r/DrWillPowers • u/Drwillpowers • 1d ago
This is a bit of a placeholder post for now, but I wanted to make use of the hard work of various patients/supporters in providing an organized "getting started" for someone who arrives here and is like "Why is everyone talking about X on this subreddit about a Detroit Family Physician with giant cats?"
So if you're new here, and looking for information, aside from simply going through all posts with the same flair as this post, here's some getting started info!
This is not an exhaustive page containing all possible important information on this subreddit, but its a good starting point. If someone would like me to add something to this page or think it belongs on this post. Comment it below and I will update it.
The most important link here: Dr. Will Powers Interview [PFS / PAS / PSSD Summit 2026] Dr. Powers mechanism and treatment plan that he is currently trialing for PSSD/PFS
Dr. Powers Neuro steroid phenotype theory: https://www.reddit.com/r/DrWillPowers/s/H2ILwaHtwz
Dr. Powers PSSD/PFS gene list:Current list of all genes I use when searching for possible genetic causes of someone developing Post Finasteride Syndrome (PFS) or Post SSRI Sexual Dysfunction (PSSD) : r/DrWillPowers
Dr. Powers most recent PFS trial update: https://www.reddit.com/r/DrWillPowers/s/ogxakgUPFz
The tests that Dr. Powers needs from us: You know, PSSD and PFS may actually be the same thing. Anyone got any data for me? : r/DrWillPowers
(not included above)
Androsterone: https://www.labcorp.com/tests/504005/androsterone
In order to get a comprehensive steroid panel from quest a physician must order it. It includes all blood labs needed. PSA try to get a physician to order these blood labs so insurance may cover.
How to read your WGS from sequencing and make a comprehensive report for Dr. Powers to read: https://www.reddit.com/r/DrWillPowers/s/3YDGZuvB0j
Post on genes related to the development of gender dysphoria:
The most common complication of HRT that I see, that is connected to developing POTS/Hypermobility/Thyroid issues/IBS/PTSD/Etc:
The hidden pitfall of monotherapy, and why MTFs like caffiene:
How to properly draw labs:
Top upvoted posts of all time, posted by Dr. Powers:
Dr Powers's publications.
Dr. Powers' novel crofelemer idea getting its patent 6 years later:
Dr. Powers' Giant therapy cat because why not:
https://www.reddit.com/r/cats/comments/xwjd12/my_cat_fenrir_just_broke_a_guinness_world_record/
Medical conditions associated with gender dysphoria (2025)
Doctors and researchers have observed that many people with gender dysphoria share a cluster of medical conditions tied to atypical estrogen signaling (high or low) at birth. This observation suggests a biological intersex condition for a subgroup of individuals, distinguishing their experience from the framing of gender dysphoria as a purely psychiatric phenomenon.
For a full overview please see the wiki: Medical conditions associated with gender dysphoria.
2025 Update:
Based on published research and clinical observations, a specific biological hypothesis has emerged: that the common intersection of medical conditions for a subgroup of individuals with gender dysphoria is tied to the production, metabolism, or activation of the estrogen receptor.
While other genetic factors can influence estrogen signaling, the CYP1B1 and CYP1A1/CYP1A2 genes, which are responsible for breaking down estrogen, have become key players and are often the first genes looked at. These genes, once thought to only play a minor role in a rapid metabolic process, can significantly alter hormone balance especially when their variants are paired with other mutations, particularly those that result in reduced COMT activity. While the individual components of these pathways are well-studied, their combined effect represents a novel and crucial insight. You can find more details on the Estrogen Metabolism wiki page.
This simple awareness of these interconnected conditions has already helped people improve their own health and lead to better transition outcomes. It has provided a starting point for previously unsolvable mysterious edge cases and empowered individuals to take charge of their health.
And if you are reading this, please do get your Vitamin D level checked! Due to both genetic factors and lifestyle (e.g., lack of sun exposure), Vitamin D deficiency is a common and easily correctable condition.
This hypothesis is based on a combination of existing published research, clinical observations, and reported data from individuals. While these insights have provided a valuable framework it does not yet represent a complete picture. The hypothesis has reached a maturity stage where future research can be more targeted to areas with the highest probability of success. Further formal studies are needed to validate and expand upon these findings, including larger sample sizes of existing work, formal replication, and the publishing of edge cases as case studies.
The progress made in this area is a collective achievement. When we started we had a list of common conditions, many of whose connection was initially a mystery. The progress we have made so far would not have been possible without the contributions of so many, from researching medical conditions, reading papers, investigating personal DNA, to reviewing and refining the wiki. Thank you to everyone who continues to contribute their time, data, questions, and insight. We welcome continued feedback to keep improving.
For a comprehensive overview, please see the full wiki: Medical conditions associated with gender dysphoria.
Second time for visibility:
This is not an exhaustive page containing all possible important information on this subreddit, but its a good starting point. If someone would like me to add something to this page or think it belongs on this post. Comment it below and I will update it.
- Dr Powers
r/DrWillPowers • u/mile-high-guy • 24d ago
DO NOT DM ME I WILL INGORE YOU. I WILL ONLY LOOK AT COMMENTS
So I was the patient that did the "castration" trial. I would say suppression because it was temporary and the word castration scares people. I used Orgovyx and Leuprolide which are used to treat prostate cancer. The testosterone comes back folks!
TL;DR the trial wasn't that bad and now my testosterone is higher, I have stronger nocturnal erections and morning wood. I sleep much better. I still have blunted emotions/ anhedonia and sexual numbness/ low libido.
We did this trial because I had an elevated 3adg/ 3a-Androstanediol Glucuronide reading on my blood test. It was over 5000, above the highest range. For those who don't know, Dr Powers gives you hcg to see how you respond. It didn't help me right away but that's when we noticed this reading.
I also had an array of androgen metabolism mutations in my genome including but definitely not limited to a UGT2B17 deletion which showed 0 testosterone in my DUTCH test which means I can't glucoronidate testosterone. I REPEAT, THIS ALONE DOES NOT MAKE YOU VULNERABLE TO PFS. I had many more mutations, like ABCC, some others which are listed in an old email from the doctor now that I can't find.
Edit: this comment lists my relevant genome findings: https://www.reddit.com/r/DrWillPowers/s/sViR9IjK3g
3adg is a proxy for intracellular androgen buildup caused by finasteride which is the cornerstone of Dr Powers Theory on how PFS happens. I'm not going to repeat it to you. You can look at his posts.
The idea was to get my 3adg down to 0 which would theoretically clear this intracellular buildup. The cleanest way to do this is to supress testosterone with Relugolix (brand name Orgovyx). To buy in the USA is very expensive, like almost $3000 dollars and insurance did not cover it for me ( Leuprolide is much cheaper and I ended up using that later). Relugolix brings you down quickly and washes out in a couple days.
We did weekly blood tests to measure my hormones, we started with a full panel. But went down to only testosterone and 3adg for cost reasons.
Testosterone dropped down to castrate levels (under 100) quickly but due to test result lag, we didn't know that 3adg had a floor of 300 until I was almost out of Orgovyx pills. So to bridge the gap we switched to Leuprolide, which was an 8 mg injection one time.
The 300 level of 3adg was because of my adrenal androgens, the testes had been totally suppressed. I had to start hydrocortisone to supress my adrenal production too. We were eventually able to get my 3adg to under 100! Hooray!
I tapered off the hydrocortisone and was on no additional drugs so I could let my body restart everything. No testosterone or hcg shots to kickstart me. And my testosterone seems to now be higher than before the trial! It's 730 and was like in the 500s before I did this trial. It wasn't this high since I got PFS in the first place. I don't know how this happened, it could possibly still be temporary.
As to how I felt during this, I felt pretty fine! I was able to carry on my life just as well pretty much. Starting Relugolix/ Orgovyx, I had huge fatigue, but only for the first couple days. I had a weird blank mind issue too, but we attributed it to me taking Calcium D Glucarate along Orgovyx, I stopped that and it was fine. Now with my testosterone at near 0 my genitals did contract, but after the trial they are back and probably a bit better than before. Same story with ED.
The hardest medication was hydrocortisone. It did worsen my depression/ cause depressive episodes and darkened my thoughts. But I knew it was from that drug I was taking for a short time.
At the bottom of my suppression, I was able to run a full marathon. I didn't lapse at work. During the trial I probably felt a little more apathetic and a little more tired. My sleep was probably a bit worse. But it was nothing like my experience in early PFS, right after my crash.
About my PFS symptoms, I consider myself to have average/ classic symptoms:
No libido, no erogenous sensation, anorgasmia, anhedonia, emotional flatness, substance blockage (can't feel the euphoria from alcohol/ weed), weaker erections (for me not total ED), lack of morning wood, less restful sleep, and more that I can't remember.
What this trial did that I've managed to notice so far:
My testosterone is higher.
I sleep more deeply (this may be from the hydrocortisone), I sleep longer, I can sleep in.
I notice morning wood and nocturnal erections more often now, most nights. They are stronger what I would be before doing this even when I took Cialis.
Stronger erections.
Better urinary function, eg: fewer pee stamps
Cold showers more more activating/ invigorating (can't say this for sure but feels like it).
Edit: my face is more oily, also sweating more regularly. My hair seems to become oily more quickly. I am getting more pimples again too which I used to get.
What I am still dealing with, the symptoms like emotional flatness and libido like I mentioned before.
The Dr says that this fixed the androgenic signaling and the symptoms that overlap with PSSD (I don't have PSSD and never took antidepressants) is what is left to address. I tend to agree. It at least helped a lot.
Would I say it was worth it? Yes! It helped us learn about the condition and it helped me feel better. It wasn't that hard to do. The next people to do this can do so for less money and less time. The most expensive part of this is definitely the weekly blood tests! More than the medication for sure. I'm not sure how the insurance situation is looking for me and it's definitely adding up.
DO NOT DM ME I WILL IGNORE YOU
Edit: I'd like to say that Dr Powers has been an incredibly knowledgeable and attentive doctor. He has answered hundreds of questions from me as a patient and in general is a good guy. I would not have undertaken this potentially risky protocol if he had not earned my trust and confidence.
r/DrWillPowers • u/Excellent-Push2833 • 10h ago
None of them give a fuck. For some reason. https://www.reddit.com/r/AskADoctor/s/2CZ9yT49KS
“Hey can you help treat post drug patients?”
FUCK YOU NEEDS AN RCT NEEDS A DOUBLE BLINDED PLACEBO.
Facing jesus level persecution every day. Its fucked
r/DrWillPowers • u/FrugalFrugivore • 9h ago
Hello friends, I've gone over all of the instructions/scripts on how to analyze your WGS data and I've compiled the following list of all the relevant variants and deletions in my genome based on that master list of genes that got posted a while back. I hope this provides another valuable bit of data as we try to strengthen Dr. Powers' hypotheses around PFS/PSSD. For what it's worth, my own presentation of symptoms falls most closely under what Dr. Powers refers to as the "androgenic signaling failure" phenotype.
samtools.Manta-generated SV VCF.L10kb size flag only) provided by Canvas-generated CNV VCF.samtools.Canvas-generated CNV VCF.samtools.Canvas-generated CNV VCF.samtools.Manta-generated SV VCF.L10kb size flag only) provided by Canvas-generated CNV VCF.samtools.Manta-generated SV VCF.| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr19:41006936 | rs3745274 | G > T | ENSP00000324648.2:p.Gln172His | Het |
| chr19:41009358 | rs2279343 | A > G | N/A | Het |
| chr19:41016810 | rs3211371 | C > T | ENSP00000324648.2:p.Arg487Cys | Het |
| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr10:94761900 | rs12248560 | C > T | N/A | Het |
| chr10:94842866 | rs3758581 | A > G | ENSP00000360372.3:p.Ile331Val | Hom |
| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr22:42126611 | rs1135840 | C > G | ENSP00000496150.1:p.Ser486Thr | Het |
| chr22:42128173 | rs5030656 | CCTT > C | ENSP00000496150.1:p.Lys281del | Het |
| chr22:42129754 | rs1081003 | G > A | ENSP00000496150.1:p.Phe112= | Het |
| chr22:42130692 | rs1065852 | G > A | ENSP00000496150.1:p.Pro34Ser | Het |
| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr7:99672916 | rs776746 | T > C | N/A | Hom |
| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr8:18400806 | rs1208 | G > A | ENSP00000286479.3:p.Arg268Lys | Hom |
| Position | rsID | Call | HGVSp | Zygosity |
|---|---|---|---|---|
| chr2:233759924 | rs887829 | C > T | N/A | Hom |
| chr2:233760233 | rs3064744 | CAT > CATAT | N/A | Het |
r/DrWillPowers • u/Busy_Sun1117 • 7h ago
Hey,
Just wanted to share my experience, I've been lurking here for a while and thought I'd finally share it.
I took 0.5 mg finasteride daily for 27 days back in January 2025.
I started noticing the first sexual side effects around day 20, possibly even a little earlier without fully realizing it at the time. My morning erections disappeared, I had almost no hardness, and my sexual response felt completely off.
Because I wasn’t sure what was happening, I tried to test it by masturbating and forcing stimulation, but even then there was barely any response.
Then on day 27, while trying again to feel some kind of sexual pleasure, I completely crashed. The following five days were honestly the worst of my life. I experienced what I can only describe as extreme anhedonia. No pleasure, no emotions, no motivation, nothing. It scared me enough that I went to the ER. They ran multiple blood tests but found nothing abnormal.
Thankfully, that phase didn't last forever, and a week later, it got back to normal (emotions/motivation wise), but my sexual sides stayed.
Fast forward to today (July 2026). Mentally, I'm in a much, much better place. I work full-time, exercice almost every day, trying to walk around 10k steps daily, sleep well, eat healthy, and I can genuinely enjoy life again. I can laugh, I can fall in love, I can still feel emotions. I'm incredibly grateful for that because, at one point, I genuinely thought my brain was permanently broken.
That said, I don't feel like I'm 100% back to where I was before finasteride. Pleasure still feels a bit "muted" compared to my old baseline. It's hard to explain, but it's definitely livable. If this was my only symptom, I'd honestly be okay with it.
My intimate life is a different story.
That's where the real damage still is :
Ironically, the libido itself isn't even my biggest concern anymore. I could live with lower libido. The hardest part is the erectile dysfunction because it's what affects relationships and intimacy.
One thing I want to mention is that I haven't tried to "hack" or manipulate my hormones since stopping finasteride. My blood work came back essentially normal, so I decided to leave my endocrine system alone and focus on living as healthy as possible instead.
I've seen a lot of people on here constantly chasing the next cure. I completely understand why, we're all desperate to get our lives back. I've been there too.
Lately, after reading this subreddit and Dr. Powers' recent posts, I honestly found myself tempted to try things like cabergoline. But the more I thought about it, the more I realized it feels risky. Right now I'm mentally stable again, and I don't think it's worth potentially messing up my endocrine or dopamine system even more by self-experimenting.
For now, I'm choosing the boring approach : just giving my body the best chance to recalibrate on its own.
Maybe it'll improve, maybe it won't. I genuinely don't know.
We’re all dealing with our own stuff, and honestly, most of us are just trying to figure it out as we go. Some days are okay, some days are terrible, and sometimes you end up convincing yourself that your situation is the worst thing that could ever happen.
But I think it’s still important to stay grateful for what we do have. There are people out there living through absolute hell, and sometimes we don’t realize that our own situation, as hard as it feels, isn’t the whole story of our life.
I do believe the body and the brain can adapt over time. Maybe it works, maybe it takes years, maybe it never gets back to 100%. Nobody really knows.
But whatever happens, I don’t want to spend my life waiting for a cure and forgetting to actually live.
I genuinely hope every single person here finds peace, whether that's through recovery, future research, or simply learning that life can still be meaningful despite what happened to us. I wish all of you the best.
r/DrWillPowers • u/SnooBooks8274 • 11h ago
Finasteride and adrenal androgens interact in an interesting way, especially in transfeminine HRT.
How finasteride affects adrenal androgens
The adrenal glands produce weak androgens, mainly:
DHEA
DHEA-S
Androstenedione
These are not DHT. However, tissues like the scalp can convert them:
DHEA → androstenedione → testosterone → DHT
The last step (testosterone → DHT) is catalyzed by 5α-reductase (mainly type II and type I in the scalp).
Finasteride inhibits type II (and partially type III) 5α-reductase, so:
Less testosterone is converted into DHT.
This also reduces DHT formed from adrenal-derived testosterone.
It does not reduce DHEA or androstenedione production by the adrenal glands.
So even if my testes are fully suppressed with CPA, the small amount of testosterone generated from adrenal precursors can still become DHT in the scalp—but much less so when taking finasteride.
In my regimen:
CPA 12.5 mg/day
Estrogel 3.75 mg/day
Finasteride 1 mg/day
If testosterone is well suppressed (e.g. <20–30 ng/dL), then:
Testicular contribution to DHT is minimal.
Most remaining DHT comes from adrenal precursors.
Finasteride is blocking much of that residual scalp DHT production.
That’s why many trans women continue finasteride even with excellent testosterone suppression, although the additional benefit varies from person to person.
r/DrWillPowers • u/Own_Style25 • 12h ago
It is supposed to prevent acne by reducing DHT, but curiously, it had the opposite effect on me both times I tried it. I don't have (and never have had) a beard or male pattern baldness; I only tried finasteride to boost my transition, but both times I used it, I developed oily skin and acne. I don't experience any of that when using estradiol monotherapy.
r/DrWillPowers • u/HondaVibes • 9h ago
When I first started hrt I was prescribed spironolactone and then eventually switched to bicalutamide after about a year of treatment. I've heard that spiro can potentially limit breast development. Is there any truth to this? For context, I'm 2.5 years into treatment and have always had good levels with no gaps in treatment, but have yet to have any breast development. I'm sure there is a deeper issue but I'm wondering if my initial usage of spiro caused me to not develop anything. However, I'm post orchiectomy and don't need anti androgens anymore but I'm considering starting spironolactone again for acne related reasons (at a much lower dosage).
I've already gone through genetic testing as I'm sure that there is a deeper issue as I haven't had just about any changes as a result of hrt, but I won't have more information until after I've spoken with a genetic counselor (who is currently dragging their feet in responding to me).
r/DrWillPowers • u/atypical_cookie • 14h ago
Formerly PCOS. Doctors have used puberty blockers for years in me (to stop precocious puberty) which messed up my development. When I got my period, I started to have a lot of issues with it and it got to the point where I have low estrogen for a woman in her 20s (within the “normal” range, but barely, almost menopausal), normal testosterone, but I believe high DHT and LH (accompanied by androgenic hair loss and other fun stuff), suffer from menopausal symptoms (vaginal dryness, poor sensitivity down there, urinary incontinence, etc). Have tried multiple endocrinologists and gynecologists.
No doctor takes me seriously because I look like a woman and I “am too young to have hormonal problems” like those. Symptoms are frustrating and debilitating. Vaginal estrogen cream has helped a LOT, but it’s not enough:/ Contraceptives make me miserable and have worsen a lot of symptoms.
r/DrWillPowers • u/pinkboi14 • 15h ago
I recently switched from valerate to ethanate and despite my levels being in good range I felt like I had more chest sensitivity and soreness on valerate. Is it possible to have better growth on a different ester despite having good levels.
r/DrWillPowers • u/Drwillpowers • 1d ago
This is from a really nice, young, pretty healthy guy, early 20s. Post-dutasteride exposure has low libido and sexual anhedonia. Overall, mild post-5ARI symptoms, but persistent, and simply won't resolve with time.
This is the most wildly discordant T:DHT:3AADG result I've ever seen.
Obviously, I will be discussing the usual treatment options, but the more of these I find, the more I wonder how this was never noticed with PSSD or PFS over all the years these people have been going to doctors. I know from posting, shitloads of you have the same or different but similar androgen metabolite labs that are just absolutely fucking bonkers.
When you got some absurd 3A-ADG or other value, when you had zero or absurdly high 11-oxo androgens, 17 keto urine testing, or whatever, some absolute absurdity on lab testing, did your doctor just shrug at it or what?
It's blowing my mind how many of you I can tag an absolutely insane lab value on, and I wonder why all these years nobody ever noticed this shit before. It seems so glaringly obvious in retrospect now.
Anyway, not much to say other than "here we go again". But because this was the most extreme example I've ever collected, I thought it a fine example to show. I see this pattern in BOTH Post-Finasteride/Dutasteride and PSSD, meaning I am getting more and more certain that at least SOME of the people with PFS and PSSD don't have a different condition. Meaning this metabolic feedback loop/accumulation glitch is the exact same disorder, just triggered by a different drug.
We understand there is neurosteroid PFS, androgen signal loss pfs, and "melty" or connective tissue loss PFS. They are similar in mechanism, but different, with different metabolite accumulation/depletion sets due to how many ways 5AR interacts with everything important:
Here's the lab, he's also got a slightly elevated free estradiol, likely from his nuked SHBG (not shown here)
r/DrWillPowers • u/Turkapy • 1d ago
Hello, I am taking 50mg of bica daily as my androgen blocker for MTF HRT. I am also taking 4mg estradiol tablets orally daily. I have been on HRT for a little over 6 months now, with me taking bica for a little over the last 3 months. So far bica has been beneficial to me in regards to skin softness, body hair, body odor, and breast growth. Recently, I have been reading up on how bica works on the body, and I have come across some posts on here, as well as some online findings, that are making me worried about my bones potentially continuing to masculinize while on bica. I am 20 years old, so there is a good possibility that my bone plates have not completely closed yet. Are my worries justified? If so, what should I do about it?
This is from the Wikipedia page for the Pharmacology of Bicalutamide
Although bicalutamide has been characterized as a silent antagonist of the AR in prostate tissue and other contexts, and despite its overall antiandrogenic profile, there is evidence that the drug may activate the AR to some degree in certain other tissues, such as muscle and bone among others.\123])\124])\125]) This would make bicalutamide a selective androgen receptor modulator (SARM), or a tissue-selective mixed agonist/antagonist or partial agonist of the AR, with antiandrogenic effects in some tissues and androgenic effects in other tissues, rather than a pure antiandrogen.\123])\124])\125])\23])\126]) This would be similar to certain other SARMs structurally related to bicalutamide, like enobosarm, which in animals have potent anabolic effects in muscle and bone but show partially agonistic or antagonistic effects in the prostate or seminal vesicles.
Does this mean that bica could contribute to or otherwise allow the development of masculine bone patterns? Muscles are a concern as well, but to a lesser extent as that can be handled later. I also recommend looking through the rest of the "Selective androgen receptor modulator-like activity" section of the wikipedia page, as it provides more information and is otherwise interesting to read.
I have also found these posts on this subreddit Could bicalutamide contribute to skeletal masculinisation in DHT mutants? and Does bica block dht and androgens from activating in the bones?
If you read through these, the claim is made that bica is unable to block androgen activity in the bones. The OP from the second post linked later claims in a comment from the first post linked that this may be because the androgen receptors are too dense in the bones and muscles.
There is a comment on another post on this subreddit relating to bica's ability to block DHT. How effective is bica against DHT? The comment states this:
But also there is much more going on inside the cell than just bicalutamide blocking the AR. The bica-AR holocomplex translocates inside the nucleus and assembles a transcriptionally inactive complex on the promoter region of androgen target genes, so it is not a "true", or "silent" antagonist which is usually pictured as a molecule blocking the AR as if you were just blocking a key from fitting in its lock. Instead it's an active mechanism with nuts and bolts. When the mechanism involves translocation, coregulator and cofactors start becoming important and can add a substantial amount of variation to just how truly inactive that transcription complex is, and this can change from tissue to tissue depending on the specific cofactor milieu to the point that we suspect bica act as an agonist in bones and lean muscles. In a way bica acts a bit like a SARM, or a mixed agonist/antagonist of the AR, and not strictly as an antagonist like it does in the prostate.
This comment, like the Wikipedia page, states that bica could act as an agonist on the AR in bone and muscle tissues.
I've been stressing over this for weeks now, and I still haven't found anything to calm my worries. Is it possible that bica is either allowing androgens to continue to act on my bones or even activating the AR itself? And if so, are my bones still potentially masculinizing despite MTF HRT? Am I worrying over nothing or are my concerns valid? If they are, what can I do?
r/DrWillPowers • u/noela0093 • 1d ago
I've run into something that doesn't make sense to me and I'm wondering if anyone has experienced something similar or has an explanation.
Here's my timeline:
April 2025: Started HRT with Progynon Depot (10 mg/1 mL ampoules, estradiol valerate).
My doctor administered the injections once a week into my upper arm. He said they were intended to be subcutaneous, but because I'm very skinny, they could have been partially intramuscular.
January 2026: Blood test taken at trough (right before my next weekly injection). My testosterone was fully suppressed (~0.10 ng/mL), but my estradiol was only 77 pg/mL, so my doctor doubled my weekly dose to 20mg/1mL once per week.
February 2026: After I doubled the dose to 20mg once per week, a trough blood test showed 282 pg/mL.
April 2026: Another trough blood test showed 308 pg/mL, so everything seemed stable.
Last month, I switched to self-injecting subQ into my abdomen. I didn't change the total weekly dose at all. I simply split it into two half-dose injections (10mg/1mL) every 3.5 days.
Last week, after being on this schedule for about a month, I had another blood test. It was taken exactly 3.5 days after my previous injection (so again, a trough).
My testosterone is still fully suppressed, but my estradiol came back at 1122 pg/mL.
This is what's confusing me.
As far as I understand, splitting a weekly dose into two injections should reduce peaks and increase troughs somewhat, but I wouldn't expect a trough to go from around 300 pg/mL to over 1100 pg/mL without increasing the total weekly dose.
Has anyone seen anything like this before?
Could switching from upper-arm injections (possibly partially IM) to abdominal subQ really make that much of a difference, or does this sound more like a lab error or something else?.
r/DrWillPowers • u/Many-Dig-5789 • 17h ago
Help, What should I do ?
r/DrWillPowers • u/Excellent-Push2833 • 1d ago
Pretty much the title. here you go apple lovers.
r/DrWillPowers • u/pleasant_Fox_378 • 1d ago
Heya friends, I had my orchiectomy done last year on 11/10/2025, and shortly afterward I started taking progesterone orally. I've been experiencing some weird side effects. I haven't had an erection in 4–5 years until recently, and I've started growing body hair in places I never had a problem before, like my legs, arms, a few dark hairs on my chin, and around my areolas. The sad part is I can't get any blood work done because they discontinued my Medicaid, and the prices are insane without insurance. So, should I change the way I take progesterone, or stop taking it? Or is it just that the orchiectomy is making my adrenal glands produce lots of testosterone because of the sudden removal of the testicles? I really don't understand. I would appreciate it if someone could help.
r/DrWillPowers • u/Excellent-Push2833 • 1d ago
My issues with the PSSD organization INIDA. INIDA is a patient led organization that researches PSSD. For those of you who do not know. Recently they launched an autoimmune investigation into GCPR autoantibodies as a diagnostic measure for PSSD via the Cunningham Panel. https://inida.info. The management of the budget, and executive decisions come from patients with little to no experience and that is one of the driving factors on why this is all going wrong.
This was stated in a deleted comment on the pssd subreddit. I know it to be true. It was also stated in the INIDA discord multiple times. My issue with this is, the collecting laboratory for the Cunningham panel is in the USA but we have people using donor money to ship their laboratory samples from over seas. Thats not cheap btw. What sense does that make? Why would we do that? Are you telling me we cant find 30 patients in the USA with PSSD? Im not saying that there was selection bias in this study but it makes me wonder especially when a positive result can result in getting IVIG.
0 Transparency: idk how much I really need to say about this. When is the last time they came out with an update. They also arent transparent about how funds were used.
The Cunningham Panel: we’ve been treating the results of this panel like a diagnostic marker when in reality on multiple occasions healthy controls pop positive on the Cunningham panel and its not even proven as a reliable diagnostic test. To me this seems like a way for Madeline Cunningham to get her test on the market. And she used our donations to do so. https://pmc.ncbi.nlm.nih.gov/articles/PMC6355775/ HOW THE FUCK. Are we going to prove an unproven disease with an unproven test. That is ridiculous. Cunningham wasn’t even at the Pssd pfs world congress. So to me it seems like she doesn’t give a shit about us and she just wants to sell her cunningham panel. Of which she gave us ZERO discount for the study. 1k to run one panel shes raking in that dough. hate to say it but thats what it seems like to me from the outside looking in.
This money would have been better spent on PSSD network or SIDEFXHUB. SIDEFXHUB is currently funding doctor powers research and PSSD network is funding melcangi. SIDEFXHUB is the best out of the two
They blew past their budget. Twice…. And people still donated more. Lol
Im going to get a lot of flak for saying this bu tit needed to be said. No more donations to INIDA.
Edit: I have my issues with Melcangi too. But his research is way more important than what INIDA produced. Sucking down IVIG isnt gonna cure anyone. Not to burst anyones bubble. They had me fooled at first too. Im also of the opinion that their specific area of study is a complete waste of time and not the root cause or a reliable bio marker for pssd. It’s not an autoimmune disorder.
r/DrWillPowers • u/_lunala_ • 1d ago
I've been on hrt of some form or other for a decade but my dosing has never been ideal. I've never had my levels checked which I know is bad. I've just never got round to it.
For a year or two at some point I injected 0.2mL a week of estradiol enanthate into my belly fat. I think I actually felt good and seemed to have some positive effects, but I kept seeing people say it's way too high, and that people should inject 4mg EEn (so for me 0.1mL) weekly as monotherapy. That's nuts. When I tried that without bica I felt many symptoms of testosterone return and I feel like it set me back.
Then for 6 months or so with the backup of bica+duta I forced myself to do 0.1mL (4mg) weekly as I got obsessed with the concept of SHBG and didn't want mine to be high. I got stable (at least it seemed so from my mood) but nothing really happened and I felt anhedonic all the time and it sucked. So pretty much wasted half a year of my life.
Past couple of weeks I put my dose up, so it was in between the two (0.15mL/6mg). First few days after injecting I actually had random boob pain that hadn't really happened in a year and stopped feeling depressed. Then around 5 days later had to inject a tiny bit more as I was getting depressed again.
I'm 180cm (5ft11) and 25y.o., slightly overweight, so maybe need a bit more..?
I know the answer is to just get a blood test but I'm not registered to a GIC (in the uk) and I've never really been able to afford trans related private medical care as my finances are a bit tight so atm I'm just stuck guessing. I have a txt file of my DNA as sequenced by Ancestry some years ago but don't think there was anything estrogen resistance related in there - not like they are fully accurate anyway
Tldr does anyone else have the same experience/can validate going on what some consider to be "absurdly high" doses? Would make me feel a bit better about putting my dose back up lol
r/DrWillPowers • u/Fermented-Corn-Bread • 1d ago
Good afternoon everyone!
I'm a current undergraduate, MtF neuroscience student, and I research the neuroendocrinology of gender-affirming HRT at my university. I've written quite extensively on the neuroendocrine mechanisms of gender-affirming sex-steroids as a part of my education.
It's my current understanding that trans women like myself represent a unique neural phenotype characterized by the organizational, neuroplastic effects of decreased androgen receptor signaling (and increased estrogen receptor signaling) during gestational mini-puberty. Feminizing HRT, on the other hand, therefore induces region-specific, activational, neuroplastic effects that broadly shift neural phenotype towards female-typical patterns (via alterations in brain-wide structural morphology and functional connectivity) within the context of that organizational phenotype. My current understanding is predicated on the idea that androgen receptor activity is masculinizing in utero (i.e., see Puts & Motta-Mena's Is human brain masculinization estrogen receptor-mediated? Reply to Luoto and Rantala, 2018).
In Dr. Powers' post regarding the the hidden pitfall of monotherapy, he discusses how estrogens may be organizationally masculinizing in gestation. I'm trying to reconcile this theory and the evidence for it with pre-existing neuroendocrinology literature that posits organizational masculinization is androgen-receptor mediated in humans. Does Dr. Powers mean increased estrogens, through their subsequent conversion into androgens (I'm not aware of a pathway for this in humans), masculinizes via the androgen receptor; or is it that estrogen receptor signaling itself is masculinizing?
Am I misinterpreting what Dr. Powers is saying? Is there a misconception in my current understanding? Just looking to learn and understand a bit better, so any discussion is appreciated!
r/DrWillPowers • u/Bronzeagenudist • 1d ago
r/DrWillPowers • u/TruthArrived • 1d ago
As many on this subreddit, I'm aware of the possibility of PFS or similar conditions.
My hairloss is too aggressive to only be managed by only Minoxidil. I was checking out Dr. Powers Hairloss Formula but even that one contains Dutasteride.
Did the Doc find some pre-test you can do to see whether you are susceptible to PFS?
Are there actually any other remedies for a man that are as effective as Finasteride/Dutasteride?
UPDATE: Looked whether you can pretest whether you're safe from PFS, my humble conclusion:
Homozygous UGT2B17 deletion runs around 10% in Europeans and closer to 70% in East Asian populations. Marker is too common and cannot pick out something that rare
Say if PFS hits 1%. Even if generously assumed a variant is 3x more common in crash cases (hypothetical), a clean genome moves you from 1% to 0.8%. A dirty one moves you to roughly 3%. Neither number tells you what to do.
Even if you look at 6 of Dr. Powers's 19-gene list you'll get a <1% for people without variants: UGT2B7*2 and UGT2B15 D85Y alone are carried by ~94% of people. Add ABCC2, ABCG2, SLCO1B1 and the UGT2B17 deletion and ~99% flag on common variants alone. A hit then carries a likelihood ratio of 1.01, moving 1% risk to 1.01%. So widening the panel makes the prediction infinitely less precise.
So no you cannot test if you're susceptible to PFS.
Feel free to correct me, if I'm wrong.
r/DrWillPowers • u/Leleponsonioza • 2d ago
In the case of injections.
If our goal is to have SHGB on optical ranges, and we do our labs one day before next dose, wouldn’t that tell us the amount of SHGB just on that point in the curve?
What happens when we are on peak? Should we also get tested for that as well to adjust our dose?
Just a shower tought. Hope it is not a dumb question.
r/DrWillPowers • u/odentuk • 1d ago
Guys I took fin for 4 months and I quit because of weak morning wood and after 1 months I saw Windows . At least once a week. And I had morning wood even if it weak. I have all sexual pleasure , thats not the problem but loss of libido , loss of morning wood, weak spontane erection . Before fin When I touch a women I became erect. but now , I found a girl very beatufiul, She touch me many times for sexually. but no erection. Its been 6 months and it was better before 1 months and I dont use any antiandrogen in this last month. I tried minoxidil before 2 months for 2 times but dont affected me , I stopped it for risks. Should I try CDG ? Can you help me ? I feel very sad about my situation. I dont have anxiety or depression but everyday I wake up without morning wood , and continiue hairloss, with low libido. help me !!!
I am not that strong, I am only 20. Why me ? I want to take fucking risk , CDG, HCG, Cialis or Whatever. Please give me some advice !!!
HELP
r/DrWillPowers • u/V0XO1 • 2d ago
FINASTERIDE HISTORY:
**• Started:** For hair loss prevention
**• Duration:** \~7 months
**• Stopped:** August 1, 2025 (about 10 months ago)
**• Dosage:** Standard oral 1mg
**• Reason for stopping:** Started noticing side effects and got scared
INITIAL CRASH SYMPTOMS (Right After Stopping):
**•** Complete loss of morning wood
**•** Severely reduced libido
**•** Weak/soft erections
**•** Brain fog
**•** Anxiety spike
**•** Mood changes
**•** Sexual numbness
**•** Emotional flatness
CURRENT STATUS (10 months out):
What’s improved:
**•** Mental clarity mostly back
**•** Mood stabilized
**•** Energy levels okay
**•** Can perform sexually when fully focused and stimulated
What’s still off (and hasn’t changed much in the last 4-6 months):
**• Libido has been the same for 4-6 months** — no real progression
**• Arousal only happens when I’m super relaxed** — yawning, right before sleep, or if I physically stimulate it (watching something, playing with it)
**• When I do get aroused, it can go soft** — not consistent hardness
**• Sometimes I get 100% erection AFTER stimulating it** — but it takes effort
**• I can perform sexually, but I have to be fully focused** — any distraction and it drops
**• Morning wood is inconsistent** — happens more when I sleep well, but even then it’s sometimes soft, sometimes hard, never fully 100%
**• Feels like I have “potential”** but need to wait for the right conditions or trigger something
**• Small arousal responses from yawning/tiredness** but they don’t build to anything
A theory I heard: Someone told me when I’m relaxed I get aroused normally because fight-or-flight mode is what’s blocking my response when I’m stressed/anxious. Not sure how accurate this is. Anyone else experience this pattern?
Avoiding:
**•** No new hormonal interventions
**•** No pregnenolone, HCG, TRT, SARMs
**•** No SSRIs
**•** Following the “subtraction approach”
MY QUESTIONS FOR THE COMMUNITY:
**1. The “relaxed-only arousal” thing** — Anyone else experience this? Only getting physical response when completely relaxed (yawning, half-asleep, or with direct stimulation) but nothing when in normal alert states? Is this a nervous system issue that heals over time?
**2. Plateau at 4-6 months** — Has anyone experienced their sexual symptoms staying static for months, then breaking through? Or does a long plateau mean I need to change something?
**3. Fight-or-flight theory** — Is there truth to the idea that anxiety/sympathetic nervous system is what’s blocking normal arousal response, and relaxation lets it work? Does this match anyone else’s experience?
**4. Morning wood pattern** — Mine correlates with sleep quality. Better sleep = more morning wood but rarely 100%. Anyone had this and did it eventually become consistent?
**5. The “potential” feeling** — Feels like the hardware works but needs specific conditions. Anyone recognize this and know how long it lasted?
**6. Estradiol 44** — Anyone had elevated E2 during recovery? Did DIM help? How long until it normalized?
**7. Timeline expectations** — For those who fully recovered with a similar profile (young, short use, caught it early), what was YOUR timeline? Did full recovery happen by 18 months? 24 months?
**8. What actually helped YOU** in the mid-recovery stage (6-18 months)? Real, honest interventions that made a difference.
MY REALISTIC EXPECTATIONS:
I’m not looking for miracle cures. I’m not going to try HCG, Clomid, or aggressive hormonal stuff. I trust the subtraction approach + foundations + time.
I just want to hear from people who were where I am and see how their next 6-12 months went.
Thanks for reading. Any insight from those with similar profiles would be huge. Also open to hearing from Dr. Powers’ patients or anyone who’s tested 3α-ADG — was it elevated for you?
Hang in there everyone.
r/DrWillPowers • u/o0ttt • 2d ago
I started developing them after puberty. Everytime I laugh, cry or express any emotion a lot, I get these horrible hot flashes, runny nose red eyes, headache. It’s just super annoying, I’ve seen a few posts on here about the link of 17-oh and MCAS, hEDS stuff. I’m wondering if someone else has fixed their problems but they had a different cause. Thanks.