New Dermaroller Study; Thoughts, comments?

[theRA]

1x/week with 1.5mm...Japanese Mint Oil (Hagina) to numb the pain (works very well)....minoxidil with no-PPG every other day or say..

when I tried the min oil it stinged alot for a couple of minutes, do you have the same expirience?

 

[hellouser]

I'd like to quote the following post from TBT and ask to you all guys what do you think (I posted this graph pages ago as well):

That was my post....

 

[albert]

That was my post....

Sorry dude, I just copied the content and closed the tab and when I was going to write the (your) name I didn't have it. I hope someone can give some feedback about your idea here as well.

 

[princessRambo]

Update from my side: Ever since the 20 or so new terminal hair that I noticed one and a half weeks ago, nothing new. I was hoping that there was more to come, but nothing as of now.

Maybe minoxidil is crucial and wounding alone doesnt cut it.

Yeah -- I wondering the same thing as I have really nothing, having been pretty much just wounding with the odd minoxidil application...There are a few vellus hairs popping up but those follicles shedded recently so they may just be hanging...the wounding may have helped them breathe a few more breath's here...

I have nothing on the slick temple that's been barren for years now...

Have I not said this before waaaay early in this thread that people only derma rolling are mainly wasting their time. I have pointed to an old study conducted in 1956 that Cotsarelis mentioned in which dermabrading alone only causes vellus hair and nothing more... I even suggested specifically you benjt doing this to at least use something else that ups PGE2 or b catenin, like castor oil, b12 topical, etc...

http://www.nature.com/jid/journal/v27/n1/full/jid195671a.html

The interest, particularly on the part of males, in the subject of human hair regeneration, is such that we feel obliged to emphasize that we have demonstrated only vellus hair formation and have not the slightest idea whether coarse terminal hair follicles can be regenerated under any circumstances. In respect to studying the latter possibility, there is the formidable technical problem, of removing or destroying the terminal hairs experimentally without the formation of a scar.

 

[Manoko]

Have I not said this before waaaay early in this thread that people only derma rolling are mainly wasting their time. I have pointed to an old study conducted in 1956 that Cotsarelis mentioned in which dermabrading alone only causes vellus hair and nothing more... I even suggested specifically you benjt doing this to at least use something else that ups PGE2 or b catenin, like castor oil, b12 topical, etc...

http://www.nature.com/jid/journal/v27/n1/full/jid195671a.html

Princess, your input is valuable, so I thought of asking you this question:

What do you think of chemical peels instead of dermarolling. Some people on other forums seem to be very hyped about it, and it makes a lot of sense to me.
The response of the body may be stronger via chemical peels than dermarolling, I mean, it removes layers of skin, not just puncture them.

I kinda see it as well as a reset switch, just like people are saying about dermarolling too.

So, what's your opinion about it, chemical peels (not strong ones to avoid scarring of course) or dermarolling ?

 

[princessRambo]

Princess, your input is valuable, so I thought of asking you this question:

What do you think of chemical peels instead of dermarolling. Some people on other forums seem to be very hyped about it, and it makes a lot of sense to me.
The response of the body may be stronger via chemical peels than dermarolling, I mean, it removes layers of skin, not just puncture them.

I kinda see it as well as a reset switch, just like people are saying about dermarolling too.

So, what's your opinion about it, chemical peels (not strong ones to avoid scarring of course) or dermarolling ?

The question is, how do deep are you going to peel. How are you avoiding scarring, there is a risk of destroying the follicle and replace it with a scar tissue, then it's bye bye forever. To all the people hyping about it, have you seen a good convincing before and after picture that is better than the indian study? At least with derma rolling you can somehow control how much damage you do, with a chemical peel I don't know how much control you have. Ask for evidence that it works first, specially convincing before pictures, don't always follow the hype, that's my take on it.

 

[odalbak]

Have I not said this before waaaay early in this thread that people only derma rolling are mainly wasting their time. I have pointed to an old study conducted in 1956 that Cotsarelis mentioned in which dermabrading alone only causes vellus hair and nothing more...

On the other hand, his observation was based on dermabrasion which doesn't go deep afaik. You said many times wounding deep was crucial in the dermarolling strategy…

 

[princessRambo]

On the other hand, his observation was based on dermabrasion which doesn't go deep afaik. You said many times wounding deep was crucial in the dermarolling strategy…

Indeed (but not more than 1.5mm, benjt study pointed this out clearly) + minoxidil used very frequently, I still maintain that we can get results as good as the indian study and I do believe even miniaturized follicle can comeback to life slowly in this way. As far as depth, some dermabrading devices can go as deep as 3mm. Quote from the study I posted above where they notice only vellus hair and nothing more using dermabrading alone:

on each of whom a two inch circular facial area was planed to an approximate depth of 2 millimeters. This method does not ordinarily allow a greater depth of removal, which is about half way through the corium of the facial skin.

 

[super]

Princess, your input is valuable, so I thought of asking you this question:

What do you think of chemical peels instead of dermarolling. Some people on other forums seem to be very hyped about it, and it makes a lot of sense to me.
The response of the body may be stronger via chemical peels than dermarolling, I mean, it removes layers of skin, not just puncture them.

I kinda see it as well as a reset switch, just like people are saying about dermarolling too.

So, what's your opinion about it, chemical peels (not strong ones to avoid scarring of course) or dermarolling ?

Dude, my doctors apply a peeling formula to my head before rolling. They do both. But they are REALLY good at skin care. So they know how much to use and for how long. Example. Only now i am doing the procedure twice a month. And the first thing my doctor looked was at how my skin was reacting to the peeling formula, in order not to hurt the skin too much. He said then that i was ok, that my skin was recovering fast enough. But some may not.

- - - Updated - - -

I also can't express enough that the hair in my temples and some others only started to grow, instead of being just vellus, after using the minoxidil. Before, only a few grew.

 

[princessRambo]

A simple addition that can make a night and day difference for the people deciding not to use minoxidil, simply crush some b12 pills into water or alcohol or both, it is soluble in both...


LINK

Vitamin B12 Activates the Wnt-Pathway in Human Hair Follicle Cells by Induction of B-Catenin and Inhibition of Glycogensynthase Kinase-3 Transcription

Concomitantly the amounts of GSK-3 were significantly reduced after stimulation with 25 ug/ml vitamin B12 (fold change compared to DMEM: 0.76 u 0.12, p < 0.05). Conclusions: Our data demonstrate a hair growth promoting effect of vitamin B12 in vitro. This effect is accompanied by the modulation of intracellular signal transduction molecules of the wnt-pathway and might promote hair growth after micrograft transplantation.

Besides upping wnt, notice what else b12 does? it significantly inhibit transcription of GSK3. You know what GSK3 is in relation to hair growth? Inhibiting it significantly enhances hair growth:

http://www.google.com/patents/WO2002066480A2

GSK3 phosphorylates and degrades β-catenin. β-catenin is an effector of the pathway for keratonin synthese. β-catenin stabilisation may be lead to increase hair development. Mice expressing a stabilised β-catenin by mutation of sites phosphorylated by GSK3 undergo a process resembling de novo hair morphogenesis (Gat et al., Cell 1998 Nov 25;95 (5):605- 14)). The new follicles formed sebaceous glands and dermal papilla, normally established only in embryogenesis. Thus GSK3 inhibition may offer treatment for baldness.

For those using minoxidil, it is even better to mix b12 with your minoxidil, they have synergic additive effect:

Topical Administration of Cyanocobalamin (Vitamin B12) Showed Suppression of Potassium Channel Inhibitor (Tolbutamide) and Induction of Murine Hair Anagen Phase and Synergistic Effect with Minoxidil

http://www.ehrs.org/conferenceabstracts/2006london/researchabstracts/14-park.htm

The grown hair weights of topical 1% minoxidil preparation (113.14 11.02 mg, p 0.001) and 0.03% cyanocobalamin (59.56
13.88 mg, p 0.05) increased significantly than that of vehicle (18.47 4.68 mg). When topically administered in mixed preparations (0.5% minoxidil and 0.03% cyanocobalamin), the more grown hair weight (87.00 8.39 mg, p 0.03 t-test with 0.05% minoxidil) by mixed preparation was observed compared to those of single 0.5% minoxidil preparation (44.33 14.96 mg) and of vehicle preparation

Also, adds castor oil as it has been shown to promote EP3 activation

http://www.ncbi.nlm.nih.gov/pubmed/18005048

This data shed new light on an underestimated complex network involved in hair growth control. Indeed most of these receptors showed a wide spectrum of expression in cultured cells and the whole hair follicle. Using IHC, we observed that expression of prostaglandin E(2) receptors (EP(2), EP(3), EP(4))

The EP3 receptor is specifically activated by castor oil:

http://www.ncbi.nlm.nih.gov/pubmed/22615395

Here we show that the EP(3) prostanoid receptor is specifically activated by ricinoleic acid and that it mediates the pharmacological effects of castor oil.

I will repeat it again, if you are not using minoxidil, why not simply use topical b12 and castor oil, they are cheap and available everywhere....

 

[albert]

I'll consider adding B12 to my Minoxidil. What else could be a safe bet to add to the dermarolling mix?

 

[buddyebsen1]

I am interested in adding B12 to minoxidil. Do you know how much I should add to a fresh bottle to make a solution which the appropriate amount?

Thanks,

 

[Koga]

How long can you keep a bottle of simple water (or is distilled water better?) with crushed B12 tablets? Won't it go bad quite fast when there's no alcohol in the solution?

 

[princessRambo]

How long can you keep a bottle of simple water (or is distilled water better?) with crushed B12 tablets? Won't it go bad quite fast when there's no alcohol in the solution?

Have u done research confirming it will go bad?

- - - Updated - - -

I am interested in adding B12 to minoxidil. Do you know how much I should add to a fresh bottle to make a solution which the appropriate amount?

Thanks,

not sure, I use 10 pills of 1000ug in a 100ml solution containing minoxidil water and egcg. Given that a single 1000ug pill is 16000% daily systemic value of b12, this might even be overkill...

 

[ganonford]

Sorry for the off-topic guys... semen question again...

PrincessRambo... do you happen to know how much does semen properties last unused?.

I know you said it may be better to let the semen stay for a couple of minutes before

applying it, but what about a couple of hours...?


Sometimes, I just can't apply it as I get, so.... do you know if I can put it inside the

refrigerator for just 2 or 3 hours, or do you think it's properties would be degraded by then?

 

[Koga]

Have u done research confirming it will go bad?

No, I did not. I just guessed any topical needs some alcohol to last several weeks (or days). B12 is water soluble; wouldn't that mean it'll disappear after a few days in plain water?

 

[princessRambo]

No, I did not. I just guessed any topical needs some alcohol to last several weeks (or days). B12 is water soluble; wouldn't that mean it'll disappear after a few days in plain water?

No, minoxidil is soluble in water and alcohol soluble and ppg soluble, your generic minoxidil bottle is mainly water and ppg as a vehicle, does that mean it disappears from the bottle after a few days? No, it means you can use those vehicles as a way for topical administration... And no, not every topical needs some alcohol to last, in fact alcohol degrades a lot of things that people use here, it's this wrong assumption that made people dissolve cetirizine in alcohol (some peeps even used vodka it seems), which completely renders it useless, and the reason why most people didn't get any effect whatsoever from using cet....in any case, the alcohol as a vehicle thing is one of those ad nauseam repeated non-nonse over and over in forums...

@zelda's #1 enemy, we should discussed this in another thread, I will reply to you in the wounding theory thread...

 

[benjt]

I got another interesting finding to report.

I just finished my latest dermarolling session - totally off schedule, I just didnt have the time recently. If I'm not mistaken it should be like 16 days after the previous rolling session, so quite a bit longer than my usual 7 to 10 days waiting.
Now, the interesting thing is: the crunching noises were back. The ones that were completely gone meanwhile during my last sessions. Today during my session they were back though not remotely as loud as during my 1st and 2nd session. Also, some other people reported that they got crunchy noises at first which then later vanished.

My theory after having gotten confirmation about this from 4 or 5 people was that the crunching noise was fibrotic tissue being penetrated, and, as the fibrotic tissue got increasingly destroyed, the crunching noises vanished.

As obviously the fibrotic tissue could not have rebuilt within 16 or 17 days, I have an alternative theory about the crunching noise: this was the "normal" noise of healthy tissue, not fibrotic tissue. If this is the case, this would indicate that 7 to 10 days between violent 1.5mm rolling sessions are indeed not enough recovery time. I really doubt that newly generated/repaired tissue can turn fibrotic that quickly, and thus I doubt that the new crunchy noises that I got are from new fibrotic tissue.

Could the other ones that reported the crunching noises extend their recovery periods to at least 14 days and check if they also get these noises back?

 

[albert]

I got another interesting finding to report.

I just finished my latest dermarolling session - totally off schedule, I just didnt have the time recently. If I'm not mistaken it should be like 16 days after the previous rolling session, so quite a bit longer than my usual 7 to 10 days waiting.
Now, the interesting thing is: the crunching noises were back. The ones that were completely gone meanwhile during my last sessions. Today during my session they were back though not remotely as loud as during my 1st and 2nd session. Also, some other people reported that they got crunchy noises at first which then later vanished.

My theory after having gotten confirmation about this from 4 or 5 people was that the crunching noise was fibrotic tissue being penetrated, and, as the fibrotic tissue got increasingly destroyed, the crunching noises vanished.

As obviously the fibrotic tissue could not have rebuilt within 16 or 17 days, I have an alternative theory about the crunching noise: this was the "normal" noise of healthy tissue, not fibrotic tissue. If this is the case, this would indicate that 7 to 10 days between violent 1.5mm rolling sessions are indeed not enough recovery time. I really doubt that newly generated/repaired tissue can turn fibrotic that quickly, and thus I doubt that the new crunchy noises that I got are from new fibrotic tissue.

Could the other ones that reported the crunching noises extend their recovery periods to at least 14 days and check if they also get these noises back?

hellouser can tell us something about what you just mentioned as he moved to dermarolling every two weeks afaik

 

[squeegee]

Keratinocyte growth inhibition through the modification of Wnt signaling by androgen in balding dermal papilla cells.

(PMID:19141591)

• Abstract
• Citations
• BioEntities
• Related Articles
• External Links

Kitagawa T, Matsuda K, Inui S, Takenaka H, Katoh N, Itami S, Kishimoto S, Kawata M

Department of Anatomy and Neurobiology, Kyoto Prefectural University of Medicine, Kawaramachi Hirokouji, Kyoto, Japan.
The Journal of Clinical Endocrinology and Metabolism [2009, 94(4):1288-1294]


Type: Journal Article, Research Support, Non-U.S. Gov't
DOI: 10.1210/jc.2008-1053

Abstract

Highlight Terms Gene Ontology(3) Diseases(1) Genes/Proteins(3) Chemicals(2)

CONTEXT/OBJECTIVE: Androgen induces androgenetic alopecia (Androgenetic Alopecia), which has a regressive effect on hair growth from the frontal region of the scalp. Conversely, Wnt proteins are known to positively affect mammalian hair growth. We hypothesized that androgen reduces hair growth via an interaction with the Wnt signaling system. The objective of this study was to investigate the effect of androgen on Wnt signaling in dermal papilla (DP) cells. DESIGN: The effect of androgen and Wnt3a on keratinocyte proliferation was measured by use of a coculture system consisting of DP cells and keratinocytes. The molecular mechanisms of androgen and Wnt pathway interactions in DP cells were examined by analyzing the expression, intracellular localization, and activity of the androgen receptor (AR) and also downstream Wnt signaling molecules. RESULTS: Wnt3a-dependent keratinocyte growth was suppressed by the addition of dihydrotestosterone in coculture with DP cells that were derived from Androgenetic Alopecia patients, but growth was not suppressed in coculture with DP cells from non-Androgenetic Alopecia males. Whereas DP cells from both scalp regions expressed AR protein, the expression levels of AR and cotranslocation with beta-catenin, a downstream Wnt signaling molecule, were higher in DP cells of Androgenetic Alopecia patients than in DP cells from non-Androgenetic Alopecia males. In addition, significant suppression of Wnt signal-mediated transcription in response to dihydrotestosterone treatment was observed only in DP cells from Androgenetic Alopecia patients.

CONCLUSION: These results suggest that Wnt signaling in DP cells is regulated by androgen and this regulation plays a pivotal role in androgen's action on hair growth.




[h=1]Keratinocyte growth factor[/h] From Wikipedia, the free encyclopedia
Jump to: navigation, search
The Keratinocyte Growth Factor (KGF), also known as FGF7, is a growth factor present in the epithelialization-phase of wound healing. In this phase, keratinocytes are covering the wound, forming the epithelium.
KGF is a small signaling molecule that binds to fibroblast growth factor receptor 2b (FGFR2b).[SUP][1][/SUP] For signalling to occur, a dimer is required between two FGF:FGFR complexes that is linked together by a molecule of heparin.
There are 23 known FGFs, and 4 FGF receptors. FGF:FGFR binding is complex and regulated by a variety of mechanisms in a tissue specific manner.
FGF10 is also known as "Keratinocyte growth factor 2".[SUP][2]




[/SUP]