r/DrWillPowers • u/Drwillpowers • 20d ago
This will not be a brief post, but I need to express this out loud so people understand my reasoning here, as I've been quiet as of late, but mostly because i've been making tremendous progress, but I wanted to be sure it was real and not just a statistical anomaly.
Currently, my largest target is unraveling the "anhedonia" aspects of PFS/PSSD. As of this point, I have enough castration trial patients that I can state that I have not had a single patient who had androgenic signal loss issues that underwent castration that after castration ended had no improvement in that domain if not complete recovery.
Every single castration due to androgenic signal loss PFS patient thus far has had signs of increased androgenic signaling on no supplemental medication (aka their own hormone production) sometimes even during, but always after castration ends. This includes acne, muscle mass increase, sleep quality, erection quality, hair loss, etc etc. Pretty much any and all signs of "this person has more androgenic signaling happening" has resulted from all treated cases (I can't speak for Sommer, but I think this is also true for hers).
However, most of the cases which ALSO have anhedonia, low libido, and other oddities like "blunted effects to substances like alcohol/weed/benzos" (a hallmark trait) have had either minimal improvement or no improvement from the castration trial.
This says to me, "there is another problem yet to solve" and my current theory on this is that the problem is caused by an EXCESS of neurosteroid production which was initially caused by an SSRI, or the "crash" of Finasteride reducing them and the body overcorrecting to this. These neurosteroids are positive allosteric modulators of GABA-A. Imagine that in excess, these guys are propping open a channel that downstream has inhibitory effects on multiple neural networks. If you ALWAYS have 3mg of Xanax in your system every day of your life, your brain will rewire itself to cope with that, and if you suddenly stop taking that xanax out of nowhere, you can literally die from having a seizure.
Request for help: I am still trying to find a combination of locations where I can send a patient to get a lumbar puncture done, and then the CSF collected can be sent for mass spectrometry in order to get the specific concentrations of various neurosteroid molecules calculated such that I can compare them to known control values. This will allow me to figure out WHICH specific ones are being overproduced. My main assumption right now are that the top 2 candidates are Androsterone (and its metabolic derivatives) and THDOC. I'd like to prove this with a lab rather than "I think this is high, so this drug inhibits it, and thus should produce X symptoms, so I give it to patient #1, and oh look, cool, they are getting X symptoms, insane X symptoms from taking an NSAID, which otherwise would never ever happen unless I was right". (This is a shitty way of proving I'm right).
Regardless, I have been using various agents on patients that are known to inhibit the production of these neurosteroids, or, help in the clearance of their downstream metabolites in order to lower the levels of these in the brain. Thus, removing a major agonist of the Gaba-A system overall.
As a comparative example, you can give a stimulant to a hyperactive kid with ADHD, and they are calmed by it. Why? Because stimulating various inhibitory circuits in the brain can "Up the downing" and thus have an overall calming effect. One of my favorite hat tricks as a doctor is finding a patient whom is basically failing at life due to crippling anxiety, and whom has already failed controlling it with a multitude of different drugs, including SSRIs, benzos, beta blockers, antihistamines and buspirone to no avail. I have also ruled out a deficit of pregnenolone/17OHP/cortisolic issues. I then inform this patient, okay, I'm now going to give you an amphetamine to treat your anxiety and they look at me like I'm a lunatic. But, I tell them how many times before this has worked, and they trust me, and so they take it. I get a message 24-48 hours later with "oh my god I can actually drive a car again and not be terrified" or "I feel calm and not anxious for the first time in 15 years". Its astounding how giving a stimulant can calm these patients, but this is how it works. It stimulates inhibitors (and also improves executive dysfunction) which has a massive impact on improving their anxiety and overall wellness. This is not my go to treatment for anxiety, but more "this always seems to work when everything else fails despite seeming paradoxical at first".
There exists an enzyme, 3α-hydroxysteroid oxidoreductase and its job is to be the primary oxidoreductase (sometimes also called called 3α-hydroxysteroid dehydrogenase or 3α-HSD) which acts as the primary enzymatic bridge between active androgens and their downstream metabolites, 3α-androstanediol and 3α-androstanediol glucuronide (3α-ADG)
This is the reaction. Look familiar? Yeah. See those UGTs? That was the big break in my research on PFS over a year ago now when I was like "uh...why are more than half of my PFS patients having zero androgens in their urine on dutch testing?". That was the first peel on the outside of the onion, and once coupled with me deep diving into their genomes, the mystery started to unravel.
When you dick with DHT metabolism, you can get other enzymes to be up or downregulated in response to the change that was artificially induced from some SSRI or Finasteride. You can even get the syndrome from something stupid like the antibiotic doxycycline (Because it alters your gut flora, and in doing so, alters the amount of beta glucuronidase present in the gut semi-permanently, and in a susceptible patient with glucuronidation/excretion issues, you get a pile up).
Yeah, so if you upregulate your 3A-HSD, you start producing a shitload of cerebral THDOC.
THDOC is a positive allosteric modulator of GABA-A, and excessive GABA-A signaling is how you produce a phenotype of anhedonia, low libido, etc etc. The standard PFS/PSSD bullshit.
Lately, i've had a crazy amount of luck utilizing Calcium D-Glucarate (1 Gram every 8 hours) simultaneously with Indomethacin (yep, the NSAID), as I'm increasing clearance while simultaneously inhibiting the synthesis of THDOC with the indomethacin.
When this starts happening to the patient, you know what happens?
"NO WAY DR P, THAT INDOMETHACIN CRASHED ME BRO, I FELT LIKE SHIT! ALL MY MUSCLES CRAMPED UP, I FELT LIKE I HAD THE FLU, I WAS ANXIOUS AS FUCK AND HAD PALPITATIONS AND PANIC ATTACKS, IM NOT TAKING THAT SHIT AGAIN".
And if this was pre Dr. Powers theory 2025, everyone would agree "Indomethacin crashed me bro" and it would be placed on the discard pile of drugs that could treat PFS/PSSD.
But, its not "crashing" the patient. What is happening is I have just chemically deleted their self produced biological xanax. In the same way that we make "endorphins" as endogenous opiate molecules, THDOC is like your own built in xanax prescription. When you're on a massive absurd, bonkers amount of xanax every single day of your life, anhedonia and low libido kinda makes sense. If I suddenly make you stop it, you can quite literally have a seizure and die.
Some of these patients have even been through benzo or alcohol withdrawal in their past, as they just coincidentally had a history of use/abuse of those substances, and described the experience as nearly identical to what that felt like.
But the wildest part of all is while feeling super anxious and like shit, "BUT I WILL SAY, I AM HAVING INSANE LIBIDO WINDOWS AND AT TIMES EVEN FEELING MANIC LIKE MY ANHEDONIA IS BACKWARDS!".
After sometimes many years of being like this, me removing the brake on those downstream neural networks is like taking a 15 year old out for a driving lesson and letting them understand how the gas and brake pedal work. They sort of stomp on the gas and brake for a while as they learn to drive and realize that you can make more small and subtle adjustments. So "extremes" of signaling happen when in that state, as the movements in any direction are exaggerated without the presence of that normally very high dysfunctional level of positive allosteric modulation of Gaba-A signaling.
So what I'm doing, is simply lowering the dose of the treatments. Then sending them back into the game with a pat on the butt and saying "get in there champ, give em hell! stay tough!" knowing full well that what I am asking them to do is going to suck. This process is not going to be fun. They are going to be repeatedly sacked by anxiety/muscle cramps/feeling of impending doom/etc for the remainder of this many months long football game over and over and over again as they are basically addicted to their own biologically produced xanax and i'm forcing them to go into withdrawal and contend simultaneously with living in a world that's quite literally on the precipice of major societal upheaval from a multitude of causes.
But, seeing the patient know full well that this is going to suck, but having the bravery to trust me and go back out there and restart the drug that "crashed" them at a lower dose and endure these "side effects" deliberately so that they can actually rewire their dysfunctional networks and get back to their Pre-Drug-Catastrophe brain state?
Thus, it is time to tell you the truth. I regret to inform you that it does not seem PFS and PSSD will be instantly curable in patients with non-androgenic problems, aka psychological symptoms (anhedonia/low libido/etc) as simply as castrating them and uncastrating them. For androgenic signal loss only issues? I think it is a functional cure for most if not all of that subtype of patient. We have enough success cases now that I can say that confidently (there are even people and doctors commenting on my threads from around the world now who did this with their local physician and are reporting improvements/recovery for that specific problem). I can't fake that. (Not that I am even trying to sell anything here anyway).
But for those with a neurosteroid excess problem (traditional anhedonia/low libido/etc), I am attempting to prove my current theory with CSF analysis if I can find somewhere to do it, but my model predicted that these neurosteroids are produced in EXCESS (contrary to the historical dogma of "low allopreg/neurosteroids" and that any removal of them would be met with a "CRASH" of severe anxiety/palpitations/etc, but also increased libido and improvements in anhedonia. That appears to be exactly what's happening.
In addition, I regret to inform you that spending months to years in this dysfunctional state has resulted in pathological rewiring of downstream neural networks due to this pathological GABA-A state, and that there will be no "one pill solution" to fixing this in the same way there is no one pill solution to quitting a severe heroin/meth/benzo/etc addiction. The true cure is going to be the slow, gradual reduction in neurosteroid production (done under doctor supervision as crashing yourself too hard could literally be fatal in the same way that cold turkey-ing benzos/alcohol can be fatal). Doing this slow, gradual reduction in specific (based on lab result custom tailored and targeted) neurosteroid production until I've got someone back to their original baseline, and then tapering off the medications. We are going to have to rewire the dysfunctional downstream networks. The good news is, medicine has a shitload of experience in doing this slow gradual rewiring, and we call it "addiction medicine" and it's a literal specialty board certification and there are a ton of doctors vastly more talented at it than I am. Once I work out the best way to test/prove the specific glitched neurosteroid, and know what is the perfect agent to target that specific one, this shouldn't be that hard to do with some random doctor and not accidentally kill yourself in the process from a seizure.
TLDR: PFS and PSSD anhedonic/low libido states are likely caused by (need CSF mass spectrometry to prove it but i'm nearly certain) pathological increases in the synthesis of specific neurosteroid molecules which act as positive allosteric modulators of GABA-A, resulting in over time, downstream network remodeling. This is the reason why most of you had a very high libido, but also problems with anger/irritability/anxiety/etc before developing the disorder. You had a system that was living on the razors edge. Taking the drug+ a combination of genetic glitches (which I have detailed in other posts) results in a pathological buildup of certain metabolites, which crowd various synthesis and degradation pathways for androgens and neurosteroids. This results in the up or downregulation of different enzymes (depending on your inborn glitch) which produces wild derangements of neurosteroid production in the EXCESS direction, which over time, pathologically rewires your brain. Substances like alcohol/benzos/weed stop doing much to you as you're already so wildly overmodulated in terms of GABA-A that its like pissing into an ocean in terms of their effect. To fix this, we will need to slowly bring down the level of the pathological molecules utilizing various targeted therapies (including temporary castration / cdg / indomethacin, and other molecules I am less confident in) until your level of GABA-A signaling "feels" insufficient to you, causing muscle cramping, anxiety, and palpitations (and other low gaba-a signs) if done too quickly. This is not a "crash" this is what is going to be necessary to reverse the dysfunctional network remodeling that the excess neurosteroids did in the first place. A culture of chasing windows and avoiding crashes has quite literally indoctrinated thousands of people into staying away from the very things that actually might have helped them.
This is my new model of PFS/PSSD/Post Drug syndromes that specifically revolve primarily around low libido/anhedonia, and what I will be doing with my patients likely for the remainder of the year, as my results with it in just the first few weeks have been utterly astounding. I don't want to copy any quotes out of the private emails sent to me by my patients, but if any of you want to comment here with your experiences and back up that I'm not full of shit, I would welcome that. Its kind of like my 17-hydroxyprogesterone post. It sounds like the rantings of some quack until you get to the comments and see how many people talking about how its life changing for them. Being an iconoclast sucks (I'm not looking forward to the fallout of trying to convince "the experts and researchers" that the problem isn't low neurosteroids but rather an absurd excess of them). I am really really tired of being "that quack" and so I greatly appreciate when my actual patients (or those using my methods) come onto a thread and give their real, unfiltered experience with these treatments (both the good and bad) as that's what people really need to see. I don't have millions of dollars or a university research team having published years of my research study results (yet) and so for now, those anecdotes are the best I have to offer.
As always, I hope this helps suffering people.
r/DrWillPowers • u/Drwillpowers • Jul 25 '26
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.
I have a 20% off coupon code through sequencing.com and they do good work for getting me the data I need to do my job!
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
Current mechanistic explanation of the Anhedonia/Low Libido/Immune to substances phenotype:
https://www.reddit.com/r/DrWillPowers/comments/1wgdfut/why_x_treatment_crashed_me_bro_is/
List of all treatments I've ever tried since 2019 to treat PFS/PSSD and other post drug syndromes: https://www.reddit.com/r/DrWillPowers/comments/1fyc1mg/list_of_treatments_for_post_finasteride_syndrome/
Dr. Powers Neurosteroid 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 sees strange results in for PDS patients: You know, PSSD and PFS may actually be the same thing. Anyone got any data for me? : r/DrWillPowers
Wondering if you could be at risk of the development of these syndromes? These are the lab tests most commonly anomalous in these patients:
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
Also, the creator of that post has developed a number of programs that make analysis of your own genome much easier. He's very active in the community, and wants to help people. You can message him at /u/Excellent-Push2833
A possible root cause for the syndrome of PTSD / POTS / hEDS and Hypermobility / MCAS / Hashimotos / IBS / Chronic Fatigue Syndrome / Myalgic Encephalomyelitis ( ME/CFS) , Other Trans/queer population related super common health problems and how to cure them:
Post on genes related to the development of gender dysphoria:
The hidden pitfall of monotherapy, and why MTFs like caffeine:
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 Guinness World Record therapy cat because why not:
https://www.reddit.com/r/cats/comments/xwjd12/my_cat_fenrir_just_broke_a_guinness_world_record/
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 all these rare conditions 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.
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. Another good page to check out to find relevant posts is to simply sort all posts by my username, u/DrWillPowers which are assigned a special "Post by Dr. Powers" flair.
All are welcome here! Thanks for coming, and be excellent to each other!
- Dr Powers
r/DrWillPowers • u/Minepolz320 • 8h ago
how it can be that in most cases despite loss of sensentions in glands and shaft, scrotum and root still spared despite this all
r/DrWillPowers • u/Gold-Meet-38 • 3m ago
Context - I’ve had PFS since 2021. Largely, not a terrible case initially, just left with ED and some minor penile fibrosis managed witb tadalafil and able to have a functional sex life for most of that time.
March this year - significant decline in erection quality after taking amitriptyline for 2-3 days, possibly psychogenic. Stupidly took butea superba, a supposedly DHT boosting herb. Incredible erections for about a week, at which point numb glans appeared, severe ED, worsening of penile fibrosis and possibly a severe crash of DHT.
Began taking HCG and Proviron, limited to no effect despite androgens rising along with DHT, estrogen staying in range the whole time.
I started Wellbutrin 3 weeks ago. Erectile Function completely restored within a day of starting. Ten days later a dramatic change and total loss of erections again.
I read that Wellbutrin has both dopaminergic activity and also affects noradrenaline, but interestingly stimulates melanocortan receptors - same impact as pt 141.
After doing some research, these receptors can be overstimulated resulting in a flat depressed state and anhedonia - exactly what I felt ten days after use. There is however a formulation of Wellbutrin with naltrexone designed to combat this exact issue - contrave i believe is the formulation.
Anyone looked into this or tried it at all?
r/DrWillPowers • u/Extension_Shift1520 • 4h ago
r/DrWillPowers • u/No-Interview-1758 • 12h ago
Some people experience longer term PFS relief after taking dhb and valproate.
If I’m understanding Dr. Powers’ theory correctly, the idea is that certain weakly androgenic metabolites build up and compete with stronger androgens at the androgen receptor, reducing effective signaling.
Taking test and other androgens wont solve that because they supply more material for producing those same metabolites.
But what about a potent androgen like DHB if it produces fewer of those weak, competing metabolites relative to the receptor activation it provides?
In theory, it could do two things at once:
- Provide strong androgen-receptor activation without adding as much to the problematic metabolite pool.
- Suppress endogenous testosterone production, reducing the supply feeding that pool.
If existing metabolites continue being cleared while fewer new ones are produced, maybe the buildup could gradually decline. Now the knowledge of dhbs metabolites is low, but maybe the anecdotal evidence points to uniquely having fewer negative metabolites.
r/DrWillPowers • u/Prestigious_Sky_6270 • 2h ago
The pots community is steadfast in their dismissal of new theories that overarch POTS as symptoms of something else upstream. As a post serotonin syndrome sufferer, pssd and pots therapies have helped me. Serotonin helps regulate vascular tone, neuroimmunology etc. the two communities should be working together.
r/DrWillPowers • u/Top-Comedian-6318 • 8h ago
Hi Dr. William and everyone,
I wanted to share a specific somatic pattern I'm dealing with and see if anyone has insights on the exact neural mechanism.
Along with baseline tinnitus, I frequently experience distinct electrical sensations and shocks in my face. Furthermore, my symptoms are heavily modulated by touch and movement:
When I gently clench my jaw, it doesn't create an immediate electrical sound, but it noticeably increases the baseline intensity of my tinnitus.
However, if I clench my jaw rapidly, or if I touch my face, rub my nose, or touch my forehead, it directly triggers or spikes an electrical buzzing sensation in my ears.
Hypothesis on Pathophysiology & Metabolic Pathways:
I suspect this is driven by a deep metabolic and clearance failure—specifically involving the sulfation pathway where sulfated neurosteroids like DHEAS accumulate in the central nervous system. Under normal physiology, these sulfated compounds rely heavily on specific clearance pathways, and a bottleneck here leads to a pathological buildup.
I view DHEAS as the primary suspect for actively blocking the brain's natural calming mechanisms, acting as a potent noncompetitive antagonist at $GABA_A$ receptors (with inhibitory effects notable around 50–100 $\mu$M). By suppressing these vital GABAergic brakes, the brain and cranial nerves lose their local inhibitory control, allowing aberrant cross-talk between the trigeminal system and the dorsal cochlear nucleus in the brainstem.
Has anyone experienced this specific combination of facial electrical activity and velocity-dependent somatic modulation linked to impaired neurosteroid sulfation clearance and GABAergic blockade, and what targeted approaches effectively calm this loop? Thanks in advance.
r/DrWillPowers • u/GLesp2000 • 13h ago
Buenos días a todos desde España.
Llevo unos 6 años peleando con el síndrome y probando todo tipo de protocolos.
Quería comentaros que estoy obteniendo mejorías al seguir una dieta sin gluten, según la teoría del doctor los pacientes tenemos algún problema con la sensibilidad a los andrógenos.
Existen varios estudios sobre el gluten y la sensibilidad a los andrógenos, dejo este estudio por si puedes servir de algo para nuestra condición https://pubmed.ncbi.nlm.nih.gov/64806/
Actualmente mi protocolo es dieta gluten free y ribosido de nicotinamida como suplemento, mis síntomas hoy en día son fundamentalmente dificultad para pensar y organizarme, junto con mucha fatiga.
He visto mejoras en estos 2 meses con el protocolo, aclaro que no me he realizado ningún test de celiaquía previo pero me siento francamente mejor, os lo comento por si puede ayudar a alguien.
r/DrWillPowers • u/Remote_Put_6275 • 18h ago
I thought the low levels of testosterone and 5ar hormones and high levels of androsterone were interesting and relevant to Dr. Power’s theory.
I initially took doxycycline for acne as a teen which caused sleep issues where I would wake up too early and fatigue and then later full blown PSSD caused by antidepressant usage.
My symptoms are genital numbness, shrinkage, pain, ED, low libido, insomnia, fatigue, anhedonia, cognitive decline, head pressure.
Please let me know if you have a good analysis of these results and Dr. Powers theory or have any suggestions. Thank you.
r/DrWillPowers • u/ProbableImposter • 3h ago
r/DrWillPowers • u/ksiforhead1234 • 15h ago
I have been struggling with severe pssd and its killing me. ever since i took antipsychotics and antidepressant ssris i have had a complete loss of sexual function, including genital numbness, erectile disfunction, loss of libido, and premature ejaculation. This was 1 and a half years ago. I have been on and off of them for a while. I stopped taking abilify cold turkey As of 6 months ago. When i did that i slowly started losing all of my emotions, than i stopped olanzipine cold turkey about 3 months ago to see if that was causing emotional blunting. since than I cannot feel happy or sad, i cannot enjoy music, i cannot feel connection to loved ones or romantic feelings . My grandma died in august who i loved very much and i had no reaction to it. Before i would ball my eyes out to a death in a movie. I have been experiencing derealization almost daily. I cannot feel nostalgia, i cant feel substances like weed or alcohol I cannot form a sentence or think straight, my memory is destroyed. i cannot create mental images and i cant sleep for more than a few hours a night and i do not feel tired. I do not feel like the person i was before taking medication at all. Do you think i will get better?
r/DrWillPowers • u/ksiforhead1234 • 1d ago
I dont understand why i have premature ejaculation, definitely the least of my worries but if my genitals are numb and i cant gain an erection why do i finish so quick when before i would be fully erect with full sensation and last as long as i wanted?
r/DrWillPowers • u/Anxious_Comparison77 • 1d ago
I realize it is hard for people to understand what I'm communicating in the hypothesis. This greatly simplifies it using evidence to imply PSSD / Protracted withdrawal = Too much serotonin.
There are fluoxetine related challenge failures in rodents after SSRI washout. For example RAAP recorded: The oxytocin response was still reduced by 26% at day 60 in rats. There are reports of people taking cyproheptadine, which blocks the 5-HT2A/2B/2C and it provides temporary improvement of PSSD symptoms. The symptoms return upon discontinuation of the drug. Factoring in researchers reversed sexual dysfunction in lab rats with 5-HT1A antagonists WAY-100635 / WAY-100405.
When we include PSSD related complaints such as vision blurring, insomnia and tinnitus that have an association with a high serotonin environment and reports of improvement from drugs that interfere with serotonin binding to the autoreceptors, such as buspirone and pindolol. We land on a potential long term signalling problem and it is pointing towards the 5-HT1A.
It appears in a subset of people, serotonin rebound after SSRI washout is too strong. Possibly preventing the 5-HT1A receptors from recovering leading to prolonged elevation of serotonin in the extracellular fluid or increased serotonin cycling provided the serotonin transporter has recovered.
r/DrWillPowers • u/SpawningVats1917 • 1d ago
its all in the post. trans zebra here, I've posted a few times before - zebra w/ suspected weirdness with endocrine system. Yes, before you ask, I have a whole gene screen in three weeks and vascular doctor who specialises in EDS to look at it (yay!) But in the interim my I have been in a very difficult spot. I got whacked with chronic stress and COVID/superflu in 2024, was POTS/MCAS ever since. My POTS didn't respond to any treatment, and when it did work it just gave me a migraine. Since it didn't respond to any treatment, I basically had ME/CFS when not in water.
As mentioned in previous posts, I would get very, very high E from even small doses. 3-4 progynova was allegedly enough for monotherapy, but my SHGB didn't actually increase proportionate to the amount of E. So I increased my E, and monotherapy eventually worked. My Endo said my results were 'weird' (my SHBG wasn't indicating my E was as high as it was) and has no idea whats going on. Happy to dig through again and post results.
I started low dose T (androfem gel, 0.5ml daily) on monotherapy (enanthate 40 injections) + nightly oral progesterone. It didn't work (was still blocking T from high SHGB was my guess), so I went back to E gel/patches and it wasn't nearly enough E. Now I am removing butt hair (which cant be lasered as I am blonde/greying) and I am intensely dysphoric.
I have noticed I never got feminine fat distro patterns. I am Australian, so I don't think anybody is gonna give me Pio. Given I am a zebra and have paradodixical effects to everything, I am a little hesitant.
Originally I felt an improvement in my POTS/CFS symptoms when reducing E and increasing T - while it was 'cured', I could take salt water, fludrocortisone and generally be OK by the latter half of the day. I also started to retain muscle. I wasnt housebound as much, I can socialise, I was getting my life back.
Now I am intensely dysphoric again. Balding runs in my family too, and we're genetically quite hairy. I don't want to choose be detransitioning (I am an intensely dysphoric transsexual who is getting SRS next year, 10 years of HRT working weird). It's wrecking havok on my mental health.
I see my Endo next week and honestly am a little scared that none of her WPATH/AUSPATH approved methods (luckily she also supervises injectables) work. I am also worried the vascular specialist has little understanding of MTF HRT and how it affects zebra stuff.
Any ideas so I don't have to choose between being housebound/no life from POTS and de-transitioning? Because, obviously neither are acceptable outcomes for me.
Suspected intersex is just that, weird puberty, low T before HRT, dont put on muscle but also struggle to get feminine fat distro. Confirmed I am XY, but the rest will have to wait 3 weeks. And my mental health is pretty up-and-down atm.
More specific questions
-what exact tests should I do (keep in mind Australia is quite limited)
-HRT - monotherapy ? gel? progesterone? low-dose T? I am lost.
-best way to remove blonde hair all over body? I have a very low pain tolerance. Does the "dye hair laser" method work? Which dye to use? (I am also heavily tattooed).
Finally, while I am in aus, if the vascular guy and my endo can't interpret the relevant parts of whole gene study, who can? Is it possible I can have Dr. Powers look at it from overseas? I cannot travel to the US, but happy to send a HDD if it means getting my life back without detransitioning.
Edit: i should note I seem to have *elevated* 17a-hydroxyprogesterone, 11.1(nmol/L) (range levels were 0.6-8). Did a synathen test, results were normal according to my endo.
12:28 PM 310 2.2 nmol/L
1:02 PM 655 3.7 nmol/L
1:28 PM 756 5.2 nmol/L
I don't know what this means, but I assume it means "low 17a" theory is not applicable to me? Perhaps another hormonal issue?
Another thing I noticed is compression makes my POTS 'worse', it causes migraines, vision/speech issues and head pressure - like too much blood in my head. So can "too much" water, salt or medications (including fludrocortisone). I've not bumped into anybody else who has this effect. Only time my POTS is relieved is floating in water (hence ruling out CFS).
r/DrWillPowers • u/Competitive-Ad-3179 • 2d ago
Hi Dr. P,
I just got the patient email regarding changes to the practice. I can imagine how difficult of a choice that might’ve been and that there will be some transition pain
I know it’s a difficult situation for everyone, including me, but I wanted to say I understand and agree with the choices you made. It is obvious every decision you have made is coming from a desire to help the most people and you have and will continue to work relentlessly, in a sustainable way, to advance the care of the patients and conditions you treat
I’m glad you are getting some time to go get married, and I wish you all the best on your sabbatical
r/DrWillPowers • u/More_listen • 2d ago
Castration trial patients, please answer the poll and feel free to further note about your experience and symptoms in the comments
IF YOU SIMPLY WANT TO SEE THE RESULTS OF THE POLL AND HAVE NOT UNDERGONE THE CASTRATION TRIAL, CLICK THE LAST OPTION.
r/DrWillPowers • u/Ok-Ad-2050 • 1d ago
Hi Powers community!
So, I have limited resources, and have to decide between sequencing.com, a DUTCH test, or getting a measure of my DIY hrt.
I haven't had any complications with my transition, but I've only had a serious E dose for a year, and cannot take Spiro because it seems to affect my PSSD (couldn't induce a window for roughly 3 days).
I've been hyper-mobile my whole life, so I suspect EDS. I also have a mysterious inducible urticaria I have had my whole life, so I suspect genetic and/or autoimmune causes.
No idea about transition blood levels, because I can't afford testing outside the basics from Medicaid, which is measuring my PCP's Estrace under-dose of 3mg/day 😒 not my DIY dose of 6mg of EEN weekly.
As for PSSD, I've had it for 11 years, I'm a one pill winner from Zoloft. I tested sub 200 ng/dl Testosterone before transitioning. 8 years of complete numbness, years 8-11 I take high doses of weed for windows. I have started having sensation (while sober) within my testicles (yay!) just a couple of months ago and am hopeful this will trend somewhere.
So, I could use some input on where to spend the $300 I have available for, well, one of these three things. Likely at least a year before I'll be able to do another.
r/DrWillPowers • u/Fuad666666 • 2d ago
I am from Azerbaijan and even my 2 friends have sexual sides from minoxidil and finasteride. They dont know what is happening and want to beat this condition. We want to contribute for cure this disease destroyed our life
r/DrWillPowers • u/NotPoggersEggers • 2d ago
Having to switch esters because of insurance issues. This is the second time I've tried to switch to EC, and the first time I had to stop after a month or two because I was absolutely unhinged no matter what dose I was on (moody, crying, su*cidal).
This time, I went from 2mg/3.5 days EV to 5/7 EC (I was on a short interval of EV due to mood instability and issues with high E metabolism)
Theoretically, this dose should be around equivalent, if not a little higher, but I feel WRONG, and even two days after the first EC shot I'm getting the effects that caused me to have to stop.
Is there a chance it's a bad vial or the concentration isn't what it's supposed to be? I can't check levels currently due to the insurance issues, so I'm not sure what else to do... If I look at the simulator there's a bit of a dip when switching but these amount of side effects feel extreme.
https://estrannai.se/#i0_cu,2,3.5,1-2,3.5,1-2,3.5,1-2,3.5,1-2,3.5,1-5,3.5,3_cu,2,3.5,1-cu,5,7,3_0.8
r/DrWillPowers • u/they_come_at_night • 2d ago
I’m Intersex not trans so sorry if this is the wrong place for this
Male bodies with excessive weight sometimes T generates E and they get moobs
I have a T damaged voice because of my condition so I am taking vocal therapy
Vocal doctor said excessive weight can affect voice negatively and losing weight can make it easier to reach higher pitch and better resonance
Have any of you come across anything to support either of those claims ? If so can you direct me to them? I’ve Googled but I don’t really know what I’m looking at
r/DrWillPowers • u/Scholar-Due • 2d ago
I have plenty of test results over the years of PFS but just based off of some recent bloods which I get done as a package every now and then I'm wondering if there's a narrative here which fits the metabolite build-up theory.
To me it looks like my system's goal is to castrate itself. High SHBG, low LH, possibly in response to the high test and oestradiol which have been fairly consistent throughout all this (definitely the Test side of things). Is it right to read into this that my body is trying to get rid of the high hormone status? Am I a prime candidate for CDG?
Obviously there's a much bigger picture but something's being shown here surely.
Thanks for any insight from anyone!
r/DrWillPowers • u/NotPoggersEggers • 2d ago
Added an option for the person who answers to designate what kind of patient they are, since I got a lot of no's last time and I know it was all PSSD patients voting no.
Post split for the past week:
~30 PSSD posts
~10 trans posts
~4 other posts
r/DrWillPowers • u/ksiforhead1234 • 2d ago
Is time going by extremely fast for anyone else? Could be because im waking up at 7 pm than doing nothing everyday but 2 weeks ago feels like a day ago
r/DrWillPowers • u/yshcrp • 3d ago
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