Reproductive compensation was originally a theory to explain why recessive genetic disorders may persist in a population. It was proposed in 1967 as an explanation for the maintenance of Rh negative blood groups. Reproductive compensation refers to the tendency of parents, seeking a given family size, to replace offspring that are lost to genetic disorders. It may also refer to the effects of increased maternal or parental investment in caring for disadvantaged offspring, seeking to compensate for genetic disadvantage. It is a theory that suggests that behavioral as well as physiological factors may play a role in the level of recessive genetic disorders in a population.
According to Andrew Overall of the University of Edinburgh, “Reproductive compensation may be particularly significant where economic or social factors mean that families are small compared to the maximum reproductive rate. Within small families, diseased infants may be more likely to be replaced. As a consequence, parents with otherwise reduced fertility have a greater influence on the frequency of recessive alleles in future generations.” 
Ian Hastings has argued that reproductive technologies such as embryo sex selection, preimplantation genetic diagnosis with in vitro fertilization, and selective termination of pregnancy may increase the frequency of genetic disorders through reproductive compensation.
More recently the reproductive compensation hypothesis has been generalized to include, not only recessive genetic disorders, but in a more general sense, the effects of parental compensation when mate selection or breeding take place under constraints. According to Patricia Adair Gowaty, “The reproductive compensation hypothesis says that individuals constrained by ecological or social forces to reproduce with partners they do not prefer compensate for likely offspring viability deficits.” In human societies, such constraints include the manipulation of female mating options, forced copulation, arranged marriages, and the trading of copulation for access to resources.
Whereas heterozygote advantage can explain the persistence of high carrier rates of lethal alleles in certain regions (e.g. sickle-cell disease in Central and West Africa), Johan Koeslag and Stephen Schach  have suggested that reproductive compensation might explain why different communities have high carrier rates for differing lethal alleles, despite living in similar or sometimes the same environment. Examples are Tay–Sachs disease amongst Ashkenazi Jews, cystic fibrosis amongst people of West European origin, and phenylketonuria among persons from Ireland.
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- Ober, C, Hyslop, T and Hauck, WW (1999). "Inbreeding effects on fertility in humans: evidence for reproductive compensation". American Journal of Human Genetics 64 (1): 225–231. doi:10.1086/302198. PMC 1377721. PMID 9915962.
- Overall, AD, Ahmad, M, and Nichols, RA (2002). "The effect of reproductive compensation on recessive disorders within consanguineous human populations". Heredity 88 (6): 474–479. doi:10.1038/sj.hdy.6800090. PMID 12180090.
- Hastings, IM (2001). "Reproductive compensation and human genetic disease". Genetics Research 77 (3): 277–283. doi:10.1017/S0016672301004992. PMID 11486510.
- Gowaty, PA (2008). "Reproductive Compensation". Journal of Evolutionary Biology 21 (5): 1189–200. doi:10.1111/j.1420-9101.2008.01559.x. PMID 18564347.
- Gowaty PA, Anderson WW, Bluhm CK, Drickamer LC, Kim YK, Moore AJ (2007). "The hypothesis of reproductive compensation and its assumptions about mate preferences and offspring viability". Proceedings of the National Academy of Sciences 104 (38): 15023–15027. doi:10.1073/pnas.0706622104. PMC 1986606. PMID 17848509.
- Koeslag JH, Schach SR (1984). "Tay-Sachs disease and the role of reproductive compensation in the maintenance of ethnic variations in the incidence of autosomal recessive disease". Annals of Human Genetics 48 (Pt 3): 275–281. doi:10.1111/j.1469-1809.1984.tb01025.x. PMID 6465844.
- Koeslag JH, Schach SR (1985). "On the perpetuation of relic genes having an inviable homozygote". Annals of Human Genetics 49 (Pt 4): 291–302. doi:10.1111/j.1469-1809.1985.tb01705.x. PMID 4073837.