Epigenetics Offer Hope For Children | Child & Family Blog

Epigenetics offer hope for disadvantaged children

By Michael Meaney and , | October 2014 

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.


 Zhang T-Y & Meaney M (2010), Epigenetics and the environmental regulation of the genome and its function, Annual Review of Psychology, 61

 Yehuda R et al. (2014), Influences of maternal and paternal PTSD on epigenetic regulation of the glucocorticoid receptor gene in holocaust survivor offspring, American Journal of Psychiatry, 171.8

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