Plasma glucose levels as predictors of diabetes: the Mexico City diabetes study

The value of diagnostic categories of glucose intolerance for predicting type 2 diabetes is much debated. We therefore sought to estimate relative and population-attributable risk of different definitions based on fasting (impaired fasting glucose [IFG]) or 2 h plasma glucose concentrations (impaired glucose tolerance [IGT]) and to describe the associated clinical phenotypes. We prospectively observed a population-based cohort of 1,963 non-diabetic participants (mean age 47 years), in whom an OGTT was performed at baseline and 7 years later. IGT was fivefold more prevalent (13.5%) than IFG. In both categories, participants were older, heavier, hyperinsulinaemic, hyperproinsulinaemic and dyslipidaemic compared with participants with normal glucose tolerance. Relative risk of incident diabetes was similar for IFG and IGT categories (3.73 [95% CI: 2.18-6.39] and 4.01 [95% CI: 3.12-5.14], respectively), but the population-attributable risk was fivefold higher for IGT (29% [95% CI: 26-32]) than for IFG (6% [95% CI: 5-7]). Isolated IFG carried no increase in risk. Lowering the threshold to 5.6 mmol/l raised the population-attributable risk of IFG to 23% (95% CI: 20-25); its contribution to diabetes progression, however, was largely due to co-existent IGT. In multivariate analysis adjusting for sex, age, familial diabetes and BMI, fasting and 2 h glucose were independent predictors. Fasting and 2 h glucose values are independent predictors of incident diabetes. Isolated IFG is not a high-risk condition; lowering the diagnostic threshold increases the population-attributable risk of IFG fourfold, but performing an OGTT captures additional diabetes progressors compared with the number identified by IFG

Data resource profile: the World Health Organization study on global AGEing and adult health (SAGE)

Population ageing is rapidly becoming a global issue and will have a major impact on health policies and programmes. The World Health Organization's Study on global AGEing and adult health (SAGE) aims to address the gap in reliable data and scientific knowledge on ageing and health in low- and middle-income countries. SAGE is a longitudinal study with nationally representative samples of persons aged 50+ years in China, Ghana, India, Mexico, Russia and South Africa, with a smaller sample of adults aged 18-49 years in each country for comparisons. Instruments are compatible with other large high-income country longitudinal ageing studies. Wave 1 was conducted during 2007-2010 and included a total of 34 124 respondents aged 50+ and 8340 aged 18-49. In four countries, a subsample consisting of 8160 respondents participated in Wave 1 and the 2002/04 World Health Survey (referred to as SAGE Wave 0). Wave 2 data collection will start in 2012/13, following up all Wave 1 respondents. Wave 3 is planned for 2014/15. SAGE is committed to the public release of study instruments, protocols and meta- and micro-data: access is provided upon completion of a Users Agreement available through WHO's SAGE website (www.who.int/healthinfo/systems/sage) and WHO's archive using the National Data Archive application (http://apps.who.int/healthinfo/systems/surveydata).

Alzheimer's disease and symbiotic microbiota: an evolutionary medicine perspective

Microorganisms resident in our bodies participate in a variety of regulatory and pathogenic processes. Here, we describe how etiological pathways implicated in Alzheimer’s disease (AD) may be regulated or disturbed by symbiotic microbial activity. Furthermore, the composition of symbiotic microbes has changed dramatically across human history alongside the rise of agriculturalism, industrialization, and globalization. We postulate that each of these lifestyle transitions engendered progressive depletion of microbial diversity and enhancement of virulence, thereby enhancing AD risk pathways. It is likely that the human life span extended into the eighth decade tens of thousands of years ago, yet little is known about premodern geriatric epidemiology. We propose that microbiota of the gut, oral cavity, nasal cavity, and brain may modulate AD pathogenesis, and that changes in the microbial composition of these body regions across history suggest escalation of AD risk. Dysbiosis may promote immunoregulatory dysfunction due to inadequate education of the immune system, chronic inflammation, and epithelial barrier permeability. Subsequently, proinflammatory agents—and occasionally microbes—may infiltrate the brain and promote AD pathogenic processes. APOE genotypes appear to moderate the effect of dysbiosis on AD risk. Elucidating the effect of symbiotic microbiota on AD pathogenesis could contribute to basic and translational research