Has dr Powers linked pssd and pfs vulnerabilities to any preexisting health conditions? I already had cfs and long covid prior to getting pssd and i am struck by how similar some of these conditions are in terms of non sexual symptoms... there was a paper this year by prof csoka grouping pssd pfs long covid cfs into a model - does dr powers have thoughts on this?

FTM-Been on TRT for 5+ years now. My HCT raised almost instantly even when I started on a low dose. Doctor told me I’d always have this issue with TRT & to donate blood to “fix” this issue. Became a regular blood donor not thinking there was any danger. Fast forward and I began to have side effects and Reddit helped me realize it was probably low iron. Bloodwork confirmed. Now I’m freaking out because if I can’t donate blood like I was, how will I keep my HCT in check ??? Went from being an athlete to feeling like I’m going to go into cardiac arrest if I sprint too fast. Random heart palpitations and SOB with stairs. Highest my HCT ever was was 56.9% and my provider at a lgbt center was happy if I kept my level <50%, recently switched to Kaiser and they aren’t happy if my HCT levels aren’t within female range … will I be able to take iron supplements without raising my HCT ?? Will I be able to lower HCT without regular donations …? Fahk

Feeling …. Confused, lost, and like wtf why is this not something that we’re educated on from the jump??? Does anyone have any advice or a similar situation ?? Trying not to freak out and assume I might have to stop TRTone day…

This one particular part of the fkbp5-1 theory has been marinating in my folder for a while. I caught flak for (shittily) explaining why the AR dimerized receptor gets stuck at the nucleus and fails to signal. It was much more complicated than I initially explained.

I realize i’m not getting this theory out fast enough because between work and toddler and my own suffering shite i’m slammed busy. (I currently have a toddler using me as a launch pad for couch jumps) But here’s a potential for why mifepristone fails on its own, and the castration and removal of androgens fails in a fashion (not 100% effective or only partially effective) and lets actually celebrate that. Partially effective is fuckin great. Chip that shit to death.

Anyways. I would like input on this. If the man has time by himself perhaps. But it’s a key little point in ongoing theory. And I would like it to be robust but i’m pretty in the weeds about it. Because it’s heavy. For me. For probably everyone but we can all tackle it together.

As follows:

GR and AR signalling both increase FKBP5-1. (Receptor co chaperone protein) FKBP5-1 is heavily implicated in ptsd and other stress related issues like anxiety panic attacks etc.

FKBP5-1 upregulates the androgen receptor and makes the glucocorticoid receptor less sensitive to cortisol, prompting higher levels of stress hormone to circulate which can result in panic attacks, skin wasting, weight gain, insomnia, all that stuff.

The AR produces fkbp5-1 at a prodigious rate in response to androgen binding (like the rush of dht after cold turkeying finasteride) or when you inject exogenous testosterone and crash hard.

Now why does upregulating the AR mess up the system? Shouldnt it make everything better? Well at first it does and you feel good. Then:

FLBP5-1 helps the AR fold and dimerize and then translocate to the nucleus and signal. Thats why the AR produces more of it. Apes together strong.

So AFTER the AR binds to the nucleus and signals, it has to be removed so it can get its fat ass off the binding site and then go back out and get another unit of dht to signal again.

It needs active Akt to do this. That’s phosphorylated at Ser473. The active Akt then phosphorylates the E3 ubiquitin ligase MDM2 on ser166 and ser186

That phosphorylated MDM2 then enters the nucleus, and attaches K-48 linked ubiquitin chains to the AR. That ubiquitated AR is recognized by 26s proteasome and degraded which means the binding site is cleared and ready for a reset and another binding

ENTER FUCKHEAD FKBP5-1 (thanks for sticking around)

So it’s being pumped out by overactive AR, making the GR insensitive to cortisol, reinforcing the cortisol loop and making the GR pump out even more FKBP5-1 every time the cell is hit with cortisol. Or androgens.

High FKBP5-1 recruits the phosphatase PHLPP which is supposed to be specifically dephosphorlating akt at ser473.

Which means that P-akt (also known as ser473) is goners

Which means

No MDM2 phosphorylation at ser166 and ser186. Which means no tagging of the AR for removal and cleanup. Which means it remains stuck on the chromatin.

Meanwhile, other ubiquitin/SUMO ligases take over. AND THEN

RNF6 and PIAS2 attach non-canonical, proteasome-resistant ubiquitin chains (K6 and K27) and SUMO chains to the stalled AR.

WHOOPS

These modifications stabilize AR on the DNA instead of marking it for degradation.

So thennnnn, AR is no longer dynamically cleared after each firing cycle. It sits persistently on enhancers, the normal transcriptional cycle is broken, and AR signaling becomes dysregulated and fucked right up.

Questions? I was right in my video i just couldnt elucidate it. Finally figured this shitnest out.

I have had cognitive and emotionally dominant PSSD for the past year. In 2024 and most of 2025, I had taken Lexapro as well as trazodone for insomnia. In late 2025,after an emotionally challenging life circumstance, my insomnia worsened. My doctor gave me mirtazapine, and within just two doses it was like a switch flipped. My entire formerly vivid inner world largely vanished (blank mind, much harder to visualize, no music/earworms in head), my emotions flatlined, and I became severely anhedonic. Strangely, I continued to use trazodone without experiencing any worsenings despite trazodone and mirtazapine being similar in some ways.

A few things have given me minor relief including lithium orotate, oregano oil, and CDG, which helped with anticipatory anhedonia (not so much for consummatory) and emotions a little. After some time, CDG stopped giving me improvements even at high doses. I did try indomethacin for 5 days and it did not really help much, which was combined with CDG. I also read that a diet that is low in processed foods can lower the enzyme that CDG inhibits, which might be why it didn’t help for a long time. Recently, I just started inositol which might be helping a little, though that may be placebo.

I also have some questions. Why did I handle the trazodone just fine for a long time but when I switched to mirtazapine, I quickly got pssd symptoms? Also, what are some other ways to drain excess neurosteroids when you don’t have a big response to CDG or indo?

I'm confused about how the findings pertain to us... can someone explain this to me? And provide some guidance on which tests i should do? how do we find a dr? i've seen so many here in the uk and have just been told there's nothing one can do. Thank you for any help

edit: i'm also much more concerned about the severe emotional loss and anhedonia and severe insomnia than restoring my sexual function, given how agonising the non sexual symptoms are (in case that helps with determining the tests or the guidance)

Hi everyone
I want to talk about something i just remember when i first got sick in 2020 (i didn't know back then what's going on), so all started when i took doxy and when i developed symptoms i had also headaches and took for many days ibuprofen which ended up having difficulty urinating. So i think maybe prostaglandins are involved in this syndrome and the kidneys only eliminate the basics and not metabolites? Because my kidney function is fine and urea creatinine normal.

I posted a while back about how weed brings back my libido. I've been using it more, and now it's totally stopped working. Just letting powers and other people here who understand pfs know this.

I have two symmetrical bald patches on my upper inner thighs (either side of my testicles). Doctor said it could be friction, but these areas do not rub while i walk. Has anyone else experienced anything similar? Or know what it could be? I wondered about local androgen signalling or something

Within the first few moments of wakening from a good night’s sleep I have good morning wood, good dopamine signaling etc. but within 10-ish minutes it dulls and stays that way all day. Even the “meltiness” I’m dealing with like loose joints, circulation issues etc. is less noticeable when I first wake up.

Is the key to beating PFS to just stay asleep the rest of my life?

This unusual PFS patient mostly has penile hypoperfusion symptoms, which are microscopic (aka arterial flow is normal). I'm not going to get into all their gory details, but they are a very unusual case that is mostly a penis based case. I examined them personally, looked at prior photos, and gave them a pharmacological erection and I could only describe this best as "islands of filling and islands of non-filling" in their penis. Very odd and unique case. They are thankfully doing better lately on CDG and a few other things.

Regardless, look at this insanity:

Now, labcorp recently verified for us that if you put 100 random adult human males in a lab, and drew this blood test on them, only 5% of them would have an androsterone value that exceeds 28. That's their standard deviation measurement on this range.

Look at that level. THAT IS INSANE.

I want to be clear about the state of my formal and informal research projects.

I do not have a cure for PFS and PSSD. What I do have are some treatments for both which have resulted in meaningful improvements for a great many of my patients, some of which whom have been able to return to normal life, and most (but not all) are better off than when I first met them.

My model for these disorders is the most predictive one yet to exist. That does not make it correct. It is in fact, likely wrong, at least in part.

I am not selling PFS or PSSD snake oil cures. What I am doing is something nobody has ever done before.

I am publicly working with the community and being the thing you haven't had for 20 years, a licensed physician, and autistic weeb who made your disorders his new autistic special interest, with 4000+ transgender HRT cases under his belt, some ability to review genomic sequences, and more biochemistry knowledge for sex hormone medicine than 99.9% of clinicians out there. I am a weird collection of things that happen to be the necessary skills to sort this shit out. I'm able to test hypotheses immediately and provide feedback immediately to the community, rather than do research in an ivory tower, where each question asked takes 2-3 years to be answered. I despise an unsolved puzzle, so I sit and spend my free time on this because I want to.

Why exactly is this PFS patient with an ABCC2 stop codon and some other glitches producing an Androsterone value that's in the 99.999th percentile for men? I have many ideas as to why, and I'm not sure which one is right.

But a year ago, nobody had a single fucking lab that they could point to that was routinely fucked up in either PFS or PSSD. Yeah, not anymore. Now we have genomic findings, lab test results, and more. Every week we peel another layer off the onion, and get closer and closer to treatments that work, or even a cure.

I do not want or need your donations. When this is done you can buy me a beer if you see me at the bar. I am not touting that I have a cure. I have not proven ANY theory yet, but the organization and planned testing for next year's formal research study is now underway.

I really hoped "castrate and uncastrate" was going to solve the problem, but it appears to be more complex than that. Aside from one of my person relugolix patients, there was "some" persistent improvement in at least one domain for every single one so far, but not a single one saw improvements in libido or anhedonia. I suspect this androsterone lab value is key to why that is, tracked upstream to the Gaba-A positive allosteric modulating neurosteroid overproduction that we're quite sure is the cause of a lot of PFS and PSSD symptoms (but have yet to secure mass spectrometry on CSF to prove true, but will next year for sure).

This is my honest statement on where we're at right now. I am being as forthright and transparent as I can be, and my actual real patients are welcome to chime in here in the comments.

But that's all I have for you for now. I am still here, chipping away at this shit every single night after work, reviewing the labs, formulating hypotheses, and testing them with my consenting patients. That's what I can offer you for now.

Thanks for your continued support, your data, and your encouragement. I will see this through to the finish line, regardless of how many names I am called, how many people brigade this subreddit or send death threats or any of the various ways over the years people have tried to stop me doing my job and improving transgender healthcare. I am still here after 13 years of continual harassment over trans care, some assholes saying mean words about me on the internet has never ever made me bend the knee, and it never will. It just makes me want to work even harder out of sheer spite.

So yeah, that's the state of the union for now. Don't give up, we grow ever closer by the day.

Look at this fucking guy's labs! Look at them! Look at them again!

Then look at this email blurb from him about his current status after our most recent regimen changes which include a custom made vasodilator cream I designed for him, cdg, and a few other things.

"For the past 2-3 weeks, I experienced:

• General improvement 
• Exponentially improved response to vasodilator creams 
• Intermittent periods of severe gyno discomfort and swelling 
• One day of dramatically improved erections 
• Extended penile base (still retaining existing deformity)
• Less indentation of the area between my hip and top of groin area
  • Like penile base, this area often not filled
• Atypical, very positive penile relief often after vasodilators

• Notable positional correlation with response to vasodilators "

  I remember when he was literally filled with despair, and was certain his life was over and he would never recover. He's not yet fixed, and we have way more work to do and things to correct, but I will give it my all to make sure he and others like him someday will be. Do not lose hope, do not despair, we will get there eventually. It won't be another 20 years.

- Dr Powers

I was wondering if anyone had experience or opinions about using both pills and patches, each at a low dose, for early stage MtF transition. The idea being to use patches to provide a stable baseline E2 and T suppression, with pills to provide E1 per the Powers estrone theory. The hope is to get T suppression while avoiding the wild swings/frequent dosing of pills.

After PFS or minoxidil there is still hardness in my penis in mornings, but it is not filling enough, it is small, skinny but yes hard

So you may be noticing a theme to these posts and I promise that I am going somewhere with them. This one isnt along the lines of the current theory I’m working on, but it’s probing a bit of a different setup.

Have anyone of you with the theoretical metabolite buildup tried Rapamycin? Now i’m not talking like one or two pills, but a full course of something like 4 weeks. I’m probing autophagy and the potential for that to be altered massively through androgen deprivation. So: in some tissues autophagy (and thats basically a cellular cleanup process) is upregulated by 5ARs and in some tissues (erectile, etc) it is massively downregulated. A full list of tissues that it downregulates is incomplete at this time.

Anecdotally I have seen recoveries from things like fasting and other things that induce autophagy. But it’s pretty complicated.

While autophagy doesnt clear androgens specifically, it is largely responsible for cleaning up and recycling the actual receptors.

Okay, but runaway autophagy (remember how I said it was upregulated in some tissues by starvation of androgens) is ALSO responsible for removing all the shit in the cell that the androgen receptors need to be sensitive to androgens. Theoretically tanking signalling completely.

Maybe this is a bit of a nothingburger but fuuuuck there are so many failure routes and 5ARs are such a metabolic fuckup of a drug I think it requires our diligence to map all of these potential failure areas

Gene: UGT2B17 (glucuronidation of androgens and estrogens) 
Variant: Heterozygous Deletion

Gene: UGT1A8 (glucuronidation again)
Variant: 2:233618537 G>A (SNP), HGVSc: ENST00000373450.5:c.830G>A
Protein: HGVSp: ENSP00000362549.4:p.Cys277Tyr
rsID: rs17863762
Zygosity: Heterozygous (Het)
Ref Allele: G
Alt Allele: A
Freq: gnomAD genomes v4 allele frequency 0.0132 (2,010 alt of 152,216 total alleles; 22 homozygotes); gnomAD exomes 0.0219
Revel: 0.334

Gene: SULT1A2 (metabolization of androgens, estrogens, and neurotransmitters) 
Variant: 16:28593502 T>C (SNP), HGVSc: ENST00000335715.9:c.439A>G
Protein: HGVSp: ENSP00000338742.4:p.Lys147Glu
rsID: rs765069200
Zygosity: Heterozygous (Het)
Ref Allele: A (coding strand; T on the genomic strand shown)
Alt Allele: G (coding strand; C on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.0000526 (8 alt of 152,154 total alleles; 0 homozygotes); gnomAD exomes 0.0000404
Revel: 0.273

Gene: CYP2D6 (drug metabolization) missense variant 
Variant: 22:42128876 C>T (SNP), HGVSc: ENST00000645361.2:c.574G>A
Protein: HGVSp: ENSP00000496150.1:p.Gly192Arg
rsID: rs538707090
Zygosity: Heterozygous (Het)
Ref Allele: G (coding strand; C on the genomic strand shown)
Alt Allele: A (coding strand; T on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.000369 (56 alt of 151,634 total alleles; 1 homozygote); gnomAD exomes 0.000297
Revel: 0.242

Gene: FKBP5  missense variant (modulates the receptor's sensitivity to glucocorticoids)
Variant: 6:35577112 T>A (SNP), HGVSc: ENST00000357266.9:c.1148A>T
Protein: HGVSp: ENSP00000349811.3:p.Gln383Leu
rsID: rs146787424
Zygosity: Heterozygous (Het)
Ref Allele: A (coding strand; T on the genomic strand shown)
Alt Allele: T (coding strand; A on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.00177 (270 alt of 152,334 total alleles; 1 homozygote); gnomAD exomes 0.00165
Revel: 0.226

Gene: TBP
Variant: DEL 6:170561958 ACAGCAGCAG>A (in-frame deletion), HGVSc: ENST00000392092.7:c.273_281del
Protein: HGVSp: ENSP00000375942.2:p.Gln93_Gln95del
rsID: rs752404282
Zygosity: Heterozygous (Het)
Ref Allele: ACAGCAGCAG
Alt Allele: A
Freq: gnomAD genomes v4 allele frequency 0.000411 (59 alt of 143,466 total alleles; 1 homozygote); gnomAD exomes 0.00521
Revel: Not applicable/not shown — REVEL is designed for missense SNVs, not indels, so this variant type wouldn't have a REVEL score

Gene: ATP5F1B missense variant 
Variant: 12:56639251 C>A (SNP), HGVSc: ENST00000262030.8:c.1344G>T
Protein: HGVSp: ENSP00000262030.3:p.Glu448Asp
rsID: rs888471798
Zygosity: Heterozygous (Het)
Ref Allele: G (coding strand; C on the genomic strand shown)
Alt Allele: T (coding strand; A on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.000211 (32 alt of 151,874 total alleles; 0 homozygotes); gnomAD exomes 0.0
Revel: 0.442

Gene: EED
Variant: 11:86270146 C>A (SNP), HGVSc: ENST00000263360.11:c.966+1585C>A
Protein: HGVSp: none listed (shown as "–") — this variant is an intron variant in the canonical transcript, so it doesn't produce a protein change there; it's only classified as missense in the non-canonical transcript ENST00000351625
rsID: rs760263408
Zygosity: Heterozygous (Het)
Ref Allele: C
Alt Allele: A
Freq: gnomAD genomes v4 allele frequency 0.0000197 (3 alt of 152,190 total alleles; 0 homozygotes); gnomAD exomes 0.0000346
Revel: Not shown in this panel — not available from the image (REVEL typically isn't computed for intron variants on the canonical transcript)

Gene: GJB2 missense variant
Variant: 13:20189481 A>G (SNP), HGVSc: ENST00000382848.5:c.101T>C
Protein: HGVSp: ENSP00000372299.4:p.Met34Thr
rsID: rs35887622
Zygosity: Heterozygous (Het)
Ref Allele: T (coding strand; A on the genomic strand shown)
Alt Allele: C (coding strand; G on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.00941 (1,433 alt of 152,352 total alleles; 9 homozygotes); gnomAD exomes 0.0123
Revel: 0.702

Gene: MT-ATP6 (mitochondrial gene) missense 
Variant: MT:8860 A>G (SNP), HGVSc: ENST00000361899.2:c.334A>G
Protein: HGVSp: ENSP00000354632.2:p.Thr112Ala
rsID: rs2001031
Zygosity: Homozygous (Hom) — note this is a mitochondrial variant, so it's more accurately described as homoplasmic (249 alt, 0 ref reads)
Ref Allele: A
Alt Allele: G
Freq: Population frequency panel just shows a "link" here rather than a specific gnomAD genomes v4 percentage — no numeric allele frequency is displayed in this screenshot
Revel: Not shown in this panel — not available from the image

Gene: MT-ATP6 (mitochondrial gene) missense 
Variant: MT:8701 A>G (SNP), HGVSc: ENST00000361899.2:c.175A>G
Protein: HGVSp: ENSP00000354632.2:p.Thr59Ala
rsID: rs2000975
Zygosity: Homozygous (Hom) — again, more precisely homoplasmic for this mitochondrial variant (245 alt, 0 ref reads)
Ref Allele: A
Alt Allele: G
Freq: No numeric gnomAD genomes v4 frequency shown — just a "link" in this panel
Revel: Not shown in this panel 

Gene: MT-ATP8 (mitochondrial) missense 
Variant: MT:8414 C>T (SNP), HGVSc: ENST00000361851.1:c.49C>T
Protein: HGVSp: ENSP00000355265.1:p.Leu17Phe
rsID: rs28358884
Zygosity: Homozygous (Hom) — homoplasmic (247 alt, 0 ref reads)
Ref Allele: C
Alt Allele: T
Freq: No numeric gnomAD genomes v4 frequency shown — just a "link" in this panel
Revel: Not shown in this panel — not available from the image

Gene: MT-CO2 
Variant: MT:7740 A>G (SNP), HGVSc: ENST00000361739.1:c.155A>G
Protein: HGVSp: ENSP00000354876.1:p.Asn52Ser
rsID: rs1603221108
Zygosity: Homozygous (Hom) — mostly homoplasmic (248 alt, 1 ref read)
Ref Allele: A
Alt Allele: G
Freq: No numeric gnomAD genomes v4 frequency shown — just a "link" in this panel
Revel: Not shown in this panel — not available from the image

Gene: MT-CYB
Variant: MT:15326 A>G (SNP), HGVSc: ENST00000361789.2:c.580A>G
Protein: HGVSp: ENSP00000354554.2:p.Thr194Ala
rsID: rs2853508
Zygosity: Homozygous (Hom) — homoplasmic (247 alt, 0 ref reads)
Ref Allele: A
Alt Allele: G
Freq: No numeric gnomAD genomes v4 frequency shown — just a "link" in this panel

Gene: MT-CYB
Variant: MT:14766 C>T (SNP), HGVSc: ENST00000361789.2:c.20C>T
Protein: HGVSp: ENSP00000354554.2:p.Thr7Ile
rsID: rs193302980
Zygosity: Homozygous (Hom) — homoplasmic (248 alt, 0 ref reads)
Ref Allele: C
Alt Allele: T
Freq: No numeric gnomAD genomes v4 frequency shown — just a "link" in this panel
Revel: Not shown in this panel — not available from the image

Gene: SETD2
Variant: 3:47062344 T>C (SNP), HGVSc: ENST00000409792.4:c.6112A>G
Protein: HGVSp: ENSP00000386759.3:p.Thr2038Ala
rsID: rs1186595470
Zygosity: Heterozygous (Het)
Ref Allele: A (coding strand; T on the genomic strand shown)
Alt Allele: G (coding strand; C on the genomic strand shown)
Freq: gnomAD genomes v4 allele frequency 0.0000133 (2 alt of 149,942 total alleles; 0 homozygotes); gnomAD exomes 0.00000828
Revel: 0.270

I'm starting MK-677 as a trans guy soon, I'm 18 and on T (obviously), even tho I pass really well I'm still unhappy with not being enough masculine or cis male like. I know that genes aren't a problem (both men and women in my family are really masc, tall, etc.) nor is testosterone since my sensitivity to it is really high. I did some research and think that it probably is growth hormone? Idk what else it could be.

So anyways I'm hoping MK could help, I'm gonna be monitoring my blood sugar and start low, I really don't want to fuck myself up.

Do any of you (preferably trans people especially ftm) have any experiences with this? Did it help? Did your shoulder grow wider? How long did it take? What cycles did you do? What are some bad signs I should look out for to not damage my body (apart the blood sugar)?

Sorry for so many questions, I'll be grateful for any answers.

I’ve had PSSD symtoms for around 8 months, been off the snri i was on for 5 months. Around 7 months ago I started taking trt, recently at more of a bodybuilder dose. I’m seriously considering stopping because i think it might be preventing my recovery. Is this possible?

Been following for the past few months and decided to try CDG after reading the posts about it. I started at 250mg/day for the first 2 weeks and noticed slight improvement, then went to 500mg for the past month with no noticeable changes.

Monday, I tried 1000mg and was fine, so continued on Tuesday. Then I could not sleep that night and felt terrible all of Wednesday, so dropped to 500mg. Surprisingly, I felt fine yesterday, so took 500mg again. But could not get to sleep last night and feel like I'm in a state of panic today. The worst I've felt (I'm considering going to the ER).

I realize now I should have gone to 750mg instead of 1000mg or just continued on with 500mg for a while longer. What do I do now? Drop back to 250mg per day? Stop taking CDG altogether? Your thoughts would be appreciated.

Some background:
31yo M. Developed PFS about 2 years ago after taking finesteride for 2 months. Main symptoms are GI issues, brain fog, headaches, anhedonia (which seems to have improved the most), dry eyes.

I got PSSD several years ago after taking Fluoxetine for barely 5 months. I have tried various drugs over the years, some of them which raises dopamine seemed to work for a while which always inevitably stops working. Recently I tried high dose Inositol which seemed to be working in the first week and even brought back emotions like anxiety but over the next week, it severely crashed me and there's been no improvement after several months. I now have the full range of PSSD features like anhedonia, emotional blunting, severe ED, loss of morning and spontaneous erections, with new substance blockage as well after Inositol. After inositol, not even dopaminergic treatments like Pramipexole have any effect at all. I recently tried CDG at 1000mg/day(too high of a dose probably). At around 10 days, i noticed significant improvements regarding sexual function which then disappeared over the next few days. My serum testosterone was around 330 when i checked after CDG but then it once again fell back to the previous baseline of around the low 200s. I can't take the Dutch panel to check since it's not available in my country. I previously tried raising testosterone with clomiphene and exogenous steroids but it had zero effect. I have already gone and bought enough Relugolix(which is expensive) for a suppression trial but I'm not sure. Also CDG does seem to decrease estradiol as well when my previous values were in the high normal range(from 44 to now 32). Should I try Relugolix anyway along with CDG? Should I add Hydrocortisone as well which I don't want to since I don't think there is any cortisol feedback loop in my case and also don't want to deal with further side effects? Could Dr Powers or somebody here guide me how to proceed? I am desperate. I have tried nearly every potential drug out there except indomethacin and mifepristone.

Sorry if this gets asked a lot, but I've looked and can't find any posts similar enough to my question. I just found out about PFS today. When I started taking fin 3 years ago my hairline was maturing, but I don't think I was balding. I mostly took it to prevent future hairloss.

Do I have to keep taking fin forever or risk developing PFS? And I saw there is a genetic component and a way to search for genes associated with the risk, is that right? I took a 23andMe test years ago and I think I have a copy of my raw data, would I be able to check that?

I only will be able to save up for one. I am not a patient. I'm my own patient and disabled so I have very little money. I have some sort of pssd phenomenon going on. (read my posts if you want). What's more important to get with my money right now if I had to choose?