The regulatory effects of androgens on haematopoiesis have been recognized since the early twentieth century. Castration of male rats causes anemia (1) which is reversible after treatment with androgens (2). A classical clinical study by Vahlquist provided indirect evidence that men had intrinsically higher haematocrit (Hct) levels when compared with women; it was observed that pre-menopausal women did not have higher Hct levels when compared with post-menopausal women, and did have an increased Hct in response to iron supplementation (3). Anecdotal data from competitive athletes suggest that androgen misuse can improve performance, partly through increasing the VO2max (Hb-mediated blood oxygen carrying capacity), albeit at the expense of an increased risk of arterial and venous thrombosis (4). Equally, women suffering from hyperandrogenic endocrinopathies such as congenital adrenal hyperplasia and Cushing’s syndrome, may exhibit relative erythrocytosis (5, 6). The above historic findings underpin the androgens on stimulating bone morrow erythropoiesis.
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Al‐Sharefi et al. (2019) studied this question.
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