A compound that induces hair growth/blocks stress hormone!

Re75

Member
Reaction score
0
A team led by researchers from UCLA and the Veterans Administration that was investigating how stress affects gastrointestinal function may have found a chemical compound that induces hair growth by blocking a stress-related hormone associated with hair loss — entirely by accident.

The serendipitous discovery is described in an article published in the online journal PLoS One.

"Our findings show that a short-duration treatment with this compound causes an astounding long-term hair regrowth in chronically stressed mutant mice," said Million Mulugeta, an adjunct professor of medicine in the division of digestive diseases at the David Geffen School of Medicine at UCLA and a corresponding author of the research.

"This could open new venues to treat hair loss in humans through the modulation of the stress hormone receptors, particularly hair loss related to chronic stress and aging."

The research team, which was originally studying brain–gut interactions, included Mulugeta, Lixin Wang, Noah Craft and Yvette Taché from UCLA; Jean Rivier and Catherine Rivier from the Salk Institute for Biological Studies in La Jolla, Calif.; and Mary Stenzel-Poore from the Oregon Health and Sciences University.

For their experiments, the researchers had been using mice that were genetically altered to overproduce a stress hormone called corticotrophin-releasing factor, or CRF. As these mice age, they lose hair and eventually become bald on their backs, making them visually distinct from their unaltered counterparts.

The Salk Institute researchers had developed the chemical compound, a peptide called astressin-B, and described its ability to block the action of CRF. Stenzel-Poore had created an animal model of chronic stress by altering the mice to overproduce CRF.

UCLA and VA researchers injected the astressin-B into the bald mice to observe how its CRF-blocking ability affected gastrointestinal tract function. The initial single injection had no effect, so the investigators continued the injections over five days to give the peptide a better chance of blocking the CRF receptors. They measured the inhibitory effects of this regimen on the stress-induced response in the colons of the mice and placed the animals back in their cages with their hairy counterparts.

About three months later, the investigators returned to these mice to conduct further gastrointestinal studies and found they couldn't distinguish them from their unaltered brethren. They had regrown hair on their previously bald backs.

"When we analyzed the identification number of the mice that had grown hair we found that, indeed, the astressin-B peptide was responsible for the remarkable hair growth in the bald mice," Mulugeta said. "Subsequent studies confirmed this unequivocally."

Of particular interest was the short duration of the treatments: Just one shot per day for five consecutive days maintained the effects for up to four months.
"This is a comparatively long time, considering that mice's life span is less than two years," Mulugeta said.

So far, this effect has been seen only in mice. Whether it also happens in humans remains to be seen, said the researchers, who also treated the bald mice with minoxidil alone, which resulted in mild hair growth, as it does in humans. This suggests that astressin-B could also translate for use in human hair growth. In fact, it is known that the stress-hormone CRF, its receptors and other peptides that modulate these receptors are found in human skin.

http://www.physorg.com/news/2011-02-str ... egrow.html?

Guys is this huge news??? Here is the mice pic..

wv39l1.jpg


Image: The CRF1/CRF2 receptor antagonist, astressin-B, injected intraperitoneally (ip) in CRF-OE mice with fully developed alopecia induces hair growth and pigmentation. Photographs: Row A: Male CRF-OE mice (4 months old) injected ip once daily for 5 consecutive days with saline at 3 days after the last injection and Row B: astressin-B (5 mg/mouse) at 3 days after the last ip injection, and Row C: the same mice as in the middle panel Row B at 4 weeks after the last ip injection. Credit: UCLA/VA
 

renordw

New Member
Reaction score
0
I think you guys are missing the point. Yes male pattern baldness is due to DHT that is unrelated to mice, but what causes the DHT to be produced in the first place? You can't just assume that hair loss is caused by one isolated compound, and there is nothing that happens before or after in the metabolic process.

I would gladly take this compound Astressin-B.
 

casperz

Experienced Member
Reaction score
25
I'd take yearly (or every six months) Astressin-B shots. I think it's possible
that the cure will be stumbled upon like this so I hope it pans out. It
sounds like it wakes up dormant follicles and there is no need for
cloning, etc. But like all new discoveries this is about 10 years out if
it is proven to work at all.

Here are some quotes and more links:

The authors suggest that temporarily blocking CRF receptors could be "a breakthrough therapy for alopecia," and might also hold potential for male pattern baldness and hair loss due to chemotherapy.

"What we can reasonably say is that the antagonist initiates the hair cycle," Million said. "In bald individuals, and in these mice, the hair follicles are in a resting stage. The antagonist awakes them. It turns on the cycle, and the growing phase starts."

Repeated experiments confirmed this accidental finding; daily injections of astressin-B over five days prompted hair re-growth that lasted about four months, quite a long time for a creature that lives only two years. And the researchers also found that they could prevent hair loss in CRF-overproducing mice if they were treated with astressin-B while they were still young.

The study: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0016377

Some interesting quotes http://abcnews.go.com/Health/Wellness/baldness-alopecia-reversed-mice/story?id=12932070
 

casperz

Experienced Member
Reaction score
25
A patent was filed for this in 2007:

http://www.wipo.int/pctdb/en/wo.jsp?WO=2007149938

http://www.faqs.org/patents/app/20080280819

The patent says this:

9. The method of claim 1, wherein the cyclic CRF antagonist peptide is administered to an area of alopecia-affected skin.

10. The method of claim 1, wherein the effective amount is from about 1 ?g/kg body weight to about 500 ?g/kg body weight.

11. The method of claim 1, wherein the subject is a human.

12. The method of claim 11, wherein the cyclic CRF antagonist peptide is administered to the scalp of the human.

They are clearly talking about using it topically on human scalp.

This could be 5 years along at this point. Are they are just now telling
people about to raise some cash to start clinical trials?
 

renordw

New Member
Reaction score
0
finfighter said:
ryandward said:
but what causes the DHT to be produced in the first place?

The Isoenzyme 5 Alpha Reductase type two metabolizes Testosterone into Dihydrotestosterone at the onset of Puberty into adulthood.....

DHT does not cause Androgenetic Alopecia by itself there are other male androgens involved, but it is the main one, it is the the most potent male androgen afterall....

Ultimately it boils down to your body's reaction to DHT, which is determined by your genetic profile.

I am pretty sure you missed the spirit of what I was saying, although you are correct. I am trying to say that it is totally feasible to break the process at a different level than the current way of treating male pattern baldness.

Cheers.
 

casperz

Experienced Member
Reaction score
25
More from the patent:

In a specific embodiment, a therapeutic agent is administered locally to an area in need of treatment or where treatment is desirable (e.g., the scalp). This may be achieved, for example, by local or regional injection or infusion, transdermal delivery (e.g., iontophoresis), topical application, and/or implantation (such as, with implants formed from porous, non-porous, or gelatinous materials, including membranes, such as sialastic membranes or fibers and the like). In one embodiment, local or regional administration can be by one or more injections (such as, subcutaneous injections) at a site or in a region where treatment is desired, such as all or part of the scalp. In particular examples, multiple subcutaneous injections (such as up to about 10, up to about 15, up to about 20, up to about 25, or even as many as 50 or 100 sc injections) are given at substantially the same time (e.g., sequentially or concomitantly) in different regions of an area to be treated, such as all or part of the scalp.

For example, 10-30 ?l of carrier (such as 20 ?l) can be administered to a rodent (such as a mouse) and 0.1 ml to 1 ml carrier (such as 0.1 ml to 0.5 ml) can be administered to larger mammals (such as a human or non-human primate) once per day for at least 5 consecutive days, such as at least 10 days, at least 30 days, or at least 60 days

I don't know if they are just talking about what is possible or what the've done but if it works it sounds like you might have injections or use it topically.

"What we can reasonably say is that the antagonist initiates the hair cycle," Million said. "In bald individuals, and in these mice, the hair follicles are in a resting stage. The antagonist awakes them. It turns on the cycle, and the growing phase starts."

Does it really matter if it's DHT or what the root cause of the hair loss is? It sounds like it wakes up the follicles and prevents them from going to sleep in the first place.
 

Cassin

Senior Member
Reaction score
78
finfighter said:
That's interesting thanks for the info. The only problem with this is that these mice suffer from an etirely different condition than the kind of androgenetic alopecia found in humans. The suppression of DHT through 5AR inhibition in males reverses hair loss in most cases, hence DHT is the main factor in adrogenetic alopecia, not corticotrophin-releasing factor (CRF). However, I do wonder if CRF plays a role in human androgenetic alopecia, if it does it is probably a much lesser role, than potent male androgens such as DHT.

yup. Great for women but not traditional male pattern baldness.
 

renordw

New Member
Reaction score
0
Would this news be feasible for those of us who have had a transplant? I am wondering if there is too much scar tissue on the implanted areas.
 

casperz

Experienced Member
Reaction score
25
There is no doubt that DHT sensitive hair is the root cause that turns
the follicles dormant, but what I take from this study is that the dormant
follicles are woken up. Yes they are dormant from another reason other
than DHT in the mice but does it matter? And it may be wishful thinking
but I sure hope it does not matter what the root cause is.

I don't think they would mention male pattern baldness if this was not the case:

The authors suggest that temporarily blocking CRF receptors could be "a breakthrough therapy for alopecia," and might also hold potential for male pattern baldness and hair loss due to chemotherapy.

"What we can reasonably say is that the antagonist initiates the hair cycle," Million said. "In bald individuals, and in these mice, the hair follicles are in a resting stage. The antagonist awakes them. It turns on the cycle, and the growing phase starts."
 

purecontrol

Established Member
Reaction score
10
ryandward said:
I think you guys are missing the point. Yes male pattern baldness is due to DHT that is unrelated to mice, but what causes the DHT to be produced in the first place? You can't just assume that hair loss is caused by one isolated compound, and there is nothing that happens before or after in the metabolic process.

I would gladly take this compound Astressin-B.


No it is not due to DHT, it is do highly sensatized ARs. Mjority of men with male pattern baldness do not have extra high levels of DHT.

Cortisol, inflamation, free radicals greatly increase that sensativity.
 

waynakyo

Experienced Member
Reaction score
464
yes i never heard of stressed induced shedding and i am not going through one right now.
 

F-M-DHT

New Member
Reaction score
0
waynakyo said:
yes i never heard of stressed induced shedding and i am not going through one right now.

Telogen Effluvium is said to be triggered by severe stress.



purecontrol said:
ryandward said:
I think you guys are missing the point. Yes male pattern baldness is due to DHT that is unrelated to mice, but what causes the DHT to be produced in the first place? You can't just assume that hair loss is caused by one isolated compound, and there is nothing that happens before or after in the metabolic process.

I would gladly take this compound Astressin-B.


No it is not due to DHT, it is do highly sensatized ARs. Mjority of men with male pattern baldness do not have extra high levels of DHT.

Cortisol, inflamation, free radicals greatly increase that sensativity.

Cortisol is released by the adrenal gland in response to stress.

I still can't see this idea being even a treatment for male pattern baldness, Telogen Effluvium possibly. Remember these are mice not humans and the stress is artificially induced probably beyond what would occur naturally.
 

Vox

Established Member
Reaction score
3
One more factor identified here:

Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells.

They were successful in recreating new hair follicles in lab:
In functional assays, analogous CD200 Itga6 cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays.

And their take on testosterone:
Testosterone is necessary for miniaturization, and 5-?-reductase type II inhibitors, which block conversion of testosterone to its more active form, dihydrotestosterone, delay progression of Androgenetic Alopecia. Little else is understood about the cause of Androgenetic Alopecia.

They have demonstrated that a defect in the conversion of hair follicle stem cells (which the bald skin does not lack) to progenitor cells play a role in male pattern baldness, but no one knows how to re-activate this mechanism.
 
Top