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Background The 10/66 Dementia Research Group developed and validated a culture and education fair battery of cognitive tests for diagnosis of dementia in population-based studies in low-income and middle-income countries including India. Aims This study examined the association between individual domains of the 10/66 battery of cognitive tests and ‘disability’ and ‘functional impairment’ in community-dwelling older adults in South India. Methods One hundred twenty-nine adults aged 60–90 years residing in Karunapura, in the city of Mysore, were interviewed in their own homes. Cognitive functioning was measured by administering the 10/66 battery of cognitive tests that composes of Community Screening Instrument for Dementia (CSI'D' COGSCORE), verbal fluency (VF) and word list memory recall (WLMR). A reliable informant was interviewed to ascertain if the subject's cognitive problems have resulted in functional impairment. Disability was measured by WHO Disability Schedule-II (DAS). Results The women had significantly lower CSI'D' COGSCORE score when compared with men (p = 0.002). The presence of ‘functional impairment’ resulting from cognitive decline was significantly associated with lower scores on VF (p = 0.03), WLMR (p = 0.03) and CSI'D' COGSCOREs (p

Background: studies since the early 1990s have shown that birth size can be a predictor of the development of Type 2 diabetes mellitus (T2DM). In the present study, we evaluated changes in the strength of associations between T2DM and birth size and maternal weight with age. Methods: in 1993–1994 (t0), 509 men and women (mean age 46 years) who had been born in Holdsworth Memorial Hospital were screened for diabetes, with increased diabetes risk identified in those who were shorter at birth and those born to heavier mothers. Ten years later (t10), the screening was repeated in 266 subjects who were non-diabetic at t0 (70% of survivors). Results: at t10, 56 new cases of diabetes were found. The incidence of diabetes decreased with increasing birth length (odds ratio (OR) = 0.90, 95% confidence interval (CI) 0.84–0.97/cm birth length; P = 0.006) after adjustment for sex, age, socioeconomic status, family history, and current body mass index. Overall, there were no significant differences in OR for the association between birth length and diabetes at t0 compared with t10, but limiting analysis to subjects with normal glucose tolerance at t0 resulted in a stronger association at t10 (OR = 0.71, 95% CI 0.58–0.87) than at t0 (OR = 0.95, 95% CI 0.86–1.05; P = 0.015 for the difference). There was a positive correlation between maternal weight and incident disease at t0 (OR = 1.08, 95% CI 1.03–1.14; P = 0.001), but not at t10 (OR = 0.98/kg, 95% CI 0.92–1.05; P = 0.6; P = 0.02 for the difference). Conclusions: short birth length remains a risk factor for diabetes. Changes in the effects of birth length and maternal weight on diabetes risk with age may indicate different causal pathways. These findings require replication in studies with more accurate dating of the onset of diabetes

The metabolic syndrome, a cluster of abnormalities including glucose intolerance, hypertension and dyslipidaemia (Reaven, 1988), has many similarities with Cushing’s syndrome which has led to the suggestion that a milder degree of hypothalamic–pituitary–adrenal (HPA) axis dysregulation may underlie this phenotype. This is supported by cross-sectional studies which show that individuals with raised blood pressure, glucose intolerance or other features of the metabolic syndrome have raised fasting plasma cortisol concentrations and increased reactivity of the HPA axis (Filipovsky et al., 1996; Phillips et al., 1998; Lee et al., 1999). The interplay between obesity and the HPA axis is complex. Tissue steroid metabolism, principally reactivation of cortisol by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in the liver, is altered in obese individuals leading to increased metabolic clearance of cortisol (Andrew et al., 1998; Stewart et al., 1999; Rask et al., 2001, 2002). As a result, although cortisol secretion is enhanced somewhat, circulating cortisol concentrations are generally normal or low in obese subjects. However, some studies suggest that a subset of individuals who maintain raised plasma cortisol concentrations in the face of obesity have a high prevalence of the metabolic syndrome. In these subjects, increased plasma cortisol concentrations or HPA reactivity add to the effect of adiposity in determining the risk of glucose intolerance, raised blood pressure and the metabolic syndrome (Phillips et al., 2000; Walker et al., 2000; Reynolds et al., 2001). South Asians have a high morbidity and mortality from coronary heart disease and the cardiovascular risk factors which comprise the metabolic syndrome are prevalent. Although South Asians have a relatively high proportion of fat, particularly visceral fat, across the body mass index (BMI) range compared with Caucasian populations, the increase in adiposity does not fully explain the high prevalence of the metabolic syndrome (McKeigue et al., 1991; Shelgikar et al., 1991; Banerji et al., 1999). A greater understanding of the mechanisms underlying this increased cardiovascular risk may allow new therapies to be developed. The role of glucocorticoids has not previously been investigated in this ethnic group. We have investigated the relationship between fasting 09·00 h cortisol concentration and cardiovascular risk factors in 509 adults from Mysore, South India to investigate the hypothesis that the high prevalence of the metabolic syndrome in South Asians is mediated by HPA axis hyperactivity.

Recent research in Europe and the USA has shown that adults who had a low birthweight or who were thin at birth with a low ponderal index (birthweight/length3) tend to be insulin resistant and have an increased risk of developing Type 2 diabetes mellitus. Low birthweight and Type 2 diabetes are common in India. We have studied glucose and insulin metabolism in 506 men and women (aged 39-60 years) born in a hospital in Mysore, South India, which kept detailed obstetric records from 1934. The prevalence of Type 2 diabetes was 15%. In contrast to Western populations, higher rates were found in men and women who were short at birth (p = 0.07) and had a high ponderal index (p = 0.05). Their mothers tended to be heavier than average during pregnancy (p = 0.004). Higher ponderal index at birth was also associated with a lower 30 minute insulin increment (p = 0.009), a marker of reduced beta cell function. We speculate that the rise in Type 2 diabetes in Indian urban populations may have been triggered by mild obesity in mothers, leading to glucose intolerance during pregnancy, macrosomic changes in the fetus, and insulin deficiency in adult life.