HEALTH NEWS

Study Title:

Early Life Stress and Disease Risk

Study Abstract

Children reared in unfavorable socioeconomic circumstances show increased susceptibility to the chronic diseases of aging when they reach the fifth and sixth decades of life. One mechanistic hypothesis for this phenomenon suggests that social adversity in early life programs biological systems in a manner that persists across decades and thereby accentuates vulnerability to disease. Here we examine the basic tenets of this hypothesis by performing genome-wide transcriptional profiling in healthy adults who were either low or high in socioeconomic status (SES) in early life. Among subjects with low early-life SES, there was significant up-regulation of genes bearing response elements for the CREB/ATF family of transcription factors that conveys adrenergic signals to leukocytes, and significant down-regulation of genes with response elements for the glucocorticoid receptor, which regulates the secretion of cortisol and transduces its antiinflammatory actions in the immune system. Subjects from low-SES backgrounds also showed increased output of cortisol in daily life, heightened expression of transcripts bearing response elements for NF-κB, and greater stimulated production of the proinflammatory cytokine interleukin 6. These disparities were independent of subjects' current SES, lifestyle practices, and perceived stress. Collectively, these data suggest that low early-life SES programs a defensive phenotype characterized by resistance to glucocorticoid signaling, which in turn facilitates exaggerated adrenocortical and inflammatory responses. Although these response patterns could serve adaptive functions during acute threats to well-being, over the long term they might exact an allostatic toll on the body that ultimately contributes to the chronic diseases of aging.

From press release:

People’s early-life experience sticks with them into adulthood and may render them more susceptible to many of the chronic diseases of aging, according to a new University of British Columbia study.

A team led by UBC researchers Gregory Miller and Michael Kobor performed genome-wide profiling in 103 healthy adults aged 25-40 years.

Those who participated in the study were either low or high in early-life socioeconomic circumstances related to income, education and occupation during the first five years of life. But the two groups were similar in socioeconomic status (SES) at the time the genome assessment was performed and also had similar lifestyle practices like smoking and drinking habits.

Their study, to be published in the Proceedings of the National Academy of Sciences, shows that among subjects with low early-life socioeconomic circumstances, there was evidence that genes involved with inflammation were selectively “switched-on” at some point. Researchers believe this is because the cells of low-SES individuals were not effectively responding to a hormone called cortisol that usually controls inflammation.

“We’ve identified some ‘biologic residue’ of people’s early-life experience that sticks with them into adulthood,” says Miller, an associate professor in the Department of Psychology and a member of the Brain Research Centre at UBC Hospital.

“The study suggests that experiences get under the skin,” says Kobor, an assistant professor in the UBC Department of Medical Genetics and a scientist at the Centre for Molecular Medicine and Therapeutics at the Child & Family Research Institute.

This pattern of responses might contribute to the higher rates of infectious, respiratory, and cardiovascular diseases as well as some forms of cancer among people who grow up in low-SES households, according to the interdisciplinary research team that also includes scientists from the University of California, Los Angeles.

“It seems to be the case that if people are raised in a low socioeconomic family, their immune cells are constantly vigilant for threats from the environment,” says Miller. “This is likely to have consequences for their risk for late-life chronic diseases.”

Study Information

Gregory E. Miller, Edith Chen, Alexandra K. Fok, Hope Walker, Alvin Lim, Erin F. Nicholls, Steve Cole, and Michael S. Kobor
Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling.
Proceedings of the National Academy of Sciences.
2009 July
University of British Columbia