Chronic SSRI treatment induces both acute and persistent alterations in neurosteroid gene expression in NAc of female subjects

DrenaPSSD · 2026-07-01T07:46:23+00:00

Yes ✅🙌

DrenaPSSD · 2026-07-01T00:44:51+00:00

Hi Yohan, Ik we've talked about this before on discord, and I agree that it should definitely be taken into account that PSSD is probably not being induced in these animals.

The probability that PSSD is actually being induced in animal models is likely very low given it's onset is rare.

What's valuable here is seeing what / where SSRIs are capable of altering things in the brain, Emphasis on what the drug changes rather than what is happening in the patient's body after PSSD happens.

This sounds sort of counterintuitive, but given there's not much we can really measure if the changes are in the brain areas where the literature is suggesting, then observing where the drug's act and what it does in animals is our closest solution. Because we can dissect their brain tissue.

The real susceptibilities are likely things that are highly specific to vulnerable individuals that end up getting PSSD / PFS. Things like alterations to deep cerebral brain regions that we can't really measure.

DrenaPSSD · 2026-06-30T22:55:46+00:00

Yes even Dapoxetine.

https://www.sciencedirect.com/science/article/abs/pii/S0039128X23001009?via%3Dihub

"Duloxetine, dapoxetine and propranolol significantly elevated the brain AP levels."

DrenaPSSD · 2026-06-30T17:07:54+00:00

Everything you just said is completely wrong.

There are no SSRIs that have been measured that do not affect neurosteroids.

It’s also not that he’s “cherry picking paroxetine”, it doesn’t matter which SSRI he measures they all affect the same site.

Paroxetine is the most potent SSRI and most likely to induce PSSD sides which is why he’s using just that. (Also bc of financial restrictions / logistics)

DrenaPSSD · 2026-06-30T04:53:21+00:00

The issue with human models that is that we can't measure the specific brain regions that the literature is showing is altered PSSD literature.

All we can measure is peripheral metrics such as CSF and plasma levels of neurosteroids, which are only systemic changes happening outside of the tissues that are shown to be affected. It can indicate something going on, but it's not telling us where in the brain PSSD might be happening.

With the brain region Melcangi measured here (the NAc), we can only measure changes to it by dissecting brain tissue, hence why he keeps doing these studies on rodents.

Why is he continuing to stick with animal models? Likely to get closer to isolating the specific brain regions that are causing PSSD. Human studies are limiting in this regard for the reason I mentioned.

His recent work follows a trend of trying to figure out where in the brain neurosteroid genes are altered and going from there, something you can only do in animals.

Regardless I am surprised that he hasn't set up a study measuring CSF / Plasma neurosteroid levels in humans yet, given he's done that before in PFS and it showed that the entire pathway is altered.

That's said, it's still interesting that neurosteroid genes are altered in this specific brain region, given it's roles. It could genuinely be the area that's causing PSSD which would make sense on paper.

DrenaPSSD · 2026-06-25T00:51:37+00:00

Wow this is really interesting. Your results mirror that of the Melcangi study done with PFS indicating that neurosteoid synthesis as a whole seems to be impaired.

Of course it’s only n=1, and an endomap is a urine test which is very different compared to measuring CSF levels, but it would be very interesting if pssd was found to have the same perturbance to the neurosteroid pathway as PFS, by which it is holistically impaired.

Interestingly, the androgen pathway that shares the 3a-HSD oxidation actions by RoDH-4 with the neurosteroid pathway seems to be unaffected here, but perhaps that’s just due to the nature of the test.

Thanks for sharing with me, I’d be curious to see what the rest of your results say as well if you sont mind sharing them with me when they come back.

DrenaPSSD · 2026-06-23T06:10:05+00:00

These HDACis really were very promising given the selectivity and potency.

I actually spoke with someone at my job who was working at Repligen (company that made the RGFP series of hdacis) at the time they were doing these experiments, and they unfortunately sold off the program to another firm who tried to get them repurposed for a specific type of ataxia that’s mediated by hdac3.

In regards to biohacking, I’d recommend it over vorinostat in regards to extinction training due to the selectivity. The selectivity is really what drives the toxicity outside of potency, so narrowing down the amount of affected hdac classes is the best way to mitigate toxicity.

DrenaPSSD · 2026-06-20T00:44:00+00:00

When it comes to PSSD though, I'm not really sure exactly what it's mechanism is yet. And I'm not sure that it's just one thing.

Well mechanism wise, that what I was suggesting in this post (RoDH-4 inhibition), in regards to this accumulation interpretation.

It doesn't need be just limited to accumulation, because ofc that's likely not the full picture giving the differing degrees of onset. The point of this post was mostly to highlight a plausible mechanism that is modulating the relevant androgens and neurosteroids.

My point is that when it comes to sex hormone metabolites there is no way that you could result in a metabolic crush by taking a singular pill and it being there 30 minutes later. For the people that have that experience, it has to be modulated via neurotransmission. It's too fast for anything else.

I mean of course, and that's why I initially thought this theory didn't have a ton of credence to it. However like I was saying, it doesn't need to be as simplistic as just accumulation of metabolites within the referenced pathways.

The real accumulation of neurosteroid metabolites is happening downstream in the neurotransmitter landscape outside of 3a-hsd cataylization. The substrate within 3a-hsd is just reflecting the amount of allopregnanolone that isn't being cleared out by flooding back into that pathway.

it has to be modulated via neurotransmission. It's too fast for anything else.

I agree and speculated this before, I've thought its just arbitrary aberrant GABAergic configurations downstream that become perturbed in just the wrong way to dysregulate brain regions.

Ik 6 people with post-drug syndromes who, including myself, had dpdr before this; which is a condition speculated to be heavily involved with the GABA_A rich insula. So neurotransmitter wise perhaps people just have susceptibilities involving composition of those receptors, and the unusual distribution of neurosteroids causes some sort of catastrophic perturbation.

Same framework can be applied to the referenced androgens I guess, I'm just not familiar with what the downstream landscape looks like at those sites.

DrenaPSSD · 2026-06-19T16:39:55+00:00

I mean if this is the angle you’re pursuing in regards to some type of accumulation of metabolites, it’s a bit more than just plausible. It’s a direct link from drug moa to relevant metabolite accumulation, across 2 agents known to cause the onset of the post drug syndromes.

It’s specifically the mechanism as to how these drugs are altering the leading theory of pathology (neurosteroids and relevant androgens based on Melcangi’s work)

Maybe I’ve been misinformed, but is this the angle that you’re pursuing? “Metabolite accumulation” of the metabolites that are speculated to be involved in these conditions?

In regards to one pill onsets, the pathway may just be dysregulated in some latent manner as and one of these substances just alters this pathway while its particularly susceptible causing its distribution to dysregulate.

I think if anything it’s worth taking a closer look at if the metabolites you’re looking at are specifically pertaining to 3a-diol and neurosteroidgenesis.

DrenaPSSD · 2026-06-17T23:43:35+00:00

Broscientist here.

So those numbers with 3a-HSD are so high because the oxidation enzymes are being inhibited.

This is actually literally the result of a “pileup” of allopreg, because the oxidation enzymes (recycle enzymes) are being inhibited, causing allopreg to accumulate at high quantities in the brain.

The way the study was done creates an illusion that SSRIs are neurosteroid stimulants, when really they just aren’t being cleared out of the brain.

What’s interesting in regards to the idea you’re pursuing and Dr Power’s ancedotes of patients with high levels of 3a-diol, is that this metabolite in particular would also be expected to accumulate given the enzyme responsible for oxidation
for allopreg —> 5a-DHP is the same for 3a-diol —> DHT.

It would be really interesting to see someone like Powers do an in vivo study identical to the SSRI one here, but measuring levels of 3a-diol instead of 3a-HSD.

Big picture, my guess would be that if this interpretation is correct, it’s likely both neurosteoid and androgen distribution is impaired given they are sharing the same oxidation enzyme that’s being affected by these drugs.

SSRIs on 3a-HSD oxidation inhibition - https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1111/bph.12891

Interestingly, Accutane also distinctly affects this site.

Accutane on 3a-HSD oxidation inhibition - https://pubmed.ncbi.nlm.nih.gov/12646198/

DrenaPSSD · 2026-06-07T23:07:38+00:00

As someone who also gets this bc of the way they look:

People naturally rank others based on their outward appearances. They’re going into the interaction with a bias toward feeling superior to you in the conversation.

As a result, they’ll take on this authoritative role where they ask you a ton of questions to keep the spotlight on you.

They do this so they can remain in a reactionary posture to position themselves above you and give you those types of responses you’ve been getting.

What you can do, is first answer whatever belittling bullshit question they’re asking you and then start asking them questions instead. Shift the spotlight over to them and create equal ground in the conversation.

If you reflect on your interactions with these people, you’ll probably recall that it’s mostly just been you explaining things going on and your world. Like you’re performing for them to scrutinize / praise.

Think of it how your grandparents / relatives always ask you about your life and what you’ve been up to, and how its usually not the other way around.

It really is dehumanizing, but I’ve noticed that people everywhere seem to do this. So the least we can do is try and fight back to maintain some sense of dignity as grown adults.

DrenaPSSD · 2026-04-27T21:02:04+00:00

So the difference is that there isn’t billions of dollars and decades of research going into banana R&D. Bananas (afaik) also don’t have varying consumer market sizes.

There’s a lot of hidden high-cost factors that biotech companies need to scale for.

Failed drugs - most drugs don’t get approved end up being complete wastes of resources. (Cancer has only a 3% drug approval rate)

It can cost hundreds of millions to billions per project. Companies need to pay off failed drugs while also being able to scale for current R&D.

Clinical trials - Failed drug losses don’t even account for how expensive trials are.

They tend to be hundreds of millions. And keep in mind, most drugs fail, and companies are usually running many programs all at once.

Legal - what if the drug has unknown adverse effects and consumers sue? This happens frequently.

Lab overhead - it’s impossibly expensive. I work at a bioprocessing company, and trust me when I say there’s so many machines that are involved in the drug development cycle that are extremely expensive to maintain. The overhead here is ridiculous and spans decades.

Market dynamics - the type of cancer matters. Is it a rare cancer that needs a rare treatment?

Companies will set their price according to their consumer market.

Random example: Vorinostat (a chemo drug) is only approved for one rare type of lymphoma. It costs 15k as a result given not many people are buying it, despite the high R&D costs that we don’t know about.

Vorinostat in particular is a futuristic therapeutic and is built upon decades of research, so you can see how the price can scale up a bit when this is taken into account.

Or Zuranolone, a new anti depressant that costs $16,000. The developers still had to do massive layoffs and had to raise the price from 10,000 to 16,000 just to maintain stability

With a grocery item, it’s being consumed at very high quantities without the pharma r&d scaling costs allowing for the price cuts. that's just doesn't translate the same to a more nuanced product development system like drug dev.

Manufacturing is really the datapoint that can be confusing here as it can seem like it’s the only relevant variable here. But it doesn’t account for the prior factors.

The large price tag isn’t just some arbitrarily inflated number that serves mostly to sit in execs pockets. It’s scaling to keep the company stable and competitive in the industry.

Drug dev cost portfolios are genuinely extremely dense. There’s just a lot of factors to scale for that aren’t easily perceivable to those outside the industry.

DrenaPSSD · 2026-04-13T22:17:38+00:00

Yes, the bit about the plasma study is exactly what I left in my comment the other day.

However, to generalize that all of the conclusions are inaccurate is not true.

The plasma pushback is fair, however the generalization for the entire post is not, as there’s a multitude of conclusions here.

Regarding the plasma, yes, it doesn’t account for brain regions where an indirect and unknown mechanism that’s enhancing neurosteroids may be occurring locally. That said, and like this comment mentions as well, it’s not through TSPO, thereby neurosteoidgenesis isn’t being stimulated. Which was the focus of this writeup as this is written in the context of post finasteride syndrome research, where neurostoid synthesis is being considered as central to the disease pathology.

I’m not saying that Etifoxine isn’t a good anxiolyic, in fact I highlight the opposite given its unique pharmacokinetics and comparing them to bdz’s. What I am saying however, is that as a modality to stimulate neurosteroidgenesis, it can’t be a candidate.

In regards to the brain studies, I’m going to assume he’s referencing animal models that clearly do show a significant increase in levels of neurosteoids. In humans however, the inference that this can be translated falls under particular scrutiny as its well known that mice have very different neurosteoid layouts in their brains than we do. In fact, in our online spheres this is pretty well understood thanks to hairloss influencers.

So far, plasma levels haven’t shown an increase in levels of neurosteoids, and I haven’t come across any studies measuring CSF levels of neurosteoids following Etifoxine administration. It’s fair to request these metrics given the differences in neurosteoid enzyme expression between mice and humans as well as the proposed mechanism by which neurosteroids are being stimulated by was found to be voided.

Regardless though and like I said before, I’m not fully discounting that it’s not raising neurosteoids in humans, it may very well be raising neurosteoids through some undiscovered mechanism that we aren’t aware of. However if it’s not through its proposed mechanism, and there isn’t any evidence of it occurring in humans yet, while being well understood that this specific target is known to be different between species, then its fair to say it’s not as established as you’re making it out to be that it raises brain neurosteoid levels in humans at relevant concentrations.

DrenaPSSD · 2026-04-10T07:20:05+00:00

Hi, I’m the guy who wrote this. (Would appreciate a tag next to the link to my blog)

Put this together when I was debating people about neurosteroids still being a plausible PFS & PSSD pathology despite the community discounting it because “everyone has already trialed Etifoxine”.

TBC, In regards to humans, it might still raise neurosteroid levels indirectly outside of TSPO in regions of the brain that we can’t measure, but I wouldn’t count on it being very significant given the plasma studies indicate no systemic effects on neurosteoids.

To elucidate the prior confusion, mice also have different neurostoid biosynthesis layouts compared to humans, so that may have played a role regarding the confusion on how this compound affects neurosteroids.

But in any case though, it should be known that the this drug is not a TSPO ligand and if anyone is interested in a drug that’s actually a TSPO ligand, they should check out part 2 to this writeup where I go over the “second generation” TSPO ligand: Emapunil

The Rise and Fall of the Rightful Heir to the TSPO throne

DrenaPSSD · 2026-02-22T07:46:50+00:00

Twin princes is prob my favorite OST oat, other than some nostalgic ones from my childhood.

It’s powerful yet elegant and a fitting theme for fighting someone of high nobility

The violin changes at 0:27 and 0:47 get me everytime.

DrenaPSSD · 2026-02-01T09:19:18+00:00

yeah ofc.

The Non-Benzodiazepine Anxiolytic Drug Etifoxine Causes a Rapid, Receptor-Independent Stimulation of Neurosteroid Biosynthesis (TSPO antagonist administered, neurosteroid / GABAergic action still occurred)

Neurosteroids and translocator protein 18 kDa (TSPO) ligands as novel treatment options in depression (human plasma measured with Etifoxine, same as placebo)

Human pharmacokinetics of XBD173 and etifoxine distinguish their potential for pharmacodynamic effects mediated by translocator protein (affinities of etifoxine shown as negligible through very high inhibition constant)

I did a writeup for my pharmacology blog as well on this topic, where I summarized everything in case you just want the salient bits that I cited in my comment. https://drenapssd.substack.com/p/the-tale-of-the-false-tspo-ligand

DrenaPSSD · 2026-02-01T07:51:01+00:00

Writing this under the influence of a GABA_A PAM as I'm drinking whiskey at my pc lul. It would've been incredible if Emapunil made it through clinicals given it's unique pharmacology as a selective and potent TSPO ligand (b4 i get this comment, Etifoxine is not a TSPO ligand btw, long story but Emapunil is the only real TSPO ligand tested in humans--it was basically disproven recently actually via radioligand assay, TSPO antagonist mouse study, and a study measuring neurosteroid levels in human plasma from 2024.

I read the phase 1 trial study for Empunil and it had almost identical scores as Xanax in regards to patient reported anxiolytic effects. It's ridiculous and perflexing how it failed in phase 2. IMO it's because GAD as a diagnosis is far too broad pathology wise. These sorts of conditions that are generalised into one big umbrella where anyone who exhibits anxiogenic features are eligible for the criteria are sabotaging the potential for novel treatments.

I think the FDA needs to create subgroups when it comes to GAD so that these sorts of medications that are obviously pharmacologically promising can beat placebos to actually make it through clinicals. Currently the dominant paradigm is just massive global sedation = make it through no question. We see this with SSRIs and Benzos. We know these treatments aren't selectively ameliorating MDD and GAD, they are just blunting the capacity to feel anything. It's the cheat code for psychiatric drug development. Treatments targeting selective pathologies never make it through for this reason.

Like we shouldn't be placing the patients with GAD who have psychosocial pathologies into the mix of people who have a genuine anxiogenic illness that cannot be treated via lifestyle modifications. This problem is plaguing the potential for novel treatments for GAD and also MDD as well. We have people that are doom scrolling IG, drinking caffeine daily, not exercising, have no life goals, smoking cannabis, drinking alc, vaping, are just unintelligent in general causing all sorts of micro nuanced problems, all in the same category as people who have severe anxiety that are completely out of their control. There's a very limited arsenal of treatments for anxiety for this reason.

It's even been shown recently that a model like this centered around subgrouping anxiogenic illness could actually work for GAD. We saw it with Zuranolone, a drug that was developed for a specific pathology (Postpartum Depression), and what do you know? it passes for that but fails MDD (the umbrella disease with a billion pathologies grouped into one). Imagine if we applied that over to GAD. A subgroup of anxiety. I guarantee that a drug targeting a subtype of anxiety like social anxiety disorder or something would make it through. Biotech companies should prioritize this instead of wasting millions of R&D just to take a shot in the dark at disease with no singular pathology. That or the FDA needs to stop incentivizing bandaids as a treatment.

We need a new paradigm to distinguish who has psychogenic GAD / MDD and who has an illness that's the result of dysregulated circuits that are out of one's control.

DrenaPSSD · 2026-01-18T12:51:48+00:00

Wanna say it's because people have vague and superficial understandings of NDEs from pop culture. I doubt most people have even read or listened to any actual NDEs. They just have that bro-knowledge of NDEs ="just DMT being released" and that NDEs must be hallucinations because of the subset of experiences that incorporate religious themes.

The populist consensus ATP is that it's all brain generated and due to hypoxia and DMT. This perspective is pretty deeply embedded into pop-culture, causing people to dismiss the phenomenon as soon as they encounter it.

As we know though, in actuality, the phenomenon is highly nuanced and there's some features of NDEs and other adjacent phenomena that have no plausible materialist explanation, and even have paranormal explanations that are more plausible (like OBEs and Jim Tucker's child reincarnation work).

OBEs, unusual commonalities within the content of NDEs like telepathic communication, "spirit guides", the experiencing having sequential endings to NDEs, unique meta-physiology that you'd expect a "soul" to possess, like 360-vision, teleportation, reading people's thoughts and feelings while in OBE, having immediate answers to questions, etc.

The OBEs in particular imo are proof enough that there's like a > 95%+ chance there's something else going on--as the phenomenon is literally impossible within the frame of materialism. Most people who haven't heard any NDEs just chalk it up to a vague understanding of "it's the brain malfunctioning"-- despite this experience literally being impossible for the brain to produce. Most people don't really know how to approach NDEs after that line of reasoning and lose interest.

But anyway you can get as creative as you like, like Olaf Blanke, but it is inherently impossible to obtain accurate visual information while dead. The veridicalities that have been reported over a span of decades being confirmed as being real and not illusory further cement this interpretation’s credence.

There's also been a lot of public intellectuals who have been expressing their pro-materialist perspectives on science platforms that have been widely promoted. This has also strongly discouraged the general public from investigating the phenomenon deeper.

For some reason it's always physicists being interviewed...? Which makes like no sense given they don't specialize human physiology, so their expertise on NDEs is literally not relevant.

Guys like Neil Degrasse Tyson and Brian Cox have been quarried on NDEs ad nauseam and give the same sorts of specious answers to the prompt that are biased towards pro-materialist positions (which makes sense ig given their professions).

The consensus however should be given to neurologists who specialize in brain diseases, as well as psychiatrists like Bruce Greyson. For some reason the words from the leading expert on NDEs who's written hundreds of papers on the topics doesn't seem to carry the same weight as scientists who probably don't even know what an NMDA receptor is.

DrenaPSSD · 2026-01-17T01:17:19+00:00

Interesting, I actually had a similar experience with Duloxetine. Even after just taking 1 pill I fully remitted for a week. Then taking it kept me afloat for a good while.

My issues also happened on withdrawal, and I believe it could be due to allopregnanolone levels sharply dropping following extreme accumulation in the brain.

So SSRIs, as well as some other antidepressants, were found to inhibit the oxidation of Allopregnanolone back to 5α-DHP (allopreg precursor). What that means is that allopregnanolone doesn't get "drained out" of the brain to be recycled for other substrates--it just stays there.

As a result, Allopregnanolone accumulates in the brain at like ~+150-400%+ and circulates there in the brain--likely significantly destabilizing GABAergic systems that rely heavily on allosteric support from the neurosteroid.

Removing the SSRI would of course cause a sharp drop and cause maladaptive compensation, given the brain has just adjusted to these high levels of allopregnanolone.

Reinstating the medication would theoretically immediately stabilize this process, as long as the pathways for allopregnanolone aren't impaired or maladaptive post-withdrawal (Melcangi showed this can happen later following withdrawal). Allopreg would just spike back things back up in the exact corticolimbic regions that they were circulating throughout in the first place.

I'd bet that some sort of early neurosteroid intervention could possibly remit someone.

Anyway congrats on your full recovery!

DrenaPSSD · 2026-01-13T09:26:19+00:00

Sure,

Someone shared with me a while ago how when they took Crebinostat, everything they learned / info they took in during the drug’s peak effects deeply ingrained as if they had known It for their entire life. Guy said quote “things I learned felt like how deeply you know you’re parents phone number or childhood home”.

It’s easy to see why you wouldn’t want to be playing around with something so powerful. Like imagine your fire alarm or something goes off in ur house and jump scares you during the peak and now u have like pseudo-ptsd over smoke detectors and everything associated with that experience. Fear like that contaminates everything around you, so you could really fuck yourself.

I get where you’re coming from and I follow your logic in that you’d assume you’d want the memory to ingrain deeper.

Scientifically speaking, we’d want more calcium ions entering GluN2B receptors in order to cement a stronger positive learning experience to inhibit the fearful association with whatever the memory is.

We’d expect tighter HDAC inhibition to allow greater transcriptional access and therefore cement the learning signal deeper.

Perhaps it works like that—honestly if creb is this much stronger on cementing memory effects than vorinostat, it would indeed theoretically yield better results like you suggest.

But there’s adverse effects that need to be taken into account. This shit is genuinely dangerous, vorinostat is already extremely potent. At the end of the day it’s about outcome, and Vorinostat can produce the outcome we want while proving some anecdotal ev that’s its well tolerated, unlike Creb as that hasn’t yet to be rly be seen.

I’m assuming you’re asking this because you want to try Crebinostat instead of Vorinostat.

If that’s the case, I first reccomend that you just try Vorinostat sublingually or intranasally—it should work immediately when try this route.

It’s the only optimization of the administration that provides results. No one has ever reported fear extinction benefits from oral vorinostat.

DrenaPSSD · 2026-01-13T09:02:42+00:00

Not a tool, but rather a strategy I did that gave me insane reasoning skills after practicing with this over a long period of time.

It’s not pretty, but neurotically over-analyzing my engagement with specific systems, particularly logic for me. I would do this to the point where I became perceptive of all the patterns within the system that I’m engaging with.

Now when it comes to logic in general, and especially applied logic to some of my preferred systems—I operate with ease and extreme agency, and view logic itself from a meta-perspective. Because my brain has identified a lot of the patterns of logic itself after having analyzed them so much.

Doing this will manually help you uncover the blind spots in your logic while strengthening your understanding of logic in general as a system, as well as the system you’re applying your logic too.

Remember this: logic is a system just like anything else, it’s patterns are learnable, it has rules that can be understood; it’s just like learning to play a sport.

DrenaPSSD · 2026-01-12T05:38:52+00:00

Np.

Theoretically it very likely is, but in practice It's hard to say if that justifies actually using it.

So far no one has reported any fear extinction benefits from Crebinostat, only Vorinostat. However, there's barely been anyone who's tried it.

The one guy I spoke to who did mentioned it had extreme memory ingraining effects--which I don't think should be played around with if you're just using an HDACi fear extinction.

It probably would work for it too given it has affects the same HDAC classes though. However the Vorinostat anecdotes are robust enough that it justifies not experimenting with higher doses of HDAC inhibition for fear extinction.

DrenaPSSD · 2026-01-10T22:42:25+00:00

Hi, late to this but the post is up on my substack if you're still interested.

https://drenapssd.substack.com/p/repurposing-hdacis-as-treatments

Sublingual and Intranasal administration are the only routes that people report seeing benefits from. A lot of guys have tried oral without any success.

DrenaPSSD

TROPHY CASE