ArticleTranslational psychiatry2019
A role for vitamin D and omega-3 fatty acids in major depression? An exploration using genomics.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 4 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 4 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- Vitamin D and depression in adults: A systematic review.Biomolecules & biomedicine · 2025Pooled it
- Vitamin D and human health: evidence from Mendelian randomization studies.European journal of epidemiology · 2024Pooled it
- Association of Vitamin D Genetic Risk Score with Noncommunicable Diseases: A Systematic Review.Nutrients · 2023Pooled it
- Applications of Mendelian randomization in psychiatry: a comprehensive systematic review.Psychiatric genetics · 2022Pooled it
- Trial
- Trial
- Supplementation-induced increase in circulating omega-3 serum levels is not associated with a reduction in depressive symptoms: Results from the MooDFOOD depression prevention trial.Depression and anxiety · 2020Trial
- Vitamin D supplementation improves anxiety but not depression symptoms in patients with vitamin D deficiency.Brain and behavior · 2020Trial
- Trial
- Omega-3 fatty acids in mental disorders: from neurobiological and metabolic mechanisms to therapeutic potential.Frontiers in nutrition · 2026Review
- Polyunsaturated fatty acids, APOE genotypes, and dementia incidence and mortality among hypertensive adults.The journal of prevention of Alzheimer's disease · 2025Article
- Genetically determined physical activity levels, sedentary behaviours, and their association with the risk of age-related macular degeneration.The Journal of international medical research · 2025Article
- The metabolome-wide signature of major depressive disorder.Molecular psychiatry · 2024Article
- Article
- Effects of Dietary Fiber, Phenolic Compounds, and Fatty Acids on Mental Health: Possible Interactions with Genetic and Epigenetic Aspects.Nutrients · 2024Review
- Omega-3 fatty acids and major depression: a Mendelian randomization study.Translational psychiatry · 2024Article
- The causal relationship between physical activity, sedentary time and idiopathic pulmonary fibrosis risk: a Mendelian randomization study.Respiratory research · 2023Article
- Metabolomic Investigation of Major Depressive Disorder Identifies a Potentially Causal Association With Polyunsaturated Fatty Acids.Biological psychiatry · 2023Article
- Shared genetic basis informs the roles of polyunsaturated fatty acids in brain disorders.medRxiv : the preprint server for health sciences · 2023Article
- Systematic comparison of Mendelian randomisation studies and randomised controlled trials using electronic databases.BMJ open · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Trials testing the effect of vitamin D or omega-3 polyunsaturated fatty acid (n3-PUFA) supplementation on major depressive disorder (MDD) reported conflicting findings. These trials were inspired by epidemiological evidence suggesting an inverse association of circulating 25-hydroxyvitamin D (25-OH-D) and n3-PUFA levels with MDD. Observational associations may emerge from unresolved confounding, shared genetic risk, or direct causal relationships. We explored the nature of these associations exploiting data and statistical tools from genomics. Results from genome-wide association studies on 25-OH-D (N = 79 366), n3-PUFA (N = 24 925), and MDD (135 458 cases, 344 901 controls) were applied to individual-level data (>2000 subjects with measures of genotype, DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th edition) lifetime MDD diagnoses and circulating 25-OH-D and n3-PUFA) and summary-level data analyses. Shared genetic risk between traits was tested by polygenic risk scores (PRS). Two-sample Mendelian Randomization (2SMR) analyses tested the potential bidirectional causality between traits. In individual-level data analyses, PRS were associated with the phenotype of the same trait (PRS 25-OH-D p = 1.4e - 20, PRS n3-PUFA p = 9.3e - 6, PRS MDD p = 1.4e - 4), but not with the other phenotypes, suggesting a lack of shared genetic effects. In summary-level data analyses, 2SMR analyses provided no evidence of a causal role on MDD of 25-OH-D (p = 0.50) or n3-PUFA (p = 0.16), or for a causal role of MDD on 25-OH-D (p = 0.25) or n3-PUFA (p = 0.66). Applying genomics tools indicated that shared genetic risk or direct causality between 25-OH-D, n3-PUFA, and MDD is unlikely: unresolved confounding may explain the associations reported in observational studies. These findings represent a cautionary tale for testing supplementation of these compounds in preventing or treating MDD.
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Registered trials
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