Interactions (not only between genes and the environment) and cardiovascular disease

Czech version

Authors: Jaroslav A. Hubáček ^1,2
Authors‘ workplace: Centrum experimentální medicíny IKEM, Praha ¹; III. interní klinika – endokrinologie a metabolismu 1. LF UK a VFN v Praze ²
Published in: AtheroRev 2025; 10(3): 178-182
Category: Reviews

Overview

Despite intensive research and extensive analysis, we are still unable to satisfactorily predict the risk of cardiovascular disease (CVD). One issue may be the way the risk is calculated, based solely on simple additive models. However, individual risk factors often interact with each other –⁠ the effect of an identical risk factor is not the same for everyone, but depends on the presence of other risk factor. Interactions between genes and diet (nutrigenetics) are often described and well documented. For example, the risk associated with some PCSK9, ANRIL (a marker at 9p21 locus) or APOA5 alleles is significantly dependent on dietary habits. Significant interactions have also been observed in relation to sex –⁠ obesity poses a much greater risk to men than to women, whereas smoking increases the risk of CVD much more in women. However, obesity and smoking do not interact –⁠ an additive model applies here when modelling CVD risk. A limitation of interaction studies is the quality of the input lifestyle data –⁠ such studies are generally less replicable than analyses based on objective, laboratory data. Nevertheless, it is evident that the analysis of inter-individual interactions should become standard in personalised medicine.

Keywords:

polymorphism – lifestyle – cardiovascular disease (CVD) – interaction

Sources

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