Justlooking
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What impact does stress have on hairloss? I mean, if you have male pattern baldness can stress increase the rate at which you lose.. or will it trigger it earlier? Has there been research about this?
What impact does stress have on hairloss?
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pleasegodno
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yes, severe stress/anxiety/panic accelerates hairloss. i know from experience. here is the best research on the phenomenon:
Am J Pathol. 2003 Mar;162(3):803-14. Related Articles, Links
Comment in:
Am J Pathol. 2003 Mar;162(3):709-12.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
Arck PC, Handjiski B, Peters EM, Peter AS, Hagen E, Fischer A, Klapp BF, Paus R.
Department of Internal Medicine, Charite School of Medicine, Humboldt University, Berlin, Germany. petra.arck@charite.de
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
J Mol Med. 2005 May;83(5):386-96. Epub 2005 Mar 10. Related Articles, Links
Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition.
Arck PC, Handjiski B, Kuhlmei A, Peters EM, Knackstedt M, Peter A, Hunt SP, Klapp BF, Paus R.
Biomedizinisches Forschungszentrum, Campus Virchow Klinikum, Charite University Medicine, Augustenburger Platz 1, 13353 Berlin, Germany. petra.arck@charite.de
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin. However, our understanding of possible SP-mast cell interactions in the skin in response to stress was limited since the receptor by which SP activates skin mast cells and the extent of mast cell mediated aggravation of SP remained to be elucidated. We now employed NK-1 receptor knockout mice (NK-1R(-/-)) and mast cell deficient W/W(v) mice and observed that stress-triggered premature induction of catagen and hair follicle apoptosis does not occur in NK1(-/-) and W/W(v) mice. Furthermore, the activation status of mast cells was less in stressed NK1(-/-) mice than in wild-type control. Additionally, stress-induced upregulation of SP positive nerve fibers was absent in both NK-1R and W/W(v) mice. These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response
Am J Pathol. 2003 Mar;162(3):803-14. Related Articles, Links
Comment in:
Am J Pathol. 2003 Mar;162(3):709-12.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
Arck PC, Handjiski B, Peters EM, Peter AS, Hagen E, Fischer A, Klapp BF, Paus R.
Department of Internal Medicine, Charite School of Medicine, Humboldt University, Berlin, Germany. petra.arck@charite.de
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
J Mol Med. 2005 May;83(5):386-96. Epub 2005 Mar 10. Related Articles, Links
Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition.
Arck PC, Handjiski B, Kuhlmei A, Peters EM, Knackstedt M, Peter A, Hunt SP, Klapp BF, Paus R.
Biomedizinisches Forschungszentrum, Campus Virchow Klinikum, Charite University Medicine, Augustenburger Platz 1, 13353 Berlin, Germany. petra.arck@charite.de
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin. However, our understanding of possible SP-mast cell interactions in the skin in response to stress was limited since the receptor by which SP activates skin mast cells and the extent of mast cell mediated aggravation of SP remained to be elucidated. We now employed NK-1 receptor knockout mice (NK-1R(-/-)) and mast cell deficient W/W(v) mice and observed that stress-triggered premature induction of catagen and hair follicle apoptosis does not occur in NK1(-/-) and W/W(v) mice. Furthermore, the activation status of mast cells was less in stressed NK1(-/-) mice than in wild-type control. Additionally, stress-induced upregulation of SP positive nerve fibers was absent in both NK-1R and W/W(v) mice. These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response
pleasegodno
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also, substance p/mast cell interactions are huge factors in the scalp itching/tingling and occasional burning/tenderness experienced during periods of stress.