Believe it or not, there are still retards on this site + IRL that genuinely believe DHT muh "masculinizes your face". It should be known by now that DHT is one of the most useless hormones when it comes to attractiveness post 16-18 years of age.
Table of Contents:
1. Molecular/Enzymatic basis
1.1. Synthesis and Potency.
1.2. Aromatization constraint.
1.3. Intracrine/paracrine compartmentalization.
2. Facial Bones
2.1. Ossification.
2.2. Androgens (more specifically androgenic morphogenesis).
2.3. Epiphyseal maturation.
3. Cellular Constraints
3.1. AR signaling
3.2. Estrogenic signaling (important)
3.3. Cofactor/Chromatin Context
4. Follicular Biology
4.1. Follicular miniaturization.
4.2. Skin Texture
4.3. Regional Specificity
1. Molecular/Enzymatic basis:
Synthesis and potency: Testosterone is converted to DHT by 5AR, basic knowledge (isoenzymes SRD5A1 and SRD5A2). DHT has around 5 x higher affinity for AR and forms a more stable AR-ligand complex, producing a MUCHHH stronger transcriptional activation at androgen response elements. This makes DHT the dominant androgenic effector in tissues with high 5AR activity (skin, hair follicle dermal papilla etc..). So now your retarded brain (doesn't apply to you if you're anti DHT) knows the basics of what we're facing.
Aromatization constraint: DHT is not a substrate for aromatase (CYP19A1) so basically it js means it cannot be converted into estradiol. AND GUESS FUCKING WHAT? ESTRADIOL IS a CENTRAL MEDIATOR of epiphyseal fusion & bone mineralization. Because DHT cannot even yield fucking estrogenic metabolites, so logically its ability to influence bone (via ER pathway) is...... NIL. NADA. ZERO.
Intracrine/paracrine compartmentalization: Androgen action is contextual, that is, local intracellular conversion and paracrine mediators (IGF1, TGF-beta (can't find symbol lol) family, Wnt/beta-catenin modulators) determine the phenotype. The scalp and facial dermis have a fuck ton of SRD5A expressions so DHT collects in soft tissues where it exerts trophic/atrophic effects depending on cell type. Bone cells express AR but their response is modulated by..... you guessed it, estrogen receptor signaling.
2. Facial Bones
Ossification: Facial bones arise mainly by direct differentiation of mesenchymal cells into osteoblasts (obv there are contributions from sutural growth + periosteal apposition). Maxillofacial size/shape are changed during puberty, obv, by a combo of endochondral growth at cranial base synchondroses + periosteal modeling. So the ossification part is clear, that's another step in understanding the final verdict (title, lol.).
Androgenic Morphogenesis: The ABSOLUTE most plastic period for changing ur face is ofc the pubertal window, when chondrocytes and osteoprogenitors are proliferative, sutures are patent and periosteal apposition rates are high. Androgens in this window help iin periosteal expansion (increasing bone breadth) by AR signaling in osteoblast lineage cells + androgen to estradiol conversion that influences endochondral maturation and death of growth plates (closure = death hehe).
Epiphyseal maturation: By 17-19 years *most* craniofacial growth centers undergo reduced chondrogenesis and sutural interdigitation increases and the proliferative capacity of osteoprogenitors gets fucked (diminishes). Once the osteogenic niche has transitioned from high turnover developmental modeling to low turnover remodeling, the capacity for ACTUAL, GOOD AMT. of periosteal expansion is pretty less/minimal/near zero or whatever. Basically by 17 you're nearing completion. This is basic knowledge but i wanted to provide a small amount of insight into the actual process.
3. Cellular Constraints
AR signaling: Osteoblasts, osteocytes nd mesenchymal progenitors express AR. DHT binding can change osteoblastic differentiation and local RANKL or OPG balance (not important to know, but if you wanna know js tell me). But a good amt. of periosteal expansion requires proliferation of osteoprogenitors which is variant and..... BOOM, age dependent. So you're done by late teens. Like 17-18-19 means it's literally 99% over.
Estrogenic signaling: A lotta anabolic skeletal effects are attributed to androgens are actually mediated by aromatization to estradiol and then, ER signaling. Because DHT bypasses aromatase (as we read in 1.2.), it lacks a HUGGEEE PART that drives bone geometry in adults.
Cofactor/Chromatin context: Whether DHT changes a cell’s behavior depends on what helper proteins and DNA regions are available for the AR to work with. In mature bone (what we're talking abt), the genes that control growth and shape are mostly fucked, and only maintenance genes stay active. Even though DHT binds the AR it can’t turn on the old growth. So even a high affinity ligand like DHT yields constrained outputs.
4. Follicular Biology
Follicular Miniaturization: AAAANNNDDDD WE HAVE REACHED THE MAIN PART. Androgenic alopecia is a classic DHT mediated phenotype. In genetically susceptible follicles (AR polymorphisms, CAG repeat length, local SRD5A expression), DHT-AR transcriptional activity upregulates paracrine mediators like TGF-beta1/2, DKK1 that induce miniaturization, which, if your retard brain doesn't understand, basically means progressive shortening of the anagen phase, reduction of the hair follicle’s dermal papilla signals and replacement of terminal hair shafts with vellus hair.
Skin Texture: DHT actuvates sebaceous gland lipogenesis by AR driven expression of enzymes of lipid biosynthesis, increasing sebum production and pore prominence. Now obviously who on the fucking planet would want that? Yup, members of the pro DHT clan. JFL at them.
Regional specificity: The same androgenic milieu can masculinize secondary sexual traits (laryngeal hypertrophy, facial hair) but in a weird way cause hair loss on the scalp. This is a dichotomy. And this dichotomy is due to region specific AR cofactor expression and differential paracrine signaling in the ffollicular units (No need to get into details as our main topic has been cleared already)
SO, I GUESS THAT'S ENOUGH TO SHUT DOWN DHT COPES? BUT, I SERIOUSLY DON'T UNDERSTAND WHY ANYONE WOULD NEED DHT POST 17. REALLY MAKES ME CURIOUS.
(and yes i posted the same thread on .org, you're welcome).
