromasin.

With adding cialis i’ll have a almost normal life ‘except sides’

Did you try to use estradiol patches ? How do you feel when you take external estrogen ?

Clomid stimulates the gonads like LH/FSH would, so it’s like a replacement for LH/FSH. Some people take hCG instead. Both drugs increase T and therefore E2.

@Crossroads
Yes I was hoping it could help solve my longstanding low E2 plight, which it modestly did at 12.5mg EOD. It raised it to 22 pg/ml, which is still low normal but I didn’t feel the benefits. Actually it felt similar to having low E2 because I read that it blocks E2 receptors at the brain and tricking it that there’s too little E2 in circulation and hence LH release. It also skyrocketed my SHBG from 40 to 72.

I should have tried combining it with 25mg Proviron (binds to SHBG) because I came across a few success stories about this specific protocol restoring libido.

@DHT
The idea of using exogenous E2 patches or even pills at such a very low dose have crossed my mind like a million times. However, my fear is that it might trigger negative feedback loop and hence lower LH output leading to lowered Testosterone production and cause femininity. The dose have to be low enough to provide E2 in the range of 22 - 45 pg/ml. I read male to female transgenders take about 2mg a day, which shoots their level to >300.

Speaking of which, it appears that Ginkgo Biloba also lowers E2.

This is from NCBI:
“Ginkgo Biloba Extract reduced the E2 levels by stimulating the E2 metabolism and inhibiting E2 synthesis, which indicates that GBE can induce antiestrogenic activity via the depletion of E2”

I suppose its E2 suppression is very minor to AI’s, though.

@doomed80 you can dissolve the pill in oil/water or alcohol and adjust the dosage.

This way you can take 0.1 mg from 2 mg pill if you normalized even for one day we can say that e2 fixed you.

Btw have you ever tried cabergoline?

I want to give it a shot what do you think?

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I’ve tried caber… I’ve barely heard any positive experiences with it and mine was not positive either. It’s one of those things that looks promising on paper but in reality lowering it some doesn’t help most people. If you have super high prolactin then sure maybe, but not for most people.

It’s worth trying but I wouldn’t have high expectations.

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Ditto. I had similar experience with bromocriptine back in the old days since I didn’t get much improvements (if any). They might prove helpful for subset of individuals, though. They’re also not a long term solution since PRL is said to exert important effects on maintaining dopaminergic neurons.

This is yet another rats study from NCBI:
"Chronic stress exposure and depressive states are known to affect neurogenesis. Neurogenesis is the process that produces new neurons throughout life. New neurons are thought to transiently increase neuronal communication. Two neurogenic niches have been recognized in the adult brain: the hippocampus and the SVZ. The hippocampus exerts a negative control on the HPA axis activity and it is involved in emotional modulation. Antidepressive treatments increase hippocampal neurogenesis and show a correlation with mood improvement (44). Olfactory bulb neurogenesis and olfactory dysfunction are also decreased by CMS exposure, a procedure that is known to induce depressive-like states (45).

Prolactin is a regulator of neurogenesis. PRL receptors are expressed in the SVZ and the hippocampus (46–48). Initial evidence of the relationship between PRL and neurogenesis has been reported by studies showing an increase in neurogenesis in the SVZ of pregnant females. This increase was found to be mediated by PRL (47), and it was hypothesized that the olfactory discrimination of odor cues related to pups is critical for maternal success. Other olfactory signals are important cues that also induce neurogenesis in the SVZ and in the hippocampus. Exposure to pheromones from a dominant male induces cell proliferation in both the olfactory bulb and the hippocampus of female mice. These effects are mediated by PRL in the olfactory bulb and luteinizing hormone in the hippocampus, and both hormones contribute to the regulation of female reproduction (49). Exposure to male pheromones increases SVZ neurogenesis and promotes maternal behavior in virgin and postpartum females (50). Injections of bromocriptine, a dopamine agonist, in female rats during the first days of pregnancy to lower PRL levels, reduces olfactory neurogenesis and induces behavioral alterations postpartum (41). These reports clearly suggest that PRL may regulate SVZ neurogenesis and play a key role in mood regulation."

Now this is purely anecdotal, but I’ve previously observed that 2-3 sauna sessions (15mins each) have elevated my libido significantly in the following day. Sauna (heat stress) is known to trigger catecholamines and prolactin release. This may have been the reason for me heightened libido.

I stumbled upon this excerpt on NCBI:
" Additionally, lower levels of IL-6 were associated with age-related increase of ED, which further confirms the hypothesis of an association between inflammation and ED. The levels of several proinflammatory cytokines are also elevated in cardiac dysfunction, and the administration of phosphodiesterase type 5 inhibitor such as sildenafil was reported to cause a sustained reduction of proinflammatory cytokines, linking the influence of proinflammatory cytokines on vasculogenic function and ED [40]."

Again, this goes to show that inflammation may be a major player in erectile dysfunction problem. I previously posted about my personal experience with certain Probiotics triggering high histamine release and resulting in increased inflammatory response (immune response) that led to absent morning erections. I’ve a strong feeling we should diagnose and treat any inflammation mainly in the gut. Gut inflammation usually represents itself as IBS.

I think I’m ruined. I probably have Sjogrens and Small Fibre Neuropathy.

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Chill out bro. Why do you think you have that?

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Because I have every single one of the non-length dependent symptoms, absolutely completely. Because the nerve pain is increasingly massively.

Update:

It’s been about 10days since I started DHEA. My baseline level was 3.93 mcg/l and lab range is 2.41 - 11.6. My DHEA-s was even lower than that before. Anyway, I used DHEA in the past and I think it helped increasing my E2 (judging by symptoms) but I need to prove it with new labs. My impression about it is that it helps me with mind clarity and boosts my mood and lifts off any left-over brain fog. It’s doing something to my libido too but I need more experimentation to be certain. I’d like to also think it modestly increased my strength at the gym (but not endurance). Having said that, there’re some downsides to DHEA and these are also totally based on anecdotal evidence so I can’t prove it just yet. One downside is increased tiredness in the early evening and needing to nap almost everyday! I never needed naps before except when stopping Corticosteroids and experiencing adrenal suppression.

I think this is due to increased Cortisol/DHEA. I’ll dial down the dose and see if evening tiredness resolves. I’ll get new set of labs to check for early morning T, E2, DHEA-s, & Cortisol so I could pass a verdict on it. The other issue with it it’s pro-inflammatory (not necessarily a problem) and stimulates immune system. My WBC always came borderline low in CBC and I think this may partially be due to low DHEA. More testing needed to draw any conclusions here.

Note: DHEA is a hormone and should be respected as such. Don’t take it if you have no labs to prove that your level is actually low and isn’t under doctor’s supervision. There’re people who got depression/irritability from it. Caveat emptor!

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Sorry bro but I still can’t follow. Can you please elaborate in layman’s terms? What’s your issue?

Hey bro! I have decided to trial Rifaximin for a week. What dosage and frequency did you use it?

I did 1600mg per day (i.e. 600 every 8hrs)for 7 days as per a study done on SIBO patients. You can find it on NCBI. Did you get the breathing test done?

I couldn’t find that test in the area I live in. However, in general my digestion, bowel movement have been kinda bad since PFS. I am planning to use 200mg per day /week.

The lowest dose I’m aware of is 200mg 3X day (i.e. 600mg). SIBO can definitely wreck havoc but it’s in my understanding a symptom of something else. Small Intestines Bacterial Overgrowth isn’t supposed to occur in first place if gut transit time is normal. Yes, I think finesteride can certainly cause it.

Go for it and see if your IBS symptoms improve. In the meantime, avoid dairy/gluten/lactose/High FODMAPs.

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This is interesting because aromatase inhibitors are sky rocketing interleukin 6 weird.
Btw I have recovered from aromasin withdrawal my libido normalized but orgasm intensity returned to pfs levels no joy :frowning: daily pde5 inhibition works well especially nocturnals are normalized but I lost spontaneous erections and visual lust.

This is far too complicated, I wish there was an easy fix. I’m now more convinced than ever that inflammation (mainly in the gut) is a major component since my bowel movements (frequency, consistency) always correlate with my symptoms in terms of erections and libido. Gut governs many inflammatory markers. Histamine should also be at a balanced point to produce a desirable effect. I’ll try very low dose pde5 inhibitor and see if they help with inflammatory markers while I work on stabilizing my gut using most-researched probiotics.

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