It's the mother!: How assumptions about the causal primacy of maternal effects influence research on the developmental origins of health and disease

Abstract

Research on the developmental origins of health and disease (DOHaD) has traditionally focused on how maternal exposures around the time of pregnancy might influence offspring health and risk of disease. We acknowledge that for some exposures this is likely to be correct, but argue that the focus on maternal pregnancy effects also reflects implicit and deeply-held assumptions that 1) causal early life exposures are primarily transmitted via maternal traits or exposures, 2) maternal exposures around the time of pregnancy and early infancy are particularly important, and 3) other factors, such as paternal factors and postnatal exposures in later life, have relatively little impact in comparison. These implicit assumptions about the “causal primacy” of maternal pregnancy effects set the agenda for DOHaD research and, through a looping effect, are reinforced rather than tested. We propose practical strategies to redress this imbalance through maintaining a critical perspective about these assumptions.

Maternal and early‐life area‐level characteristics and childhood adiposity: A systematic review

“…All studies adjusted for either maternal smoking during pregnancy or maternal weight at various time points (with the exception of Kim et al), factors that have been associated with offspring adiposity in previous research, improving the robustness of the studies reviewed herein. Only one study included measures of paternal smoking or weight, which is a limitation because paternal genetics, attitudes, and behaviours likely also affect childhood adiposity, and their exclusion from models overemphasizes the effect of maternal factors . The exclusion of preterm and low birthweight babies in some studies may have affected the estimates as these outcomes may be on the causal pathway between the environment and childhood adiposity, given evidence of links between the environment, birth outcomes, and infancy catch‐up growth for preterm and small babies .…”

“…6 These findings suggest that there is some inconsistency in how these mea- 45 which is a limitation because paternal genetics, attitudes, and behaviours likely also affect childhood adiposity, and their exclusion from models overemphasizes the effect of maternal factors. 66 The exclusion of preterm and low birthweight babies in some studies 47,48,51 may have affected the estimates as these outcomes may be on the causal pathway between the environment and childhood adiposity, given evidence of links between the environment, birth outcomes, 42 and infancy catch-up growth for preterm and small babies. 44,67 Residual confounding may also occur at the area-level, where certain environments experience multiple forms of disadvantage in terms of suitability for healthy weight gain, for example, areas with limited park access tend to have fewer outlets selling healthy foods.…”

What’s in a name? The three genealogies of the social in social epigenetics

“…Lastly, recent social science investigations show that the 'molecularization' of environments at work in epigenetic research labs is expanding in new directions. In particular, while research in epigenetics still tends to overstudy maternal transmissions (Sharp, Lawlor & Richardson, 2018), there is now a significant interest in the father's influence. However, as this research reduces paternal influence to 'father-as-sperm influence' -i.e.…”

“…First, they criticize this research for viewing food as an individual choice rather than as a set of culturally, economically and socially embedded practices. They also denounce the possible conflation between association -between maternal nutrition and health outcomes in the offspring -and causation, because of unobserved confounders (Sharp, Lawlor & Richardson, 2018). However, these critics express less an upfront rejection of this area of social epigenetics than a certain disillusion towards its initial promises.…”

Proxy gene-by-environment Mendelian randomization study confirms a causal effect of maternal smoking on offspring birthweight, but little evidence of long-term influences on offspring health

“…The developmental origins of health and disease hypothesis proposes that early life experiences, 61 including those in utero, can have long-term health effects, and maternal pregnancy exposures are 62 important to long-term health of offspring (1). Heavier maternal smoking in pregnancy is known to 63 be causally associated with lower offspring birthweight (2-6), but its other effects in offspring are 64 less clear.…”