whats the proof that DHT directly causes hairloss, and not just through its opposition to estrogen?
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Yeah its strange how people get stuck on finasteride and min especially on reddit. Can i dm you about my regimen?
Sure
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I would say the proof is in the fact that finasteride works.
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There is a lot to cover here, but I will just throw in some stuff I have saved recently. Firstly we are dealing with a relative increase of T & DHT in relation to epitestosterone, a native antiandrogen...
We conclude that EpiT was effective as an antiandrogen and had no intrinsic androgenic activity in the hamster flank organ. It probably functions both as a competitive inhibitor of the androgen receptor and as a 5 alpha-reductase inhibitor.
(https://pubmed.ncbi.nlm.nih.gov/3598212/)
The CYP17 promoter polymorphism may partly explain high natural (>4) T/E ratios. Our data indicate that 5-androstene-3beta, 17alpha-diol is an important precursor of epitestosterone and that CYP17 is involved in its production.
(https://pubmed.ncbi.nlm.nih.gov/18496127/)
(https://www.sciencedirect.com/science/article/pii/S0022202X15411169)
The level of dihydrotestosterone (DHT) and the ratio of testosterone to epitestosterone (T/E ratio) in vertex hair from premature baldness subjects were higher than in the sample of non-baldness subjects (P<0.001, 0.001), whereas the levels of androgens in occipital hair from the same baldness group were not different. In addition, we discovered the levels of DHT, testosterone, and DHT/T ratio in plasma from premature male pattern baldness were higher than in those of control subjects (P<0.001, 0.001, 0.005).
(https://pubmed.ncbi.nlm.nih.gov/14757277/)
(https://www.jidonline.org/article/S0022-202X(15)36130-3/fulltext)
Unfortunately I cannot find a study comparing estradiol levels in hair of balding and non-balding men but I would say that unless there is shown to be a significant difference I would not say that raising estradiol 'fixes' the pathology of male pattern baldness but rather that it helps offset the direct damage of androgens.
Regarding androgens and how they damage hair, we also need to be careful because studies which add DHT in isolation in a petri dish are bullshit and don't really replicate the environment found in vivo in the actual human hair follicle. For instance this study compares the effect of DHT on hair at different levels of oxidative stress and in my opinion this is HUGE:
Tissue culture is routinely carried out at atmospheric levels of 21% O2, vastly higher than the physiological levels of 1–5% O2 found within the dermis in vivo. These supraphysiological levels of oxygen accelerate the fibroblast transition into a postmitotic, senescence state (Alalufet al., 2000; Chen, 2000). Our findings highlight that this is also the case for DPCs and demonstrate that these cells should be cultured under hypoxic conditions(2% O2).
Androgens have been shown to stimulate TGF-b1 secretion in AR-transfected BDPCs (Inuiet al., 2002). In our study, DHT stimulated TGF-b secretion from DPCs only at 21% O2, suggesting that oxidative stress is an essential component of androgen response in Androgenetic Alopecia. ...
AR-transfected BDPCs but not ODPCs respond to synthetic androgen R-1881 by producing TGF-b1 (Inuiet al., 2002). In contrast, we also show that at 21% O2 ODPCs also secrete TGF-b1 and TGF-b2 in response to DHT.
(https://core.ac.uk/download/pdf/82360493.pdf)
And what this basically shows is that at normal oxygen levels balding follicles do not react negatively to DHT, whereas at supraphysiological oxygen levels EVEN occipital (non balding) follicles react by releasing negative growth factors in the presence of DHT.
Honestly read all these f*****g papers, I simply can't quote all of the relevant important information here, it would be too much...
We conclude that EpiT was effective as an antiandrogen and had no intrinsic androgenic activity in the hamster flank organ. It probably functions both as a competitive inhibitor of the androgen receptor and as a 5 alpha-reductase inhibitor.
(https://pubmed.ncbi.nlm.nih.gov/3598212/)
The CYP17 promoter polymorphism may partly explain high natural (>4) T/E ratios. Our data indicate that 5-androstene-3beta, 17alpha-diol is an important precursor of epitestosterone and that CYP17 is involved in its production.
(https://pubmed.ncbi.nlm.nih.gov/18496127/)
Another interesting observation was the remarkable increase in T/E ratios in the hair of balding fathers and their sons. These elevated T/E ratios were the results of a significant decrease in epitestosterone and a slight increase in testosterone (Figure 1b,c). In comparing the T/E ratio between the balding group and nonbalding group (Figure 2), we found that the sons of the balding group showed a ratio three times higher (mean 35.83, range 30.37–42.54, p <0.001) than that of the control group (10.47, 6.39–15.95). The difference between the fathers of the two groups was more clear – the T/E ratio of the balding fathers (mean 46.41, range 32.99–68.34, p <0.001) was about five times that of the nonbalding fathers (9.17, 6.34–11.41).(https://www.sciencedirect.com/science/article/pii/S0022202X15411169)
The level of dihydrotestosterone (DHT) and the ratio of testosterone to epitestosterone (T/E ratio) in vertex hair from premature baldness subjects were higher than in the sample of non-baldness subjects (P<0.001, 0.001), whereas the levels of androgens in occipital hair from the same baldness group were not different. In addition, we discovered the levels of DHT, testosterone, and DHT/T ratio in plasma from premature male pattern baldness were higher than in those of control subjects (P<0.001, 0.001, 0.005).
(https://pubmed.ncbi.nlm.nih.gov/14757277/)
Of the 12 steroids studied, 9 steroids extracted from the vertex hair showed group differences (Table 1). The balding groups in both populations had significantly higher DHT levels (mean=6.48ngg−1 (P<0.0002) for Koreans and 4.59ngg−1 (P<0.004) for Caucasians) than the control groups (3.56ngg−1 for Koreans and 1.51ngg−1 for Caucasians). T levels were also increased in both balding groups (14.48ngg−1 (P<0.02) for Koreans and 5.87ngg−1 (P<0.02) for Caucasians) compared with their corresponding control groups. Balding Caucasians had 2-fold increased epitestosterone (Epi-T) levels compared with normal Caucasians (P<0.007), but only slight increases compared with normal Koreans, which might suggest different androgen metabolisms between the races. In addition, 5β-dihydroprogesterone (5β-DHP) levels were significantly increased in balding Koreans (P<0.0003) compared with normal Koreans, but were not significantly different from those in the Caucasian groups.(https://www.jidonline.org/article/S0022-202X(15)36130-3/fulltext)
Then this last study is also pretty interesting. It shows that Epitestosterone seems to be a larger factor for Caucasians (despite it actually being higher in balding follicles, T & DHT seem to go up more), and not so much for Asians. An increase in T & DHT in relation to epitestosterone seems universal in both races however. And then we also have levels of some other hormones which seem to be distorted, indicating overall alteration in steroid metabolism.Unfortunately I cannot find a study comparing estradiol levels in hair of balding and non-balding men but I would say that unless there is shown to be a significant difference I would not say that raising estradiol 'fixes' the pathology of male pattern baldness but rather that it helps offset the direct damage of androgens.
Regarding androgens and how they damage hair, we also need to be careful because studies which add DHT in isolation in a petri dish are bullshit and don't really replicate the environment found in vivo in the actual human hair follicle. For instance this study compares the effect of DHT on hair at different levels of oxidative stress and in my opinion this is HUGE:
Tissue culture is routinely carried out at atmospheric levels of 21% O2, vastly higher than the physiological levels of 1–5% O2 found within the dermis in vivo. These supraphysiological levels of oxygen accelerate the fibroblast transition into a postmitotic, senescence state (Alalufet al., 2000; Chen, 2000). Our findings highlight that this is also the case for DPCs and demonstrate that these cells should be cultured under hypoxic conditions(2% O2).
Androgens have been shown to stimulate TGF-b1 secretion in AR-transfected BDPCs (Inuiet al., 2002). In our study, DHT stimulated TGF-b secretion from DPCs only at 21% O2, suggesting that oxidative stress is an essential component of androgen response in Androgenetic Alopecia. ...
AR-transfected BDPCs but not ODPCs respond to synthetic androgen R-1881 by producing TGF-b1 (Inuiet al., 2002). In contrast, we also show that at 21% O2 ODPCs also secrete TGF-b1 and TGF-b2 in response to DHT.
(https://core.ac.uk/download/pdf/82360493.pdf)
And what this basically shows is that at normal oxygen levels balding follicles do not react negatively to DHT, whereas at supraphysiological oxygen levels EVEN occipital (non balding) follicles react by releasing negative growth factors in the presence of DHT.
Honestly read all these f*****g papers, I simply can't quote all of the relevant important information here, it would be too much...
It's not strange, it's because people listing 15 suppliments/topicals and still getting non-obvious or "copyable" results. If literally anything else showed tangible results, the conversation would shift quickly away from finasteride.
Even people who use RU/other topical AAs can't show it's obvious efficacy as a stand alone treatment.
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Just a note here with personal info. I have pretty high Testosterone (1150) High E (88) and low DHT (2.4) I was a dense dense NW0 at 42 and I’m almost bald at 44 in treatments - Propecia, Topical Dutasteride, oral minoxidil, RU.
also getting sides. I’m in great shape.
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you probably have high systemic e but low tissue e
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How come that deathdiss guy is banned, why do so many people on here get banned? what rules are they breaking?
Their definitely getting maintenace with AAor at least most people, but regrowth is a different game sadly.
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Almost bald? Will you stop ffs
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I'm directly descended from genghis Khan via a traceable royal lineage from the crimean khanate yet I am/was balding aggressively lmao
Even genghis khan can't save you
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The genetic recombination pill has destroyed me tbh
How so, besides hair loss?
Frontiers | Dihydrotestosterone Regulates Hair Growth Through the Wnt/β-Catenin Pathway in C57BL/6 Mice and In Vitro Organ Culture
Dihydrotestosterone (DHT) is the most potent androgen that regulates hair cycling. Hair cycling involves cross-talk between the androgen and Wnt/β-catenin pa...
www.frontiersin.org
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As you age DHT and Estrogen declines, and hair follicles' dht resistance declines.
Follicles become even more sensitive with age, by then only a few dht is enough to cause male pattern baldness.