Paternity is well established at the oldest age so the natural history of male fertility is concluded only by death. By contrast, female fertility, terminating naturally at menopause, occupies only half of average adult life expectancy. Despite the enduring fertility potential, fathers older than 50 years are responsible for only *1% of births in developed countries. Communal procreative patterns are determined by the similarity of couple's age and the overwhelming age-restriction of female fertility. Nevertheless, fertility concerns of men cannot be disregarded at any set age particularly with increasing remarriage to younger women.

Unfortunately the biomedical literature usually regards male fertility evaluation as synonymous with semen analysis. Such reductive logic risks overlooking important details of the whole picture and, coupled with the fact that men only provide semen samples when concerned about their fertility (Handelsman 1997), virtually all research on human sperm involves convenience samples inherently unrepresentative of the general male population. Tunnel vision in appraising the limitation of such research leads predictably to grievous misunderstanding (Handelsman 2000).

In evaluating age effects on male fertility, it is necessary to note that male fertility is measured by counting conceptions, not sperm. Consequently, estimation of male fertility has been largely the domain of demographers. They, in turn, focus almost exclusively on female fertility, for reasons only partly explained by the simplistic axiom that only maternity is ascertainable. The little evidence available suggests that male fertility declines modestly with age (Anderson 1975, Ford et al 2000). In these studies, it remains unclear if attempts to adjust for the highly correlated effects of wife's age are sufficient to exclude that the modest decline in male fertility is only illusory. If real, such modest declines in male fertility may be due to age-related reduction in coital rate, sperm production or function, none being easy to study in the general population.

Apart from indirect evidence from paternity, the few studies of sperm output available are restricted to small convenience samples of infertile, older men. These suggest sperm output is undiminished up to the age of 50 years but systematic studies of any quality are limited beyond that age to small convenience samples. Similarly, as both testicular histology and sperm function require biopsy and semen samples, respectively, there are equally no valid population-based data to evaluate age effects on spermatogenic histology or sperm function.

Given the difficulties of evaluating spermatogenesis by studies requiring semen analysis, valid surrogate variables would be useful. Indeed, semen analysis itself is an imperfect surrogate marker for male fertility for which questionnaire instruments have been developed (Levine 1988, Joffe 1997). Testicular volume provides an excellent surrogate marker of spermatogenesis because seminiferous tubules comprise the bulk of testis volume as noted in the clinical observation that testicular atrophy reliably connotes impaired spermatogenesis in infertile men. Lacking any longitudinal studies of testis size, the largest cross-sectional study indicates that testis volume is little affected by age until the eighth decade, if the effects of terminal illness or vascular disease (Regadera et al 1985) are distinguished (Handelsman & Staraj 1985). Smaller post-mortem (Johnson 1986) and ultrasound (Lenz et al 1993) studies are consistent with these observations. Cross-sectional studies showing consistently that blood follicle-stimulating hormone (FSH) increases and inhibin B decreases progressively with advancing age while their inverse relationship is maintained suggest that these hormone markers, together with testis ultrasound, could constitute useful surrogate markers of spermatogenesis for future population-based studies of human ageing.

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