The research, published in the journal Biology of Sex Differences, tested 130 newborn infants, each examined only hours after delivery. The team, based at the University’s Autism Research Centre, presented the babies with two videos shown side by side. One was a social stimulus: a human face moving naturally. The other was a non-social stimulus: a Newton’s cradle, the familiar desk toy in which a row of metallic balls swings under gravity and their mechanical properties, transferring momentum from one end of the row to the other. Neither stimulus carried cultural meaning; one simply depicted a person, the other depicted moving objects.

The central finding was that, regardless of sex, newborn infants generally preferred to look at the social stimulus. Human faces, it seems, exert a powerful pull on attention from the very start of life. But when the researchers compared the two sexes, a consistent on-average difference emerged. Female infants spent a greater proportion of their looking time on the face, while male infants spent a greater proportion of their time on the swinging balls. The effect is a difference in averages between groups, not a categorical split, and the researchers are explicit that there is substantial variation within each sex and considerable overlap between them.

The result matters because of its timing. Within hours of birth, an infant has had almost no exposure to gendered clothing, toys, parental expectations or any of the countless cultural signals that shape development in the months and years that follow. If differences in social attention are already measurable at this point, the authors argue, then prenatal biological factors that differ between the sexes during pregnancy, such as sex hormone levels and genetic influences, are likely to contribute to them. That does not mean biology determines everything; rather, it suggests that prenatal factors set up early tendencies that later interact with experience.

The study is, in an important sense, a replication. In 2000, researchers at the University of Cambridge published a study reporting that newborn girls, on average, looked longer at faces while newborn boys, on average, looked longer at objects. That finding was influential but also contested, and scientists in the field called for it to be repeated under more rigorous conditions. Until now, no team had attempted it. The reason is practical as much as scientific: carrying out controlled experimental research on newborn infants is extraordinarily difficult. Recruitment must happen around unpredictable deliveries, testing windows are measured in hours, and every aspect of the procedure has to be gentle enough for babies only recently out of the womb.

The new study was designed to answer those methodological criticisms. Compared with the original 2000 experiment, it used more controlled experimental testing conditions and a more reliable method for monitoring infant gaze. Crucially, the researchers who analysed the videos of the babies’ eyes were blind to two things: the sex of each baby, and whether the baby was looking at the social or the non-social stimulus. This double-blinding of the analysis stage ensured that the expectations of the people coding the data could not bias the results, a safeguard that addresses one of the most common sources of concern in observational infant research.

Yumnah Khan, a PhD student at the Autism Research Centre and the lead researcher on the study, placed the finding in the context of the lab’s broader research programme. Our recent research has also shown that on-average sex differences are present in brain structure at birth and emerge prenatally, she said. This new study tells us that there are not only on-average sex differences in the brain but also in attention and behaviour. In other words, the structural and the behavioural evidence now point in the same direction: some differences between the sexes are detectable before postnatal experience could plausibly have produced them.

Professor Sir Simon Baron-Cohen, Director of the Autism Research Centre, who supervised the study, framed the result as a contribution to one of psychology’s oldest arguments. This study addresses the age-old question of whether nature plays any role at all in shaping sex differences in the human mind and brain, he said. The fact that we observe these differences within hours of birth, before extensive postnatal experience has occurred, suggests that prenatal factors play a role, and that these prenatal factors, sex hormones and/or genes, go on to interact with postnatal experience. In other words, it’s nature and nurture, not nature or nurture. That formulation is a deliberate rejection of the binary framing that has often dominated public discussion of the topic, in which commentators are asked to choose between a fully biological and a fully cultural account.

Other members of the team emphasised the limits of what the study can claim. Dr Alex Tsompanidis, Assistant Research Professor at the Autism Research Centre, noted that sex differences at birth are important as starting points, but that they do not fully determine how children learn and develop in later life, because biological and social factors always interact, contributing to the rich diversity of human societies. Professor Carrie Allison, Deputy Director of the Centre, stressed the statistical character of the finding: the differences do not apply to all male or all female infants, and are only seen when groups are compared on average. Our future research needs to better understand that variation, she said, pointing to the overlap between the sexes as a key target for further work.

The team’s next step is a longitudinal follow-up study, already underway and funded by the K. Lisa Yang Centre for Autism Research at Cambridge, part of the Yang Tan Collective. By following the same children over time, the researchers hope to determine whether these earliest differences in attention contribute to later differences in children’s minds, brains and behaviour. The stakes extend beyond the nature-versus-nurture debate itself. Girls, on average, learn to talk earlier and develop social skills faster than boys, and conditions such as autism, which is diagnosed about twice as often in boys as in girls, may be connected to the same developmental pathways. The researchers hope that by understanding the origins of the earliest sex differences, scientists can better understand neurodiversity and the conditions in which it is expressed. The original study was supported by the Wellcome Trust, the Simon Foundation Autism Research Initiative and a PhD studentship from Trinity College, Cambridge and the Cambridge Trust.

Subject of Research: Sex differences in newborn social attention and their prenatal origins

Article Title: Sex differences in attention are present at birth, study finds

Article References: Sex differences in attention are present at birth, study finds. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: newborn infants, sex differences, social attention, prenatal factors, Autism Research Centre, University of Cambridge, Biology of Sex Differences, face preference, nature and nurture, infant gaze, autism, hormones

At the heart of the disagreement lies a deceptively simple question: how much of the variation observed between individual epigenomes is actually driven by genes rather than by environment? Zaina’s reply leaned heavily on evidence that genetic differences between individuals exert a powerful influence on epigenetic patterns, particularly DNA methylation, the chemical modification of cytosine bases that is the most widely studied epigenetic mark. He pointed to studies such as work by Husquin and colleagues, published in Genome Biology, which explored the genetic basis of human population differences in DNA methylation and their causal impact on immune gene regulation. If, as Zaina contends, the individual characteristics of the epigenome are for the vast majority dependent on interindividual genetic differences, he asks whether the field should really invest so heavily in understanding the social and environmental ramifications of those differences.

Zaina’s answer is a firm no, and he offers two distinct reasons for it. The first is that he believes there is little to be learnt from studies of environmentally driven variation in epigenetic predispositions to disease, because what he calls the grip of genetics over epigenetics is so strong that the field should, in his view, be renamed paragenetics. The term is deliberately provocative: it suggests that epigenetics is not an autonomous discipline studying environmental regulation of the genome, but essentially a satellite of genetics, a layer of molecular detail whose variation is predetermined by underlying DNA sequence. The second reason is more subtle and more philosophical. Zaina warns that by calling for a complexification of the biosocial tools of epigenetics, researchers run the risk of reifying the social differences under study, converting them into the genetic differences that supposedly have a grip on them. In other words, the very act of tracing social disparities to molecular marks might end up naturalizing those disparities as biological facts.

Chiapperino and Paneni’s response does not dismiss these concerns. They concede that Zaina’s reading of the relationship between genetics and epigenetics contains several elements of truth, and they note that these elements can also be found in a well-established thread of philosophical, historical and sociological scholarship on the subject. Epigenetic differences, they acknowledge, may not simply be the marks, the product, or the biological correlates of one’s unique exposures to ecological, material and social environments. The epigenome is also the result of developmental trajectories, meaning the timing of events during an organism’s development, and of individual genetic differences, meaning variation in DNA sequence. The authors are explicit that they never intended to suggest otherwise, and they credit Zaina for acknowledging that dialogue around the biosocial aspects of epigenetics is worth the community’s effort.

But the authors argue that a wrong conclusion is often drawn from this acknowledgment. Claiming that the presence of genetics’ grip on the epigenome proves either that environmental determinants are unimportant, or that the epigenome is in essence under the control of the genome, is, in their view, just as problematic as the opposite claim that the epigenome sits entirely at the mercy of its environments. The reason, they insist, is that this is not an either/or matter. Drawing on extensive scholarship in developmental epigenetics and on decades of analysis of the nature-nurture debate, they argue that the dichotomous framing itself is the problem. Genetic and non-genetic factors, they write, constitute a dynamic, mutually dependent, relational developmental system within which different components and levels of organization coact to promote the emergence, maintenance, or modification of phenotypic traits. On this view, asking whether genes or environment matter more is a category error, because both are constitutive of the developmental process rather than competing causes of it.

From this diagnosis flows what Chiapperino and Paneni describe as a pragmatic call towards methodological symmetry. Their complaint is not that epigenetics ignores biology, but that the sophistication of its methods, tools and questions is strikingly lopsided. When researchers study biological variables of developmental systems, they deploy elaborate molecular assays, statistical models and experimental designs of considerable complexity. Yet when it comes to socio-environmental variables and their biological ramifications, the same level of methodological rigor is rarely matched. Why, the authors ask, should the measurement of social exposures, life conditions and environmental contexts remain so comparatively crude when the molecular readouts they are supposed to explain have become so refined? This asymmetry, they suggest, is a genuine scientific weakness, not merely a sociological observation, because poorly characterized environmental variables undermine the very inferences that epigenetic studies are designed to support.

The second half of their reply tackles Zaina’s warning about reification more directly. Chiapperino and Paneni state plainly that they do not believe the complexity of the phenotypes and human conditions studied in epigenetics will ever be amenable to genetic differences, let alone be bound to be reframed as genetics-related phenomena. Crucially, their reasoning is not that misinterpretation is impossible. They fully acknowledge that genetic or epigenetic differences can be misread as privileged informational sources, obscuring the deep social, historical and environmental ramifications behind them, and they cite a body of critical scholarship that has repeatedly raised the alarm about risky revivals of sociobiological ideas within epigenetics. Scholars such as Maurizio Meloni, who has written on race in an epigenetic time, and Dupras, Saulnier and Joly, who surveyed the ethical, legal and social dimensions of the field, have hammered this nail on its head, in the authors’ words. The concern that epigenetics could become a vehicle for old biological determinism dressed in new molecular clothing is taken seriously rather than waved away.

Instead, the authors ground their confidence in a different principle: the impossibility of reducing complex phenotypic differences to either one of their components, whether the genome or the environment. There may be specific phenotypes for which a genetic difference is more instructive for understanding the roles and contributions of a given epigenetic difference, including those relating to environmental exposures or developmental trajectories. Yet even these phenotypes, they argue, must ultimately be explained as the product of the biosocial components of the system, that is, of the organism as a whole embedded in its conditions of life. Once this distinction is recognized, the authors write, they cannot share Zaina’s caution about the risk of affirming the primacy of the genome through the epigenome. A risk of misinterpreting the biosocial dimensions of the epigenome certainly exists, but they pose a pointed counter-question: is that risk enough of a reason to give up on what Zaina himself called the noble and useful enterprise of reducing the daylight between epigenetics and fine-grained mapping of the social milieu?

The exchange closes on a note that is part challenge and part invitation. Experimenting with the epistemic foundations and political undertones of a biosocial epigenetics, the authors concede, is no easy task, and it may carry a controlled and relative risk of discomfort. But they believe there exist few alternatives to walking into this territory, a peregrination metaphor they borrow from Zaina himself, without taking that risk of thinking and writing about these issues with colleagues from different trajectories, if not different worldviews. It may be far from the comfort zone of pipettes and tubes, they write, but it may nonetheless be a productive and exciting stroll. Their closing line, urging scientists to take a walk on the wild side, captures the stakes of the debate: whether epigenetics will retreat into a purely molecular, genetically anchored discipline, or embrace the harder, messier work of integrating rigorous social science into its study of how lives become biology. The correspondence, published as open access in Epigenetics Communications and supported by a Swiss National Science Foundation Ambizione grant, makes clear that this conversation is far from over, and that its outcome will shape how a generation of researchers interprets the molecular traces of human difference.

Subject of Research: The debate over genetic versus environmental influences on epigenetic variation and the biosocial ambitions of epigenetics

Article Title: Walk on the wild side: a response to Zaina

Article References: Chiapperino, L., & Paneni, F. (2023). Walk on the wild side: a response to Zaina. Epigenetics Communications, 3(1), Article 3. https://doi.org/10.1186/s43682-023-00019-z

Image Credits: AI Generated

DOI: 10.1186/s43682-023-00019-z

Keywords: epigenetics, DNA methylation, biosocial science, nature and nurture, developmental epigenetics, genetics, gene-environment interaction, social epigenetics, biological determinism, Epigenetics Communications, Chiapperino, Zaina

The dispute began with Chiapperino and Paneni’s earlier paper, Why epigenetics is (not) a biosocial science and why that matters, which examined whether and how epigenetic research can genuinely capture the entanglement of biological and social processes in health and disease. Dupras responded with a critical assessment, reading their argument as a call for less reductionism and more holistic methods in the field. That reading, the two authors now insist, misrepresents their intent. They never claimed that epigenetics should be assimilated to nurture while genetics stands for nature, nor did they seek to draw a sharp line between biosocial epigenetics and a supposedly non-biosocial genetics.

At the heart of the reply is a reframing of the central question. The authors argue that the problem is not whether the processes of development, health differentiation, and evolution are either natural or social, either biosocial or not. Instead, they ask to what extent the methods, tools, and study designs of epigenetics can capture the interactions that necessarily occur between nature and nurture, between biological and social processes. This developmental version of epigenetics, which they align with work by researchers such as Robert Lickliter and David Witherington, is explicitly designed to move beyond the inherited dichotomies of the nature-nurture debate rather than reproduce them under a new molecular vocabulary.

The authors also reject the charge that they are demanding a wholesale turn to holism. They acknowledge that the full complexity of biosocial processes may be incommensurable with the methods of the biomedical sciences, yet they explicitly disavow any foundational endeavor toward an all-encompassing holistic biosocial science. Drawing on the history, philosophy, and social anthropology of science, including the work of Hans-Jörg Rheinberger, John Law, and Annemarie Mol, they contend that the reductionism-holism dichotomy is itself inadequate for understanding postgenomic scientific practice. The point, they write, is not whether epigenetic methods are reductionist, since they plainly are, but how they operate most prolifically at the fuzzy boundary between the trivial and the complex.

To make this abstract argument concrete, Chiapperino and Paneni turn to the measurement tools that dominate epigenetic studies of psychosocial environments: stress scales and allostatic load indices. These instruments, widely used to link adversity to molecular change, have drawn sustained criticism for lacking definition, standardization, and fidelity, and for what anthropologist Jörg Niewöhner has called the molecularization of biography and milieu. The authors concede that such methods are certainly reductionist. But they ask whether reductionism necessarily dooms these tools to a poor picture of the environmental embeddedness of health, and their answer is a qualified no.

The problem, they argue, lies less in the instruments than in the study designs that house them. Much epigenetic research reproduces a simplistic linearity: exposures, objectified through stress or allostatic load measurements, produce biological differences readable in the epigenome, which are in turn linked to disease through mechanistic or statistical associations. A different configuration employing the very same reductionist tools could avoid this pitfall. Repeated longitudinal measures of psychological and physiological scales, for example, could reveal the multidirectional effects of stress, its biological embodiment over time, and the biopsychosocial looping effects through which people respond to and reshape their own conditions. Such designs would leave the reductionist qualities of the methods untouched while dramatically complexifying the account of the phenomenon they can offer.

The reply also addresses Dupras’s defense of ambitious large-scale initiatives such as the International Human Epigenome Consortium. Chiapperino and Paneni are careful to state that they do not question the consortium’s importance for advancing standards, methods, reference knowledge, and a sense of global community among epigeneticists. Nor do they deny that the boundary between epigenetics and genetics is blurred, a definitional controversy that continues to occupy commentators such as Bernhard Horsthemke. Yet they maintain that a theoretically modest point remains highly relevant for any endeavor seeking to build reference epigenomes for the understanding of health and disease.

That point comes into sharp focus around ethnicity and DNA methylation. Few researchers hold that interindividual differences in the epigenome can be fully recapitulated by genetic variation, including variation across so-called genetic ancestry groups. The authors cite a study by James Galanter and colleagues showing that, across the genome, genetic ancestry accounts for roughly three-quarters of the association between ethnicity and methylation differences, with the remaining quarter attributed to shared environmental, social, and cultural factors within groups. In that residual quarter lies evidence that both ancestry and the social construction of ethnic difference shape epigenetically measurable disparities in disease prevalence and health trajectories. This finding, they argue, validates ongoing calls to diversify reference epigenomic maps and epigenome-wide association studies beyond their current overrepresentation of participants of European ancestry, but it also demands more than genetic imputation alone.

Here the authors pose a pointed question to the global epigenetics community: what is currently on the agenda to account for the share of health disparities across social groups that stems from differences in social and environmental exposures rather than genetic ancestry? They suggest that the biosocial dimensions of ethnic differences in the epigenome likely lack a fixed ontology, being neither purely biological nor purely social. For some traits, reference epigenomes may prove highly sensitive to genetic differences across ancestry groups; for others, they may be more open to varied developmental trajectories, local contexts, and culturally situated practices. They caution, following Maurizio Meloni and colleagues, that even simplistic cause-effect models can constitute a problematic form of biosocial determinism around epigenetic differences.

Ultimately, Chiapperino and Paneni frame their reply as a call to symmetry: a demand that the development of epigenetic tools, methods, and study designs refrain from overlooking either side of the biosocial continuum. They do not claim to offer a unique path, nor to certify whether epigenetics is or is not a holistic biosocial science. The simplistic stance, they suggest, belongs to those who feel compelled to pick a side in what is ultimately a fabricated dichotomy between the biological and social origins of epigenetic differences. In a field increasingly asked to explain how poverty, discrimination, and stress become embodied, that insistence on balance may prove more consequential than any single methodological prescription, reminding researchers that the most rigorous science of the epigenome may be the one that refuses to let nature and nurture compete for exclusive ownership of it.

Subject of Research: The role of reductionist and holistic methods in capturing biosocial interactions in epigenetic research

Article Title: In medio stat virtus? A reply to Dupras

Article References: Chiapperino, L., & Paneni, F. (2023). In medio stat virtus? A reply to Dupras. Epigenetics Communications, 3(1), Article 5. https://doi.org/10.1186/s43682-023-00017-1

Image Credits: AI Generated

DOI: 10.1186/s43682-023-00017-1

Keywords: epigenetics, biosocial science, reductionism, holism, DNA methylation, allostatic load, genetic ancestry, health disparities, International Human Epigenome Consortium, nature and nurture, study design, philosophy of science