Why the study?
Although lower height is linked to higher CAD and T2D risk, it remains unclear whether these associations are causal, direct, or mediated by other factors.
Does genetically determined higher height reduce the risk of coronary artery disease and type 2 diabetes in a general population cohort?
Does genetically determined higher height reduce the risk of coronary artery disease and type 2 diabetes in a general population cohort?
Genetically determined taller height is causally associated with a lower risk of coronary artery disease, an effect that appears to be primarily mediated by lung function rather than traditional cardiometabolic risk factors.
Answers are grounded in this paper and cite their sources.
Genetically taller height should not alter CAD risk assessment; leaves open lung function mediation for prospective validation.
There is evidence that lower height is associated with a higher risk of coronary artery disease (CAD) and increased risk of type 2 diabetes (T2D). It is not clear though whether these associations are causal, direct or mediated by other factors. Here we show that one standard deviation higher genetically determined height (~6.5 cm) is causally associated with a 16% decrease in CAD risk (OR = 0.84, 95% CI 0.80-0.87). This causal association remains after performing sensitivity analyses relaxing pleiotropy assumptions. The causal effect of height on CAD risk is reduced by 1-3% after adjustment for potential mediators (lipids, blood pressure, glycaemic traits, body mass index, socio-economic status). In contrast, our data suggest that lung function (measured by forced expiratory volume [FEV1] and forced vital capacity [FVC]) is a mediator of the effect of height on CAD. We observe no direct causal effect of height on the risk of T2D.
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Marouli et al. (2019) studied this question.
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