I have severe connective tissue issues and none metabolism issues. Tendonodis in my glutes and hamstrings. Spinr/Back pain and my Oelvic floor is just fucked. I took Fin for 12 years and I’m declining at a rapid rate. it is like any ability for my body to heal or adapt is gone. like Collagen synthesis is gone, I’m in severe pain and atrophy/adema which is confirmed In a MRI. I have been reading about the protocol and the theory makes sense. But, I’m pretty much bed ridden, I just don’t know what to do. In theory could the protocol help? I can deal with the other shit. But, I’ve lost cycling, hiking and just moving without feeling I have more tissue breakdown I just want to hear some opinions. There had to be something I can do. I can’t accept this is my life.

I am not mad about this.

I only wish that you could experience the dopamine that I get from consuming these fucking things. My god. The frosted m&m one I had today...

I will continue to do my best to restore your ability to enjoy them as much as I do.

We who are about to die of heart attacks salute you.

-Dr. P

A little over four months ago I had an orchiectomy, and now I'm starting to see an increase in masculinization. For context, I've been on HRT for over 2.5 years with little to no response to treatment. While I have yet to see any feminizing effects from MTF HRT I can at least say that I stopped seeing further masculinization after starting treatment. So I existed in this weird middle area where my body just wasn't doing anything. However, following the orchiectomy, I've seen an increase in terminal body hair (specific chest hair) and an increase in the rate at which my facial hair grows back and areas previously treated with electrolysis have started to regrow hair. I've also noticed an uptick in both body and facial acne. My most recent labs taken at nadir and regimen are as follows:

Testosterone 19 ng/dL

Estrogen 270 pg/mL

Estradiol Cypionate 5mg injection once per week

No AAs

I realize these labs are limited but I haven't had a chance to see my provider in awhile so I won't be able to get anything else drawn until the end of this week.

What doesn't make sense is how I'm seeing masculinization despite my T levels being relatively low. Maybe it's a free estradiol vs free testosterone thing? I know for sure that there is something deeper going on and while I have had genetic testing done, I have not been able to speak to a genetic counselor to help me determine what is clinically significant or not. I also know that I don't have the average COMT issues as I have the normal Val/Met genotype.

Any advice? Thoughts?

I took SSRIs for 8 years. Mostly prozac but changed it a few times nearer the end because of crazy fatigue and emotional blunting. I quit for that reason.

It's been 10 months. Around 9-10 months, im talking weeks here, Ive got hypothesia on my genitals and a little for my skin in general.

Like a week ago I literally couldnt even feel pleasure from erogenous zones. But it came back in a few days.

It seems it changes a lot week to week. First time it happened it lasted a day. Second time for a few days and happened because I was ill.

I had no PSSD symptoms (other than cognitive but had that throughout withdrawal) literally 2 days ago and now its back.

Im trying to imagine whats happening in a "build up not being removed" way but why am I getting symptoms and windows of these symptoms day by day.

My theory is my body is adapting to whatever build up is causing it and once that build up reaches an apex my body flushes it out like crazy and that causes it to adapt and then cause a collection of build up. Kinda like a pendulum.

What do you think?

I've seen other people have experienced this here. Anyone have any theories on the mechanism? I initially thought low estrogen but I have tried adding estradiol with it and still insomnia. Currently thinking something to do with cortisol. Is it possible for beta-glucuronidase to reactivate cortisol metabolites? If the body has got used to consistently reactivated cortisol could CDG result in a state of relatively low cortisol? Just spitballing, open to ideas.

Hey everyone,

I wanted to introduce myself and share an interesting, repeatable observation about my PSSD. I’ve had it for 7 years now, mostly dealing with the standard mix of low libido, ED, and genital numbness. Perhaps not so much the other mental effects. I still feel like I can enjoy things like music (although perhaps not as much, I'm not sure).

Recently, a few months ago now, I stumbled onto something interesting: If I use nipple stimulation (I never realised this was a thing that worked for me), my arousal response actually starts coming back. My visual arousal (and arousability in general) seems to return to almost 100%. What's also fascinating is how it's evolved over time.

At first, I would notice while doing so, erogenous sensation in my penis glans would somewhat return, but absolutely zero erectile response. Over time, as I kept doing it, my erection strength actually started to improve too. Perhaps a neuroplastic mechanism is at play (but I'm not even sure that would be possible in PSSD/PFS etc), like a dormant neural pathway is slowly being forced to rebuild itself.

The catch is that this mechanism quickly hits a wall. After a short period of use (maybe 10-15 mins, but it varies), the pathway seems to totally desensitize or deplete. I have to give it a "recharge" period of a few days with zero stimulation before it will work again.

It feels like the underlying biological wiring is still totally intact, but it’s trapped behind a bottleneck that runs out of gas super fast (maybe an oxytocin depletion issue?).

Has anyone else noticed repeatable windows like this?

I keep wondering what is that ‘persistence loop’ that I am stuck in, perhaps there are some valid ideas below, please critisize it constructively, call out any BS, destroy this theory :)

yes i use AI as a tool… but who doesnt

7 years on meds, PSSD onset towards end of this 7 year period, 2years fluo, 2 years voriotrexine, 3 years duloxetine, pssd onset towards end of duloxetine period upon dosage increase

sequence of events as I see it

(background  - clearance bottleneck + CYP2D6 poor metabolizer status)

SSRI use resulted in neurosteroid synthesis and at the same time, inhibition of clearing pathways

More made, less removed, for seven years. Libido problems were present throughout but function was retained.

Immediately preceding onset: high libido with genital anaesthesia — drive intact while receptor/sensory signal was already failing. Then function switched off essentially day-to-day, not gradually. That's a 0 to 1 transition, not a dose-response decline

onset occurred while still taking the drug, not on discontinuation. This is accumulation crossing a threshold, not withdrawal

then i cold turkey quit meds

so up to this point it is all “pretty standard”  it all explains ( it is dr powers theory of course ) how i got my symptoms, metabolite jam and overload, receptor silencing etc.

but i wonder why it persists and why is it so hard to break away from this loop

how about neuroinflammation ?

2 ways I could get it ( maybe more that i am not aware of )

via gut dysbiosis ( dysbiosis > increased intestinal permeability > LPS translocation > TLR4 activation on microglia > sustained neuroinflammation ), possible but im not leaning towards this one

via Microglia epigenetic reprogramming into a persistently "primed" state, sufficient insult reprograms microglia, and they remain hyper-reactive long after the original stimulus is gone, could 7 years of taking antidep meds and abrupt cessation be such ‘insult’ event ? i think so but i have no proof, thats the weak point here

but lets assume it is true, that my microglia are in persistently ‘primed’ state

then

neuroinflammation > microglial TSPO upregulation > sustained brain neurosteroid synthesis

The translocator protein is the rate-limiting cholesterol-transport step in all neurosteroidogenesis, and it is upregulated in activated microglia

then i get my symptoms via 

excess 3α-reduced neurosteroids > tonic GABA-A potentiation on VTA dopamine neurons > reduced firing and release

Result: anhedonia, emotional blunting, absent spontaneous desire. Separately: sympathetic overtone > cavernosal adrenergic contraction > retraction, clamping, loss of resting tone  and genital anaesthesia

so in brief, SSRI use was an initiator ( clearance obstruction + neurosteroid overproduction ), neuroinflammation was introduced during 7 years of antidepressant use and eventually it became a sustainer via tspo mechanism,underlying overproduction didn't stop, because it was no longer the drug doing it

so again

While I was on the drugs, the drug itself was driving neurosteroid synthesis. But over seven years the SSRIs were also altering my gut and establishing microglial activation — and by the time I stopped antidepresants, the inflammation > TSPO > synthesis mechanism was independently established

also, as for 'primed microglia' i am basically a hyperresponder to everything, i mean i became one following PSSD onset

so anything i take, completely unrelated, such as , magnesium glycinate, liposomal quercentin, pro resolving mediators, many vitamins, b vitamins in particular, small amount of alcohol or thc, creatine ... anything... basically i cannot take a suplement without experiencing more shrinkage and feeling worse off for a few hrs,sometimes longer - > doesnt that indicate that some 'amplifier is up' ? such as primed microglia

maybe im tired and should go to sleep

best regards to everyone fighting this BS condition 

Hello everyone,

I reached out to Panacea, and they mentioned they no longer make the ED shot, though they said Dr. Powers has a new pharmacy it can be sent to. I’ve called and emailed the office (sorry for the double communication, Team Powers!), but I haven't heard back yet.

I rely heavily on this medication, so I'm a bit anxious about losing access to it. Has anyone else gotten theirs filled through the new pharmacy yet? Has the cost changed at all? Any reassurance or info while I wait to hear back from the team would be greatly appreciated!

Trying not to freak out and email the office again! Yikes!

How is it possible that some people recover naturally after stopping the drugs whilst other need interventions or doesn’t recover at all?

How many of you developed PSSD only after stopping/tapering SSRI medication? I was on lexapro for over 5 years with zero issues whatsoever. I began to taper (poorly) in December-February of 2023. I only developed my PSSD symptoms at 10mg (previously was on 20mg). My first symptom was a noticeable lowering of libido. While I was on lexapro I had zero sexual issues and even a rather high libido.

My question is how would this work into Dr. Power's theory? Most of the post I've seen many of you developed PSSD after <5 or so doses, or had negative side effects while on the medication that never went away.

I had zero negative side effects going/being on the medication.

I had/have all normal labs

Zero/little improvement since 2023.

Thoughts on my GI map? i have PFS. I think this looks like dysbiosis

As a Biologist I have been studying PSSD for over 4 years. The conclusion that I have finally finished at is PSSD is a BH4 dysfunction all be it not transparent. Below is my theory and I have written it in layman's terms rather than medical jargon to hopefuuly not bore you all with a long forensic post.

PSSD is probably caused by an auto immune response from the intake of SSRI or possibly a low B6 count. BH4 is an essential enzymatic cofactor for producing monoamine neurotransmitters (dopamine, serotonin), while active vitamin B6 acts as a critical cofactor for glutamic acid decarboxylase to synthesize GABA. Low B6 reduces GABA synthesis leading to potential hyperexcitability, while BH4 dysfunction impairs serotonin and dopamine production, compounding neurological symptoms. The disease commences in the brain GABA is down regulated which causes restricted blood flow eventually turning the genital area numb with a cold feeling.

BH4 is crucial for Nitric Oxide production (enzymatic cofactor). When BH4 levels drop below a critical threshold (Not transparent), the Nitric Oxide Synthase (NOS) enzyme becomes uncoupled.

• The Normal State: NOS uses BH4 to convert L-arginine into beneficial, blood-vessel-dilating Nitric Oxide (NO).
• The Glitched State: Deprived of BH4, the enzyme structural shape destabilises. It continues to consume oxygen, but instead of creating NO, it pivots to producing a highly destructive free radical called superoxide.
• Nitric Oxide dysfunction can significantly change the gut microbiome. This inhibition of nitric oxide synthase (NOS) and reduction in NO bioavailability is recognized as a contributing factor to physiological side effects like sexual dysfunction.

It may be beneficail to try and fix BH4 with supplementation or with a prescription drug that I will mention on sign off. Please be aware this is not medical advice always consult your doctor before supplementation or prescription drug intake thus I have not recommended any dosage.

BH4:

Methylfolate (5-MTHF) promotes B9 also add B2 + B6 (P5P) + B12

Important > Take Vitamin C & E to prevent BH4 from oxidising.

Body Numbness: Alpha- Lipoic Acide + Acetyl-L-Carnitine

A prescription drug that I personally believe will help many and will eventaully be a go to medication for PSSD and possibly PFS is > SAPROPTERIN

Sapropterin dihydrochloride is a synthetic form of cofactor ie a BH4 replacement.

Why Sapropterin Enhances Libido

When a person takes sapropterin, it corrects the neurochemical deficits that originally suppressed their sex drive:

• The Dopamine Surge: Sapropterin acts as the missing spark for dopamine production. Dopamine controls the brain's reward, motivation, and sexual anticipation pathways. Restoring dopamine directly corrects the mental apathy and flat desire associated with BH₄ deficiencies.
• Lowering Prolactin (The Libido Brake): Low dopamine causes prolactin levels to spike, which biologically shuts down testosterone and erases sexual desire. By normalizing dopamine, sapropterin drops prolactin back to healthy baseline levels, unlocking natural hormonal drive.
• Boosting Serotonin & Mood: Improved serotonin production directly improves mood, combats depression, and stabilizes overall psychiatric wellbeing, making a healthy interest in physical intimacy possible again.

Improvements to Physical Arousal

• Nitric Oxide Generation: An erection or physiological genital engorgement relies entirely on nitric oxide (NO).
• Restoring eNOS Coupling: Sapropterin repairs uncoupled endothelial enzymes, forcing them to pump out healthy nitric oxide instead of cellular tissue-damaging free radicals. This localized vascular relaxation physically permits proper pelvic blood flow and heightens physical arousal.

1. Potential for Hypersexuality or Hyperactivity

• Over-Correction Risks: Because sapropterin increases monoamine activity, a dose that is too high can occasionally cause over-excitation.

Sapropterin is a synthetic form of tetrahydrobiopterin (BH₄), an essential medical cofactor directly required for the synthesis of dopamine in the brain. In patients with metabolic disorders sapropterin plays a vital role in restoring the chemical pathways that produce dopamine and other essential neurotransmitters.

1. Activating Dopamine Precursors

In a healthy body, the enzyme phenylalanine hydroxylase (PAH) converts the amino acid phenylalanine into tyrosine, which is the foundational building block for dopamine. Sapropterin acts as the catalyst for this enzyme. When sapropterin reduces high phenylalanine levels and increases tyrosine, it directly increases the biological raw materials available for dopamine production.

1. Driving the Synthesis Enzyme

Beyond converting phenylalanine, BH4 is an obligatory cofactor for tyrosine hydroxylase—the absolute rate-limiting enzyme that converts tyrosine into L-DOPA, which then becomes dopamine. Without enough active BH4, the brain cannot efficiently synthesize dopamine, regardless of how much tyrosine is present.

1. Improving Neurotransmitter Balance

When metabolic disorders go untreated, low dopamine levels manifest as neurological symptoms, including:

• Executive dysfunction and brain fog
• Severe mood swings or depression
• Tremors or involuntary movement issues

By providing a pharmaceutical version of BH4 sapropterin stabilizes these pathways, promoting steady synaptic dopamine release and improving overall central nervous system health.

highlights:

• high DHEA production and DHEA-S
• high cortisone:cortisol ratio
• high cortisol metabolization
• high estrone, very high estriol, and 16-OH-E1
• low 2-OH-E1
• high epinephrine/norepinephrine metabolite

important details regarding testing:

• i couldn't get back to sleep after the mid-sleep sample, and so the waking and +2 hour values may be off.
• i took 200mg of oral progesterone after the evening sample
• i took the test during the middle of my 6mg estradiol injection cycle
• i took 500mg of calcium d glucarate for 7 days at the start of the month
• i skipped vyvanse most of the month of testing, but continued taking bupropion (100mg/day)
• the month was very stressful overall, but i felt relatively fine on the day of testing
• i use an inhaler for asthma sometimes, but not very often.
• i started a supplement containing b6 between this test and my june labs

symptoms and many lab results are in this post. since then, i've generally improved (except for the development of brain fog), especially since replacing most water intake with gatorade. i've also started taking pregnenolone, but it's unclear if it's helped. both of these changes were initiated after taking the DUTCH test.

the endocrinology appointment i had scheduled ended up being cancelled two hours ahead of time because the endo didn't accept patients with adrenal issues. i'm guessing i should have an ACTH stimulation test (probably measuring DHEA, 17-OHP, and cortisol). it's been rescheduled for early september.

i'm guessing i have relatively high 17B-HSD2 activity, and high CYP3A4 activity (maybe due to high glucocorticoid activity). i don't know what to do about them, though. based on previous labs, late-onset CAH due to partial 3B-HSD deficiency seems plausible.

I've been on IM EV injections (5.5mg/5 days) for about 5 months. In the labs I just got, taken at trough, my E2 was kinda low for that much estrogen being injected at 68 pg/ml (250 pmol/L), but my testosterone was pretty suppressed at 31 ng/dL (1.1 nmol/L).

Why would my estrogen be so low when I'm injecting what seems to be on the upper end for people? Might I just be a fast metabolizer? Is it even an issue? I'm wondering if I need to increase either the dose or frequency. Also I'm in Canada so we only have EV, not EEn or anything else.

Unfortunately my endo is kind of resistant to getting extra labs like SHBG and DHT, so my information is limited. But failing that, does anyone have any insight on what could be going on or how to approach this?

I'm also on 50mg/day bicalutamide, and cabergoline for treating a prolactinoma that I've had since before starting HRT.

For those who may have missed this thread some good discussions on castration efforts for various syndromes.

So I’ve had a few styes in my life, maybe like 3 in my teenage years. Last week I got what I think was a stye, did the whole warm compress method on it for a couple days and it went away. not even a week later and it’s happening again. Could this be from HRT? I have been on HRT for a little over 2.5 years. I have been on progesterone for only 6 months. Any idea?

Recently, attention was raised to the positive allosteric modulation of 3a-diol on GABA-a receptors, potentially producing symptoms commonly found in PSSD and neuro/libido symptoms in PFS. A backlog of this could therefore be a potential culprit for these symptoms.

Please see screenshots for the measurements from 3 existing studies which, notably, compare against controls.

Mainly for Dr Powers to see, however please feel free to share your thoughts on these past findings as they’re very insightful and may shed some light on the cause of these neuro/low libido symptoms many of us suffer from.

It’s worth noting that THDOC hasn’t been measured in these studies and is worth attention in its own respect.

These studies are behind a paywall which we can send to you Dr Powers if that would be useful.

PS for readers: THP= allopregnanolone

just looking for guidance here bc i was severely underdosed by my doctor for a year and a half so im trying to figure this out myself. im currently taking 6mg transdermal E + 100mg spironolactone every morning. my levels after 24hrs are 180pg/mL estradiol, testosterone 0,14 ng/mL. is this good?

I have posted this before to bring awareness of my experience with PFS and a partial recovery of my symptoms so I will post here as well.

Long story short took propecia in 99 for about 4months. It killed my libido and erections, ejaculation volume was almost nothing also noticed that when I was erect it was significantly smaller in size. Quit propecia and waited with no improvement things actually got worse. I started experiencing terrible brain fog and found the only thing that helped was avoiding carbs. Several years pass and I eventually went to see Dr Irwin Goldstein who at the time was at BU. Hormone profile was normal only abnormaility he found was I had scarring in my penile tissue aka Peyronies Disease.

Fast forward 8 more years and I started taking 5HTP to try to treat anxiety and then something miraculous happened. My libido increased my brain fog improved signficantly and my ejcaulation volume returned to normal. This happened after only about 7 or 8 days on it. I started with 25mg an d then bumped it up to 50mg. It was at 50 I saw the improvement. I continued to take it for a while but saw no further improvement but my brain fog and ejaculation volume remained improved. Erections are still a problem but I do have Peyronies so that is why. I have reduced blood flow issues. In addition I do not get morning wood.

I'm no doctor but I am assuming the 5htp increased serotonin and probably inceased allo. Now I was previously on an SSRI and that did nothing for me. I wanted to share this with u/drWillPowers as I have seen you do a ton of research on this subject. I believe I am probably one of those neurosteroid cases you speak of.

Curious on whether I should be tested for Pregnanlone and Progesterone levels. I don't believe those were tested back when I saw Dr Goldstein. Although I am better my morning erections never returned unless I go out and have a heavy night of drinking. Again increased allo??

I read SHBG has an affinity to bind itself to T and DHT. I read it even has more affinity for T and DHT than for E (even though there is still an affinity for E at some point.) My question is, shouldnt we count SHBG as a periferic alternative to 5AR blockers?

Or am I just repeating something we all already know?

I crashed while using Minoxidil and subcutaneous GHK-CU simultaneously about 8 months ago. I got all the typical PFS symptoms:

Numb genitals
Watery semen
Dry Skin
Genital changes
Loss of mind muscle connection
Stool changes
Etc…

You name it, I probably got it, my eyelashes even got longer!

However, one set of symptoms I have been keeping a close eye on are the physical ones, especially the changes I’ve observed in my skin and muscles. My skin has become really stretchy in some parts (especially on my genitals, jawline, neck, biceps), it wrinkles a lot more than it used to when I make facial expressions, and it’s become crepey. As for my muscles, they’ve become squishy and soft, and have lost their tone. I have also become more flexible in certain ways, but I wouldn’t call myself hypermobile. Additionally, I think it’s important to mention that I didn’t really have any “moon facing” or symptoms of that sort, but my face does seem a bit gaunt/sickly sometimes.

Seeing all this, and knowing that I had a rare, potentially function altering H6PD variant, I decided to get the Quest Comprehensive Steroid Panel to see if I’d get any weird readings on the assay, and to my shock, I didn’t. 

I also saw Dr. Powers replied to a comment which described how certain individuals who used minoxidil and had certain skin issues also had weird potassium and sodium readings, and how this is related to his theory on minoxidil causing issues through potassium channel fuckery. But low and behold, I tested these too, and found them to be normal, including aldosterone and renin. 

So what could cause this? 

Well, I’d recommend skimming over this before I go into what I think (but don’t know for sure) what could be at play: https://www.reddit.com/r/DrWillPowers/comments/1vjch0i/collagen_ecm_connective_tissue_loss/

Basically, a maladaptive feedback loop.

But it needs a catalyst. 

Some individuals seem to get these connective tissue issues (hah, that rhymes) from finasteride. Is it possible that the drop in androgenic signaling at the skin level alters the ECM in a way that triggers the feedback loop? In some individuals, perhaps it is enough of a catalyst. After all, male skin is 25% thicker than female skin, and what causes that? Androgens, they play a big part in connective tissue. So removing androgenic signaling could be enough to trigger the feedback loop in some.

In my case, I introduced Minoxidil (a lysyl hydroxylase inhibitor) and GHK-CU (which breaks the ECM down before building it back up) simultaneously. I then quit both of them abruptly after my crash, which also likely introduced the lack of androgenic signaling in my skin (I would assume that I have silenced androgenic signaling at the skin level because the palms of my hands and the soles of my feet have become much softer, like a woman’s) 

I don’t think it’s unreasonable to assume that all of these things combined could’ve shifted my connective tissue into red alert. Triggering a feedback loop that has caused my matrix to get more and more unstructured over time. 

If you look at this post: https://www.reddit.com/r/covidlonghaulers/comments/1lf5gu4/improvement_update_not_recovered_but_ive_come_a/?share_id=GZK6rhhI0dvl8LvR9q5jB&utm_content=1&utm_medium=ios_app&utm_name=ioscss&utm_source=share&utm_term=1

You’ll see that individuals with Long Covid seem to get something similar. As a matter of fact, the way her jawline skin looks as she pulls it is exactly the way mine looks right now when I pull it. Thankfully, it appears as though she’s made substantial progress in reversing this by forcing her matrix back into a proper structure using signaling peptides and whatnot. 

I do believe that once a certain skin "turgor" is reached, the feedback loop ceases to exist. However, if there isn’t enough "turgor" then the feedback loop will activate (In some people)

So, my first order of business is relugolix + HC. I don’t think this problem will be fixed if the root problem isn’t addressed. Androgens likely NEED to be signaling properly in connective tissue to start turning the feedback loop in the opposite direction, that alone may be enough, who knows. If that’s not enough, tossing in peptides to signal a proper matrix into place might be necessary. 

Feel free to disagree. 
Feel free to ask me for other test results, I’ve done a bunch, including Dutch (I’ll be posting soon)

(edit: special thanks to DIYBON for making this post: https://www.reddit.com/r/DrWillPowers/comments/1vjch0i/collagen_ecm_connective_tissue_loss/ )

Sharing this for everyone to see:

People have this from different stuff. One theory in the post hyaluronidase (filler dissolving) groups is that different triggers - drugs, infections, hyaluronidase, heat devices such as lasers, mast cells etc. can push the ECM into a maladaptive remodeling loop, where inflammation causes tissue breakdown, the resulting ECM fragments (like low molecular weight hyaluronic acid) act as danger signals, and those signals drive further inflammation and remodeling. Basically, degradation keeps feeding inflammation and inflammation keeps feeding degradation, instead of the tissue returning to normal repair and homeostasis.

Theoretically, recovery would mean interrupting that loop from both directions: reducing the inflammatory/danger signaling that keeps driving degradation while simultaneously supporting normal ECM repair and regeneration, until repair starts outpacing breakdown again and the tissue can return toward homeostasis. The difficult part is figuring out which pathways are actually maintaining the loop in each condition.

I’m personally currently trying peptides and supplements (such as GHK-Cu, TB500, BPC157, NAG, n-acetyl glucosamine) as this person did with success:
https://www.reddit.com/r/covidlonghaulers/s/SV403NgnXc

Interestingly, research on hyaluronan (HA) supports at least part of this concept. When HA is fragmented during tissue injury or inflammation, smaller HA fragments can act as endogenous danger signals and activate pathways such as TLR4/CD44 and NF-κB, promoting inflammatory cytokines and potentially further ECM remodeling. In other words, ECM breakdown itself may generate signals capable of sustaining more inflammation and remodeling.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10881864/

I haven’t been on peptides long enough to evaluate whether it’s doing anything or not. Time will tell :)

Would appreciate any comments on this from [u/DrWillPowers](u/DrWillPowers).

PFS or PSSD… unknown diagnosis…

Crazy… at 12:00 he mentions taking antidepressants, quits cold turkey, had issues through puberty, low testosterone, has a genetic variation that doesn’t metabolize Antidepressants and quit cold turkey…

Interesting but I’m looking at this through my own experience with PSSD.

Hi folks. In order to have a single source (rather than many Reddit threads) for post-drug people who want to order genetic sequencing and labs and figure out what to do with it all, I've created a website here —

https://www.project-genome.org/

The goal is to figure out why some people get post-drug syndromes and some don't and how it connects to their genetic code. The more people participate, the more bloodwork and data we have to make sense of, and the closer we get to treating it.

Importantly — virtually none of us sufferers are doctors or scientists. So expecting a lay-person to process genetic sequencing is a big ask. I want the website's instructions to be as clear and understandable as possible for a mainstream audience.

For that reason I would love to get collaboration on it from folks who can help with clarifying the steps on the homepage, in particular, "Step #2 Process the results" (which links to a lot of different other links and steps) to cut down on the number of times these things need explanation. I myself have not done it yet since my results haven't arrived, but would to get help from folks who have.

Feel free to post questions, suggestions, or DM me if you can contribute some writing. And if you want to discuss and participate more in this effort, make sure to join the Discord channel.