New Dermaroller Study; Thoughts, comments?
- Thread starter Jlyncher
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hi jason, i'm happy for your "awesome results".
will you add new pics this week?
I hope so, i am really courius about your story so as the others readers.
Thx!
odalbak
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what for?
Aurelio
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To induce regrowth in this area
jason5
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Here is a photo I took recently that is showing somewhat of a hairline and hair filling in. This is a big change for me. I will post proper high rez top pics in about a week. Will see what dropping minoxidil will cause, hopefully I can maintain and continue to increase density without its use.
u rolled on the whole head or only on 1 temple?looks like ur left temple is muuuch bigger then ur right oneHere is a photo I took recently that is showing somewhat of a hairline and hair filling in. This is a big change for me. I will post proper high rez top pics in about a week. Will see what dropping minoxidil will cause, hopefully I can maintain and continue to increase density without its use.
Sparky4444
Senior Member
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minoxidil screws with me...my eyes, especially...I'm going to go the castor oil route for topical....The science now shows that oils are extremely beneficial, not harmful, for your scalp and hair
Im wondering if we get more subcutanous fat with dermarolling or less?i have no clue why DR shouldnt lead to less subcutanous fat?
btw just saw this article,dunno if it was posted here alrdy
http://archderm.jamanetwork.com/article.aspx?articleid=524193
btw just saw this article,dunno if it was posted here alrdy
http://archderm.jamanetwork.com/article.aspx?articleid=524193
I just bought some 1% B12 powder from bulksupplements, thought I would mix it with my minoxidil. Turns out the other 99% is mannitol. I originally planned on using a filter to extract the B12 to add to minoxidil. I found out that mannitol is soluble in water. This means if I try to filter the B12, I will also dissolve the mannitol and it won't work. Anyone know if mannitol would be bad to apply topically? What should I do to get the B12 into my minoxidil 
jason5
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My entire head of course. Have you seen my before picture ? I was basically bald, so this is a huge improvement. I've always had that one temple balding ahead of the other, so I didn't expect it to get much improvement till later.
DesperateOne
Banned
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So I added a few B12 pills into minoxidil and it turned pink. Should I filter the thing?
We might need to get into string theory in order to solve male pattern baldness
We might need to get into string theory in order to solve male pattern baldness
K
karankaran
Guest
LOL, this cracked me up!
Jason, about the reason why you are stopping minoxidil... have you been applying it immediately after rolling? or did you wait the 24h as in the study? Also, how much time have you been on it before dermarroling?
closetmetrosexual
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Possibly this.
I have no experience with the product myself.
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I've never heard of DMSO helping against hair loss.
Just make sure you keep it away from minoxidil!
DMSO will pull minoxidil (and pretty much anything else) directly into your bloodstream. Be careful.
squeegee
Banned
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Is this why Minoxidil works in the first place??
Nitric oxide inhibits androgen receptor-mediated collagen production in human gingival fibroblasts.
Lin SJ, Lu HK, Lee HW, Chen YC, Li CL, Wang LF.
Source
Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan Periodontal Department, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Abstract
Lin S-J, Lu H-K, Lee H-W, Chen Y-C, Li C-L, Wang L-F. Nitric oxide inhibits androgen receptor-mediated collagen production in human gingival fibroblasts. J Periodont Res 2012; 47: 701-710. © 2012 John Wiley & Sons A/S Background and Objective: In our previous study, we found that flutamide [an androgen receptor (AR) antagonist] inhibited the up-regulation of collagen induced by interleukin (IL)-1β and/or nifedipine in gingival fibroblasts. The present study attempted to verify the role of nitric oxide (NO) in the IL-1β/nifedipine-AR pathway in gingival overgrowth. Material and Methods: Confluent gingival fibroblasts derived from healthy individuals (n = 4) and those with dihydropyridine-induced gingival overgrowth (DIGO) (n = 6) were stimulated for 48 h with IL-1β (10 ng/mL), nifedipine (0.34 μm) or IL-1β + nifedipine. Gene and protein expression were analyzed with real-time RT-PCR and western blot analyses, respectively. Meanwhile, Sircol dye-binding and the Griess reagent were, respectively, used to detect the concentrations of total soluble collagen and nitrite in the medium. Results: IL-1β and nifedipine simultaneously up-regulated the expression of the AR and type-I collagen α1 [Colα1(I)] genes and the total collagen concentration in DIGO cells (p < 0.05). IL-1β strongly increased the expression of inducible nitric oxide synthase (iNOS) mRNA and the nitrite concentration in both healthy and DIGO cells (p < 0.05). However, co-administration of IL-1β and nifedipine largely abrogated the expression of iNOS mRNA and the nitrite concentration with the same treatment. Spearman's correlation coefficients revealed a positive correlation between the AR and total collagen (p < 0.001), but they both showed a negative correlation with iNOS expression and the NO concentration (p < 0.001). The iNOS inhibitor, 1400W, enhanced IL-1β-induced AR expression; furthermore, the NO donor, NONOate, diminished the expression of the AR to a similar extent in gingival fibroblasts derived from both healthy patients and DIGO patients (p < 0.05). Conclusion: IL-1β-induced NO attenuated AR-mediated collagen production in human gingival fibroblasts. The iNOS/NO system down-regulated the axis of AR/Colα1(I) mRNA expression and the production of AR/total collagen proteins by DIGO cells.
A role for the androgen receptor in collagen content of the skin.
Markova MS, Zeskand J, McEntee B, Rothstein J, Jimenez SA, Siracusa LD.
Source
Division of Rheumatology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Abstract
Collagen, the major macromolecular component of skin, is responsible for maintaining the structural integrity of the tissue as well as for providing important functional characteristics, such as pliability and thickness. We have been studying the structure and regulation of collagen in mouse mutations affecting the skin. In the course of these studies, we found that there are significant differences in collagen content between the skin of wild-type male and female mice, which become evident at puberty. Furthermore, male mice with an X-linked mutation in the androgen receptor gene (formerly called testicular feminization and abbreviated as Ar(Tfm)) showed decreased levels of collagen, indicating that the androgen receptor pathway contributes to the observed differences. These findings demonstrate that there are striking differences in the collagen content of skin between male and female mice, and provide a biochemical explanation for these differences.
Action of androgen on fibroblast collagen synthesis: a receptor-dependent response.
C Loire[SUP]1[/SUP], B Kern[SUP]1[/SUP] and Ch Sultan[SUP]1[/SUP]
[SUP]1[/SUP]INSERM U.58, MONTPELLIER and CNRS GR.40, CRETEIL, France.
Top of pageAbstract
Several groups are still investigating an "in vitro" biological response of androgen action. The purpose of this study was to determine whether dihydrotestosterone (DHT) influences the secretion of collagen by cultured foreskin fibroblasts raised from patients with normal or undetectable DHT-binding activity (complete androgen resistance). Collagen synthesis and secretion were evaluated by [SUP]3[/SUP]H-proline incorporation in newly synthetized collagen by confluent fibroblasts alone, or in the presence of DHT (10[SUP]−5[/SUP] to -10[SUP]−10[/SUP]M). Production of collagen is expressed as a ratio between tritiated OH-proline and OH-proline plus proline,within the cells or in the culture medium.
These data show that : -in control cells,DHT significantly increases production of collagen released in the culture medium (p < 0.001), -In complete androgen resistance with no detectable androgen binding activity, DHT does not modify basal collagen synthesis. These results strongly suggest that this hormonal response is mediated via a DHT-receptor or is receptor-dependent. This could be used as a biological response of androgen action in patients with androgen resistance associated with a "post-receptor" defect.
“During the hair cycle the follicle has to be rebuilt from stem cells,” explains Dr Bruno Bernard, director of research for life sciences at L’Oreal. “Stem cells in human hair follicles are localised in two different reservoirs – one is in the upper part of the follicle and the other in the lower part.
“The cells in the lower part are required to activate the cells in the upper part and so help to maintain the follicle function. The thickening of collagen in the connective tissue sheath, which sits around the base of the hair follicle, prevents the movement of stem cells from the lower reservoir to the upper reservoir. Bit by bit, the follicle is squeezed and causes the follicles to grow smaller and smaller.” Indeed, research from The Rockefeller University in New York suggests movement between the two groups of stem cells is crucial in normal hair growth.
http://www.telegraph.co.uk/science/8470168/The-cures-for-baldness-around-the-corner.html
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so Fibrosis is really the bad guy in hairloss..
Formation of fibrous tissue or fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the
miniaturization. Involution of the pilosebaceous unit in this form of baldness and sustained microscopic
follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of androgenetic alopecia. However, till date, the
inflammatory component has not been explored in developing treatment protocols for androgenetic
alopecia.
http://www.hairlosstalk.com/interac...w-Dermaroller-Study-Thoughts-comments/page142
Nitric oxide inhibits androgen receptor-mediated collagen production in human gingival fibroblasts.
Lin SJ, Lu HK, Lee HW, Chen YC, Li CL, Wang LF.
Source
Shin-Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan Periodontal Department, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Abstract
Lin S-J, Lu H-K, Lee H-W, Chen Y-C, Li C-L, Wang L-F. Nitric oxide inhibits androgen receptor-mediated collagen production in human gingival fibroblasts. J Periodont Res 2012; 47: 701-710. © 2012 John Wiley & Sons A/S Background and Objective: In our previous study, we found that flutamide [an androgen receptor (AR) antagonist] inhibited the up-regulation of collagen induced by interleukin (IL)-1β and/or nifedipine in gingival fibroblasts. The present study attempted to verify the role of nitric oxide (NO) in the IL-1β/nifedipine-AR pathway in gingival overgrowth. Material and Methods: Confluent gingival fibroblasts derived from healthy individuals (n = 4) and those with dihydropyridine-induced gingival overgrowth (DIGO) (n = 6) were stimulated for 48 h with IL-1β (10 ng/mL), nifedipine (0.34 μm) or IL-1β + nifedipine. Gene and protein expression were analyzed with real-time RT-PCR and western blot analyses, respectively. Meanwhile, Sircol dye-binding and the Griess reagent were, respectively, used to detect the concentrations of total soluble collagen and nitrite in the medium. Results: IL-1β and nifedipine simultaneously up-regulated the expression of the AR and type-I collagen α1 [Colα1(I)] genes and the total collagen concentration in DIGO cells (p < 0.05). IL-1β strongly increased the expression of inducible nitric oxide synthase (iNOS) mRNA and the nitrite concentration in both healthy and DIGO cells (p < 0.05). However, co-administration of IL-1β and nifedipine largely abrogated the expression of iNOS mRNA and the nitrite concentration with the same treatment. Spearman's correlation coefficients revealed a positive correlation between the AR and total collagen (p < 0.001), but they both showed a negative correlation with iNOS expression and the NO concentration (p < 0.001). The iNOS inhibitor, 1400W, enhanced IL-1β-induced AR expression; furthermore, the NO donor, NONOate, diminished the expression of the AR to a similar extent in gingival fibroblasts derived from both healthy patients and DIGO patients (p < 0.05). Conclusion: IL-1β-induced NO attenuated AR-mediated collagen production in human gingival fibroblasts. The iNOS/NO system down-regulated the axis of AR/Colα1(I) mRNA expression and the production of AR/total collagen proteins by DIGO cells.
A role for the androgen receptor in collagen content of the skin.
Markova MS, Zeskand J, McEntee B, Rothstein J, Jimenez SA, Siracusa LD.
Source
Division of Rheumatology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Abstract
Collagen, the major macromolecular component of skin, is responsible for maintaining the structural integrity of the tissue as well as for providing important functional characteristics, such as pliability and thickness. We have been studying the structure and regulation of collagen in mouse mutations affecting the skin. In the course of these studies, we found that there are significant differences in collagen content between the skin of wild-type male and female mice, which become evident at puberty. Furthermore, male mice with an X-linked mutation in the androgen receptor gene (formerly called testicular feminization and abbreviated as Ar(Tfm)) showed decreased levels of collagen, indicating that the androgen receptor pathway contributes to the observed differences. These findings demonstrate that there are striking differences in the collagen content of skin between male and female mice, and provide a biochemical explanation for these differences.
Action of androgen on fibroblast collagen synthesis: a receptor-dependent response.
C Loire[SUP]1[/SUP], B Kern[SUP]1[/SUP] and Ch Sultan[SUP]1[/SUP]
[SUP]1[/SUP]INSERM U.58, MONTPELLIER and CNRS GR.40, CRETEIL, France.
Top of pageAbstract
Several groups are still investigating an "in vitro" biological response of androgen action. The purpose of this study was to determine whether dihydrotestosterone (DHT) influences the secretion of collagen by cultured foreskin fibroblasts raised from patients with normal or undetectable DHT-binding activity (complete androgen resistance). Collagen synthesis and secretion were evaluated by [SUP]3[/SUP]H-proline incorporation in newly synthetized collagen by confluent fibroblasts alone, or in the presence of DHT (10[SUP]−5[/SUP] to -10[SUP]−10[/SUP]M). Production of collagen is expressed as a ratio between tritiated OH-proline and OH-proline plus proline,within the cells or in the culture medium.
These data show that : -in control cells,DHT significantly increases production of collagen released in the culture medium (p < 0.001), -In complete androgen resistance with no detectable androgen binding activity, DHT does not modify basal collagen synthesis. These results strongly suggest that this hormonal response is mediated via a DHT-receptor or is receptor-dependent. This could be used as a biological response of androgen action in patients with androgen resistance associated with a "post-receptor" defect.
“During the hair cycle the follicle has to be rebuilt from stem cells,” explains Dr Bruno Bernard, director of research for life sciences at L’Oreal. “Stem cells in human hair follicles are localised in two different reservoirs – one is in the upper part of the follicle and the other in the lower part.
“The cells in the lower part are required to activate the cells in the upper part and so help to maintain the follicle function. The thickening of collagen in the connective tissue sheath, which sits around the base of the hair follicle, prevents the movement of stem cells from the lower reservoir to the upper reservoir. Bit by bit, the follicle is squeezed and causes the follicles to grow smaller and smaller.” Indeed, research from The Rockefeller University in New York suggests movement between the two groups of stem cells is crucial in normal hair growth.
http://www.telegraph.co.uk/science/8470168/The-cures-for-baldness-around-the-corner.html
- - - Updated - - -
- - - Updated - - -
so Fibrosis is really the bad guy in hairloss..
Formation of fibrous tissue or fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the
miniaturization. Involution of the pilosebaceous unit in this form of baldness and sustained microscopic
follicular inflammation with connective tissue remodeling, eventually resulting in permanent hair loss, is
considered a possible cofactor in the complex etiology of androgenetic alopecia. However, till date, the
inflammatory component has not been explored in developing treatment protocols for androgenetic
alopecia.
http://www.hairlosstalk.com/interac...w-Dermaroller-Study-Thoughts-comments/page142
DesperateOne
Banned
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lol, which part? The pink minoxidil, or the string theory.
jason5
Member
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I've decided that I may reduce it to 0.1ml (a few drops) twice a day before giving up on it. If I still get issues with it, I'll drop it. No, I waited about 14 hours but will now wait 24 hours. I started it with the dermarolling so about 2 months ago. I did use it 2 years ago but had basically no results and dropped it after 6 months since I was getting dark eyes. The heart palpitations is what concerned me recently, thus why I want to stop it.
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