Innovation Ecosystem

A deep dive into early life adversity

Researcher Daniel Keating details what he sees as an epidemic of toxic stress

Photo by Richard Asinof

Dan Keating, left, presenting his talk about the lifelong impact of early adversity at Brown University on May 4.

By Richard Asinof
Posted 5/8/17
Dan Keating delivered a detailed analysis of the latest research on early adverse events and toxic stress and how it has created a stress epidemic in America.
To break the vicious cycle of early adversity, does it require a different approach to medical and social work education around toxic stress? How does identification of epigenetic changes in the brain’s wiring require new kinds of approaches to mental health interventions? Is there a way to begin to address ways to remediate brain danger from lead, mercury and other heavy metals and toxicants? When will interventions to remove lead from housing stock in Rhode Island be seen as one of the most effective interventions to improve reading skills?
While Dan Keating seemed to be very much aware of the research work that Barry Lester has been involved with in epigenetics at Brown, the conversation around toxic stress and early adversity often seems to focus on the practice of good social work interventions to support parenting and nurturing as the best way to break the cycle. Is there a need to broaden the conversation to talk about the diseases of despair and the relationship to addiction? And, to include in the conversation endocrine disruptors and environmental toxicants as a potential major factor in stress dysregulation? Does there need to be some kind of legal intervention to hold corporations, where applicable, to the health costs of such health disruptors, as a way to break the cycle?

PROVIDENCE – The lecture by Daniel Keating on May 4 at Brown University on “The Lifelong Impact of Early Adversity and How To Break the Cycle” was a wonkish look into what Keating described as the vicious circle of early life adversity and stress.

Keating, a professor of Psychology, Psychiatry and Pediatrics at the University of Michigan, spoke in a rapid-fire delivery, attempting to cram a book-length presentation into an hour talk, to an audience of about 50, including students, professors, policymakers and practitioners in the field of early childhood development.

The talk, which was co-sponsored by Brown University and Rhode Island Kids Count, was the 2017 Lipsitt-Duchin Lecture on Child and Youth Behavior Development.

Keating’s talk was followed by a response panel that included Susan Dickstein, a psychologist at Bradley Hospital, and Blythe Berger, the chief of the center for Perintatal and Early Childhood Health at the R.I. Department of Health.

The basic gist of Keating’s presentation was to better understand the connective story around early adverse events, sometimes referred to as toxic stress, and the best ways to intervene to break the vicious cycle.

“The reason we need to understand the mechanism, is that without understanding how the system operates, we won’t know where the points of leverage are for change,” Keating said.

As Keating described the cycle, early life adverse stress leads to bio-embedding and epigenetic changes in the brain, which leads to stress dysregulation, which leads to lifelong harm to developmental health, which leads to social inequity and what he termed “the stress epidemic,” which leads to stress contagion and harsh social environments, and then back to the next generation of early life stress.

The effects of early adversity are pervasive, according to Keating, based upon a growing body of research. It results in childhood problems in development and behavior, deficits in adolescent achievement and health, adult diseases of many types, and a decrease in life expectancy. Worse, according to Keating, is that the effects are portable: they can persist across changing contexts, and they are life-long.

There are multiple pathways, Keating continued, for the effects of adverse events and stress to “get under the skin,” as he described the process.

These include the ways that the brain “listens” to the environment, in what he called neural sculpting, synaptic pruning in early childhood, resulting in life course consequences.

Brains can also “listen” to the environment, causing epigenetic modification of gene expression, citing the work of Brown researcher Barry Lester. [See link to ConvergenceRI story below.]

The research has found that there is a strong potential for transgenerational transmission of stress-related changes, creating what Keating called “an enduring population burden.

In response to the multiple reasons for an infant with what’s termed “social dysregulation” – whether from a high stress pregnancy, epigenetic inheritance, genetic vulnerability, or high stress in early infancy, Keating suggested that research showed that sustained and persistent positive interactions can generate resilience, what he called “supernurturing.”

“A stress dysregulated infant is a difficult infant to raise,” Keating explained. “The standard things that we expect to see as we’re parenting a newborn to bring the infant into a calmer state – maybe they are hungry, or need a diaper change, or they need to be held – and eventually they calm down and are soothed – imagine if you never get to that point. You’re dealing with this infant and you can’t get them out of it.”

Keating suggested that some of the supports for parents with stress dysregulated infants include: co-parenting, allo-parenting from extended family or others, and programs to provide support through high-quality childcare and home visiting.

While the system to respond to stress is essential for survival, excess or toxic levels of stress during pregnancy or an infant’s first year of life can rewire the brain and cause epigenetic changes, according to Keating.

He characterized it as an “environmental” signal that could be encapsulated in the phrase: “Live fast, live hard, as you are likely to die young.”

No magic bullets
Keating cautioned that resilience after early adversity remains a challenge, with no evidence that the stress physiology changes, despite the mitigation and work-arounds. As a result, the research pointed to the need for systemic change that interrupts the cycle at the start.

Based on Centers for Disease Control and Prevention data, Keating postulated that there was evidence of a stress epidemic underway, looking at increases beginning about 1980 in the number of stress-related disorders and diseases, including obesity, diabetes, metabolic and sleep disorders in the 20 percent to 25 percent range. Self-reported data findings, Keating continued, showed a related pattern, increasingly for younger cohorts.

Connections to inequality, low resilience
Keating showed a slide that looked at the difference in countries that had low inequality and high resilience, compared to countries with high inequality and low resilience. The countries in the latter category included Australia, Canada, Ireland, New Zealand, the United Kingdom and the U.S., which Keating suggested might be related to a history of colonialism.

Toxicants as catalysts for stress
In the question and answer period that followed the talk, ConvergenceRI asked Keating about how lead and other toxicants fit into his adverse events model.

Keating replied that the research showed that lead had impacts on cognitive development as well as on regulator capabilities, emotions, attention deficits and behavior regulations.

“I’m pretty persuaded that if you look at the degree of lead in bodies and do an analysis of the changes in violent criminal activity, you get a pretty clear picture,” Keating said, referring the peak of the crime wave in the mid 1990s and its decrease, following the banning of lead in gasoline.

“We are exposing ourselves to an extraordinary number of toxins, about whose effects we just don’t know,” he continued. “The long answer is, boy, it’s complex; let’s try and keep as much of it out of us that we don’t need, right?”

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