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For Boston Baldy, on the DKK-1 front, and wound-healing, etc


#1

BB, look at this:

L8. Dihydrotestosterone (DHT)-inducible DICKKOPF 1 from scalp dermal papilla cells causes apoptosis in follicular keratinocytes.
Young-Kwar Sung, Mi-Hee Kwack, Moon-Kyu Kim, Jung-Chul Kim; Department of Immunology, School of Medicine, Kyungpook National University, Daegu, Korea.

Paracrine factors induced by dihydrotestosteron (DHT) are thought to influence the activity of the follicular cells. RT-PCR analysis and ELISA showed that DICKKOPF 1 (DKK-1) is up-regulated and secreted to conditioned media upon DHT exposure. In addition, in vitro co-culture system by using dermal papilla cells (DPCs) and outer root sheath keratinocytes (ORS) showed that DHT inhibits ORS growth and neutralizing antibody against DKK-1 significantly attenuates DHT-induced growth inhibition of ORS cells. Flow cytometry analysis showed DHT induces substantial apoptosis in co-cultured ORS and caspase inhibitor attenuates DHT-induced growth inhibition of ORS. Altogether, this study shows that secreted DKK-1 from DPCs by DHT causes apoptosis in keratinocytes and suggests that DHT-inducible DKK-1 is responsible for the hair growth inhibition.

BB,
I have a few thoughts on this and what “baldness” might really come from and start out at. We know for a fact that the first inflammation seen in baldness is strangely near the infidulum, or the opening in the dermis where the hair comes out. It really seemed to make no sense to me (or anyone else) why that was, but now I think I see the correlation. The EHRS article above states that DHT-inductible DKK-1 leads to apoptosis (cell death) in keratinocyte cells. The speed of cell division in keratinocyte cells determines how “big” a hair follicle that one has. Hair growth only speeds up so much with treatments, and the speed at which the length of hairs grow out of the little “keratinocyte factory” which makes the long-cylinders of keratin that we know as “hair shafts” seems somewhat “fixed”. Fast cell division in the keratinocytes correlate with big, thick mature hairs.

Well then, if DKK-1 leads to “cell death” (apoptosis) directly in these cells, the [b-dead-cells are going to be “in there” with the keratinocytes, no doubt “break off” and travel along the hair shaft as it exits the infidulum (that ‘hole’ in the dermis where the hair departs). We have wondered openly for years on discussion forums as to “why does the immune system attack our hair” and why aren’t we like apes, who can get terrific regrowth out of finasteride, minox,and especially RU58841? We know that there is no immuno component to primate balding, but there is to ours (which is why its so hard to reverse vs. primates). I think I may see why the immune system attacks now. Its perfectly natural. The travelling T-cells that scavenge the body looking for “foreign invaders” would notice the dead keratinocyte cells a while after they were killed, but not before they completely leave the body. This would seemingly be why the immuno attack would first be noticeable at the infidulum. All the stuff that happens later, the collagen deposistion around the hair follicle, etc. might very well be the hair follicle trying to “defend” itself from the inflammatory acids, oxides, killer cells, etc. the immune system continually sends at the “foreign invader” near the top of the dermis.

You mentioned that caffeine was a wnt-upping substance, but what Im wondering is is topical caffeine just inhibits or binds DKK-1, http://search.comcast.net/?q=caffeine+dkk-1&cat=Web&con=preview?
I know that there is a big difference in alot of compounds before/after the enter the digestive system, and this is why caffeine might be of a topical benefit, but no internal benefit. Curcumin analogues are being developed by a company called Androscience to block androgen receptors and literally inhibit their very expression in targeted tissues, but internal curcumoids obviously dont do this—or eating curry would be like taking flutamide.

This makes me want to go back and re-look at the alpecin product and how it might be designed to work. I have found some more topical anti-androgens (DHT inhibitors) via this study:

Activity of herbal extracts on the control of sebum secretion.Accession number;04A0230063
Title;Activity of herbal extracts on the control of sebum secretion.
Author;UCHIUMI YOICHIRO(Maruzen Pharm. Co., Ltd., JPN) YAMAMOTO SUSUMU(Maruzen Pharm. Co., Ltd., JPN) MIZUTANI KENJI(Maruzen Pharm. Co., Ltd., JPN)
Journal Title;Fragr J

Journal Code:G0987B

ISSN:0288-9803

VOL.32;NO.3;PAGE.53-57(2004)
Figure&Table&Reference;TBL.4, REF.13
Pub. Country;Japan
Language;Japanese
Abstract;Potential activity of herbal extracts on sebum secretion was studied. Among the herbal extracts tested, polyol-soluble licorice extract P-U (product name) derived from Glycyrrhiza inflata showed the most potent testosterone 5 .ALPHA.-reductase inhibition, androgen receptor binding inhibition and antimicrobial activities, which are closely related to sebum secretion. In addition to the findings on polyol-soluble licorice extract P-U, clove extract and peppermint extract showed testosterone 5 .ALPHA.-reductase inhibition, arnica extract and rose fruit extract showed androgen receptor binding inhibition, alpinia speciosa root extract and scutellaria root extract showed estrogen receptor agonists, and sophora root extract showed antimicrobial activity. (author abst.)

“Menthol” can be synthetic of course, but its been shown to inhibit alpha five reductase and decrease sebum in human skin. Alpecin has menthol, caffeine. I wonder if this is what they are up to…a topical anti-androgen, and an attempt to inbibit DKK-1 signalling so that keratinocytes dont “die” and induce and immunological response? I know that DKK-1 inhibits wnt signalling, and if we could stop it, wnt signalling might “start again” in the scalp to some extent, http://www.nature.com/onc/journal/v23/n52/abs/1207892a.html

It would seem if one were inclined to try the “needling” or whatnot, topical caffeine along with a DHT-inhibitor might be something to try anyway. BTW-anymore news on that front?

One more thingy…on one of the other anti-androgens mentioned in that Japanese study. Licorice, like green tea, inhibits angiogenesis or new blood vessel formation. At first glance it would seem that these should be whoop-ass anti-androgens, but I dont know if once could/or couldn’t induce terrific topical hair RE-growth by blocking new capillaries needed for the new hairs. I wonder. Do you know folks who claim great success with topical green tea? The ECGC should block androgen receptors and be quite anti-androgenic and in hamster flank organ studies it is incredibly effective against even topical DHT administration in keeping the flank organ from growing at all, even well over spironolactone.


#2

Hey Benji,

Great post, as always. And I completely agree with your theory on the origins of inflammation in hair loss. Indeed, the more I read about hair loss the more I strongly believe that inhibiting DKK-1 and upregulating the WNT/beta-catenin pathway is the “cure” for hair loss. In reality inhibiting DHT or creating anti-inflammatory conditions, while useful, are clumsy, indirect ways of dealing with hair loss in humans.

I’m actually familiar with the article you posted on DHT upregulating DKK-1. It’s really not all that surprising, though, but confirms what we already know about the origins of hair loss. It’s been known for at least 5 years now that DKK-1 is possibly the most important inhibitor of hair follicle development. For example, see here:

  1. DKK-1 prevents follicular neogenesis:
    http://stke.sciencemag.org/cgi/content/abstract/sigtrans;2007/387/tw176

  2. DKK-1 is a potent inhibitor of the WNT pathway:
    http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WW3-45VDCF6-J&_user=10&_coverDate=05%2F31%2F2002&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=38940d5563df9c6d6e4ededc3b47849b

  3. DKK-1 inhibits melanocyte function:
    http://www.nature.com/jid/journal/v127/n5/abs/5700636a.html

  4. DKK-1 reduces overall hair follicle spacing:
    http://www.sciencemag.org/cgi/content/abstract/sci;314/5804/1447

  5. And many, many more (just go to scholar.google.com). Note that almost all articles use the word “potent” in describing the role of DKK-1 in inhibiting the WNT/beta-catenin pathway.

So the question is: what can we do to inhibit DKK-1? (Another question would be about what would up-regulate WNT/beta-catenin, but that’d be a slightly different question with slightly different answers.)

Possible DKK1 inhibitors:

  1. R-Spondin1 (aka NU206): a new product which is being marketed by a company called Nuevlo for gastrointestinal cancer; still in Phase I trials so not currently available; but shown to have inhibitory effects on DKK1.
    http://www.pnas.org/cgi/content/full/104/37/14700

  2. Bortezomib: anti-cancer drug; must be taken intravenously and may have significant side-effects (e.g., neuropathy); but shown to reduce serum concentrations of DKK1.
    http://www.ingentaconnect.com/content/bsc/bjh/2006/00000135/00000005/art00013

  3. Lithium: upregulates WNT pathway (i.e., it upregulates Bax and suppresses Bcl-2, neutralizing GSK-3b); lithium also has many positive functions on inflammation and reducing sebum production (it’s more effective than ketoconazole for seborrheic demratitis). I haven’t seen anything on DKK1 inhibition but it might be effective, no?
    http://www.freepatentsonline.com/20050084494.html

  4. DMSO: boosts WNT signaling, beta-catenin, and increases absorption of lithium as a nice bonus. I haven’t seen any research on DKK1 inhibition, though.

Etc.

Okay, I’m getting sleepy and must go to bed. But this is the beginning of a fruitful discussion, I hope… any other possible DKK1 inhibitors out there (besides via DHT inhibition)?

Best,
BB

P.S. Lithium chloride plus DMSO as a topical is great. It has reduced all itchiness and sebum production. I don’t know about hair growth – too early to tell. But it’s certainly not hurting.


#3

oh just shut up already

»


#4

BB,

You mentioned this: DKK-1 prevents follicular neogenesis:
http://stke.sciencemag.org/cgi/cont...abstract/sigtrans;2007/387/tw176

  1. DKK-1 is a potent inhibitor of the WNT pathway:
    http://www.sciencedirect.com/scienc...38940d5563df9c6d6e4ededc3b47849b

  2. DKK-1 inhibits melanocyte function:
    http://www.nature.com/jid/journal/v127/n5/abs/5700636a.html

  3. DKK-1 reduces overall hair follicle spacing:
    http://www.sciencemag.org/cgi/content/abstract/sci;314/5804/1447

Me again…My interest is in caffeine because it apparenlty “binds” DKK-1 somehow and inhbits it from exerting nearly as much influence in the dermal papilla. My understanding of baldness is this: We all have male hormone that binds to androgen receptors, and the dermal papilla’s in some of us produce negative growth factors which suppress hair follicle cellular activity. Ive wondered what or which negative growth factor is “the one” that gets the immune system involved. I remember reading that by placing RU58841 with hair follicles, a 16% increase in their activity was observed. Thats not exactly the uptick one would expect. We know that cyclosporine regrows a good deal of hair in humans, and more than finasteride. It would seem the immuno problems are the greater part of baldness. DKK-1 is the one dermal papilla inhibitor whose by product, dead keratinocyte cells, would be in the area of the first inflammation that is seen in male pattern baldness…the area near the infidulum where the dead keratinocyte cells would naturally be on their way out of the body. It kinda makes sense anyway. Finding out DKK-1 is suppressive of WNT is “icing on the cake”, but DMSO and lithium are just shown to up WNT, but not decrease DKK-1. If DKK-1 isn’t present, one would imagine that WNT would go back up to natural levels found in non-bald scalp. I guess what Im suggesting in a round-about way is that the alpecin product might really be helpful if one is also inhibiting DHT (finasteride) or blocking androgen receptors along with it in really regrowing a pretty good clip of hair and definitely not losing more of it. Also, if one were going to try the “wounding” on themselves, the caffeine would seemingly be a way to ensure that some wnt signalling was taking place

The other DP-negative growth factors that I know of are FGF-5, thrombospondin, TGF-beta, tnf-alpha, Protien Kinease C.

Ive wondered what results folks who tried the wounding have had thusfar? I haven’t kept up with them, but am suprised a few men havent made a handful of wounds in a bald area and seen what ensued with a lithium chloride or DMSO up there.


#5

» BB,
»
» You mentioned this: DKK-1 prevents follicular neogenesis:
» http://stke.sciencemag.org/cgi/cont...abstract/sigtrans;2007/387/tw176
»
» 2. DKK-1 is a potent inhibitor of the WNT pathway:
» http://www.sciencedirect.com/scienc...38940d5563df9c6d6e4ededc3b47849b
»
» 3. DKK-1 inhibits melanocyte function:
» http://www.nature.com/jid/journal/v127/n5/abs/5700636a.html
»
» 4. DKK-1 reduces overall hair follicle spacing:
» http://www.sciencemag.org/cgi/content/abstract/sci;314/5804/1447
»
»

»
»
» Me again…My interest is in caffeine because it
» apparenlty “binds” DKK-1 somehow and inhbits it from exerting nearly as
» much influence in the dermal papilla. My understanding of baldness is
» this: We all have male hormone that binds to androgen receptors, and the
» dermal papilla’s in some of us produce negative growth factors which
» suppress hair follicle cellular activity. Ive wondered what or which
» negative growth factor is “the one” that gets the immune system involved.
» I remember reading that by placing RU58841 with hair follicles, a 16%
» increase in their activity was observed. Thats not exactly the uptick one
» would expect. We know that cyclosporine regrows a good deal of hair in
» humans, and more than finasteride. It would seem the immuno problems are
» the greater part of baldness. DKK-1 is the one dermal papilla inhibitor
» whose by product, dead keratinocyte cells, would be in the area of the
» first inflammation that is seen in male pattern
» baldness…the area near the infidulum where the dead
» keratinocyte cells would naturally be on their way out of the body. It
» kinda makes sense anyway. Finding out DKK-1 is suppressive of WNT is
» “icing on the cake”, but DMSO and lithium are just shown to up WNT, but
» not decrease DKK-1. If DKK-1 isn’t present, one would imagine that WNT
» would go back up to natural levels found in non-bald scalp. I guess what
» Im suggesting in a round-about way is that the alpecin product might
» really be helpful if one is also inhibiting DHT (finasteride) or blocking
» androgen receptors along with it in really regrowing a pretty good clip of
» hair and definitely not losing more of it. Also, if one were going to try
» the “wounding” on themselves, the caffeine would seemingly be a way to
» ensure that some wnt signalling was taking place
»
»
» The other DP-negative growth factors that I know of are FGF-5,
» thrombospondin, TGF-beta, tnf-alpha, Protien Kinease C.
»
»
»
» Ive wondered what results folks who tried the wounding have had thusfar? I
» haven’t kept up with them, but am suprised a few men havent made a handful
» of wounds in a bald area and seen what ensued with a lithium chloride or
» DMSO up there.

Hmm, i keep reading about the positive effects of ‘wounding’. Procedures such as dermabrasion seem to do wonders for aging skin, what if a balding man were to have dermabrasion performed on his scalp? Would that signal something in the skin to start producing hair?


#6

Cotsarelis’s research is the best way!!!

http://www.manticeye.com/article.php?id=1142_0_2_0_C

http://www.associatedcontent.com/article/248593/cure_for_baldness_linked_to_wnt_gene.html

http://www.nahrsmembers.org/home/Publications/tabid/70/Default.aspx


#7

If caffeine supposdly inhibits DKK1 i will tell you that it doesnt work
i drink about a 2 liter of diet cola every day for 20 yrs
my hair is still balding same rate


#8

http://www.associatedcontent.com/article/248593/cure_for_baldness_linked_to_wnt_gene.html

It says that the new hair were think BUT Colorless = white ??


#9

Hangin,

I think in the above post he made clear why topical caffien is far more effective than ingested caffien.


#10

» BB,
»
» You mentioned this: DKK-1 prevents follicular neogenesis:
» http://stke.sciencemag.org/cgi/cont...abstract/sigtrans;2007/387/tw176
»
» 2. DKK-1 is a potent inhibitor of the WNT pathway:
» http://www.sciencedirect.com/scienc...38940d5563df9c6d6e4ededc3b47849b
»
» 3. DKK-1 inhibits melanocyte function:
» http://www.nature.com/jid/journal/v127/n5/abs/5700636a.html
»
» 4. DKK-1 reduces overall hair follicle spacing:
» http://www.sciencemag.org/cgi/content/abstract/sci;314/5804/1447
»
»

»
»
» Me again…My interest is in caffeine because it
» apparenlty “binds” DKK-1 somehow and inhbits it from exerting nearly as
» much influence in the dermal papilla. My understanding of baldness is
» this: We all have male hormone that binds to androgen receptors, and the
» dermal papilla’s in some of us produce negative growth factors which
» suppress hair follicle cellular activity. Ive wondered what or which
» negative growth factor is “the one” that gets the immune system involved.
» I remember reading that by placing RU58841 with hair follicles, a 16%
» increase in their activity was observed. Thats not exactly the uptick one
» would expect. We know that cyclosporine regrows a good deal of hair in
» humans, and more than finasteride. It would seem the immuno problems are
» the greater part of baldness. DKK-1 is the one dermal papilla inhibitor
» whose by product, dead keratinocyte cells, would be in the area of the
» first inflammation that is seen in male pattern
» baldness…the area near the infidulum where the dead
» keratinocyte cells would naturally be on their way out of the body. It
» kinda makes sense anyway. Finding out DKK-1 is suppressive of WNT is
» “icing on the cake”, but DMSO and lithium are just shown to up WNT, but
» not decrease DKK-1. If DKK-1 isn’t present, one would imagine that WNT
» would go back up to natural levels found in non-bald scalp. I guess what
» Im suggesting in a round-about way is that the alpecin product might
» really be helpful if one is also inhibiting DHT (finasteride) or blocking
» androgen receptors along with it in really regrowing a pretty good clip of
» hair and definitely not losing more of it. Also, if one were going to try
» the “wounding” on themselves, the caffeine would seemingly be a way to
» ensure that some wnt signalling was taking place
»
»
» The other DP-negative growth factors that I know of are FGF-5,
» thrombospondin, TGF-beta, tnf-alpha, Protien Kinease C.
»
»
»
» Ive wondered what results folks who tried the wounding have had thusfar? I
» haven’t kept up with them, but am suprised a few men havent made a handful
» of wounds in a bald area and seen what ensued with a lithium chloride or
» DMSO up there.

So where can you get this topical caffeine. Hell I’m willing to give it a shot.


#11

Number one: Saw palmetto has no effect on serum levels of DHT. Im going to show you the sometimesdifferences in certain substances taken internally vs. being used topically.

"Summary: Using prostate tissue samples obtained by needle biopsy, researchers compared tissue levels of testosterone (T) and dihydrotestosterone (DHT) in men with symptomatic benign prostatic hyperplasia (BPH) taking finasteride, placebo, or a saw palmetto herbal blend (SPHB).

A total of 244 prostate samples were analyzed - 40 from the prostate adenomectomy group, 44 from the finasteride study, and 160 from the SPHB trial. In men taking finasteride, prostate tissue levels of DHT were decreased significantly when compared to untreated men (p < 0.01). Conversely, prostate tissue levels of T were significantly increased - five to ten times - in those taking finasteride compared to untreated controls (p < 0.01). While serum (i.e., bloodstream) levels of T remained similar, serum levels of DHT were also significantly reduced in men taking finasteride compared to controls (p < 0.01).

Men taking SPHB had a significant decrease in prostate tissue levels of DHT from baseline to 6 months of treatment (p = 0.005). However, this reduction was not statistically significant when compared to the placebo group. The 6-month decline in DHT for the SPHB group was 32%. In comparison, the finasteride effect on prostate tissue levels of DHT was an 80% reduction compared to untreated men. Treatment with SPHB led to no changes in prostate tissue levels of T or in serum levels of T or DHT. Of particular interest, serum levels of prostate-specific antigen (PSA) decreased by approximately 50% in men taking finasteride compared to no change in men taking SPHB."

ME AGAIN HANGIN’,…you are probably asking yourself, “but why?”. Saw Palmetto is composed of some of the free form fatty acids (palmitic, oleic, etc.) that have been shown to have some five alpha reductase inhibition in test tubes, right? Yup, they sure are in there, HOWEVER, these free-form fatty acids get changed in all likelihood in digestion and depending on whatever esle one might have on their stomach when eating them. Changing free form fatty acids back to triglycerides (which do nada for five alpha reductase) may or may not be the reason that serum levels of DHT are unchanged with taking saw palmetto. Saw Palmetto probably works becuase of its sterol content, which can indeed sit on androgen receptors------------------THEREFORE TOPICALLY SAW PALMETTO, BY BYPASSING DIGESTION AND ALL THE ACIDS IN YOUR STOMACH MIGHT BE MORE EFFECTIVE. Caffeine very well might work in a similar way. The alpecin researchers claimed one would have to drink sixty cups of coffee a day to put as much of it around the follicles as using it topically would do.

Personally, I have no idea why you dont just take finasteride, which has been used for over 20 years now in the form of proscar. Ive taken it for 11 with no ill side effects whatsoever.

This is why diet coke, even if you drink a bunch of it, probably does not effect the dermal papilla’s release of DKK-1 or any genetic upregulation associated with it. We DO KNOW THIS though Hangin, the first inflammation seen in baldness is near the opening in the dermis where the hair emerges onto the skin. The travelling T-cells sent by the immune system to look for “foreign-looking” bodies in the human body are seeing something in this area that trouble them enough to mount an auto-immune response. Dr. Peter Proctor, a doctor and pharmacologist who has studies baldness since the early 80’s has wrote on his website that “baldness really looks like organ rejection” and that the best drug we have seen for its treatment is unfortunately an immuno-suppressant, organ rejection drug, cyclosporine. SO, if we can find what explicitly is causing the immune system to see the follicles as “foreign”, we might be able to stop the immuno attack.

Bryan Shelton, who knows alot more about baldness and its etiology than anyone Ive encountered on message boards, posted as excerpt a long time ago detailing how RU58841, which regrows hair very impressively in stumptailed macaques–and better than finasteride—only supressed human beard hair growth something like 16 percent in an ex vivo (outside the body) culture and increased head hairs studied the same way by about the same percentage. In other words, alone, male hormone does not seemingly do enough to just destroy hair follicles, the immuno component might be an even larger part of the equation. Researchers have been looking for exactly what the immune system wants to attack.

There are some candidates that have been discussed, such as the increased TGF-beta signalling in and around the follilce and that pathways presence in other auto-immune disorders, the outnumbering of positive growth factors released by the follicle by negative growth factors over time, and now this latest negative growth factor that has been found…DKK-1.

Ive not had time to look into whether the other negative growth factors secreted by your dermal papilla’s ALSO KILL CELLS like Dkk-1 apparently does to keratinocyte cells. I know that cell division in various follicle cells has been shown to SLOW DOWN, but NOT DIE in response to other negative growth factors like FGF-5, thrombospondin, TGF-beta, PKC, etc. There are probably one or two more that haven’t even been discovered yet. Apoptosis, or cell death in cells, would indeed lead to some dead cells being in the body and this probably would invite negative responses from travelling immuno cells looking for all things foreign. Do you see now why some of us might be interested in something like this as a way to hang onto the hair we have?

By the way…menthol, which is in alpecin, slows the metabolization of caffeine. If one just put coffee on their head, it would likely be metabolized fairly quickly and therefore would not be very effective.

If your interested in things that have been shown to topically reduce alpha five reductase activity in human skin, and not test tubes, here is a brief study from Japan:

http://sciencelinks.jp/j-east/article/2 … 230063.php

Activity of herbal extracts on the control of sebum secretion.Accession number;04A0230063
Title;Activity of herbal extracts on the control of sebum secretion.
Author;UCHIUMI YOICHIRO(Maruzen Pharm. Co., Ltd., JPN) YAMAMOTO SUSUMU(Maruzen Pharm. Co., Ltd., JPN) MIZUTANI KENJI(Maruzen Pharm. Co., Ltd., JPN)
Journal Title;Fragr J

Journal Code:G0987B

ISSN:0288-9803

VOL.32;NO.3;PAGE.53-57(2004)
Figure&Table&Reference;TBL.4, REF.13
Pub. Country;Japan
Language;Japanese
Abstract;Potential activity of herbal extracts on sebum secretion was studied. Among the herbal extracts tested, polyol-soluble licorice extract P-U (product name) derived from Glycyrrhiza inflata showed the most potent testosterone 5 .ALPHA.-reductase inhibition, androgen receptor binding inhibition and antimicrobial activities, which are closely related to sebum secretion. In addition to the findings on polyol-soluble licorice extract P-U, clove extract and peppermint extract showed testosterone 5 .ALPHA.-reductase inhibition, arnica extract and rose fruit extract showed androgen receptor binding inhibition, alpinia speciosa root extract and scutellaria root extract showed estrogen receptor agonists, and sophora root extract showed antimicrobial activity. (author abst.)


#12

http://www.manticeye.com/article.php?id=1142_0_2_0_C

"“We’re testing various different dermatological procedures and drug interventions to maximize the effect,” said Steinberg, whose company has licensed the technology developed by Cotsarelis. “We’ll be testing in humans within a year.”

If all goes well, Steinberg said, bald men will be able to undergo the procedure at doctor's offices within a couple of years. 

 Because the procedure would involve derm abrasion or other less-invasive methods of removing the top layer of skin and then applying growth-inducing drugs, Steinberg said: "This is definitely a don’t-try-this-at-home kind of thing."

Follica, founded in September 2005, has just a handful of employees and is one of eight businesses backed by Boston's Puretech Ventures, but the study’s results are 'huge for us," Steinberg said. 

"The hair growth market is between $2 billion and $4 billion, with nothing out there that actually works all that well," said Steinberg. That includes hair transplants, drug treatments, laser procedures and "all the late-night infomercial stuff"</em>

Me again: If they actually start testing in humans in one year, we should know where this stands rather quickly. I know some folks who have eagerly anticipated HM for so many years on the board would almost feel ‘betrayed’ if something like this out of nowhere were to actually work, but one has to allow for the strange alliance of Kurt Stenn to this project along with Costarialis. Stenn is affiliated with Follica. Now Stenn might be wanting to pump something to this new company and get share prices up and cash out his options, but has his career really been indicative of that kind of behavior taking his years at Harvard and Johnson&Johnson into consideration? Costarialis has tried HM before and fell short (but so did everybody back then), but I dont know if he would be attempting something like this if he didn’t beleive in its possible human efficacy. Im of the opinion that these two men at least believe this may be efficous as far as treating alopecia–despite many questions of androgenic-suceptibility in the new hair or its spacing, quaility, etc. But that IS WHAT TESTING IS FOR. I wish em’ all the damned luck in the world, just as I wish ICX, Aderans, Shishedo, and Phoenixbio luck also.

BB, I also found this to be interesting:

"Removing the epidermis layer from small sections of laboratory mice, stimulated stem cell activity. This new activity actually produced new hair follicles.
The human hair follicle has always thought to die and never regrow. In the mice, the hair follicles grew back.

Further research revealed the gene WNT. Scientists discovered that suppressing this gene also suppressed hair follicle growth. Adding a booster of WNT, produced even more hair.

Dr George Cotsarelis revealed the hair that grew back was white. He joked that maybe one could dye it. The hair was very healthy and thick. This showed the follicle to be healthy, as well" http://www.associatedcontent.com/article/248593/cure_for_baldness_linked_to_wnt_gene.html

BB, when they mention “removing the epidermis layer” it sort of makes me feel that they are removing deeper sections of skin than we might be completely aware of. I have a feeling this is deeper than a scratch in other words, but a good removal of skin. In fact one might have to “scoop out” a bit of skin if you think about it. The mention of “dermabrasion plus a topical” might be good for PR, but I wonder if the wounding may be a little more traummatic than what we might be hoping for? The thought of “dermabrasion” would market very well with the public because hey, if the gals can take it, so can we right? At this point, it might be better for folks who are nosy (like me) to wait and see rather than needling my scalp more than one to three little pin pricks in deference to scarring. Do you know of anyone who is REALLY trying any of this?


#13

Horseshit


#14

Funny how all you “experts” who cant even save their own hair and maintain what they have, and have to hold out for HM, come on here and analyze my regimen, cracks me up

Saw Palmetto has been shown to NOT REDUCE blood levels of DHT yes, that is a GOOD THING,

it works by preventing the existing DHT from binding to the base of the hair follicles, also the same way it prevents this DHT from binding to the prostate

Propecia HAS BEEN SHOWN to reduce serum blood levels of DHT which I believe is part of the reason it has noticeable strange side effects in some guys, messing with your blood hormone levels is not good

Saw Palmetto
is perhaps the weakest 5 AR inhibitor on my regimen

Nettles, Pygeum and beta sis are much more effective and when combined with saw Palmetto they work great also


#15

» If caffeine supposdly inhibits DKK1 i will tell you that it doesnt work
» i drink about a 2 liter of diet cola every day for 20 yrs
» my hair is still balding same rate

Ive done quite abit of research on hair loss and one of the products that keeps showing up is aspartame, which is found in diet soda. Do a search of ‘aspartame and hair loss’ and theres enough articles out there to at least cause us to be cautious about this product.I think diet plays a crucial role in hair loss, which can in part explain why baldness has crept in Asian male population relatively over night. ‘westernization’ of certain societies has allowed them to trade in their healthy lifestyles and diets with a western one.As far as topical caffeine is considered, would brewing a very potent cup of tea and applying to hair be of any good use?


#16

» Hangin, if youre interested in DHT at all, you might find this interesting,

Very interesting study here:

http://jn.nutrition.org/cgi/content/full/133/2/516

Quote:
Mice treated with black tea tended to have a greater serum testosterone concentration (34.4%, P = 0.50) and had a 72% lower DHT concentration than controls (P < 0.05), suggesting that black tea may contain components that inhibit the activity of 5-reductase, an enzyme that converts testosterone to the more bioactive DHT.

I know that mice, rats, monkeys, and humans have two isoforms of alpha five reductase, type 1 and type 2. Mice have been tested with very large doses of finasteride to check for side effects and because the pharmacology is assumed to be much the same with them.
The study above noted that black tea was given as the only beverage for mice and that prostate DHT as well serum DHT was reduced. The serum DHT was reduced slightly more than what finasteride would have done in the mice.

Could it be that by drinking a few glasses of black tea a day might inhibit alpha five just as well as finasteride?

You are relying on the sterols in pygeum, nettles, beta sis, and palmetto to block androgen receptors, and they will. But doesn’t this lead to side effects that are unpleasant. I mean hell, why not just take flutamide and block them all. An androgen receptor is an androgen receptor is an androgen receptors. There is no “dht”-receptor that only takes DHT only. DHT binds with several times the affinity to the receptor site that regular testosterone does, and it does so more “solidly” and for “longer” or so its thought due to more chemical stability or whatnot, and thus elicits more negative downstream mitochondrial responses.

Topical saw palmetto oil would probably be much better than taking it internally as it would most likely inhibit the alpha five reductase enzyme located in the innermost portion of the outer root sheath of the hair follicle, where almost all of the DHT that actually gets uptaken by the follicle is made as DHT gets bound by globulin when it enters the blood stream when made elsewhere in the body all but .8 percent of the time. Less than one percent of circulating serum DHT is “unbound” if your globulin levels are normal in other words. Then again, I see you use topical ketoconazaole, which probably does sit on your androgen receptors.

By the way…Ive kept my hair for years hanging, and have a pretty damn good head of hair with some temporal recession. Im not bald or anything, far from it.

ApeSmith,the thing with topical caffeine is it needs to be administered with a topical menthol as menthol “time releases” the caffeine and slows the absorption in the dermis.http://www.springerlink.com/content/w1avju32k62xyuhd/
This is why one simply cannot pour tea on their heads and have the effect. Also, high amounts of the caffeine had diminishing returns in experiments at the two German Universities. There would be, like anything else in pharmacology, an ‘optimum amount’. You mentioned aspartame…we have Donald Rumsfeld to thank for aspartame because when he was at the Food and Drug Adminstration he pushed that stuff through. Its a stimulant that had bad effects on lab animals for years. Alot of people at the FDA were miffed at its approval, but money (as usual) won out. Its not much good for people at all.


#17

» » If caffeine supposdly inhibits DKK1 i will tell you that it doesnt work
» » i drink about a 2 liter of diet cola every day for 20 yrs
» » my hair is still balding same rate
»
» Ive done quite abit of research on hair loss and one of the products that
» keeps showing up is aspartame, which is found in diet soda. Do a search of
» ‘aspartame and hair loss’ and theres enough articles out there to at least
» cause us to be cautious about this product.I think diet plays a crucial
» role in hair loss, which can in part explain why baldness has crept in
» Asian male population relatively over night. ‘westernization’ of certain
» societies has allowed them to trade in their healthy lifestyles and diets
» with a western one.As far as topical caffeine is considered, would brewing
» a very potent cup of tea and applying to hair be of any good use?

my dad balded at the same age same exact pattern as me
aspartame was not even invented back then


#18

» » Hangin, if youre interested in DHT at all, you might find this
» interesting,
»
»
» Very interesting study here:
»
»
» http://jn.nutrition.org/cgi/content/full/133/2/516
»
»
» Quote:
» Mice treated with black tea tended to have a greater serum testosterone
» concentration (34.4%, P = 0.50) and had a 72% lower DHT concentration than
» controls (P < 0.05), suggesting that black tea may contain components that
» inhibit the activity of 5-reductase, an enzyme that converts testosterone
» to the more bioactive DHT.
»
»
»
» I know that mice, rats, monkeys, and humans have two isoforms of alpha
» five reductase, type 1 and type 2. Mice have been tested with very large
» doses of finasteride to check for side effects and because the
» pharmacology is assumed to be much the same with them.
» The study above noted that black tea was given as the only beverage for
» mice and that prostate DHT as well serum DHT was reduced. The serum DHT
» was reduced slightly more than what finasteride would have done in the
» mice.
»
» Could it be that by drinking a few glasses of black tea a day might
» inhibit alpha five just as well as finasteride?
»
»
»
» You are relying on the sterols in pygeum, nettles, beta sis, and palmetto
» to block androgen receptors, and they will. But doesn’t this lead to side
» effects that are unpleasant.

NO, I Have never experienced side effects, but I am not saying it does not happen in isolated cases
most guys on naturals experience increased libido, opposite of fin

I mean hell, why not just take flutamide and
» block them all. An androgen receptor is an androgen receptor is an
» androgen receptors. There is no “dht”-receptor that only takes DHT only.
» DHT binds with several times the affinity to the receptor site that
» regular testosterone does, and it does so more “solidly” and for “longer”
» or so its thought due to more chemical stability or whatnot, and thus
» elicits more negative downstream mitochondrial responses.
»
»
» Topical saw palmetto oil would probably be much better than taking it
» internally as it would most likely inhibit the alpha five reductase enzyme
» located in the innermost portion of the outer root sheath of the hair
» follicle, where almost all of the DHT that actually gets uptaken by the
» follicle is made as DHT gets bound by globulin when it enters the blood
» stream when made elsewhere in the body all but .8 percent of the time.
» Less than one percent of circulating serum DHT is “unbound” if your
» globulin levels are normal in other words. Then again, I see you use
» topical ketoconazaole, which probably does sit on your androgen
» receptors.
»

I have had good experience with the internal natural 5 ar inhibitors, some guys see zero effect

»
» By the way…Ive kept my hair for years hanging, and
» have a pretty damn good head of hair with some temporal recession. Im not
» bald or anything, far from it.
»
»
»
»
»
»
»
» ApeSmith,the thing with topical caffeine is it
» needs to be administered with a topical menthol as menthol “time releases”
» the caffeine and slows the absorption in the
» dermis.http://www.springerlink.com/content/w1avju32k62xyuhd/
» This is why one simply cannot pour tea on their heads and have the effect.
» Also, high amounts of the caffeine had diminishing returns in experiments
» at the two German Universities. There would be, like anything else in
» pharmacology, an ‘optimum amount’. You mentioned
» aspartame…we have Donald Rumsfeld to thank for aspartame
» because when he was at the Food and Drug Adminstration he pushed that
» stuff through. Its a stimulant that had bad effects on lab animals for
» years. Alot of people at the FDA were miffed at its approval, but money
» (as usual) won out. Its not much good for people at all.
»


#19

» » » If caffeine supposdly inhibits DKK1 i will tell you that it doesnt
» work
» » » i drink about a 2 liter of diet cola every day for 20 yrs
» » » my hair is still balding same rate
» »
» » Ive done quite abit of research on hair loss and one of the products
» that
» » keeps showing up is aspartame, which is found in diet soda. Do a search
» of
» » ‘aspartame and hair loss’ and theres enough articles out there to at
» least
» » cause us to be cautious about this product.I think diet plays a crucial
» » role in hair loss, which can in part explain why baldness has crept in
» » Asian male population relatively over night. ‘westernization’ of
» certain
» » societies has allowed them to trade in their healthy lifestyles and
» diets
» » with a western one.As far as topical caffeine is considered, would
» brewing
» » a very potent cup of tea and applying to hair be of any good use?
»
» my dad balded at the same age same exact pattern as me
» aspartame was not even invented back then

I am not saying it might not have some effect negatively on the hair
however all the years my hair recovered aftet i started on the saw palmetto etc, i did not change my aspartame habits

if mine was caused by aspartame it would have had no effect, my regimen, since i did not reduce my aspartame


#20

» Funny how all you “experts” who cant even save their own hair and maintain
» what they have, and have to hold out for HM, come on here and analyze my
» regimen, cracks me up
»
» Saw Palmetto has been shown to NOT REDUCE blood levels of DHT yes, that is
» a GOOD THING,
»
» it works by preventing the existing DHT from binding to the base of the
» hair follicles, also the same way it prevents this DHT from binding to the
» prostate
»
» Propecia HAS BEEN SHOWN to reduce serum blood levels of DHT which I
» believe is part of the reason it has noticeable strange side effects in
» some guys, messing with your blood hormone levels is not good
»
» Saw Palmetto
» is perhaps the weakest 5 AR inhibitor on my regimen
»
» Nettles, Pygeum and beta sis are much more effective and when combined
» with saw Palmetto they work great also

Hangin

That was SO pathetic! OH man! Totally lame move. Just casually interjecting your nonsense in a thread after you were warned not to show your face for a while. Just.casually.interjecting.your.tired rhyme. Ha! I know the obsessed baldies get a little into it. But your lame attempt to regain your status on the board is transparent and weak. Complete lolz. Don’t take any crap. You 'ol rebel you.