Perceived psychosocial stressors and inflammatory biomarkers among urban-dwelling older Black adults.

BACKGROUND

Older Black adults experience a high prevalence of cardiovascular conditions and psychosocial stress, both linked to systemic inflammation. However, few studies have examined their combined influence. We tested whether associations between psychosocial stressors (PS) and cardiovascular conditions are linked to inflammatory proteins in older Black adults.

METHODS

We quantified 92 proteins in blood from 642 older Black adults. Cardiovascular burden and PS (financial burden, perceived stress, and discrimination including unfair treatment and personal rejection subscales) were assessed. Linear models tested associations between each PS and protein, adjusting for cardiometabolic factors, demographics, and interactions. An exploratory false discovery rate adjustment was applied (q < 0.10).

RESULTS

Participants had a mean age of 75 years (SD = 6.4) and 15 years of education (SD = 3.3); 19.3% were men. Cardiovascular burden included BMI (mean = 30.6, SD = 6.4 kg/m2), hypertension (80.1%), type 2 diabetes (25.1%), and heart disease (6.8%). Median stress scores were: financial burden = 5 (IQR = 4-6), discrimination = 1 (IQR = 0-2) [unfair treatment = 0 (IQR = 0-1), personal rejection 0 (IQR = 0-1)], and perceived stress 0.75 (IQR = 0.25-1.25). Several proteins were associated with BMI, hypertension, and type 2 diabetes. PS effects depended on cardiovascular burden: financial burden × heart disease (11 proteins), discrimination × heart disease (20 proteins), unfair treatment × heart disease (14 proteins), and discrimination × BMI (1 protein, HGF). We found one significant interaction for IL-17C when exploring financial burden × sex interactions. No other main effects or interactions were significant. Exploratory network analyses suggested coordinated immune signaling; pathway enrichment was not significant.

CONCLUSIONS

The effects of psychosocial stress-inflammation associations are complex and may depend on cardiovascular burden. Replication is needed to establish temporality and clinical relevance.