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Spermatogenesis is a complex process and one of the few examples of a continuous proliferation of highly specialised cells in the adult human organism. Because of the fast reproduction and the high degree of cell differentiation spermatogenesis is particularly susceptible to noxious influences and stressors. The underlying idea of the thesis is that spermatogenesis and its dysfunction might indicate the exposure of the male organism to noxae. If certain co-morbidities were excluded, an impairment of the spermatogenesis, expressed through subnormal sperm counts, might serve as an indicator of the health status of the male body. In consequence, men that have an impaired spermatogenesis corresponding to their bad health in general should die earlier than men with undisturbed spermatogenic functions. There should be an association between the lifespan of an individual and its sperm counts or fertility status.
Data base were the medical records of men who attended the fertility and sterility office at the University Hospital in Marburg, Germany. The examinations took place between 1949 and 1985. Most of the men had asked for consultation because of an assumed fertility problem and therefore a spermiogram had been carried out. With the help of public registration offices as well as the data set of a health insurance the vital status of the former patients, i.e. ‘dead’ versus ‘alive’, was traced. In the case of the deceased men, the exact date of death also was registered. Information about the last occupation of the cases served as an indicator of the socioeconomic status. Following the WHO guidelines, the cases were divided into three fertility classes: normozoospermic (sperm count ≥ 20 x 106/mL), oligozoospermic (< 20 x 106/mL) und azoospermic (no sperms).
A life table analysis allowed to plot the survival functions of the fertility groups and revealed a higher mortality for oligozoospermic than for normozoospermic cases. A semiparametric Cox regression as well as other parametric regression models, e.g. the Gompertz-Makeham model, allowed to quantify this difference and to model the influence of the fertility status on lifetime mortality, while controlling for several covariates. Here, the mortality risk of the oligozoospermic men was twice as high as the risk of the normozoospermic cases. The mortality risk of the azoospermic patients was not elevated, neither in comparison with the normozoospermic cases nor in comparison with the oligozoospermic patients. The regression models revealed no influence of the sperm concentration on the lifetime mortality of the individuals. That leads to the conclusion that the association between spermatogenesis and mortality is not expressed in a quantitative way in terms of a dose-response-relationship, but in a rather qualitative way as a lower or higher mortality risk in case of a “better” or “worse” physiological function.
To explain the higher mortality risk of the men with a subnormal sperm count several approaches are discussed. (1) Effects of childlessness on health and mortality: (Involuntary) childlessness increases the risk of getting divorced and it is associated with a less healthy life style, lower social support and a higher morbidity. (2) Conditions in utero and in early childhood: Adverse circumstances can affect both, the health status in general and reproductive functions, e.g. spermatogenesis, at the same time. (3) genetic dispositions which mediate the connection between reduced fertility on the one hand and elevated mortality on the other hand.