"The Actual Cure For Male Pattern Baldness"

lampofred

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Feb 13, 2016
Messages
2,980
@GorillaHead

I read that vitamin A lowers excess 5a reductase and increases androgens while lowering the "end-of-chain" hormones like DHT. I think low vit A is definitely a player in MPB but it's involved in extremely complicated biochemical processes so IDK if it's safe to supplement. It can greatly increases oxidative stress, iron/PUFA-related damage, blood pressure, etc. if your system can't handle it.
 

GorillaHead

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Oct 21, 2018
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USA
@GorillaHead

I read that vitamin A lowers excess 5a reductase and increases androgens while lowering the "end-of-chain" hormones like DHT. I think low vit A is definitely a player in MPB but it's involved in extremely complicated biochemical processes so IDK if it's safe to supplement. It can greatly increases oxidative stress, iron/PUFA-related damage, blood pressure, etc. if your system can't handle it.


Based on everything i am reading. All signs point to too much vitamin a being the problem or something related to its metabolism and its interaction with fatty acids or even vdr in the skin cause it To be detrimental to hair on the scalp
 

fathom

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Aug 18, 2020
Messages
12
so does potassium bicarbonate work??

I'm at 2 1/2 months now, have gone the oral route much more so that the topical one. So far, nothing but within the next month if I notice no signs, I will switch to a more heavy topical regime. I'll see this through and prove or disprove it.
 

tim333

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Joined
Feb 27, 2020
Messages
197
@GorillaHead

I read that vitamin A lowers excess 5a reductase and increases androgens while lowering the "end-of-chain" hormones like DHT. I think low vit A is definitely a player in MPB but it's involved in extremely complicated biochemical processes so IDK if it's safe to supplement. It can greatly increases oxidative stress, iron/PUFA-related damage, blood pressure, etc. if your system can't handle it.
I'd be interested in your sources. Adequate vA is important, the problem is that most get too much which definitely promotes balding.

Millions of middle aged men in poor countries have full heads of hair and are borderline vA deficient.
 

johnwester130

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Aug 6, 2015
Messages
2,924
I'm at 2 1/2 months now, have gone the oral route much more so that the topical one. So far, nothing but within the next month if I notice no signs, I will switch to a more heavy topical regime. I'll see this through and prove or disprove it.

do you think fungus causes baldness?

so far i have in my fungal program

daktarin cream - basically nizoral
selsun blue
zinc pyrithion shampoo
alpecin 4 in1 - contains 4 antifungal ingredients
 

Inaut

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Joined
Nov 29, 2017
Messages
2,223
@johnwester130 Why only topical and not solving the fungal issue internally? I think baldness is caused by this issue and it cascades into hormone disruption and over active adrenals, under active thyroid etc... leading to baldness. I'm testing something out as my hair thinning quite obviously now (I've also tried countless topical methods which is probably adding to the problem tbh...) Reducing my supplements to only a few with a focus on fungal/bacteria elements and resistant starch for fixing colon. Healthwise I'm feeling amazing these days. Optimistic regardless of what awaits me outside my door (covid/lock down/political theatre)
 

tim333

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Feb 27, 2020
Messages
197
I lost most of my hair when I was consuming a WAPF diet that included liver and cod liver oil. After I gave that up my hairloss slowed down to almost nothing. I haven't grown back what I lost though. I had my serum vA tested 12 months after going on a low vA diet, it was still high. At 18 months, the same level. It may take a couple more years to deplete my liver reserves. My target is between 30 and 40 mcg/dL, that is not a deficient range. In that range your body still has plenty of vA to use, most children are in that range. As far as I'm concerned there is nothing to lose by reducing serum vA to that range and everything to gain. An elevated level of retinoic acid is strongly associated with hair loss, it also depletes other nutrients whose deficiencies are associated with hairloss such as biotin, riboflavin, vD and K2.
 

ilhanxx

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Joined
Feb 26, 2019
Messages
259
I am on rob's massage technic and wow (pinching and finger clawning) . lots of baby hairs everywhere, I spend much time about 35 40 min a day. oral or topical medicals doesn't cure fibrose tissue tightness/hardness. I realize that when the scalp going softer and elastic, sebum or itching problems has gone.
 

tim333

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Joined
Feb 27, 2020
Messages
197
I am on rob's massage technic and wow (pinching and finger clawning) . lots of baby hairs everywhere, I spend much time about 35 40 min a day. oral or topical medicals doesn't cure fibrose tissue tightness/hardness. I realize that when the scalp going softer and elastic, sebum or itching problems has gone.
Are you sure there are new hairs or are you just studying your scalp more closely and seeing them because of that?

I massage but wow 40 mins a day? My scalp would look nasty after that.

If scalp calcification is a major player then lowering vA and allowing K2 to work will help a lot. Not sure how fibrosis and calcification is connected though.
 

mrchibbs

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Nov 22, 2017
Messages
2,459
Location
Atlantis
Are you sure there are new hairs or are you just studying your scalp more closely and seeing them because of that?

I massage but wow 40 mins a day? My scalp would look nasty after that.

If scalp calcification is a major player then lowering vA and allowing K2 to work will help a lot. Not sure how fibrosis and calcification is connected though.

Calcification follows fibrosis. Ray has several newsletters on this. It's roughly inflammation -> edema -> fibrosis -> calcification
 

md_a

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Aug 31, 2015
Messages
268
Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla

Abstract

Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.

Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla - PubMed



Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia

Abstract

Background

Several interactions between retinoids and immune system exist. Current evidences suggest a role of retinoic acid in controlling hair cycle. Retinol-binding protein 4 (RBP4) belongs to the lipocalin family and is the specific carrier for retinol (vitamin A) in the blood. It delivers retinol from the liver stores to the peripheral tissues. The pathogenesis of alopecia areata (AA) may be related to increased serum RBP4 level.

Objective

To assess the level of RBP4 in patients with AA.

Patients and methods

This comparative study was conducted on 60 participants who were divided into three groups: group A consisting of 20 patients with active AA; group B consisting of 20 patients with androgenetic alopecia, selected as an example of noninflammatory hair loss; and group C consisting of 20 normal healthy controls. Blood samples were collected from all participants and RBP4 level was measured using enzyme-linked immunosorbent assay.

Results

RBP4 mean value was found to be 38.37±2.83, 37.27±5.05, and 32.10±2.28 μg/ml for groups A, B, and C, respectively. Healthy control group had statistically significant lower value of RBP4 than did the other two groups, but there were no significant difference between AA patients and androgenetic alopecia patients. In AA group, there was no significant relation between number of lesions and the level of RBP4.

Conclusion

The level of RBP4 was found to be increased in serum of both AA and androgenetic alopecia patients. The role of RBP4 may be as a nonspecific molecule leading to hair loss or miniaturization through controlling hair cycle. However, the exact role of RBP4 in the hair cycle and its clinical significance in treatment of AA remains to be elucidated.

Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia



Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia

Abstract

Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.

In conclusion, our findings provide a new link between PGC1a and hair development. Further study will be required to understand the mechanisms regulating hair growth and AGA pathogenesis albeit the complexity in PPAR signaling pathways. It is important to establish the role of interactions between AR, PPAR and retinoid pathways in hair differentiation. The new insights and knowledge of this publication can lead to new ways for AGA prediction, early diagnosis and new treatments to delay or avoid hair miniaturization. In any case this publication proves that the hair growth and differentiation is a very complicated and multifaceted process and it requires knowledge of all the key players to understand and support hair growth.
Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia | Scientific Reports



Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla

Abstract

Androgenetic alopecia (AGA) is characterized by vellus transformation of scalp hairs, corresponding to hair follicle miniaturization during repeated hair cycles with shortened anagen phase. This phenomenon is mediated mainly by androgen. Then, the multi-step molecular pathway of androgen can be involved in the pathogenesis of AGA. The expression of type II 5α-reductase is higher in dermal papilla cells from AGA and beard than those from other sites. On the other hand, type I 5α-reductase expression is relatively low. Next, hormone binding assays and RT-PCR demonstrated that androgen receptor (AR) expression is significantly higher in bald dermal papilla cells than non-bald cells. Additionally, AR coactivator Hic-5/ARA55 is highly expressed in dermal papilla cells of hair follicles from androgen-sensitive sites such as AGA and beard. Collectively, the enhanced expression of type II 5α-reductase, AR and Hic-5/ARA55 can upregulate sensitivity to androgen of dermal papilla cells in AGA. Furthermore, in the coculture of AR-overexpressing human dermal papilla cells from AGA and normal human keratinocytes, R1881 suppresses keratinocyte growth through androgen-inducible TGF-β1, indicating that TGF-β1 is one of the key players in pathogenesis of AGA. TGF-β2 and DKK-1 has been reported to be androgen-induced suppressor of growth of follicular epithelial cells. We expect that more pathogenic mediators will be identified in the future, enabling easier understanding of AGA pathogenesis and providing new therapeutic targets from aspect of andrology.

Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla - PubMed



Dickkopf 1 promotes regression of hair follicles

Abstract

Recently, we suggested that Dickkopf 1 (DKK-1) is a pathogenic mediator involved in male pattern baldness. As premature catagen onset is a key characteristic of male pattern baldness, in this study, we evaluated whether DKK-1 has a role as a catagen inducer in hair cycling. Herein, we report that recombinant human DKK-1 (rhDKK-1) injection into the hypodermis of mice during anagen caused premature onset of catagen, whereas neutralizing DKK-1 antibody delayed anagen-to-catagen transition in mice. Moreover, treatment with rhDKK-1 led to a decrease in final hair follicle length, whereas DKK-1 antibody led to an increase compared with control animals. In addition, DKK-1 and DKK-1 messenger RNA expression is most upregulated in follicular keratinocytes of late anagen in depilation-induced hair cycle progression. Moreover, we observed that rhDKK-1 blocks canonical Wnt-mediated activation of β-catenin signaling and induces the proapoptotic protein Bax, resulting in apoptosis in outer root sheath keratinocytes. Taken together, our data strongly suggest that DKK-1 is involved in anagen-to-catagen transition in the hair cycle by regulating the activity of follicular keratinocytes.

Dickkopf 1 promotes regression of hair follicles - PubMed



Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression

The stress-related neurohormones including glucocorticoids (GCs) are secreted by hair follicles (HFs), and GCs suppress murine hair growth in vivo. In this study, we found that dexamethasone (Dex), a synthetic GC, increased the expression of dickkopf-1 (DKK1), a known catagen inducer, in dermal papilla (DP) cells, but not in follicular keratinocytes. The neutralizing DKK1 antibody significantly attenuated the Dex-induced inhibition of human hair shaft elongation. In addition, the neutralizing Dkk1 antibody delayed Dex-induced catagen in mice. Collectively, our data strongly suggest that stress-related neurohormones cause DP cells to secrete DKK1, thereby leading to stress-associated disturbances in hair growth.

Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression - PubMed

...

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes

Abstract

Recent studies suggest that androgen-driven alteration to the autocrine and paracrine factors produced by scalp dermal papilla (DP) cells may be a key to androgen-potentiated balding. Here, we screened dihydrotestosterone (DHT)-regulated genes in balding DP cells and found that dickkopf 1 (DKK-1) is one of the most upregulated genes. DKK-1 messenger RNA is upregulated in 3-6 hours after 50-100 nM DHT treatment and ELISA showed that DKK-1 is secreted from DP cells in response to DHT. A co-culture system using outer root sheath (ORS) keratinocytes and DP cells showed that DHT inhibits the growth of ORS cells, and neutralizing antibody against DKK-1 significantly reversed the growth inhibition of ORS cells. Analysis of co-cultured ORS cells showed a significant increment of sub-G1 apoptotic cells in response to DHT. Also, recombinant human DKK-1 inhibited the growth of ORS cells and triggered apoptotic cell death. In addition, DHT-induced epithelial cell death in cultured hair follicles was reversed by neutralizing DKK-1 antibody. Moreover, immunoblotting showed that the DKK-1 level is up in the bald scalp compared with the haired scalp of patients with androgenetic alopecia. Altogether, our data strongly suggest that DHT-inducible DKK-1 is involved in DHT-driven balding.

https://pubmed.ncbi.nlm.nih.gov/17657240/



A Potential Suppressor of TGF- Delays Catagen Progression in Hair Follicles

TGF-beta plays important roles in the induction of catagen during the hair cycle. We examined whether TGF-beta2 could activate a caspase in human hair follicles. Using active caspase-9 and -3 specific antibodies, we found that TGF-beta2 activated these caspases in two regions, the lower part of the hair bulb and the outer layer of the outer root sheath. In addition, we searched for a plant extract that can effectively suppress TGF-beta action. We found that an extract of Hydrangea macrophylla reduced synthesis of a TGDbeta-inducible protein. We confirmed that the extract has a potential to promote hair elongation in the organ culture system. Furthermore, it delayed in vivo progression of catagen in a mouse model. Our results suggest that the induction of catagen by TGF-beta is mediated via activation of caspases and that a suppressor of TGF-beta could be effective in preventing male pattern baldness

https://www.researchgate.net/public..._Delays_Catagen_Progression_in_Hair_Follicles

https://ugro.com/hydrangea-macrophy...t extract may,enter the telogen resting stage.



sFRP-1

sFRP-1 (secreted frizzled-related protein 1) is an inhibitor of Wnt signaling pathway. A recent study demonstrated that sFRP-1 regulates intrafollicular canonical Wnt/β-catenin activity through the inhibition of Wnt ligand effects in the human hair bulb (Hawkshaw et al., 2018). sFRP-1 secretions from the dermal papilla control human hair follicle cycling and hair shaft production by interacting with Wnt ligands in the immediately adjacent hair follicle epithelium. sFRP-1 enhanced the emigration of dermal papilla fibroblasts to the connective tissue sheath, which occurs upon Catagen induction, leading to a reduced dermal papilla volume (Kloepper et al., 2010; Tobin et al., 2003). Conversely, inhibition of sFRP1 activity enhanced hair shaft production, hair shaft keratin expression, and inhibition of spontaneous hair follicle regression.

https://korea.in-cosmetics.com/__novadocuments/656371?v=637116672107930000



Characteristics of healthy and androgenetic alopecia scalp microbiome: Effect of Lindera strychnifolia roots extract as a natural solution for its modulation

Abstract

Objective: The human scalp harbours a vast community of microbiotal mutualists. Androgenetic alopecia (AGA), the most common form of hair loss in males, is a multifactorial condition involving genetic predisposition and hormonal changes. The role of microflora during hair loss remains to be understood. After having characterized the scalp microbiota of 12 healthy male subjects and 12 AGA male subjects (D0), the aim of this investigation was to evaluate the capacity of Lindera strychnifolia root extract (LsR) to restore a healthy bacterial and fungal scalp microflora after 83 days (D83) of treatment.


Material and methods: The strategy used was based on high-throughput DNA sequencing targeting the encoding 16S ribosomal RNA for bacteria and Internal Transcribed Spacer 1 ribosomal DNA for fungi.


Results: Test analysis of relative abundance comparing healthy and AGA subjects showed a significant increase of Cutibacterim acnes (P < 0.05) and Stenotrophomonas geniculata (P < 0.01) in AGA subjects. AGA scalp condition was also associated with a significant (P < 0.05) decrease of Staphylococcus epidermidis relative abundance. A lower proportion of Malassezia genus in samples corresponding to AGA scalps and an increase of other bacterial genera (Wallemia, Eurotium) were also noted. At the species level, mean relative abundance of Malassezia restricta and Malassezia globosa were significantly lower (P < 0.05) in the AGA group. Eighty-three days of treatment induced a significant decrease in the relative abundance of C. acnes (P < 0.05) and S. geniculata (P < 0.01). S. epidermidis increased significantly (P < 0.05). At the same time, LsR treatment induced a significant increase in the proportion of M. restricta and M. globosa (P < 0.05).


Conclusion: Data from sequencing profiling of the scalp microbiota strongly support a different microbial composition of scalp between control and AGA populations. Findings suggest that LsR extract may be a potential remedy for scalp microbiota re-equilibrium.

https://pubmed.ncbi.nlm.nih.gov/32803888/
 

Ableton

Member
Joined
Nov 21, 2019
Messages
1,272
Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla

Abstract

Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.

Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla - PubMed



Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia

Abstract

Background

Several interactions between retinoids and immune system exist. Current evidences suggest a role of retinoic acid in controlling hair cycle. Retinol-binding protein 4 (RBP4) belongs to the lipocalin family and is the specific carrier for retinol (vitamin A) in the blood. It delivers retinol from the liver stores to the peripheral tissues. The pathogenesis of alopecia areata (AA) may be related to increased serum RBP4 level.

Objective

To assess the level of RBP4 in patients with AA.

Patients and methods

This comparative study was conducted on 60 participants who were divided into three groups: group A consisting of 20 patients with active AA; group B consisting of 20 patients with androgenetic alopecia, selected as an example of noninflammatory hair loss; and group C consisting of 20 normal healthy controls. Blood samples were collected from all participants and RBP4 level was measured using enzyme-linked immunosorbent assay.

Results

RBP4 mean value was found to be 38.37±2.83, 37.27±5.05, and 32.10±2.28 μg/ml for groups A, B, and C, respectively. Healthy control group had statistically significant lower value of RBP4 than did the other two groups, but there were no significant difference between AA patients and androgenetic alopecia patients. In AA group, there was no significant relation between number of lesions and the level of RBP4.

Conclusion

The level of RBP4 was found to be increased in serum of both AA and androgenetic alopecia patients. The role of RBP4 may be as a nonspecific molecule leading to hair loss or miniaturization through controlling hair cycle. However, the exact role of RBP4 in the hair cycle and its clinical significance in treatment of AA remains to be elucidated.

Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia



Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia

Abstract

Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.

In conclusion, our findings provide a new link between PGC1a and hair development. Further study will be required to understand the mechanisms regulating hair growth and AGA pathogenesis albeit the complexity in PPAR signaling pathways. It is important to establish the role of interactions between AR, PPAR and retinoid pathways in hair differentiation. The new insights and knowledge of this publication can lead to new ways for AGA prediction, early diagnosis and new treatments to delay or avoid hair miniaturization. In any case this publication proves that the hair growth and differentiation is a very complicated and multifaceted process and it requires knowledge of all the key players to understand and support hair growth.
Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia | Scientific Reports



Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla

Abstract

Androgenetic alopecia (AGA) is characterized by vellus transformation of scalp hairs, corresponding to hair follicle miniaturization during repeated hair cycles with shortened anagen phase. This phenomenon is mediated mainly by androgen. Then, the multi-step molecular pathway of androgen can be involved in the pathogenesis of AGA. The expression of type II 5α-reductase is higher in dermal papilla cells from AGA and beard than those from other sites. On the other hand, type I 5α-reductase expression is relatively low. Next, hormone binding assays and RT-PCR demonstrated that androgen receptor (AR) expression is significantly higher in bald dermal papilla cells than non-bald cells. Additionally, AR coactivator Hic-5/ARA55 is highly expressed in dermal papilla cells of hair follicles from androgen-sensitive sites such as AGA and beard. Collectively, the enhanced expression of type II 5α-reductase, AR and Hic-5/ARA55 can upregulate sensitivity to androgen of dermal papilla cells in AGA. Furthermore, in the coculture of AR-overexpressing human dermal papilla cells from AGA and normal human keratinocytes, R1881 suppresses keratinocyte growth through androgen-inducible TGF-β1, indicating that TGF-β1 is one of the key players in pathogenesis of AGA. TGF-β2 and DKK-1 has been reported to be androgen-induced suppressor of growth of follicular epithelial cells. We expect that more pathogenic mediators will be identified in the future, enabling easier understanding of AGA pathogenesis and providing new therapeutic targets from aspect of andrology.

Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla - PubMed



Dickkopf 1 promotes regression of hair follicles

Abstract

Recently, we suggested that Dickkopf 1 (DKK-1) is a pathogenic mediator involved in male pattern baldness. As premature catagen onset is a key characteristic of male pattern baldness, in this study, we evaluated whether DKK-1 has a role as a catagen inducer in hair cycling. Herein, we report that recombinant human DKK-1 (rhDKK-1) injection into the hypodermis of mice during anagen caused premature onset of catagen, whereas neutralizing DKK-1 antibody delayed anagen-to-catagen transition in mice. Moreover, treatment with rhDKK-1 led to a decrease in final hair follicle length, whereas DKK-1 antibody led to an increase compared with control animals. In addition, DKK-1 and DKK-1 messenger RNA expression is most upregulated in follicular keratinocytes of late anagen in depilation-induced hair cycle progression. Moreover, we observed that rhDKK-1 blocks canonical Wnt-mediated activation of β-catenin signaling and induces the proapoptotic protein Bax, resulting in apoptosis in outer root sheath keratinocytes. Taken together, our data strongly suggest that DKK-1 is involved in anagen-to-catagen transition in the hair cycle by regulating the activity of follicular keratinocytes.

Dickkopf 1 promotes regression of hair follicles - PubMed



Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression

The stress-related neurohormones including glucocorticoids (GCs) are secreted by hair follicles (HFs), and GCs suppress murine hair growth in vivo. In this study, we found that dexamethasone (Dex), a synthetic GC, increased the expression of dickkopf-1 (DKK1), a known catagen inducer, in dermal papilla (DP) cells, but not in follicular keratinocytes. The neutralizing DKK1 antibody significantly attenuated the Dex-induced inhibition of human hair shaft elongation. In addition, the neutralizing Dkk1 antibody delayed Dex-induced catagen in mice. Collectively, our data strongly suggest that stress-related neurohormones cause DP cells to secrete DKK1, thereby leading to stress-associated disturbances in hair growth.

Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression - PubMed

...

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes

Abstract

Recent studies suggest that androgen-driven alteration to the autocrine and paracrine factors produced by scalp dermal papilla (DP) cells may be a key to androgen-potentiated balding. Here, we screened dihydrotestosterone (DHT)-regulated genes in balding DP cells and found that dickkopf 1 (DKK-1) is one of the most upregulated genes. DKK-1 messenger RNA is upregulated in 3-6 hours after 50-100 nM DHT treatment and ELISA showed that DKK-1 is secreted from DP cells in response to DHT. A co-culture system using outer root sheath (ORS) keratinocytes and DP cells showed that DHT inhibits the growth of ORS cells, and neutralizing antibody against DKK-1 significantly reversed the growth inhibition of ORS cells. Analysis of co-cultured ORS cells showed a significant increment of sub-G1 apoptotic cells in response to DHT. Also, recombinant human DKK-1 inhibited the growth of ORS cells and triggered apoptotic cell death. In addition, DHT-induced epithelial cell death in cultured hair follicles was reversed by neutralizing DKK-1 antibody. Moreover, immunoblotting showed that the DKK-1 level is up in the bald scalp compared with the haired scalp of patients with androgenetic alopecia. Altogether, our data strongly suggest that DHT-inducible DKK-1 is involved in DHT-driven balding.

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes - PubMed



A Potential Suppressor of TGF- Delays Catagen Progression in Hair Follicles

TGF-beta plays important roles in the induction of catagen during the hair cycle. We examined whether TGF-beta2 could activate a caspase in human hair follicles. Using active caspase-9 and -3 specific antibodies, we found that TGF-beta2 activated these caspases in two regions, the lower part of the hair bulb and the outer layer of the outer root sheath. In addition, we searched for a plant extract that can effectively suppress TGF-beta action. We found that an extract of Hydrangea macrophylla reduced synthesis of a TGDbeta-inducible protein. We confirmed that the extract has a potential to promote hair elongation in the organ culture system. Furthermore, it delayed in vivo progression of catagen in a mouse model. Our results suggest that the induction of catagen by TGF-beta is mediated via activation of caspases and that a suppressor of TGF-beta could be effective in preventing male pattern baldness

https://www.researchgate.net/public..._Delays_Catagen_Progression_in_Hair_Follicles

https://ugro.com/hydrangea-macrophylla-for-hair-loss-captures-the-attention-of-scientists/#:~:text=The hydrangea plant extract may,enter the telogen resting stage.



sFRP-1

sFRP-1 (secreted frizzled-related protein 1) is an inhibitor of Wnt signaling pathway. A recent study demonstrated that sFRP-1 regulates intrafollicular canonical Wnt/β-catenin activity through the inhibition of Wnt ligand effects in the human hair bulb (Hawkshaw et al., 2018). sFRP-1 secretions from the dermal papilla control human hair follicle cycling and hair shaft production by interacting with Wnt ligands in the immediately adjacent hair follicle epithelium. sFRP-1 enhanced the emigration of dermal papilla fibroblasts to the connective tissue sheath, which occurs upon Catagen induction, leading to a reduced dermal papilla volume (Kloepper et al., 2010; Tobin et al., 2003). Conversely, inhibition of sFRP1 activity enhanced hair shaft production, hair shaft keratin expression, and inhibition of spontaneous hair follicle regression.

https://korea.in-cosmetics.com/__novadocuments/656371?v=637116672107930000



Characteristics of healthy and androgenetic alopecia scalp microbiome: Effect of Lindera strychnifolia roots extract as a natural solution for its modulation

Abstract

Objective: The human scalp harbours a vast community of microbiotal mutualists. Androgenetic alopecia (AGA), the most common form of hair loss in males, is a multifactorial condition involving genetic predisposition and hormonal changes. The role of microflora during hair loss remains to be understood. After having characterized the scalp microbiota of 12 healthy male subjects and 12 AGA male subjects (D0), the aim of this investigation was to evaluate the capacity of Lindera strychnifolia root extract (LsR) to restore a healthy bacterial and fungal scalp microflora after 83 days (D83) of treatment.


Material and methods: The strategy used was based on high-throughput DNA sequencing targeting the encoding 16S ribosomal RNA for bacteria and Internal Transcribed Spacer 1 ribosomal DNA for fungi.


Results: Test analysis of relative abundance comparing healthy and AGA subjects showed a significant increase of Cutibacterim acnes (P < 0.05) and Stenotrophomonas geniculata (P < 0.01) in AGA subjects. AGA scalp condition was also associated with a significant (P < 0.05) decrease of Staphylococcus epidermidis relative abundance. A lower proportion of Malassezia genus in samples corresponding to AGA scalps and an increase of other bacterial genera (Wallemia, Eurotium) were also noted. At the species level, mean relative abundance of Malassezia restricta and Malassezia globosa were significantly lower (P < 0.05) in the AGA group. Eighty-three days of treatment induced a significant decrease in the relative abundance of C. acnes (P < 0.05) and S. geniculata (P < 0.01). S. epidermidis increased significantly (P < 0.05). At the same time, LsR treatment induced a significant increase in the proportion of M. restricta and M. globosa (P < 0.05).


Conclusion: Data from sequencing profiling of the scalp microbiota strongly support a different microbial composition of scalp between control and AGA populations. Findings suggest that LsR extract may be a potential remedy for scalp microbiota re-equilibrium.

Characteristics of healthy and androgenetic alopecia scalp microbiome: Effect of Lindera strychnifolia roots extract as a natural solution for its modulation - PubMed
hi sh#kelberg. how is it going?
 

johnwester130

Member
Joined
Aug 6, 2015
Messages
2,924
I'm at 2 1/2 months now, have gone the oral route much more so that the topical one. So far, nothing but within the next month if I notice no signs, I will switch to a more heavy topical regime. I'll see this through and prove or disprove it.

what about topically in a bottle of ethanol?
 

tim333

Member
Joined
Feb 27, 2020
Messages
197
Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla

Abstract

Diffuse hair loss ranks among the most frequent and psychologically most distressing adverse effects of systemic therapy with retinoids, which severely limits their therapeutic use even where clinically desired. Since the underlying mechanisms of retinoid-induced effluvium are as yet unknown, we have investigated the influence of the prototypic retinoid all-trans retinoic acid (ATRA, tretinoin) on the growth of human scalp hair follicles (HF) in culture. HF in the anagen VI stage of the hair cycle were cultured in the presence of 10(-8) or 10(-10) M ATRA. Compared with controls, hair shaft elongation declined significantly already after 2 d in the ATRA-treated group, and approximately 80% of the ATRA-treated HF had prematurely entered catagen-like stage at day 6, compared with 30% in the control group. This corresponded to an upregulation of apoptotic and a downregulation of Ki67-positive cells in ATRA-treated HF. Since transforming growth factor (TGF)-beta has been implicated as a key inducer of catagen, we next studied whether ATRA treatment had any effect on follicular expression. TGF-beta2 immunoreactivity was detected in the outer root sheath of anagen VI scalp HF. In catagen follicles, TGF-beta2 was also expressed in the regressing epithelial strand. After 4 d of ATRA treatment, TGF-beta2 was significantly upregulated in anagen HF in the dermal papilla (DP) and the dermal sheath, 7, and TGF-beta neutralizing antibody partially abrogated at RA induced hair growth inhibition. Real-time PCR confirmed a significant upregulation of TGF-beta2 transcripts in ATRA-treated hair bulbs. This study is the first to provide direct evidence that ATRA can indeed induce a catagen-like stage in human HF and suggests that this occurs, at least in part, via upregulation of TGF-beta2 in the DP. Therefore, topical TGF-beta2/TGF-beta receptor II antagonists deserve to be explored for the prevention and management of retinoid-induced hair loss.

Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla - PubMed



Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia

Abstract

Background

Several interactions between retinoids and immune system exist. Current evidences suggest a role of retinoic acid in controlling hair cycle. Retinol-binding protein 4 (RBP4) belongs to the lipocalin family and is the specific carrier for retinol (vitamin A) in the blood. It delivers retinol from the liver stores to the peripheral tissues. The pathogenesis of alopecia areata (AA) may be related to increased serum RBP4 level.

Objective

To assess the level of RBP4 in patients with AA.

Patients and methods

This comparative study was conducted on 60 participants who were divided into three groups: group A consisting of 20 patients with active AA; group B consisting of 20 patients with androgenetic alopecia, selected as an example of noninflammatory hair loss; and group C consisting of 20 normal healthy controls. Blood samples were collected from all participants and RBP4 level was measured using enzyme-linked immunosorbent assay.

Results

RBP4 mean value was found to be 38.37±2.83, 37.27±5.05, and 32.10±2.28 μg/ml for groups A, B, and C, respectively. Healthy control group had statistically significant lower value of RBP4 than did the other two groups, but there were no significant difference between AA patients and androgenetic alopecia patients. In AA group, there was no significant relation between number of lesions and the level of RBP4.

Conclusion

The level of RBP4 was found to be increased in serum of both AA and androgenetic alopecia patients. The role of RBP4 may be as a nonspecific molecule leading to hair loss or miniaturization through controlling hair cycle. However, the exact role of RBP4 in the hair cycle and its clinical significance in treatment of AA remains to be elucidated.

Assessment of retinol-binding protein 4 in patients with alopecia areata and androgenetic alopecia



Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia

Abstract

Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.

In conclusion, our findings provide a new link between PGC1a and hair development. Further study will be required to understand the mechanisms regulating hair growth and AGA pathogenesis albeit the complexity in PPAR signaling pathways. It is important to establish the role of interactions between AR, PPAR and retinoid pathways in hair differentiation. The new insights and knowledge of this publication can lead to new ways for AGA prediction, early diagnosis and new treatments to delay or avoid hair miniaturization. In any case this publication proves that the hair growth and differentiation is a very complicated and multifaceted process and it requires knowledge of all the key players to understand and support hair growth.
Progressive expression of PPARGC1α is associated with hair miniaturization in androgenetic alopecia | Scientific Reports



Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla

Abstract

Androgenetic alopecia (AGA) is characterized by vellus transformation of scalp hairs, corresponding to hair follicle miniaturization during repeated hair cycles with shortened anagen phase. This phenomenon is mediated mainly by androgen. Then, the multi-step molecular pathway of androgen can be involved in the pathogenesis of AGA. The expression of type II 5α-reductase is higher in dermal papilla cells from AGA and beard than those from other sites. On the other hand, type I 5α-reductase expression is relatively low. Next, hormone binding assays and RT-PCR demonstrated that androgen receptor (AR) expression is significantly higher in bald dermal papilla cells than non-bald cells. Additionally, AR coactivator Hic-5/ARA55 is highly expressed in dermal papilla cells of hair follicles from androgen-sensitive sites such as AGA and beard. Collectively, the enhanced expression of type II 5α-reductase, AR and Hic-5/ARA55 can upregulate sensitivity to androgen of dermal papilla cells in AGA. Furthermore, in the coculture of AR-overexpressing human dermal papilla cells from AGA and normal human keratinocytes, R1881 suppresses keratinocyte growth through androgen-inducible TGF-β1, indicating that TGF-β1 is one of the key players in pathogenesis of AGA. TGF-β2 and DKK-1 has been reported to be androgen-induced suppressor of growth of follicular epithelial cells. We expect that more pathogenic mediators will be identified in the future, enabling easier understanding of AGA pathogenesis and providing new therapeutic targets from aspect of andrology.

Molecular basis of androgenetic alopecia: From androgen to paracrine mediators through dermal papilla - PubMed



Dickkopf 1 promotes regression of hair follicles

Abstract

Recently, we suggested that Dickkopf 1 (DKK-1) is a pathogenic mediator involved in male pattern baldness. As premature catagen onset is a key characteristic of male pattern baldness, in this study, we evaluated whether DKK-1 has a role as a catagen inducer in hair cycling. Herein, we report that recombinant human DKK-1 (rhDKK-1) injection into the hypodermis of mice during anagen caused premature onset of catagen, whereas neutralizing DKK-1 antibody delayed anagen-to-catagen transition in mice. Moreover, treatment with rhDKK-1 led to a decrease in final hair follicle length, whereas DKK-1 antibody led to an increase compared with control animals. In addition, DKK-1 and DKK-1 messenger RNA expression is most upregulated in follicular keratinocytes of late anagen in depilation-induced hair cycle progression. Moreover, we observed that rhDKK-1 blocks canonical Wnt-mediated activation of β-catenin signaling and induces the proapoptotic protein Bax, resulting in apoptosis in outer root sheath keratinocytes. Taken together, our data strongly suggest that DKK-1 is involved in anagen-to-catagen transition in the hair cycle by regulating the activity of follicular keratinocytes.

Dickkopf 1 promotes regression of hair follicles - PubMed



Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression

The stress-related neurohormones including glucocorticoids (GCs) are secreted by hair follicles (HFs), and GCs suppress murine hair growth in vivo. In this study, we found that dexamethasone (Dex), a synthetic GC, increased the expression of dickkopf-1 (DKK1), a known catagen inducer, in dermal papilla (DP) cells, but not in follicular keratinocytes. The neutralizing DKK1 antibody significantly attenuated the Dex-induced inhibition of human hair shaft elongation. In addition, the neutralizing Dkk1 antibody delayed Dex-induced catagen in mice. Collectively, our data strongly suggest that stress-related neurohormones cause DP cells to secrete DKK1, thereby leading to stress-associated disturbances in hair growth.

Dickkopf-1 is involved in dexamethasone-mediated hair follicle regression - PubMed

...

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes

Abstract

Recent studies suggest that androgen-driven alteration to the autocrine and paracrine factors produced by scalp dermal papilla (DP) cells may be a key to androgen-potentiated balding. Here, we screened dihydrotestosterone (DHT)-regulated genes in balding DP cells and found that dickkopf 1 (DKK-1) is one of the most upregulated genes. DKK-1 messenger RNA is upregulated in 3-6 hours after 50-100 nM DHT treatment and ELISA showed that DKK-1 is secreted from DP cells in response to DHT. A co-culture system using outer root sheath (ORS) keratinocytes and DP cells showed that DHT inhibits the growth of ORS cells, and neutralizing antibody against DKK-1 significantly reversed the growth inhibition of ORS cells. Analysis of co-cultured ORS cells showed a significant increment of sub-G1 apoptotic cells in response to DHT. Also, recombinant human DKK-1 inhibited the growth of ORS cells and triggered apoptotic cell death. In addition, DHT-induced epithelial cell death in cultured hair follicles was reversed by neutralizing DKK-1 antibody. Moreover, immunoblotting showed that the DKK-1 level is up in the bald scalp compared with the haired scalp of patients with androgenetic alopecia. Altogether, our data strongly suggest that DHT-inducible DKK-1 is involved in DHT-driven balding.

Dihydrotestosterone-inducible dickkopf 1 from balding dermal papilla cells causes apoptosis in follicular keratinocytes - PubMed



A Potential Suppressor of TGF- Delays Catagen Progression in Hair Follicles

TGF-beta plays important roles in the induction of catagen during the hair cycle. We examined whether TGF-beta2 could activate a caspase in human hair follicles. Using active caspase-9 and -3 specific antibodies, we found that TGF-beta2 activated these caspases in two regions, the lower part of the hair bulb and the outer layer of the outer root sheath. In addition, we searched for a plant extract that can effectively suppress TGF-beta action. We found that an extract of Hydrangea macrophylla reduced synthesis of a TGDbeta-inducible protein. We confirmed that the extract has a potential to promote hair elongation in the organ culture system. Furthermore, it delayed in vivo progression of catagen in a mouse model. Our results suggest that the induction of catagen by TGF-beta is mediated via activation of caspases and that a suppressor of TGF-beta could be effective in preventing male pattern baldness

A Potential Suppressor of TGF- Delays Catagen Progression in Hair Follicles | Request PDF

https://ugro.com/hydrangea-macrophylla-for-hair-loss-captures-the-attention-of-scientists/#:~:text=The hydrangea plant extract may,enter the telogen resting stage.



sFRP-1

sFRP-1 (secreted frizzled-related protein 1) is an inhibitor of Wnt signaling pathway. A recent study demonstrated that sFRP-1 regulates intrafollicular canonical Wnt/β-catenin activity through the inhibition of Wnt ligand effects in the human hair bulb (Hawkshaw et al., 2018). sFRP-1 secretions from the dermal papilla control human hair follicle cycling and hair shaft production by interacting with Wnt ligands in the immediately adjacent hair follicle epithelium. sFRP-1 enhanced the emigration of dermal papilla fibroblasts to the connective tissue sheath, which occurs upon Catagen induction, leading to a reduced dermal papilla volume (Kloepper et al., 2010; Tobin et al., 2003). Conversely, inhibition of sFRP1 activity enhanced hair shaft production, hair shaft keratin expression, and inhibition of spontaneous hair follicle regression.

https://korea.in-cosmetics.com/__novadocuments/656371?v=637116672107930000



Characteristics of healthy and androgenetic alopecia scalp microbiome: Effect of Lindera strychnifolia roots extract as a natural solution for its modulation

Abstract

Objective: The human scalp harbours a vast community of microbiotal mutualists. Androgenetic alopecia (AGA), the most common form of hair loss in males, is a multifactorial condition involving genetic predisposition and hormonal changes. The role of microflora during hair loss remains to be understood. After having characterized the scalp microbiota of 12 healthy male subjects and 12 AGA male subjects (D0), the aim of this investigation was to evaluate the capacity of Lindera strychnifolia root extract (LsR) to restore a healthy bacterial and fungal scalp microflora after 83 days (D83) of treatment.


Material and methods: The strategy used was based on high-throughput DNA sequencing targeting the encoding 16S ribosomal RNA for bacteria and Internal Transcribed Spacer 1 ribosomal DNA for fungi.


Results: Test analysis of relative abundance comparing healthy and AGA subjects showed a significant increase of Cutibacterim acnes (P < 0.05) and Stenotrophomonas geniculata (P < 0.01) in AGA subjects. AGA scalp condition was also associated with a significant (P < 0.05) decrease of Staphylococcus epidermidis relative abundance. A lower proportion of Malassezia genus in samples corresponding to AGA scalps and an increase of other bacterial genera (Wallemia, Eurotium) were also noted. At the species level, mean relative abundance of Malassezia restricta and Malassezia globosa were significantly lower (P < 0.05) in the AGA group. Eighty-three days of treatment induced a significant decrease in the relative abundance of C. acnes (P < 0.05) and S. geniculata (P < 0.01). S. epidermidis increased significantly (P < 0.05). At the same time, LsR treatment induced a significant increase in the proportion of M. restricta and M. globosa (P < 0.05).


Conclusion: Data from sequencing profiling of the scalp microbiota strongly support a different microbial composition of scalp between control and AGA populations. Findings suggest that LsR extract may be a potential remedy for scalp microbiota re-equilibrium.

Characteristics of healthy and androgenetic alopecia scalp microbiome: Effect of Lindera strychnifolia roots extract as a natural solution for its modulation - PubMed
Thank you. Retinoic acid seems to antagonize androgen receptors, do you have any thoughts on the interactions going on here and how they might relate to hair loss?
 

tallglass13

Member
Joined
Dec 29, 2015
Messages
528
Thank you. Retinoic acid seems to antagonize androgen receptors, do you have any thoughts on the interactions going on here and how they might relate to hair loss?
I do have a thought on this, and I've been trying to put together more evidence for this, but it seems that testosterone may be good for the hair, while dihydrotestosterone causes the damage. As we know finasteride and dutasteride significantly lower scalp DHT levels, but raise scalp testosterone levels. . The European drug Permixin which is saw palmetto, was shown to work as well by increasing scalp testosterone levels. A study in 1975 by Christopher Papa, showed increased hair growth in 65% of the subjects by applying topical testosterone. I know Danny Roddy has a before and after picture of one of the subjects and one of his articles. So if vitamin A antagonizes androgen receptors, it may be lowering the scalp testosterone level, causing more hair loss. Teenage boys and young men with high testosterone levels usually have pretty thick hair. As they get older into their early twenties, I think a lot of men become hypogonadal through certain activities ;-) and begin using more adrenal steroids such as DHEA and androstenedione, and they become deficient in testicular pure testosterone.
It appears that the ratio of pure testosterone to DHT might be an issue. Or just DHT binding in low testosterone States. I think the prostate and the hair follicles want testosterone, but in a low testosterone State dht ends up binding to The receptors and expressing. I have read that older men have higher DHT to testosterone ratio, that is why they grow hair an unwanted places such as the back and ears. This may be due to high total estrogen levels that antagonize the adrenals to produce more DHT and Androstedione.
 
Last edited:

ilhanxx

Member
Joined
Feb 26, 2019
Messages
259
Are you sure there are new hairs or are you just studying your scalp more closely and seeing them because of that?

I massage but wow 40 mins a day? My scalp would look nasty after that.

If scalp calcification is a major player then lowering vA and allowing K2 to work will help a lot. Not sure how fibrosis and calcification is connected though.
Henry choy has some work (detumescence therapy), if you success to transform your scalp tissue marshmellow softness, it will regrowth completely, but it need to very much time and hard dicipline. I massage 40min every day, scalp tissue turning white. I tested pufa. yesterday, I eat some sunflower seed, My scalp turned fibrosis and itchy. pufa is real poison. first of all pufa must be eliminated. hormones and medications don't work after a meanwhile, because body show resistance. the equation and answers are so complex. But there is a result. the result is degenerate/tight/fibrin tissue. If we take enough calorie and eliminate inflamattive food (ray diet) and correct method massage will lead to good result.
 

mrchibbs

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Joined
Nov 22, 2017
Messages
2,459
Location
Atlantis
Henry choy has some work (detumescence therapy), if you success to transform your scalp tissue marshmellow softness, it will regrowth completely, but it need to very much time and hard dicipline. I massage 40min every day, scalp tissue turning white. I tested pufa. yesterday, I eat some sunflower seed, My scalp turned fibrosis and itchy. pufa is real poison. first of all pufa must be eliminated. hormones and medications don't work after a meanwhile, because body show resistance. the equation and answers are so complex. But there is a result. the result is degenerate/tight/fibrin tissue. If we take enough calorie and eliminate inflamattive food (ray diet) and correct method massage will lead to good result.

I absolutely agree regarding the PUFAs, they are the root cause of the micro-inflammation of the hair follicle which leads to the fibrosis and then calcification. Regarding the Henry Choy paper, I think the ideas are valid, but the article itself is probably bogus, as no one has ever been able to contact the author or verify the study results. There are other papers which provide evidence for mechanical stimulation of the scalp, however, and Rob has done a good job generating evidence that it can work.
 
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