Vitamin D deficiency, depression severity, and suicide risk: evidence from patients with major depressive disorder
Background/aim Major depressive disorder (MDD) is a common psychiatric condition characterized by depressive symptoms and suicide-related clinical features. Vitamin D status has been investigated as a potential clinical correlate of depression and suicidal ideation, but the direction and specificity of these associations remain uncertain. This cross-sectional study aimed to examine the associations among serum 25-hydroxyvitamin D [25(OH)D] levels, depressive symptom severity, suicidal ideation, and suicide-related cognitive–affective dimensions in adults diagnosed with MDD. Materials and methods This cross-sectional study included 97 adults aged 18–65 years who were diagnosed with MDD according to DSM-5 criteria. Depressive symptom severity and suicide-related outcomes were assessed using the Hamilton Depression Rating Scale (HDRS), Suicidal Ideation Scale (SIS), and Suicide Probability Scale (SPS). Vitamin D status was classified as deficient (<20 ng/mL), insufficient (20–29 ng/mL), or sufficient (≥30 ng/mL). Associations were examined using multivariable generalized linear models adjusted for available sociodemographic and clinical covariates. Results Vitamin D deficiency was observed in 61.9% of participants and the mean serum 25(OH)D level was 18.4 ± 11.9 ng/mL. Lower serum 25(OH)D levels were significantly associated with higher HDRS, SIS, and SPS total/subscale scores. In adjusted models, higher serum 25(OH)D levels remained inversely associated with HDRS scores, SIS scores, and total SPS scores. Parental status was also associated with lower SIS scores, while a history of suicide attempts was associated with higher SPS–Suicidal Ideation scores. Conclusion Lower serum 25(OH)D levels were associated with greater depressive symptom severity and higher suicide-related scale scores in adults with MDD, particularly across cognitive–affective domains relevant to suicide probability. However, given the study’s cross-sectional single-center design, absence of a healthy control group, modest sample size, and adjustment limited to available covariates, these findings should be interpreted as associations rather than evidence of causality, directionality, or established biomarker utility.