title: Developmental origins of health and disease: a paradigm for understanding disease cause and prevention.
abstract: OBJECTIVE
  Although diseases may appear clinically throughout the lifespan, it is clear that many diseases have origins during development. Altered nutrition, as well as exposure to environmental chemicals, drugs, infections, or stress during specific times of development, can lead to functional changes in tissues, predisposing those tissues to diseases that manifest later in life. This review will focus on the role of altered nutrition and exposures to environmental chemicals during development in the role of disease and dysfunction.
  
  
  RESULTS
  The effects of altered nutrition or exposure to environmental chemicals during development are likely because of altered programming of epigenetic marks, which persist across the lifespan. Indeed some changes can be transmitted to future generations.
  
  
  CONCLUSIONS
  The evidence in support of the developmental origins of the health and disease paradigm is sufficiently robust and repeatable across species, including humans, to suggest a need for greater emphasis in the clinical area. As a result of these data, obesity, diabetes, cardiovascular morbidity, and neuropsychiatric diseases can all be considered pediatric diseases. Disease prevention must start with improved nutrition and reduced exposure to environmental chemicals during development.
authors: aDivision of Extramural Research and Training, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina bDivision of Environmental Health Sciences, School of Public Health, University of Massachusetts, Amherst, Massachusetts, USA.
authors: Jerrold J
authors: JJ
authors: Heindel
authors: Laura N
authors: LN
authors: Vandenberg
mesh_terms: D002648:Child; D004781:Environmental Exposure / Q000009:adverse effects*; D004785:Environmental Pollutants / Q000633:toxicity*; D057890:Epigenomics; D005260:Female; D059647:Gene-Environment Interaction; D006801:Humans; D008297:Male; D009747:Nutritional Physiological Phenomena; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology / Q000517:prevention & control*; D011634:Public Health
chemical_list: D004785:Environmental Pollutants
references: J Nutr. 2005 Jun;135(6):1382-6
references: 15930441
references: Endocrinology. 2006 Jun;147(6 Suppl):S43-9
references: 16690803
references: Adv Exp Med Biol. 2014;791:67-81
references: 23955673
references: Lancet Neurol. 2014 Mar;13(3):330-8
references: 24556010
references: J Intern Med. 2007 May;261(5):412-7
references: 17444880
references: Endocrinology. 2012 Jan;153(1):42-55
references: 22109888
references: Environ Health Perspect. 2011 Aug;119(8):1196-201
references: 21507777
references: Reprod Toxicol. 2011 Apr;31(3):337-43
references: 21055462
references: Environ Health. 2012 Jun 27;11:42
references: 22715989
references: Reprod Toxicol. 2013 Apr;36:104-16
references: 23453003
references: Reprod Toxicol. 2012 Dec;34(4):708-19
references: 22975477
references: Ann Nutr Metab. 2014;64 Suppl 1:26-34
references: 25059803
references: Endocrinology. 2012 Sep;153(9):4097-110
references: 22733974
references: Endocrinology. 2006 Jun;147(6 Suppl):S11-7
references: 16690809
references: Hum Reprod Update. 2014 Jan-Feb;20(1):63-75
references: 24082037
references: J Environ Pathol Toxicol Oncol. 2014;33(3):239-45
references: 25272062
references: Nat Rev Cancer. 2012 Jun 14;12(7):479-86
references: 22695395
references: Am J Physiol Endocrinol Metab. 2013 Nov 15;305(10):E1195-207
references: 24045869
references: Science. 2014 Jul 11;345(6193):121
references: 25013035
references: J Clin Endocrinol Metab. 2011 Oct;96(10):3056-8
references: 21832106
references: Proc Nutr Soc. 2014 Aug;73(3):413-21
references: 25027290
references: Science. 2013 Jan 25;339(6118):448-52
references: 23223451
references: Nutrients. 2014 Jun 02;6(6):2165-78
references: 24892374
references: PLoS One. 2013;8(1):e55387
references: 23359474
references: Environ Health Perspect. 2013 Mar;121(3):359-66
references: 23322813
references: Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19351-6
references: 18042717
references: Obstet Gynecol. 2013 Oct;122(4):931-935
references: 24084567
references: Science. 2014 Aug 15;345(6198):1255903
references: 25011554
references: Trends Cell Biol. 2014 Nov;24(11):664-74
references: 25242115
references: Environ Health Perspect. 2011 Aug;119(8):1189-95
references: 21507776
references: BMC Med. 2013 Oct 23;11:228
references: 24228800
references: Cell. 2014 Mar 27;157(1):95-109
references: 24679529
references: Reprod Toxicol. 2012 Dec;34(4):694-707
references: 23041264
references: J Exp Zool B Mol Dev Evol. 2014 Jun;322(4):208-20
references: 24719220
references: Lancet. 2013 Jan 5;381(9860):3-4
references: 23290956
references: Environ Health Perspect. 2011 Aug;119(8):1182-8
references: 21507778
references: Endocrinology. 2012 Aug;153(8):3828-38
references: 22707478
references: Brain Behav Immun. 2014 Mar;37:30-44
references: 24184474
references: Acta Obstet Gynecol Scand. 2014 Nov;93(11):1090-8
references: 24835110
references: Am J Phys Anthropol. 2013 Dec;152 Suppl 57:79-93
references: 24249592
references: Mol Cell Endocrinol. 2014 Dec;398(1-2):31-5
references: 25218215
references: Mol Cell Endocrinol. 2012 May 6;354(1-2):3-8
references: 22020198
references: Environ Health Perspect. 2012 Jun;120(6):779-89
references: 22296744
references: Cell Metab. 2014 Jun 3;19(6):941-51
references: 24794974
references: Endocr Rev. 2009 Jun;30(4):293-342
references: 19502515
references: PLoS One. 2013 Sep 12;8(9):e72670
references: 24069155
references: PLoS One. 2012;7(5):e36129
references: 22570695
references: Endocr Rev. 2011 Apr;32(2):159-224
references: 20971919
references: Best Pract Res Clin Endocrinol Metab. 2012 Oct;26(5):667-76
references: 22980048
references: Proc Nutr Soc. 2013 Aug;72(3):317-25
references: 23312451
references: Sci Am. 2014 Aug;311(2):44-51
references: 25095468