Vellus hairs and Donora area hairs equal when transplanted to mice

Stem cell; cell based hair therapy
21

Hangin,

I never said that the shampoo was BETTER than the cream. The cream is almost assuredly better…but the shampoo has been shown to be helpful in AGA.

My “regimine” for the most part is finasteride (never had any side effects), nizoral about twice a week, and copper peptides (usually prox-n after the shower). My results are that my hair has gotten darker over the years Ive done this. I rotate tricomin in with the prox-n (cheaper) also. Ive kept what I have had since about 03’ very well, but haven’t regrown my temples. I like to spray a blast of tricomin mist in my face-----it helps you look younger.

Im not saying keto cream isn’t effective…I know its effective. I just dont want more than about one topical. The anti-androgenic effect of both finas and nizoral are probably “enough” to keep what one has. Im not diggin’ on your regimine. I do however, disagree with the assertion that nizoral is useless or that shampoo isn’t an acceptable way to get an indication to the dermis. Its not as effective as a cream or foam or spray, but it can indeed get some effect. Chuck Fraiser has NANO shampoo pictures and you can tell he got thickening on it -alone-with no other treatment. They are on HLT.

No flames…Im tired. The board is “tired”. Just trying to find out as much as possible and bounce it off what others have been able to pick up and show with studies or reason. Thats all we have at this point. :ok:

22

» »we are humans and not immunosuppressed mice which can do
» » that.
»
» It’s not quite the same thing. The one study showed that pre-existing
» balding follicles could grow and enlarge again, similar to control hairs
» that were also transplanted onto these mice. If Follica is creating new
» hair follicles, and if these new follicles are not immediately sucseptible
» to AGA, I think they’ll grow fine on the human scalp, just like the hair at
» the back and sides.
»
» I think the real question here is what phenotype the newly created
» follicles take on. They can start ‘balding’ immediately or soon afterward
» (similar to follicles already on the way out due to AGA), they could
» ‘bald’ over a long period of time (similar to our existing follicles,
» which are good for at least 15-20 years after they are created in utero),
» or they never bald (similar to hair at the back and sides of the head.)

IM guessing that they, if they have the same genetic makeup of the hairs that were “there” would bald a few years afterwards because of the adult levels of androgen that they would face…Its hard for me to imagine that they would get a “second” childhood period of twelve years or whatever where they are just fine.

I must admit about using anti-androgens during the “making” process though. High androgens in fetal development are linked with long ring fingers on males and females. More aggression and althletic performance (females) are linked with this statistically. Fluridil and Cyteperone Acentate and spiro are mentioned in the patent. Perhpas if androgens are low enough during these hairs development, perhaps the defective androgen receptor gene would not form in such a way as to lead to later baldness? Fluridil was shown to down the very presence of androgen receptor sites over time…

Science would be getting a “second change” to make hair during the follica process if its “doable”. Perhaps the precise genes that lead to baldness could be “blocked” during this time? Im hopeful for this approach…and honestly have considered trying it on myself after really delving into the patent. Lithium chloride is cheap and obtainable and pure apple juice has polyphenols that block the EGF receptor. NO-mimetics like argnine and minox are available to us. I wish they’d get the ball rolling at follica and test some guys. If you cant tell, Im anxious for human baldness to be a thing of the past…for all of us.

23

Has anyone heard of this stuff?

Part III.Wound Healing, Inflammation, and Fibrosis
Thymosin Beta 4 Induces Hair Growth via Stem Cell Migration and Differentiation

DEBORAH PHILPa, SHARLEEN ST-SURINa, HEE-JAE CHAa, HYE-SUNG MOONa, HYNDA K. KLEINMANa AND MICHAEL ELKINa

a Cell Biology Section, NIDCR, NIH, Bethesda, Maryland, USA

Key Words: cell migration • hair follicle growth • angiogenesis • wound healing • stem cells • cell survival • inflammation • gene expression • laminin-5 • proteases • zyxin • endothelial cells • thymosin beta 4 • keratinocytes • MMPs • TIMPs

Address for correspondence: Hynda K. Kleinman, Ph.D., Cell Biology Section, NIH, NIDCR, Building 30, Room 433, 30 Convent Dr. MSC 4370, Bethesda, MD 20892. Voice: 301-496-4069; fax: 301-402-0897. hkleinman@dir.nidcr.nih.gov

Thymosin beta 4 is a small 43-amino-acid molecule that has multiple biological activities, including promotion of cell migration angiogenesis, cell survival, protease production, and wound healing. We have found that thymosin beta 4 promotes hair growth in various rat and mice models including a transgenic thymosin beta 4 overexpressing mouse. We have also determined the mechanism by which thymosin beta 4 acts to promote hair growth by examining its effects on follicle stem cell growth, migration, differentiation, and protease production.

Part III.Wound Healing, Inflammation, and Fibrosis
Thymosin Beta 4 Induces Hair Growth via Stem Cell Migration and Differentiation

DEBORAH PHILPa, SHARLEEN ST-SURINa, HEE-JAE CHAa, HYE-SUNG MOONa, HYNDA K. KLEINMANa AND MICHAEL ELKINa

a Cell Biology Section, NIDCR, NIH, Bethesda, Maryland, USA

Key Words: cell migration • hair follicle growth • angiogenesis • wound healing • stem cells • cell survival • inflammation • gene expression • laminin-5 • proteases • zyxin • endothelial cells • thymosin beta 4 • keratinocytes • MMPs • TIMPs

Address for correspondence: Hynda K. Kleinman, Ph.D., Cell Biology Section, NIH, NIDCR, Building 30, Room 433, 30 Convent Dr. MSC 4370, Bethesda, MD 20892. Voice: 301-496-4069; fax: 301-402-0897. hkleinman@dir.nidcr.nih.gov

Thymosin beta 4 is a small 43-amino-acid molecule that has multiple biological activities, including promotion of cell migration angiogenesis, cell survival, protease production, and wound healing. We have found that thymosin beta 4 promotes hair growth in various rat and mice models including a transgenic thymosin beta 4 overexpressing mouse. We have also determined the mechanism by which thymosin beta 4 acts to promote hair growth by examining its effects on follicle stem cell growth, migration, differentiation, and protease production.

24

» Hangin,
»
» I never said that the shampoo was BETTER than the cream. The cream is
» almost assuredly better…but the shampoo has been shown
» to be helpful in AGA.
»
» My “regimine” for the most part is finasteride (never had any side
» effects), nizoral about twice a week, and copper peptides (usually prox-n
» after the shower). My results are that my hair has gotten darker over the
» years Ive done this. I rotate tricomin in with the prox-n (cheaper) also.
» Ive kept what I have had since about 03’ very well, but haven’t regrown my
» temples. I like to spray a blast of tricomin mist in my face-----it helps
» you look younger.
»
»
»
» Im not saying keto cream isn’t effective…I know its
» effective. I just dont want more than about one topical. The
» anti-androgenic effect of both finas and nizoral are probably “enough” to
» keep what one has. Im not diggin’ on your regimine. I do however, disagree
» with the assertion that nizoral is useless or that shampoo isn’t an
» acceptable way to get an indication to the dermis. Its not as effective as
» a cream or foam or spray, but it can indeed get some effect. Chuck Fraiser
» has NANO shampoo pictures and you can tell he got thickening on it
» -alone-with no other treatment. They are on HLT.
»
»
»
» No flames…Im tired. The board is “tired”. Just trying
» to find out as much as possible and bounce it off what others have been
» able to pick up and show with studies or reason. Thats all we have at this
» point. :ok:

if you can keep what you have that is , way more difficult than most guys realize.
If most guys on the board could just keep what they have, no regrowth, they would be ecstatic

However
in order to even keep what you have, you must cure a lot of the problems that are causing the problem in the first place, example clean out a lot of DHT with prop, fin, natural 5 ar blockers, etc which is what I did, and that in turn causes a lot of thickening and regrowth. in thinning areas, the bald areas are almost impossible to fix though, with any regimen short of a hair transplant

if you are not on super hair vitamin, i think you might want to try it, I have heard nothing but positive feedback on it, and I havce taken them for 20 yrs. I would never stop taking them, i think they help tremendously with hair strength, growth rate, keeps hair from breaking off, etc etc etc. overall hair health. They will cause some regrowth in the early stages of thinning, but not in the later stages if you have high DHT accumulation

25

» Lithium chloride is cheap and obtainable
» and pure apple juice has polyphenols that block the EGF receptor.

Shoot, I have tons of lithium. In the past, I was considering taking a piece of sandpaper and abrading a very small section of skin on my stomach or side, and then applying some lithium daily to see what happens. I wouldn’t know what dose to use, though. When i get really bored, I’ll play around.

26

» » Lithium chloride is cheap and obtainable
» » and pure apple juice has polyphenols that block the EGF receptor.
»
» Shoot, I have tons of lithium. In the past, I was considering taking a
» piece of sandpaper and abrading a very small section of skin on my stomach
» or side, and then applying some lithium daily to see what happens. I
» wouldn’t know what dose to use, though. When i get really bored, I’ll play
» around.

Ive looked at the patent. The re-epilithialization period for human skin is much shorter than in mouse skin. Human hair germs were detected in seven days after wounding. Ive seen a picture that I cant link to the rest of the board, but it was very impressive. The guy who runs “tressless.com” had the photo and sent it to me in my email at HLT. I dont have the link, but ALOT of new hair was forming in the mouse skin and it was impressive.

I think by reading the patent, they will add the wnt from 3 to 5 days POST wounding, along with the egf-receptor blocker. Did you know lithium chloride used to be considered as a replacement for table salt? It tastes like table salt. It has long-term toxicity, but I imagine just eating some of it on an apple might get enough in the blood stream to get to the scalp (Im always amazed at just how little a finasteride pill is, and the fact that .2mgs is almost as effective as 1 full pill—and how it can do what it does to scalp hair). I am just hoping it can “make” hair in the donor area—to give us more donor hair so it can be moved up front. If your donor area was 50% thicker, just think of how much one could transplant without having an un-natural thinness (have seen this in person several times) in the back? It would be a de facto “solution” for most all of us unless one was way up on the norwood scale. The patent “schedule” looked like this…pluck hair-wait three days…abrade-wait 3 to 5 days…apply topical or take internals until 9 days after wound date. That was it. The epilithial layer was all that had to be removed until skin was pink, shiny, and smooth. There was no blood.

If one done this, I wouldn’t expect the hair made to differ from the hair that occured in whatever body part it was done on though…

To remove hair, they simply plucked hair, wait three days…abrade…and apply epidermal growth factor after skin re-epilithialized. No more hair. That might be something they could do if they hit “a home run” and it worked wonderfully to get rid of the vellus hairs one has in balding areas (and their respective full-sized sebaceous glands), but that is of course getting way ahead of the game. Im wishing them luck, but temper my expectations until I see in vivo human proof. But I AM glad someone is trying this, as I hate to put all my eggs in the HM basket in case its not doable.

27

»
»
» To remove hair, they simply plucked hair, wait three
» days…abrade…and apply epidermal growth factor after skin
» re-epilithialized. No more hair. That might be something they could do if
» they hit “a home run” and it worked wonderfully to get rid of the vellus
» hairs one has in balding areas (and their respective full-sized sebaceous
» glands), but that is of course getting way ahead of the game. Im wishing
» them luck, but temper my expectations until I see in vivo human proof. But
» I AM glad someone is trying this, as I hate to put all my eggs in the HM
» basket in case its not doable.

What is the purpose for plucking the hair… what biological mechanism does this provoke?

28

» Your implication that the shampoo works better because of absorbing into
» a wet scalp, although on its face it may appear valid, does not hold true,
» since the study subjects all applied the cream immediately after
» shampooing, thus onto a WET SCALP,
»
»
» http://www.hairsite.com/hair-loss/forum_entry-id-6113-page-4-category-3-order-last_answer.html
»
»
»
» Ketoconazole (KCZ), an imidazole anti-fungal agent, is known to be
» effective for the treatment of seborrheic dermatitis and dandruff. In
» addition, 2% KCZ shampoo was found to improve hair density and the size and
» proportion of anagen follicles in androgenetic alopecia (AGA) [1] and, in
» combination with finasteride, to have an additive effect for AGA [2].
» Recently, it has been reported that topical application of KCZ stimulates
» hair growth in C3H/HeN mice [3]. However, whether topical KCZ is effective
» enough to improve the clinical appearance of AGA is not yet clear. We
» therefore carried out an open trial of topical 2% KCZ lotion (Nizoral®) in
» combination with shampoos. Furthermore, to identify the mechanism, which
» can explain the clinical effect of KCZ on AGA, we performed transient
» transfection assays using CV-1 cells transfected with androgen receptors
» (AR).
»
» The six Japanese males from 23 to 51 years old were enrolled in this study
» with their written informed consent. They presented with grade II vertex to
» IVa AGA according to the Hamilton–Norwood classification [4]. The subjects
» applied topical 2% KCZ lotion (Nizoral®) almost every day during or
» immediately after hair washing with their own unmedicated shampoos. When
» they revisited our clinic every several months, clinical pictures were
» obtained to determine the efficacy of the treatment. Two of the men, one 23
» years old with grade II vertex and the other 25 years old with Va AGA,
» showed remarkable hair regrowth after 6 and 10 months, respectively (Fig.
» 1). The 23-year-old male stopped using KCZ and 3 months later hair loss
» recurrence on the vertex was noted (Fig. 1c). When he started using KCZ
» again during shampooing, hairs on the vertex grew again after 3 months
» (Fig. 1d). These findings constitute evidence of the clinical efficacy of
» KCZ for AGA. A 41-year-old male showed a slight increase in vertex hair
» growth after 1 year. Other three of the men, 31, 38 and 51 years old did
» not show significant improvement. These findings suggest that topical KCZ
» with shampoo can be effective for some males with AGA.
»
»
»
» Fig. 1. A 23-year-old Japanese man who used 2% ketoconazole (KCZ) lotion
» during shampooing everyday. Six months later, hair regrowth was attained
» (b) in comparison with the pre-treatment condition (a). Suspension of use
» for 3 months, however, caused recurrent hair loss (c). Renewed use of KCZ
» induced renewed growth of vertex hair (d). A 25-year-old Japanese man with
» AGA (e) applied 2% KCZ lotion immediately after shampooing everyday. Ten
» months later, hair regrowth was apparent (f).
»
» To identify the mechanism, which can explain the effect of KCZ on AGA, we
» performed transient transfection assays using an androgen-responsive
» synthetic promoter for CV-1 cells transfected with AR. At 50–70% confluency
» in a 24-well plate, the CV-1 cells, maintained in Dulbecco’s modified
» Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum, were
» transfected with the transfection reagent Fugene-6 (Roche Diagnostics
» Corp., Indianapolis, IN, USA) according to the manufacturer’s instructions.
» For luciferase assays, we transfected 0.1μg of the reporter plasmid,
» pGL2-GRE3-bG-luc [5], 12.5ng of pCI-neo-BamX-AR(Gly23) [5] and 0.2μg
» of the pRL-CMV vector, the Renilla luciferase control reporter vector
» driven by the CMV immediate-early enhancer/promoter, as the internal
» controls. At 24h after transfection, we added fresh DMEM supplemented with
» 10% charcoal-treated fetal bovine serum with methyltrienolone (R1881, a
» stable synthetic androgen) or ethanol as a mock vehicle. The cells were
» also treated with KCZ (Janssen, L.P., Titusville, NJ) or ethanol as a mock
» vehicle. At 48h after transfection, the cells were harvested for luciferase
» assays. Luciferase activities were measured with a luminometer using the
» Dual-Luciferase™ reporter assay system (Promega, Madison, WI). The results
» were summarized from three independent sets of transfections and presented
» as mean±S.D.; statistical significance was tested with Student’s t-test.
» The results demonstrated that 10 or 20μg/ml KCZ reduced luciferase
» activity to 67.5% (p<0.01) or 49.9% (p<0.03), respectively, reflecting its
» suppressive action on AR (Fig. 2). This finding suggests that KCZ improves
» AGA through the suppression of AR activity.
»
»
»
» Fig. 2. KCZ effect on R1881-induced AR transcactivity in CV-1 cells
» transfected with AR. We used the transfection reagent Fugene-6 (Roche
» Diagnostics Corp., Indianapolis, IN, USA) to transfect 0.1μg of the
» reporter plasmid, pGL2-GRE3-bG-luc, 12.5ng of pCI-neo-BamX-AR(Gly23) and
» 0.2μg of pRL-CMV vector (lanes 1–6) into CV-1 cells cultured at 50–70%
» confluency in a 24-well plate. The infected cells were treated with
» 10−9M R1881 (lanes 2–6) or ethanol as a mock vehicle (lane 1). After
» overnight incubation, KCZ at the indicated concentration was added to the
» cultures. The activities of the various reporter genes were compared with
» the luciferase activity in the presence of R1881 and the absence of KCZ
» (lane 2).
»
» Dermal papilla cells are the main targets for androgen in hair follicles,
» as evidenced by immunohistochemistry [6] and reporter assays [7] for the
» detection of AR. Deep penetration of KCZ into dermal papilla is therefore
» necessary to realize the suppressive action on androgen in vivo. The use of
» KCZ in combination with detergent containing shampoos in this study may
» enhance KCZ penetration. On the other hand, a recent study demonstrated
» that KCZ stimulates hair growth in mice [3], suggesting that its effect on
» hair is androgen independent. To summarize, KCZ may exert its effect on AGA
» in both an androgen-dependent and -independent manner.
»
»
»
»
» References
» return to Article Outline
»
» [1]. [1]Pierard-Franchimont C, De Doncker P, Cauwenbergh G, Pierard GE.
» Ketoconazole shampoo: effect of long-term use in androgenic alopecia.
» Dermatology. 1998;196:474–477. MEDLINE | CrossRef
»
» [2]. [2]Khandpur S, Suman M, Reddy BS. Comparative efficacy of various
» treatment regimens for androgenetic alopecia in men. J Dermatol.
» 2002;29:489–498. MEDLINE
»
» [3]. [3]Jiang J, Tsuboi R, Kojima Y, Ogawa H. Topical application of
» ketoconazole stimulates hair growth in C3H/HeN mice. J Dermatol.
» 2005;32:243–247. MEDLINE
»
» [4]. [4]Norwood OT. Male pattern baldness: classification and incidence.
» South Med J. 1975;68:1359–1365. MEDLINE
»
» [5]. [5]Inui S, Nakao T, Itami S. Modulation of androgen receptor
» transcriptional activity by anti-acne reagents. J Dermatol Sci.
» 2004;36:97–101. Abstract | Full Text | Full-Text PDF (135 KB) | MEDLINE |
» CrossRef
»
» [6]. [6]Itami S, Kurata S, Sonoda T, Takayasu S. Interaction between
» dermal papilla cells and follicular epithelial cells in vitro: effect of
» androgen. Br J Dermatol. 1995;132:527–532. MEDLINE
»
» [7]. [7]Inui S, Itami S, Pan HJ, Chang C. Lack of androgen transcriptional
» activity in human keratinocytes. J Dermatol Sci. 2000;23:87–92. Abstract |
» Full Text | Full-Text PDF (106 KB) | MEDLINE | CrossRef

So was this the shampoo they used that grew the hair or the cream after?? I use 2% Keto for like 2 weeks now…3x a week…makes my hair thicker and fuller…but do i need to use a cream nizoral after?? Can some one explain it to me…??

29

What if we move our vellus hair (from the MPB area) back to the donor area ? will it grow back ? If it does all we have to do is a process of getting the donor to the balding areas and visversa…should I file for a Patent ???

30

» What if we move our vellus hair (from the MPB area) back to the donor area
» ? will it grow back ? If it does all we have to do is a process of getting
» the donor to the balding areas and visversa…should I file for a Patent ???

when do you think you can have something on the market?5 years?

31

I believe in the Secret and asked the “Universe” what the missing link to Benji’s question is and it said the answer is related to viruses , polarity and electromagnetism…

http://jeffsutherland.com/complementary/2004/10/why-do-people-go-bald.html

Intrigued by comments on hair loss and frequency effects I analyzed many different cases of Alopecia Areata. Recently, my son returned from Baghdad with an itchy scalp and sure enough, he picked up the “bald head virus!” It was a good opportunity to test him carefully and update the frequencies.

In every case of complete hair lost I found a virus with frequency 365466 and in most cases of partial hair loss, I found the bacterial form of the virus predominated with frequency 254466. As you will recall from previous postings with a photo of the SV40 virus attacking a cell, there are four components of a virus that can be seen in the photo. So you need four frequencies.

In testing a few people with little hair loss I found the same organism so the virus is quite widespread. I suspect that the observed genetic predisposal to hair loss is confounded by the fact that familial infections are common.

In any event, the following F100 program wipes out the virus. If you have a plasma device that only operates below 10000hz, then devide the frequencies by 64.

repeat 60
dwell 60
duty 50
pulse 64 75
converge 23 1
365466
254456
155646
65636
end repeat

posted by Jeff Sutherland

32

» » What if we move our vellus hair (from the MPB area) back to the donor
» area
» » ? will it grow back ? If it does all we have to do is a process of
» getting
» » the donor to the balding areas and visversa…should I file for a Patent
» ???
»
» when do you think you can have something on the market?5 years?

lol :smiley: , We dont really know, we are doing everything we can.

33

Could we use Daktarin Gold?

34

I think you guys are worrying too much over this mice & immune issue. I don’t see what this issue changes about the Folica situation.

Regardless of the immune system suppression results, the bottom line is that the mice with human skin grafts are producing some entirely new human hair follicles that didn’t previously exist. Maybe they needed immune suppression to form, but we can do that temporarily on ourselves too if we have to.

These are gonna be new follicles. They won’t have 20 years of DHT exposure. I see no reason to assume the immune system would eat the new follicles alive like androgen-wrecked ones as soon as it gets back online. No more than it was eating the original follicles before the DHT got to them, and no more that it’s currently eating you donor wreath follicles right now.

The immune response attack is PROPORTIONAL to the amount of androgen damage in the follicle, remember? It’s not just an on/off thing. You’ve always had a raging-poweful immune system, but it was only partially miniaturizing certain follicles for years in your teens, remember?

If you time-traveled and transplanted one of your current (balded) follicles onto your head back 10 years ago, then think of what would happen: Your 1998 self’s immune system would still immeidately attack the 2008-sourced follicle down to its 2008 level of miniaturization, while leaving the rest of the 1998 follicles much less miniaturized at the time.

Likewise, a no-androgen-exposure follicle sprouted on your head in 2008 would get only a childhood-level immune attack, even though the existing follicles alongside it might still be getting chewed down to nothing because of the long term androgen damage.

So I think as long as we can get a new batch of these goddamn follicles fully formed right in the first place, they shouldn’t rely on immune system suppression just for their continued survival.

35

my idea is topical antibiotic (doxycycline or penicilin).

Supposedly 2 applications are enough to get the hair growing for 6 months or longer.

Other than that, if its not the DHT (even 100% reduction of DHT wont get your hair back), and if immuno suppresed mice can regrow miniaturized hair, then its either:

  • the immune system
  • the mice

that make the difference.

IF we consider that there are some ppl who claim that immunosupressives grow your hair back the best,

then I’d conclude its the immune system that makes the difference.

there is something that makes the follicle unloved by your immune system. shut this up and you’ll have hair again.

36

I agree.

I have no doubt that whacking the immune system temporarily should work to regenerate some hairs for us.

The only questions to my mind (and they’re big ones) is whether we can controllably get the hair good enough for our purposes, and whether the hairs will remain viable once immune system activity returns to the area.

Anecdotal real world cases and Folica-spoken indications seem to say yes to both issues. My fingers remain firmly crossed.

I think the situation with Folica’s impact on pre-existing hairs is still a great big blank page though.

Will Folica make the body fix them? Get rid of them? How does their presence and condition affect the regeneration and qualities of the all-new follicles?

We’ve been talking about this stuff for a couple of years now when you count people just paying attention to research in general. And I still don’t think we’ve concluded much of anything about this aspect of Folica.

37

very interesting research! Are there anymore studies that back this up?

Why don’t the scientists just study balding & non-balding follicles i.e. do a genetic comparison? if the both follicles are from same person, than it should be much easier to identify the key genetic differences between balding & non-balding follicles. And once we have a complete list of genetic differences, it might also be easier to find the real cause and fix it.

38

The genes are identical in balding and non-balding follicles in one person. That’s how they use DNA to identify people. If your genes were different throughout the body, they wouldn’t be able to use DNA to identify somebody. It’s just how the genes are expressed that causes some follicles to bald. That’s why they compare genes from different people to try and find genetic causes of diseases (including baldness).

39

» 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?

I don’t understand one thing: Why do you think that a slick balled head, is actually filled with small hairs? sure when I look at dad’s head I see a few small hairs here and there, but if all his hairs were there, only very small, surely i would see them. So is these hypothesis that follicles never die based on any thing?

40

A 'slick bald head" is filled with tiny hairs from the original follicles. This is not a theory, it’s a simple fact. Examine your head with a magnifying glass or something powerful enough, and they’ll be there.

Balded follicles don’t “die.” They don’t vanish. The follicles would still be there if you took a dead cadaver’s bald scalp and dissected it looking for them.

The balded follicles are just effectively shut down by the body. Unplugged. All signs point to the method of shutting them down being an immune system attack that holds them perpetually out of action.