Introduction: The relationship between androgens and beard growth has been the subject of extensive research, but the underlying mechanisms remain complex and not fully understood. The following article explores the nuanced ways in which androgens, particularly testosterone and its 5α reductase metabolite dihydrotestosterone (DHT), influence beard growth, terminal hair development, and paradoxical responses in various hair follicles.
Androgen Dependence in Facial and Body Hair: Facial and body hair growth is known to be androgen-dependent, but variation in total testosterone in the blood stream alone does not account for differences in hair density and patterning across different ethnic groups. Somehow, the combined effects of testosterone and DHT, both binding to the same intracellular androgen receptor on cells, are responsible for androgenic activation of terminal beard hair follicles on the face.
Pubertal Transformation: At puberty, the rise in plasma androgens leads to the transformation of tiny, pale, vellus hairs into terminal hairs in the beard region. The hair follicles enlarge gradually over several hair cycles to accommodate these dramatic changes. The complete response can take until the age of around 30 in men before the full beard growth affect is achieved. While both sexes can experience this transformation, males exhibit much higher androgen levels leading to more significant terminal hair development. For women, significant transformation of beard hair follicles usually only occurs as a result of a medical issue that causes abnormally high levels of androgen hormones to be produced, such as with polycystic ovary syndrome (PCOS).
The Paradox of Androgen Regulated Hair Growth: Androgens stimulate growth of terminal hair on the face and underarm axilla during puberty, yet beard growth persists into old age for men, whereas axillary hair growth in both sexes starts to decline from around 30 years of age. Yet it is the same androgen hormones and the same androgen receptors that produce the hair follicle regulating signals. These variations in hair growth response over time illustrate the complex and still poorly understood mechanisms of androgen action within hair follicles.
Androgens and Dermal Papilla Cells: Dermal Papilla (DP) cells at the base of hair follicles in the beard region express androgen receptors, facilitating androgen binding and signalling that can either increase or decrease hair follicle growth activity. However, the same signalling mechanism producing such divergent responses, as seen with scalp hair follicles, remains an intriguing paradox.
Investigations in vitro and in vivo: Studies with cultured DP cells have replicated the paradoxical in vivo response. Both androgen-stimulated beard cells and androgen-inhibited balding scalp cells contain higher levels of androgen receptors compared to control non-balding scalp DP cells (as seen in hair follicles around the sides and back of the head). This suggested that androgens act on DP cells through the same receptor yet they exert contrasting effects – even when the cells are isolated in culture and exposed to the same androgens in a controlled way.
Studies on testosterone metabolism also revealed distinctions, with beard, pubic, and scalp cells all containing testosterone and androstenedione (another type of androgen hormone) intracellularly. However, significantly, only beard cells produced 5α-dihydrotestosterone. This likely reflects an essential role of 5α-reductase activity in beard growth. Notably, men with a genetic 5α-reductase type 2 deficiency do not grow beards, but their scalp hair is normal. It’s rather circumstantial evidence, but it seems that the local activity of 5α-reductase in the beard follicles is particularly active and might at least partly explain the strong response of beard follicles to androgen hormones.
The Mitogenic Factors: In beard cells, testosterone stimulates the secretion of more mitogenic factors, influencing DNA synthesis at physiological levels. Conversely, testosterone reduced DNA synthesis by balding scalp DP cells. The presence or absence of 5α-reductase activity in different cell types further complicates this mechanism.
Overall though, it appears that only beard dermal papilla cells have the ability to respond to testosterone, at least in vitro, by producing new mitogenic factors. Even more interestingly, only beard cells are able to positively respond to the same mitogenic factors. This suggests that these mitogenic factors may play a role in the gradual increase in dermal papilla size caused during the androgen-mediated enlargement of hair follicles.
Underlying Mechanisms of Different Reactions: Recent studies have emphasized that the paradoxical effects of androgens on human hair follicles are most likely due to intrinsic differential gene expression within individual cells. Since the androgen receptors appear consistent in androgen-stimulated beard and inhibited balding follicles, these are unlikely to be the source of the different reactions. Instead, differences in the levels of intracellular 5α-reductase type 2 and the ability to metabolize circulating androgens into potent 5α-dihydrotestosterone play a pivotal role in defining the different follicular characteristics.
Post Receptor Level Specificities: There also seem to be specific differences at the post receptor level between various types of androgen-stimulated follicles. Both underarm axilla follicles (characteristic of both sexes) and beard follicles (normally restricted to men) respond similarly to androgens, despite intrinsic differences. These observations hint at distinct post-receptor mechanisms governing the hair growth responses.
Gene Availability and Embryonic Patterning: The paradox of androgen effects on balding and beard growth appears to involve not only androgen receptors and 5α-reductase type 2, but also the genes available for expression within each cell type. These differences in gene availability are likely determined during embryonic patterning mechanisms, contributing to the intricate landscape of hair growth across different body sites. In other words, some as yet unknown genes are available to be activated in beard DP cells or in balding scalp DP cells and these gene determine whether the hair follicles respond with increased hair growth or hair follicle miniaturization. These genes seem to function downstream of the androgen – androgen receptor signalling inside the DP cells.
Conclusion: The influence of androgens on beard hair growth remains a multifaceted and intriguing area of research. While the role of androgens like testosterone and DHT in promoting terminal hair development is clear, the intricate and paradoxical mechanisms within the hair follicles still need further exploration. The understanding of these processes may have wider implications for hair and skin disease research. Future studies focusing on the paracrine factors produced by dermal papilla cells, particularly those altered by androgens, could lead to improved treatments for hair disorders and beard growth.
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