Advances in Developmental Psychology - Vol. 2

By Michael E. Lamb; Ann L. Brown | Go to book overview

3
Paternal Effects on Reproductive Outcome and Developmental Risk

Virginia Gunderson and Gene P. Sackett
University of Washington


INTRODUCTION

The social role of fathers as well as mothers figures prominently in current theory and research on human development (e.g., Lamb, 1981; Parke, 1979). Biological influences of paternal factors on pregnancy and postnatal development have fared less well as either theoretical or research topics. Experimental and epidemiological literature concerning pregnancy outcome, prenatal determinants of behavior, and developmental risk factors has dealt almost exclusively with maternal variables. Prominent among these are age, parity, socioeconomic status, growth of the mother during her own development, exposure to drugs and teratogens, physiology before and during pregnancy, perinatal complications and psychological stress and psychopathology (e.g., Bell & Smotherman, 1980; Friedman & Sigman, 1981; Shepard & Fantel, 1979). This emphasis comes from the prevailing--and certainly intuitive--view that such biological effects must originate in maternal disorders. Thus, in the report on the national perinatal study ( Niswander & Gordin, 1972), not a single protocol or finding among the 528 pages of procedures and results relates to any paternal factor.

This lack of concern for paternal effects as potentially significant biological determinants of reproductive outcome in humans seems puzzling. It is clear that female and male factors can underlie failures to conceive (e.g., Cockett & Urry, 1977). Thus, males have not been ignored as important contributors to sterility among human couples. However, this paper does not deal with the large literature on sterility and other disorders that prevent conception. Our concern is with paternal factors determining the developmental fate of offspring after conception has occurred. Some of these factors might directly affect the anatomy and physiology of developing embryos and fetuses. Others may affect the intrauterine environment, producing suboptimal conditions for implantation and perhaps for placental development or function. Potential paternal influences range from direct and indirect genetic effects, through immunological incompatibilities between mates, to environmental variables such as paternal drugs, poisons, or diseases. Our contention is that such paternal factors, like those known to be of maternal origin, may affect fetal loss, growth abnormalities, and risk for deviant postnatal behavioral development. Given ignorance about potential paternal contributions, such effects would appear to be caused only by maternal factors.

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