To examine the association of low-grade systemic inflammation with diabetes, as well as its heterogeneity across subgroups, we designed a case-cohort study representing the ϳ9-year experience of 10,275 Atherosclerosis Risk in Communities Study participants. Analytes were measured on stored plasma of 581 incident cases of diabetes and 572 noncases. Statistically significant hazard ratios of developing diabetes for those in the fourth (versus first) quartile of inflammation markers, adjusted for age, sex, ethnicity, study center, parental history of diabetes, and hypertension, ranged from 1.9 to 2.8 for sialic acid, orosomucoid, interleukin-6, and C-reactive protein. After additional adjustment for BMI, waist-to-hip ratio, and fasting glucose and insulin, only the interleukin-6 association remained statistically significant (HR ‫؍‬ 1.6, 1.01-2.7). Exclusion of GAD antibody-positive individuals changed associations minimally. An overall inflammation score based on these four markers plus white cell count and fibrinogen predicted diabetes in whites but not African Americans (interaction P ‫؍‬ 0.005) and in nonsmokers but not smokers (interaction P ‫؍‬ 0.13). The fully adjusted hazard ratio comparing white nonsmokers with score extremes was 3.7 (P for linear trend ‫؍‬ 0.008). In conclusion, a low-grade inflammation predicts incident type 2 diabetes. The association is absent in smokers and African-Americans. Diabetes 52:1799 -1805, 2003 T ype 2 diabetes is a leading cause of morbidity and mortality. Prevention of diabetes and its associated burden, primarily cardiovascular morbidity and mortality, have become major health issues worldwide (1). Obesity has also become a public health priority, given its growing worldwide epidemic and its vast health consequences. Thus, the pathogenesis of so-called "diabesity"-type 2 diabetes in the milieu of obesity-has recently received increased attention.Although insulin resistance and ␤-cell failure continue to be recognized as the central causal processes in the development of type 2 diabetes, other paradigms have evolved. Influenced by findings indicating an inflammatory basis for cardiovascular diseases and following the "common soil" hypothesis of coronary heart disease and type 2 diabetes, we investigated the association between inflammation markers and incident diabetes, reporting in 1999 that a low-grade inflammation precedes and predicts diabetes development in adults participating in the Atherosclerosis Risk in Communities (ARIC) Study (2). Several reports investigating various markers of inflammation in different population groups have confirmed this association (3-11). The marked variation in magnitude of these reported associations and the frequently modest correlations found between markers of inflammation highlight the difficulty of characterizing this low-grade systemic inflammatory state on the basis of a single analyte.Thus, the purpose of this study is to evaluate the association of incident type 2 diabetes with several markers of inflammation, examined individu...

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The aim of this study was to investigate the relationship between feeding practices in the first year of life and the occurrence of severe early childhood caries (S-ECC) at 4 years of age. A birth cohort study (n = 500) was conducted in children who were born within the public health system in São Leopoldo, Brazil. Feeding practices were assessed using standardized methods at 6 and 12 months of age. A total of 340 children were examined at 4 years of age. S-ECC was defined as recommended by an expert panel for research purposes: ≧1 cavitated, missing or filled smooth surfaces in primary maxillary anterior teeth or d₁₊ mfs ≧5. Poisson regression with robust variance was used in order to determine the early feeding practices which represent risk factors for the occurrence of S-ECC at 4 years of age. The multivariable model showed a higher adjusted risk of S-ECC for the following dietary practices at 12 months: breastfeeding ≧7 times daily (RR = 1.97; 95% CI = 1.45–2.68), high density of sugar (RR = 1.43; 95% CI = 1.08–1.89), bottle use for liquids other than milk (RR = 1.41; 95% CI = 1.08–1.86), as well as number of meals and snacks >8 (RR = 1.42; 95% CI = 1.02–1.97). Mother’s education ≤8 years was also associated with the outcome. The present study identified early feeding practices which represent risk factors for caries severity in subsequent years. These findings may contribute to developing general and oral health interventions, with special attention to families with low maternal education.

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Aims/hypothesis The aim of this study was to investigate the association of leptin levels with incident diabetes in middle-aged adults, taking into account factors purportedly related to leptin resistance. Subjects and methods We conducted a case-cohort study (570 incident diabetes cases and 530 non-cases) representing the 9-year experience of 10,275 participants of the Atherosclerosis Risk in Communities Study. Plasma leptin was measured by direct sandwich ELISA. Results In proportional hazards models adjusting for age, study centre, ethnicity and sex, high leptin levels (defined by sex-specific cut-off points) predicted an increased risk of diabetes, with a hazard ratio (HR) comparing the upper with the lower quartile of 3.9 (95% CI 2.6-5.6). However, after further adjusting additionally for obesity indices, fasting insulin, inflammation score, hypertension, triglycerides and adiponectin, high leptin predicted a lower diabetes risk (HR=0.40, 95% CI 0.23-0.67). Additional inclusion of fasting glucose attenuated this protective association (HR=0.59, 95% CI 0.32-1.08, p<0.03 for linear trend across quartiles). In similar models, protective associations were generally seen across subgroups of sex, race, nutritional status and smoking, though not among those with lower inflammation scores or impaired fasting glucose (interaction p=0.03 for both). Conclusions/interpretation High leptin levels, probably reflecting leptin resistance, predict an increased risk of diabetes. Adjusting for factors purportedly related to leptin resistance unveils a protective association, independent of adiponectin and consistent with some of leptin's described protective effects against diabetes.