Although humans are considered to be nonseasonal mammals, we are undoubtedly sensitive to photoperiod (9), as exemplified by seasonal affective disorder and by seasonal trends in the frequency of births and in the incidence of twins. Such effects are most obvious in northern Europe, where photoperiodic changes are most extreme (10). Furthermore, both longitudinal and cross-sectional studies have demonstrated that sperm counts in men are consistently approx 30% lower in summer than in winter (11,12), although not all studies have reported such effects, and they may be less apparent or absent in tropical countries (13). An alternative explanation is that it is exposure to the higher summer temperature that is responsible for lowering sperm production (see section on scrotal temperature), although temperature changes do not account for all of the seasonal trends in births, especially in northern Europe (3). If the reported seasonal changes in sperm counts are an echo from our seasonally breeding ancestors, then this may be variable in its effect and, in most men, is unlikely to exert any major effect on their fertility. Studies in seasonally breeding animals have established the key pathways by which daylight length can regulate the reproductive axis, and melatonin secreted by the pineal gland plays a pivotal role (1,2). Therefore, it is curious that young men with hypogonadotropic hypogonadism show abnormal blood levels of melatonin, being increased in men with idiopathic hypogonadotropic hypogonadism
(IHH) and decreased in men with Kallmann syndrome, when compared with controls (14). However, in both groups of patients, melatonin levels were normalized by testosterone replacement therapy, implying that the abnormal melatonin level was a consequence rather than a cause of the hypogonadotropic hypogonadism (14).
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