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      Exposure to the Chinese Famine in Early Life and the Risk of Hyperglycemia and Type 2 Diabetes in Adulthood

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          Abstract

          OBJECTIVE

          Early developmental adaptations in response to undernutrition may play an essential role in susceptibility to type 2 diabetes, particularly for those experiencing a “mismatched rich nutritional environment” in later life. We examined the associations of exposure to the Chinese famine (1959–1961) during fetal life and childhood with the risk of hyperglycemia and type 2 diabetes in adulthood.

          RESEARCH DESIGN AND METHODS

          We used the data for 7,874 rural adults born between 1954 and 1964 in selected communities from the cross-sectional 2002 China National Nutrition and Health Survey. Hyperglycemia was defined as fasting plasma glucose ≥6.1 mmol/l and/or 2-h plasma glucose ≥7.8 mmol/l and/or a previous clinical diagnosis of type 2 diabetes.

          RESULTS

          Prevalences of hyperglycemia among adults in nonexposed, fetal exposed, early-childhood, mid-childhood, and late-childhood exposed cohorts were 2.4%, 5.7%, 3.9%, 3.4%, and 5.9%, respectively. In severely affected famine areas, fetal-exposed subjects had an increased risk of hyperglycemia compared with nonexposed subjects (odds ratio = 3.92; 95% CI: 1.64–9.39; P = 0.002); this difference was not observed in less severely affected famine areas (odds ratio = 0.57; 95% CI: 0.25–1.31; P = 0.185). The odds ratios were significantly different between groups from the severe and less severe famine areas ( P for interaction = 0.001). In severely affected famine areas, fetal-exposed subjects who followed an affluent/Western dietary pattern (odds ratios = 7.63; 95% CI: 2.41–24.1; P = 0.0005) or who had a higher economic status in later life experienced a substantially elevated risk of hyperglycemia (odds ratios = 6.20; 95% CI: 2.08–18.5; P = 0.001).

          CONCLUSIONS

          Fetal exposure to the severe Chinese famine increases the risk of hyperglycemia in adulthood. This association appears to be exacerbated by a nutritionally rich environment in later life.

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          Most cited references 14

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          The thrifty phenotype hypothesis.

          The thrifty phenotype hypothesis proposes that the epidemiological associations between poor fetal and infant growth and the subsequent development of type 2 diabetes and the metabolic syndrome result from the effects of poor nutrition in early life, which produces permanent changes in glucose-insulin metabolism. These changes include reduced capacity for insulin secretion and insulin resistance which, combined with effects of obesity, ageing and physical inactivity, are the most important factors in determining type 2 diabetes. Since the hypothesis was proposed, many studies world-wide have confirmed the initial epidemiological evidence, although the strength of the relationships has varied from one study to another. The relationship with insulin resistance is clear at all ages studied. Less clear is the relationship with insulin secretion. The relative contribution of genes and environment to these relationships remains a matter of debate. The contributions of maternal hyperglycaemia and the trajectory of postnatal growth need to be clarified.
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            Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959-1961.

            Schizophrenia is a common major mental disorder. Intrauterine nutritional deficiency may increase the risk of schizophrenia. The main evidence comes from studies of the 1944-1945 Dutch Hunger Winter when a sharp and time-limited decline in food intake occurred. The most exposed cohort conceived during the famine showed a 2-fold increased risk of schizophrenia. To determine whether those who endured a massive 1959-1961 famine in China experienced similar results. The risk of schizophrenia was examined in the Wuhu region of Anhui, one of the most affected provinces. Rates were compared among those born before, during, and after the famine years. Wuhu and its surrounding 6 counties are served by a single psychiatric hospital. All psychiatric case records for the years 1971 through 2001 were examined, and clinical and sociodemographic information on patients with schizophrenia was extracted by researchers who were blinded to the nature of exposure. Data on number of births and deaths in the famine years were available, and cumulative mortality was estimated from later demographic surveys. Evidence of famine was verified, and unadjusted and mortality-adjusted relative risks of schizophrenia were calculated. The birth rates (per 1000) in Anhui decreased approximately 80% during the famine years from 28.28 in 1958 and 20.97 in 1959 to 8.61 in 1960 and 11.06 in 1961. Among births that occurred during the famine years, the adjusted risk of developing schizophrenia in later life increased significantly, from 0.84% in 1959 to 2.15% in 1960 and 1.81% in 1961. The mortality-adjusted relative risk was 2.30 (95% confidence interval, 1.99-2.65) for those born in 1960 and 1.93 (95% confidence interval, 1.68-2.23) for those born in 1961. Our findings replicate the Dutch data for a separate racial group and show that prenatal exposure to famine increases risk of schizophrenia in later life.
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              Towards a new developmental synthesis: adaptive developmental plasticity and human disease.

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                Author and article information

                Journal
                Diabetes
                diabetes
                diabetes
                Diabetes
                Diabetes
                American Diabetes Association
                0012-1797
                1939-327X
                October 2010
                9 July 2010
                : 59
                : 10
                : 2400-2406
                Affiliations
                1National Institute for Nutrition and Food Safety, Chinese Center for Disease Control and Prevention, Beijing, China;
                2Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts;
                3Division of Human Nutrition, Wageningen University, Wageningen, the Netherlands;
                4Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts;
                5Departments of Epidemiology and Pediatrics, Erasmus MC, Rotterdam, the Netherlands.
                Author notes
                Corresponding authors: Yanping Li, liyanping72@ 123456yahoo.com ; or Guansheng Ma, mags@ 123456chinacdc.net.cn ; or Frank B. Hu, nhbfh@ 123456channing.harvard.edu .

                Y.L. and Y.H. contributed equally to this study.

                Article
                0385
                10.2337/db10-0385
                3279550
                20622161
                © 2010 by the American Diabetes Association.

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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                Categories
                Metabolism

                Endocrinology & Diabetes

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