Several risk factors are known to be associated with increased risk of type 2 diabetes, including increasing age, obesity (especially central obesity), dietary excess, dietary factors such as increased intake of animal fats and sugar- sweetened beverages, sedentary lifestyle, positive family history, history of gestational diabetes, polycystic ovary syndrome, presence of hypertension, hyperlipidaemia, or other cardiometabolic risk factors (Figure 1). Many of these risk factors are associated with a Westernized lifestyle and increase with increasing urbanization and mechanization. The recognition of the role of these factors in the pathogenesis of type 2 diabetes has led to recommendations for selective screening for type 2 diabetes in people with these risk factors.

Fig1. Risk factors in the development of type 2 diabetes. HDL, high- density lipoprotein cholesterol; PCOS, polycystic ovarian syndrome; TG, triglycerides.

Several large studies, including the Nurses’ Health Study in the USA and the InterAct Study in Europe, have contributed to improved understanding of the role of dietary factors and the risk of incident type 2 diabetes. Dietary factors that increase the risk for type 2 diabetes include the following:

• Increased fat intake.

 • Increased intake of red and processed meat.

• Consumption of fried food.

• Increased intake of white rice.

 • Consumption of sugar- sweetened beverages.

Dietary factors that decrease the risk for type 2 diabetes include the following:

• Increased fruit and vegetable intake.

 • A Mediterranean diet pattern.

• Consumption of fermented dairy products.

• Intake of oily fish.

• Drinking tea.

Obesity accounts for 80–85% of the overall risk of developing type 2 diabetes, and underlies the current global spread of the disease. The risk of type 2 diabetes increases as the body mass index (BMI) increases above 24 kg/m², although the risk appears to be present with a lower BMI in Asians. Although central obesity is a particularly strong factor, it can impart further risk regardless of the overall level of general obesity. This obesity- related risk is more marked in certain ethnic populations such as Pima Indians, Black Africans, South Asians, Chinese, and other Asian populations, and may be related to increased visceral adiposity. Obesity, particularly central adiposity, is associated with insulin resistance and also β- cell dysfunction, partly through increased free fatty acids and lipotoxicity. Obesity is also associated with other metabolic abnormalities such as dyslipidaemia and hypertension.

The clustering of some of the risk factors, namely hypertension, elevated blood glucose, elevated triglyceride, low high- density lipoprotein (HDL) cholesterol, and abdominal obesity, is termed the metabolic syndrome. Presence of the metabolic syndrome, according to the definition, is associated with a two- to fivefold increased risk of developing diabetes in most populations.

A positive family history is an important risk factor for type 2 diabetes. In the InterAct case–cohort study, a family history of type 2 diabetes was associated with a 2.7- fold risk of incident diabetes. There have been advances in our understanding of the genetic basis of type 2 diabetes over the last few years, with more than 1000 genetic variants so far identified as being associated with type 2 diabetes. Nevertheless, the identified genetic variants explain <10 % of the heritability of type 2 diabetes. In the InterAct study, a genetic risk score composed of known genetic variants for type 2 diabetes explained only 2% of the family history–associated risk of the disease, suggesting that there are still unexplained factors that contribute to the association between family history and type 2 diabetes, including yet to be identified genetic factors, shared environment and behaviour, epigenetic factors, and possibly other factor. Most of the known genetic variants for type 2 diabetes were identified in European populations. Although several type 2 diabetes–associated genetic variants have been identified in other populations, including East Asians and South Asians, our current knowledge of genetic variants associated with type 2 diabetes cannot explain the marked geographical and ethnic variations in diabetes prevalence.

Traditional risk factors such as increasing age, adiposity, physical inactivity, dietary factors, positive family history, and presence of other cardiometabolic risk factors are well- recognized factors for diabetes and many are considered to be on the causal pathway. Current approaches to diabetes prevention are mostly focused on addressing these risk factors, in particular unhealthy diet and physical inactivity. In the prospective Whitehall II study, it was estimated that traditional modifiable risk factors such as health behaviour and obesity, when measured repeatedly over time, explain approximately half of the social inequalities in incidence of type 2 diabetes.

Emerging risk factors

Sugar- sweetened beverages

Consumption of sugar- sweetened beverages is now recognized as an important contributor to the recent rapid escalation in obesity and diabetes. Sugar- sweetened beverages include carbonated soft drinks, fruit juices, iced tea, and energy and vitamin water beverages, and are similar in having high sugar content, low satiety, and low nutritional value. The intake of such beverages has increased markedly over recent decades, and consumption trends often mirror those of obesity and diabetes prevalence in different parts of the world. Sugar- sweetened beverages contain added sugars in the form of fructose, chronic exposure to which can lead to hepatic steatosis, insulin resistance, central obesity, and metabolic abnormalities.

Decreased sleep

 In addition to changes in diet and physical activity, it is increasingly recognized that there is a U- shaped relationship between sleep duration and diabetes risk, with short sleep duration, another facet of our modern lifestyle, being an important contributor to the increasing prevalence of type 2 diabetes. Early seminal work highlighted the detrimental effects of sleep deprivation on glucose tolerance and insulin sensitivity. Subsequent cross- sectional studies have suggested an association between short sleep duration and diabetes and obesity. In a prospective study of >70000 women in the Nurses’ Health Study, short sleep duration was associated with a ~57% increase in diabetes risk over the 10- year study period. Similar data were obtained from the First National Health and Nutrition Examination Survey (NHANES I), which noted that people with a sleep duration of ≤5 hours had a 47% increase in incident diabetes over a 10- year period. The exact mechanism whereby sleep restriction increases diabetes risk is unclear, although it may be related to activation of the sympathetic nervous system, decrease in cerebral glucose utilization, changes in the hypothalamic–pituitary–adrenal axis, and other neuroendocrine dysregulation. In addition to short duration, other sleep disturbances and altered circadian rhythm, for example during shift work, are associated with an increased risk of diabetes.

Depression and treatment of depression

There is a bidirectional relationship between depression and diabetes and impaired glucose tolerance. The incident rate of type 2 diabetes is modestly higher among those with baseline depressive symptoms. Once type 2 diabetes was diagnosed, there was a positive association with depressive symptoms, illustrating the emotional burden of having diabetes. The use of second- generation antipsychotic agents, commonly referred to as atypical antipsychotics, has been linked with hyperglycaemia and diabetes. A complex association exists between mental illness, use of psychiatric medications, and diabetes.

Drug- induced metabolic changes

 There is increasing recognition that some commonly used medications may be associated with adverse metabolic effects and increased risk of diabetes. High- dose thiazide diuretics worsen insulin resistance and β- blockers can impair insulin secretion. The increasing use of highly active antiretroviral therapy (HAART) has dramatically reduced the mortality of people with human immunodeficiency virus (HIV) infection. However, protease inhibitors and, to a lesser extent, nucleoside reverse transcriptase inhibitors are associated with insulin resistance, deranged glucose and lipid metabolism, and an increased risk for type 2 diabetes. The growing use of such agents will likely have a significant impact on the epidemiology of diabetes in areas where HIV/AIDS is endemic, such as Africa.

Environmental toxins

Whereas most studies on the increasing burden of diabetes with a Westernized lifestyle have focused on changes in dietary patterns and increasingly sedentary behaviour, some studies suggest that environmental pollutants may represent a previously unrecognized link between urbanization and diabetes. For example, there is a strong cross- sectional association between serum concentrations of chlorinated persistent organic pollutants with diabetes and also components of the metabolic syndrome. Brominated flame retardants, bisphenol A, and perfluorinated compounds have emerged as other classes of organic pollutants that are associated with diabetes. These environmental toxins may accumulate in adipose tissue and act as endocrine disruptors, leading to dysregulation of glucose and lipid metabolism.

Low birth weight and fetal malnutrition

 There is a relationship between the intrauterine environment, fetal malnutrition, and the risk of diabetes and cardiovascular disease later in life. Maternal undernutrition and low infant birth weight, along with rapid postnatal growth, are associated with increased risk of diabetes in the offspring. This mismatch of a metabolic phenotype programmed during intrauterine development and the nutritionally rich postnatal environment may be most important in regions that are undergoing rapid economic development, and may be an important factor contributing to the rapid rise in diabetes in Asia and the Pacific region.

Maternal obesity, maternal hyperglycaemia, and other factors in early development

Offspring of women with obesity or women with diabetes have an increased risk of diabetes and cardiometabolic abnormalities. This is partly caused by the effects of maternal overnutrition and of intrauterine hyperglycaemia on fetal growth, although it may also involve epigenetic changes. With increasing numbers of women with obesity or young- onset diabetes, this is likely to exacerbate the epidemic of diabetes further by setting up a vicious cycle of diabetes begetting diabetes. There is also increasing interest in the potential link between assisted reproduction technology and risk of diabetes and obesity in the offspring, though this remains an area of controversy, with limited and conflicting data.

Despite the increasing recognition of these novel risk factors, the main risk factors associated with diabetes remain the traditional ones such as increasing age, adiposity, physical inactivity, dietary factors, positive family history, and presence of other cardiometabolic risk factors, as outlined in Figure 1.

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