Vellus hairs and Donor area hairs equal transplanted to mice

[michael barry]

Note: Performing your original search, vellus hairs mice alopecia, in PubMed will retrieve 6 citations.




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1: J Am Acad Dermatol. 2003 May;48(5):752-9. Links
Transplants from balding and hairy androgenetic alopecia scalp regrow hair comparably well on immunodeficient mice.Krajcik RA, Vogelman JH, Malloy VL, Orentreich N.
Orentreich Foundation for the Advancement of Science Inc, Cold Spring-on-Hudson, New York 10516, USA. ofas1@juno.com

Human hair follicles were grafted onto 2 strains of immunodeficient mice to compare the regeneration potential of vellus (miniaturized, balding) and terminal (hairy, nonbalding) follicles from males and a female exhibiting pattern baldness. Each mouse had transplants of both types of follicles from a single donor for direct comparison. Grafted follicles from 2 male donors resulted in nonsignificant differences in mean length (52 mm vs 54 mm) and mean diameter (99 microm vs 93 microm) at 22 weeks for hairs originating from balding and hairy scalp, respectively, corresponding to 400% versus 62% of the mean pretransplantation diameters. Follicles from the female donor transplanted to several mice also resulted in nonsignificant differences in length (43 mm vs 37 mm) for hairs from balding and hairy scalp, respectively, during a period of 22 weeks. The mean diameter of the originally vellus hairs increased 3-fold, whereas the terminal hairs plateaued at approximately 50% of pretransplantation diameter, resulting in a final balding hair volume double that of the nonbalding hairs. This report shows that miniaturized hair follicles of pattern alopecia can quickly regenerate once removed from the human scalp and can grow as well as or better than terminal follicles from the same individual.

PMID: 12734505 [PubMed - indexed for MEDLINE]




That is fukking humiliating. We move our vellus hairs to mice, and they can regrow.......................dammit. Dutasteride wont get them back though. God is kicking us in the balls.

 

[michael barry]

When one really considers the fact that vellus hairs from male pattern bald me can grow as well or even better than donor area hair when moved to an immuno deficient mouse's back.................it makes me want to chuck all studies in mice.


Lets see................castrates dont lose anymore hair, so we know that male hormone is causing the hair loss.

But castrates only grow back a little of what was recently lost----about like guys on dutasteride or finasteride.


So what then is keeping our miniaturized hairs small on our own heads. Why wont they grow back if you are on finasteride and shampoo with nizoral? Does the immune system keep attacking them when they are small..........there has got to be a reason for them not- re-enlarging like they do on these mice.


Anybody got any ideas?

 

[PersonGuy]

f*** I wish I was smarter and then I'd have input. Anybody else? I'm interested to hear feedback on this topic myself.

 

[bornthisway]

When one really considers the fact that vellus hairs from male pattern bald me can grow as well or even better than donor area hair when moved to an immuno deficient mouse's back.................it makes me want to chuck all studies in mice.


Lets see................castrates dont lose anymore hair, so we know that male hormone is causing the hair loss.

But castrates only grow back a little of what was recently lost----about like guys on dutasteride or finasteride.


So what then is keeping our miniaturized hairs small on our own heads. Why wont they grow back if you are on finasteride and shampoo with nizoral? Does the immune system keep attacking them when they are small..........there has got to be a reason for them not- re-enlarging like they do on these mice.


Anybody got any ideas?

Regarding that study, it just points to a topical immunosuppressant or immunomodulatory (which have been discussed on HairLossTalk.com already). I did come across one that was discussed which a steroid user with male pattern baldness was using that reversed his hair loss..

NOTE: I am not suggesting anyone use any of these, there are inherent problems with drugs of this nature.

"Tacrolimus is the current best drug for hair loss in my opinion unfortunately it is not commonly available in topical form though the drug company Fujisawa has an NDA awaiting for tacrolimus for it's use in atopic dermatitis (eczema).

Currently the only place which carries tacrolimus is http://www.communitydrug where it is priced at $130 for 30 mls this price will significantly drop when the official form of the drug from the manufacturer Fujisawa is FDA approved later this year.

Tacrolimus for me personally has regrown so much of the hair I have lost over the past few years making my hair loss become hardly noticeable.

In the studies it has been used at only once or twice a week I myself have opted to use it 1ml every other day.

This is the first drug which works in a way completely aside from hormonal manipulation or through the potassium k channel openers (minoxidil is a drug of this class) and is the best current way to treat hair loss."

Again, this drug I mentioned is not the route to take for male pattern baldness, but there is potential with these class of drugs or at least a specific class of inhibitors...

Regarding Tacrolimus: The long-term safety of Tacrolimus Ointment has not been determined. Because rare cases of cancer (eg, lymphoma, skin cancer) have been reported, continuous long-term use should be avoided and the application of Tacrolimus Ointment should be limited to the affected areas. Tacrolimus Ointment should not be used in children younger than 2 years of age.

 

[alkulk]

Tacrolimus is suspected to cause cancer.

 

[bornthisway]

Now, regarding the immune system attacking hair follicles... the whole idea of hair loss being indicative of potential cancer seems quite plausible to me.. here's a medical hypothesis on the subject.

Androgenic alopecia may have evolved to protect men from prostate cancer by increasing skin exposure to ultraviolet radiation.

Peter Kabai

Department of Ecology, Faculty of Veterinary Science, AOTK, SZIE, Szent István University, P.O. Box 2, H-1400 Budapest, Hungary

Received 27 July 2007;

Summary:

Androgenic alopecia affects populations adapted to colder climate, and individuals at an age and hormonal status susceptible to prostate cancer. Male pattern baldness enhances absorption of UV radiation on the top of the head, an area directly exposed to sunlight during everyday activities. Ultraviolet radiation is reported to reduce the risk of advanced prostate cancer. Here I propose that progression of androgenic alopecia rather than being a risk factor is a finely tuned mechanism evolved to protect against prostate cancer.

Introduction:

Ethologists perceive androgenic alopecia (Androgenetic Alopecia) as a social signal evolved to indicate senescence [1], whereas in the medical literature it is discussed as an abnormal benign condition with no physiological effect [2].

Social signal theory has been supported by image manipulation experiments, where pictures of bald men are perceived older than the same faces with full hair [3]. The exact nature of the information conveyed, however, has been debated. Some believe that baldness is a signal of social competence and aggressive dominance [4], others suggest it indicates maturity and a non-threatening form of dominance [1].

In any case, young women perceive bald men sexually less attractive and less active [1]. As Androgenetic Alopecia affects about 30% of Caucasian males at the age of 30 years [5], signalling senescence at the age of the highest reproductive potential might be premature and therefore costly for many men. Even though the social signal theory has not been incorporated into mainstream medical science, the notion that Androgenetic Alopecia is not simply a disordered condition but has specific functions deserves attention, considering the genetically pre-programmed nature of the process.

Hair follicles react to androgens in a site-specific manner. In man, with genetic predisposition to Androgenetic Alopecia, terminal hairs in the temporal and frontal regions and later over the vertex of the scalp are miniaturized into vellus hairs, whereas follicles at other areas are not affected under the influence of androgens. Such differential reaction to the same hormone is pre-programmed in the individual follicles: follicles transplanted from non-balding areas to the bald vertex develop into full hair. Although the mechanism of differential reaction of hair follicles to androgens is not fully understood [6], it is very likely that Type 2 5a reductase (5aR-2) converting testosterone to more potent dihydrotestosterone in the follicles is involved. Besides hair follicles, 5aR-2 is expressed in the prostate, testes, seminal vesicles, and the liver. Inherited deficiency in 5aR-2 activity prevents Androgenetic Alopecia and results in small prostate. Finasteride, a 5aR-2 inhibitor has been useful in the treatment of Androgenetic Alopecia as well as prostatic hypertrophy [7]. As changes in the level of 5aR-2 activity affect Androgenetic Alopecia and prostatic hyperplasia in a similar manner, Androgenetic Alopecia as a risk factor for prostate cancer has been a target of epidemiological studies. Although findings have been inconsistent, one of the largest study including 1446 prostate adenocarcinoma cases and 1390 controls depicted an association between vertex baldness and prostate cancer [8].

Another line of epidemiological studies suggest reduced risk of prostate cancer associated with sun exposure, outdoor activity, highly active vitamin D receptor variants [9], high level of vitamin D [10], childhood sunburn, regular foreign holidays, sunbathing score, high exposure to UVR [11] or living at lower latitude [12], results all pointing at the protective role of sun exposure.

The hypothesis:

Male pattern baldness exposes a relatively large skin area to sunlight during everyday activity performed in a vertical position. I propose that Androgenetic Alopecia evolved to elevate UV absorbance and thus to provide some protection against prostate cancer. Moreover, the shared androgen pathways leading to Androgenetic Alopecia and prostate cancer indicate a finely tuned mechanism of inducing baldness in men susceptible for prostate cancer at an age preceding the predicted onset of the disease. According to this interpretation if baldness is a social signal, then it has gained this function secondarily.

This hypothesis comprises two testable relations. Whether Androgenetic Alopecia was positively selected for in populations susceptible for prostate cancer can be directly tested when genetic background of Androgenetic Alopecia as well as of predisposition to prostate cancer are known. Indirect evidence of shared genetic control might be revealed by possible genetic correlations between Androgenetic Alopecia, sun exposure and prostate cancer in family history studies. The possible protective role of Androgenetic Alopecia against prostate cancer can be easily resolved. Epidemiological studies on risk factors for prostate cancer should involve questions on Androgenetic Alopecia status as well as on the level, and surface area exposed to sunlight.

Consequences of the hypothesis:

This hypothesis might be relevant for the design of epidemiological studies as well as for the treatment of Androgenetic Alopecia and prostate cancer. Epidemiological studies on the link between Androgenetic Alopecia and prostate cancer can be confounded by the varying level of sun exposure of bald men with high or low outdoor activity, wearing or not wearing a sun protective hat, and living at lower or higher altitudes. Similarly, sun exposure measured as difference in pigmentation between areas protected or not protected from the sun without considering the surface area exposed may weaken the power of testing the cancer-protective role of UV radiation. Controlling for both Androgenetic Alopecia and sun exposure in both lines of studies might reveal stronger associations between sun exposure and lower risk of non-skin cancers.

Benign prostatic hyperplasia has been treated with finasteride, a potent 5aR-2 inhibitor [7]. As such treatment also halts or reverses Androgenetic Alopecia, treated men with prostatic hyperplasia might receive less UV radiation during everyday activities than without finasteride treatment. Careful studies are needed so that advice on compensating for reduced sunlit areas could be given to patients. As association between low level of sun exposure with various forms of non-skin cancers, coronal heart disease, and hypertension has been suggested [13,14], links between predisposition to baldness and such conditions would be worthy to seek.

Acknowledgement:

I am grateful to T.O’Keeffe for his valuable comments.

References:

[1] Muscarella F, Cunningham MR. The evolutionary signifi-
cance and social perception of male pattern baldness and
facial hair. Ethol Sociobiol 1996;17:99–117.

[2] Sinclair RD. Male androgenetic alopecia. JMGH 2004;1(4):
319–27.

[3] Henns R. Social perceptions of male pattern baldness. A
review. Dermatol Psychosom 2001;2:63–71.

[4] Keating CF, Mazur A, Segall MH. A cross-cultural exploration
of physiognomic traits of dominance and happiness. Ethol
Sociobiol 1981;2:41–8.

[5] Hamilton JB. Patterned loss of hair in man: types and
incidence. Ann NY Acad Sci 1951;53:708–28.

[6] Trüeb RM. Molecular mechanisms of androgenetic alopecia.
Exp Gerontol 2002;37:981–90.

[7] D’Amico AV, Roehrborn CG. Effect of 1 mg/day finasteride
on concentrations of serum prostate-specific antigen in
men with androgenic alopecia: a randomised controlled
trial. Lancet Oncol 2007;8:21–5.

[8] Giles GG, Severi G, Sinclair R, English DR, McCredie MRE,
Johnson W, et al. Androgenetic alopecia and prostate
cancer: findings from an australian case-control study.
CEPB 2002;11:549–53.

[9] John EM, Schwartz GG, Koo J, Van Den Berg D, Ingles SA.
Sun exposure, vitamin D receptor gene polymorphisms, and
risk of advanced prostate cancer.
Cancer Res 2005;65:5470–9.

[10] Giovannucci E, Liu Y, Rimm EB, Hollis BW, Fuchs CS,
Stampfer MJ, et al. Prospective study of predictors of
vitamin D status and cancer incidence and mortality in
men. J Natl Cancer Inst 2006;98:451–9.

[11] Luscombe CJ, Fryer AA, French ME, Liu S, Saxby MF, Jones
PW, et al. Exposure to ultraviolet radiation: association
with susceptibility and age at presentation with prostate
cancer. Lancet 2001;358(9282):641–2.

[12] Hanchette CL, Schwartz GG. Geographic patterns of pros-
tate cancer mortality: evidence for a protective effect of
ultraviolet radiation. Cancer 1992;70:2861–9.

[13] Schwartz GG, Skinner HG. Vitamin D status and cancer: new
insights. Curr Opin Clin Nutr Metab Care 2007;10:6–11.

[14] Grimes DS. Are statins analogues of vitamin D? Lancet
2006;368(9529):83–6.

 

[michael barry]

Bornthisway.............................DAMN, that might just be right. Very fukkking depressing. Im going to post that in some other places. Thanks

 

[bornthisway]

NP. I'll make a thread for this in this section.

 

[tino]

So what then is keeping our miniaturized hairs small on our own heads. Why wont they grow back if you are on finasteride and shampoo with nizoral? Does the immune system keep attacking them when they are small..........there has got to be a reason for them not- re-enlarging like they do on these mice.


Anybody got any ideas?

Mice do not have mutations in other genes.For example TERC(see below)



viewtopic.php?f=32&t=44593


abridged telomere repair via Telomerase, or shortened Telomeres are associated with many pathological degenerative processes.One of them is the idiophatic pulmonary fibrosis.Families which show mutations in TERC or TERT genetic,tend to develop pulmonary fibrosis.

http://nar.oxfordjournals.org/cgi/reprint/35/22/7406


http://www.pnas.org/cgi/content/full/104/18/7552


Pulmonarys fibrosis is basically TGF-ß mediated(http://www.ncbi.nlm.nih.gov/pubmed/1796 ... d_RVDocSum),and in the first line male(gender) specific.Androgenes(DHT) intracts whith the Tgf-beta gen, by activating his expression...maybe in general, and not only tissue specific.The androgenic mediated Tgf-beta expression, must be created by a evolutionary history...there must be a use in the broader sense.Possibly his function is to attack tissue which shows impurity.....induced by genetic.To what extent the tissue will be detected as impurely.....it may depend on the presence of ROS too.Some organs glands and tissues produce more ros than other.For example the thyroyd gland and the process of melanin synthesis in the hair follicle.So if there is a genetic impurity,and a additional burden(like smoking),androgenes may increase the tgf-beta expression there, to make the tissue metabolic inactive.Not only tgf-beta.....more apoptotic factors.The reason and mistake in the case of degenerative fibrotic and apoptotic desorders.may be protection from cancer.Androgenic/TGF-beta induced Apoptosis and Fibrosis,may subject to the idea of destroy cancer vulnerable tissue.

In the genetic pure tissue of mouses,there may be no reason to attack growth and regeneration.

There are more hormones and factors than androgenes which are known as tgf-beta inducers.For example Aldosteron/the mineralocorticoid-Receptor), or angiotensin.Men who develop male pattern baldness, are known to develop high blood pressure too.

Tino

 

[sphlanx2006]

michael would you say that this raises doubts about the possible success of Follica's potential treatment?

 

[michael barry]

splanx,

it certainly is the biggest concern.

the only possible thing that might be able to counteract the human immune system (if it presents a problem) might be a couple of weeks of cyclosporin from the wounding date until new hair follicle germs form in the skin I'd guess. If that didn't work, then perhaps it just wont work for people


Quite frankly, this is about the only thing I imagine we could have in the relatively near future. Nothing else seems to be on the horizon.

 

[sphlanx2006]

I am afraid that having to take such a strong drug even for a few weeks, would scare many people, to the extent of making Follica's people decide not to launch their procedure, even if it would have a nice result with cyclospirin. I know that me, and many other people who give great importance to their hair would be willing to stay indoors and be very careful for a couple of weeks (while on cyclospirin) but this is an extreme that is not suitable for the majority of people.

 

[abcdefg]

Its the immune system. Its not god doing anything. We are vastly more intelligent, more complex, and have more complex immune systems. The immune system as we all know is the major critical factor in male pattern baldness not androgens. You would have to be stupid to take any immune system altering drug. To think science has any real understanding of the immune system would be a stupid thing to think. That wont stop people from doing it though. People are stupid in general.