Journal of psychiatric research · 2026
Association between C-reactive protein and depression among alcohol users in the United States: A population-based analysis of National Health and Nutrition Examination Survey (NHANES) 2015-2020.
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Rita-Venugopal Lekshmi, Varghese M Tom, Kc Madhav
Аннотация
BACKGROUND: Inflammation and alcohol use are linked to depression, but whether their effects are independent or interactive remains unclear.
OBJECTIVE: To examine inflammation as an independent correlate of depression among U.S. adults who consume alcohol and a modifier of the alcohol-depression association.
METHODS: Cross-sectional analysis of NHANES 2015-2020 including adults aged ≥18 reporting past-year alcohol use(n = 3019). Depression was assessed using the PHQ-9, with scores categorized as no depression(0), minimal(1-4), mild(5-9), and moderate-severe(10-27). Inflammation was measured using high-sensitivity CRP, categorized as low(≤1 mg/L), average(1-3 mg/L), and high(>3 mg/L). Alcohol use was classified as light, moderate, or heavy based on drinks/week and binge frequency. Modified Poisson regression with robust variance estimated prevalence ratios for depressive symptoms across CRP levels, adjusting for covariates (alcohol severity, age, sex, race/ethnicity, income, BMI, smoking, physical activity, sleep, comorbidities, drug use). Survey-weighted GLM models tested CRP-alcohol interactions.
RESULTS: High CRP was associated with 13% higher mild and 22% higher moderate-severe depression prevalence (p < 0.0001) vs. low CRP. CRP-alcohol interactions were statistically significant with high CRP associated with increased depression prevalence among light drinkers (PR = 1.06,95% CI:1.05-1.07) and moderate drinkers (PR = 1.03,95% CI:1.01-1.04). Among heavy drinkers, high CRP showed an 8.2% increase, not statistically significant, likely due to limited power and dilution by acute inflammation. Sensitivity analyses excluding CRP >10 mg/L showed stronger effects (6-11% increase); high CRP × heavy drinking became significant (PR = 1.11,95% CI:1.05-1.18, p < 0.0001).
CONCLUSION: CRP was associated with higher depression and modified alcohol-depression associations. Inflammation amplified depression risk across drinking levels.
OBJECTIVE: To examine inflammation as an independent correlate of depression among U.S. adults who consume alcohol and a modifier of the alcohol-depression association.
METHODS: Cross-sectional analysis of NHANES 2015-2020 including adults aged ≥18 reporting past-year alcohol use(n = 3019). Depression was assessed using the PHQ-9, with scores categorized as no depression(0), minimal(1-4), mild(5-9), and moderate-severe(10-27). Inflammation was measured using high-sensitivity CRP, categorized as low(≤1 mg/L), average(1-3 mg/L), and high(>3 mg/L). Alcohol use was classified as light, moderate, or heavy based on drinks/week and binge frequency. Modified Poisson regression with robust variance estimated prevalence ratios for depressive symptoms across CRP levels, adjusting for covariates (alcohol severity, age, sex, race/ethnicity, income, BMI, smoking, physical activity, sleep, comorbidities, drug use). Survey-weighted GLM models tested CRP-alcohol interactions.
RESULTS: High CRP was associated with 13% higher mild and 22% higher moderate-severe depression prevalence (p < 0.0001) vs. low CRP. CRP-alcohol interactions were statistically significant with high CRP associated with increased depression prevalence among light drinkers (PR = 1.06,95% CI:1.05-1.07) and moderate drinkers (PR = 1.03,95% CI:1.01-1.04). Among heavy drinkers, high CRP showed an 8.2% increase, not statistically significant, likely due to limited power and dilution by acute inflammation. Sensitivity analyses excluding CRP >10 mg/L showed stronger effects (6-11% increase); high CRP × heavy drinking became significant (PR = 1.11,95% CI:1.05-1.18, p < 0.0001).
CONCLUSION: CRP was associated with higher depression and modified alcohol-depression associations. Inflammation amplified depression risk across drinking levels.