Hair is the second-fastest-growing tissue of the human body. Normal hair fall is 50-100 hair per day; if hair fall exceeds this limit, it is termed according to a case-control study; stress may be the primary reason for unexplained hair loss as ‘balding’ or alopecia. There are many reasons why men and women lose their hair, but when a person is under stress, hair can go into the telogen (fall-out) phase. Most common forms of hair loss in females include female pattern hair loss (FPHL), telogen effluvium (diffuse temporary hair loss typically manifested 2-3 months after severe stressful event such as childbirth, severe disease, major surgery, crash diets, severe emotional stress and certain drugs), trichotillomania (impulse control disorder having compulsive urge to pull one’s hair, more common in adolescent girls), iron deficiency hair loss, frequent styling techniques causes hair breakage, traction alopecia, and central centrifugal alopecia. Among the skin appendages, hair has an undeniable importance in the feminine personality, making hair loss one of their biggest problems with many psychosocial implications. As a high level of stress is bound to affect female medical students, the association between stress and hair fall and to examine a relationship between stress and hair fall in these medical students.
Attempts to define clinical outcomes for the study of deleterious psycho-social stress have occupied multiple researchers over the past decades. The skin contains a mini-organ, the hair follicle (HF), which is subjected to life-long remodeling via the hair cycle. Experimental animal models suggest that perceived stress can trigger neuroendocrine-immune changes, which interfere with the organism’s tissue regenerative capacity such that in young female mice, prolonged noise- or restraint stress paradigms provoke neurogenic inflammation and subsequent HF regression (catagen).
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In humans, hair loss is often reported clinically during periods of excessive stress. Hair loss may indicate underlying organic disease, however, frequently no organic disturbances can be found, which can be disturbing for hair loss patients and their doctors. It was therefore hypothesized that analogous to the animal models, in humans, stress activates neuroendocrine-immune circuits, which terminate hair growth in the absence of other clinically noticeable health disturbances. Such circuits in mice involve the dense peptidergic innervations of organs at the self-environment interface (e.g. skin, gut, lungs) and its interaction with mast cells. The subsequent activation of the later is a common mechanism in response to a wide variety of stressors, including psychosocial stress. In the wake of stressful events, cytokines that regulate innate and adaptive immune responses are released. These include tumor necrosis factor-alpha (TNFα) or interferon-gamma (IFNγ). Under conditions of stress, they participate in cellular adaptive immune responses traditionally addressed as T-helper cell Type 1 (TH1). As a consequence, in response to prolonged stress-exposure in otherwise healthy animals, epithelial and mesenchymal cells in the skin are driven into apoptosis or senescence and premature termination of hair growth occurs which leads to weakness of hair and ultimately they fall early.