Homemade Follicular Neogenesis

I agree with you on this JTR. As a matter of fact, Dr. Gho uses stem cells in his cellular HM research and feels that since the stem cells come from the MPB-resistant area, they result in follicles that are also resistant to MPB. Keep in mind that Dr. Gho does not inject a dermal component in his cellular HM research; thus, the resulting follicles’ dermal component comes 100% from the balding area. And we know that the dermal component is the part of the follicle that gets whacked out by DHT and is also responsible for building the dermal component of new or regenerating follicles.

IOW, according to ICX/ARX, DHT-resistant mesenchymal cells are capable of building DHT resistant follicles. But according to Gho, epithelial stem cells can, under the proper circumstances, trump the signals sent via the dermal component.

Obviously nobody knows the answer to this for certain, but my gut feeling is that stem cells from the balding area coupled with the dermal component from the balding area will result in MPB-prone follicles. I mean you have a lose-lose situation there. And as far as the theory that the MPB characteristics are removed due to the embryonic reaction of the new follicle growing (in the Cotsarelis technique), keep in mind that this same embryonic reaction occurred in the balding area when the MPB-prone follicles originally grew there. This is proof that the presence of WNT doesn’t magically make the MPB environment favorable to building DHT resistant follicles. (but having said that, maybe someday a cell signaler will be found that will).

So IMO, the question of the hour is–how long can these new follicles hold out in a heavily DHT-laden environment? My guess is that it will be absolutely NW-level dependent. IOW, if a person is a NW7 at age 19, the new follicles are not going to last long on his head. OTOH, if the person is a NW3 at age 40, the follicles could last for quite some time.

But I’m speaking of the clinical research method here and not of the bathtub coctail version. As I said before, I don’t put much faith in the bathtub coctail version of this research. But that is just my personal opinion.

» I agree with you on this JTR. As a matter of fact, Dr. Gho uses stem cells
» in his cellular HM research and feels that since the stem cells come from
» the MPB-resistant area, they result in follicles that are also resistant
» to MPB. Keep in mind that Dr. Gho does not inject a dermal component in
» his cellular HM research; thus, the resulting follicles’ dermal component
» comes 100% from the balding area. And we know that the dermal component is
» the part of the follicle that gets whacked out by DHT.

Honestly, I’m very tempted to agree with you JB. But what’s keeping me back are the anecdotes on wounding and hair growth on bald people. For example, the father of a friend of mine was in a severe car accident and had several large scars on his BALD head. But lo and behold – dark hairs generated from these large wounds. Not many, mind you, but hairs obviously different from vellous hairs on the rest of his scalp. Maybe I’m crossing my fingers, eh??

» I agree with the above comment. I think the “homemade follicular
» neogenesis” is at best only an approximation of a baldness cure. However,
» it is a total solution if it works! As far as DHT sensitibity, I disagree.
» The cell lines are embryonic in the wounding plus WNT activation
» and follicular neogenesis starts from scratch, so to speak. Of course
» these were done with mice, so no one knows with complete certainty.

I think the cell lines are NOT embryonic. What they are doing is mimicking an embryonic pathway to create a new follicle, but the cell lines that are doing this are DHT-susceptible. There is a fine nuance of difference here, but I think it makes all the difference in the world.

» I agree with you on this JTR. As a matter of fact, Dr. Gho uses stem cells
» in his cellular HM research and feels that since the stem cells come from
» the MPB-resistant area, they result in follicles that are also resistant
» to MPB.

Yes, but I think that it’s not necessarily the stem cells that are determining the DHT-susceptibility of the new follicles, but the keratinocytes, DP cells, etc. from the area where the new follicles are being grown. These cells are the “building blocks” of the new follicles, per se, while the stem cells are kind of acting as “inducers”. They FACILITATE the process, but in the end, the new follicle will bear the genotype (and thus the phenotype) of the building blocks uses. If the new follicle is being grown from DHT-susceptible raw materials, then it will have the phenotype of these raw materials.

Of course, the stem cells will ultimately (partly) differentiate into follicular components as well, and then, they, too, will bear the genotype and phenotype of the part of the head what brung 'em.

» Honestly, I’m very tempted to agree with you JB. But what’s keeping me
» back are the anecdotes on wounding and hair growth on bald people. For
» example, the father of a friend of mine was in a severe car accident and
» had several large scars on his BALD head. But lo and behold – dark hairs
» generated from these large wounds. Not many, mind you, but hairs obviously
» different from vellous hairs on the rest of his scalp. Maybe I’m crossing
» my fingers, eh??

OK, but do you know for certain that these wonderful hairs are not DHT-susceptible? Just because hairs grow and look great for a few months, a year, or a few years, doesn’t mean they will not eventually succumb to DHT.

You were just looking at hairs; you weren’t looking at a map of their DNA.

» Obviously nobody knows the answer to this for certain, but my gut feeling
» is that stem cells from the balding area coupled with the dermal component
» from the balding area will result in MPB-prone follicles.

Exactly. And well said.

Of course, the big picture point here is that why would these doctors even risk this, when they can easily use cells from the DHT-resistant “donor area” to accomplish the same thing? Follicles grown in this way, in vitro, can then be implanted into the scalp.

After all we now know, it’s not a big stretch of the imagination to see that happening.

» Of course, the big picture point here is that why would these doctors even
» risk this, when they can easily use cells from the DHT-resistant “donor
» area” to accomplish the same thing? Follicles grown in this way, in
» vitro, can then be implanted into the scalp.
»
» After all we now know, it’s not a big stretch of the imagination to see
» that happening.

But I’d like to point out that this is NOT what Cotsarelis and the rest of the Follica team have been talking about in public – they’ve talked about wounding the scalp with a laser and then applying a WNT-promoting lotion. Hmmm… I’m going to email some people and see if I can get some ideas about Cotsarelis’ procedure and DHT sensitivity…

» But I’d like to point out that this is NOT what Cotsarelis and the rest of
» the Follica team have been talking about in public – they’ve talked about
» wounding the scalp with a laser and then applying a WNT-promoting lotion.

Sure, and that’s great to prove the concept that new hairs can be grown, and that is exactly what they’ve done.

But when this thing shakes out as a real medical procedure, my bet is they’ll use cell lines from the back of the head to induce DHT-resistant follicles.

Have you read the original document of Cotsarelis et al? See here:
http://nahrsmembers.org/home/Publications/tabid/70/Default.aspx

I tried the DMSO thing once and found that other people were complaining about a terrible odour emanating from my body. My breath and my whole body was stinking yet I couldn’t smell it myself. I had to stop the DMSO treatment because I was paranoid about this side effect.

» Have you read the original document of Cotsarelis et al? See here:
» http://nahrsmembers.org/home/Publications/tabid/70/Default.aspx

The WNT/wounding study was done in mice, right?

And mice don’t get MPB, right?

Then how can they know that MPB in humans won’t affect the new hairs, if the new hairs are grown in MPB areas using MPB-affected cell lines?

» Granted, a 60 year-old would not have the same testosterone levels of a 20
» year-old.

BTW wouldn’t there be more to balding than testosterone levels?

Sme men don’t go bald until they are middle aged–a time when they have less testosterone than when they were younger (one possible reason: it would be a combo of how much over how long that causes hair to fall out, and that could vary from person to person).

» But I don’t see how they would get the cells to revert to a youthful or
» embryonic state. Inducing new follicles to grow, in my view, is not the
» same as turning back the genetic clock in the cell nucleus. Instead,
» you’re basically recreating an embryonic process but using adult building
» blocks to do it.

OK–I didn’t realize that the newly generated follicles don’t start over again from square one, so to speak.

However–perhaps this could give someone a second chance at saving his hair from the effects of DHT, by creating new follicles and taking Avodart.

Or maybe something like this stuff could be used to create more donor hair on the back of the head to use for HTs.

I’d do this, sounds crazy enough. A 3x3 mm test area on the temple, why not.

Two questions though:

Didn’t the mice in question develop tumors from too much signalling?

Anybody can recommend a source of lithium orotate?

» BTW wouldn’t there be more to balding than testosterone levels?

Of course, but testosterone levels determine how much DHT can be in circulation, because testosterone is converted into DHT by the reductase enzyme. So if you have genetic receptor sensitivity to DHT, and high testosterone levels, you’ll express MPB. But if you have genetic receptor sensitivity plus very low testosterone levels (as in females or most males of advanced age), even with the genetics in place, you’ll probably express MPB very weakly.

» Sme men don’t go bald until they are middle aged–a time when they have
» less testosterone than when they were younger (one possible reason: it
» would be a combo of how much over how long that causes hair to fall out,
» and that could vary from person to person).

Yes, it’s a combination of a lot of things:

  1. The testosterone levels in your body, which determine DHT levels.

  2. Your genes – genetics determine the sensitivity of your cell receptors to DHT. So, lots of men who have huge testosterone levels, and thus huge DHT levels, still don’t go bald because they have great genetics.

  3. Your genetics also determines the AGE at which your genetically-determined receptor sensitivity to DHT kicks in, if at all. So, in some men it’s 18, in others it’s 25, in others it may be 35 or 50.

In general, a general rule is that, apart from senescent baldness, the later in life the receptor sensitivity genes kick in, the LOWER the man’s ultimate Norwood level will be when it stabilizes.

So, if a man’s receptor sensitivity MPB genes kick in at 15, there’s a much higher chance he’ll stabilize at a NW 7. But if his receptor sensitivity genes kick in much later, say at 40, then there’s a much higher chance that he’ll stabilize at, say, NW 2 or 3.

This is largely (but not only) because, as he gets older, his testosterone levels are declining, so less DHT is being produced.

»Anecdotally, a 47 year-old man named “hatchet” at regrowth.com reports
» using the wounding/LiCi/DMSO procedure and having new hair follicles grow
» for the first time in his life (he’s been balding since 19). Several
» others report some growth, but most of thee posters are just starting out
» on this procedure. So we will have to wait and see what happens…

      One thing i know about regrowth.com: in contrast with other hair loss sites ,there pretty much everybody is having ``this huge regrowth``,``my temples are filling in`` or ``new hair follicles grow for the first time in his life (he's been balding since 19)``.   but everybody`s camera is broken or not home or ``i dont know how to post a pic.Nobody posted a single freakin pic.My opinion is that they are a bunch of liars.... 

People, if you are making SENSATIONAL claims be prepared to back it with pics .

PUT UP OR SHUT UP

Hey Ivory,

I don’t know a good source of lithium orotate, but I’d google it. As far as tumors, lithium appears very safe as a topical AND oral supplement. It is being used in a number of clinical trials for its anti-cancer properties. There appears to be a major difference between genetically programming WNT pathways and adjusting WNT pathways through topicals and oral supplements.

Four provisos, however:

  1. Is needling enough? I.e., will this create the wounding needed to engender stem cell like conditions that foster new hair growth? (I certainly wouldn’t recommend dermabrasion on the scalp to anyone – at least not yet.) But at the very least needling is a good idea b/c it will increase the absorption of topicals AND increase collagen production.
  2. Smell problems with DMSO. DMSO may make you smell bad – it’s a sulfur compound so this is an obvious side effect.
  3. Be careful with caffeine. People report getting headaches if they apply too much caffeine. Everyone has different levels of sensitivity.
  4. I’d consider throwing in 3 other compounds. Just buy pills of green tea, grapeseed, and apply polyphenols. Add several pills to the mixture. These are fairly potent anti-androgens and appear to regular the WNT pathway in ways that may be beneficial for hair loss.

Best,
BB

» I’d do this, sounds crazy enough. A 3x3 mm test area on the temple, why
» not.
»
» Two questions though:
»
» Didn’t the mice in question develop tumors from too much signalling?
»
» Anybody can recommend a source of lithium orotate?

BB wrote:

-lithium appears very safe as a topical AND oral supplement-

Please stay away from lithium!!!
Lithium is used in the drug therapy of major depression. It is well known for its very narrow therapeutic range and its strong side-effects. It should not be used as an oral supplement.

I don´t know about topical application but I would stay away from it as well.

Should be hard to get too…

I don’t recommend taking lithium as an oral supplement for hair loss – no evidence that it can help with hair loss. In fact, in high doses lithium carbonate can actually CAUSE hair loss. In lower doses it is considered safe by the medical establishment for the treatment of mood disorders, however.

But like I said lithium actually has ANTI-cancer properties. Since most of us have MPB, which is strongly correlated with prostate cancer, here’s an interesting article:

Sun A, Shanmugam I, Song J, Terranova PF, Thrasher JB, Li B. Lithium
suppresses cell proliferation by interrupting E2F-DNA interaction and
subsequently reducing S-phase gene expression in prostate cancer.
Prostate. 2007 Apr 17; [Epub ahead of print]
PMID: 17440966 [PubMed - as supplied by publisher]

"BACKGROUND: Lithium is an existing drug for bipolar disorder
and its uptake was recently linked to reduced tumor incidence
compared to the general population. The major target of lithium
action is glycogen synthase kinase 3 (GSK-3). Since GSK-3
expression and activation are associated with prostate cancer
progression, the anti-cancer potential of lithium on prostate
cancer was investigated in this study. METHODS: Multiple
prostate cancer cell lines were treated with lithium chloride
(LiCl). Cell proliferation and cell cycle distribution were
analysed. DNA replication was determined using BrdU labeling
assay. Genome-wide screening of gene expression was performed
using cDNA microarray assay. GSK-3beta gene-specific silencing
was conducted using small interferencing RNA (siRNA)
transfection. E2 factor (E2F) transactivation was evaluated
using reporter gene assay and E2F-DNA interaction was
determined with chromatin-immunoprecipitation assay (ChIP).
RESULTS: LiCl significantly inhibited cell proliferation, which
was associated with reduced DNA replication and S-phase cell
cycle arrest. LiCl significantly decreased the expression of
multiple DNA replication-related genes, including cell division
cycle 6 (cdc6), cyclin A, cyclin E, and cdc25C, which are
regulated by E2F factor during cell cycle. A novel GSK-3-
specific inhibitor TDZD-8 and GSK-3beta siRNA also suppressed
the expression of these E2F target genes, indicating that LiCl-
induced anti-cancer effect was associated with GSK-3beta
inhibition. Furthermore, LiCl suppressed E2F transactivation by
interrupting the interaction of E2F1 factor with its target
gene promoter. CONCLUSIONS: These data indicated that LiCl
suppresses cancer cell proliferation by disrupting E2F-DNA
interaction and subsequent E2F-mediated gene expression in
prostate cancer. Prostate (c) 2007 Wiley-Liss, Inc." 

Isn’t it interesting how finasteride also limits the spread of prostate cancer?

» BB wrote:
»
» -lithium appears very safe as a topical AND oral supplement-
»
» Please stay away from lithium!!!
» Lithium is used in the drug therapy of major depression. It is well known
» for its very narrow therapeutic range and its strong side-effects. It
» should not be used as an oral supplement.
»
» I don´t know about topical application but I would stay away from it as
» well.
»
» Should be hard to get too…

On Sept. 25, Intercytex will hold a big press conference and, after initial remarks by Dr. Kemp, from behind a curtain will step out one man:

Bruce Willis.

:wink: