+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Critical windows for nutritional interventions against stunting 1 2 3

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          An analysis of early growth patterns in children from 54 resource-poor countries in Africa and Southeast Asia shows a rapid falloff in the height-for-age z score during the first 2 y of life and no recovery until ≥5 y of age. This finding has focused attention on the period −9 to 24 mo as a window of opportunity for interventions against stunting and has garnered considerable political backing for investment targeted at the first 1000 d. These important initiatives should not be undermined, but the objective of this study was to counteract the growing impression that interventions outside of this period cannot be effective. We illustrate our arguments using longitudinal data from the Consortium of Health Oriented Research in Transitioning collaboration (Brazil, Guatemala, India, Philippines, and South Africa) and our own cross-sectional and longitudinal growth data from rural Gambia. We show that substantial height catch-up occurs between 24 mo and midchildhood and again between midchildhood and adulthood, even in the absence of any interventions. Longitudinal growth data from rural Gambia also illustrate that an extended pubertal growth phase allows very considerable height recovery, especially in girls during adolescence. In light of the critical importance of maternal stature to her children's health, our arguments are a reminder of the importance of the more comprehensive UNICEF/Sub-Committee on Nutrition Through the Life-Cycle approach. In particular, we argue that adolescence represents an additional window of opportunity during which substantial life cycle and intergenerational effects can be accrued. The regulation of such growth is complex and may be affected by nutritional interventions imposed many years previously.

          Related collections

          Most cited references 28

          • Record: found
          • Abstract: found
          • Article: not found

          Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. MRC Vitamin Study Research Group.

          A randomised double-blind prevention trial with a factorial design was conducted at 33 centres in seven countries to determine whether supplementation with folic acid (one of the vitamins in the B group) or a mixture of seven other vitamins (A,D,B1,B2,B6,C and nicotinamide) around the time of conception can prevent neural tube defects (anencephaly, spina bifida, encephalocele). A total of 1817 women at high risk of having a pregnancy with a neural tube defect, because of a previous affected pregnancy, were allocated at random to one of four groups--namely, folic acid, other vitamins, both, or neither. 1195 had a completed pregnancy in which the fetus or infant was known to have or not have a neural tube defect; 27 of these had a known neural tube defect, 6 in the folic acid groups and 21 in the two other groups, a 72% protective effect (relative risk 0.28, 95% confidence interval 0.12-0.71). The other vitamins showed no significant protective effect (relative risk 0.80, 95% Cl 0.32-1.72). There was no demonstrable harm from the folic acid supplementation, though the ability of the study to detect rare or slight adverse effects was limited. Folic acid supplementation starting before pregnancy can now be firmly recommended for all women who have had an affected pregnancy, and public health measures should be taken to ensure that the diet of all women who may bear children contains an adequate amount of folic acid.
            • Record: found
            • Abstract: found
            • Article: not found

            A life course approach to diet, nutrition and the prevention of chronic diseases.

            To briefly review the current understanding of the aetiology and prevention of chronic diseases using a life course approach, demonstrating the life-long influences on the development of disease. A computer search of the relevant literature was done using Medline-'life cycle' and 'nutrition' and reviewing the articles for relevance in addressing the above objective. Articles from references dated before 1990 were followed up separately. A subsequent search using Clio updated the search and extended it by using 'life cycle', 'nutrition' and 'noncommunicable disease' (NCD), and 'life course'. Several published and unpublished WHO reports were key in developing the background and arguments. International and national public health and nutrition policy development in light of the global epidemic in chronic diseases, and the continuing nutrition, demographic and epidemiological transitions happening in an increasingly globalized world. RESULTS OF REVIEW: There is a global epidemic of increasing obesity, diabetes and other chronic NCDs, especially in developing and transitional economies, and in the less affluent within these, and in the developed countries. At the same time, there has been an increase in communities and households that have coincident under- and over-nutrition. The epidemic will continue to increase and is due to a lifetime of exposures and influences. Genetic predisposition plays an unspecified role, and with programming during fetal life for adult disease contributing to an unknown degree. A global rise in obesity levels is contributing to a particular epidemic of type 2 diabetes as well as other NCDs. Prevention will be the most cost-effective and feasible approach for many countries and should involve three mutually reinforcing strategies throughout life, starting in the antenatal period.
              • Record: found
              • Abstract: found
              • Article: not found

              Epigenetics and transgenerational transfer: a physiological perspective.

              Epigenetics, the transgenerational transfer of phenotypic characters without modification of gene sequence, is a burgeoning area of study in many disciplines of biology. However, the potential impact of this phenomenon on the physiology of animals is not yet broadly appreciated, in part because the phenomenon of epigenetics is not typically part of the design of physiological investigations. Still enigmatic and somewhat ill defined is the relationship between the overarching concept of epigenetics and interesting transgenerational phenomena (e.g. 'maternal/parental effects') that alter the physiological phenotype of subsequent generations. The lingering effect on subsequent generations of an initial environmental disturbance in parent animals can be profound, with genes continuing to be variously silenced or expressed without an associated change in gene sequence for many generations. Known epigenetic mechanisms involved in this phenomenon include chromatin remodeling (DNA methylation and histone modification), RNA-mediated modifications (non-coding RNA and microRNA), as well as other less well studied mechanisms such as self-sustaining loops and structural inheritance. In this review we: (1) discuss how the concepts of epigenetics and maternal effects both overlap with, and are distinct from, each other; (2) analyze examples of existing animal physiological studies based on these concepts; and (3) offer a construct by which to integrate these concepts into the design of future investigations in animal physiology.

                Author and article information

                Am J Clin Nutr
                Am. J. Clin. Nutr
                The American Journal of Clinical Nutrition
                American Society for Nutrition
                May 2013
                3 April 2013
                3 April 2013
                : 97
                : 5
                : 911-918
                [1 ]From the Medical Research Council (MRC) International Nutrition Group, London School of Hygiene & Tropical Medicine, London, United Kingdom (AMP, SEM, and AJF); MRC Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge, United Kingdom (KAW, GRG, and AP); and the MRC, Keneba, The Gambia (AMP, GRG, LMJ, AJF, and AP).
                Author notes

                Supported by the UK Medical Research Council (MC-A760-5QX00, U105960371, U123261351, and G0700961).

                [3 ]Address correspondence to AM Prentice, MRC International Nutrition Group, London School of Hygiene & Tropical Medicine, Keppel Street, London, WC1E 7HT, United Kingdom. E-mail: andrew.prentice@
                © 2013 American Society for Nutrition

                This is a free access article, distributed under terms ( which permit unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


                Nutrition & Dietetics


                Comment on this article