Hot off the Press: Early Childhood Adversity and the Accelerated Epigenetic Clock

Feb 21

For decades, people have wondered how biology interacts with life experiences to shape long-term health. One of the ways that “nature” and “nurture” are thought to come together is through the epigenome. The epigenome is the term used to describe the heritable chemical modifications that can occur to DNA and that can affect gene functioning.

Scientists hypothesize that the chemical “marks” left on our epigenome may be the result of our life experiences, including exposure to childhood adversity. As we describe in a previous blog post, childhood adversities can cause serious trauma and stress in the early stages of life.

In this “Hot off the Press” blog post, we summarize the results of a recent paper examining the connection between exposure to early childhood adversity and a relatively new measurement tool based on the epigenome called the epigenetic clock. The paper was recently published in Psychoneuroendocrinology and is entitled: Adversity exposure during sensitive periods predicts accelerated epigenetic aging in children

What is the epigenetic clock?

Normally, age is calculated by counting the days or years since your birthday. This is referred to as your chronological age. The epigenetic clock is designed to predict your age based on a set of epigenetic marks, which are thought to capture the cellular aging process of cells. When a person’s epigenetic clock runs faster than their chronological clock, the thinking is that they might be more at risk for poor health because they are cellularly older than their chronological age.

In this study, we analyzed data from 973 children in the Avon Longitudinal Study of Parents and Children (ALSPAC). Our goal was to answer four mains questions about the relationship between exposure to childhood adversity and the epigenetic clock.

Figure 1. How life experiences can shape biology. Here we show how environmental factors can lead to the addition of chemical tags (here, shown as flags) that are added to the DNA sequence. The addition of these chemical tags changes how our genes function, causing them to turn on or off. These changes in gene functioning can have different biological consequences

What did we find? Let’s unpack it!

1. Is there a link between exposure to different types of adversity and accelerated epigenetic aging? In other words, are kids who are exposed to adversity cellularly older than their unexposed peers?

We found that the epigenetic age, of children who experienced sexual or physical abuse when they were young (at the age of 3), was accelerated as compared to children who were unexposed. Specifically, these children were cellularly older by about 1 month. Similarly, we found that financial hardship or neighborhood disadvantage at age 7 was also associated with epigenetic age acceleration by about one month. Although one month may not seem like a lot, keep in mind that these are children. Interestingly, these results are also consistent with other studies(Lawn et al., 2018) looking at epigenetic aging in adulthood.

2. For each type of adversity, did timing matter? In other words, how did the age at exposure to adversity influence epigenetic aging?

We saw that there were two periods in early and middle childhood when adversity was particularly impactful. During this sensitive period, the connection between adversity and epigenetic age was stronger than other time periods, indicating that the age when children are exposed to adversity matters. Specifically, we found that this sensitive period model fits best at two separate age groups and for separate sets of exposures. At age three and a half years old, in children exposed to sexual or physical abuse, a sensitive period was found. At seven years old, in children exposed to financial hardship and neighborhood disadvantage, a sensitive period was found.

3. Is this sensitive period affected by the accumulation of events over time or to the recency of the event?

After seeing evidence for these sensitive periods, we wondered if these results might actually be explained by other aspects of time. In other words, was it possible that more recently-occurring exposures were more harmful? Or that children who were exposed more often had worse epigenetic aging scores? In digging into these possibilities, we found that the association between exposure to three types of adversities (abuse, financial hardship, and neighborhood disadvantage) and epigenetic age acceleration was indeed best explained by a sensitive period and not by these other aspects of time.

4. How does all of this stuff play-out for boys and girls? Are they similar or different in terms of their response to adversity?

We split our sample into two (485 boys and 488 girls) and then ran the analysis again. These results showed that adversity could affect epigenetic age acceleration in boys and girls differently. For example, we found that by age 7, girls who were exposed to abuse were epigenetically older than their unexposed peers by 2 months. This finding does not conflict with the results described above, but it does suggest that these results might be stronger for girls.

Take away:

We think this paper helps to shed light on how adversity and experiences of hardship can “get under the skin” or become biologically apart of us. It is also important in showing that when these experiences happen may be particularly important. If these results replicate in other studies, they suggest that intervention strategies occurring before or during sensitive periods in development could be a helpful approach to prevent the development of mental health problems and other disorders as early in life as possible.

Erin Dunn