Inflammation, Social Disadvantage, and Heart Disease Risk in Women

A groundbreaking study reveals how chronic inflammation links social deprivation, aging, and increased heart disease risk in women, offering new avenues for targeted prevention.
Recent research from King's College London, in partnership with the University of Nottingham, highlights the significant role of chronic inflammation in connecting frailty, social deprivation, and increased cardiovascular disease (CVD) risk among women. The study, published in Communications Medicine, suggests that persistent low-grade inflammation, often called "inflammaging," may serve as a biological link between aging, social inequality, and health outcomes.
Frailty, characterized by a decline in physical resilience with age, is associated with a higher likelihood of developing health issues such as heart disease. It has been observed that individuals living in socioeconomically deprived areas or experiencing social disadvantages tend to be more frail and at greater risk of cardiovascular problems. However, the biological pathways underlying these associations were not fully understood.
To explore this, researchers analyzed blood samples from over 2,000 women aged 37 to 84 years, all part of the TwinsUK cohort. They examined 74 inflammation-related proteins to understand how these markers relate to frailty, area-level deprivation, and cardiovascular risk. Their findings revealed ten inflammatory proteins associated both with social disadvantage and frailty. Notably, four proteins—TNFSF14, HGF, CDCP1, and CCL11—were also linked to a higher likelihood of cardiovascular disease.
In particular, the protein CDCP1 showed a strong association with future heart disease events such as artery blockage or narrowing. These discoveries suggest that specific inflammatory proteins could serve as biological markers connecting social inequality, aging, and cardiovascular health.
The team validated their results in an independent cohort from the Nottingham Osteoarthritis Study, confirming the consistency across different populations. Dr. Yu Lin, the study’s lead author, highlighted that social hardship might trigger harmful inflammation, which over time damages health. The findings open the possibility for novel interventions focusing on reducing inflammation and addressing social inequalities to lower CVD risk.
Furthermore, these inflammation-related proteins could help healthcare providers identify individuals at elevated risk for heart disease, enabling targeted preventive strategies. The researchers are now investigating other factors, such as the gut microbiome, which might influence inflammation and cardiovascular risk, especially in deprived communities where microbial diversity appears lower.
Overall, this research underscores the importance of both social and biological factors in cardiovascular health and suggests that comprehensive approaches integrating medical treatment and social policy could effectively reduce disease burden in vulnerable populations.
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