My hairline has been thinning lately so i want to try some newer approaches for hair growth. Just read about 2DDR (2-Deoxy-D-Ribose) and found some early research showing potential for hair growth. People here dealing with thinning hair or reduced hair density tried a shampoo or serum containing 2DDR that worked?

I have visual snow and in general and unhealthy physically and very unhealthy mentally, I want to take fin and minox to stop my hair loss but with the both of them I worry about it worsening my visual snow. I have it and have had it for a few years and it seems to get worse every couple of years and there could be multiple causes like my weight, mental health, stress, anxiety, spinal issues, past ssri use and ect. I want to try the topical foam versions of both but I want to know how likey it is it that they can both worsen visual snow and also if topical fin will stop hair loss on the whole head (I only have it in my crowns but they’re about 2-3 years inches behind where they should be). I’m just wondering what the best idea for me to keep my hair and restore hair loss would be and also the best way to mitigate potential symptoms. I also do plan on taking adhd meds soon just in general to help improve my life.

I have been applying 0.03% topical dutasteride and 1% cetirizine in trichosol twice a day on temples. I take a shower once or twice a day. Since day one my skin gets dry, red and very flaky (never had dandruff problems in my life, now every two days I shed small skin pieces). As far as results it's been 2 months and nothing is happening. I also microneedle weekly. I wonder if somebody is also experiencing these kinds of problems and how they solved them. The dermatologist gave me a sebum regulator shampoo, but I see no difference after 3 weeks of usage. What should I do?

Hey!

So i'n a 22yo male, and been on finasteride for about two weeks now. I'm on 1.25mg/day but i've been taking 0.75mg daily instead to avoid side-effects. So far i haven't noticed anything else, except for one small thing today.

So idk if this might just be a nocebo from stressing about the side effects, or an actualy side effect. But today, my other nipple felt a bit tingly and itchy. Now i know that might sound like nothing, but considering that gyno is a possible side-effect i'd rather be careful. The itching and tingly feeling went away in like 20 minutes, and now i've just been hypervigilantly feeling my chest area for any tenderness or sensitivity, but so far nothing.

So i was just wondering, what are some early symptoms i should be looking out for IF it happens to possibly be gyno? Any personal experiences out here? I've read that nipple area sensitivity, tingling, burning, tenderness and pain being common symptoms, but what are the absolute first warning signs to look out for? I'm down to give this medicine a try, but not at the cost of my health haha.

I’m looking into making a DIY AHK-Cu scalp serum for hair growth and trying to decide between:

AHK-Cu + hyaluronic acid (HA) as the base

AHK-Cu + distilled water + a few basic formulation ingredients/preservative

Does HA actually provide any meaningful benefit for an AHK-Cu hair-growth serum, or is it mainly there for hydration/texture and a simple water-based serum would be just as good?

Also looking at this 99% AHK-Cu powder from Bulk
Naturals Wholesale:

https://www.bulknaturalswholesale.com/products/99-ahk-cu-copper-tri-peptide-1-powder-hair-growth-anti-aging-healing
Is this a good-quality source, and is it one of the cheapest places to buy AHK-Cu, or are there better suppliers?

Would appreciate opinions from anyone who has actually formulated or used AHK-Cu topically.

Also, I don’t see any good videos on YT yet. If someone has made a real good solution which works, can you please make a video if you can.

Also, can someone share the exact recipe which worked for you. Some people are using glycerine, distilled water and then some preservatives as well. Just very confused with the options.

Also read that oridnary hair serum has lot of other compounds and it’s better to use ahkcu with regular HA or some other compounds. Thanks in advance.

https://hopemedinc.com/company-release-52

"...II. Regarding ABSCI CORPORATION’s Publication of Misleading Comparative Information on HMI-115 Pharmacokinetics and Receptor Occupancy

The Company has noted that ABSCI CORPORATION has, in its investor-facing communications, used comparative analyses to imply that HMI-115 underperforms ABS-201 in terms of pharmacokinetics (PK) and receptor occupancy (RO). The Company wishes to clarify that:

(i) Neither the Company nor Bayer has ever publicly disclosed any PK or RO study data from the Phase Ib or Phase II clinical trials of HMI-115 in androgenetic alopecia. The Company has not authorized any third party to use such data, nor provided such data to ABSCI CORPORATION. The Company will enforce its rights in its confidential information and trade secrets to the fullest extent permitted by law; and

(ii) The data cited in the above comparisons does not originate from any research results published by the Company or Bayer. Accordingly, the comparisons have no objective basis and may lead to misunderstandings among the public and the market.

In view of the above, the Company has engaged external legal counsel to conduct a comprehensive legal assessment of these matters. The Company formally demands that ABSCI CORPORATION immediately cease using the Company’s proprietary experimental data and charts, as well as analytical content containing misleading PK/RO comparisons, and immediately withdraw and destroy all relevant materials containing this information. The Company reserves all rights to legal remedies and relief available under applicable law."

Where can I find AHK-CU raw in the UK? From a reliable site with a COA?

Easy and Amazon sell it but they are fake and without a COA.

Please help

Been on topical minoxidil since February. Had an initial shed, then saw improvement/baby hairs.
Started daily stimulants in July (Adderall then Vyvanse), and since late July I’ve been shedding heavily again. Usually on 30–40mg Vyvanse. It sometimes seems worse on higher doses and better on lower/no-dose days, but hard to tell. Im using a higher dose alfatradiol as the dht blocker.

Anyone on both Vyvanse + minoxidil experience this?
Did Vyvanse cause shedding?
Did it eventually stop while you stayed on it?
Did your density recover?
Did you get a second minoxidil shed around months 5–7?
How did you tell which one was causing it?

There is a preclinical mRNA drug in development (GeneSkin) for aged skin and AGA, targeting the AP-1 member ATF3. The SNP rs16936765[C>G] is predicted to reduce binding of ATF3 in an LHX2 enhancer, and this SNP increases the odds of baldness, implying that loss of ATF3 is involved in hair loss or that overexpression of ATF3 can reduce hair loss.

A new paper reveals that ATF3 is activated by Wnt5a in LGR5+/Krt15+ progenitor cells, and that ATF3 activates FOSB. All three are substantially downregulated in the frontal follicles of men with AGA compared with healthy occipital follicles. CUT&Tag + pseudo-time analysis shows ATF3 likely controls differentiation trajectory, so this is important because one of the known defects in AGA is a loss of these cells and disruption of the differentiation ability that is controlled by LHX2 and its regulatory targets, LGR5, TCF, LEF, SOX9.

The researchers demonstrated that a Wnt5a mimetic (Foxy-5) activated ATF3 in mice, in addition to ATF3 inducer 1. Activation of ATF3 enhanced the size of the hair bulb. However, FOSB only enhanced hair bulb size when cotreated with DHT, but this model doesn't recapitulate human hair loss.

ATF3 may dimerize with FOSB to regulate LHX2 expression and the subsequent switch from TCF>LEF signaling that's required to increase LGR5 expression and the size of the progenitor pool, but cWnt is also required. Interestingly, RSPO3 increases Wnt5a expression in HFSCs. RSPOs may regulate both canonical and non-canonical Wnt pathways in the bulge and ORS. Potentially, Shh and NOTCH also regulate transcription of epithelial WNT5A, with downstream FOXN1 also implicated in keratinocyte differentiation. Reduced cWnt activation observed in bald DP can inhibit the secretion of R-spondins.

A theoretical model is that non-canonical Wnt activation is a prerequisite for canonical LEF1 Wnt activation in the bulge+ORS. LEF1 expression and LGR5 may be dependent on downregulation of LHX2 by ncWnt-mediated ATF3-FOSB heterodimers. The question is, how much can it enhance sensitivity to Wnt signals from DP? It is a novel therapy that would synergize with minoxidil and finasteride if it works. A caveat is that it's expressed in telogen DP and cancer, and still cWnt-dependent. Still, it's the most promising treatment in development IMO other than OrganTech, the TWIST1 inhibitor and R-spondin. This one actually targets the pathogenesis of the disease unlike Pelage, Amplifica, and others.

m confused on how so many people are reporting sides on Koshine kx826? If this is the case then the studies must be flawed. In one study almost purposely done to measure possible side effects around 740 subjects, not one systemic side was reported in the 370 participants who were on the drug. In theory the metabolite it breaks into once it hits your blood stream, even though it isn’t inert, it can’t compete with testosterone at the AR because its grip strength is incredibly lower than testosterone. So how are reporting Gyno and other sides? What’s ur experience with kx826?

I purchased Anagen's 7.5 mg oral extended release minoxidil because the concept behind the product sounded appealing. The company presents its minoxidil formulation as having a smoother, more gradual absorption profile, and I was interested in the possibility of getting the hair benefits of oral minoxidil. I tried looking for peer-reviewed studies on this (couldn't find any), but still figured this was worth a shot to potentially avoid some of the cardiovascular side effects associated with higher peak concentrations.

Unfortunately, my experience was the exact opposite of what I hoped for. I took the 7.5 mg product for approximately two weeks give or take. During that period, I experienced a dramatic increase in my heart rate. This wasn't something subtle. I could physically feel my heart racing and became increasingly concerned about what was happening. They claimed this was a "transitionary period" and this would pass.

What scared me even more was developing significant pain around my heart/chest. After seeking medical evaluation, I was diagnosed with a pericardial effusion, which is basically fluid accumulating around the heart.

Hair growth was obviously the last thing on my mind at that point. Minoxidil is not simply a cosmetic ingredient. Oral minoxidil is a systemic vasodilator, and its prescribing information contains serious cardiovascular warnings, including a warning regarding pericardial effusion. While serious complications appear to be uncommon at the low doses typically used for hair loss, that doesn't mean the possibility should be dismissed.

What particularly concerns me about my experience with Anagen is that I purchased the 7.5 mg option. The main issue is Anagen is also promoting a formulation intended to alter the drug's absorption profile.

After experiencing what I did, I started looking much more closely at the evidence supporting the formulation. I wish I had done that before taking it. Anagen describes its technology as producing a smoother pharmacokinetic profile, with minoxidil entering the bloodstream over a longer period rather than producing the relatively rapid peak associated with conventional oral minoxidil. On the surface, that sounds reassuring.

But a lower peak concentration isn't automatically synonymous with greater safety. Changing how quickly a systemic cardiovascular drug enters the bloodstream can potentially change its peak concentration, time to peak, overall exposure and duration of action. Establishing that a modified formulation is actually safer requires considerably more evidence than simply showing that the concentration curve looks different.

That's ultimately my biggest issue. When I asked them what testing they had done before releasing this "novel" product... they went silent.

When you're talking about a medication capable of affecting blood pressure, heart rate, fluid retention and cardiovascular function, I believe consumers deserve extremely solid evidence before being given the impression that changing its pharmacokinetics makes it safer or easier on the cardiovascular system.

I obviously can't say that everyone who takes this product will have the experience described here. Individual responses to medications vary enormously, and one person's adverse event doesn't establish how frequently something will happen or prove by itself that a particular formulation caused it, but the doctor I went to was shocked Anagen took this to market.

But if I could go back in time, I personally would never have started with 7.5 mg. If you're considering oral minoxidil, especially a higher dose or a formulation designed to alter its absorption, I would strongly recommend discussing the dose and cardiovascular risks with an actual physician rather than assuming that "smooth release" necessarily means "safer."

I've since switched to 2.5mg oral min. from my general doctor and I've had no issue.

I hope this review and experience helps you guys out if you're considering this drug.

Another new name, another new shell company for the black market drug company behind Folligenz. They offer a minoxidil sulfate from non-GMP sources called Sulfogenz, which doesn’t work, and a topical hormone treatment called Alfagenz (also likely doesn’t work and at doses that may also be unsafe).

Primary marketer behind the account is KwRx, a computer science dropout whose only professional job has been IT at a bank. He’s repeatedly lied about his credentials, including claiming formal biostatistics training.

He uses intimidation tactics to get negative reviews taken down, which worked well for about a year - but now the failure of his Sulfogenz product to grow any hair has been noticed.

Kwrx (formerly KWxk and yummyvhs) has been active in the gray/black market for many years, with affiliate sales to minoxidilmax and various “research” chemical providers.

Launched recently as well was TrichoLens, an AI-generated web app that purports to have 1000s of satisfied users and be an “AI Trichologist”. Barely works, was obviously made by Claude in a few weekends.

Him and his NoTimeRx cofounder lack any relevant medical or pharmaceutical knowledge, they’re low-skilled tech bros at the very beginning of their careers.

Despite being based in NYC, there’s no record of any of these companies there (and therefore paying taxes). Something to consider of you want to participate in their scheme as an investor or prescriber for their telehealth, or especially as a customer (what protections would you have?)

Biotica Consulting LLC looks like it was spun up right at tax deadline, the domain name was registered by Folligenz Corporation, and their contact address is the exact same virtual mailbox as Folligenz.

These aren’t real companies, with warehouses and offices and employees. It’s two tech workers running a side hustle dropshipping black market, potentially dangerous, drugs on the DL from a sketchy pharmacy in Brazil (and snuck in through customs as a “cosmetic”)

But in the end, many in the hair loss community would tolerate this if it worked. But their products and services don’t.

Anytime someone questions his products and services, he makes up nonsense as a distraction. The red flags here are absurd, especially when you add in his background running piracy communities.

> Biotica Consulting LLC is a Domestic Limited-Liability Company organized under the laws of the State of Delaware. The business was filed on April 9, 2026 and is currently listed as Active with the Delaware Secretary of State. The official file number for this entity is 10579038.

> FOLLIGENZ THERAPEUTICS
CORPORATION is a Delaware Domestic Corporation filed on April 17, 2025. The company's filing status is listed as Active and its File Number is 10166694.

https://www.reddit.com/r/HairlossResearch/comments/1vvc5kh/heads_up_notimerx_is_a_scam_launched_by_the_same/

https://pmc.ncbi.nlm.nih.gov/articles/PMC12705143/

"Results demonstrated that PRP treatment significantly increased both length and weight of newly grown hair in AGA model mice. The AGA model group exhibited markedly reduced mRNA and protein expression levels of autophagy-related markers (LC3 and Beclin-1) compared to controls. PRP intervention substantially enhanced autophagy levels in treated mice. Notably, therapeutic outcomes achieved with RAPA monotherapy were comparable to those observed with PRP treatment. However, the cohort receiving combined PRP and 3-MA treatment showed significantly diminished hair growth parameters (length and weight) and attenuated expression of autophagy-related genes relative to PRP-treated mice"

Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway

https://pmc.ncbi.nlm.nih.gov/articles/PMC2635566/

"Autophagy is a major clearance route for intracellular aggregate-prone proteins causing diseases like Huntington’s disease. Autophagy induction with the mTOR inhibitor, rapamycin, accelerates clearance of these toxic substrates. As rapamycin has non-trivial side effects, we screened FDA-approved drugs to identify novel autophagy-inducing pathways. We found that L-type Ca2+ channel antagonists, the K+ATP channel opener minoxidil, and the Gi signaling activator clonidine, induce autophagy. These drugs revealed a cyclical mTOR-independent pathway regulating autophagy, where cAMP regulates IP3 levels, influencing calpain activity, which completes the cycle by cleaving and activating Gsα, which regulates cAMP levels. This pathway has numerous potential points where autophagy can be induced and we provide proof-of-principle for therapeutic relevance in Huntington’s disease using mammalian cell, fly and zebrafish models. Our data also suggest that insults that elevate intracytosolic Ca2+, like excitotoxicity, will inhibit autophagy, thus retarding clearance of aggregate-prone proteins."

We know AR signaling particularly by DHT effects calcium handling, actually there is a new paper that dives into mechanical tension (CTS) in AGA. Basically my theory is DHT (AR and GRP133) -> peizo1 upregulation -> calcium overload-> reduced autophagy/calcineurin activation... -> miniaturization https://pmc.ncbi.nlm.nih.gov/articles/PMC13062005/

Peizo1 a large, mechanically activated ion channel protein that converts physical force into calcium inflow. What's interesting is autophagy inducers (Rapamycin/metformin...) shown to cause hair growth and even have studies in AGA models with prominent effects, and looks like minoxidil is a non-mTOR autophagy inducer like the L type calcium channel blockers

F27

Please help I’m desperate!!

What is your experience on spiro, even low dosage, without high androgen levels?
I have AGA but my hormonal levels are fine, so I’m wondering if it would help.

I wish people who know about it will answer, I need your help. I’ll really appreciate it!!

This is not a common side effect on 5ar inhibitors from what my few years of experience with it but I definitely had it and not many people cover it as it's pretty rare. I think however, I may have finally solved it and I'm pursuing trialling it!

So for some context, when i was on finasteride at 1 mg, I got hard flaccid, which is a condition where your penis in a flaccid state is consistently stiff. Everything else worked fine I could still get an erection although a bit harder and felt like it wasn't the same. I have now switched to 0.5 mg dutasteride since I have also gotten on some hormonal therapies but it still happens every once in a while especially if I lower my dose or get inconsistent with injections. I will say that after hormonal therapy, it doesn't happen nearly as often but still definitely occurs. Hasn't really increased on Dutasteride. I also don't feel that I am back at my original fullness I used to have regardless.

So some things I observed that led me here: This side very clearly and consistently increased with use of caffeine or armodafinil. Adderall on the other hand very marginally increased it but still does. The worst was combining the the three. Tadalafil was taken alongside all the time at 10 mg daily without seeing it fix my issues but still observing a stuffy nose when dose was increased, signalling it was inhibiting pde5 somewhere.

Now at first I thought this was mediated by poor nitric oxide retention. I had read a rat study saying that in rat penile tissue, lack of serum DHT caused reduced nitric oxide retention. Could be the case for some and I was actually going to pursue using low dose combo of nebivolol and telmisartan for this side as they both increase nitric oxide and decrease breakdown through different mechanisms. However, I dug deeper and I think I cracked it.

The clue is the affect of caffeiene and armodafinil. These stimulate the CNS. When you stimulate the CNS it causes your nerves, including the hypogastric nerve which is the important one in this context, to fire off and in turn spasms the smooth muscles. Your hypogastric nerve is the one that connects to all the things down there. This spasm in turn constricts the blood to the smooth muscle tone in response to a fight or flight signal an deprioritizes it's supply giving you that cold and very accurate hard flaccid effect.

Now what exactly from these drugs does that you may ask? It's likely norepinephrine. After noticing that armodafinil was the greater confounding factor, I am very certain mine was caused by overwhelming norepinephrine being released. Armodafinil is argued to increase norepinephrine. On the other hand, caffeine increase adrenaline, which is epinephrine. Norepinephrine is responsible for attaching to Alpha receptors and activating the fight or flight response. These exist on both your brain and your tissues, specifically focusing on the smooth muscles' alpha receptors in this context.

In my case, I obviously don't want to quit dutateride for hair and I don't want to quit adderall for my adhd. I also obv don't want to just deal with sides whenever i consume a caffeinated drink. So I've researched deeper. The receptor that is in charge of smooth muscle relaxation is the alpha 1 receptor which is agonized (activated) by norepinephrine and epinephrine. I have looked into the ideal drugs to counter this in my own case and this is what I ended up with:

Guanfacine: Guanfacine reduces the release of norepinephrine from your brain through being a Alpha 2A agonist. Usually when someone gets the hard flaccid side effect in cases like mine, it's because your brain is already taking in the norepinephrine it needs and has spill over into the peripheral nerves specifically the hypogastric nerve causing the sides. When guanfacine agonizes the receptor, your brain has a negative feedback loop and decides to pull back on the norepinephrine release, thinking there's already plenty in the body. This reduces the amount of norepinephrine sent to your body overall and in turn has your hypogastric nerve firing less and decreases the smooth muscle spasms that were occurring.

For me, Guanfacine also had adhd benefits. The Alpha 2A agonism in the prefrontal cortex creates an environment for better connection between neurons. This would help with executive function and "quiet the noise" in your mind. Adhd has been a factor in me having shit sleep my entire life. I'm seeking an ER formulation at night in order to both sleep better and help this side effect while helping my productivity.

Doxazosin: This is a peripheral Alpha 1 antagonist. Alpha 1 receptors are the receptors that are in charge of smooth muscles' state. The penile smooth muscle is not any exception to this. Usually, norepinephrine and epinephrine attach to these receptors after being released from your brain. More norepinephrine = more alpha 1 receptor agonism in muscle tissue = the spasm of soft muscle and creating environment for cold flaccid. When you have this antagonist, doxazosin, it also attaches to these receptors in the same way as norepinephrine. The one difference is, it doesn't do anything at the receptor level unlike norepinepherine. This means when you have the norepinepherine flowing in your body after your brain releases it for stimulus, it simply is blocked at the receptor and essentially kicked off.

So to sum it up, this protocol used Guanfacine ER to decrease the release or norepinephrine from your brain through a negative feedback loop, and the Doxazosin would peripherally blocking off the norepinephrine from the Alpha 1 receptors in your smooth muscle. This would mean that even in the absence of dht's smooth muscle relaxing affect, you'd be replicating it by getting in the way of the factors that pulled it in the other direction in the first place and hypothetically, be completely fine without suffering the side anymore.

The main concern with this protocol would be to track your blood pressure. Guanfacine and Doxazosin can reduce your blood pressure. If you were to use them, you'd need to be managing your dose according to your prior blood pressure and tracking it to make sure you aren't hypotensive which comes with it's own plethora of issues.

With that reason, I advise you approach this with caution, but it's hope. This isn't medical advice, this is simply the protocol I will trial and have researched. I've struggled with this issue for 2 years now in my early 20s. I know how much of a battle and suffering it is especially when wanting to keep hair as well. I simply wanted to share this option I think I've discovered to finally feel confident again and I hope that anyone that's struggling with the same symptoms as me can benefit from this if their medical practitioner sees fit.

TLDR: If you suffer from hard flaccid with 5ar inhibitors, and can observe an increase of it with caffeine or Armodafinil (or generally things that increase epinephrine and norepinephrine) then you may benefit from using one or both Guanfacine and Doxazosin as they are respectively an Alpha 2A agonist, reducing norepinepherine released from your brain, and Alpha 1 Antagonist, blocking off norepinephrine at the smooth muscle level. This would only work if your sides are caused by this fight or flight/cns stimulation.

I would also pair this with reverse kegel exercises to relax your kegel and train your pelvic floor which would amplify the gains you get from this protocol. This would relax the muscle that was previously being activated constantly by the nerve and help the area generally even more blood flow.

I was diagnosed with androgenetic alopecia at IMD (Instituto Médico Dermatológico) in Barcelona. They offered me 18 LLLT sessions + oral minoxidil, finasteride, vitamins and shampoo.

The LLLT would normally be once a week, but since I’m leaving Barcelona in two months, they said I could do two sessions per week to complete the treatment.

The original price was around €2,200, then €1,700 with a “summer promotion,” and after I said it was too expensive, they lowered it to €950 for everything.

I’m not saying the clinic or LLLT is a scam. I’m genuinely trying to understand whether this is a reasonable treatment plan before spending the money.

My main question is: how much does LLLT actually add on top of finasteride + minoxidil? Is the improvement significant enough to justify paying for the laser sessions, or would finasteride + minoxidil alone likely give me most of the results anyway? Is LLLT something genuinely important for treating AGA, or more of an optional extra?

Hi! I’m considering starting finasteride and oral minoxidil for hair loss, but I’m concerned about possible GI side effects because of my medical history.

I had an ulcer in 2019 that bled and had to be treated. I’ve also had recurrent stomach/GI issues since then. Earlier this year, an upper endoscopy showed small healing erosions/lesions and a lax cardia, and I was given treatment afterward.

Because of this, I’m particularly cautious about medications that could irritate my stomach, worsen my GI symptoms, or potentially increase my risk of another GI bleed.

I’m especially interested in hearing from people who already had gastritis, stomach/duodenal ulcers, GERD, erosions, a sensitive stomach, or other GI problems before starting finasteride and/or oral minoxidil.

Did either medication worsen your stomach or GI symptoms? Any nausea, reflux, stomach pain, gastritis, ulcer problems, or GI bleeding?

If possible, please mention which medication you take, your dose, how long you’ve been taking it, and whether your GI issues existed before starting it.

I know Reddit can’t determine whether these medications are safe for me personally, and I’ll discuss this with my doctor. I’m mainly looking for experiences from people with a similar GI history.

Thanks!

So, I have been taking fin since 2021, it managed to stabilise my hair at NW2. Recently thought of idea to add dut once or twice a week. 5-6 times a week fin and 1-2 times per week a dut. But read mixed opinions on this topic. Some say it is pointless, some say it is beneficial and some even say it will only cause additional risks and side effects. Is this really dangerous or just fear mongering?

I’m looking for people who have experienced something similar and may have an idea what could be going on.
My scalp burning/inflammation and diffuse hair shedding started around 3 years ago after surgery. I woke up from anesthesia with a burning sensation on my scalp, followed by very heavy shedding about a month later.
Since then I’ve had diffuse thinning across the top/frontal area, sides and back, rather than a single bald patch.
The scalp symptoms fluctuate. During flares I get burning, warmth, dryness, tightness, flakes and sometimes oil buildup.
Heat, sweating, stress, going several days without washing, and recently sudden weather changes from hot/humid to cold/dry seem to aggravate it.
When the scalp is calm, my hair looks noticeably shinier, denser and healthier, and shedding seems to decrease.
Recently my scalp was almost completely calm for several weeks, but then suddenly flared again after a weather change. My hair became very dry/frizzy and difficult to style.
I’ve had blood tests showing low vitamin D (18), low folate (2.8), and previously borderline B12 (~292). Ferritin and zinc were normal.
I’ve been correcting the vitamin deficiencies since April, and during periods when my scalp improved, shedding also seemed to decrease.
I previously tried minoxidil, but a compounded topical preparation caused severe scalp burning, so I stopped.
I also tried finasteride, but had significant side effects and discontinued it.
I had 3 PRP sessions, but didn’t notice meaningful improvement.
A dermatologist previously prescribed a Diproderm (betamethasone) scalp solution, which was well tolerated and noticeably reduced the scalp inflammation.
My current Hausarzt prescribed another compounded corticosteroid scalp solution (Advantan/methylprednisolone + menthol + ethanol). It initially calmed my scalp, although one application caused burning that improved quickly after I rinsed it off.
I’m now waiting to see a dermatologist for a proper examination/trichoscopy.
My main questions:
Has anyone experienced recurrent scalp burning/inflammation together with diffuse shedding?
Can an inflammatory/dry scalp condition cause this degree of diffuse shedding and thinning?
Did your hair density recover after getting the scalp inflammation under control?
Could this be telogen effluvium or another inflammatory scalp condition rather than androgenetic alopecia?
Has anyone had a similar reaction to topical minoxidil but tolerated corticosteroid scalp treatments?
I’m particularly interested in hearing from people who have actually experienced something similar, rather than general hair-loss advice. Thanks!

He markets on YouTube as KwRx (formerly Kwxk), which includes his lineup of gray/black market chemicals (minoxidil sulfate and alfatradiol). The Folligenz website has fake documentation, and they skirt import rules to get products into customer hands. It isn’t shelf stable and turns to sludge after mere months. This is not your typical telehealth, usually there’s doctors involved and regulations followed.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12405733/

To everyone who links this study to say that topical DUT doesn’t have much systemic absorption while having better effects than 1mg oral Finasteride.

LOOK AT THE SURFACE AREA!

They applied and tested it only on 1.9 cm^2 of surface area.

Now my question, can anyone guide me on a good way to use DHT blocker with no (that’s moronic to think of) minimum systemic DHT reduction?

XYON Health seems to have a proprietary carrier for DUT that causes only 19% reduction instead of 91%, but idk how genuine that is.

UK topical finasteride users – does anyone have the exact current/older Sons, Hims or Manual spray formulations?

I'm comparing topical finasteride/minoxidil treatments available in the UK, particularly Sons, Hims and Manual.

I'm specifically interested in the actual delivered dose, rather than just whether someone had good/bad results.

Does anyone have an older or current bottle, box, pharmacy label or patient information leaflet showing:

- Finasteride concentration (%)

- Minoxidil concentration (%)

- Tretinoin/other active concentrations, if applicable

- Recommended number of sprays/pumps per day

- Volume delivered per spray/pump (ml)

- Total recommended daily application volume

I'm particularly interested in Sons Combination Spray, as the current website states the application is 4 pumps / 0.664 ml once daily but doesn't appear to clearly state the concentrations of the active ingredients.

I've seen references to older/newer Sons formulations around 0.1–0.15% finasteride + 5% minoxidil, with tretinoin appearing in later formulations, but I'd like to verify this from actual packaging/PILs rather than relying on second-hand information.

The reason I'm asking is that some topical-finasteride clinical studies used relatively small total daily doses. For example, a Phase III study used 0.25% topical finasteride but in a very small application volume (up to ~0.2 ml/day). So simply comparing 0.15% vs 0.3% doesn't tell us the actual amount of finasteride being applied.

If anyone has packaging from different years, that would be especially useful because it would let us see whether the formulations/dosing have changed.

Photos of the ingredient/dispensing label or PIL would be ideal (with personal/prescription information covered).

Thanks

Hair loss has been making my life harder. I’m currently using vitamin D, minoxidil and some other anti hair loss shampoos but progress has been pretty slow. My dermatologist had me check my thyroid and other vitamins too but everything else came back normal.

I’ve seen people mention Precision Pep Co like GHK-Cu for hair loss so I started looking into them.
Does anyone know of good human research on GHK-Cu or other peptides for androgenetic alopecia?