Childhood obesity and insulin resistance

Insulin resistance (IR) in childhood has importance to the understanding and prevention of the growing epidemic of insulin resistance syndrome (IRS) in adults with attendant obesity, type 2 diabetes (T2DM), atherosclerotic diseases, hypertension, gout, non-alcoholic, steato-hepatitis (NASH), gall bladder disease, nephropathy, polycystic ovarian disease (PCOS), infertility and premature senility. The severity of IR and its’ complications in children unfortunately and usually progresses in their pubertal transition to adulthood; affected young children are more likely than adults to have underlying causal monogenic disorders; the sequence of natural history and events give insights into disease pathogeneses, and optimal life style choices that last are best made during the early formative years. Some features of IR in children discussed herein are: a strong tendency to low birth weight for gestational age, adverse effects of adrenarche and therapeutic steroid therapy, predisposition to premature pubarche, acanthosis nigricans, tall stature despite pituitary GH suppression, allergic diathesis, hyperandrogenism and PCOS, dyslipidemia and fatty liver disease, and diagnosis by clinical and biochemical markers of IR including insulin regulated hepatic hormonal binding proteins such as IGFBP-1. The national preoccupation with the “metabolic syndrome” T2DM and obesity, should be appropriately directed to an improved understanding of IR in children and their management, if the looming health crisis in affected adults is to be seriously addressed. The nation is facing its’ first generation of children who will be less healthy and die younger than the previous generation (Marks (2005) Presentation to the American Association of Diabetes Educators 32nd Annual Meeting and Exhibition, August 10–13, Washington, DC).     

Childhood influences on youth obesity

We develop a model to estimate the influence of child and parental characteristics on the likelihood that a child will become an obese or overweight youth. We use this model to test whether it is possible to forecast obesity and overweight among youth. Comparing Receiver Operating Characteristic (ROC) scores from these forecasts, we find that a model using childhood covariates does as well in forecasting youth obesity and overweight as a model using the covariate values contemporaneous with the youth obesity and overweight outcomes. The datasets used in this paper, the National Longitudinal Survey of Youth (NLSY79) and the NLSY79 Children and Young Adults, provide data from 1986 to 2002, allowing for the study of a child's transition to and from obesity or overweight over a long period. Explanatory variables that significantly influence the likelihood of youth obesity or overweight outcomes include the mother's obesity status and education, the youth's mental health, and certain demographic features including race, sex, and family size. These factors provide potential targets for policies that could be implemented early in life among children most likely to become obese or overweight.     

Childhood conditions and adult height

Self-reported height and childhood conditions among 1711 Danish male general workers born between 1923 and 1940 were analysed. No significant associations were found between adult height and father's occupation, growing up with both parents, paternal unemployment, sickness among the parents, parents receiving disability pension, economical problems in childhood, area of residence in childhood, and years at school. The study therefore provides no support for the hypothesis that poor childhood conditions are the cause of low adult height in this socially very homogeneous sample.     

Childhood obesity: genetic and environmental overlap with normal-range BMI

Objective: To understand the overlap between the etiology of obesity and normal variation in BMI in children. Methods and Procedures: Height and weight data were available from a large UK representative sample of twins: 2,342 same‐sex pairs at 7 years and 3,526 same‐sex pairs at 10 years. The twin method and model‐fitting techniques were used to estimate genetic and environmental contributions to BMI. DeFries‐Fulker (DF) extremes analysis was used to investigate genetic and environmental influences on the mean difference between obese and normal‐weight children. Obesity was classified using the International Obesity Task Force (IOTF) criteria. Results: At both ages, BMI and obesity were highly heritable (0.60–0.74) and only modestly influenced by shared environmental factors (0.12–0.22). Extremes analyses indicated that genetic and environmental influences on obesity are quantitatively and qualitatively similar to those operating across the range of BMI. Discussion: Obesity is the extreme of the same genetic and environmental factors responsible for variation throughout the distribution of BMI. This finding implies that genes that influence obesity will also be associated with BMI in the normal range, and similar environmental influences will affect BMI in the clinical and normal range. Knowing that obesity is influenced by the same genetic and environmental factors that affect weight at all levels has implications for investigating the mechanisms for weight gain and developing interventions for weight control.     

Covariates and prevalence of obesity among adult North Indian population

The present study was aimed to investigate the prevalence of obesity and its covariates including age among adult Khatri males and females. A total of 805 subjects (male = 381, female = 424) between age of 18 yr to 71 + yr residing in Shahjahanpur city, Uttar Pradesh, India were studied cross sectionally. The study highlights the trend of obesity in the population and also discusses in detail, the factors that cause it. An inverse relationship was obtained between level of physical activity and different relative weight categories based on body mass index in both the sexes. Similar association was observed in case of television watching time and overweight/obesity. With increase in hours of television watching the prevalence of overweight/obese also increased among both Khatri males and females.     

Non-shivering thermogenesis and obesity in adult diabetic Wistar fatty rats

1. Characteristics of resting and of norepinephrine (NE)-stimulated thermogenesis, and the glycemic response to NE were determined in adult male Wistar Fatty rats. Rats were maintained on Purina chow No. 5001 until 22 weeks of age, and fed semisynthetic diets containing 54% carbohydrate, 20% protein, 16% mixed fats, plus essential vitamins, minerals, and non-nutritive fiber from 22 until 30 weeks of age. 2. Obese rats were 50% heavier than lean throughout the study. Phenotype effects (obese greater than lean) were present for retroperitoneal (RP) and dorsal (DOR) white fat depot weight, adipocyte number per depot, and adipocyte lipid content. Epididymal mass and cellularity were similar in both phenotypes. 3. Interscapular brown adipose tissue (IBAT) mass, adipocyte size, and adipocyte number were greater in obese than in lean. Resting metabolic rates (RMR) of obese rats were lower than in lean, and increased 79% in lean but only 33% in obese animals following NE (200 micrograms/kg BW, s.c.) stimulation. 4. The glycemic response to NE occurred normally in both phenotypes, and resulted in a 3-fold increment in plasma glucose in lean rats and a 5-6-fold increase in plasma glucose in obese rats. 5. The results of this study are consistent with hyperplasia and hypertrophy of IBAT, RP and DOR depots, and indicate that the capacity for non-shivering thermogenesis is impaired in the obese phenotype of this strain in spite of peripheral sensitivity to NE and greater mass and cellularity of brown adipose tissue.     

Childhood respiratory infection and adult chronic bronchitis in England and Wales.

The high mortality from chronic bronchitis in England and Wales and the excess of urban over rural mortality are unexplained. On dividing England and Wales into 212 local authority areas a strong geographical relation was found between death rates from chronic bronchitis and emphysema in 1959-78 and infant mortality from bronchitis and pneumonia during 1921-5. It was concluded that this relation provided strong evidence of a direct casual link between acute lower respiratory infection in early childhood and chronic bronchitis in adult life. Regression analysis suggested that infection in early childhood had a greater influence than cigarette smoking in determining the geographical distribution of chronic bronchitis. National time trends reflected the influence of both factors. Chronic air pollution in adult life may be less important a cause of chronic bronchitis than previously supposed.