Biological science can at last predict vulnerability, allowing families and governments to intervene pre-emptively and effectively.

The US epidemic of childhood mental illness recalls the crisis of Philip Roth’s “Nemesis.” Set in 1944 Newark, Roth’s novel portrays polio inexplicably sweeping the city, particularly the poorer neighborhoods. Today’s childhood mental illnesses—such as depression, anxiety, attention deficit hyperactivity disorder (ADHD) and drug addiction — also hit mainly the disadvantaged. As with polio, no one can predict who will fall victim, who will escape or why. No child, rich or poor, is completely safe from mental illnesses whose transmission mechanisms are only partially understood and whose debilitating impacts are often life-long.

Yet all this could change thanks to better understanding of epigenetics – the process by genes are switched on and off. These studies hold the promise of identifying, early on, which children will probably become mentally ill. Families and governments will then have the opportunity to take pre-emptive, targeted and effective action.

By 1955, identification of the polio virus and introduction of a vaccine put an end to repeated epidemics. Likewise, today, biological science is poised to resolve the apparent randomness of childhood mental illness. The big question is: which children are most vulnerable and why? Tests could soon spot children at risk even before a single symptom appears. As a result, many childhood mental illnesses could, like polio, cease to be unpredictable mysteries that inexplicably afflict some children and not others. Mental illness, once anticipated, could be alleviated through early interventions before it takes hold.

“Tests could soon spot susceptibility before a single symptom is manifest – even in babies. Many childhood mental illnesses, like polio, could soon cease to be unpredictable mysteries. Mental ill-health, once anticipated, could then be alleviated dramatically.”

We now know that childhood adversity, associated often but not always with poverty, can turn genes on and off and thus inhibit healthy responses to stress, leaving children vulnerable to mental illnesses that can last a lifetime. The big breakthrough in epigenetics arises from recent discoveries that these biological effects leave chemical markers, which can be measured simply, even in newborns, by using swabs to collect saliva and a few cells from inside the cheek.

The chain of experiences leading to personal mental illness can be long. Our research has isolated biological markers of mental health vulnerability in blood from the adult offspring of Holocaust survivors, sometimes decades after those survivors died. These markers reveal that this particular trauma affected the mental health not only of the initial victims, but also of their children. The markers in the blood of the offspring generation further show that the legacy can be passed even onto grandchildren – perhaps biologically (we can’t prove this yet) but, highly likely, through living with parents who are themselves not mentally well.

The challenge for intervention programs is to assess the impact of adversity at the level of the individual child – epigenetic measures will likely achieve this goal. The implications of finding these markers for individual children are considerable. First, public agencies can take pre-emptive action to support those most prone to depression, anxiety, ADHD and drug addiction. Better targeting is more efficient and effective, focusing resources on children at risk.

Second, biological information can empower poorer families and communities where stress and childhood adversity, associated with being poor, can seriously compromise brain development. Poverty typically undermines the mental health of parents, imperiling the quality of parental care and thus children’s own mental health. But some children are unaffected. Knowing precisely which ones are at risk can encourage parents to act. Cohesive families, even among the very poorest, can help children to be more resilient, buffering them from mental health risks. Difficult family circumstances need not dictate a child’s destiny. Parents living in even the most impoverished conditions can effectively protect their children. Indeed, the same biological tests that highlight vulnerability could also confirm when good parenting is working and is reducing a child’s mental frailty.

The biological sciences are challenging policy makers and practitioners to spot the vulnerable early and to act swiftly and effectively. Worldwide, the leading health burden is mental illness, not diabetes or heart disease. Many US families – rich and poor — recognize this reality all too readily. And whereas heart disease generally shows some mercy by arriving later in life, mental disorders most commonly appear in later childhood or adolescence, derailing individuals in their prime.

Our next step must be to develop not only effective “markers” of high risk for individual children but to put them into use in community settings or pediatric clinics at pre-school ages. That’s when interventions are most effective. Think of all the polio cases – and the accompanying lifelong tragedies – that have been prevented. We can do this for childhood mental illness.

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Understanding how genes are turned on and off may help us identify the most vulnerable young people and tailor supports that work best for each child.

The gold standard, for those seeking to make real improvement in children’s lives, is to provide the right intervention at the right time in the right place for the right child. But how do you achieve this when children differ so much? There is immense variability not only in their vulnerabilities but also in their susceptibility to support that might be available. The answer is to understand what lies at the root of those vulnerabilities and susceptibilities.

Our research has identified a key, early environmental factor which produces enduring biological changes in brain development and changes in behaviour that are crucial to lifetime outcomes. We have found that the biological process is potentially reversible, holding out considerable hope that children’s lives can be dramatically improved through well-targeted supports. Our findings suggest that social policy could soon be on a par with general medicine in being able to structure help that is appropriate to the needs, biology and responsiveness of each child.

Our central finding is that early parenting styles have a profound and enduring impact on human genes, switching some on and some off in the early years. The reversibility of this process of epigenetics, by which the expression of human genes is influenced by environmental factors, offers options for tailored interventions to engineer more positive outcomes.

“Social policy could soon be on a par with general medicine in being able to structure help that is appropriate to the needs, biology and responsiveness of each child.”

How have we established that switching genes on and off is important in this field of child development? The first clue is that human health is clearly not simply a function of a person’s genetic sequence. Identical twins have more or less the same genetic material, but their health may differ greatly. Something else operates at the genome level. The process is “epigenetic”—the Greek prefix “epi” means “over” or “above”—and signals clinical modifications to genetic material, turning some genes on, silencing others.

The changes that epigenetic signals make are graphically illustrated at the level of human cells. My body produces over 200 cell types, including liver, brain and muscle cell types. Each has exactly the same DNA, yet they look and function very differently. The liver metabolizes glucose, while the brain can play chess. Epigenetic signals have activated different genes in the liver than those in the brain so they can operate differently.

Our research has examined whether environmental conditions can alter the epigenetic signals that control the operation of genetic sequences—the human genome. We studied “Mom”—one of the most influential of all environmental signals. Mom defines one’s environment almost completely until one is born, and she continues to influence experience during the early formative years. We wanted to know whether a mother’s behaviour toward her child alters the epigenetic signals that influence the function of the child’s genome and thus individual differences in personality traits.

We began with the rat, a highly social species. Surprisingly, mother rats differ considerably in the levels of care they afford their offspring. We found that variation in maternal care altered epigenetic signals that control the activity of genes in the rat brain that regulate the stress response. These epigenetic signals are potentially very stable chemically, which helps us understand the biological basis for the enduring influence that parental care seems to exert on development, stress responses and health.

Could these same processes be occurring in humans? We obtained post-mortem tissue from humans, taking the samples from the same brain region as in the rats. We knew the developmental history and status of the humans whose tissue we examined. Our study found that people with a history of early childhood maltreatment showed alteration in these same epigenetic signals on the same genes in the same brain region that we had discovered in the rats.

As I’ve said, the stable chemistry of epigenetic signals help us explain the observation that early social environments seem to persistently influence the function of the brain and individual mental health over a lifespan. However, everything we know about how the environment influences these epigenetic signals would suggest that these signals are reversible. So we examined the evidence by joining studies of programs that focused specifically on improving parental care.

We found that when we looked at people’s cells, we could detect the influence of these treatment programs across the genome even 25 years after their exposure to them. This finding suggests that, although the early social environment has a profound influence, if that environment is restructured, the epigenetic marks are, at least in some sites, plastic and therefore open to social intervention. This issue of reversibility in later life is of paramount importance to those who hope to improve human lives, especially those of children.

Exploring epigenetic signals has also given us insight into human resilience, which is vital in helping us focus treatments on those who really need them. We know that the impact of the environment varies for different people. So, for example, some people who have experienced childhood maltreatment suffer mental depression, whereas others do not. Why? Often, people’s genetic background determines their sensitivity to these environmental conditions. In other words, the impact of an environmental factor on epigenetic signals varies, depending on a person’s genetic makeup. So genes not only affect resilience to adversity, they also influence susceptibility to treatment and support. This fits with considerable evidence that some children, by virtue of their genetic makeup, respond to interventions better than other children.

What does all this add up to? It helps us tackle that crucial challenge: to provide the right intervention at the right time in the right place for the right child. Currently, we tend to target help at children we consider disadvantaged, equating that group with the most vulnerable. But poverty and birth outcome are actually inadequate predictors of well-being long-term. Certainly, poverty is a disadvantage, but many children raised in poverty grow up to enjoy generally healthy outcomes.

To focus simply on environmental conditions, such as poverty, is to cast too wide a net. Our current research is exploring whether epigenetic signals, which reflect the actual impact of adversity at the level of individual children, might be more effective indicators of truly vulnerable individuals. The great virtue of personal assessment using epigenetic signals is that these markers reflect not only levels of environmental influences, but also their interaction with a person’s genetic background. So they might be a better way to capture vulnerability at the level of the individual child.

Acquiring this information is also relatively straightforward. A few cells taken from the inside of the cheek allow us to study epigenetic signals. This research might also help us understand why certain interventions work better with some children and how we might better shape intervention programs to the needs of individuals.

We have already made some progress in this direction. Our first paper on this subject looked at US combat veterans. We were able to show that an epigenetic signal on a gene that regulates stress responses predicted how well psychotherapy would work. We could, in short, use chemical analysis to predict which veterans were likely to get better.

Hopefully, the same approach can be used to predict which treatments work better for which children. Success in this research could mean much better targeting of help, making it more effective. By allowing us to distinguish the vulnerable from the resilient among disadvantaged people, it might also give us better insight into the true impact of support programs. We can also understand better why one size does not fit all children, recognizing that different biology may require different levels of interventions. In summary, we hope in time to be able to provide much more effective support policies for children both financially and in terms of outcomes for the next generation.

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