Adapted from Born Anxious: The Lifelong Impact of Early Life Adversity—and How to Break the Cycle, by Daniel P. Keating. Published by St. Martin’s Press. Copyright © 2017 Daniel P. Keating. Reprinted with permission of the publisher, St. Martin’s Press. All rights reserved.

By the late 1990s, our group at the Canadian Institute for Advanced Research had identified robust connections between early adversity and lifelong anxiety and stress, leading to problems in social relationships and mental and physical health—and even to shorter lives. What we needed was an explanation for why this was happening: How does early-life stress “get under the skin”?

Enter Michael Meaney, a professor at McGill University who specialized in neurology, stress, maternal care, and gene expression. He had been studying rodents displaying stress dysregulation (SDR), who were over-reactive to stressors and stayed in a stressed-out state longer. He had discovered physiological differences and behavioral problems in rats who’d been deprived of maternal nurturing, which aligned with previous studies, but he also arrived with a brand-new and as yet unpublished finding. He had actually found a biological mechanism—a process that seemed to explain why those who experienced stress early in life had so much trouble thereafter. As he explained what he had learned, we suddenly realized that this was the missing piece of our puzzle.

Meaney’s lab had been studying the link from deficiencies in early nurturing to SDR for some time and had been seeking the underlying biology of why this happened. A chance meeting at a conference with a McGill colleague, Moshe Szyf, provided the inspiration. A pioneer in the growing field of epigenetics, Szyf suggested that an epigenetic change to genes that control the stress system might be worth exploring. Up to this point, nearly all the work on epigenetics had looked at it in terms of normal fetal development—where it plays a major role in controlling how and when genes work—or in response to physical inputs throughout life. The spark here was to explore whether social experiences—in this case, early nurturing—could have a similar effect.

Ordinarily, our stress response system amps up or powers down proportionate to threats we face. If there’s a lion about to pounce, or a man with a gun walking our way, the system releases cortisol, which puts us on high alert. When the threat passes, the cortisol is shut off. Well, it turned out that when Michael’s newborn rats experienced the stress of poor or missing maternal nurturance at a high enough level, something happened that prevented the cortisol from being shut off.

This process is what’s known as an epigenetic change: a gene’s function is altered—either switched on or switched off—by an external factor. In this case, the external factor was extreme childhood stress without comfort, and it caused an epigenetic change called “stress methylation.” Methylation means that a methyl group—a specific type of chemical molecule—has attached itself to the on-off switch that is a part of every gene. In the particular case of stress methylation, the gene whose job it is to tell the HPA axis, which controls the body's response to stress, to stand down—to shut off the flow of cortisol—is silenced. High levels of stress experienced in early life can methylate the key gene that controls this stress system. When this happens, we live as if constantly facing the pouncing lion or the man with the gun.

There it is, I thought, there’s our answer: stress can get under the skin, changing the very way our genes function. I was far from alone in recognizing how this changed the landscape of how to look at early life stress. As my colleague, Clyde Hertzman, who had a penchant for pithy and pointed conclusions, remarked on first hearing about this new social epigenetic story of the biological embedding of SDR in early life: “It’s a way of getting a message to a newborn that it’s a dangerous world out there, so you’d better live hard, live fast, and, very probably, die young.”

The minute we learned of this epigenetic effect we realized the potential implication for understanding not just people at the lower end of social status, but all of us. Clearly, it fit with the social inequality story we had been pursuing for a decade. Low socioeconomic status (SES) as a marker of early life adversity, with the lifelong consequences we had come to understand, was a natural fit for this new story. But it went well beyond that. Difficulties in early nurturing arise from many other sources than economic and social disadvantage. In the modern world, the stresses of managing dual careers or the worries about the hypercompetitive world that one’s children may face can interfere with the kind of nurturing that infants need. At a later point, we learned that this epigenetic change could follow another social pathway: If the mother is hyper-stressed during pregnancy, the same stress methylation can follow. Parents from lower SES groups may have a greater risk of stressful pregnancies or stressed-out early parenting, but it can happen at any level of SES—which was entirely consistent with our findings on how stress can show up at any level of society: it can happen to anyone.

Our team was not alone in grasping the profound implications of this dramatic new science; soon researchers around the world joined this exploration, revolutionizing the way we look at child development. We can say with certainty that stress can change the way our genes work, with consequences across the lifespan. And beyond. It turns out that this epigenetic change—which doesn’t affect the DNA at all—can be passed down to the next generation; this has been found in animal studies, but there is recent evidence that it happens to us, too. This remarkable finding means that the social experience of early adversity can make a change that becomes part of our biology—and part of our biological inheritance: nurture becoming nature.