RSSDI Update–2015 Sarita Bajaj, Manoj K Srivastava
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Diabetes Epidemiology

Culprits in the Diabetes Epidemic: Role of Dietary FactorsChapter 1

Brig MK Garg,
Namita Mahalle
Diabetes mellitus (DM) is one of the major causes of morbidity and mortality in the world. Epidemiological studies have recorded a high prevalence of DM. The prevalence of DM is high among Asians, including Indians, and is rising, particularly due to change in modern lifestyle. India has the highest number of population with diabetes and cardiovascular disease, which will increase in future.
Though increase prevalence of DM has been attributed to various genetic factors, these changes are unable to explain sudden rise of DM in past century. Genetic changes occur over centuries. Epigenetic changes and maternal malnutrition have also been implicated. Genetic and epigenetic changes usually take many generations to show their effect. In the absence of obvious shift in the genetic pool, the present spiraling epidemic of DM has most likely been triggered by environmental factors. Hence, environmental factors become more important on the background of genetic changes. Among environmental factors, the most widely studied are lifestyle changes, dietary factors, and environmental pollutants.1
Our diet has changed drastically in recent past from fruit, vegetable, and protein-based diet to increase carbohydrate and fat-based diet. These dietary factors may explain changing pattern of DM in recent times. Insulin resistance and subclinical inflammation are identified as being a central pathophysiological process behind the DM. Recently, there have been rise in interest to study relation of dietary factors with oxidative stress, insulin resistance, and inflammation. Dietary factors like carbohydrate, fat, dietary fibers, and micronutrients like vitamins and minerals have been reported to be related to insulin resistance and inflammation.15
This chapter explores the relation of various macronutrient and micronutrient dietary factors with insulin resistance and inflammation.
Carbohydrate consumption has been a critical factor blamed for weight gain, obesity, and diabetes. The literature on intake of sugar-sweetened beverages and weight gain has been systematically reviewed and 10 prospective cohort studies were identified. In most of these studies, increase in sugar-sweetened soft drink consumption was associated with weight gain. Several short-term clinical trials have provided insights into the metabolic consequences of ingesting sugar-sweetened beverages. Studies have shown increase in body weight and visceral fat. In large scale human observational studies among various populations, diets with a high glycemic index were associated with increased risk of developing type 2 diabetes mellitus (T2DM). A significant positive association between white rice consumption and risk of diabetes was observed among two cohorts of Chinese and Japanese women although the association was not significant for Japanese men. A dose-response analysis showed that each serving per day of white rice consumption was associated with an 11% increase in risk of diabetes in the overall population.6 The results of this systematic review and meta-analysis indicate that total carbohydrate is associated with an increased risk of T2DM. This association seems to be stronger for Asians 2than for Western populations. A study from southern part of India also reported a positive association of refined grain intake with the risk of type 2 diabetes.7
High carbohydrate intake has been associated with increased C-reactive protein (a marker of inflammation), increased generation of reactive oxygen species, nuclear factor-κB, activating protein-1 (AP-1) and raised levels of inflaammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-18. Yajnik et al. reported increase in inflammatory markers in urban slum dwellers, which was associated with increased insulin resistance.8 Most of calories in low income group are consumed in the form of rice or wheat contents of which are mainly carbohydrate and may explain this observation. In our study among Indians, carbohydrate was positively correlated and associated with insulin resistance and inflammatory markers.1
Lower total fat intake leads to small but statistically significant sustained reductions in body weight in adults in studies with baseline fat intakes of 28%–43% of energy intake and durations from 6 months to over 8 years. Although the role of fat intake in the development of obesity has been widely discussed in the literature, uncertainties remain because of conflicting results reported by cross-sectional and prospective studies. This could be partially explained by the phenomenon of underreporting when using self-reported dietary intake. An energy-dense, low-fiber, high-fat diet is associated with higher fat mass and greater odds of excess adiposity in childhood in children participated in the Avon Longitudinal Study.
Studies of general populations consuming diets high in fat, particularly saturated fat, have shown increased risk of diabetes. Total and saturated fat intake were associated with a higher risk of type 2 diabetes, but these associations were not independent of body mass index (BMI). Consumption of energy-dense, nutrient-poor foods has contributed to the rising incidence of obesity and may underlie insulin resistance and β-cell dysfunction. In animal studies, saturated fat intake worsens insulin resistance, effects in humans may depend on type of fat consumed and associated other dietary factors. Studies from India including ours showed that dietary fat intake was positively related with insulin resistance.1,9 Both free fatty acids and inflammatory markers have been shown to predict type 2 diabetes independent of known risk factors.
A high score for vegetable protein was inversely associated with type 2 diabetes in Health Professionals Follow-up study. Impaired β-cell proliferation and islet vascularization at later stages are implicated in low-protein fetuses. An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produced significant weight loss. This is hypothesized to be mediated by increased central nervous system leptin sensitivity. Elevated thermogenesis and glucagon-like peptide-1 appear to play a role in protein-induced satiety. We have shown that dietary protein is inversely related with insulin resistance and inflammatory markers in Indian population.1,3
High-fiber diets have received considerable attention in recent years due to their association with decreased incidence of several metabolic disorders such as hypertension, diabetes, obesity, as well as heart disease and colon cancer. The mechanisms behind the reported effects of dietary fiber on metabolic health is speculated to be a result of changes in intestinal viscosity, nutrient absorption, rate of passage, production of short-chain fatty acids, and production of gut hormones. Fibers help to lose and maintain weight, prevent obesity, and improve glucose tolerance (by reducing insulin resistance), thus lowering diabetes. A high-fiber diet may help to promote a negative energy balance by causing early satiety secondary to gastric distention. Many cross-sectional studies conducted worldwide observed inverse associations between fiber intake and BMI. Total grain, wholegrain, total dietary fiber, cereal fiber, and dietary magnesium intakes showed strong inverse associations with incidence of diabetes in a prospective cohort study of 35,988 older Iowa population. Several cross-sectional epidemiologic studies reported inverse associations of serum insulin, insulin resistance with fiber intake. We have also observed inverse relation of dietary fibers with inflammatory markers.1,3
Micronutrients are vitamins and minerals are required in small quantities for specific functions, such as essential coenzymes and cofactors, for metabolic reactions and required to maintain energy production and life. In our study, dietary vitamins showed diverse pattern, but 3essentially a negative correlation with insulin resistance and inflammatory markers. Fruit and vegetables are main source of vitamins. There are several studies which showed negative correlation of intake of fruit and vegetables with insulin resistance and inflammatory markers.
Dietary vitamin B12 deficiency is a severe problem in India due to vegetarianism and causes hyperhomocysteinemia. High prevalence of hyperhomocysteinemia has been reported in Indian population. Yajnik et al. reported vitamin B12 deficiency and hyperhomocysteinemia in 81% and 79% of urban middle-class population. Serum vitamin B12 levels had significant negative association with homocysteine levels. In our study, though homocysteine was positively correlated with insulin resistance and inflammatory markers in study population, serum vitamin B12 levels were not.2
We have also observed negative association of dietary mineral intake with insulin resistance and inflammatory markers. The mechanisms by which particular elements or their compounds may affect heart disease risk are not clear, but it is likely that they involve effects on enzymes, hormones, and messenger molecules. Among minerals, magnesium and zinc showed significant relationship with both parameters, whereas chromium was only related to inflammatory markers. There is strong inverse relationship between dietary magnesium and inflammation.
Change of diet from aboriginal age which was full of protein, vitamin, and mineral to modern diet rich in refined starches, sugar, and unhealthy lipids poor in fiber, vitamins, and minerals may facilitate activation of the innate immune system, most likely by an excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. This imbalance may favor the generation of a proinflammatory milieu, which in turn may produce insulin resistance in the peripheral tissues and endothelial dysfunction at the vascular level, and ultimately predispose susceptible people to an increased incidence of DM.10,11 This may explain partly recent epidemic of obesity, DM, and cardiovascular disease.
  1. Mahalle N, Kulkarni MV, Naik SS, Garg MK. Dietary factors responsible for insulin resistance and inflammation in subjects with coronary artery disease in Indian population. J Diabetes Complications. 2014;28:536–41.
  1. Mahalle N, Kulkarni MV, Garg MK, Naik SS. Vitamin B12 deficiency and hyperhomocysteinemia as a correlates of cardiovascular risk factors in Indian subjects with coronary artery disease. J Cardiol. 2013;61(4):289–94.
  1. Mahalle N, Garg MK, Kulkarni MV, Naik SS. Differences in traditional and non-traditional risk factors with special reference to nutritional factors in patients with coronary artery disease with or without diabetes mellitus. Indian J Endocrinol Metab. 2013;17:844–50.
  1. Mahalle N, Garg MK, Naik SS, Kulkarni MV. Relation of magnesium with insulin resistance and inflammatory markers in subjects with known coronary artery disease. JCDR. 2014;5:22–9.
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  1. Hu EA, Pan A, Malik V, Sun Q. White rice consumption and risk of type 2 diabetes: meta-analysis and systematic review. BMJ. 2012;344:e1454.
  1. Mohan V, Radhika G, Sathya RM, Tamil SR, Ganesan A, Sudha V. Dietary carbohydrates, glycaemic load, food groups and newly detected type 2 diabetes among urban Asian Indian population in Chennai, India (Chennai Urban Rural Epidemiology Study 59). Br J Nutr. 2009;102:1498–506.
  1. Yajnik CS, Joglekar CV, Lubree HG, Rege SS, Naik SS, Bhat DS, et al. Adiposity, inflammation and hyperglycaemia in rural and urban Indian men: Coronary Risk of Insulin Sensitivity in Indian Subjects (CRISIS) Study. Diabetologia. 2008;51:39–46.
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  1. Yajnik CS. Nutrition, growth, and body size in relation to insulin resistance and type 2 diabetes. Curr Diab Rep. 2003;3:108–14.