Newly Discovered Factor in Androgenetic Alopecia. The Cure is Near?

Armando Jose

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Thank you squeegee for the study, this one from 1979 ;)

Here more information about this issue:
Effects of Tocotrienol Supplementation on Hair Growth in Human Volunteers
Tropical Life Sciences Research, 21(2), 91–99, 2010
In conclusion, this trial demonstrated that supplementation with tocotrienol capsules increases hair numbers in volunteers suffering from hair loss as compared to the placebo group. A possible explanation for the effects could be due to the potent antioxidant activity of tocotrienols that help to reduce lipid peroxidation and oxidative stress in the scalp, which are known to be associated with alopecia.
http://ernd.usm.my/journal/journal/TLSR 21-2-8-(91-99).pdf

Also
Glutathione, Glutathione S-Transferase and Reactive Oxygen Species of Human Scalp Sebaceous Glands in Male Pattern Baldness
Journal of Investigative Dermatology (1996) 107, 154–158
These results support the hypothesis that reactive oxygen species are involved in the pathogenesis of sebaceous gland hyperplasia in male pattern baldness.

http://www.nature.com/jid/journal/v107/n2/pdf/5610424a.pdf

One more
Int J Mol Med. 2008 Dec;22(6):725-9.

Lipid peroxides induce early onset of catagen phase in murine hair cycles.
Naito A, Midorikawa T, Yoshino T, Ohdera M.

http://www.spandidos-publications.com/ijmm/article.jsp?article_id=ijmm_22_6_725



And this doctorate thesis in 1987 in Spain, it is very interesting
Contribución al estudio de la fisiopatología androgénica. Aplicación a la alopecia seborreica masculina
Contribution to the study of the pathophysiology androgenic. Application to seborrheic alopecia male
http://digibug.ugr.es/handle/10481/13996
It is possible read the complete text, in Spanish language, in pdf

“Ask which was born first the hen or the eggâ€￾
 
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Sparky4444

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Forget Toco's for hair growth -- it does NOTHING for male pattern baldness...if it didn't work for me, it doesn't work...if it doesn't work for you, it doesn't work...period...
 

Armando Jose

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Hair regrowth very is difficult if not impossible, you have to try to get it to stop the process.
 

squeegee

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Never forget guys that Prostaglandins are lipids! Every baldy have shiny heads. There is a reason why Tocotrienol, L carnitine or Miconazole treatments are working.. Elevated ROS, inflammation, lipid oxidation.
 

squeegee

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Br J Dermatol. 2012 May;166(5):1035-42. doi: 10.1111/j.1365-2133.2012.10856.x.
[h=1]Hair follicle stem cell differentiation is inhibited through cross-talk between Wnt/β-catenin and androgen signalling in dermal papilla cells from patients with androgenetic alopecia.[/h]Leirós GJ, Attorresi AI, Balañá ME.
[h=3]Source[/h]Fundación Pablo Cassará, Instituto de Ciencia y Tecnología Dr César Milstein, Consejo Nacional de Investigaciones Científicas y Técnicas, Ciudad de Buenos Aires, Argentina.

[h=3]Abstract[/h][h=4]BACKGROUND:[/h]Hair follicle (HF) regeneration begins when signals from the mesenchyme-derived dermal papilla cells (DPC) reach multipotent epidermal stem cells in the bulge region. Wnt/β-catenin signalling is known to affect mammalian hair growth positively. In androgenetic alopecia (Androgenetic Alopecia), androgens cause HF miniaturization through a mechanism that remains unclear. Circulating androgens act on DPC and alter paracrine factors that influence hair epithelial cells.
[h=4]OBJECTIVES:[/h]To elucidate the role of androgens in dermal papilla-induced differentiation of HF stem cells.
[h=4]METHODS:[/h]HF stem cell differentiation was evaluated in a coculture model with DPC or culturing with media conditioned by DPC after activation of androgen and Wnt/β-catenin signalling pathways. To study the molecular cross-talk between the androgen and Wnt signalling pathway in DPC, we analysed the expression and activation of downstream Wnt signalling molecules in the presence of androgens.
[h=4]RESULTS:[/h]In a coculture model with human DPC from patients with Androgenetic Alopecia and HF stem cells, we observed that androgens abrogate hair differentiation evaluated by hair-specific keratin 6 expression. Wnt signalling activation restored the ability of androgen-treated DPC to induce differentiation. Androgen treatment revealed a significant decrease in the cytoplasmic/total β-catenin protein ratio and upregulation of the activity of glycogen synthase kinase-3β in DPC, indicative of canonical Wnt pathway inhibition.
[h=4]CONCLUSIONS:[/h]These results suggest that androgens deregulate DPC-secreted factors involved in normal HF stem cell differentiation via the inhibition of the canonical Wnt signalling pathway.
© 2012 The Authors. BJD © 2012 British Association of Dermatologists.

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Endocrinology. 2010 May;151(5):2373-80. doi: 10.1210/en.2009-1474. Epub 2010 Mar 16.
[h=1]A mouse model of androgenetic alopecia.[/h]Crabtree JS, Kilbourne EJ, Peano BJ, Chippari S, Kenney T, McNally C, Wang W, Harris HA, Winneker RC, Nagpal S, Thompson CC.
[h=3]Source[/h]Department of Tissue Repair, Wyeth Research, Collegeville, Pennsylvania 19426, USA.

[h=3]Abstract[/h]Androgenetic alopecia (Androgenetic Alopecia), commonly known as male pattern baldness, is a form of hair loss that occurs in both males and females. Although the exact cause of Androgenetic Alopecia is not known, it is associated with genetic predisposition through traits related to androgen synthesis/metabolism and androgen signaling mediated by the androgen receptor (AR). Current therapies for Androgenetic Alopecia show limited efficacy and are often associated with undesirable side effects. A major hurdle to developing new therapies for Androgenetic Alopecia is the lack of small animal models to support drug discovery research. Here, we report the first rodent model of Androgenetic Alopecia. Previous work demonstrating that the interaction between androgen-bound AR and beta-catenin can inhibit Wnt signaling led us to test the hypothesis that expression of AR in hair follicle cells could interfere with hair growth in an androgen-dependent manner. Transgenic mice overexpressing human AR in the skin under control of the keratin 5 promoter were generated. Keratin 5-human AR transgenic mice exposed to high levels of 5alpha-dihydrotestosterone showed delayed hair regeneration, mimicking the Androgenetic Alopecia scalp. This effect is AR mediated, because treatment with the AR antagonist hydroxyflutamide inhibited the effect of dihydrotestosterone on hair growth. These results support the hypothesis that androgen-mediated hair loss is AR dependent and suggest that AR and beta-catenin mediate this effect. These mice can now be used to test new therapeutic agents for the treatment of Androgenetic Alopecia, accelerating the drug discovery process.

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[h=1]Keratinocyte Growth Inhibition through the Modification of Wnt Signaling by Androgen in Balding Dermal Papilla Cells[/h]
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682470/
ontext/Objective: Androgen induces androgenetic alopecia (Androgenetic Alopecia), which has a regressive effect on hair growth from the frontal region of the scalp. Conversely, Wnt proteins are known to positively affect mammalian hair growth. We hypothesized that androgen reduces hair growth via an interaction with the Wnt signaling system. The objective of this study was to investigate the effect of androgen on Wnt signaling in dermal papilla (DP) cells.Design: The effect of androgen and Wnt3a on keratinocyte proliferation was measured by use of a coculture system consisting of DP cells and keratinocytes. The molecular mechanisms of androgen and Wnt pathway interactions in DP cells were examined by analyzing the expression, intracellular localization, and activity of the androgen receptor (AR) and also downstream Wnt signaling molecules.
Results: Wnt3a-dependent keratinocyte growth was suppressed by the addition of dihydrotestosterone in coculture with DP cells that were derived from Androgenetic Alopecia patients, but growth was not suppressed in coculture with DP cells from non-Androgenetic Alopecia males. Whereas DP cells from both scalp regions expressed AR protein, the expression levels of AR and cotranslocation with β-catenin, a downstream Wnt signaling molecule, were higher in DP cells of Androgenetic Alopecia patients than in DP cells from non-Androgenetic Alopecia males. In addition, significant suppression of Wnt signal-mediated transcription in response to dihydrotestosterone treatment was observed only in DP cells from Androgenetic Alopecia patients.
Conclusion: These results suggest that Wnt signaling in DP cells is regulated by androgen and this regulation plays a pivotal role in androgen’s action on hair growth.
 

Jacob

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I'm not sure how anyone using tocotrienols is going to say- it's working for me. At least I'd hope anyone on them would be taking/using a variety of other things..so it'd be hard to say- yep, it's the tocos!
 

salar_s

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hi folks
i am new to forum ,so forgive me ,because i couldn't find appropriate topic to ask my question.
so this is my story ,i had massive hairloss(even in sides and donor area) in last 2 years because of stress ,depression and severe disease,i am 21 year old,and my father and my uncles didn't suffer from hairloss,and my elder brother have great hair.
there is a lot of thin hair in my frontal head,so how can i thicken them ?which lotion or medicine you suggest ?
thanks and forgive me for my poor english
 

Armando Jose

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Your hair loss is not common baldness or androgenetic alopecia (hair loss only in certains areas of scalp), then the solution couldn`t be finasteride and/or minoxidil....
The better way is eliminate stress, depression and severe disease
If you want some specific product for hair, a natural lotion it is possible
Take care and good luck
 

Beardedpt

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Never forget guys that Prostaglandins are lipids! Every baldy have shiny heads. There is a reason why Tocotrienol, L carnitine or Miconazole treatments are working.. Elevated ROS, inflammation, lipid oxidation.

Hey Squgee. Could you point me in the direction of this protocol?
 

Sparky4444

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Never forget guys that Prostaglandins are lipids! Every baldy have shiny heads. There is a reason why Tocotrienol, L carnitine or Miconazole treatments are working.. Elevated ROS, inflammation, lipid oxidation.

And I've seen guys who have shiny scalps but still have their hair....
 

shivers20

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I wonder what cox-2 inhibitor was being used that regrew hair in mice.

Cyclooxygenase-2 overexpression in the skin of transgenic mice results in suppression of tumor development

David K. Bol; R. Bruce Rowley; Ching-Ping Ho; Brigette Pilz; Janet Dell; Mavis Swerdel; Kaoru Kiguchi; Stephanie Muga; Russell Klein; et al. (Profiled Author: Susan M. Fischer)
Cancer Research 2002;62(9):2516-2521.
Scopus
AbstractSignificant evidence has accumulated suggesting that the inducible form of cyclooxygenase (COX-2), a central enzyme in the prostaglandin biosynthetic pathway, plays an important role in tumor development. To better understand the role of COX-2 in tumorigenesis, we generated transgenic mice that overexpress COX-2 under control of the human keratin 14 promoter, which allows for expression in the epidermis and some other epithelia. Transgenic mice, referred to as K14.COX2 mice, were readily distinguished from their nontransgenic littermates by the appearance of significant alopecia. Administration of a specific COX-2 inhibitor restored hair growth, indicating that the alopecia was attributable to elevated COX-2 enzymatic activity. Unexpectedly, COX-2 overexpression was found to protect, rather than sensitize, K14.COX2 mice to skin tumor development induced by an initiation/promotion protocol. K14.COX2 transgenics developed tumors at a much lower frequency than did their littermate controls (3.3% versus 93%, respectively, on a FVB background and ∼25% versus 100%, respectively, on an ICR background) and presented with significantly reduced tumor burdens (average, 0.03 versus 12.7 tumors/mouse, respectively, on a FVB background and 0.5 versus 7.1 tumors/mouse, respectively, on an ICR background). Mice fed a COX-2 inhibitor in utero and as weanlings up to the time of promotion also showed a significant resistance to tumor development. These results clearly raise questions regarding the role of COX-2 and elevated prostaglandin levels in skin tumor development.
 

squeegee

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:pc:
 

Jojje

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I have read 30 pages and the topic has became a little messy. Anyone can list the available treatments in the thread?
+1

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I live in Europe and here they sell Zyrtec( Cetirizine) in the form of oral drops solution. It contains the same ingredients as the pills, but unlike the pills you don't have to go through all the mess with making them suitable for topical application. Anyway I am going to try that together with my generic minoxidil. Also I wanted to ask, since here people support the opinion that inflammation is a crucial factor in male pattern baldness, what are your thoughts on using corticosteroids instead of antihistamines like cetirizine? There is a (in)famous doctor who is known for discovering retin-a (tretinoin) who also conducted experiments on humans.. but he has a patent for treating alopecia with a combination of minoxidil and antiinflamatory agent ( hydrocortisone). His name is Albert Kligman and here is a link to his method:

http://patft.uspto.gov/netacgi/nph-...&f=G&l=50&d=PALL&RefSrch=yes&Query=PN/5026691

I know corticosteroids are not as safe to use as antihistamines, but what if they prove to be more effective? There are many success stories of people suffering form alopecia areata who have been treated with corticosteroids. I'm still thinking on adding corticosteroids to my regimen, but first I'll try the liquid Zyrtec

I have a strong corticosteroid that i wil be testing on scalp.. 7 days then a break for 3 weeks etc and continue on. Could report back if its interesting to hear.
Needs break because of strength. Its called Betnovat (Betametason)
 

Hoppi

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hm, this is an interesting one :)

I actually stumbled upon this thread because I was looking into histamine's possible role in male pattern baldness, actually in relation to the HPA axis. I was learning that histamine is capable of stimulating the HPA axis, which could therefore possibly cause or increase hair loss.

So, I was learning about histamine receptors and receptor antagonists.

Apparently there are 4 histamine receptors, and drugs like diphenhydramine (Benadryl), cetirizine and loratadine are all H1 antagonists and seem to work to some degree when taken internally for hair loss. Loratadine surprised me because apparently it does not penetrate the blood-brain barrier much, which implies they really are working either directly by reducing inflammation around the follicles or via some other mechanism stimulating the HPA axis.

I'm unsure of the role of the other receptors but H1 antagonists seem to have the most success.
 
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