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Nat. Rev. Cardiol. doi:10.1038/nrcardio.2017.78 Figure 6 Mendelian randomization of a time-dependent and cumulative exposure Figure 6 | Mendelian randomization of a time-dependent and cumulative exposure. a | The genetic variant-to-disease (multiple sclerosis) association reflects lifetime associations (including causal effects mediated through vitamin D that only occur during adolescence). Therefore, Mendelian randomization might provide evidence of a causal effect when this effect actually only occurs during a critical time period. b | The genetic variant alters the heparin-binding domain of extracellular superoxide dismutase (ecSOD), meaning that it cannot bind to the external membrane of endothelial cells, and cannot prevent nitric oxide (NO) from being degraded by superoxide anions. Less NO results in vasoconstriction and increased risk of coronary heart disease (CHD). c | Genetic variants instrumenting LDL cholesterol (LDL-C) have large effects on risk of CHD. Given that CHD is a disease that develops over decades, the effect estimates are equivalent to the estimates that would be derived from lifelong lowering of LDL-cholesterol levels. These figures are schematic representations and should not be interpreted as formal directed acyclic graphs. Holmes, M. V. et al. (2017) Mendelian randomization in cardiometabolic disease: challenges in evaluating causality Nat. Rev. Cardiol. doi:10.1038/nrcardio.2017.78