Is there increased fertility in adult males with the sickle cell trait?

Different proposals have been offered to explain the polymorphism of the sickle cell hemoglobin gene. One of these proposals (Eaton and Mucha 1971) suggested that differential fertility of male subjects with the sickle cell trait contributes to the persistence and stability of the sickle cell gene frequency. Eaton and Mucha claimed that oligospermia, induced by hyperpyrexia, is a less common problem in these subjects because they probably have milder and shorter episodes of fever from malaria infection than subjects with a normal genotype. We have looked for evidence to support this hypothesis by comparing the testicular function, testicular size, and serum concentrations of the reproductive hormones in adult male subjects with the sickle cell trait and in an age-matched group of subjects with normal hemoglobin genotype. The mean serum concentration of testosterone, luteinizing hormone, follicle-stimulating hormone, and prolactin of both groups, measured by radio-immunoassay, were not statistically different from each other. Also, there was no detectable difference in any of the common indexes of semen quality between the two groups. The testicular volume index and several anthropometric indexes of subjects with the sickle cell trait and subjects with the normal hemoglobin genotype were also statistically similar. The results suggest that gonadal function is similar in adult males with the normal genotype and those with the sickle cell trait. Any increase in fertility observed in the latter group is probably due to extragonadal factors.