Nature 2021; 592: 428432https://www.nature.com/articles/s41586-021-03417-2
These authors report that in mice the stress hormone corticosterone (the rodent equivalent of cortisol in humans) acts on dermal papillae to suppress expression of Gas6 (encoding growth arrest specific 6) and thereby cause hair follicle stem cell (HFSC) quiescence and reduced hair growth. They show that in chronic stress, high levels of corticosterone prolong HFSC quiescence and maintain hair follicles in an extended resting phase.
There is much anectodal evidence that chronic stress can lead to hair loss. Here, these researchers from Harvard University confirmed such a link and identified that the underlying mechanism involves our endocrinology. Hair follicles naturally cycle between growth and rest, reflecting whether HFSCs are in an active phase or in quiescence, when growth is slowed and hairs are easily shed. The authors show that these states are determined by corticosterone levels acting on the dermal papilla cells, which lie just beneath the HSFCs. By understanding the downstream mechanisms they show that, without reducing the high corticosterone levels induced by chronic stress, restoring Gas6 expression from dermal papilla cells is sufficient to overcome the stress-induced inhibition and drives HFSCs into frequent regeneration cycles, with no observable long-term adverse effects. The same team also recently identified a similar process whereby chronic stress activates the sympathetic nervous system and depletes melanocyte stem cells, leading to premature hair graying.
These novel findings have potential broad relevance for understanding how chronic stress may accelerate biological ageing and reduce lifespan, possibly also by stimulating glucocorticoid secretion and the sympathetic nervous system to inhibit stem cell activity.