MadSci Network: Medicine |
Hi Mikael! What a great question! Hair whitening has been extensively studied in gerontobiology. I must admit that there is no immediate answer to your question but after a quick search in PubMed I think I can provide you with some thoughts in this issue. A short answer to your question is “yes”, stress “can probably contribute” to hair whitening in some genetically predisposed individuals. But then why? What is the link? First of all we must consider the histophysiology of hair follicles. A hair follicle is a sheath of epidermal cells and connective tissue that surrounds the root of a hair. The root of the hair, beneath the surface of the skin (scalp), is expanded at its base to form the bulb, which contains a matrix of dividing cells. As new cells are formed the older ones are pushed upwards and become keratinised to form the root and shaft of the hair. Hair pigments, like all other visible pigment in mammals, result from synthesis and distribution of melanin, in this case, in the hair bulbs. The melanins are produced in melanocytes from tyrosine and can be of two basic types: eumelanins, which are brown or black; and phaseomelanins, which are red or yellow. Black human hair contains approximately 99% eumelanin and 1% phaseomelanin, brown and blond hair contain 95% eumelanin and 5% phaseomelanin; and red hair contains 67% eumelanin and 33% phaseomelanin. However, The hair follicle and skin epidermal melanogenic systems are broadly distinct. The primary distinguishing feature of follicular melanogenesis, compared to the continuous melanogenesis in the epidermis, is the tight coupling of hair follicle melanogenesis to the hair growth cycle. The hair growth cycle consists of a growth phase (anagen) for 2-3 years, followed by a transitional stage (catagen) and resting phase (telogen), each of which lasts for about 2 weeks. On average about 85% of hairs are in anagen and hence actively growing. Hair follicle is a regenerating system. By traversing the phases of the cycle (growth, regression, resting, shedding, then growth again), the follicle demonstrates the unusual ability to completely regenerate itself. The basis for this regeneration rests in the unique follicular epithelial and mesenchymal components and their interactions. This hair growth cycle appears to involve periods of melanocyte proliferation (during early anagen), maturation (mid to late anagen) and melanocyte death via apoptosis (during early catagen). Thus, each hair cycle is associated with the reconstruction of an intact hair follicle pigmentary unit ellipsis at least for the first 10 cycles or so. Thereafter, grey and white hairs appear, suggesting an age-related, genetically regulated exhaustion of the pigmentary potential of each individual hair follicle. Melanocyte aging may be associated with reactive oxygen species-mediated damage to nuclear and mitochondrial DNA with resultant accumulation of mutations with age, in addition to dysregulation of anti-oxidant mechanisms or pro/anti-apoptotic factors within the cells. Now how does “stress” relate to this? First of all, stress (e.g. fight, fright, flight, pain, hypoglycaemia, etc.) induce the secretion of adrenocorticotrophic hormone (ACTH) form the anterior pituitary profoundly. Indeed, the practical definition of a “stressful event” is anything that cause an increased secretion of ACTH. ACTH is a peptide hormone synthesized as a pre-prohormone pro-opiomelanocortin (POMC). This large protein is processed in the anterior pituitary to form a number of peptide hormone, including ACTH, lipotrophic hormone, endorphins, and importantly melanocyte stimulating hormone (MSH). Thus when ACTH is secreted by the anterior pituitary, MSH is also secreted! MSH, as its name suggests, stimulate the melanocytes and cause them to form and distribute the pigment melanin. In fact, injection of MSH into a person 8-10 days can greatly increase darkening of the skin, esp. in light-skinned people. ACTH, because of its similarity to MSH, has about 1/30 as much melanocyte- stimulating effect as MSH. Furthermore, because the quantities of pure MSH secreted in human being are extremely small, whereas those of ACTH are large, it is likely that ACTH normally is more important than MSH in stimulating melanocytes. Although I have not seen any research data confirming the causal relationship between stress, ACTH, and hair whitening, it is not difficult for one to speculate that under chronic stress, the body may respond to the “stress” by increasing secretion of ACTH. This increased ACTH level, if sustained for a prolonged period, may somehow over-stimulate the melanocytes in the hair bulb, and disrupt the normal coupling of follicular melanogenesis and hair growth cycle. This might then contribute to the age-related, genetically regulated exhaustion of the pigmentary potential of each individual hair follicle and subsequently resulting in hair whitening. I hope this has shed some lights in how stress might relate to hair whitening. Joshua Chai Medical Student University of Cambridge, UK Reference: 1. Hearing VJ, Tsukamoto K, “Enzymatic control of pigmentation in mammals”, FASEB J 1991 Nov;5(14):2902-9 2. Borges CR, Roberts JC, Wilkins DG, Rollins DE, “Relationship of melanin degradation products to actual melanin content: application to human hair.”, Academic Press 2001 3. Tobin DJ, Paus R., “Graying: gerontobiology of the hair follicle pigmentary unit.”, abstract from PubMed 4. Stenn KS, Paus R., “Controls of hair follicle cycling.”, abstract from PubMed 5. Guyton & Hall, “Textbook of Medical Physiology”, Saunders
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