Key result
Top 1% genetic risk linked to ~5-fold higher odds of CAD.
Why the study?
Most studies examining gene-lifestyle interactions in CAD are small-scale candidate gene studies lacking replication, while evidence from robust genetic risk score or genome-wide interaction approaches remains limited.
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Effect estimate: OR 4.83 (95% CI 4.25–5.46)
p-value: p=1×10−132
Genetic risk and lifestyle factors have a log-additive effect on coronary artery disease risk, emphasizing that a healthy lifestyle remains crucial even for individuals with high genetic risk.
May aid CAD risk stratification; extends G×L observational data but leaves open causal effects and practice change.
Genetic risk and combined lifestyle factors and behaviors have a log-additive effect on the risk of developing CAD. First, we describe genetic and lifestyle factors associated with CAD and then focus on G×L interactions. The majority of G×L interaction studies are small-scale candidate gene studies that lack replication and therefore provide spurious results. Only a few studies, of which most use genetic risk scores or genome-wide approaches to test interactions, are robust in number and analysis strategy. These studies provide evidence for the existence of G×L interactions in the development of CAD. Further G×L interactions studies are important as they contribute to our understanding of disease pathophysiology and possibly provide insights for improving interventions or personalized recommendations.
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Said et al. (2019) conducted a null in Coronary Artery Disease. combined genetic and lifestyle risks was evaluated on Risk of developing coronary artery disease with varying genetic and lifestyle risks (OR 4.83, 95% CI 4.25–5.46, p=1×10−132). Individuals in the top 1% of the genetic risk distribution had nearly 5-fold higher odds of coronary artery disease compared to those in lower risk categories.
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