Favorable adiposity, statins, vitamin D, dried fruit linked to lower ovarian cancer risk in MR meta-analysis

Photo by Markus Spiske / Unsplash

Journal of public health (Oxford, England) Published June 2, 2026 Medically reviewed June 2, 2026 Study authors: Yalew Melaku, Lumsden Amanda L, Mulugeta Anwar, Madakkatel Iqbal, Lee Sang Hong, Oehler Martin K, Mä… PubMed ↗ DOI ↗ By Dr. Julia Lee, PhD · Oncology, Genomics & Drug Development

Key Takeaway

Interpret these MR findings as genetic associations, not causal evidence; do not infer clinical benefit from statins or vitamin D supplementation.

This systematic review and meta-analysis of Mendelian randomization (MR) studies examined the genetic evidence linking various exposures to ovarian cancer risk. The analysis pooled data from multiple MR studies to assess associations between genetically predicted exposures and ovarian cancer.

Key findings include a protective association for favorable adiposity (OR per SD 0.35, 95% CI 0.20-0.61), HMG-CoA reductase inhibitor genetic proxies (OR 0.66, 95% CI 0.53-0.82), serum vitamin D (OR 0.88, 95% CI 0.82-0.95), and dried fruit intake (HR 0.61, 95% CI 0.41-0.91). These associations were all in the direction of lower ovarian cancer risk.

The authors note that while genetic evidence supports these associations, causality is not definitively established. The associations between vitamin D and HMG-CoA reductase inhibition with ovarian cancer risk warrant further study. Importantly, these findings should not be interpreted as evidence that statins or vitamin D supplementation reduce ovarian cancer risk, as only genetic proxy associations were reported. No clinical recommendations can be made from this genetic evidence alone.

Study Details

Study typeMeta analysis

EvidenceLevel 1

PublishedJun 2026

PMID42127414

View Original Abstract ↓

BACKGROUND: Ovarian cancer (OC) remains a major global health issue, often diagnosed late and lacking effective screening. METHODS: MR studies until 11 September 2023 were identified by a systematic search across nine databases. We complied with PRISMA guidelines and included different OC subtypes and all exposures studied, conducting meta-analyses where feasible to combine estimates from non-overlapping samples. RESULTS: We identified 120 articles examining genetic evidence for an association between 230 exposures and OC risk. Endometriosis, late age at menopause, and several adiposity measures were robustly associated with greater OC risk. In contrast, late age at menarche, higher adiponectin, and body fat without adverse metabolic profile were associated with lower risk (favourable adiposity: meta-analysis OR per SD 0.35, 95% CI 0.20-0.61). Meta-analyses on lipid-lowering drug target HMG-CoA reductase inhibitor (OR 0.66, 95% CI 0.53-0.82), serum vitamin D (OR 0.88, 95% CI 0.82-0.95), and dried fruit intake (HR 0.61, 95% CI 0.41-0.91) were supportive of protective associations. CONCLUSIONS: Genetic evidence confirms OC risks associated with endometriosis, and age at menarche and menopause. While greater overall adiposity increases the risk, fat without an adverse metabolic profile appears protective. Associations between vitamin D and HMG-CoA reductase inhibition with OC risk warrant further study.