Black boys facing chronic adversity show signs of early genetic aging

A new study finds that certain genetic variations influence how much childhood poverty shortens and frays the ends of chromosomes called telomeres.
(Christina House / For the Los Angeles Times)

By the time they have reached the fourth grade, African American boys who have run a childhood gantlet of poverty, shifting family structure, harsh parenting and a mother’s low mood and educational attainment will have signs of premature genetic aging that can deepen their vulnerability to mental and physical illness, says a new study.

And the toll of environmental stresses on a child’s cells is even more pronounced when that child has inherited a constellation of genetic variations that make him more sensitive to privation or privilege, the authors of this new research have found.

The latest research underscores that poverty exacts its wages on a person’s health early and at the most profound levels. The authors of the study looked at the telomeres -- the string of regular gene sequences that sit at the tail end of an individual’s chromosomes -- of 40 9-year-old African American boys. The boys were drawn from a larger study and represented two extremes: half came from the poorest, most splintered African American families in which harsh parenting and maternal depression were present; the other half came from the study’s most affluent African American families, in which family stability, nurturing care and maternal mental health were the order of the day.

Sometimes called a “mitotic clock,” telomeres grow a tiny bit more ragged each time a cell divides -- a process that is sped up by illness, stress and chronic adversity. Like the ends of a shoelace, a newborn’s telomeres start long and clean and strong, but grow ragged with wear and tear. The length and integrity of an individual’s telomeres are increasingly seen as a signpost of his or her genetic age and susceptibility to a broad range of illnesses.


Existing research has drawn a line between environmental stresses and shorter, more frayed telomeres. But the current study appears to be the first to establish that certain genetic variations will exaggerate (or mitigate) the fraying effects of social hardship in childhood on an individual’s telomere length.

Researchers looked at genetic variations that influence the production and activity of two key neurochemicals -- dopamine and serotonin -- which play important roles in a variety of things, including mood, heart health, metabolism, movement and motivation. When the boys had two or more of the genetic variations checked by researchers, their telomeres were more dramatically shortened by the experience of childhood adversity. Those same variations made children of relative affluence and stability even more sensitive to the positive effects of their circumstances. Relative to children without the “sensitizing” genetic variation, the telomeres of children who had it maintained extra length and integrity.

The study, published Monday in the journal PNAS, also offers insight into the range of environmental factors linked to poverty that corrode a child’s health. The latest study shows that low family income relative to needs had the most indisputable effect on telomere length. But it also demonstrates that the child who weathers one or more instances of family splintering is likely to have measurably shortened telomeres, and that a mother’s education has a measurable effect in both directions: When mom has completed high school or done some college work, her 9-year-old son was likely to have longer, more intact telomeres; when she left school before completing 12th grade, her child’s telomeres were markedly shorter.