Category: General
Posted by: agohaircom
J Behav Ther Exp Psychiatry. 2010 Jul 14.
Movement decoupling: A self-help intervention for the treatment of trichotillomania.
Moritz S, Rufer M.
Trichotillomania (TTM) is classified as an impulse control disorder characterized by the recurrent urge to pull out one's own hair resulting in noticeable hair loss. Cognitive-behavioral therapy, involving habit reversal training, currently represents the treatment of choice. The present study assessed the feasibility and effectiveness of a novel self-help technique, entitled decoupling (DC). DC aims at attenuating TTM by performing movements that decouple the behavioral elements involved in hair pulling. A total of 42 subjects with TTM were recruited via self-help forums for TTM and were randomized either to DC or progressive muscle relaxation (PMR). After four weeks, participants were asked to fill out the same questionnaires as before and rate the effectiveness of the intervention. The completion rate was high and the reliability of the assessments at least satisfactory. The DC group showed a significantly greater decline on the Massachusetts General Hospital - Hair-Pulling Scale, which served as the primary outcome, relative to PMR indicating a medium to strong effect size. Declines on scales tapping depression and obsessive-compulsive disorder were comparable between the two groups. Despite some methodological limitations and the need for replication including follow-up and expert ratings, the present study suggests that DC may prove beneficial to a substantial number of individuals affected with TTM.
Movement decoupling: A self-help intervention for the treatment of trichotillomania.
Moritz S, Rufer M.
Trichotillomania (TTM) is classified as an impulse control disorder characterized by the recurrent urge to pull out one's own hair resulting in noticeable hair loss. Cognitive-behavioral therapy, involving habit reversal training, currently represents the treatment of choice. The present study assessed the feasibility and effectiveness of a novel self-help technique, entitled decoupling (DC). DC aims at attenuating TTM by performing movements that decouple the behavioral elements involved in hair pulling. A total of 42 subjects with TTM were recruited via self-help forums for TTM and were randomized either to DC or progressive muscle relaxation (PMR). After four weeks, participants were asked to fill out the same questionnaires as before and rate the effectiveness of the intervention. The completion rate was high and the reliability of the assessments at least satisfactory. The DC group showed a significantly greater decline on the Massachusetts General Hospital - Hair-Pulling Scale, which served as the primary outcome, relative to PMR indicating a medium to strong effect size. Declines on scales tapping depression and obsessive-compulsive disorder were comparable between the two groups. Despite some methodological limitations and the need for replication including follow-up and expert ratings, the present study suggests that DC may prove beneficial to a substantial number of individuals affected with TTM.
J Dermatol Sci. 2010 Apr;58(1):43-54. Epub 2010 Feb 16.
Laminin-511, inducer of hair regrowth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia.
Imanishi H,Abstract
BACKGROUND: Chemotherapy-induced alopecia (CIA) has a devastating cosmetic effect, especially in the young. Recent data indicate that two major basement membrane components (laminin-332 and -511) of the skin have opposing effects on hair growth. OBJECTIVE: In this study, we examined the role and localization of laminin-332 and -511 in CIA. METHODS: We examined the expression of laminin-332 and -511 during the dystrophic catagen form of CIA induced in C57BL/6 mice by cyclophosphamide (CYP) treatment. RESULTS: Our data indicate that both laminin-332 and its receptor alpha 6 beta 4 integrin are up-regulated (both quantitatively and spatially) after mid to late dystrophic catagen around the outer root sheath (ORS) in the lower third of hair follicles in CIA. This up-regulation also occurs at the transcriptional level. In contrast, laminin-511 is down-regulated after mid dystrophic catagen at the protein level, with transcriptional inactivation of laminin-511 occurring transiently at the early dystrophic catagen stage in both epidermal and ORS keratinocytes. Laminin-511 expression correlates with expression of alpha 3 integrin in CIA and we also demonstrate that laminin-511 can up-regulate the activity of the alpha 3 integrin promoter in cultured keratinocytes. Injection of a laminin-511 rich protein extract, but not recombinant laminin-332, in the back skin of mice delays hair loss in CYP-induced CIA. CONCLUSIONS: We propose that abrupt hair loss in CIA is, at least in part, caused by down-regulation of laminin-511 and up-regulation of laminin-332 at the transcriptional and translational levels. (c) 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
Laminin-511, inducer of hair regrowth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia.
Imanishi H,Abstract
BACKGROUND: Chemotherapy-induced alopecia (CIA) has a devastating cosmetic effect, especially in the young. Recent data indicate that two major basement membrane components (laminin-332 and -511) of the skin have opposing effects on hair growth. OBJECTIVE: In this study, we examined the role and localization of laminin-332 and -511 in CIA. METHODS: We examined the expression of laminin-332 and -511 during the dystrophic catagen form of CIA induced in C57BL/6 mice by cyclophosphamide (CYP) treatment. RESULTS: Our data indicate that both laminin-332 and its receptor alpha 6 beta 4 integrin are up-regulated (both quantitatively and spatially) after mid to late dystrophic catagen around the outer root sheath (ORS) in the lower third of hair follicles in CIA. This up-regulation also occurs at the transcriptional level. In contrast, laminin-511 is down-regulated after mid dystrophic catagen at the protein level, with transcriptional inactivation of laminin-511 occurring transiently at the early dystrophic catagen stage in both epidermal and ORS keratinocytes. Laminin-511 expression correlates with expression of alpha 3 integrin in CIA and we also demonstrate that laminin-511 can up-regulate the activity of the alpha 3 integrin promoter in cultured keratinocytes. Injection of a laminin-511 rich protein extract, but not recombinant laminin-332, in the back skin of mice delays hair loss in CYP-induced CIA. CONCLUSIONS: We propose that abrupt hair loss in CIA is, at least in part, caused by down-regulation of laminin-511 and up-regulation of laminin-332 at the transcriptional and translational levels. (c) 2010 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
Ann Dermatol. 2009 May;21(2):142.
The therapeutic effect and the changed serum zinc level after zinc
supplementation in alopecia areata patients who had a low serum zinc level.
Park H, Kim CW, Kim SS, Park CW.
Department of Dermatology, College of Medicine, Hallym University, Seoul, Korea.
BACKGROUND: It has been reported that some alopecia areata patients have zinc
deficiency. There have also been several reports published concerning oral zinc
sulfate therapy, with encouraging results, in some alopecia areata patients.
OBJECTIVE: The purpose of this study was to evaluate the therapeutic effects of
oral zinc supplementation for twelve weeks in alopecia areata patients who had a
low serum zinc level. METHODS: Oral zinc gluconate (50 mg/T/day) supplementation
was given to alopecia areata patients without any other treatment for twelve
weeks. The serum zinc level was measured before and after zinc supplementation. A
four-point scale of hair regrowth was used to evaluate the therapeutic effect of
oral zinc supplementation in these patients. RESULTS: Fifteen alopecia areata
patients were enrolled in this study. After the therapy, the serum zinc levels
increased significantly from 56.9 microg/ to 84.5 microg/dl. Positive therapeutic
effects were observed for 9 out of 15 patients (66.7%) although this was not
statistically significant. The serum zinc levels of the positive response group
increased more than those of the negative response group (p=0.003). CONCLUSION:
Zinc supplementation needs to be given to the alopecia areata patients who have a
low serum zinc level. We suggest that zinc supplementation could become an
adjuvant therapy for the alopecia areata patients with a low serum zinc level and
for whom the traditional therapeutic methods have been unsuccessful.
The therapeutic effect and the changed serum zinc level after zinc
supplementation in alopecia areata patients who had a low serum zinc level.
Park H, Kim CW, Kim SS, Park CW.
Department of Dermatology, College of Medicine, Hallym University, Seoul, Korea.
BACKGROUND: It has been reported that some alopecia areata patients have zinc
deficiency. There have also been several reports published concerning oral zinc
sulfate therapy, with encouraging results, in some alopecia areata patients.
OBJECTIVE: The purpose of this study was to evaluate the therapeutic effects of
oral zinc supplementation for twelve weeks in alopecia areata patients who had a
low serum zinc level. METHODS: Oral zinc gluconate (50 mg/T/day) supplementation
was given to alopecia areata patients without any other treatment for twelve
weeks. The serum zinc level was measured before and after zinc supplementation. A
four-point scale of hair regrowth was used to evaluate the therapeutic effect of
oral zinc supplementation in these patients. RESULTS: Fifteen alopecia areata
patients were enrolled in this study. After the therapy, the serum zinc levels
increased significantly from 56.9 microg/ to 84.5 microg/dl. Positive therapeutic
effects were observed for 9 out of 15 patients (66.7%) although this was not
statistically significant. The serum zinc levels of the positive response group
increased more than those of the negative response group (p=0.003). CONCLUSION:
Zinc supplementation needs to be given to the alopecia areata patients who have a
low serum zinc level. We suggest that zinc supplementation could become an
adjuvant therapy for the alopecia areata patients with a low serum zinc level and
for whom the traditional therapeutic methods have been unsuccessful.
01/05: Hair regrowth and vitamin D
Category: General
Posted by: agohaircom
Dermatol Online J. 2010 Feb 15;16(2):3.
Does D matter? The role of vitamin D in hair disorders and hair follicle cycling.
Amor KT, Rashid RM, Mirmirani P.
Department of Dermatology, University of Texas and MD Anderson Cancer Center, Houston, Texas, USA. rashidrashid.mdphd@yahoo.com
Hair regrowth and hair cycle
The formation of the hair follicle during embryogenesis requires reciprocal signaling between the epithelium and mesenchymal cells. The major epithelial-derived signaling molecules involved in the early stages of hair follicle morphogenesis include fibroblast growth factors (FGF), bone morphogenic proteins (BMP), and sonic hedgehog (SHH) [9, 10].These signals result in elongation of the hair follicle in embryogenesis. The first hair cycle after birth is unique because it represents the completion of the embryological development of the hair follicle and it is not dependent on the factors required for the maintenance of the hair follicle postnatally [11]. Therefore, deficiencies in factors required for maintenance of the hair regrowth cycle are not evident until the first hair is shed.
The maintenance of the hair follicle postnatally is dependent on the integrity of the dermis, epidermis, and the normal hair cycle. The hair cycle consists of three phases: anagen, catagen, and telogen. The anagen phase is the growth phase of the hair cycle. Anagen is initiated by signals from the mesodermal dermal papilla cells, which are at the base of the hair follicle, to the keratinocyte/hair follicle stem cells, which are located in the bulge of the hair follicle. These signals stimulate the follicular stem cell to proliferate and differentiate into a mature hair follicle, which consists of an outer root sheath, the inner root sheath, and the hair shaft. Approximately 85 percent of hairs are in anagen phase at one time, and this phase lasts two to six years. The catagen phase is the transition phase, which occurs when the anagen follicle receives a signal ends the growth phase. In catagen, apoptosis of the lower part of the hair follicle, located below the bulge, occurs. The dermal papilla cells also break away from the hair follicle and enter a rest stage. The catagen phase lasts one to two weeks. At the conclusion of the catagen phase, the hair follicle is one-sixth its original diameter. Telogen is the final phase of the hair cycle. It is also known as the resting phase. This phase lasts five to six weeks, until anagen is initiated again.
Does D matter? The role of vitamin D in hair disorders and hair follicle cycling.
Amor KT, Rashid RM, Mirmirani P.
Department of Dermatology, University of Texas and MD Anderson Cancer Center, Houston, Texas, USA. rashidrashid.mdphd@yahoo.com
Hair regrowth and hair cycle
The formation of the hair follicle during embryogenesis requires reciprocal signaling between the epithelium and mesenchymal cells. The major epithelial-derived signaling molecules involved in the early stages of hair follicle morphogenesis include fibroblast growth factors (FGF), bone morphogenic proteins (BMP), and sonic hedgehog (SHH) [9, 10].These signals result in elongation of the hair follicle in embryogenesis. The first hair cycle after birth is unique because it represents the completion of the embryological development of the hair follicle and it is not dependent on the factors required for the maintenance of the hair follicle postnatally [11]. Therefore, deficiencies in factors required for maintenance of the hair regrowth cycle are not evident until the first hair is shed.
The maintenance of the hair follicle postnatally is dependent on the integrity of the dermis, epidermis, and the normal hair cycle. The hair cycle consists of three phases: anagen, catagen, and telogen. The anagen phase is the growth phase of the hair cycle. Anagen is initiated by signals from the mesodermal dermal papilla cells, which are at the base of the hair follicle, to the keratinocyte/hair follicle stem cells, which are located in the bulge of the hair follicle. These signals stimulate the follicular stem cell to proliferate and differentiate into a mature hair follicle, which consists of an outer root sheath, the inner root sheath, and the hair shaft. Approximately 85 percent of hairs are in anagen phase at one time, and this phase lasts two to six years. The catagen phase is the transition phase, which occurs when the anagen follicle receives a signal ends the growth phase. In catagen, apoptosis of the lower part of the hair follicle, located below the bulge, occurs. The dermal papilla cells also break away from the hair follicle and enter a rest stage. The catagen phase lasts one to two weeks. At the conclusion of the catagen phase, the hair follicle is one-sixth its original diameter. Telogen is the final phase of the hair cycle. It is also known as the resting phase. This phase lasts five to six weeks, until anagen is initiated again.
08/01: Dr Proctor treats hair loss
Dr Proctor treats hair loss
Category: General
Posted by: agohaircom
Clin Genet. 2009Oct;76(4):332
Hereditary hair loss and the ancient signaling pathways....
Van Raamsdonk CD.
....hair, teeth, and nails, begin as a thickening of the ectoderm, called a placode. The placode arises from a primary induction signal that is sent from the underlying mesenchyme. The arrangement of hair follicles is due to the amount and distribution of signals that promote and inhibit hair placode formation. Continued development of a hair follicle after placode formation requires a complex cross-talk. Here, I will review recent studies in humans and mice that have increased our understanding of the role of these signaling pathways...in hereditary hair loss syndromes.....
Hereditary hair loss and the ancient signaling pathways....
Van Raamsdonk CD.
....hair, teeth, and nails, begin as a thickening of the ectoderm, called a placode. The placode arises from a primary induction signal that is sent from the underlying mesenchyme. The arrangement of hair follicles is due to the amount and distribution of signals that promote and inhibit hair placode formation. Continued development of a hair follicle after placode formation requires a complex cross-talk. Here, I will review recent studies in humans and mice that have increased our understanding of the role of these signaling pathways...in hereditary hair loss syndromes.....
27/11: Stroke,tempol, and Uric acid
Some of the same processes and agents that figure in hair loss and hair loss treatment also figure in stroke. All of this is at a very basic level of pathogenesis. E.g., see Dr proctor's paper on uric acid and stroke. Effective in both experimental animals of neuroprotection in stroke and in preventing uric-acid-induced kidney damage, TEMPOL (e.g.,) is effective in radiation-induced hair loss.
17/11: Hair loss blog
15/11: Hair regrowth and minoxidil
Minoxidil in hair loss treatment
Minoxidil stimulates hair regrowth. Sites of action include the papilla or matrix cells or possibly both. Biopsies from patients with male pattern hair loss show that the primary response is miniaturization. This is accompanied by shortening of the hair regrowth cycle. There is no evidence of follicular neogenesis. The site of action in hair loss treatment and hair regrowth is probably the papilla.
Minoxidil stimulates hair regrowth. Sites of action include the papilla or matrix cells or possibly both. Biopsies from patients with male pattern hair loss show that the primary response is miniaturization. This is accompanied by shortening of the hair regrowth cycle. There is no evidence of follicular neogenesis. The site of action in hair loss treatment and hair regrowth is probably the papilla.
07/11: Organic semiconductor
Category: General
Posted by: agohaircom
Not directly related to hair loss treatment. However, Dr Proctor has an early organic semiconductor device in the smithsonian Institution collection.
