Journal
CIRCULATION
Volume 137, Issue 7, Pages 653-661Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCULATIONAHA.117.030898
Keywords
blood pressure; cardiovascular diseases; genetic predisposition to disease; genetics; healthy lifestyle; risk
Funding
- British Heart Foundation [SP/13/2/30111]
- Medical Research Council [MR/L01341X/1, MR/L01632X/1]
- Public Health England [MR/L01341X/1]
- National Institute of Health Research Biomedical Research Center at Imperial College Healthcare National Health Service Trust
- Imperial College London
- National Institute of Health Research Health Protection Research Unit in Health Impact of Environmental Hazards [HPRU-2012-10141]
- UK Dementia Research Institute from UK Dementia Research Institute Ltd - UK Medical Research Council
- Alzheimer's Society
- Alzheimer's Research UK
- British Heart Foundation [SP/13/2/30111] Funding Source: researchfish
- Medical Research Council [G9521010, MC_qA137853, HDR-2002, G0600237, MR/L01632X/1, MR/K006584/1] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0512-10113] Funding Source: researchfish
- MRC [G0600237, MR/L01632X/1, G9521010] Funding Source: UKRI
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BACKGROUND: High blood pressure (BP) is a major risk factor for cardiovascular diseases (CVDs), the leading cause of mortality worldwide. Both heritable and lifestyle risk factors contribute to elevated BP levels. We aimed to investigate the extent to which lifestyle factors could offset the effect of an adverse BP genetic profile and its effect on CVD risk. METHODS: We constructed a genetic risk score for high BP by using 314 published BP loci in 277 005 individuals without previous CVD from the UK Biobank study, a prospective cohort of individuals aged 40 to 69 years, with a median of 6.11 years of follow-up. We scored participants according to their lifestyle factors including body mass index, healthy diet, sedentary lifestyle, alcohol consumption, smoking, and urinary sodium excretion levels measured at recruitment. We examined the association between tertiles of genetic risk and tertiles of lifestyle score with BP levels and incident CVD by using linear regression and Cox regression models, respectively. RESULTS: Healthy lifestyle score was strongly associated with BP (P<10(-320)) for systolic and diastolic BP and CVD events regardless of the underlying BP genetic risk. Participants with a favorable in comparison with an unfavorable lifestyle (bottom versus top tertile lifestyle score) had 3.6, 3.5, and 3.6 mm Hg lower systolic BP in low, middle, and high genetic risk groups, respectively (P for interaction=0.0006). Similarly, favorable in comparison with unfavorable lifestyle showed 30%, 31%, and 33% lower risk of CVD among participants in low, middle, and high genetic risk groups, respectively (P for interaction=0.99). CONCLUSIONS: Our data further support population-wide efforts to lower BP in the population via lifestyle modification. The advantages and disadvantages of disclosing genetic predisposition to high BP for risk stratification needs careful evaluation.
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