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Endemic disease, nutrition and fertility in developing countries

Published online by Cambridge University Press:  31 July 2008

C. G. N. Mascie-Taylor
Affiliation:
Department of Biological Anthropology, University of Cambridge

Extract

The two main ways in which disease and nutrition can influence fertility are by reducing fecundity or by extending the birth interval. Fecundity refers to reproductive ability, that is the potential to breed, as compared to fertility which denotes actual childbearing (McFalls & McFalls, 1984). Reduced fecundity, which is usually referred to as subfecundity, results from impairment of any of the biological aspects of reproduction, including coital inability, conceptive failure as well as pregnancy loss. Subfecundity is only one factor operating to reduce fertility; other factors include those governing mate exposure (both formation and dissolution of unions as well as exposure to intercourse within unions) and birth control.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1992

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References

Barrett-Connor, E. (1969) Infections and pregnancy: a review. Southern med. J. 62, 275.CrossRefGoogle ScholarPubMed
Belsey, M. (1979) Biological factors other than nutrition and lactation which may influence natural fertility: additional notes with particular reference in sub-Saharan Africa. In: Natural Fertility. Edited by Leridon, H. & Meaker, J.. Ordina, Liège.Google Scholar
Eaton, J. & Mucha, J. (1971) Increased fertility in males with sickle cell trait. Nature, Lond. 231, 456.CrossRefGoogle ScholarPubMed
Epelboin, S. & Epelboin, A. (1979) Dangers of infection, pain and death. People, 6, 26.Google Scholar
Frisch, R. E. (1990) Body fat, menarche, fitness and fertility. In: Adipose Tissue and Reproduction. Edited by Frisch, R. E.. Karger, Basel.Google Scholar
McFalls, J. A. & McFalls, M. H. (1984) Disease and Fertility. Academic Press, Orlando.Google Scholar
Muir, D. & Belsey, M. (1980) Pelvic inflammatory disease and its consequences in the developing world. Am. J. Obstet. Gynec. 138, 913.CrossRefGoogle ScholarPubMed
Schrifin, B., Erez, S. & Moore, J. (1973) Teen-age endometriosis. Am. J. Obstet. Gynec. 116, 973.Google Scholar
Soong, Y-K., Lee, P-S., Kau, S-M., Lee, C-J. & Pao, C-C. (1990) Endocervical chlamydial deoxyribomucleic acid in infertile women. Fert. Steril. 54, 815.CrossRefGoogle ScholarPubMed
Spangler, D., Jones, G. & Jones, H. (1971) Infertility due to endometriosis. Am. J. Obstet. Gynec. 109, 850.CrossRefGoogle ScholarPubMed
Tau-Cody, K. R., Campbell, W. F., Dodson, M. G. & Minhas, B. S. (1988) Progesterone markedly enhances Chlamydia trachomatis inclusions in vitro and results in increased inflammation and productive infection in vivo. Fert. Steril. 50, S29.Google Scholar
Wolff, H., Newbert, U., Zebhauser, M., Bezold, G., Korting, H. C. & Mewer, M. (1991) Chlamydia trachomatis induces an inflammatory response in the male genital tract as associated with altered semen quality. Fert. Steril. 55, 1017.CrossRefGoogle ScholarPubMed