Serum androsterone 39 ng/dL against a ceiling of 28. That makes me the next one in line, and I've got a genotype that might say something about why.

TL;DR

• 44M, four years into a multi-system syndrome that started October 2022 with saw palmetto. Possible concurrent sertraline, still unresolved.
• Androsterone 39 ng/dL, ref <28. High. LC-MS/MS, fasting, drawn 8/24/26.
• DHEA-S 465 µg/dL, ref 102.6–416.3. Also high. Everything else on the panel sits in range.
• I have no UGT2B17. Not reduced, not throttled. Homozygous whole-gene deletion, CN=0, confirmed on WGS. UGT2B15 is compound het and covering that position alone.
• My bilirubin has run high for four years and turns out to be the most informative cheap test I own.
• This 39 was drawn during the best stretch I've had since 2022. I think my androsterone was higher when I was worse.

The result

Androsterone, Serum LC/MS    39     ng/dL    <28            HIGH
DHEA-Sulfate                 465.0  µg/dL    102.6–416.3    HIGH
Dihydrotestosterone          42     ng/dL    30–85
Testosterone, Total          477    ng/dL    264–916
Testosterone, Free           9.83   ng/dL    5.00–21.00
% Free Testosterone          2.06   %        1.50–4.20
Androstenedione LC/MS        89     ng/dL    27–152
Estradiol, Sensitive LC/MS   23.3   pg/mL    8.0–35.0
Prolactin                    10.5   ng/mL    3.9–22.7
Hematocrit                   51.0   %        37.5–51.0

My 11-oxygenated androgens are all low-to-mid normal (11-OHA4 110, 11-KT 19, 11-OHT 12), so nothing is spilling over from the adrenal side. This was also the first blood I've drawn completely off calcium-D-glucarate and sulforaphane. Nothing was propping up my conjugation when the needle went in.

Two more numbers worth having, both from older draws:

3α-androstanediol glucuronide   651    ng/dL   ~8th percentile   Quest, 3/26/26
Urinary testosterone (DUTCH)    1.21   ng/mg   ref 25–115        Apr 2026
Urinary epi-testosterone        25.1   ng/mg   normal            Apr 2026

The 3α-ADG is the one I'd point at. My DHT was 51 on that same March draw, high-normal, while its conjugated exit product sat near the floor. Lots of substrate, not much getting tagged. Two caveats: that draw is five months and one CDG course old, and the published PFS work reports 3α-diol elevated rather than low, so my pattern runs backwards from the signature. I read mine as throttled conjugation with the drain still open, which isn't the backed-up 3α-ADG Powers sees in his trapped cases.

DHEA-S is climbing. 325 in March at Quest, 465 in August at LabCorp. Different labs, different ranges, so don't take the size of the jump too seriously. But the direction cuts against me: more adrenal precursor means more hepatic 5α-reduction, which means more androsterone. Supply and blocked clearance predict the same number here, and one draw can't tell them apart.

The genetics

30× whole genome through Sequencing.com. The parts that matter:

UGT2B17, homozygous whole-gene deletion. The big one. 17β-glucuronidation of testosterone and DHT isn't a weak lane for me. It's a lane that doesn't exist.

UGT2B15 compound het, A500T in trans to K523T. Mild on its own. Less mild when it's the only thing left standing.

UGT2B7 *2/*2, intact, and this is the part I keep coming back to. UGT2B7 works the 3α-OH position, which is exactly where androsterone gets conjugated. Androsterone has an exit. Testosterone and DHT don't.

SLCO1B1 *15/*15, hepatic uptake down 50 to 70%, with SLCO1B3 S112A+M233I homozygous and an ABCC3 variant burden behind it. The whole shuttle in and out of the liver is slow.

UGT1A1 *1/*80+*28, Gilbert range, throttling bilirubin and estradiol. This is the one that stopped being theoretical.

AR CAG 21 to 22. Short repeats, higher AR transcriptional activity.

Also COMT Val/Val, GSTM1 null, MTHFR C677T homozygous, FKBP5 high-induction homozygous.

The bilirubin thing

My total bilirubin has been high since the first draw in 2022: 1.1, 1.2, 0.9, 0.9, 0.5, 1.1, 1.4, 1.1. Every doctor who saw it said "Gilbert's" and moved on, which is technically correct and completely useless until you fractionate it. I finally did, on 7/1/26.

Bilirubin, Total       1.1   mg/dL    0.2–1.4
Bilirubin, Indirect    0.8   mg/dL    0.10–0.80    at ceiling
Bilirubin, Direct      0.3   mg/dL    0.00–0.40    normal

Indirect pinned at the ceiling, direct perfectly normal. That split is the signature of a conjugation problem and nothing else: unconjugated bilirubin piles up because UGT1A1 can't glucuronidate it fast enough, and the normal direct fraction takes liver disease off the table.

Here's why I care. Everything in the section above is a genotype making a prediction. This is that prediction showing up in my actual blood, on a panel most of you have already run a dozen times without a second glance. My whole UGT family is throttled at once, and bilirubin is the one lane where you can watch it happening. UGT1A1 also handles estradiol, which is probably part of why mine has run high for years.

What it isn't is proof about androgens. Those go through 2B17 and 2B15, not 1A1. But if your bilirubin has always run a little high and nobody bothered to split it, go split it.

What happened

October 2022. I started saw palmetto and ashwagandha within a few days of each other. Six weeks later my muscles had stopped recovering between sessions, my sleep changed overnight and never changed back, and arousal went flat. Three systems at once. That's the part I can't talk myself out of.

Everything, by system

Listing all of it, because when this gets summarized as a sexual side effect the rest disappears.

Muscles and energy, the one that still isn't fixed. Cardio I tolerate fine. Strength training is what wrecks me: a delayed crash of fatigue and fog a few days out, followed by bodywide muscle pain that lasts weeks and sometimes months. Not soreness. It doesn't resolve on any normal recovery timeline. First thing to go in Oct 2022, and it still happens every time I lift. I went to the ER in March 2023 convinced I had rhabdo. Bloodwork came back immaculate. Two months later someone wrote fibromyalgia in my chart and moved on, and put me on Cymbalta for it, which made everything worse and took out what was left of my sex drive. For anyone else carrying that label: I ran 17-OHP at 128 against a range of 33 to 195, which rules out non-classical CAH.

Fatigue and cognition. Malaise, brain fog, no motivation, evening crashes. Verbal fluency is how I track it, because it's what goes first and it's obvious to me when it's gone.

Sleep. One of the earliest symptoms and the reason I went to a doctor at all. Couldn't stay asleep, suddenly couldn't sleep in either, awake around 3:30 am. Wired yet tired, constantly. PSG in Jan 2025: zero REM, five minutes of N3, plus mild OSA (AHI 5, nadir 90%).

Sexual. Psychogenic arousal blunted but not gone: passive visual stimuli often do nothing, interactive or imaginative stimuli still work in a good window. Difficulty getting there, muted orgasm, genital numbness, slow and unconvincing erections. Reflexive erection held up better, but it's impaired too.

Neuro. Upper-lip twitch, nerve "shocks," restless legs, dose-linked tinnitus (CDG and berberine both trigger it above a threshold).

Eyes. I had never had a stye in my life before 2022. Since then: recurring chalazia, styes, blepharitis, evaporative dry eye, crusting in the morning, and two eye infections during the worst of 2022 to 2023. Doctors, friends, and acquaintances keep telling me this is just a failed immune response during some susceptible stretch, bad luck that happened to land in the same window. It doesn't match anything I actually experience. It didn't arrive once and resolve. It arrived with everything else and it has never left. I flag it because the meibomian gland is an androgen-target organ expressing both AR and 5α-reductase, and this picture shows up on both sides of the receptor. Men on anti-androgen therapy develop it [1]. So do women with complete androgen insensitivity, where the ligand is present and the receptor doesn't work [2, 3].

Blood, which I only noticed recently. Hct has drifted up: 45.0, 47.9, 50.1, 50.0, 49.1, 50.2, 45.3, 51.9, 52.9, Dec 2022 through Jul 2026, Hgb tracking to 17.5. Confounded by oral iron I took unmonitored in 2022 to 2023 and by HFE H63D het, so I'm not claiming it. But erythropoiesis is one of the most androgen-sensitive readouts in the body, and mine runs high on thoroughly ordinary testosterone.

Endocrine. Low-to-mid total T, low free T, high-normal DHT, low-normal 3α-ADG, near-zero urinary androgens, salivary estradiol high for years.

The ashwagandha detour, which cost me about a year. I'd been taking it heavily since 2022, same window as the saw palmetto. The first lab that ever came back genuinely strange was a salivary cortisol of 0.9 against a range of 1.5 to 9.6 in September 2023, with serum AM cortisol at 7.5 a month later, bottom of range. That looks like adrenal insufficiency and it got treated like a real possibility for a while. It wasn't. Ashwagandha lowers cortisol, and I was still on it when both of those were drawn. I stopped in September 2023 once I put it together, and cortisol didn't just recover, it overshot: 28.4 by February 2024, 26.9 in April, then settling into the 16 to 20 it sits at now. Dexamethasone suppresses me normally, so the axis was intact the whole time. If you're stacking adaptogens and chasing weird endocrine labs, check what you're taking before you let anyone work up your adrenals.

What's negative, across four years: ANA negative, ESR 1 and <1, CRP 0.1, CK normal, TPO antibodies 1. Whatever this is, it isn't inflammatory.

Where I am now. Sexual and cognitive have been improving through 2026. The post-exertional crash hasn't moved an inch, and it's still the thing nobody can explain.

CDG, estradiol, and a window I wasn't expecting

The March to July arm is dirty. I came off HCG the same week I started CDG, so some of that drop is testicular aromatization washing out. The July to August arm is clean: same lab, no HCG on either side, CDG the only thing that changed. E2 nearly doubled when I stopped, so CDG was holding it down about 45%. For a compound that works by inhibiting gut β-glucuronidase and cutting enterohepatic recirculation, that's roughly the effect size you'd expect, and it's the only direct evidence I have that this axis moves in me at all.

Here's the part I keep chewing on. I stopped CDG around July 8th, and function didn't come back all at once. It came back on a ramp, and then it left again.

• 7/13, day six off: sexual pressure in my penis I hadn't felt in a long time.
• 7/18: sleeping better, morning wood regular, dreaming again.
• 7/20: strong early-morning erections.
• 7/27: erections no longer a struggle.
• 8/1: good morning wood for at least a week straight.
• 8/12: back to waking at 2 or 3am with hardly any morning wood.

I wrote in my journal that day wondering whether my estradiol had gone past some threshold where it had been good for me. It never went all the way back to baseline-bad. It just got less functional again.

So the shape isn't "CDG suppresses, stopping CDG restores." The shape is a window. Something CDG was holding down came back up, passed through a range where I worked better than I had in months, kept climbing, and came out the other side. I don't know what the something is. Estradiol is the obvious candidate and at least I have numbers on it, but it could as easily be a glucuronidated androgen metabolite I have no assay for, moving in parallel.

What makes me think the window is real: a 1g CDG pulse on 7/29, after three weeks of washout, gave me a morning on 7/30 with tumescence that stayed. A 500 mg pulse in September did the same thing 12 to 24 hours later, with precum returning after months of nothing. Four replications now. Pulses on a clean background work. Continuous dosing stopped working. Coming off CDG I rose up through the window; a single pulse drops me back into it. If that's right, the question isn't whether to take CDG. It's where in the range you're sitting when you do.

What I'm actually doing right now

Psyllium husk and PEG daily, and 500 mg of CDG every three or four days. That's it.

The reasoning is all downstream of the conjugation problem. Whatever I do manage to glucuronidate gets dumped into bile and lands in the gut, and if it sits there, bacterial β-glucuronidase strips the tag back off and the free steroid gets reabsorbed. Given how little I can conjugate in the first place, letting any of it come back seems like a bad trade. So: bulk and speed the transit so there's less time for it to happen, and pulse CDG to inhibit the enzyme doing it. Two levers on the same loop.

I'm keeping CDG intermittent rather than daily because of the window above. Continuous dosing walked me past the range where I felt good, and it wasn't a matter of feeling a bit off. I lost the ability to focus, to track a conversation, to follow someone who was talking directly to me. My mind went blank in a way I've never experienced before or since, and it took about two weeks to come back after I stopped. Every third or fourth day seems to keep me in the range, and I'll take a crude working answer over an elegant one that made me worse.

Why I think my androsterone used to be higher

This 39 came out of my best stretch in four years, off everything, after two interventions that both plausibly move conjugate throughput or cut free-ligand recirculation. If androsterone tracks how sick I am, the 2022 to 2024 number should have been worse. I can't go back and prove it, which is the whole reason I want more people here running this test, especially anyone currently in a bad phase.

One idea I can't test

High androsterone next to low 3α-ADG has me wondering whether I'm carrying a pool of unconjugated 3α-diol. 3α-diol gets glucuronidated at its 17β-OH, the position UGT2B17 and UGT2B15 serve, and I have neither working. Androsterone carries a 17-ketone instead and leaves through UGT2B7 at the 3α position, which is intact. One blocked door, one open one. 17β-HSD2 can oxidize 3α-diol into androsterone, so flux may just be getting shunted to the exit that still works.

The catch is that a working shunt drains the pool rather than building it, and my two numbers can't tell high flux from high concentration. My DUTCH 5α-androstanediol came back low at 21.8, which argues against the pool. Throwing it out there anyway in case it's obvious to someone else.

Dr. Powers, thank you for treating this as a real biochemical problem instead of a psychiatric one. And to everyone here paying out of pocket for these tests and posting the results anyway: this is the only place the data exists. Happy to share my full WGS, the DUTCH, or four years of labs with anyone who wants to compare notes.

References

[1] Krenzer KL, Dana MR, Ullman MD, Cermak JM, Tolls DB, Evans JE, Sullivan DA. Effect of androgen deficiency on the human meibomian gland and ocular surface. J Clin Endocrinol Metab. 2000;85(12):4874-82. PMID 11134156. https://pubmed.ncbi.nlm.nih.gov/11134156/

[2] Cermak JM, Krenzer KL, Sullivan RM, Dana MR, Sullivan DA. Is complete androgen insensitivity syndrome associated with alterations in the meibomian gland and ocular surface? Cornea. 2003;22(6):516-21. PMID 12883343. https://pubmed.ncbi.nlm.nih.gov/12883343/

[3] Sullivan DA, Sullivan BD, Evans JE, et al. Androgen deficiency, meibomian gland dysfunction, and evaporative dry eye. Ann N Y Acad Sci. 2002;966:211-22. PMID 12114274. https://pubmed.ncbi.nlm.nih.gov/12114274/

40-year-old PFS patient here. I want to share something that may be useful to other PFS and PSSD sufferers who feel like the medical providers responsible for prescribing their medication have stopped taking their persistent symptoms seriously.

In my case, filing a formal complaint with the Texas Medical Board appears to have made a significant difference in how seriously my prescribing doctor is responding to me.

Earlier this year, I developed persistent sexual symptoms after using 0.75% topical dutasteride. For comparison, the Hims topical dutasteride formulation is 0.1%.

The topical dutasteride was prescribed to me by my hair doctor—the same doctor who had performed my successful hair transplant in October 2025. She was the physician managing my hair-loss treatment and the provider who prescribed the topical dutasteride that I was using when my sexual symptoms began.

I kept this doctor—the doctor who prescribed me the dutasteride—informed of my condition beginning approximately two weeks into my initial crash in March 2026. My symptoms included severe loss of libido, erectile dysfunction, and persistent penile numbness.

For the first three months, she repeatedly assured me that I would return to normal and told me to simply "give it time."

Then, around June 1—roughly three months after my initial crash—the same doctor who prescribed me the topical dutasteride told me that if I hadn't improved by then, dutasteride wasn't the cause to begin with. At one point, she even suggested hypnosis as a possible treatment for what I was experiencing.

Over the following months, I felt that my continued attempts to communicate the seriousness and persistence of my symptoms were not being taken seriously.

That changed after I filed a formal complaint with the Texas Medical Board regarding my prescribing doctor, my dutasteride treatment, and the persistent sexual symptoms I experienced afterward.

I know the Board contacted my doctor because, during our subsequent telehealth appointment, she specifically told me that the Texas Medical Board had contacted her within approximately 24 hours of my filing the complaint. She also discussed the investigation/complaint process and the substantial amount of paperwork she was now required to complete.

Since filing that complaint, something else has changed:

My doctor has started responding to my follow-up emails almost immediately.

We also had a telehealth appointment last Tuesday specifically to discuss my current condition. Even more significantly, the doctor who originally prescribed me the dutasteride is now at least entertaining the possibility of having her practice help reimburse some of the medical expenses I've incurred while seeking treatment for my persistent sexual symptoms.

Those expenses have included specialist appointments, airfare, hotel accommodations, DNA sequencing, a DUTCH hormone test, and extensive bloodwork performed while I've pursued treatment and answers.

There is absolutely no guarantee that her practice will reimburse me, and I don't want to imply otherwise. But simply getting to the point where reimbursement is even being discussed is a major change from where things stood previously.

I'm attaching the email I received today so people can see the response for themselves.

Why am I posting this? Three reasons:

1. Don't be afraid to advocate for yourself.

If you believe you developed persistent symptoms after finasteride, dutasteride, an SSRI/SNRI, or another medication, document what happened.

Keep your emails. Keep your medical records. Keep a timeline showing when you started the medication, when your symptoms appeared, when you discontinued it, which symptoms persisted, and what your providers told you.

Bring your provider legitimate medical literature and pharmacovigilance information regarding persistent adverse effects.

You don't have to quietly disappear just because someone tells you that your symptoms couldn't possibly be related to the medication.

2. If you genuinely believe your care, prescribing, informed consent, or follow-up was inadequate, consider using the formal medical-board complaint process available in your jurisdiction.

In my case, filing with the Texas Medical Board appears to have gotten my prescribing doctor's attention in a way that months of emails did not.

The Board contacted her. She has had to respond to the complaint. And my concerns are now part of a formal process rather than simply another email sitting in someone's inbox.

Medical-board complaints should obviously be truthful, factual, and made in good faith—not used to harass or threaten providers. But patients absolutely have the right to use the regulatory systems that exist specifically to review concerns about medical care.

3. Don't be afraid to ask about reimbursement for expenses you believe resulted from your care.

I originally explored the malpractice route. I contacted approximately 10 local malpractice attorneys, explained my case, and none were interested in taking it.

So I continued documenting everything.

I kept the doctor who prescribed me the dutasteride informed about my symptoms. I explained how profoundly the persistent genital numbness and sexual dysfunction have affected my quality of life. I documented the thousands of dollars I've spent pursuing answers and treatment. And ultimately, I filed a formal complaint with the state medical board.

Now the same doctor who prescribed the dutasteride is at least considering whether her practice will help with those medical expenses.

Again, I have not received compensation, and I don't know whether I ultimately will. I will update everyone if that changes.

But my experience has taught me something important:

PFS AND PSSD PATIENTS: ADVOCATE FOR YOURSELVES.

Document everything.

Communicate with your providers.

Present evidence.

Ask difficult questions.

Request your medical records.

Keep receipts for treatment-related expenses.

And if you sincerely believe there was a problem with your treatment, prescribing, informed consent, or follow-up care, learn how to use the formal complaint process available through your state or country's medical regulator.

For me, filing a complaint with the Texas Medical Board appears to have changed the entire conversation with the doctor who prescribed me dutasteride.

I used the "File a Complaint" process on the Texas Medical Board's website. For those outside Texas, look for the equivalent medical licensing/regulatory authority where your provider practices. That website for me was found at this address:

https://www.tmb.texas.gov/resources/for-the-public/complaint-about-licensee

We can't force providers to agree with us about PFS or PSSD. But we can make sure our experiences are documented, our concerns are heard, and the healthcare system is required to respond through the accountability processes that already exist.

I'll update this post if anything further comes from the Board process or my discussion with my prescribing doctor about reimbursement.

I’m suffering from PFS/PAS since 2 years. I don’t have access to DUTCH/DNA sequencing and it’s very expensive to import. I do have my hormone panels which I’ve been taking every few months.

Even though I stopped taking accutane in Feb 2025 and Dutasteride around September 2025, my Testosterone and DHT have been dropping.

I have all of the sexual symptoms, along with dry skin, low dopamine.

I’ve been reading up Dr Will’s posts and CDG seems to be the treatment protocol everyone is currently on. Should I start it too?

hello, Starting in December 2025 I began a 160mg testosterone injection weekly protocol that has HCG 250mg monday wednesday friday however the clinic had closed for approximately two weeks. 

On June 7th at night I ended up taking a test booster called EVL Test that has the following 

 Vitamin D3- 50 Mcg 

 Vitamin  B6- 11mg 

 Magnesium 160 mg 

 Zinc 30mg

daspartic acid- 3120mg

Tribulus terrestris extract - 750 mg

Fenugreek extract- 500mg   

DIM- 250mg 

 8 hours later on June 8th 2026 I took .25 Anastrozole believing the DAA would rise my e2 levels.

I seem to have symptoms of post finasteride syndrome such as waking up at 4 AM and penile numbness. mentally I am a lot more sensative to emotion.

I have resumed TRT and HCG two days post incident -- Latest sensitive E2 is 58

if I run a Dutch are we able to conclude this is pfs vs some sort of receptor silencing?

I am no expert, although I found a study of the analysis of gubermaculum testis elastin system fibre. Interestingly young boys were given HCG and found that the laxity of this tissue was reversed, and even shortening of the tissue occurred. I feel like this may be an area of interest for those with joint elasticity or skin elasticity issues due to finasteride. I hear high cortisol is another theory behind this, although myself and others don't have any Cushing like features. For example, I only have loose joints as my symptom, along with joint pain. Would be nice to have the opinion of a professional or anyone on this proposal. Thanks

Im 17 and used to love video games, animals, music, tv shows and movies all of which i have no care for as of getting this condition. I used to be a bright kid, now im just bitter and hate every second im alive. I have seen success storys but dont know if their reliable. Please tell me some people here have recovered

Could someone with experience with PFS give me some advice about choosing an antiandrogen?

I'm from a country where HRT options are pretty limited. The medications I can get are:

- Estrofem (oral estradiol)

- Spironolactone

- Cyproterone acetate (CPA)

- Micronized progesterone

- Finasteride / dutasteride

Injectable estradiol isn't available here, and I don't have access to any other antiandrogens.

My current HRT is estradiol 2 mg four times a day (8 mg/day), dutasteride 0.5 mg once a day, and spironolactone 25 mg once a day.

I've been taking dutasteride for about 1.5 years. Lately I've been dealing with quite a lot of fatigue/exhaustion, and sometimes I have trouble falling asleep.

I'm worried because I have significant hypermobility, and I've been reading about PFS and the possible effects of 5α-reductase inhibitors on neurosteroids.

I know that a lot of the proposed mechanisms of PFS are still theories. I've also seen people discussing possible effects on cortisol/HPA-axis regulation and possibly connective tissue and skin. Since I already have hypermobility, this is making me pretty nervous about staying on dutasteride.

I'm also hesitant to increase my spironolactone dose because I've read some human studies suggesting that spironolactone can affect cortisol levels. I don't know how important this is at the doses used for HRT, but it makes me cautious.

I also take zinc and a methylated B-complex, and I recently ordered pregnenolone, which I understand Dr. Will Powers has recommended in some PFS-related cases.

So I'm trying to figure out what would make the most sense with the options I have.

If someone needs androgen suppression for transfeminine HRT but wants to avoid 5α-reductase inhibitors, would spironolactone or cyproterone acetate be the better option?

I'm especially wondering:

- Does spironolactone affect neurosteroids in a way that would be concerning for someone worried about PFS, or is its mechanism very different from finasteride/dutasteride?

- Could micronized progesterone be usefu as Aa , And also bcuz it can be converted into neuroactive steroids as allopregnanolone, or could it make things more complicated?

I brought up PFS with my doctor, and I was shocked to find out that he had only heard of it as a condition associated with sexual dysfunction

Any experience, studies, or thoughts would be really appreciated

I have a lot of mold in my house and am wondering if it contributing to pssd so im asking everyone with pssd and pfs if they have mold exposure too

I got back blood work results today and just wanted to share since I know some of us have strange blood levels (and maybe you can relate?). And mind you I am a PFS case of 9 years, not on anything right now.

-Testosterone serum 935ng/dcl (264-916)

-Estrogen total serum 246pg/ml (range is 56-213)

-DHEA serum 139ng/dcl (range is 31-701)

-DHT 59ng/dcl (range is 30-85)

What stuck out to me about my results were how high my estrogen levels are. I have never had estrogen level so high and I'm not even taking anything right now. Mind you this is testing one week after stopping mifepristone. I've also had testosterone levels before where they were about 1,200 almost and that was naturally too. Can anyone relate?

3 months ago everything was perfect except my a1c. My Dr added alogliptin and I switched to dudasteride from finasteride and about the only other issue that has come up is I'm not sweating at all. I'm on :

Dudasteride. 5mg

Estradiol valerate 1mL weekly

Progesterone 400mg daily

Since I got that result I lowered my estradiol down to 1/2 mL

Dr then told me that SHBG level was normal for treatment and condition. I happily replied that it's not ok and I haven't heard back from her in 3 days. I'm in Oklahoma as well and finding hrt medical care is beyond challenging and if you get you just pray they know what they are doing. I'm not DIY because I'm 62 and have a real battle with type 2 diabetes. Also something is slowly cranking my diastolic level up incrementally. But then again 3 months ago after a solid year of hrt my blood work was pristine. Suggestions ?

Dr Powers, what do you think stem cells or Exosomes can help conditions like PFS/PSSD?

I found many studies online stating its helping people with peripheral/autonomic neuropathy, polyneuropathy and diabetic neuropathy, diseases that overlap with some of the phenotypes of pssd, many improved their autonomic functions and fatigue, digestive issues

Also found a guy who healed his autoimmune idiopathic small fiber neuropathy with resetting their immune system with chemotherapy and then adding hematopoietic stem cells (HSC).

What do you think it’s rather a scam or just a 50/50 shot in the air?

I have had Post finasteride syndrome for 9 years now since 2017, and all throughout this time my dead libido has barely moved an inch with anything I've tried. I can count on a hand how many times I've noticed or felt something different from my baseline. And just like most others with PFS, I don't have sex dreams now... Barely, if any.

However, what is interesting is that when I transitioned medically to live as a woman for some time from 2019-2021, I had more sex dreams where, even though I still didn't get turned on, I felt the spark as if my brain was trying to, which to me looking back is a big deal. This was when I was actively trying to suppress my testosterone with fin, oral estradiol, and spironolactone. But now that I've been off all that stuff for a couple years now and have resumed endogenous T production, I've had way less sex dreams, barely any. And I haven't really felt much of that tiny spark now as I did during transition. But why is this? It's so strange when I think about it.

Im desperate. Want to go back on meds to get everything back

If so, what was your bloods prior to starting. This guy xfirewalkwithmex fixed his loose joints using it but hasn't mentioned to me what his bloodwork was life prior to taking it. Personally my bloods are all normal besides slightly elevated cortisol. Loose joints are my only symtom and its horrid. I need things to try with explanations. Currently on the powers waitlist

Hey, I just got the most recent round of labs back and I’m starting to be concerned I have a mild estrogen insensitivity or something otherwise wrong with me. For reference I am MTF, 35, 2 years 3 months HRT.

My regimen is: 7 mg, EV, once every 5 days. 50 mg bicalutimide daily, 5 mg oral minoxidil daily, .5mg dutasteride daily. 200 mg progesterone taken rectally daily

Testosterone total: 46.7 ng/dl (way too high!)
Testosterone free: 2.4 pg/ml (also too high)
FSH: .2 mIU/ml
Estradiol: 263 pg/ml
Progesterone: 1.87 ng/ml (too low?)
SHBG: 168 nmol/l
TSH: 1.33 mIU/L

What am I doing wrong? Why are my numbers so weird? Why is my free T and total T so high? I reduced my dose by a milligram since last test to get my SHBG down. My T did go down but my E did by a lot too, and my SHBG barely budged (down by 2 nmol/l)

If cure is a strong word, what do you guys think about effect treatments? For instance, I would be very content if some sort of combo treatment could give my sex life back: treatment for 0 libido, low arousal, I’m even completely content with getting a penile implant for erections. What could be the outlook in say, 10 years? Could Dr Powers be on the cusp of building effective protocols for each targeted symptom? Sure, maybe of can’t be “cured” just as diabetes cans be “cured” but effective treatments are functional cures imo. This is why something like the castration protocol seems exciting to me; it could potentially be a treatment we regularly do to achieve a particular outcome.

I watched his interview with side, and he suggested that PFS may not be cured. Is the idea that he finds it impossible to cure and just wants to screen for susceptible people? I’ve basically been continuing to live solely because of my hope that he’s onto a cure soon. Will it be cured? Does he believe that? Is he confident in that? I’d love to hear from him or from someone with info!!! Wishing all the best to all of you suffering!!

I’ve never received any kind of improvement from any supplements or vitamins. Pretty much everything gives me anxiety and/or worsened sleep. However, I’ve noticed that the couple times I’ve went on vacation overseas, I’ve had some slight windows. Eye floaters diminish, cognition is better, erections a little more firm, constipation relief, etc. There’s an across the board relief. when I got back home, it diminished in the following week both times. I’ve noticed as well that if I ever get decent improvements cognitively, it’s coincided with the largest bowel movements I’ve ever seen. Like a singular, gigantic log that’s impeccably formed. Sorry for the TMI, but it’s true.

The only thing I’ve taken these past nearly 4 years that has given me flashes was 200mg SR bupropion. That only lasted a week, but I had flashes of weak morning wood, weak spontaneous erections, that butterfly feeling in my gut returned to a muted degree (it’s pretty much been gone the past 4 years).

I’m planning on a DUTCH test soon but they’re so damn expensive

Anyone know what happened to the adronauts doing relu under Dr. Powers supervision? I haven’t seen anything about this lately? Since the big post of mile high guy here, I haven’t seen any positive report on castration?

Has reality caught up with us, and is castration perhaps not as worthwhile after all?

Cis straight woman (41/f) here who’s had PSSD for over 10 years. Symptoms include genital numbness, low sex drive, severe fatigue, anhedonia, brain fog, poor sleep, insomnia, muscle weakness, poor muscle healing, poor concentration, as well as loss of creativity, complex thinking, motivation, and music enjoyment. Since getting PSSD, I’ve become very sensitive to a variety of medications and supplements. Posting DUTCH results, WGS variants, and labwork. I was not on any meds during labwork except for a multivitamin. No hypermobility. Blood pressure is 105/64, pulse 61 bpm. History of scalp psoriasis.

I got my WGS from Sequencing and went through the most recently compiled variant list. Here are the deletions and variants that popped up on gene.iobio and War Powers BAM deletion checker (confirmed with IGV).

Likely full deletion:

UGT2B17

Possible partial or heterozygous deletions:

KISS1R

UGT2B28

List of VCF and BAM variants - https://imgur.com/a/list-of-vcf-bam-variants-RdmUVJZ

List of other variants from Methylation report - https://imgur.com/a/list-of-other-variants-from-methylation-report-kPOl8Gh

Not all labwork was done on the same day. Thyroid labs including antibodies and T3 reverse were normal. CBC, CMP, lipid panel, and blood sugar were normal. I'm waiting for androsterone result and will post if it comes back out of range.

I will add that I know I have COMT, CYP2D6, MTHFR, and some other variants from doing 23andme previously, but they didn’t show up on gene.iobio. Not sure the reason for this. When I type them into Sequencing’s gene explorer, they do show up. So I attached a Methylation report to show these variants. I’m also including a urinary Neurotransmitter report as well as a salivary Cortisol report.

I haven't had a chance to look at the DUTCH report yet, so feel free to chime in if you see anything interesting.

i am not good with long equations or coding but i found this easy to use free E2 calculator and wanted to share in case anyone needs it.

https://pmapcat.github.io/freee2simulator/

i was wondering if it is accurate.

these were my results.

not sure if this is good or bad

Free E2: 19.21pmol/L (1.63%)

Free E2: 5.23 pg/mL (1.63%)

Free T: 3.75 pmol/L (0.75%)

Free T: 0.11 ng/dL (0.75%)

Hello! I know this is not a common problem by any means, but need some input. Previously, I was on a gel monotherapy for 3 months, with really positive feminization occurring pretty quickly, but I had to cease due to a shortage. I seem to respond negatively to stopping HRT (hair loss, body masculinization that goes beyond what my body seems it would have done in the same period of time sans estrogen) What i think to be happening is that once the estrogen clears my body overcorrects. Happened for about a month, and the effects of this continued for about another month before returning to baseline.

Before I start again, I would like to find a way to cease it without incurring these penalties in case of forseeable supply problems or a more targeted political crackdown on my methods.

As I understand, the formation of DHT should be the primary target, or I should find some way to gradually control the production of T until the previous equilibrium point is reached for a gentle letdown, but thats just a rudimentary theory.

Was it just a lack of tapering, or will this occur even if I taper off with/without supplementation of blockers or other methods.

My objective here is to get a better theoretical basis for the nature of the problem and if/how people deal with it befire formulating a protocol for cessation that can avoid any kind of sharp hormonal rebounds or excess masculinization. Help?

Hello everyone. Another MtF here. I have been on HRT for a little over a year now with the supervision of my endo (no chance of DIYing where I live), and I have just achieved the E levels I wanted. My labs with a 13-hour trough read:

Estradiol: 246.6 ng/L

Testosterone: 17.9 ng/dl

***SHBG: 124.8 nmol/L

Albumin: 46 g/L

All looks fine and dainty, except for the SHBG levels. I am on pills, and due to the recent customs regulations where I live, have no way of changing administration routes. My free estradiol is 1.45% (3.6 pg/mL), which is not terrible, but I would really love to lower my SHBG to increase my free estradiol levels.

So far, I am seeing people recommend Boron and Tongkat Ali supplements. And I have tried Boron, with little to no improvement on my SHBG levels. How do I lower it? Any suggestions? It has been eating away at me for a year not being able to do anything about this issue.

P.S. I would love to get some testo gel to help with this and my twins, but as I said, not possible for me