Yang Guangli, Zhang Siyuan, Wang Yanhe, Han Bingyu, Sun Dongsheng
Department of General Surgery, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Department of Neurology, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
BMC Public Health. 2025 Sep 30;25(1):3161. doi: 10.1186/s12889-025-24346-z.
Evidence on the association between viral hepatitis, particularly hepatitis B and C, and depressive symptoms remains limited. This cross-sectional study aimed to evaluate this relationship.
We analyzed data from the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2018. HBV or HCV infections were identified through serological testing, and depressive symptoms were measured using the Patient Health Questionnaire-9 (PHQ-9). Weighted multivariable logistic regression models were used, with additional subgroup and interaction analyses. Additionally, viral hepatitis was categorized as never infected, previously infected, or actively infected to compare risks by infection status.
Among 25,635 participants, 456 had HBV or HCV infection. Compared with uninfected individuals, those with viral hepatitis had higher odds of depressive symptoms (OR = 1.72, 95% CI: 1.22-2.43). When depressive symptoms were categorized by severity, viral hepatitis was associated with mild (OR = 1.46, 95% CI: 1.01-2.10), moderate (OR = 1.96, 95% CI: 1.25-3.09), and severe depression (OR = 1.74, 95% CI: 1.08-2.81). Viral hepatitis was also associated with higher PHQ-9 scores (β = 1.06, 95% CI 0.36-1.77). No significant effect modification was detected across age, sex, race/ethnicity, education level, marital status, poverty-income ratio, body mass index, smoking status or alcohol use (all p for interaction > 0.05). When infection status was further stratified, only active infection was significantly associated with depressive symptoms (OR = 1.67, 95% CI: 1.19-2.33).
Viral hepatitis was independently associated with depressive symptoms, and this relationship was driven primarily by active infection. As causality cannot be inferred from cross-sectional data, longitudinal studies are warranted.