The Maternal Footprint: The Contested Science of Maternal-Fetal Effects Sarah S. Richardson Univ. Chicago Press (2021)
Like me, my grandmother lived with anxiety, even though she would not have described it that way. Unlike me, she fled Poland under false papers at the start of World War II, knowing that her twin sister and her beloved mother-in-law remained in the occupied country.
When I read the media coverage of Rachel Yehuda’s 2016 study claiming that children of Holocaust survivors have epigenetic changes at a particular site in the genome, and these changes make them more susceptible to stress (R. Yehuda et al. Biol. Psychiatry 80, 372-380; 2016), that asked me questions. Did my grandmother’s traumatic experiences lead to changes in the regulation of her DNA that her body passed on to my father when she was pregnant, ultimately contributing to my anxiety? Or was my anxiety due to genetics, culture, education, or the scary knowledge that something terrible had happened to my loved ones? Or was it all of the above?
Yehuda’s study has often been criticized for its small sample size, small control group, and oversized causation claims, although you might not know it from the media coverage. Sarah Richardson’s book The maternal imprint broadens this criticism to the field of human transgenerational epigenetics more generally. She argues that social assumptions about maternal responsibility give ideas in this area more credibility than they deserve based on the data. Her argument will be of interest to researchers, pregnant nerds, and policy makers, although it could have best shown her working.
Epigenetics are the chemical changes in DNA that do not alter the sequence itself, but affect the way genes are regulated; such a change is called methylation. Richardson deals only with transgenerational epigenetics, the kind that can be passed on to a gamete or an embryo. This is distinct from the epigenetic changes relayed between cells in a person’s body. The latter is strongly supported and has a significant effect on the genomes of cancer cells, for example.
The first half of the book is a long tour of theories of maternal and paternal contributions to heredity since the end of the 19th century. Richardson, historian of science, shows how the beliefs of each era shaped his theories.
The dominant thought has turned around several times. In the 1880s, the “germplasm” theory held that sperm and ovum contributed equally to heredity. Between the 1880s and the early 1900s, a subgroup of eugenics in the United States rejected these ideas and thought that a mother’s mental state during pregnancy would be permanently imprinted on her child. For example, an 1882 book by educational reformer Georgiana Bruce Kirby told pregnant women that in order to influence their fetuses well, they should do math and play music every day instead of doing “household chores.” Such as “making jam” and “hemming skirts”. ”. Then, in the 1910s, it was thought that males carried the lion’s share of the risk to offspring, due to their more dangerous jobs and their greater likelihood of drinking alcohol.
Finally, Richardson discusses his central critique of the work on human epigenetics. She digs many holes in three study groups: Suzanne King’s work on pregnant babies during a 1998 ice storm in Quebec, Canada; Yehuda’s studies of Holocaust survivors and their children; and research on babies born during the Dutch famine of the hunger winter of 1944-45.
The studies of ice storms only included 34 children and did not have a control group. The Holocaust work only had eight parental controls and nine offspring controls. The Dutch studies included 811 descendants – a large enough sample, including many controls. Still, Richardson points out that the effect sizes they found were small: differences in DNA methylation levels between 0.7% and 2.7%. None of the studies took biological samples from infants at birth. Without these, argues Richardson, they cannot rule out “reverse causation.” In other words, they can’t determine whether the epigenetic changes caused, say, increased susceptibility to stress, or whether susceptibility to stress caused the epigenetic changes.
Epigenetic studies typically use blood samples, but epigenetics vary by cell type, so if you’re interested in the effects on the brain, it’s not clear that you’ll learn anything from the changes in the blood. . And studies rarely collect much, if any, information about paternal contributions to the effects studied. One theory maintains that maternal obesity during pregnancy leads to higher rates of obesity in children; studies that have broadened the search have found that paternal height better explains the variation.
Richardson makes a lot of good points, but the references and counterpoints are too thin on the pitch. What is more problematic is that it does not engage in the growing body of work designed to fill some of the gaps in Dutch studies – efforts such as the Avon Longitudinal Study of Parents and Children in the UK – Uni, and at least seven others covered by the Pregnancy and Childhood Epigenetics Consortium which has samples in the thousands and collects umbilical cord blood to combat reverse causation. Richardson never explains how she selected the three study groups she focuses on to the exclusion of the others.
Her key claim is that poor epigenetic results can hold too stubbornly a hold because our culture teaches us to assume that mothers bear the blame. It’s true, women are far too easy to blame. But to make a strong argument, other interpretations must be addressed, such as the general frenzy for DNA-based explanations, or the cult of personal responsibility over social responsibility.
Richardson is right, however, about how cultural assumptions diminish the possibilities. As public health specialist Liana Winett wrote: “Asking, ‘What would a woman do today if she wanted to help her baby avoid chronic disease?’ is very different and much more limiting than asking, “What would our society do and offer if we wanted to be the healthiest place to be born?” “
The author declares no competing interests.