Telomeres: harsh childhood 'makes chromosomes age early'

One implication of study could be that chronic stress in early life could lead to shorter-than-expected lifespan for some boys

Steve Connor
Tuesday 08 April 2014 18:59
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Children brought up in severely deprived backgrounds are more likely to show ageing in their chromosomes compared to more privileged children, according to a new study
Children brought up in severely deprived backgrounds are more likely to show ageing in their chromosomes compared to more privileged children, according to a new study

Children as young as nine who are brought up in severely deprived backgrounds are more likely to show ageing in their chromosomes compared to more privileged children according to a study suggesting that environmental stress in early life can have long-term impacts on a person's genetic makeup.

A study of 40 African-American boys shows that those who came from socially disadvantaged homes had telomeres - the structural "tips" at the end of the chromosomes - that were on average about 20 per cent shorter than boys from more stable, nurturing backgrounds.

But it also found that the effect depended on the kind of gene variants for neurotransmitters in the brain that the boys had inherited. Some gene variants were linked with significantly shorter telomeres in disadvantaged children but the same gene variants were linked with longer telomeres when the boys came from a more privileged background.

Telomeres generally get shorter with age so one of the implications of the study could be that chronic stress in early life could increase the ageing process and so lead to a shorter-than-expected lifespan for boys with a particular genetic makeup. However, the researchers emphasised that the study only shows an association and has not proved that a deprived childhood directly causes the telomeres to become shorter.

Daniel Notterman of Pennsylvania State University, who led the study published in the Proceedings of the National Academy of Sciences, said that the differences in telomere length between the boys from different social background were exacerbated by the gene variants involved in the production of two chemical "messengers" in the brain, dopamine and serotonin.

"I'm not surprised we found such a relationship and I'm not surprised by the gene interaction. I'm surprised by the magnitude of the association," Dr Notterman said.

The shortening of the telomeres by the age of nine may not be irreversible and the findings support the idea of early intervention to stop any long-lasting damage to a child's health and wellbeing in later life, Dr Notterman said.

"The demonstration that telomere length is shortened by age nine supports the idea of early intervention," he said.

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