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. Author manuscript; available in PMC: 2018 May 28.
Published in final edited form as: Obesity (Silver Spring). 2016 Aug;24(8):1630–1638. doi: 10.1002/oby.21554

Figure 3. Mendelian randomisation; the use of genetic proxy measures of risk factors to allow causal inference.

Figure 3

(A) In general, a genotype of use to this study is associated with the exposure, is independent of measured or unmeasured confounders and can only influence outcome via the causal effect of the exposure.

(B) The presence or absence of association between the BMI associated genotype and disease risk (from existing genomewide association study data sets) give evidence that the BMI is a causal risk factor for disease.

(C) Here genotype acts as a proxy measure for an exposure potentially affecting the BMI in a reciprocal analysis. This type of reciprocal analysis allows for a triangulation or network approach to the assessment of the effects of and effects on BMI.