Accelerated biological aging (GOLD BioAgeDiff) and depressive symptoms in US adults: NHANES 2005–2018

Apr 5, 2026Journal of affective disorders

Faster biological aging linked to depression symptoms in US adults (2005-2018)

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Abstract

Among 14,318 adults, each 1-SD increase in GOLD BioAgeDiff (≈5.05 years) was associated with higher odds of moderate-to-severe depressive symptoms.

Higher GOLD BioAgeDiff was linked to greater depressive symptom burden, as indicated by increased odds of moderate-to-severe symptoms.
In the primary analysis, each standard deviation increase in GOLD BioAgeDiff corresponded to an odds ratio of 1.14 for moderate-to-severe depressive symptoms.
The association between GOLD BioAgeDiff and depressive symptoms decreased when adjusting for cardiometabolic factors.
GOLD BioAgeDiff was also correlated with higher continuous PHQ-9 scores, indicating more severe depressive symptoms.
Exploratory analyses suggested potential differences in the association based on coronary heart disease and smoking status.

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BACKGROUND: Accelerated biological aging may link depressive symptoms with broader somatic morbidity, yet associations with mortality-validated phenotypic aging metrics remain understudied. We examined the association between Gompertz Law-Based Biological Age Difference (GOLD BioAgeDiff) and depressive symptoms in U.S. adults.

METHODS: NHANES 2005-2018 participants (≥18 years) with complete PHQ-9 and biomarker data were analyzed. GOLD BioAgeDiff was defined as biological age minus chronological age. Survey-weighted logistic regression evaluated moderate-to-severe depressive symptoms (PHQ-9 ≥10), and linear regression evaluated continuous PHQ-9 scores. Primary models adjusted for sociodemographic and behavioral factors; fully adjusted models additionally included BMI, physical activity, diabetes, and coronary heart disease.

RESULTS: Among 14,318 adults, 1228 had PHQ-9 ≥10. Each 1-SD increase in GOLD BioAgeDiff (≈5.05 years) was associated with higher odds of moderate-to-severe depressive symptoms in the primary model (OR 1.14, 95% CI 1.06-1.24; P = 0.001), attenuated in the fully adjusted model (N = 13,760; OR 1.09, 95% CI 1.00-1.19; P = 0.063). GOLD BioAgeDiff was also associated with higher PHQ-9 scores (primary β = 0.25, 95% CI 0.14-0.36; P < 0.001; fully adjusted β = 0.15, 95% CI 0.04-0.26; P = 0.009). Spline analyses showed borderline evidence of deviation from linearity in the primary model (P = 0.067) but no evidence supporting nonlinearity in the fully adjusted model (P = 0.396). Exploratory subgroup analyses suggested possible heterogeneity by CHD and smoking status.

LIMITATIONS: Cross-sectional design limits temporality and causal inference.

CONCLUSIONS: Higher GOLD BioAgeDiff was associated with greater depressive symptom burden. Estimates were attenuated after cardiometabolic adjustment, and subgroup findings require cautious interpretation and longitudinal confirmation.

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Accelerated biological aging (GOLD BioAgeDiff) and depressive symptoms in US adults: NHANES 2005–2018

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