closetmetrosexual
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The heart palpitations is what concerned me recently, thus why I want to stop it.
Are you sure the heart palpitations are from the minoxidil?
The heart palpitations is what concerned me recently, thus why I want to stop it.
Are you sure the heart palpitations are from the minoxidil?
I cannot be 100% sure, but I've never had anything like that before, I also was starting to feel fatigued so those 2 symptoms began to scare me. I'm getting amazing results so I really don't want to stop, so I will further reduce and wait and see. I really hope minoxidil isn't the key reason for all this great regrowth. Just looking at my hair today I'm seeing more growth so something is working very well.
You're going to hate me saying this but it could be all in your head. I first started minoxidil 2 or so years ago and thought I began experiencing shortness or breath after reading up on oral minoxidil and was freaking out. Long short I quit for two years and re-started minoxidil this year because of severe thinning as of recently and I just carried on with my life normally. So far, I have not experienced any symptoms. I said earlier that topical(not oral) has an excellent safety record. This is because so little of the drug is absorbed into the blood stream. In fact, in studies where they applied minoxidil twice daily, blood levels of the drug were undetectable in 7 out of 13 and so incredible minor in the remaining 6 test subjects. Most importantly, vital signs like heartbeat and blood pressure remained constant throughout the myriad of studies done in the clinical stages.
Systemic cardiovascular effects during chronic treatment with topical minoxidil vs placebo were evaluated using a double-blind, randomized design for two parallel groups (n = 20 for minoxidil, n = 15 for placebo). During 6 months of follow-up, blood pressure did not change, whereas minoxidil increased heart rate by 3-5 beats min-1. Compared with placebo, topical minoxidil caused significant increases in LV end- diastolic volume, in cardiac output (by 0.751 min-1) and in LV mass (by 5 g m-2). We conclude that in healthy subjects short-term use of topical minoxidil is likely not to be detrimental. However, safety needs to be established regarding ischaemic symptoms in patients with coronary artery disease as well as for the possible development of LV hypertrophy in healthy subjects during years of therapy.
What do you think about this study?
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
I cannot be 100% sure, but I've never had anything like that before, I also was starting to feel fatigued so those 2 symptoms began to scare me. I'm getting amazing results so I really don't want to stop, so I will further reduce and wait and see. I really hope minoxidil isn't the key reason for all this great regrowth. Just looking at my hair today I'm seeing more growth so something is working very well.
lol, which part? The pink minoxidil, or the string theory.
This is a posting from another thread a number of years which I believe makes some valid points.What do you think about this study?
But getting rid of fibrosis isnt enough to get all hair back..
So we need to take dht reducing things to not rebuild fibrosis again?
Article: Perifollicular fibrosis: pathogenetic role in androgenetic alopecia. Source: Biol Pharm Bull. 2006 Jun;29(6):1246-50. Author(s): Yoo HG, Kim JS, Lee SR, Pyo HK, Moon HI, Lee JH, Kwon OS, Chung JH, Kim KH, Eun HC, Cho KH Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging and Hair Research, Clinical Research Institute, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University. |
Androgenetic alopecia (Androgenetic Alopecia) is a dihydrotestosterone (DHT)-mediated process, characterized by continuous miniaturization of androgen reactive hair follicles and accompanied by perifollicular fibrosis of follicular units in histological examination. Testosterone (T: 10(-9)-10(-7) M) treatment increased the expression of type I procollagen at mRNA and protein level. Pretreatment of finasteride (10(-8) M) inhibited the T-induced type I procollagen expression at mRNA (40.2%) and protein levels (24.9%). T treatment increased the expression of transforming growth factor-beta 1 (TGF-beta1) at protein levels by 81.9% in the human scalp dermal fibroblasts (DFs). Pretreatment of finasteride decreased the expression of TGF-beta1 protein induced by an average of T (30.4%). The type I procollagen expression after pretreatment of neutralizing TGF-beta1 antibody (10 mug/ml) was inhibited by an average of 54.3%. Our findings suggest that T-induced TGF-beta1 and type I procollagen expression may contribute to the development of perifollicular fibrosis in the Androgenetic Alopecia, and the inhibitory effects on T-induced procollagen and TGF-beta1 expression may explain another possible mechanism how finasteride works in Androgenetic Alopecia. “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. Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, Cotsarelis G. Source Department of Dermatology, Kligman Laboratories, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA. Abstract Androgenetic alopecia (Androgenetic Alopecia), also known as common baldness, is characterized by a marked decrease in hair follicle size, which could be related to the loss of hair follicle stem or progenitor cells. To test this hypothesis, we analyzed bald and non-bald scalp from Androgenetic Alopecia individuals for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin15 (KRT15), CD200, CD34, and integrin, α6 (ITGA6) were quantitated via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small cell size and quiescence. These KRT15(hi) stem cells were maintained in bald scalp samples. However, CD200(hi)ITGA6(hi) and CD34(hi) cell populations--which both possessed a progenitor phenotype, in that they localized closely to the stem cell-rich bulge area but were larger and more proliferative than the KRT15(hi) stem cells--were markedly diminished. In functional assays, analogous CD200(hi)Itga6(hi) cells from murine hair follicles were multipotent and generated new hair follicles in skin reconstitution assays. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of Androgenetic Alopecia. http://www.ncbi.nlm.nih.gov/pubmed/21206086 |
Before mine was very pale, now the scalp seems more alive and and got sort of a tan.Guys, a general question : does your scalp change color and pigment with DRing ? also , does it become less flashy ? i have been on supplements and nizoral and planning to start DR in 2 days, but i have been seeing my existing bald spot thickened... the color is changing and it has been sort of brown... also during flash , i no longer see a shiny light on scalp and the "shiny"ness is greatly reduced....
squeegee the lighting in those photos pisses me off so deeply.
Guys, a general question : does your scalp change color and pigment with DRing ? also , does it become less flashy ? i have been on supplements and nizoral and planning to start DR in 2 days, but i have been seeing my existing bald spot thickened... the color is changing and it has been sort of brown... also during flash , i no longer see a shiny light on scalp and the "shiny"ness is greatly reduced....