Clinical Review

Prevention of Type 2 Diabetes: Evidence and Strategies

Journal of Clinical Outcomes Management. 2017 April;24(4)

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Risk Factors and Screening for T2DM

Identifying risk factors for diabetes is a necessary step in screening individuals and taking measures to prevent diabetes ( Table 1 ). Nonmodifiable risk factors include age (≥ 45 years), family history of diabetes in a parent or a sibling, personal history of gestational diabetes, history of polycystic ovary syndrome, and ethnicity (ie, Native American, African American, Hispanic American, or Pacific Islanders). Obesity, physical inactivity, dyslipidemia, hypertension, smoking, impaired fasting glucose (IFG), and impaired glucose tolerance (IGT) constitute modifiable risk factors for T2DM [5]. Excessive weight, specifically abdominal obesity, is thought to be a major contributor to the rising prevalence of T2DM across different ethnic and age groups [6]. Indeed, obesity is at the core of the metabolic syndrome, which manifests with increased waist circumference, high blood pressure, high triglycerides, low high-density lipoprotein (HDL) cholesterol, and/or abnormal glucose metabolism. The association between metabolic syndrome and an increased risk for diabetes is very well established [7].

The American Diabetes Association (ADA) recommends screening all adults for prediabetes by assessing for diabetes risk factors [8]. Glucose testing is recommended in individuals aged 45 years or older, and should be considered in adults of any age who are overweight or obese (body mass index [BMI] ≥ 25 kg/m ² or ≥ 23 kg/m ² in Asian Americans) and have 1 or more additional risk factors for diabetes. Testing also should be considered in children and adolescents who are overweight or obese and who have 2 or more additional risk factors. If tests are normal, repeat testing carried out at a minimum of 3-year intervals is suggested [8].

Prediabetes

Abnormalities in glucose metabolism progress along a continuum through various stages before T2DM develops. Years before the development of overt diabetes, and especially in the presence of excessive visceral fat, cellular sensitivity to insulin gradually decreases, leading to a compensatory increased insulin secretion [9]. With time, and under continuous increased demand, pancreatic beta cell function declines and ultimately fails to overcome insulin resistance and maintain a normal glucose metabolism, resulting in prediabetes followed by the development of diabetes. This early beta cell dysfunction was illustrated by the decreased beta cell volume observed on autopsy of obese patients with IFG or T2DM, when compared to obese individuals with normal glucose tolerance [10]. It is estimated that around 40% to 70% of beta cell function is already lost by the time diabetes is clinically diagnosed. This relatively slow pathophysiologic process allows the identification of at-risk patients well before their blood glucose levels reach the diabetic diagnostic thresholds, and therefore presents an opportunity for prevention.

Diagnostic Criteria

The ADA guidelines released in 2003 define prediabetes as IFG (fasting blood glucose [FBG] levels of 100–125 mg/dL), IGT (glucose levels of 140–199 mg/dL at 2 hours during an oral glucose tolerance test [OGTT] following an oral load of 75 g of dextrose), or both. Additionally, hemoglobin A1C (A1C) was introduced as a diagnostic tool for prediabetes in 2010, with values between 5.7% and 6.4% indicating prediabetes [8]. Most of these thresholds were chosen due to their association with increased rates of complications, notably retinopathy and cardiovascular disease.