Abstract
The consumption of sugar-sweetened beverages (SSB), which includes soft drinks, fruit drinks, and other energy drinks, is associated with excess energy intake and increased risk for chronic metabolic disease among children and adults. Thus, reducing SSB consumption is an important strategy to prevent the onset of chronic diseases, and achieve and maintain a healthy body weight. The mechanisms by which excessive SSB consumption may contribute to complex chronic diseases may partially depend on an individual’s genetic predisposition. Gene–SSB interaction investigations, either limited to single genetic loci or including multiple genetic variants, aim to use genomic information to define mechanistic pathways linking added sugar consumption from SSBs to those complex diseases. The purpose of this review is to summarize the available gene-SSB interaction studies investigating the relationships between genetics, SSB consumption, and various health outcomes. Current evidence suggests there are genetic predispositions for an association between SSB intake and adiposity; evidence for a genetic predisposition between SSB and type 2 diabetes or cardiovascular disease is limited.
Highlights
Sugar-sweetened beverages (SSBs), such as sodas, fruit-flavored drinks, and sports drinks, are a significant source of dietary added sugars and a major contributor to excess energy intake [1]
Observational data suggest that higher sugar-sweetened beverages (SSB) consumption is linked to a host of chronic diseases, including cardiovascular disease (CVD), type 2 diabetes (T2D), obesity, non-alcoholic fatty liver disease (NAFLD), and gout [7,8,9,10,11]
Olsen and colleagues generated four genetic risk scores including variants associated with BMI, waist circumference, waist-to-hip ratio, and a combined score, and assessed SSB consumption in relation to annual changes in body weight, waist circumference, and waist circumference adjusted for BMI for three cohort studies [28]
Summary
The consumption of sugar-sweetened beverages (SSB), which includes soft drinks, fruit drinks, and other energy drinks, is associated with excess energy intake and increased risk for chronic metabolic disease among children and adults. The mechanisms by which excessive SSB consumption may contribute to complex chronic diseases may partially depend on an individual’s genetic predisposition. Gene–SSB interaction investigations, either limited to single genetic loci or including multiple genetic variants, aim to use genomic information to define mechanistic pathways linking added sugar consumption from SSBs to those complex diseases. The purpose of this review is to summarize the available gene-SSB interaction studies investigating the relationships between genetics, SSB consumption, and various health outcomes. Current evidence suggests there are genetic predispositions for an association between SSB intake and adiposity; evidence for a genetic predisposition between SSB and type 2 diabetes or cardiovascular disease is limited
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