Most of us have fond memories of our childhood homes, so it’s hard to imagine the lives of less fortunate kids. But far too many youngsters spend their earliest years in homes that are ravaged by poverty and neglect. Many of these children are physically and emotionally abused by parents who are at their wits’ end, who quarrel and drink and sometimes disappear or turn to crime. These parents’ demons take over the home, leaving little room for nurturance and love.
Life is doubly unfair for these neglected and abused kids, because they are also much more likely to continue suffering as adults. Early adversity is strongly linked to later, chronic inflammation, a biological process implicated in a number of serious adult diseases, like heart disease. It’s assumed that childhood stress is the culprit, but the pathways from adversity to disease remain a mystery. Scientists have been trying to understand this connection, in hopes that they and intervene and salvage these kids’ lives.
Psychological scientists call this “getting under the skin”—as in, how do experiences of childhood translate into biological processes that eventually cause illness? Much of the work has focused on what is assumed to be a neurobiological cascade of events, which leads from stress to cellular malfunction of some kind to inflammation. In order to zero in on this crucial link, scientists have been very careful to control for the behavior, so that things like poor eating and smoking don’t skew the insights.
But what about lifestyle itself? Isn’t it possible that the kids’ own smoking and heavy drinking and poor eating habits—as teenagers and beyond—might actually be the pathway—or a pathway—from early misfortune to heart disease? In a way, this seems obvious—that kids from dysfunctional homes would themselves go on to lead unhealthy lives with untoward consequences, but in fact the connection between these lives and inflammation has never been demonstrated. A team of psychological scientists, led by UCLA’s Elizabeth Raposa and involving colleagues at Emory and the University of Queensland, Australia, decided to explore this provocative idea.
To do so, the scientists drew participants from a very large, ongoing longitudinal study of new mothers and their children. The children were selected at age 15 from mostly lower income homes in around Queensland. The mothers had earlier in the study described their home lives, at several points beginning during pregnancy and finally when their children turned five. Childhood adversity was a composite measure that included low family income; parental quarreling; harsh discipline; criminal behavior on the part of either parent; and mother’s psychopathology, primarily depression. The least fortunate of the kids experienced all of this.
The kids themselves described their lives at around age 20. They reported how many cigarettes they smoked on a typical day and how many drinks they consumed. They also completed an inventory of depressive symptoms, and listed any current stressful experiences—problems in romantic relationships, financial woes, work problems, and so forth.
Finally, somewhere between the ages of 22 and 25, all the subjects provided blood samples. The scientists were looking for two key indicators of chronic inflammation—one called CRP and the other TNF. The scientists also measured the subjects’ height and weight, so they could calculate their Body Mass Index, or BMI.
The results were striking. As described in an article to appear in the journal Psychological Science, the kids who had experienced the worst adversity before age five went on to be heavier smokers, which in turn predicted higher levels of TNF in early adulthood. Similarly, these unfortunate kids were more likely to be overweight or obese as young adults, and unhealthy weight in turn was linked to higher levels of both inflammation markers. What’s more, the kids with the worst lives went on to lead more stressful lives as adults, and this continuing stress appeared to explain their unhealthy lifestyles, at least in part.
There were some surprises. For one, drinking does not seem to be a pathway from lousy home life to inflammation and disease. It’s possible that clinical levels of alcohol abuse might play such a role, but this study didn’t sort that out. Also, although adversity did lead to a lot of depression in adulthood, depression had a negligible effect on inflammation. Finally, the scientists found no direct connection between early adversity and inflammation, though that may be because the subjects were still quite young. It’s possible, they say, that the expected cascade of biological effects, leading directly from adversity to inflammation, simply did not yet have time to do its damage at the cellular level.
Taken together, these findings highlight an important and previously unreported link between early misfortune, unhealthy living and serious health risks in early adulthood. It’s not to suggest that this is the only mechanism at work, but these hopeful findings identify actual behavioral targets. The ultimate goal is to eradicate the poverty and other social conditions that darken kids’ lives, but these findings suggest interventions that could save lives now.
Follow Wray Herbert’s reporting on psychological science in The Huffington Post and on Twitter at @wrayherbert.