Encyclopedia of Evolutionary Psychological Science

Living Edition
| Editors: Todd K. Shackelford, Viviana A. Weekes-Shackelford

Hormone Effects on Human Fetal Development

  • Catherine DeSotoEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-16999-6_3630-1

Keywords

Evolutionary Psychology Hormonal Exposure Excess Cortisol Hormone Cortisol Psychology Framework 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Prenatal Programming, Cortisol

The evidence that phenotype is set partially based on prenatal hormonal exposure is overall strong. Such effects make sense within the evolutionary psychology framework.

Hormone levels that a developing fetus experiences can result in long-lasting phenotypic differences in the individual. Because the maternal blood supply is the route by which a fetus will be exposed, mother’s levels – and her experiences – can affect development.

High levels of stress during pregnancy result in higher levels of the hormone cortisol as does exogenous ingestion of certain medicines (e.g., steroids) or certain foods (i.e., licorice). In any case, there is evidence that exposure of the fetus during prenatal development will alter early programming, causing differences in metabolism and other physiological parameters. The effects are long term or permanent. Combined with experimental methods employing animal models (see Weinstock 2008), there is converging evidence implicating a causal pathway for human development. The human placenta features 11beta-hydroxysteroid type 2 (HSD2) that works as a barrier to prevent excess cortisol exposure for a fetus; the enzyme converts the active form into an inactive form when it crosses the placental barrier. Animal research suggests that this enzyme can be more or less active due to starvation, various kinds of inflammation, or general stress, thus altering fetal exposure to glucocorticoids. Broadly, high levels of glucocorticoids in the mother result in lower birth weight and increase in HPA activity and changes in the overall metabolic profile. For example, increased cortisol, higher susceptibility to diabetes, and cardiovascular risk have all been well documented (see Reynolds 2010; Reynolds 2013). The general patterns suggest that more cortisol encountered prenatally results in generally more cortisol when there is not an acute stressor present and a blunted increase during times of acute stress (O’Connor et al. 2013). Also of considerable interest are the effects on the developing brain. McEwen in 1999 demonstrated a definite susceptibility of the developing brain to glucocorticoids. Since that time, several key findings have emerged. Buss et al. (2012) have found evidence for an early window of sensitivity to cortisol in girls. Specifically, early exposure to high cortisol during gestation was associated with significantly increased size of the amygdala in seven-year-old girls. The amygdala is associated with linking and responding to fear or anxiety-producing external stimuli. Research has documented that levels of cortisol (measured in utero) predict later impairments in measured cognitive development (Bergman et al. 2010).

Evolutionary psychologists generally conceptualize an individual as a combination of genotype framing allowing for a range of final outcomes that are fine-tuned based on expected or encountered environmental circumstances. As a whole, it appears that prenatally experienced increased cortisol leads to alterations of the offspring’s HPA, thus causing myriad changes, including low birth weight and altered glucose processing (e.g., later susceptibility to type 2 diabetes) and altered response to experienced stressors throughout life. From an evolutionary psychology perspective, it is interesting to observe that deleterious effects may be most pronounced when a mismatch between utero environment programming and experienced adult environment is likely greatest. For example, low birth weight in tandem with adulthood obesity was a stronger risk factor than either variable alone (Li et al. 2010). This suggests the possibility that the function of prenatal programming may be to somehow prepare for adult environment most likely to be encountered.

Conclusion

Certainly, the environment encountered determines which behaviors and phenotypes are the most adaptive. Hormones may serve as a signal to alter the developing fetus toward a phenotype more adaptive to expected circumstances. Alteration of the physiology and behavior of offspring via the levels of maternal corticoids could be plausible vehicle for such fine-tuning to occur. In any event, evidence that hormonally based prenatal programming alters the phenotypic outcome of the individual, especially glucocorticoids, is strong.

References

  1. Bergman, K., Sarkar, P., Glover, V., & O’Connor, T. G. (2010). Maternal prenatal cortisol and infant cognitive development: Moderation by infant mother attachment. Biological Psychology, 67(11), 1026–1032.CrossRefGoogle Scholar
  2. Buss, C., Poggi-Davis, E., Shahbaba, B., Pruessner, J. C., Head, J., & Sandman, C. A. (2012). Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems. Proceedings of the National Academy of Sciences, 109, 1312–1319.CrossRefGoogle Scholar
  3. Li, Y., He, Y., Qi, L., Jaddoe, V. W., Feskens, E. J. M., Yang, X., Ma, G., & Hu, F. B. (2010). Exposure to the Chinese famine in early life and the risk of hyperglycemia and type 2 diabetes in adulthood. Diabetes, 59, 2400–2406.CrossRefPubMedPubMedCentralGoogle Scholar
  4. O’Connor, T. G., Bengman, K., Sorkar, P., & Glover, V. (2013). Prenatal cortisol exposure predicts infant cortisol response to acute stress. Developmental Psychobiology, 55(2), 145–155.CrossRefPubMedGoogle Scholar
  5. Reynolds, R. M. (2010). Corticosteroid mediated programming and the pathogenesis of obesity and diabetes. Journal of Steroid Biochemistry and Molecular Biology, 122, 3–9.CrossRefPubMedGoogle Scholar
  6. Reynolds, R. M. (2013). Glucocorticoid excess and the developing origins of disease: Two decades of testing the hypothesis. Psychoneuroendocrinology, 38, 1–11.CrossRefPubMedGoogle Scholar
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Copyright information

© Springer International Publishing AG 2017

Authors and Affiliations

  1. 1.PsychologyUniversity of Northern IowaCedar FallsUSA

Section editors and affiliations

  • Jennifer Byrd-Craven
    • 1
  1. 1.Oklahoma State UniversityStillwaterUSA