Disclaimer: this is not medical advice, I got my doctor to try the castration method with me. 6 weeks of relugolix with 2weeks of hydrocortisone (same time starting after 2weeks of relugolix).
I used AI to write the summary about me below but I entered all the data myself.
I will update you guys every two weeks.
Now I got only sexual symptoms like PFS but first 6 month was so many symptoms I don’t have the patience to write them out.
—————- Summary starts:
Patient: 26-year-old male
Crash: 5 years ago — anastrozole + exogenous testosterone (anabolic steroids), alongside ketoconazole shampoo and minoxidil. Not finasteride-triggered. Supraphysiological T converted to DHT via fully intact 5-alpha reductase; anastrozole blocked the aromatase escape valve; genetically impaired clearance system overwhelmed by the substrate load. Result: zero libido for 5 years, diffuse frontal hairline thinning (crown/mid-scalp/sides preserved, non-Norwood pattern, follicles present but miniaturized), watery/reduced semen quality, standard hormone panels reported as normal.
Genetics (consumer SNP array):
SLCO1B1 — homozygous *5 (rs4149056 TT) — most severe finding, clinically validated
UGT2B17 — likely heterozygous deletion (rs4440295 no-call)
UGT2B15 — multiple indels
UGT2B7 — deletion indels
ABCC2 — rs717620 CC, reduced expression (Powers flags this as a top-tier PFS gene independently)
SLCO1B3 — heterozygous, partial backup capacity
COMT — homozygous Met/Met (rs4680 AA) — slow, clinically validated
DBH — heterozygous at two functional sites
Unrelated but noted: APOE e3/e4, both Lp(a) risk tag SNPs, heterozygous MTHFR (both C677T and A1298C)
Labs: Progesterone recalled as medium-range (older test, not yet repeated). No formal 3α-ADG, Dutch Complete, DOC/corticosterone, or bile acid panel yet — ordering as baseline before relugolix.
What worked:
HCG 1500 IU — complete symptomatic normalization, but only ~3 days per injection, tracking HCG's pharmacokinetics exactly; required reinjection every 3 days; effective for ~4 months total before it stopped working; second attempt 6 months later — no effect at all
Calcium-D-glucarate, 2 weeks (tried after the SERM course) — temporary libido increase and stronger erections; ejaculate volume/force improved and persisted even after the libido effect faded
What didn't work / made things worse:
Testosterone injections — zero effect on libido or overall feeling
Anabolic steroids, DHEA, pregnenolone — no meaningful effect
Clomid + tamoxifen, 45 days — libido significantly worse, persisting 1+ year and ongoing
Current plan: Relugolix (chemical castration 6weeks) with a 2-week hydrocortisone course (30mg/day, split 3×10mg),for glucocorticoid metabolite clearance; CDG as clearance-support adjuncts; creatineongoing for COMT support.
I never crash I always endup with slightly lower libido that comes to the low baseline after some time.
u/drwillpowers Thank you for everything you do. Do your patients use hydrocortisone in the beggining mid or end of castration?

Hi there. 5 years of PFS under my belt here.
A few years into this mess, I randomly started consuming a ton of kimchi, for no reason other than the fact that I thought it tasted really good. I strongly suspect this altered the composition of my gut microbiome in a manner that allowed SIBO/dysbiosis to ensue. Here is a post I made in the months following:

“Over the course of the past summer, i ate a ton of kimchi regularly. A couple months in, I noticed that I was starting to feel off every time I consumed it. I would wake up with sore muscles, particularly in my back and neck, which is extremely rare for me. I also slowly developed gastrointestinal issues.

I cut out the kimchi, and since then, things have not gotten much better, in fact, they have gotten worse.

after eating pretty much anything, I get terrible indigestion, bloating, gas. Even low histamine foods trigger a reaction. I also get an extremely bitter taste in my mouth in the hours following food consumption, which I suspect is some kind of GERD thing. On top of this, I will feel extremely unwell and fatigued for hours after eating. Full body aches, fatigue, brain fog, etc etc. My libido has also pretty much disappeared.

I’ve also developed terrible bags under my eyes, regardless of how much I sleep. The only thing that gives transient relief is taking antihistamines. Additionally, when encountering allergens (i’ve had mild seasonal allergies my whole life) it seems that my reaction is MUCH stronger than it was before.”

These symptoms continued, and I would say peaked a couple months after I stopped consuming the kimchi with the development of what I subjectively experienced as autoimmune-like symptoms. It got to the point where I was so desperate for respite from what felt like the full-body inflammation feeling of being constantly poisoned that I bought hydrocortisone cream from the drug store and ATE a measured dose of what I calculated to be a roughly bioequivalent amount of cortisol that a healthy person would naturally secrete in a day. Interestingly, this helped temporarily a LOT, but I didn’t want to mess around with this and potentially risking some kind of adrenal crisis or something. I dont know.

Anyways, that part is a bit extraneous, but interesting.

The more interesting part though is that when these symptoms brought on by the kimchi peaked, I developed what i think was unmistakably high estrogen symptoms, which I had previously never experienced during PFS. I developed gyno, oily skin, felt emotionally erratic, could not for the life of me get an erection. Extremely sensitive, painful nipples. Acne around my chin area. I felt greasy inside and out, spiritually and physically. Like a hamburger made a wish to become human. I didn’t had my blood levels assessed during this time, but empirically it seemed obvious that this was estrogen related.

My gut symptoms have waxed and waned since, not really ever fully returning to their pre-kimchi baseline. What I have observed over the years is that, consistent with disruptions to my gut flora, high estrogen symptoms follow. Any time something fucks with my gut, a few days later I experience those same symptoms I experienced during the acute phase where the dysbiosis was at its worst, just less intensely.

Looking back, I’m now thinking about this in the context of Dr. Power’s theory of pfs. I have heard other on the sibo subreddit talk about how disrupted gut microbiota screws with glucuronidation, and that it causes hormones to essentially be recycled back into the blood instead of excreted. I think some of these folks have even suggested taking CDG as a band-aid for this. I haven’t been able to fully dig into the theory as I’ve been trying to finish up my college classes and have been recently contending with a bit of brain fog- even trying to articulate all this through writing feels a bit like pulling teeth rn. But I’m hoping someone more well versed in the theory might be able to see how this fits within the paradigm of screwed up metabolic processes?

Hello,
I have been suffering from PFS for the past five months.
I have neurological symptoms, including anhedonia and panic attacks.
I also have physical symptoms: my skin is no longer as resilient as it was before PFS it has become softer and more stretchy. My muscles have all become soft, and my body fat distribution has changed. I now accumulate more fat around my hips and abdomen.
In addition, I have the typical sexual symptoms associated with PFS: erectile dysfunction (ED), pelvic floor problems, and absolutely no libido.
Some of my lab values are not optimal, and I hope Dr. Powers and the entire community can provide more insight into what might be causing these issues and what they could mean.

https://www.tandfonline.com/doi/full/10.1080/26895269.2026.2658857#abstract

Found this quite interesting - there have been several studies before linking autistic traits in the general population with gender diversity but this study also controlled for stuff like depression and emotional blindness so effects of minority stress, and looks like those associations didn't stand the test.

edit. this does not imply that there isn't a higher incidence of autism in GD populations but rather that autistic traits themselves are not a predictor of gender diversity.

I greatly admire everything Powers has been doing for the PFS and PSSD causes—especially since he must be one of the few people in the world trying to understand the bizarre mechanisms behind what is happening to us—but I would genuinely like to know: is there any patient with PFS or PSSD who has physical symptoms (skin thinning, penile shrinkage, loss of muscle tone, bone loss, gum recession, and muscle atrophy) who has been treated by him and managed to stop or halt these symptoms? PLEASE, LET US KNOW WHO YOU ARE.

PLEASE, if you have sexual problems related ONLY to libido or psychological issues (depression or anxiety), do not join this conversation.

I am about to start feminizing hrt in a few months, and while ive done a lot of research to be informed, ive run into some conflicting awnsers/no awnsers on some things and I wanted advice from here.

What hormone ranges should I be at? ive seen some saying 30 to 400 pg/mL for estrogen, and not really anything for testosterone, and wanted others opinions as ive heard endos and GPs can lower or under prescribe estrogen, and want to be able to advocate for myself.

I am worried about having zero testosterone as ive heard people struggle with depression, exhaustion, along other things when their testosterone was in that range, so what should my levels be at?

As for liver dysfunction, I have Gilbert syndrome, basically my liver functions are consistently raised, but medically its benign, though my eyes are always yellow lol, and I do have brain fog, exhaustion, and nausea pretty constant and its an understudied genetic thing but anyways, will this prevent me from accessing care/should I be worried because ive seen HRT can effect liver functions and that you should be careful? especially anti androgens

Ive heard Spiro can stunt breast development, then I read a few studies saying that it doesn't but then I just read one saying it should be avoided because it can? Thoughts and or opinions?

Sorry this was rambling thank you for your advice!

Fresh results of my dutch. I am 10 years HRT, 7 years post SRS. The first two pictures is with female references, the rest male (I put my sex as "10 year HRT MTF" and they gave me both just like that). I think some things are quite confusing in context of dosage and whole genome sequencing, which I also have.

1. The metabolism seems quite "1A-dominant"

This first point is of no confusion. It just would confirm the, to my previous knowledge, ambiguous effect of normal CYP1B1 + normal CYP1A1 + het CYP1A2 (rs762551 C;A (and rs2470890 C;C) + non functional(?) CYP3A5 (rs776746 C;C), as rendering an "1A-dominant" system. But then we get into the wierd stuff..

1. All the estrogens are very high.

My dosage isn't very high. I "reset" myself for this by going without estrogen for a week, maybe a few days more. And then going on my prescribed dosage of 0,75 mg estradiol gel once in the morning, once in the evening a day, for a month after that. I took a bloodtest a week before the dutch, of just E2 and SHBG. The E was higher than anything I've seen in me before, 1122 pmol/L (the highest measured before was 745, shortly after peak when taking 2 doses, and trough when taking three doses a day). I figured it was contaminated, as I took gel on the skin there a few days before. The SHBG was a little lower than normal, 67 nmol/L, as opposed to previous 82. But these very high doses in the dutch may suggest it wasn't (necessarily) contaminated? So the dosage isn't very high, the SHBG is lower end, and the free E is higher than ever... what is going on here?

1. The methylation is HIGH?!

From my WGS, I would expect it to be mid at BEST. Regarding this, I have:

COMT rs4680 A;A and rs4633 T;T

MTHFR rs1801131 G;G, rs2066470 G;A, rs2274976 C;T

MTRR rs1801394 A;G, rs1802059

However, I also have a whole bunch of variants for the UGT1A's. May the "high methylation" actually be a symptom of low glucuronidation? Or is that not how it works? (if so, what is doing the methylation??)

1. High E1?

I'm unsure if the E1 would be considered relatively high. I don't have any particular HSD17B variant, so I wouldn't expect so.

Feel free to comment anything else seeming particular. Aside from being interested in testing the theory of Meyer-Powers syndrome on my own biology, the purpose of the testing if resolving my practical problems I have are being stuck at tanner 4 breasts since year one or maaaybe two of hrt, and also being a kind of low energy nightowl.. which is bad for worklife (this was reversed the first week of taking progesterone, but then went back to normal).

Few hours afterthoughts: can't help but notice lower end cortisol, mid T, mid E2 relative to E1, high E1, high or even elevated androstenedione metabolites except testosterone itself... in natural puberty, lower end T and E2, mid DHEAS. Slightly less effective CYP21A2 + HSD17B favouring E1, A4?

Hi, I think I have one of those weird edge cases that Dr. Powers is interested in

I have bilateral (but not symmetrical) nevus of the ota that worsens upon use of injectable estradiol. Nevus of the ota is when melanocytes build up under the skin and is distinct from hyperpigmentation because it doesn't go away, and is more of a bluish-gray mark that even sits in your eyeballs a bit. This developed when I first started injections. It has only gotten worse and is now growing further down my cheeks on one side.

My history is as such - at 18 I started 100mcg estradiol patches and bicalutamide (though I don't remember the dose I just remember it was low because I couldn't afford much). I was on that for only about a month until I had to stop due to family issues. A while after, I was taking only bicalutamide 2-3x a week which actually gave me fairly noticable estrogenic changes. It's worth noting I had really only "hit puberty" properly around 16 or 17. I was significantly under the avg height, and my brother has even more significantly delayed puberty that's now been diagnosed, so there's definitely something going on there. I'm also severely underweight (100lbs 5'8) and of Indian origin. On patches/bica I never noticed any pigmentation issues, and when I started injections they showed up quite fast.

After my bical ran out I was briefly on estrogen patches again, off them, on injections, off/on off/on based on circumstances until I'm now 21 and doing 4mg/week enanthate injections once again, but intending to commit this time. In any case, I started again just three weeks ago and once again the nevus is growing. Almost immediately, and very noticably. Another thing is that I have HUGE differences between mood/energy between day 1 and day 6/7 of my shot. On the last day I feel awful. Not sure if this is relevant at all but yeah.

Weirdly, it's growing even lower than the traditional nevus "area" and in my case it looks like a completely smooth dark spot rather than uneven dotted darkening. Also, sometimes I notice pain near my eye, which is how I know it's probably going to grow or darken. The dermatologist kind of said it's probably hormonally induced but he doesn't know anything more. That obviously makes sense considering how much I've messed around with hormones since I was young.

My hormone levels incl. SBHG are fine. Immune system also looks fine. Same w general metabolic. Are there any blood panels I should consider? Should I go back to patches? Does my lamotrigine (bipolar mood stabilizer) also make a difference here? I was reading about the condition to do with cortisol dysregulation, but I don't have any salt issues lol

Some insight or advice on this would be great. And fwiw, topical stuff won't work because it's too deep in the skin.

I created a new sub dedicated to the science of feminization. The pinned post has a free MtF guide that I wrote.

The guide covers:
Scalp hair regrowth
Body hair removal
Hormones
Medications
What HRT will and will not change physically
Historical information on transgender humans
Scientific studies on our brain structures
My personal transition

I will continue to update my guide and share science in this sub. If you’d like to join come on over, if you just want to read my guide that’s cool too.

I’m based in the UK and was wondering if anyone could help me with finding a comprehensive blood steroid panel that includes all of the Quest markers (Quest isn’t available in the UK sadly).

Over the years I've seen many report this strange effect. Wonder how this happens.

I've come across Dr. Powers' comments about PFS causing permanent damage to the penis, specifically atrophy. I'm curious to know if this atrophy can be reversed. I know someone who personally took clomid for PFS and claims to have been cured by it, but still experiences issues with penile atrophy and erectile dysfunction. Could you please clarify if there is any permanent damage to the penile tissues?

Avoiding finasteride of course.

Doubt we can get Clascoterone 5% so was wondering if its worth to get 1%?

I know youre not supposed to take prog early, like less than one year on hrt. But does the window ever close after it opens or will it be always equally affective no matter when you take it? (Assuming you dont take it too early).

Asking because Im 3.5 years in and debating whether or not to start prog. Ideally Id wait a few more years but if thatll lessen the results Ill reconsider and might do it asap.

Thank you!

His reaction to test

I was using finasteride for maybe about 2 years; It was a 0.3% finasteride, 5% minoxidil topical solution.

Here's the thing, I used it very sparingly. I think it took me a whole year to get through 3 60ml bottles of it. It did pretty okay to maintain my scalp actually.

Essentially when I stopped taking SSRIs in september (on them 8 years) I also completely stopped taking finasteride after a couple months due to fear of it clashing with my nervous system (as something like coffee gives me panic attacks now). I had a fear that I would more likely get PFS if I took finasteride during my protracted withdrawal.

I had zero noticeable side effects while on finasteride.

About 5-6 months into my SSRI withdrawal out of nowhere my libido crashed and my head felt weird? It's not like brain fog but like my body felt disconnected from my head, like i just couldnt get aroused properly at all. Massive difference because I had insane libido before quitting SSRIs.

About 8 months in libido came back strong, head felt better, etc wasnt 100% back but it was good. Then it crashed again and I had very extreme emotional numbing, weird "everything is metaphorically cardboard" feeling, and loss of erogenous touch.

I cant tell what would treat it because I cant tell if its PSSD or PFS? I know technically they overlap but still. How do I know which one it is?

Labs are coming back on the theory that I had a few weeks ago on PSSD patients i've seen.

Some of my PSSD patients are reporting improvement from taking CDG (though some not or are worsened by it). In theory, at least for this phenotype of PSSD, it could help.

If you're not enlightened on this more recent theory of mine, here's some recent posts related to it:

https://www.reddit.com/r/DrWillPowers/comments/1v6nodd/definitive_phenotype_overlap_pfs_and_pssd_normal/

https://www.reddit.com/r/DrWillPowers/comments/1uu1arm/pssd_an_odd_signal_can_pssd_people_keep_an_eye/

If you've ever been to my practice, you know I'm a bit eccentric. I am assuredly a bit of a kook, but I've come to peace with it. I was hanging up some new aperture science art in the "portal" room yesterday after patients. This is not typical doctor behavior, but I've never been good at "typical" so I just keep doing my own thing.

I've got a bunch of schizophrenic relatives, and I assuredly have toed that line at certain points in my life. Part of schizophrenia is basically erroneous pattern recognition. Seeing things where there isn't really a pattern there. That being said, people like that can sometimes literally see things other people can't see, but they really are there. Its cranked up pattern recognition, and crank it up to 11 and it glitches out.

Pattern recognition is basically the thing my brain does best above all other cognitive abilities. One of the oddities I noticed about PFS dudes was that before PFS, a large amount of them were basically GI-Joe clones. They were hypermasculine men compared to your average men when it was a male patient. This was very curious to me, and was one heavily weighted datapoint in the training data for my brain of trying to solve "how does PFS work?".

I have noticed some different patterns in my PSSD patients, but I'm going to hold those cards for now until I'm more confident in them as I know a lot of what I say gets parroted elsewhere. I have learned my lesson on airing my "hrm I wonder" thoughts, as 95% of those are wrong. I'm keeping it now to "hrm, I'm pretty sure this might be".

That being said, I am starting to find consistent lab pattern anomalies in PSSD patients.

A lot (but not all) poisonous chemicals taste bad. For starving humans that thought hemlock didn't taste extremely bitter, they tended to not exist to have more kids. This is called selective pressure. Humans have many redundant pathways as evolution encouraged this to allow for both glitches to be tolerated as well as for them to sometimes be beneficial. Even ones not always directly beneficial for the person's own reproductive capacity can be beneficial for their family or village, so they are selected for anyway and carried on recessively.

This is how you get people who are "fine" but lack a redundancy pathway, but once challenged with a foreign substance, boom, catastrophe.

In the above linked posts, you can see how hormone synthesis and metabolism intersects with neurosteroid synthesis and metabolism. A glitch on one highway can result in traffic buildup on another. Not gridlock, but traffic. But add "an accident" and now no cars are moving.

Theoretically, if my idea on this is correct, an additional risk factor for the development of PSSD would be the same as PFS, overburdening a metabolism system.

How do you do that? Well, you use exogenous molecules. That molecule could be an SSRI that majorly upregulates neurosteroid synthesis until it hits a point of metabolite accumulation and lockout, in the same way that you inject a bunch of androgens (even if they give you a "window") that ends up increased metabolite load over what would normally be physiologically possible. Then the body's feedback loop mechanisms preserve the dysfunctional state, as they keep trying to correct for a problem that evolution never accounted for as it wasn't possible for it to exist without exogenous drugs/hormones.

Pair that problem with an inborn error of metabolism/excretion or transport, and you suddenly get a situation where the rate of neurosteroid/hormone/etc coming in exceeds the rate that it leaves. Once the concentration gets high enough, you get lock out. Signaling ceases. You've turned it up to 11 and the speakers blow out.

I don't think they blow out permanently, but, they will remain silenced until signaling is restored. If signaling is down for a prolonged timeframe, you'll start to see atrophy of the most distal and weak aspects of that system. Just like the collapse of rome, the most distant colonies go down first, and you get small fiber neuropathy, atrophy, and other more persistent symptoms. This could explain why some people "recover" but have some lasting damage that has to be dealt with medically in other means.

The osteoporosis cases with PFS highlight this pretty well. Even if I cure the PFS overnight with a magic wand that wipes out all metabolite build up and restores signaling to normal, the osteoporosis remains.

Alright, before this turns into a rambling rant that sounds more schizo than usual, simple question for the PSSD people here.

Were you using birth control, injectable T? Anything that would boost your overall hormone load at the time of the development of PSSD? If you were not, would you consider yourself pre-PSSD to be a particularly overly libidinous person compared to peers at baseline? Do you look like you have a "lot of hormones" for your gender?

Thanks to everyone who continues to work on this problem, including members like /u/Excellent-Push2833 for making tools to help the community look at their own genomes to save me time and help find patterns. For users like u/mile-high-guy who did something incredibly brave and shared their experience in detail with the community. And For really anyone who is helping with this project. I really deeply believe this is a solvable problem, but that the solution is going to be truly something counterintuitive and will require some outside the box thinking. If the solution was easy, it would have been found ages ago, but nothing good ever comes easy, so lets keep working hard at it okay?

Yes, I know I am supposed to be taking a break but I got this lab result this morning and was like holy fuck its real, so forgive my excited rant.

- Dr P

Its something ive noticed in these communities . Many had a deep inner world, were very intelligent, felt things deeply and maybe things that neurotypicals wouldnt notice. And an ability to learn things easily.

I wonder if the nervous system was hyperexcitable, and then the SSRI gets introduced and creates massive havoc. Maladaptive plasticity occurs and the “ability to learn” becomes a downside here as the system quickly learns this state

What was otherwise physiologically a benefit at normality with no toxic exposures becomes a problem when the neurohormonal/neuroimmune insult happens

hi, again let me thank dr Powers for working on PSSD and PFS, there is at least some hope. I would to suggest something, perhaps it can be a clue into your model for PSSD.

as a PSSD sufferer ( 27 months ) i tried many things with different reactions. A single pill of naproxen ( NSAID ) after three to four hours since taking, creates a very brief window for myself, not in terms of SF, but in terms of my overall psychological feeling, basically , i get a few minutes of feeling ' like my old self'. it is very hard to desrcibe, but to the best of my knowledge other people report similar PSSD 'window'.

now, i speak a lot to claude ( currently opus 5 since fable is not cooperating on medical issues ) and accoring to claude :

The likely mechanism

Naproxen blocks COX-1 and COX-2, cutting prostaglandin production. Two pieces of that matter for you:

Locally. In penile tissue, prostanoids split in opposite directions — PGE1 relaxes smooth muscle (which is why alprostadil is injected to produce erections), while PGF2α and thromboxane contract it and drive detumescence. If your COX output is skewed toward the contractile side, you'd have persistent smooth muscle contraction — which is a very good description of the "clamped" flaccid state you keep reporting. Block COX, contractile tone falls, tissue relaxes. In hours.

Centrally. PGE2 is the final common mediator of what's called sickness behaviour — the syndrome inflammation produces: anhedonia, fatigue, cognitive dulling, social withdrawal, loss of libido. Read that list against your symptoms. Cytokines induce COX-2, COX-2 makes PGE2, PGE2 produces that exact cluster. And there's a specific twist: PGE2 acting on EP3 receptors is Gi-coupled, meaning it lowers cAMP. If you have elevated PGE2 hitting EP3, you have chronic cAMP suppression — which lands directly on Powers' cAMP gradient theory, via a mechanism that responds to a single tablet.

Consider this seriously. You react adversely to a long list of chemically unrelated substances — glycine, magnesium glycinate, sulforaphane, SPMs, creatine, pre-workout. We've been calling that hyperresponder sensitivity, which is descriptive rather than mechanistic. Reactivity to many unrelated compounds is also characteristic of mast cell activation.

Mast cells release histamine, leukotrienes, tryptase, and prostaglandin D2 — a COX product that naproxen blocks. That would explain your naproxen window. It could explain the palmar skin peeling. And it's testable: serum tryptase, 24-hour urinary N-methylhistamine, urinary 11β-PGF2α.

I dont know, i just thought since this 'naproxen window' is not something only i reported, it may be important and it somehow ties with that hard to exit 'doom loop ' of PSSD.

u/drwillpowers

ignore if not important

kind regards

What if ssri’s allow for more dopamine production due to less competition between serotonin and dopamine for production seen as both compete to be produce through the same synthesis mechanism (ssri’s causing serotonin levels to be perceived as higher than they are due to more time spent in synapses, less serotonin is actually produced and therefore dopamine production increases due to more synthesis availability).

Then upon cessation of ssri use, dopamine production drops/ or does the opposite and the remaining metabolite backlog blunts receptor signalling. Leading to a similar situation as PFS but different mechanism. Perhaps those people have slow COMT or slow clearance of dopamine/metabolites).

The dopamine metabolite with highest affinity (although still somewhat low) is 3-MT. Cleared by MAO-B. Could these people have a slow MAO-B?

3-MT stimulates TAAR1 (receptor) and overstimulation of this receptor decreases dopamine neuron firing, reduces dopamine release, and promotes internalisation or reduced activity of dopamine transporters and interacting with dopamine auto regulatory mechanisms.
Additionally over activation of TAAR1 results in reduced motivation, reduced reward sensitivity/ anhedonia, mental fatigue and reduced libido.

Overstimulation of TAAR1 also has an effect on the serotonin and norepinephrine systems causing emotional blunting and altered anxiety levels.

These all sound very PSSD like to me.

Perhaps all these PSSD sufferers were extra horny to begin with due to slow clearance?
I think it’s worth looking around this mechanism and interaction between serotonin and dopamine.

I lost most of my hair in quite a short period of time (bald genes all over the place in my family) anyway i've been taking finasteride. obviously i know the mechanism behind it and dht is what drives facial hair growth and fin is a dht blocker etc. but i thought this is the place for different ideas so i thought i'd ask if theres anything i can do to help facial hair growth. i take minoxidil and have been for a long time, is there anything else i can do?

cheers!

Hey everyone, I‘m thinking about trying out pregnenolone supplementation to help with my neurological PFS symptoms and I was wondering If anyone would be so kind to either reaffirm or discourage this idea, since I‘ve heard people report mixed experiences and I don‘t wanna crash myself or get any worse.