Womb with a View: On the Science of Maternal Effects

By Meredith ReichesApril 17, 2022

Womb with a View: On the Science of Maternal Effects

The Maternal Imprint: The Contested Science of Maternal-Fetal Effects by Sarah S. Richardson

IN AN ARTICLE entitled “How to Have the Best Pregnancy Ever,” published in 2013 on the feminist news site Jezebel, Tracie Egan Morrissey offers advice to her readers. “Doctors say that a glass of wine a day will not harm your unborn baby, or its IQ,” she writes, referring to a study in the British Journal of Obstetrics and Gynæcology. “That being said,” Morrissey continues, citing an article in PLOS ONE, “even one glass of wine in your entire pregnancy could lower your baby’s IQ.” What follows is a gleeful onslaught of contradictory and sometimes absurd guidance, much of it supported by peer-reviewed research. Don’t eat fatty foods! Don’t sleep on your back! Rub almond oil all over your taint! The drumbeat of directives and prohibitions will be familiar to any reader who has ever been pregnant. So might the ability of that drumbeat to keep the pregnant person on high alert. In 2022, it goes almost without saying that injunctions and warnings of this kind take aim at one party: the womb-bearing parent.

In a world where the CDC recommends that all women of childbearing age take birth control or abstain from drinking on the off chance that they might become pregnant, it may be difficult to imagine that the gestating parent wasn’t always on the hook for the quality of the baby. To the contrary: Fathers, genetic chance, and the child-rearing environment each took a star turn. As historian and philosopher of science Sarah S. Richardson writes in The Maternal Imprint: The Contested Science of Maternal-Fetal Effects, the very idea that the parent contributing the egg plays an equal role in heredity to the parent contributing the sperm was radical, constituting something of a revolution on the scientific front and in ideas about gender. In the 1880s, German biologist August Weismann demonstrated that eggs and sperm contain equal quantities of hereditary material. He also showed that this material doesn’t change as a result of its carrier’s life experiences. Before then, however, educated thinkers of all stripes believed that egg-bearers and sperm-bearers brought qualitatively and quantitatively different elements to shaping offspring. They also thought that what happened to prospective parents in the course of their lives could affect the hereditary material they passed to their offspring. According to Descartes, for example, mothers had nothing to do with a fetus’s internal organs. Rather, they telegraphed through the umbilical cord what its body ought to look like. And either parent leading a dissipated life would, in the view of some 19th- and early 20th-century physicians, impart deficits to an embryo at conception. Physician and eugenicist Frederick Walker Mott railed especially at the “race poisons,” alcohol and syphilis, which could make sperm “degenerate.”

These ideas weren’t merely the result of technical constraints on what scientists could see and describe. Researchers enlisted evidence at the cellular level to support the story of separate reproductive roles for males and females. Biologists who observed sperm under a microscope concluded that the heroic, wriggling gametes “rejuvenated” eggs, infusing the lineage with vim and vigor. Even granting that eggs and sperm contributed the same amount of hereditary material, some researchers, like American zoologist William Keith Brooks, maintained that the egg carried instructions for a general species type — what makes a fetus recognizable as, say, a human — while the sperm contained the blueprint for a unique individual. Scottish biologists Patrick Geddes and J. Arthur Thomson took the division of labor further: ova were responsible for passive maintenance, they insisted, while sperm built and synthesized. Eggs, in effect, furnished raw material, while sperm served as both the architectural visionaries and the contractors realizing the vision. In all these accounts, whatever genius a child might possess is clearly derived from the male parent.

This is not to say that mothers were ever in the clear, particularly with respect to damaging a fetus. Even when Weismann’s theory of sex equality in heredity was ascendant, many respected researchers, clinicians, and members of the public continued to understand the bodies of pregnant women as dangerously porous. Against this backdrop, the idea that women could influence their developing fetuses for good — that the behaviors and attitudes of gestating parents could make children healthy, pious, and intelligent — was hailed by some as progressive. Eugenic thinkers of a feminist bent and their followers seized on this possibility as creating an arena where women had agency. They used claims that women could gestate an improved race to argue that women should have the freedoms and resources to realize that potential.

If you’re detecting a war of the sexes coursing through debates about how heredity works, you’re not wrong. Gender politics, Richardson makes clear, at once spring from and are embedded in European and American theories of heredity. Late 19th- and early 20th-century thinkers wrote frankly about the premise that, on the cellular stage, the relationship between eggs and sperm played out the balance of power between the sexes. On the side of Weismann and the androgynous germ plasm, philosophical thinkers like Simone de Beauvoir cited equality in gametes as proof that the sexes themselves had to be equal in some fundamental way. Disciples of complementarity theories of egg and sperm, meanwhile, saw reflected under their microscopes the self-evident truth that males were active and original, igniting creation and driving innovation, while females were passive and inertial, warehousing nourishment and conserving traits through time.

Like other scientific theories, ideas about how parents influence their unborn children did not and do not emerge out of social vacuums. Richardson is the latest in a series of thinkers, including anthropologist Emily Martin, to identify how theories of heredity locate intuitions about causality in authoritative knowledge, however it might be defined in a particular time and place. That is to say, if an account feels true — if so-called common sense suggests that it is true — then it can be difficult for empirical evidence to dislodge the master narrative it is enlisted to support, whether with regard to the formation of a blastocyst or the readout from a PCR. The scientific and medical workers in Maternal Imprint were steeped in such master narratives. They appealed to and drew from the microscope — and from the observations and lived experiences of everyday people. And their spheres of influence extended beyond the learned community and into Chautauqua tents, popular pamphlets, and amphitheaters, sometimes creating echo chambers in which popular belief and quantitative data reinforced one another.

It's well and good to call out logical fallacies and wishful interpretations of data in disciplines that have long since lost scientific legitimacy — phrenology and eugenics, for instance. But the stakes are much higher when critics of science identify suspect master narratives at work in fields that are cutting-edge today. At the heart of Richardson’s book is just such a critique of the burgeoning world of epigenetics. Epigenetics, the field of biology concerned with how DNA is expressed or silenced, has been welcomed as emancipating us from the tyranny of genetics — our fate is no longer carved in stone in our genes — and as a call to personal responsibility. As the CDC website on epigenetics puts it, “Since your environment and behaviors, such as diet and exercise, can result in epigenetic changes, it is easy to see the connection between your genes and your behaviors and environment.” Statements like these make the relationship between environment, behavior, and epigenetic change sound straightforward. Richardson takes on three prominent case studies in epigenetics to demonstrate that it is anything but.

Each case takes as its departure point a “stressor” — a stimulus with the potential to knock a body out of biological equilibrium — experienced by women of childbearing age. In two scenarios, the Dutch famine winter of 1944–1945 and the 1998 ice storm in the Montérégie region of Quebec, researchers focus on pregnancies that took place during or shortly after an acute challenge. They believe that gestating parents’ bodily experiences, like hunger and cold, and their psychological experiences, like anger and fear, leave epigenetic traces on the genomes of their children. The third case study, led by neurogeneticist Rachel Yehuda, seeks to explain through epigenetics how high cortisol levels in Holocaust survivors correlate with relatively low cortisol levels in their children. All three studies claim to have discovered an effect of the stressor on gene expression patterns in offspring. They also assert that these epigenetic changes cause deficits, including higher body mass indices among children gestated during the Dutch famine and the Quebecois ice storm and attenuated stress responses among the children of Holocaust survivors.

How big are these changes, and how worried should prospective parents be? (It would seem that our pregnant Jezebel readers now have epigenetics to add to the list of threats!)

Richardson points to major grounds for caution when interpreting the results of epigenetic studies. The first red flag is that the effects identified are subclinical, meaning that they wouldn’t register at a doctor’s visit where a care provider is looking for signs that something’s wrong. Richardson refers to such effects as “cryptic.” By contrast, she notes, “Previous eras of research […] focused on severe, gross prenatal deprivations causing visible, macroscopic outcomes.” While research in the past was concerned with issues like folate deficiency causing spina bifida or thalidomide getting in the way of fetal limb formation, the biological traces of epigenetic difference aren’t at all obvious.

Setting aside health effects, the epigenetic changes measured in humans often fall well below the threshold of what scientists consider worth talking about in animal research. Studies of epigenetic changes in rats and mice show methylation levels, a metric of epigenetic change, between 20 and 100 percent at the locus of interest. Significant epigenetic changes like these do result in readily detectable changes in offspring bodies and behavior, whether it is in fur color or response to novel environments. Human studies, on the other hand, often report methylation differences under 10 percent.

The concerns pile on. Most researchers don’t look at the entire epigenome, instead zeroing in on portions contained in pre-designed and commercially available “chips,” so the range of changes that might turn up in a study is limited from the outset. Epigenetic changes are measured in tissue, and it happens to matter what tissue you choose for measurement, since methylation patterns differ across the blood, skin, and internal organs within each person. Even a single tissue, like blood, contains many types of cells carrying information from all over the body. Their epigenetic signals might be responding to circumstances far removed from, say, a trauma experienced in utero. In fact, methylation patterns at some sites change on time scales ranging from hours to years. Not only is the tissue itself important, but it matters when in the life course you collect it — if you don’t get a sample at birth, it’s possible that the changes you observe took place at a later time and weren’t caused by experiences during gestation.

Then there are all the possible explanations for epigenetic differences that studies don’t consider. Genes and epigenetics aren’t unrelated; your genes have a lot to say about your methylation patterns, so it may be that your biological family has more impact on your epigenetic profile than your lived experience. This is particularly noteworthy because studies focus almost exclusively on gestating parents, meaning that genetic, epigenetic, behavioral, and psychological data from the sperm-contributing parent are missing. And, as in all studies of variation, sample size matters. The smaller the data set, the more influence any single data point has on the story you tell.

People are invested in epigenetic narratives, just as they were invested in the self-evident truths of phrenology and the aspirational rallying cries of eugenics. And for good reason. Biological evidence, carrying with it deep forms of authority, confers legitimacy on experience: if it’s in the genes, it really happened. Recently, I described Richardson’s doubts about the epigenetics of Holocaust survival to a colleague. He had heard Yehuda speak some years prior. His mother-in-law, he explained, was a Holocaust survivor, and the description Yehuda offered of the psychology of survivors mapped perfectly onto his own family’s lived experience. The framework Yehuda proposed to explain the transmission of trauma across generations offered him and his wife a profound sense of relief; the anxiety his wife carried, and the anxiety they observed in their children, now felt inevitable and thus worthy of forgiveness. It had released them from the story that their suffering resulted from bad parenting. No thoughtful or rigorous critique, he told me, with a mix of gentle humor and deep seriousness, would persuade his family to relinquish the explanatory lifeline Yehuda had thrown to them.

In this anecdote, we find the crux of the issue: stories about heredity are maps of responsibility. They can function therapeutically or punitively, attributing problems to supposedly immutable sources like biology or to theoretically flexible causes like behavior. (Neither explanation, of course, is inherently progressive — just ask LGBTQ-plus rights activists about the possibilities and perils of “born this way.”) What they often also do, as Richardson illustrates, is stick the gestating parent with the proverbial bill. No matter that the circumstances under investigation were out of pregnant people’s control: no gestating parent could be blamed for a famine in the middle of a war, an ice storm, or attempted genocide. The pathway of action for these catastrophes, according to scientists, is the maternal body. The gestating parent, therefore, becomes the locus of surveillance and intervention, the site of infinite possibility and infinite frustration in the quest for some elusively optimal way to be.

As an anthropologist who studies reproduction, I run in circles, biological and political, with colleagues about the role of the mother in reproductive outcomes. Entire professional organizations, including the International Society for the Developmental Origins of Health and Disease, convene on the premise that the gestating body — or indeed, the potentially gestating body — is the place to intercede to promote the birth of healthy children who grow into productive members of society. Here, I think we could benefit from turning back to the writer of the Jezebel article, Tracie Egan Morrissey, who has wisdom to offer on the question of how much any individual can steer reproductive destiny. “Don’t have asthma or allergies,” she writes. “Don’t live near pollution. […] Don’t be poor.”

What would it mean for theories of heredity if we were to turn away from the individual as the site of intervention and focus instead on addressing human needs to eat, have safe shelter, and be free from persecution? What if we were to create a world in which gestating did not entail a nine-month passage through an environmental minefield? Then we might put what Richardson describes as “the long reach of the womb” in perspective and allow the womb-equipped among us a centuries-overdue sigh of relief.


Meredith Reiches is an associate professor of Anthropology at the University of Massachusetts, Boston.

LARB Contributor

Meredith Reiches is associate professor of anthropology at the University of Massachusetts Boston. She is at work on an essay collection, Heteroskeptical.


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