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      Maternal and child undernutrition: consequences for adult health and human capital

      review-article
      a , * , e , b , a , d , f , c , for the Maternal and Child Undernutrition Study Group
      Lancet
      Lancet Publishing Group

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          Summary

          In this paper we review the associations between maternal and child undernutrition with human capital and risk of adult diseases in low-income and middle-income countries. We analysed data from five long-standing prospective cohort studies from Brazil, Guatemala, India, the Philippines, and South Africa and noted that indices of maternal and child undernutrition (maternal height, birthweight, intrauterine growth restriction, and weight, height, and body-mass index at 2 years according to the new WHO growth standards) were related to adult outcomes (height, schooling, income or assets, offspring birthweight, body-mass index, glucose concentrations, blood pressure). We undertook systematic reviews of studies from low-income and middle-income countries for these outcomes and for indicators related to blood lipids, cardiovascular disease, lung and immune function, cancers, osteoporosis, and mental illness. Undernutrition was strongly associated, both in the review of published work and in new analyses, with shorter adult height, less schooling, reduced economic productivity, and—for women—lower offspring birthweight. Associations with adult disease indicators were not so clear-cut. Increased size at birth and in childhood were positively associated with adult body-mass index and to a lesser extent with blood pressure values, but not with blood glucose concentrations. In our new analyses and in published work, lower birthweight and undernutrition in childhood were risk factors for high glucose concentrations, blood pressure, and harmful lipid profiles once adult body-mass index and height were adjusted for, suggesting that rapid postnatal weight gain—especially after infancy—is linked to these conditions. The review of published works indicates that there is insufficient information about long-term changes in immune function, blood lipids, or osteoporosis indicators. Birthweight is positively associated with lung function and with the incidence of some cancers, and undernutrition could be associated with mental illness. We noted that height-for-age at 2 years was the best predictor of human capital and that undernutrition is associated with lower human capital. We conclude that damage suffered in early life leads to permanent impairment, and might also affect future generations. Its prevention will probably bring about important health, educational, and economic benefits. Chronic diseases are especially common in undernourished children who experience rapid weight gain after infancy.

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          Most cited references144

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          Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales.

          Although the rise in ischaemic heart disease in England and Wales has been associated with increasing prosperity, mortality rates are highest in the least affluent areas. On division of the country into two hundred and twelve local authority areas a strong geographical relation was found between ischaemic heart disease mortality rates in 1968-78 and infant mortality in 1921-25. Of the twenty-four other common causes of death only bronchitis, stomach cancer, and rheumatic heart disease were similarly related to infant mortality. These diseases are associated with poor living conditions and mortality from them is declining. Ischaemic heart disease is strongly correlated with both neonatal and postneonatal mortality. It is suggested that poor nutrition in early life increases susceptibility to the effects of an affluent diet.
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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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              Is Open Access

              The world health report 2001 - Mental health: new understanding, new hope

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                Author and article information

                Contributors
                Journal
                Lancet
                Lancet
                Lancet
                Lancet Publishing Group
                0140-6736
                1474-547X
                26 January 2008
                26 January 2008
                : 371
                : 9609
                : 340-357
                Affiliations
                [a ]Universidade Federal de Pelotas, Pelotas, Brazil
                [b ]MRC Epidemiology Resource Centre, University of Southampton, Southampton, UK
                [c ]Sitaram Bhartia Institute of Science and Research, New Delhi, India
                [d ]Hubert Department of Global Health, Emory University, Atlanta, USA
                [e ]University of North Carolina at Chapel Hill, Chapel Hill, USA
                [f ]Human Sciences Research Council, Durban, South Africa
                Author notes
                [* ]Correspondence to: Cesar Victora, Universidade Federal de Pelotas, CP 464, 96001-970, Pelotas, Brazil cvictora@ 123456terra.com.br
                [‡]

                Members listed at end of paper

                Article
                LANCET61692
                10.1016/S0140-6736(07)61692-4
                2258311
                18206223
                33efa261-a92a-43d1-b9dc-efc35e4b8269
                © 2008 Elsevier Ltd. All rights reserved.

                This document may be redistributed and reused, subject to certain conditions.

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                Medicine
                Medicine

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