IMPORTANCEThe term prediabetes is used to identify individuals at increased risk for diabetes. However, the natural history of prediabetes in older age is not well characterized.OBJECTIVES To compare different prediabetes definitions and characterize the risks of prediabetes and diabetes among older adults in a community-based setting. DESIGN, SETTING, AND PARTICIPANTS In this prospective cohort analysis of 3412 older adults without diabetes from the Atherosclerosis Risk in Communities Study (baseline, 2011-2013), participants were contacted semiannually through December 31, 2017, and attended a follow-up visit between January 1, 2016, and December 31, 2017 (median [range] follow-up, 5.0 [0.1-6.5] years). EXPOSURES Prediabetes defined by a glycated hemoglobin (HbA 1c ) level of 5.7% to 6.4%, impaired fasting glucose (IFG) level (FG level of 100-125 mg/dL), either, or both. MAIN OUTCOMES AND MEASURES Incident total diabetes (physician diagnosis, glucose-lowering medication use, HbA 1c level Ն6.5%, or FG level Ն126 mg/dL). RESULTS A total of 3412 participants without diabetes (mean [SD] age, 75.6 [5.2] years; 2040 [60%] female; and 572 [17%] Black) attended visit 5 (2011-2013, baseline). Of the 3412 participants at baseline, a total of 2497 participants attended the follow-up visit or died. During the 6.5-year follow-up period, there were 156 incident total diabetes cases (118 diagnosed) and 434 deaths. A total of 1490 participants (44%) had HbA 1c levels of 5.7% to 6.4%, 1996 (59%) had IFG, 2482 (73%) met the HbA 1c or IFG criteria, and 1004 (29%) met both the HbA 1c and IFG criteria. Among participants with HbA 1c levels of 5.7% to 6.4% at baseline, 97 (9%) progressed to diabetes, 148 (13%) regressed to normoglycemia (HbA 1c , <5.7%), and 207 (19%) died. Of those with IFG at baseline, 112 (8%) progressed to diabetes, 647 (44%) regressed to normoglycemia (FG, <100 mg/dL), and 236 (16%) died. Of those with baseline HbA 1c levels less than 5.7%, 239 (17%) progressed to HbA 1c levels of 5.7% to 6.4% and 41 (3%) developed diabetes. Of those with baseline FG levels less than 100 mg/dL, 80 (8%) progressed to IFG (FG, 100-125 mg/dL) and 26 (3%) developed diabetes. CONCLUSIONS AND RELEVANCEIn this community-based cohort study of older adults, the prevalence of prediabetes was high; however, during the study period, regression to normoglycemia or death was more frequent than progression to diabetes. These findings suggest that prediabetes may not be a robust diagnostic entity in older age.

Aims/hypothesis Ideal cardiovascular health (CVH) is associated with lower diabetes risk. However, it is unclear whether this association is similar across glycaemic levels (normal [<5.6 mmol/l] vs impaired fasting glucose [IFG] [5.6-6.9 mmol/l]). Methods A secondary data analysis was performed in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study. Incident diabetes was assessed among 7758 participants without diabetes at baseline (2003-2007) followed over 9.5 years. Baseline cholesterol, blood pressure, diet, smoking, physical activity and BMI were used to categorise participants based on the number (0-1, 2-3 and ≥4) of ideal CVH components. Risk ratios (RRs) were calculated using modified Poisson regression, adjusting for cardiovascular risk factors. Results Among participants (mean age 63.0 [SD 8.4] years, 56% female, 73% white, 27% African-American), there were 891 incident diabetes cases. Participants with ≥4 vs 0-1 ideal CVH components with normal fasting glucose (n = 6004) had 80% lower risk (RR 0.20; 95% CI 0.10, 0.37), while participants with baseline IFG (n = 1754) had 13% lower risk (RR 0.87; 95% CI 0.58, 1.30) (p for interaction by baseline glucose status <0.0001). Additionally, the magnitude of the association of ideal CVH components with lower diabetes risk was stronger among white than African-American participants (p for interaction = 0.0338). Conclusions/interpretation A higher number of ideal CVH components was associated with a dose-dependent lower risk of diabetes for participants with normal fasting glucose but not IFG. Tailored efforts that take into account observed differences by race and glycaemic level are needed for the primordial prevention of diabetes.

BackgroundMechanistic studies suggest that aldosterone impairs glucose metabolism. We investigated the cross‐sectional associations of aldosterone and plasma renin activity with fasting plasma glucose, insulin resistance (IR), β‐cell function, and longitudinal association with incident diabetes mellitus among adults in MESA (the multiethnic study of atherosclerosis) prospective cohort study.Methods and ResultsHomeostatic model assessment of IR (HOMA2‐IR) and HOMA2‐β were used to estimate IR and β‐cell function, respectively. Incident diabetes mellitus was defined as fasting plasma glucose ≥126 mg/dL or anti‐diabetic medication use at follow‐up. Linear regression was used to examine cross‐sectional associations of aldosterone with fasting plasma glucose, HOMA2‐IR and HOMA2‐β; Cox regression was used to estimate hazard ratios (HR) for incident diabetes mellitus with multivariable adjustment. There were 116 cases of incident diabetes mellitus over 10.5 years among 1570 adults (44% non‐Hispanic white, 13% Chinese American, 19% Black, 24% Hispanic American, mean age 64±10 years, 51% female). A 100% increase in log‐aldosterone was associated with a 2.6 mg/dL higher fasting plasma glucose, 15% higher HOMA2‐IR and 6% higher HOMA2‐β (P<0.01). A 1‐SD increase in log‐aldosterone was associated with a 44% higher risk of incident diabetes mellitus (P<0.01) with the greatest increase of 142% (P<0.01) observed in Chinese Americans (P for interaction=0.09 versus other ethnicities). Similar cross‐sectional findings for log‐plasma renin activity existed, but log‐plasma renin activity was not associated with incident diabetes mellitus after full adjustment.ConclusionsAldosterone is associated with glucose homeostasis and diabetes mellitus risk with graded associations among Chinese Americans and blacks, suggesting that pleiotropic effects of aldosterone may represent a modifiable mechanism in diabetes mellitus pathogenesis with potential racial/ethnic variation.