got.daim
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Ultimate Hair Loss Guide
Thread Song:
How to avoid becoming Baldcels and/or
Thread Song:
How to avoid becoming Baldcels and/or
"Just be confident, own your hair loss and baldness!"
To start, here are a few examples of bottomless copes from Blue Pill Normies / Oofie Doofies who believe their Becky girlfriend / Foidin would still love them if they looked like that?
Medical history / Investigation of causes
First and foremost, you need to know if you have been afflicted with the most common form of alopecia
Several names are established for androgenetic alopecia: abbreviated AGA (male pattern baldness), and male pattern baldness
They all describe the same etiology and pathogenesis (for those unfamiliar with Latin, "cause" and "development")
Other types of hair loss
At this point, only a number of the very, I emphasize VERY rare, causes of hair loss in men will be mentioned as examples.
This list is expressly INCOMPLETE
Telogen effluvium : diffuse shedding after stress, weight loss, infection, surgery, nutritional deficiencies, or medication
Endocrine causes
- Disorders of your thyroid function
- Hypogonadism
- Hypoparathyreoidismus
- Systemic form of lupus erythematosus
- Red lichen planus
- Syphilis (Not possible for incels and sub-5s anyway)
- Various mycoses = fungal infections
DHT and what it is
The underlying cause, as the name suggests, lies with an androgen
Androgenetically, it's a steroid hormone belonging to the androgens, a male sex hormone
And genetically , it's a genetic predisposition of the hair follicles
Dihydrotestosterone (DHT) is the sex hormone that drives the development
It's a metabolite of the more well-known testosterone
How is DHT produced? By an enzyme called 5-alpha reductase
In humans, this enzyme exists in three isoenzymes
In short: Isoenzymes are different variants of an enzyme that catalyze the same chemical reaction but differ in their structure
- 5α-Reductase Type 1: Predominantly active in the skin, sebaceous glands and the liver
- 5α-Reductase type 2: Mainly active in the prostate, seminal vesicles and hair follicles
- 5α-Reductase type 3: Is also expressed in various tissues
But daim, why the hell do we produce this hormone if it turns a good portion of us into absolute subhumans and not slaying bastards?
DHT actually plays an important role in physiology and development during puberty
What does it do?
Physiological role in men:
—> Before and during puberty, DHT is crucial for the development of male sexual characteristics, especially the external genitalia (penis, scrotum) and the prostate, as well as for the development of body hair
During puberty, it also enhances the androgen effect in the skin and hair follicles (e.g., beard growth, sebum production)
—> After puberty, DHT no longer assumes a "vital" new function, but primarily continues to affect androgen dependent tissues such as the prostate, skin, and hair follicles
This continued effect is precisely the reason why DHT is associated with benign prostatic hyperplasia (BPH) and androgenetic alopecia (AGA) in adulthood
Testosterone | Dihydrotestosterone |
Spermatogenesis and fertility | Prostate enlargement and increased risk of prostate cancer (carcinoma = CANCER, you academic subhumans lol) |
Male muscle and skeletal development | Growth of facial, underarm, pubic and body hair |
Voice deepening | Androgenetic alopecia |
Increased libido and erections |
The mechanism behind DHT and your hair loss
Cellular level of hair loss and miniaturization of hair follicles
Now let's get to the reason why you start looking like your unemployed uncle who goes to brothels at 19 kek
In androgenetic alopecia, DHT doesn't simply have a direct "toxic" effect on the hair follicle, but primarily alters the behavior of the dermal papilla, which acts as a kind of "control center" for hair growth
When DHT binds to the androgen receptor in these cells, they release increased amounts of inhibitory signaling molecules such as TGF-β and DKK-1
These signals lead to the inhibition of growth promoting pathways (especially Wnt/β-catenin), and the hair cycle transitions more quickly into the regression phase ( catagen )
As a result, each subsequent hair becomes thinner, shorter, and less pigmented, the follicle gradually shrinks ("miniaturization") , but often remains structurally intact
Importantly , the stem cells of the follicle are frequently not completely destroyed, but their activation is disrupted, which is why reversibility is theoretically possible in early stages
So what does this mean for us? To a certain extent, we can not only act preventively, but are also able to partially recover lost ground, (PREVENTION, is what I would urgently recommend to each of you from the slightest sign of AGA, because it is important to maintain the status quo, protect hair that is still healthy, or in other words, prevent DHT from having its effect, this is 100 times easier than trying to resurrect already damaged follicles or bald patches from the dead)
The Norwood Scale
The following diagram might even look familiar to some of you
It's the most common way to classify AGA (androgenetic alopecia) in men
It's important to note that this is a rough guideline for how DHT-induced hair loss usually progresses
Therefore , different patterns can emerge , such as the Vertex variant shown here
It's named after its two originators, James Hamilton and O'Tar Norwood (hence the well-known joke in our community, "Norwood Reaper")
Another graphic is also included (this one illustrates the phenomenon of "diffuse thinning" much better , meaning the diffuse thinning of hair in men with a partially stable hairline)
As you can see, the hair loss pattern does NOT HAVE to strictly follow the Norwood pattern
As always in nature, nuances, exceptions, and overlaps are more common
Possible solutions
Drug therapy, hair transplantation, "Just Shave it Bro"
5-alpha reductase inhibitors
Those of you who don't have the attention span of a goldfish will surely remember the enzyme 5-alpha reductase
As we recall, it converts testosterone to DHT in our hair follicles, where it binds to androgen receptors (ARs) and initiates the cascade that ultimately leads to miniaturization
The pharmaceutical industry has given us two candidates from the group of inhibitors: finasteride and dutasteride
They differ in that finasteride only inhibits isoenzyme 1, while dutasteride blocks all three isoenzymes
Now you need to understand this:
DHT is measured in blood plasma, and DHT is measured in the scalp through tissue biopsies
When taken orally (as tablets), they are significantly more potent than when applied topically and can also have more side effects because the medication acts systemically
Here is a list of the different dosages and their effect on plasma and scalp DHT levels
We are only interested in the change in the tissue of the scalp
Source: Dutasteride and Finasteride Scalp DHT Reduction. Olsen et al (2006). The American Academy of Dermatology
1. Finasteride
Mechanism : Selective 5α-reductase type II inhibitor, reduces the conversion of testosterone to DHT Less DHT means less AR stimulation in androgen-sensitive follicles
Status : Oral 1 mg is approved in the US for male pattern baldness; Label: men only
Evidence : Large randomized trials showed slowed progression and an increase in hair growth over 2 years; long-term data over 5 years showed sustained benefit.
Molecular/Pharmacological : Reduces serum and scalp DHT, acting upstream before AR-dependent DP signaling changes become maximally effective. This is closer to the underlying cause than purely cosmetic stimulation.
Side effects:
Sexual side effects are known: decreased libido, erectile dysfunction, ejaculation dysfunction. Regulatory warnings also highlight psychiatric side effects and the fact that sexual problems can persist or have been reported after discontinuation. This doesn't mean that this is common, but it's also not responsible to dismiss it as mere internet myth.
In summary: Finasteride is effective for many men and generally well-tolerated, but the discussion about side effects should be neither hysterical nor trivialized
Sources :
Kaufman KD et al. Finasteride in the treatment of men with androgenetic alopecia. J Am Acad Dermatol. 1998.
Trost L et al. Side Effects of 5-Alpha Reductase Inhibitors. Rev Urol. 2013.
2. Dutasteride
Mechanism : Inhibits 5α-reductase types I and II and lowers DHT more effectively than finasteride.
Status : Not approved for AGA everywhere; according to recent reviews, approved for male AGA in South Korea, Japan, and Taiwan, but off-label in many other countries.
Evidence : Randomized trials showed better hair regrowth than placebo and, in some comparisons, stronger effects than finasteride, with a similar but potentially more relevant side effect profile due to greater DHT suppression.
Side effects : In principle, similar to finasteride, but often require more careful consideration due to higher potency and longer half-life. This is particularly relevant when weighing the benefits against the risks.
Quellen:
Arif T et al. Dutasteride in Androgenetic Alopecia: An Update. Dermatol Ther. 2017.
Shanshanwal SJS et al. Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia. J Cosmet Dermatol. 2017.
Hair revival
Minoxidil it's usually not enough on its own.
Topical:
Topical minoxidil is not an antiandrogen. Therefore, it does not lower DHT, but rather improves the growth conditions of the follicle. Minoxidil is a prodrug and is converted in the follicle by sulfotransferase to the active minoxidil sulfate; this promotes anagen, influences potassium channels, and acts on dermal papilla cells and growth factors such as VEGF. In simpler terms: It makes the follicle more efficient, even if the underlying cause of the DHT persists.
Topical minoxidil + microneedling:
Microneedling is often used as an add-on to topical minoxidil. It likely helps in two ways: first, by improving penetration of the topical agent, and second, by creating a controlled micro-injury that activates wound healing and growth programs, including evidence of Wnt/β-catenin-associated signaling pathways. Overall clinical evidence suggests that the combination may be superior to minoxidil alone, but studies are not all methodologically rigorous, and precise parameters such as needle length, frequency, and technique are not yet fully standardized.
Sources:
Kumar MK et al. A randomized controlled, single-observer blinded study of topical minoxidil plus microneedling vs topical minoxidil alone. Int J Trichology. 2018.
Bao L et al. Randomized trial of electrodynamic microneedling combined with 5% minoxidil in androgenetic alopecia. J Dermatol. 2020/2022.
Abdi P et al. Topical minoxidil and microneedling for AGA: systematic review and meta-analysis. Arch Dermatol Res. 2023.
Oral minoxidil
often works better for patients who have insufficient minoxidil sulfotransferase in their scalp. Minoxidil sulfotransferase is otherwise highly concentrated in the human liver, which is why non-responders often respond better to oral minoxidil. Anecdotal reports also indicate that 2.5 mg and 5 mg of oral minoxidil are significantly more effective than topical minoxidil. While the literature has not shown it to be superior to the 5% foam, many physicians report greater success with oral minoxidil in their patients. It is also considerably easier to administer.
Mechanism : systemic variant of the same principle; often used when topical minoxidil is not tolerated or is not consistently applied.
Status : mostly off-label for AGA. Expert consensus from 2024/2025 considers LDOM a relevant option for selected patients.
Side effects : most common is hypertrichosis. Furthermore, edema/fluid retention, headache, dizziness, palpitations/tachycardia, and blood pressure effects may occur; severe cardiac side effects are less frequent at low doses, but there is no zero risk.
Classification : effective, but more systemic than topical minoxidil. It is not a lifestyle supplement, but a genuine blood pressure medication with hair loss as a side effect, repurposed for therapeutic use
RU58841
Mechanism : Experimental topical AR antagonist. Principle: DHT may be present, but become less effective locally at the receptor.
Evidence : The problem is not that the mechanism is implausible, but that robust, modern long-term human data are lacking. Much is based on older preclinical data, animal models, and forum reports.
Status : Not approved, not an established drug standard.
Classification : Scientifically interesting, but practically a gray area. Anyone selling RU as a "safe topical alternative" is massively exaggerating the evidence.
Sources:
Battmann T et al. RU 58841, a new specific topical antiandrogen. J Steroid Biochem Mol Biol. 1994.
De Brouwer B et al. A controlled study of the effects of RU58841 on human hair growth in the nude mouse model. Br J Dermatol. 1997.
Breezula
Mechanism : Topical androgen receptor antagonist. Unlike finasteride/dutasteride, clascoterone does not lower DHT upstream, but blocks it locally at the androgen receptor in the target tissue. This is conceptually elegant: instead of suppressing hormone production systemically, it attenuates the target response at the follicle locally.
Status:
Clascoterone 1% cream is approved for acne in the USA.
Breezula / Clascoterone 5% solution for AGA is not yet officially approved based on Phase III topline data from 2025/2026, but the data are positive and marketing authorization applications have been announced or prepared.
Side effects : predominantly local reactions so far, low systemic exposure, favorable safety profile in the published Phase I/II trials and in the most recent Phase III reports. Nevertheless, complete long-term, real-world safety data are naturally still lacking.
Classification : one of the most interesting candidates, especially for people who want to avoid systemic DHT reduction. I personally will include it in my stack as soon as the EMA allows it.
Sources:
Rosette C et al. Cortexolone 17α-propionate (clascoterone) is an androgen receptor antagonist under investigation for androgenetic alopecia. J Am Acad Dermatol. 2019.
ClinicalTrials.gov, CB-03-01 solution in male AGA.
Pyrilutamide (KX-826)
Mechanism : also a topical nonsteroidal AR antagonist.
Status : investigational. In March 2026, positive Phase III results and pending approval steps were reported in China; however, global standard approval is not yet in place.
Classification : mechanistically similar to clascoterone, but not yet established in regulatory and widespread use.
Sources:
Zhou C et al. Efficacy and Safety of topical KX-826 in Male Subjects with Androgenetic Alopecia: multicenter randomized double-blind placebo-controlled phase II study. J Invest Dermatol abstract/PDF. ClinicalTrials.gov, KX-826 phase III and phase I/PK studies.
TL;DR:
Are you under 18? Trytopical minoxycycline and microneedling.
If it's really aggressive, get blood work done at a lab and get a 5-alpha reductase inhibitor. Maybe you can find a doctor who understands your emotional distress and will write you a prescription. I'm not encouraging anyone to buy illegal medication on the black market, especially minors.
Go to a dermatologist who is familiar with androgenetic alopecia and takes your problems seriously. If you're 18 or older, try finasteride. If you have side effects, you can try taking only 0.5mg or 0.25mg. Then, use a pill cutter to cut the pill into 1/2 or 1/4 pieces, depending on how many mg you want to take.
You can also take it every other day. Let's say you experience a loss of libido after 2 weeks at 1mg every day
(Sorry for any errors, I am half awake running off of some substances and I will edit this tomorrow)
@gato @Flint