How DHT and Androgens Drive Acne Formation

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Androgens are a key factor in acne pathogenesis. Lawrence Green, MD, FAAD discusses how hormones help drive the skin disease.

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How DHT and Androgens Drive Acne Formation​


Androgens are integrally associated with acne development. Acne originates in the sebaceous gland, which is under androgen control. Among androgens, dihydrotestosterone (DHT) is the most potent, and it plays a central role in acne pathogenesis.


DHT's Role in Sebaceous Gland Activation​


DHT activates the sebaceous glands by binding to the androgen receptor. However, it's important to note that while DHT stimulates these glands, it does not cause them to proliferate. In other words, sebaceous hyperplasia (an increase in the number or size of sebaceous glands) is not under androgen control. What DHT does do, unfortunately, is promote acne through multiple mechanisms.


Abnormal Keratinization and Clogging of the Follicle​


Once DHT binds to androgen receptors—both in sebocytes (cells in sebaceous glands) and keratinocytes—several events are triggered. In the hair follicle, DHT alters keratinization, leading to abnormal follicular desquamation. This abnormal shedding results in the formation of a clog within the pilosebaceous unit (the hair follicle and its associated sebaceous gland).


Without retinoid therapy to normalize this process, the clog creates an anaerobic environment within the follicle.


Proliferation of​


This clogged, low-oxygen environment becomes ideal for the proliferation of Cutibacterium acnes (C. acnes), the commensal anaerobic bacterium that resides in the follicle. Once overgrown, C. acnes initiates a cascade of inflammatory responses.


  • C. acnes breaks down sebum lipids, leading to an increase in free fatty acids and triglycerides.
  • These free fatty acids attract neutrophils, amplifying inflammation.
  • Meanwhile, increased sebum production—also stimulated by androgen activity—adds to the inflammatory state.

The Full Acne Cascade​


So, through DHT activation of androgen receptors:


  • Keratinization is disrupted, leading to clogging.
  • Anaerobic conditions allow C. acnes to thrive.
  • Inflammation is triggered by both bacterial activity and increased sebum.
  • Comedogenesis (formation of comedones) and acne progression follow.

Essentially, DHT and androgen receptor activation initiate and perpetuate nearly every step in the acne pathway—all within the hair follicle.


Targeting the Androgen Receptor for Acne Treatment​


Given this mechanism, it becomes clear why hormonal therapies that modulate or block androgen receptor activity are a theoretically strong and effective treatment strategy for acne.
 
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Hey everyone! Androgens and acne, what a combo, right? Dr. Green really hit the nail on the head discussing how hormones play a role in this skin struggle. It's something many of us can relate to. Speaking of skin issues, I've had my fair share of battles, especially with melasma. It's been quite the journey finding effective treatments. Recently, I stumbled upon a melasma treatment that showed promising results. Pico laser worked wonders for me, offering a ray of hope in this ongoing battle.
 
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While the explanation given in the video seems like accurate information, it only represents a small piece of the puzzle. For example, the acne that men on TRT experience often responds to E2 management, and in these cases, has apparently nothing to do with DHT.
Yes how do we control e2 and acne, I guess lower dose or take an ai. Although daily of eod cialas controls estrogen aswell. I find all of this helps when acne flares up.. mostly after taking hcg after a couple of weeks
 
While the explanation given in the video seems like accurate information, it only represents a small piece of the puzzle. For example, the acne that men on TRT experience often responds to E2 management, and in these cases, has apparently nothing to do with DHT.
Is that your experience? I guess it's the fluctuation of hormones or the adjustment to a new normal. And as always genetics.
I had mild acne during puberty that subsided and vanished.
On TRT with androgel and now TU I haven't had acne. Maybe a bit more oily forehead now, however I had also a oily forehead while T deficient.
 
Is that your experience? I guess it's the fluctuation of hormones or the adjustment to a new normal. And as always genetics.
I had mild acne during puberty that subsided and vanished.
On TRT with androgel and now TU I haven't had acne. Maybe a bit more oily forehead now, however I had also a oily forehead while T deficient.
Yes - chest and back acne eliminated with anastrazole.

Another big component with acne is insulin and IGF-1: The Relationship Between Acne Vulgaris and Insulin Resistance

SAD diet is devastating for acne while keto/carnivore is very helpful.
 
No acne during puberty. No acne during many years of drinking or doing drugs, partying, not sleeping for days and destroying my body. Also no acne while low T with crashed e2. No acne while hardcore bodybuilding for 15 years and running up to 500mg ( i know pussy #s given todays brainless kids) of androgens ( test + deca + some oldschool Russian methandrestenolone) and no acne on TRT. Basically never. But I never eaten SAD diet because I'm Eastern European and been eating pretty good since I've rolled out. So my take its genetics, plus food and maybe being athletic as been involved in various forms of sport since early teens. But I had my share of other pretty harsh issues while growing up which faded with years so probably outgrew.

I'm actually eager to test my DHT as I've never tested it as its so expensive.

My 2 cents.
 
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*Acne vulgaris (AV) is a chronic inflammatory and immune-mediated skin condition characterized by the presence of noninflammatory (open and closed comedones) and inflammatory (papules, pustules, and nodules) lesions, primarily on the face, chest, upper back, and shoulders (1,2).

*AV is a multifactorial disease with 4 key interrelated processes driving pathophysiology: inflammation, increased sebaceous gland activity, and sebum production, follicular hyperkeratinization, and colonization of proinflammatory strains of Cutibacterium acnes (C.acnes) (1,6,7)
 
Acne is multifactorial and not a typical symptom of high e2, yes it can play a role but DHT let alone sensitivity of the AR to DHT plays a big role.

High estradiol is not the main driver here.

Non aromatizable androgens can cause acne!

Androgenicity of the compound is key here!
 
While the explanation given in the video seems like accurate information, it only represents a small piece of the puzzle. For example, the acne that men on TRT experience often responds to E2 management, and in these cases, has apparently nothing to do with DHT.
You mean anastrozole can be used as an acne treatment?
 
 
 

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