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Ali Abbasi

information to fill the evidence gap due to unmeasured confounding or reverse causality (4, 5, 6, 7) . It has been successfully shown that a complementary analysis of genetic data, termed ‘Mendelian randomization,’ has additive value to infer a causal

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Julia Kubiak, Per Medbøe Thorsby, Elena Kamycheva and Rolf Jorde

results from Mendelian randomization analyses should be viewed with caution as the genes involved may not only affect serum 25(OH)D, but the production of other metabolites as well. The relation to serum 25(OH)D could also simply be co-variation since the

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Stefan Pilz, Armin Zittermann, Christian Trummer, Verena Theiler-Schwetz, Elisabeth Lerchbaum, Martin H Keppel, Martin R Grübler, Winfried März and Marlene Pandis

study designs including, apart from classic observational studies, also Mendelian Randomization (MR) studies ( 157 ). These MR studies evaluate whether genetically determined serum 25(OH)D levels are associated with outcome and have the advantage over

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Xiaomin Nie, Yiting Xu, Xiaojing Ma, Yun Shen, Yufei Wang and Yuqian Bao

population ( 5 , 6 ). A Mendelian randomization study indicated that higher BMI or FM played a causal role in increasing FT3 levels ( 17 ). Simple obesity indexes, such as BMI have been widely used in these studies. There have been few studies of

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Zhen-yu Song, Qiuming Yao, Zhiyuan Zhuo, Zhe Ma and Gang Chen

deficient concentrations of serum vitamin D ( 50 , 51 ). In the contrast, one Mendelian randomization study showed null relationship between vitamin D and risk of prostate cancer ( 52 ). Other studies also failed to find a positive relationship between

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Karolien Van De Maele, Jean De Schepper, Jesse Vanbesien, Monique Van Helvoirt, Ann De Guchtenaere and Inge Gies

D and effective weight loss. Studies based on bi-directional Mendelian randomization analysis argue that vitamin D deficiency is rather a cause of the obesity than an actual modulator of the weight loss process ( 23 ). Since the serum 25-OH-D changes

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Christian Trummer, Stefan Pilz, Verena Schwetz, Barbara Obermayer-Pietsch and Elisabeth Lerchbaum

that results derived from a Mendelian Randomization study suggest that low 25(OH)D levels are a consequence of obesity, but it is unlikely that vitamin D deficiency causes obesity ( 37 ). Interestingly, the observed association between vitamin D

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Shenglong Le, Leiting Xu, Moritz Schumann, Na Wu, Timo Törmäkangas, Markku Alén, Sulin Cheng and Petri Wiklund

, population-based study in young adults found that SHBG was associated with multiple circulating metabolites reflecting the degree of adiposity and insulin resistance, but the Mendelian randomization analyses suggested weak causal effects ( 31 ), which support

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Elisabet Einarsdottir, Minna Pekkinen, Kaarel Krjutškov, Shintaro Katayama, Juha Kere, Outi Mäkitie and Heli Viljakainen

Experimental Medicine 2015 8 14977 – 14984 . 26628980 3 Vimaleswaran KS Berry DJ Lu C Tikkanen E Pilz S Hiraki LT Cooper JD Dastani Z Li R Houston DK , Causal relationship between obesity and vitamin D status: bi-directional Mendelian randomization

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Magnolia Ariza-Nieto, Joshua B Alley, Sanjay Samy, Laura Fitzgerald, Francoise Vermeylen, Michael L Shuler and José O Alemán

.1016/j.metabol.2014.05.001 ) 10.1016/j.metabol.2014.05.001 24933398 24 Yaghootkar H Lamina C Scott RA Dastani Z Hivert MF Warren LL Stancakova A Buxbaum SG Lyytikainen LP Henneman P , Mendelian randomization studies do not support a causal role for