Abstract
Poor semen quality is an attribute of the human condition that we share with our closest primate ancestors and may be part of our evolutionary inheritance. This characteristic may also reflect the lack of selection pressure on male fertility in advanced societies that have gone through the demographic transition. In the future, such trends may be further exacerbated by the widespread use of ART, which will impair the elimination of low fecundity genotypes from the human gene pool. Environmental pollutants may also be influencing male fertility, however, neither the chemical identity of these factors nor their mechanism-of-action are fully understood. Over 20 years ago, Carlsen et al.1 published a highly cited paper in the British Medical Journal which purported to detect a significant decline in sperm counts over a period of 60 years (1934–1996). This was followed shortly afterwards by the Skakkebaek and Sharpe hypothesis,2 published in Lancet, which argued that the increasing incidence of reproductive abnormalities in the human male may be related to increased oestrogen exposure in utero, citing maternal exposure to diethylstilbestrol (DES) during pregnancy as evidence for such a link. These classic papers have now become inextricably linked in the global consciousness and have led to a public misconception that male fertility is declining as a consequence of fetal exposure to environmental estrogens.3 In the 20 years that have elapsed since these landmark papers were published, a great deal of data has appeared that seem to support and refute their validity in equal measure, resulting in a state of confusion. The European Science Foundation4 has recently published a review of the current status of male reproductive health. Using this summary as a guide we are now in an excellent position to dissect some of the key arguments and formulate questions for future consideration.
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