Utilization of an early-life risk factor score to determine later life type 2 diabetes risk

Longitudinal association of cumulative risk factors in early life, genetic risk, and healthy lifestyles during adulthood with the risk of type 2 diabetes 

1. In this prospective cohort study, a higher early-life risk factor score (ERS) was associated with a dose-dependent increased risk of developing type 2 diabetes (T2D) later in life. 

Evidence Rating Level: 1 (Excellent) 

Type 2 diabetes (T2D) cases have been rising worldwide, with 90% of the diabetes population classified as type 2 diabetics. The “Developmental Origins of Health and Disease” (DOHaD) theory postulates that early life experiences may impact metabolic development, leading to T2D onset. While several early life risk factors have been identified, it remains difficult to modify these behaviours as people have not reached independence, in contrast to the recommended later cardiovascular-focused lifestyle changes. This study aimed to examine combined early life effects on T2D onset and examine the impact of genetic factors as well as lifestyle modifications on T2D rates. The early development risks examined were breastfeeding, maternal smoking and birth weight. An early life risk factor score (ERS) was constructed and weighed based on factors. Modifiable healthy lifestyle factors (MHS) assessed were sleep health, nicotine exposure, diet and physical activity. Each metric was assessed and categorized into healthy, moderate and unhealthy. T2D incidences that were already prevalent as well as onset during the study. The standard polygenic risk score (PRS) for genetic predisposition for T2D was used in assessment, with participants being classified into low, medium and high risk tertiles. A total of 7,408 individuals had or developed T2D across the study, or 4.98% of the population. ERS was correlated with a higher risk of T2D (P <0.001).  Those with 3 ERS had the greatest risk of developing T2D compared to those with 0 ERS (hazard ratio [HR]: 1.93, 95% confidence interval [CI]: 1.65, 2.26). Participants with a higher MHS showed a 53% lower risk of T2D (HR: 0.47; 95% CI: 0.44, 0.51). While ERS across all MHS showed increased risk, no significant interaction was observed (P=0.113). Overall, EHS was associated with an increased risk of T2D onset in a dose-response relationship, without significant changes from MHS or PRS, indicating the need for early intervention in T2D prevention.

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