Abstract
Abstract Objective: Different adiposity traits may be causally related to hypertension in different ways. By using genetic variants as randomly allocated proxies for studying the effect of modifying adiposity traits, the Mendelian randomization approach can be used to investigate this. Design and method: In this study, we used four different genetic risk scores (GRSs: GRS-BMI565, GRS-WHR324, GRS-VAT208, GRS-BF81) including hundreds of single nucleotide polymorphisms (SNPs) associated with Body Mass Index (BMI), Waist to Hip Ratio (WHR), Visceral Adipose Tissue (VAT), and Body Fat (BF), respectively, using risk alleles and weight from largest available GWAS meta-analyses. These were applied as instrumental variables (IVs) in Mendelian Randomization analyses. Two Swedish urban-based cohort studies, the Malmö Diet and Cancer (MDC) and the Malmö Preventive Projects (MPP; subjects evaluated both at baseline and after an average follow-up of 23 ± 4.7 years), were used to obtain genetic association estimates with blood pressure (BP). Results: In both the MPP and MDC, with the exception of that for BF, all the GRSs were significantly associated with systolic BP and diastolic BP, but with different magnitude.: In particular, each standard deviation (SD) increase in the GRS-WHR324 doubled the likelihood of hypertension prevalence at MDC or MPP baseline exam. However, only the GRS-BMI565 was significantly associated to BP and with hypertension incidence during 23.6 ± 4.3 years of follow-up in MPP. Conclusions: In conclusion, we have confirmed a causal link between genetically mediated adiposity, especially WHR and BMI, and BP-related traits including hypertension prevalence and, for the first time to our knowledge, hypertension incidence. The differences in magnitude between these associations might suggest different mechanisms by which different adiposity traits mediate their effect on BP/hypertension and consequently may indicate that tailored interventions are needed to reduce cardiovascular risk.
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