Lifestyle

Your Neighborhood May Be Aging You At The Cellular Level

Researchers have determined that neighborhood conditions may be driving aging at the cellular level.

Their study in Social Science and Medicine finds that people living in neighborhoods with fewer social and economic opportunities such as jobs and stable housing are more likely to have an abundance of CDKN2A RNA, a measure of cellular aging.

This article was written by Rachel Harrison and originally published by Futurity.

“Our health is shaped not only by individual behaviors, but also by the environments we live in,” says Mariana Rodrigues, a PhD student at New York University’s School of Global Public Health and the study’s first author.

“This study suggests that structural conditions may become biologically embedded and influence aging processes over time.”

Neighborhood factors such as green spaces, clean air, jobs, well-resourced schools, and affordable housing can influence our well-being. Studies show that people living in areas lacking these opportunities have a higher risk of chronic disease and shorter life expectancies, but less is known about the impact on health and aging at a cellular level.

As cells age, they stop dividing but remain metabolically active and secrete substances that fuel inflammation. These cellular changes are connected to frailty and aging-related diseases. Measures of cellular senescence—an indicator of biological aging—include: CDKN2A RNA abundance, which is involved in halting cell division; DNA damage response, reflecting genomic instability; and senescence-associated secretory phenotypes, which activate inflammatory pathways.

To understand the connection between neighborhood factors and cellular aging, the researchers analyzed data from 1,215 American adults in the Midlife in the United States (MIDUS) study, including blood samples measuring four molecular markers of cellular aging. They also assessed neighborhood opportunity based on a participant’s census tract using the Childhood Opportunity Index 3, which calculates 44 location-specific measures of education (e.g., test scores and graduation rates), health and environment (e.g., air and water quality, walkability, and health insurance coverage), and social and economic resources (e.g., employment, homeownership, and income).

The researchers found that people living in low-opportunity neighborhoods had significantly elevated CDKN2A RNA, even after accounting for other socioeconomic, health, and lifestyle factors. The association between neighborhood opportunity and CDKN2A expression was strongest for social and economic factors, meaning that cellular senescence may be driven by a neighborhood’s lower social and economic opportunity rather than by a lack of education, health, or environmental factors.

“Stressors related to income, jobs, and housing are not occasional, but persistent conditions that shape daily life,” says Adolfo Cuevas, associate professor of social and behavioral sciences at NYU School of Global Public Health and the study’s senior author.

“Our findings suggest that chronic stress caused by economic deprivation and limited mobility may be the primary driver of cellular aging.”

The researchers hope that future studies will hone in on community-related factors that could buffer against health risks and continue to examine how neighborhood conditions influence aging over time, which could help pinpoint critical windows of exposure.

However, they note that many environmental factors that influence health are structural—”not things we can fix as individuals, but rather, what we should be addressing as a society,” noted Rodrigues.

“Improving neighborhood conditions, particularly social and economic resources, may be important for promoting healthy aging and reducing health disparities, but if we really want to address health disparities and improve health for everyone, it’s important to consider what needs to be changed at the structural level,” says Rodrigues.

Additional study authors are from the NYU School of Global Public Health as well as the University of California, Los Angeles.

Support for this work came from the National Institute of Diabetes and Digestive and Kidney Diseases.

Source: New York University

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