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Inflammation may link frailty to heart disease

Chronic inflammation may help explain how frailty and social deprivation increase the risk of heart disease in women, researchers have suggested.

The findings could support more targeted efforts to reduce cardiovascular risk in vulnerable groups.

Researchers from King’s College London and the University of Nottingham analysed blood samples from more than 2,000 women aged 37 to 84 who are part of the TwinsUK cohort.

They examined 74 inflammation-related proteins to explore how frailty, area-level social deprivation and cardiovascular disease may be biologically connected.

The team identified ten proteins associated with both frailty and living in deprived areas. Four of these – TNFSF14, HGF, CDCP1 and CCL11 – were also linked to an increased risk of heart disease.

One protein in particular, CDCP1, was strongly associated with future cardiovascular events such as blocked or narrowed arteries.

Dr Yu Lin is research associate in the Department of Twin Research & Genetic Epidemiology at King’s College London.

The researcher said: “To better understand how frailty and deprivation contribute to heart disease, we took a data-driven approach, screening a large number of inflammatory proteins in the blood.

“By identifying overlapping biological markers linked to both social and health vulnerability, we were able to uncover a potential shared pathway between these risk factors.”

Frailty is a clinical condition defined by the body’s reduced ability to recover from physical or medical stress.

Previous studies have shown that people who are frail or living in disadvantaged areas tend to experience poorer cardiovascular outcomes.

The biological pathways connecting these risks have remained unclear.

This research suggests that certain inflammatory proteins may form a biological link between social inequality, ageing and heart disease.

Dr Cristina Menni is senior lecturer in molecular epidemiology at King’s College London.

She said: “Frailty, social disadvantage and heart disease often go hand in hand, but the biological mechanisms linking them are not yet fully understood.

“Our findings suggest that the stress of socioeconomic hardship may trigger harmful inflammation that damages health over time.

“If confirmed, this could open up new ways to prevent disease, not only through medical treatments that reduce inflammation, but also through social policies that address health inequalities.”

The findings were validated in a separate group of women from the Nottingham Osteoarthritis Study to confirm consistency across different populations.

The proteins identified could serve as biomarkers to help clinicians detect those at greater cardiovascular risk.

The study supports combining clinical strategies to reduce inflammation with wider policy changes aimed at tackling inequality.

The research team now plans to explore how other factors – such as gut microbiome composition – may influence inflammation and cardiovascular risk.

Early evidence suggests that people in deprived areas may have lower gut microbial diversity, which could contribute to chronic inflammation.

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