Globalization of diabetes: the role of diet, lifestyle, and genes

Abstract

Type 2 diabetes is a global public health crisis that threatens the economies of all nations, particularly developing countries. Fueled by rapid urbanization, nutrition transition, and increasingly sedentary lifestyles, the epidemic has grown in parallel with the worldwide rise in obesity. Asia's large population and rapid economic development have made it an epicenter of the epidemic. Asian populations tend to develop diabetes at younger ages and lower BMI levels than Caucasians. Several factors contribute to accelerated diabetes epidemic in Asians, including the "normal-weight metabolically obese" phenotype; high prevalence of smoking and heavy alcohol use; high intake of refined carbohydrates (e.g., white rice); and dramatically decreased physical activity levels. Poor nutrition in utero and in early life combined with overnutrition in later life may also play a role in Asia's diabetes epidemic. Recent advances in genome-wide association studies have contributed substantially to our understanding of diabetes pathophysiology, but currently identified genetic loci are insufficient to explain ethnic differences in diabetes risk. Nonetheless, interactions between Westernized diet and lifestyle and genetic background may accelerate the growth of diabetes in the context of rapid nutrition transition. Epidemiologic studies and randomized clinical trials show that type 2 diabetes is largely preventable through diet and lifestyle modifications. Translating these findings into practice, however, requires fundamental changes in public policies, the food and built environments, and health systems. To curb the escalating diabetes epidemic, primary prevention through promotion of a healthy diet and lifestyle should be a global public policy priority.

Figure 1

Time trends of diabetes prevalence in Chinese adults. Data are based on population-based cross-sectional surveys conducted in China (Chan et al. [3] and Yang et al. [4]).

Figure 2

Multivariate RRs (with 95% CIs) of type 2 diabetes according to ascending quintiles of intake of cereal fiber (A); the ratio of polyunsaturated fat intake to saturated fat intake (B); intake of trans fat (C); and glycemic load (D). Each of the RRs was adjusted for the other 3 dietary variables and for age (in 5-year categories); time (8 periods); the presence or absence of a family history of diabetes; menopausal status and the use or nonuse of postmenopausal hormone therapy; smoking status (never smoked; former smoker; current smoker, 1–14 cigarettes per day or current smoker, ≥15 cigarettes per day); BMI (<23.0, 23.0–24.9, 25.0–29.9, 30.0–34.9, or ≥35.0); weekly frequency of moderate-to-vigorous exercise (<0.5 h, 0.5–1.9 h, 2.0–3.9 h, 4.0–6.9 h, or ≥7.0 h); and daily alcohol consumption (0 g, 0.1–5.0 g, 5.1–10.0 g, or ≥10.0 g) (11).

Figure 3

Percentage changes in risk of developing type 2 diabetes among nondiabetic women associated with TV watching, other sedentary behaviors, and walking. Adjusted for age, smoking, alcohol consumption, family history of diabetes, and dietary covariates. All sedentary behavior variables are included simultaneously in the model. Other sitting includes reading, eating meals, and time spent sitting at a desk. Error bars indicate 95% CIs. d, day. Adapted from Hu et al. (26).

Figure 4

ORs of diabetes risk according to joint classification of Western dietary pattern scores (in quartiles, Q) and genetic risk scores (<10, 10–11, and ≥12). ORs and 95% CIs were calculated by using an unconditional logistic regression model. The analyses were adjusted for age, BMI, smoking, alcohol consumption, physical activity, family history of diabetes, and total energy intakes (P for interaction = 0.02). From Qi et al. (45).