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      Metabolic syndrome in Spanish adolescents and its association with birth weight, breastfeeding duration, maternal smoking, and maternal obesity: a cross-sectional study

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          Prenatal origin of obesity and their complications: Gestational diabetes, maternal overweight and the paradoxical effects of fetal growth restriction and macrosomia.

          Pregestational (PGDM) and gestational (GDM) diabetes may be associated with a variety of fetal effects including increased rate of spontaneous abortions, intrauterine fetal death, congenital anomalies, neurodevelopmental problems and increased risk of perinatal complications. Additional problems of concern are fetal growth disturbances causing increased or decreased birth weight. Optimal control of maternal blood glucose is known to reduce these changes. Among the long lasting effects of these phenomena are a high rate of overweight and obesity at childhood and a high tendency to develop the "metabolic syndrome" characterized by hypertension, cardio-vascular complications and type 2 diabetes. Similarly, maternal overweight and obesity during pregnancy or excessive weight gain are also associated with increased obesity and complications in the offspring. Although there are different causes for fetal growth restriction (FGR) or for fetal excessive growth (macrosomis), paradoxically both are associated with the "metabolic syndrome" and its long term consequences. The exact mechanism(s) underlying these long term effects on growth are not fully elucidated, but they involve insulin resistance, fetal hyperleptinemia, hypothalamic changes and most probably epigenetic changes. Preventive measures to avoid the metabolic syndrome and its complications seem to be a tight dietary control and physical activity in the children born to obese or diabetic mothers or who had antenatal growth disturbances for other known or unknown reasons. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Association of weight gain in infancy and early childhood with metabolic risk in young adults.

            Early postnatal life has been suggested as an important window during which risks for long-term health may be influenced. The aim of this study was to examine the independent associations between weight gain during infancy (0-6 months) and early childhood (3-6 yr) with components of the metabolic syndrome in young adults. This was a prospective cohort study (The Stockholm Weight Development Study). The study was conducted in a general community. Subjects included 128 (54 males) singletons, followed from birth to 17 yr. None of these young adults met the full criteria for the metabolic syndrome. We therefore calculated a continuous clustered metabolic risk score by averaging the standardized values of the following components: waist circumference, blood pressure, fasting triglycerides, high-density lipoprotein cholesterol, glucose, and insulin level. Clustered metabolic risk at age 17 yr was predicted by weight gain during infancy (standardized beta = 0.16; P < 0.0001) but not during early childhood (standardized beta = 0.10; P = 0.23), adjusted for birth weight, gestational age, current height, maternal fat mass, and socioeconomic status at age 17 yr. Further adjustment for current fat mass and weight gain during childhood did not alter the significant association between infancy weight gain with the metabolic risk score (standardized beta = 0.20; P = 0.007). Rapid weight gain during infancy (0-6 months) but not during early childhood (3-6 yr) predicted clustered metabolic risk at age 17 yr. Early interventions to moderate rapid weight gain even at very young ages may help to reduce adult cardiovascular disease risks.
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              Determination of body composition of children from skinfold measurements.

              C. Brook (1971)
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                Author and article information

                Journal
                European Journal of Nutrition
                Eur J Nutr
                Springer Science and Business Media LLC
                1436-6207
                1436-6215
                June 2015
                July 23 2014
                June 2015
                : 54
                : 4
                : 589-597
                Article
                10.1007/s00394-014-0740-x
                25052543
                9e1dca64-64e0-4c81-99d4-7cf7764234a2
                © 2015

                http://www.springer.com/tdm

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