Okay
atrophicpyra i looked at the studies and your claim it's wrong, first of all:
The studies were performed on mice in vitro cells, specifically MC3T3-E1 cells (Which are non transformed pre osteoblast cells derived from C57BL/6 in mouse newborns skull.
studies showed that it increased proliferation, differentiation and mineralization markers.
also that it reduced resorption activity, TRAP / cathepsin B and direct androgen receptor signaling. which in simple terms, it showed that DHT shifts the bone turnover towards a more “bone-preserving” state.
Now the issue with claiming this will grow bone is as it follows
Study used rats with hormone deficiencies and osteoporosis.
Your logic is also flawed as your argument was "If bone formation increases and resorption decreases bones will grow larger", this is simply not true as it only displays that DHT works by mildly and locally aiding the maintenance of bone density not causing elongation or growth, bone balance control density, not growth, it's a homeostasis mechanism, now you will say, well, doesn't that mean that dut and fin will affect BMD? actually, quite the opposite, which ill address at the end.
Important to mention bone modeling and remodeling are far from the same, bone remodeling (which is osteoblast-osteoclast turnover) regulates the bone density, this doesn't mean it grows bones at all, whereas
bone modeling is the real responsible for changes in bone size and shape.
To actually cause real bone enlargement and jaw growth or overall growth you need growth plates or active sutures, spatial remodeling signals, mechanical forces, coordinated tissue resorption
and deposition in specific directions, the study you cited actually used none of this and only used isolated cell activity level.
The strongest argument you cited is that the studies found dht to have "anti resorptive properties", the issue with is that this means in a best case scenario that bone turnover slows, and bone is preserved, not that it enhances anabolism, actually scientific literature shows that androgens are mainly anti resorptive with very limited anabolic potential in vivo cells, which renders the theory useless.
The in vitro thing also has several problems, as the studies cited used mouse osteoblast cells in a dish and avian / isolated osteoclasts, this scenario and environment is highly unrealistic because it doesn't take into account real variables to consider such as that there was no endocrine system, no competing hormones and also no structural constraints, the fact cells behave a certain way doesn't mean it will grow localized projection the way you want it to.
Now let's talk about the point i made in the older threads about fin and dut having no effect whatsoever at BMD and actually increased circulating test levels and increased BMD, this is mainly because DHT itself play a tertiary role when it comes to regulating BMD and bone density overall, it's over run by test and E2 specifically as the most important hormone for preserving it, this mainly because estrogen is the primary inhibitor of osteoclasts, also not to mention DHT cannot aromatize unlike Testosterone which does convert to estrogen making it the main protective pathway and the reason why no BMD loss was shown, test and e2 go up when inhibiting test to DHT conversion cause it increases circulating test levels and it increases as well E2 (already explained the importance), this actually destroys the whole claim as the studies where performed not only in real humans (which they also were young healthy men) and also because the studies showed an increased of BMD,
if DHT was a main factor for growth it would've shown a decrease of BMD and not the opposite which was shown, yet again if that theory of DHT growing bones and being “muh crucial” was true facial shrinkage would've been noticed clinically as well as BMD loss which wasn't noticed at all, if not the opposite ill quote the study “Circulating DHT does not appear to have a clinically significant role in modulating bone mass", this meaning the circulating test and e2 increase compensates for the loss of DHT and avoid the BMD loss and even go as far as to improve it, proving AGAIN how dht plays a tertiary role for bone density rather than a main role like E2 does.
anyways, point is If DHT were a important and crucial driver of bone growth, the long term suppression would result in measurable bone loss or craniofacial changes, which AGAIN neither of which are observed clinically.
studies:
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/
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The study you cited again proves you wrong jfl, the study also used Beta DHT "beta-DHT (normally inactive) still affects osteoclasts" was mentioned in the studies, now what does this actually imply? ohhh, it implies that bone cells may respond through non standard pathways which makes the effect to be cell specific
and also non generalizable, this meaning that osteoclast responses may involve atypical or cell specific receptor interactions, limiting the extrapolation to systemic physiology in humans.
studies used
(Osteoblast proliferation, differentiation and mineralization on (MC3T3-E1))
studies:
https://pubmed.ncbi.nlm.nih.gov/7819831/
https://pubmed.ncbi.nlm.nih.gov/15694414/
(Explanation of the need for cofactors and synergy)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5294959/
(Dut and finasteride study)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2684818/
https://pubmed.ncbi.nlm.nih.gov/9892663/ (study cited by you)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5651475/ ( yes the studies you cited debunk your own claim)
syna link that one dht nigga again i want him to explain how this is possible if there is little 5ar activity in bone
and “muh permanent heightmaxx”
