Damn, Norwood is ruthless



For comparison, the pic everyone has seen:

He's only bald because the prison food isn't vegan so its adding chemicals to his body so its messing up his DHT levels

I thought eating organic would help with balding

DHT doesn't cause balding, free testosterone apparently does. DHT and testosterone are ok


https://sci-hub.scihubtw.tw/https://...jpa.1330880106

DHT is responsible for balding, its just some peoples hair follicles are more sensitive to it than others.

What you think fin does? It reduces DHT levels.

Studies have found that 5αR2 is more highly expressed in the AGA balding scalp and beard HFs in males than in nonbalding AGA scalps (Price, 1999), so we speculated that the region-specific expression of 5αR2 induces the distinct effects of androgens on HF growth. However, it is difficult to assess the influence of 5αR2 on HF growth because 5αR cannot be maintained in culture systems in vitro. Therefore, we used DHT in our study. We found thatDHT at concentrations of 10-5 mol/L and 10-6 mol/L significantly inhibited HF growth, while 10-7 mol/L DHT promoted HF growth compared with 10-8 mol/L DHT. Moreover, the effect of DHT on hair growth in C57BL/6 mice is similar to that on in vitro HFs. These results suggest that different concentrations of DHT greatly contribute to androgen-induced HF development. Many scholars have demonstrated that the scalp skin DHT concentration in AGA is significantly higher than that in hair-containing scalp (Price, 1999), which is consistent with the results of our experiments showing that high-dose DHT inhibits HF growth. However, after treatment with finasteride, the scalp skin DHT levels decreased, and AGA progression was delayed (Bang et al., 2004; Buchanan and Robaire, 2010; Prahalada et al., 2015). In our study, we found a similar phenomenon:when the DHT concentration decreased from 10-6 mol/L to 10-7 mol/L, the HFs grew much better than in the presence of higher DHT concentrations. In fact, the results suggest that an appropriate level of DHT is required for normal androgen-sensitive HF growth. Once the DHT concentration decreased from 10-7 mol/L to 10-8 mol/L, the HF growth rate showed no significant difference from that in the control group, which explains why beard growth is weaker in castrated males.

Activation of the Wnt/β-catenin pathway is important for HF regeneration and hair shaft growth. It has been reported that HFs cannot form when β-catenin, a key signaling molecule in this pathway, is mutated in the hair substrate of mice. When the mutant is induced in normal mice, the HFs do not enter the next hair growth cycle (Huelsken et al., 2001). Moreover, the loss of β-catenin activity directly leads to a block in the differentiation of HFSCs into HF cells (Povelones and Nusse, 2002; Furlong, 2005). Thus, we concluded that DHT affects HF growth differently by regulating the translocation of β-catenin, which is mediated by GSK3β. GSK3β activity is determined by several factors, and it has been demonstrated that phosphorylation at ser-9 is essential for decreasing GSK3β activity (Shimizu and Morgan, 2004; Mulholland et al., 2005). As expected, the Wnt/β-catenin pathway is negatively influenced by high levels of DHT (10-5 and 10-6 mol/L) in cultured HFs. Our results are in agreement with those of Leirós GJ et al., who found that DHT can downregulate the expression of p-GSK3β (ser9) and β-catenin in HFs from AGA patients (Leirós et al., 2012). Notably, HFs treated with 10-7 mol/L DHT showed an obvious increase in the nuclear expression of β-catenin in the hair matrix. Therefore, we hypothesized that 10-7 mol/L DHT promotes HF growth by activating the Wnt/β-catenin signaling pathway, while high levels of DHT have the opposite effect. In the normal hair follicle cycle, immunofluorescence staining indicated that AR is expressed in the dermal papilla cells and hair matrix cells, so we speculate that DHT might regulate Wnt/β-catenin signaling pathway by binding with AR in these two types of cells. However, the exact mechanism needs to be further confirmed.

To further demonstrate the role of the Wnt signaling pathway in HF growth, we used IM12 and 21H7 to mimic the effects of activating and inhibiting the Wnt signaling pathway (Schm?Le et al., 2010; Tsai et al., 2014). In the presence of IM12, a β-catenin-specific activator that impacts GSK3β, the growth rate of HFs in vitro was significantly accelerated. Overwhelming evidence has shown that the activation of β-catenin is necessary to induce HFs (Celso et al., 2004). However, the addition of the β-catenin inhibitor 21H7 markedly inhibited the growth of HFs. David Enshell-Seijffers et al. also found that ablation of β-catenin in HFs results in dramatic hair shortening and thinning (Enshell-Seijffers et al., 2010). A similar positive effect of IM12 on HFs was observed upon cotreatment with 10-6 mol/L DHT. Considering both of these results, it is conceivable that DHT is involved in regulating HF growth by modulating the translocation of β-catenin to the nucleus. From our results, we conclude that the effects of DHT are closely related to its concentration; actually, DHT can activate the Wnt pathway at an appropriate concentration.

Functional cross-talk between the androgen and Wnt/β-catenin signaling pathways has been described in this study. Our results indicate that DHT can regulate the expression of molecules necessary for HF development, and some of these factors involved in androgen-induced hair growth are encoded by target genes of the Wnt/β-catenin pathway. We found that an appropriate concentration of DHT resulted in an increase in p-GSK3β (ser-9) levels in cultured HFs, followed by β-catenin translocation into the nucleus and activation of the transcription of downstream target genes (here means activate Wnt/β-catenin pathway), which prompted faster HF growth. As shown in our study,high-dose DHT had a negative effect on HFsthat was diminished by cotreatment with a β-catenin activator.

Previous studies have found that androgen has different effects on hair follicles in different regions, andappropriate concentrations of androgens can promote hair growth, while excessive concentrations of androgens can inhibit hair growth(Itami and Inui, 2005)
https://www.frontiersin.org/articles...019.01528/full