NEW YORK – New research has highlighted genetic risk scores for cardiovascular disease (CVD) in individuals in China, including scores that can be combined with lifestyle information to predict risks of early-onset coronary artery disease (CAD), late-onset CAD, and ischemic stroke (IS) in this population.
Their findings, published in the journal Nature Human Behaviour on Wednesday, provided potential clues to the previously reported rise in CVD in individuals between the ages of 15 and 49 years old, along with declining rates of CVD in individuals over 50 around the world during the past few decades.
"Early-onset CVD is affecting a growing number of younger adults, underscoring the urgent need for effective prevention," co-senior and co-corresponding authors Jun Lv and Liming Li, public health researchers at Peking University and the Key Laboratory of Epidemiology of Major Diseases, and their colleagues wrote.
While past studies suggest early-onset heart conditions appear to have both genetic and environmental contributors, they noted that CAD genetic risk scores established in European populations tend to show little to no clinical utility for individuals from East Asia, prompting a search for variants that can be used for predicting early-onset CAD and other forms of CVD in these populations.
With that in mind, members of the China Kadoorie Biobank Collaborative Group brought together data for 96,400 adult individuals enrolled through a prospective study in China. By combining polygenic risk score (PRS) clues from past CVD-related genome-wide association studies in individuals of East Asian or European ancestry, the researchers came up with trait-specific "MetaPRSs" for coronary artery disease (CAD), ischemic stroke (IS), and intracerebral hemorrhage (ICH).
The team initially assessed the 3.7 million-variant MetaPRS for CAD, a MetaPRS encompassing 4.8 million variants involved in IS risk, and an ICH MetaPRS spanning some 2.1 million variants in a training set of 24,251 Chinese participants before evaluating the performance of the three risk scores in another 72,149 individuals from China.
By incorporating participants' self-reported lifestyle data — ranging from smoking and dietary habits to physical activity, body mass index, and waist circumference measures — the investigators saw an interplay between genetic risk and lifestyle factors, particularly when it came to the risk of early-/late-onset CAD and IS.
"We observed additive interactions between genetic risk and lifestyles on early-onset CAD and IS and late-onset CAD," the authors wrote.
The investigators found that individuals at high genetic risk of early-onset CAD had a far greater reduction in their risk of disease by shifting to favorable lifestyle factors than did individuals at low risk of early-onset CAD. They estimated that favorable lifestyle factors would dial down risk by roughly 14.7-fold in the genetically high-risk group compared to a group at low genetic risk.
Similar, albeit less-dramatic risk reductions turned up when the team considered lifestyle effects on the genetic risk of late-onset CAD and IS, where individuals with high genetic risk were expected to reduce their absolute risk of each disease by 2.6-fold and 2.5-fold, respectively, if positive lifestyle changes were achieved.
"With genetic tests becoming affordable and popular, lifestyle improvements may be of greater interest to young adults at high genetic risk and have larger public health consequences," the authors suggested, calling it a "vision of precision prevention."