My Long PFS Journey

Note that SHBG goes down when people are taking supplemental testosterone. And I agree with Nelson Vergel that too low SHBG is bad and works against the T.

@Crossroads
Great note bro. Those with low SHBG need to check liver, thyroid, & pancreas (diabetes type 1&2). Low SHBG means more unbound sex hormones are available for body processes, which may seem a good thing at a first glance, but bioavailable T doesn’t last long in the body (1 - 8 hrs) before being metabolized resulting in lower level and thus low T symptoms. People with low SHBG and are on trt need smaller and more frequent T shots to maintain good T level.

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I almost had every PFS symptom in the book. There were times when I recovered 100% but those were short lived. I noticed a pattern between recovery and relapse periods. I’m now in full remission but I’ve to wait it out to make sure it lasts (no relapses).

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I’m having a lot of mini recoveries myself recently, my baseline does seem to be improving with time, I hope you continue to feel good.

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@AaronF
Mini recoveries is a subtle sign you’re on the right path bro. It means you’re in the fine tuning process to true recovery. Try and observe the specific pattern during the good times. Daily journal can be very helpful.

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This is really weird exact opposite of my situation… yet we get same symptoms.
I quit from aromasin I crashed a little bit.
Sensitivity loss, pleasureless orgasm and late ejaculation returned.
May be i am in withdrawal from ai i am trying to endure it.

Hormones take a while to balance out. Trick is to give it sometime because it usually get worse before it gets better. We’re all biochemically different so “one size fits all” rule doesn’t apply here especially for us with longstanding PFS. It’s better to get needed tests regularly and try and draw a pattern to see the big picture. Only then you’ll truly know what to attack.

Most weird thing is if I can become hard achieving orgasm will be difficult. If I am
flaccid then I’ll have an satisfactory orgasm with powerful ejaculation. What the hell is wrong I do not understand.

@DHT
Not sure how to explain this, this is my PURE speculation: I was under the impression that lower Estrogen (higher T/E2) may result in harder erections, but mediocre orgasms and higher estrogen (lower T/E2) may result in softer erections, but massive loads. Since you’re on AI I’d surmise your hormones (including E2) is on a rollercoaster.

Having said that, there’re far too many things to count that are inexplicable to me to this day. How are you feeling?

I was on Aromasin I shouldn’t get any rebound.

I feel okay on mental part i feel more relaxed and anger subsided. Also i feel un easy like hyper active.

Visual lust and libido destroyed completely i started to feel something today but erections are all 30 percent even with daily pde5 inhibitor. If i became hard then achieving orgasm is like a running a marathon.
There are no bad sides like joint pains but i prefer them to this castrated feeling.

If this will continue i will either kill my self or restart ai yet, like you said this must be imbalance and i am hopeful that it will be normalized in time.

I am also thinking about serotonin receptor interactions between 5HT1A and 5HT2A / 2C might have changed.

Estradiol directly influences interaction between serotonin and 5HT2A receptors.
1A modulates orgasm and ejaculation but inhibits Erections and 2A enhances Erections.

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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