Abstract
Background: The development of diabetes mellitus has been closely linked to multiple risk factors, of which modifiable factors are of particular interest for disease prevention. Yet few studies have assessed the system of pathways though which risk factors lead to diabetes, and how the different groups of risk factors may interact,both as independent or mediating factors. Methods: We aimed to develop a broad pathway model for diabetes risk with modifiable lifestyle risk factors as the start point, hypothesising that Lifestyle Risk (physical inactivity, smoking, poor diet and insufficient sleep) would impact Diabetes Risk (HbA1c) through the mediating factor of Physiological Load (BMI, resting pulse rate, CRP, systolic and diastolic blood pressure). The lifestyle and physiological factors were grouped via principal components analysis and a summary index respectively. Non modifiable risk factors, such as sociodemographics were specified as covariates. We used structural equation modeling to test this model, first using Wave 5 data from the Indonesian Family Life Survey (IFLS), as this was the only wave that collected all indicators of interest. To fit in longitudinal data from an earlier wave (IFLS4), we further tested a smaller model with the two Lifestyle Risk indicators available. Results: Both models showed indirect effects of Lifestyle Risk on Diabetes Risk via Physiological Load, with the cross-sectional model also showing a direct effect. The effect sizes were within the range of other studies that assessed the variables separately. Conclusion: Taken together, the results support the model of an indirect effect of Lifestyle Risk on Diabetes through Physiological Load. Specifying Lifestyle Risk as an observable, composite variable incorporates the cumulative effect of risk behaviour and differentiates this study from previous studies assessing it as a latent construct. We were able to assess causality with retrospective cohort data. Finally, the parsimonious model groups and summarises the multifarious risk factors and illustrates parsimonious and modifiable pathways that could be applied in chronic disease prevention efforts.