Prenatal Stress and Development: Beyond The Single Cause and Effect Paradigm

Abstract

Our awareness of the causes of stress-induced developmental dysfunction has increased dramatically over the past decade, and it is becoming increasingly clear that a number of factors can have considerable impacts on the developing fetus. Although there is a tendency in investigations of developmental teratogens to attribute specific causes to adverse fetal outcomes, it is important we recognize that for most developmental dysfunctions it is unlikely a single cause, but yet a series of environmental insults combined with genetic predisposition that ultimately leads to a disease state. Nonetheless, a number of developmental teratogens, such as maternal psychological stress and chemical exposures, have been shown to increase the likelihood of developmental defects. These defects can manifest during development, leading to observable birth defects, or could become evident long after birth, even into adulthood. In addition, epigenetic mutations in the germline can alter the phenotype of successive generations through transgenerational inheritance, and in this way environmental factors can alter the developmental outcomes and disease predispositions of future generations. Understanding this complexity is essential to interpretations of causality in the studies of stress-induced developmental dysfunction and needs to be fully considered to more effectively interpret potential outcomes.

An Epigenetics-Based, Lifestyle Medicine–Driven Approach to Stress Management for Primary Patient Care: Implications for Medical Education

“…39,40 Epigenetically induced biochemical changes can also cause transgenerational effects such as tendencies or predispositions toward certain diseases in offspring. [41][42][43][44][45][46] More narrowly stated, epigenetically induced biochemical reactions continuously shape, and/or are shaped by, behavioral, psychological, lifestyle, and environmental factors. Examples of these factors include poor nutrition, 34,47,48 obesity, 49,50 tobacco, 51,52 alcohol consumption, 53,54 psychosocial stress, [55][56][57] sleep deprivation, 58,59 and environmental pollution.…”

Early life course determinants of psychopathology

“…Lastly, by recognising the importance of moderating and mediation effects among environmental and genetic factors, comes the implicit recognition that these risk factors do not act in isolation, but are complexly interrelated with later disease risk (344). Furthermore, these risk factors are not related to discrete or specific psychiatric disorders in later life, but are instead predictive of a range of neurodevelopmental outcomes, with their role in specific disorders representing one point in a complex causal pathway (202).…”

“…Furthermore, these risk factors are not related to discrete or specific psychiatric disorders in later life, but are instead predictive of a range of neurodevelopmental outcomes, with their role in specific disorders representing one point in a complex causal pathway (202). Thus while in reality the data at hand will necessitate a reductionist approach to the problem, as exemplified by the testing of a number of individual directional hypotheses in the current work, future research should be designed with the capacity to better account for the multifaceted causal pathways among a number of exposures and outcomes (344).…”