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      Impact of ethnicity on gestational diabetes identified with the WHO and the modified International Association of Diabetes and Pregnancy Study Groups criteria: a population-based cohort study

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          Abstract

          Objective

          The International Association of Diabetes and Pregnancy Study Groups (IADPSG) recently proposed new criteria for diagnosing gestational diabetes mellitus (GDM). We compared prevalence rates, risk factors, and the effect of ethnicity using the World Health Organization (WHO) and modified IADPSG criteria.

          Methods

          This was a population-based cohort study of 823 (74% of eligible) healthy pregnant women, of whom 59% were from ethnic minorities. Universal screening was performed at 28±2 weeks of gestation with the 75 g oral glucose tolerance test (OGTT). Venous plasma glucose (PG) was measured on site. GDM was diagnosed as per the definition of WHO criteria as fasting PG (FPG) ≥7.0 or 2-h PG ≥7.8 mmol/l; and as per the modified IADPSG criteria as FPG ≥5.1 or 2-h PG ≥8.5 mmol/l.

          Results

          OGTT was performed in 759 women. Crude GDM prevalence was 13.0% with WHO (Western Europeans 11%, ethnic minorities 15%, P=0.14) and 31.5% with modified IADPSG criteria (Western Europeans 24%, ethnic minorities 37%, P< 0.001). Using the WHO criteria, ethnic minority origin was an independent predictor (South Asians, odds ratio (OR) 2.24 (95% confidence interval (CI) 1.26–3.97); Middle Easterners, OR 2.13 (1.12–4.08)) after adjustments for age, parity, and prepregnant body mass index (BMI). This increased OR was unapparent after further adjustments for body height (proxy for early life socioeconomic status), education and family history of diabetes. Using the modified IADPSG criteria, prepregnant BMI (1.09 (1.05–1.13)) and ethnic minority origin (South Asians, 2.54 (1.56–4.13)) were independent predictors, while education, body height and family history had little impact.

          Conclusion

          GDM prevalence was overall 2.4-times higher with the modified IADPSG criteria compared with the WHO criteria. The new criteria identified many subjects with a relatively mild increase in FPG, strongly associated with South Asian origin and prepregnant overweight.

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          Most cited references24

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          Type 2 diabetes across generations: from pathophysiology to prevention and management.

          Type 2 diabetes is now a pandemic and shows no signs of abatement. In this Seminar we review the pathophysiology of this disorder, with particular attention to epidemiology, genetics, epigenetics, and molecular cell biology. Evidence is emerging that a substantial part of diabetes susceptibility is acquired early in life, probably owing to fetal or neonatal programming via epigenetic phenomena. Maternal and early childhood health might, therefore, be crucial to the development of effective prevention strategies. Diabetes develops because of inadequate islet β-cell and adipose-tissue responses to chronic fuel excess, which results in so-called nutrient spillover, insulin resistance, and metabolic stress. The latter damages multiple organs. Insulin resistance, while forcing β cells to work harder, might also have an important defensive role against nutrient-related toxic effects in tissues such as the heart. Reversal of overnutrition, healing of the β cells, and lessening of adipose tissue defects should be treatment priorities. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            Is Open Access

            Effect of Treatment of Gestational Diabetes Mellitus on Obesity in the Next Generation

            OBJECTIVE Gestational diabetes mellitus (GDM) may cause obesity in the offspring. The objective was to assess the effect of treatment for mild GDM on the BMI of 4- to 5-year-old children. RESEARCH DESIGN AND METHODS Participants were 199 mothers who participated in a randomized controlled trial of the treatment of mild GDM during pregnancy and their children. Trained nurses measured the height and weight of the children at preschool visits in a state-wide surveillance program in the state of South Australia. The main outcome measure was age- and sex-specific BMI Z score based on standards of the International Obesity Task Force. RESULTS At birth, prevalence of macrosomia (birth weight ≥4,000 g) was 5.3% among the 94 children whose mothers were in the intervention group, and 21.9% among the 105 children in the routine care control group. At 4- to 5-years-old, mean (SD) BMI Z score was 0.49 (1.20) in intervention children and 0.41 (1.40) among controls. The difference between treatment groups was 0.08 (95% CI −0.29 to 0.44), an estimate minimally changed by adjustment for maternal race, parity, age, and socio-economic index (0.08 [−0.29 to 0.45]). Evaluating BMI ≥85th percentile rather than continuous BMI Z score gave similarly null results. CONCLUSIONS Although treatment of GDM substantially reduced macrosomia at birth, it did not result in a change in BMI at age 4- to 5-years-old.
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              Learning to live with complexity: ethnicity, socioeconomic position, and health in Britain and the United States.

              G D Smith (2000)
              The relation between ethnicity, socioeconomic position, and health is complex, has changed over time, and differs between countries. In the United States there is a long tradition of treating ethnic group membership simply as a socioeconomic measure, and differentials in health status between African Americans and groups of European origin have been considered purely socioeconomic. A contrary position sees the differences as either "cultural" or due to inherent "racial" differences. Although conventional socioeconomic indicators statistically explain much of the health difference between African Americans and Americans of European origin, they do not tell the full story. Incommensurate measures of socioeconomic position across ethnic groups clearly contribute to this difference. Additional factors, such as the extent of racism, are also likely to be important. The interaction of ethnicity, social position, and health in Britain is similarly complex. Studies that inadequately account for socioeconomic circumstances when examining ethnic-group differences in health can reify ethnicity (and its supposed correlates); however, the reductionist attribution of all ethnic differences in health to socioeconomic factors is untenable. The only productive way forward is through studies that recognize the contingency of the relations between socioeconomic position, ethnicity, and particular health outcomes.
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                Author and article information

                Journal
                Eur J Endocrinol
                Eur. J. Endocrinol
                EJE
                European Journal of Endocrinology
                BioScientifica (Bristol )
                0804-4643
                1479-683X
                February 2012
                10 November 2011
                : 166
                : 2
                : 317-324
                Affiliations
                [1 ]Department of Endocrinology Oslo University Hospital HF, Aker PO Box 4959 Nydalen, N-0424, OsloNorway
                [2 ]Faculty of Medicine University of Oslo OsloNorway
                [3 ]Oslo and Akershus University College of Applied Sciences PO Box 4, St. Olavs plass, N-0130, OsloNorway
                [4 ]Department of Child and Adolescents Medicine Akershus University Hospital N-1478, LørenskogNorway
                [5 ]Department of Obstetrics and Gynecology Oslo University Hospital HF, Rikshospitalet PO Box 4950 Nydalen, N-0424, OsloNorway
                [6 ]Stovner Municipality Karl Fossums Vei 30, N-0985, OsloNorway
                [7 ]Department of Public Health, Sport and Nutrition University of Agder PO Box 422, N-4604, KristiansandNorway
                [8 ]Department of Oncology and Medical Physics Haukeland University Hospital BergenNorway
                [9 ]Department of Pediatrics Oslo University Hospital HF, Ullevål PO Box 4956 Nydalen, N-0424, OsloNorway
                [10 ]Unit of Biostatistic and Epidemiology Oslo University Hospital HF, Ullevål PO Box 4956 Nydalen, , N-0424, OsloNorway
                [11 ]Department of Preventive Medicine Oslo University Hospital HF, Ullevål PO Box 4956 Nydalen, N-0424, OsloNorway
                [12 ]Diabetes Unit King Edward Memorial Hospital, Rasta Peth Pune, 411011India
                Author notes
                (Correspondence should be addressed to A K Jenum at Department of Endocrinology, Oslo University Hospital; Email: a.k.jenum@ 123456medisin.uio.no )
                [*]

                (A K Jenum and K Mørkrid are first authors)

                Article
                EJE110866
                10.1530/EJE-11-0866
                3260695
                22108914
                0263f45f-f6ee-4130-9aad-e4a20a8e2429
                © 2012 European Society of Endocrinology

                This is an Open Access article distributed under the terms of the European Journal of Endocrinology's Re-use Licence which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 5 October 2011
                : 22 November 2011
                Funding
                Funded by: The Research Council of Norway
                Categories
                Clinical Study

                Endocrinology & Diabetes
                Endocrinology & Diabetes

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