[Childhood obesity and coronary artery disease: a Mendelian randomization study]

Area of Science:

• Genetics
• Cardiovascular Disease Epidemiology
• Pediatric Health

Background:

• Childhood obesity is a growing public health concern.
• The long-term cardiovascular consequences of childhood obesity require further investigation.
• Establishing a causal link between childhood obesity and adult coronary artery disease (CAD) is crucial for preventative strategies.

Purpose of the Study:

• To determine the causal effect of childhood obesity on the risk of developing coronary artery disease (CAD) in adulthood.
• To utilize the Mendelian randomization (MR) method for robust causal inference.
• To quantify the association between childhood body mass index (BMI) and adult CAD risk.

Main Methods:

• Employed Mendelian randomization (MR) analysis using genetic variants associated with childhood BMI as instrumental variables.
• Utilized large-scale genetic data from the Early Growth Genetics Consortium and the Genetic Investigation of Anthropometric Traits Consortium.
• Assessed potential pleiotropy using MR-Egger regression and conducted primary analysis with the mode-based estimate method.

Main Results:

• No significant pleiotropy was detected among the selected genetic variants (MR-Egger intercept: -0.008 to 0.018).
• A 1-unit increase in childhood BMI (kg/m²) was associated with a 37% average increase in the risk of adult CAD (OR=1.37, 95% CI: 1.09-1.72).
• The findings provide strong evidence for a causal relationship.

Conclusions:

• Childhood obesity is causally linked to an increased risk of developing coronary artery disease (CAD) in adulthood.
• This study reinforces the importance of early life weight management for long-term cardiovascular health.
• The Mendelian randomization approach offers a reliable method for investigating such causal associations.