Evidence map›Paper›PMID 30597039›Full record

ArticleInternational journal of epidemiology2019

Circulating vitamin D concentrations and risk of breast and prostate cancer: a Mendelian randomization study.

Xia Jiang, Niki L Dimou, Kawthar Al-Dabhani, Sarah J Lewis, Richard M Martin, Philip C Haycock, Marc J Gunter, Timothy J Key, Rosalind A Eeles, Kenneth Muir and 12 more

Abstract read
In one paragraph

Article in International journal of epidemiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 6 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. Pooled it
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  7. The double disparity: Vitamin D deficiency and lethal prostate cancer in black men.The Journal of steroid biochemistry and molecular biology · 2025
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  10. Advances in laboratory medicine · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors.

Xia JiangProgram in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Niki L DimouDepartment of Hygiene and Epidemiology, School of Medicine, University of Ioannina, Ioannina, Greece.
Kawthar Al-DabhaniDepartment of Epidemiology and Biostatistics, The School of Public Health, Imperial College London, London, UK.
Sarah J LewisDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Richard M MartinDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Philip C HaycockDepartment of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK.
Marc J GunterNutritional Epidemiology Group, Nutrition and Metabolism Section, International Agency for Research on Cancer, Lyon, France.
Timothy J KeyCancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Rosalind A EelesDivision of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
Kenneth MuirInstitute of Population Health, University of Manchester, Manchester, UK.
David NealNuffield Department of Surgery, University of Oxford, Oxford, UK.
Graham G GilesCancer Epidemiology & Intelligence Division, Cancer Council Victoria, Melbourne, VIC, Australia.
Edward L GiovannucciDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Meir StampferDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Brandon L PierceDepartment of Public Health Sciences, The University of Chicago, Chicago, IL, USA.
Joellen M SchildkrautDepartment of Public Health Sciences, University of Virginia, Charlottesville, VA, USA.
Shaneda Warren AndersenDivision of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Deborah ThompsonDepartment of Public Health and Primary Care, Centre for Cancer Genetic Epidemiology, University of Cambridge, Strangeways Research Laboratory, Worts Causeway, Cambridge, UK.
Wei ZhengDivision of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN, USA.
Peter KraftProgram in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Konstantinos K TsilidisDepartment of Hygiene and Epidemiology, School of Medicine, University of Ioannina, Ioannina, Greece.
PRACTICAL, CRUK, BPC3, CAPS and PEGASUS consortia

Funding

Statistical Methods for Analysis of Massive Genetic and Genomic Data in Cancer ResearchR35CA197449 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI XIHONG LIN · 2015 to 2026
$10.9M
Vitamin D and colorectal cancer risk: an integrated molecular and genetic epidemiologic studyR00CA207848 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WARREN ANDERSEN, SHANEDA · 2018 to 2020
$601k
Cancer Research UK 19169Cancer Research UK 19170Cancer Research UK C18281/A19169Department of HealthNCI NIH HHS R00 CA207848NCI NIH HHS R35 CA197449World Health Organization 001
6 · The paper itself

Abstract

backgroundObservational studies have suggested an association between circulating vitamin D concentrations [25(OH)D] and risk of breast and prostate cancer, which was not supported by a recent Mendelian randomization (MR) analysis comprising 15 748 breast and 22 898 prostate-cancer cases. Demonstrating causality has proven challenging and one common limitation of MR studies is insufficient power.

methodsWe aimed to determine whether circulating concentrations of vitamin D are causally associated with the risk of breast and prostate cancer, by using summary-level data from the largest ever genome-wide association studies conducted on vitamin D (N = 73 699), breast cancer (Ncase = 122 977) and prostate cancer (Ncase = 79 148). We constructed a stronger instrument using six common genetic variants (compared with the previous four variants) and applied several two-sample MR methods.

resultsWe found no evidence to support a causal association between 25(OH)D and risk of breast cancer [OR per 25 nmol/L increase, 1.02 (95% confidence interval: 0.97-1.08), P = 0.47], oestrogen receptor (ER)+ [1.00 (0.94-1.07), P = 0.99] or ER- [1.02 (0.90-1.16), P = 0.75] subsets, prostate cancer [1.00 (0.93-1.07), P = 0.99] or the advanced subtype [1.02 (0.90-1.16), P = 0.72] using the inverse-variance-weighted method. Sensitivity analyses did not reveal any sign of directional pleiotropy.

conclusionsDespite its almost five-fold augmented sample size and substantially improved statistical power, our MR analysis does not support a causal effect of circulating 25(OH)D concentrations on breast- or prostate-cancer risk. However, we can still not exclude a modest or non-linear effect of vitamin D. Future studies may be designed to understand the effect of vitamin D in subpopulations with a profound deficiency.

Indexed as

AgedBreast NeoplasmsCausalityFemaleGenome-Wide Association StudyHumansMaleMendelian Randomization AnalysisMiddle AgedPolymorphism, Single NucleotideProstatic NeoplasmsReceptors, EstrogenRisk FactorsVitamin DReceptors, EstrogenVitamin DbreastmalignancyMendelian randomizationprostateserum vitamin D concentrations

Identifiers

PMID30597039
PMCPMC6934026

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.