Semin Reprod Med 2018; 36(03/04): 177-182
DOI: 10.1055/s-0038-1675779
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Developmental Origins of Health and Disease: The History of the Barker Hypothesis and Assisted Reproductive Technology

Olivia J. Carpinello
1   Program in Reproductive Endocrinology and Gynecology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland
,
Alan H. DeCherney
1   Program in Reproductive Endocrinology and Gynecology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland
,
Micah J. Hill
1   Program in Reproductive Endocrinology and Gynecology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland
2   Division of Reproductive Endocrinology and Infertility, Walter Reed National Military Medical Center, Bethesda, Maryland
› Author Affiliations
Further Information

Publication History

Publication Date:
13 March 2019 (online)

Abstract

Since Barker's publication of “The fetal and infant origins of adult disease” in 1990, significant emphasis has been placed on the intrauterine environment and its effect on adult disease. Historical events such as the Dutch Famine and the 1918 Flu Pandemic have provided organic data about the epigenetic changes that can result from famine, infection, and stress. Mechanisms that allow for intrauterine survival may predispose to adult disease states when the fetus enters a world of abundance. As the field of in vitro fertilization (IVF) has developed and evolved, little attention has been paid to subtle yet significant differences in IVF offspring. Offspring of assisted reproductive technology (ART) have been reported to have higher rates of preterm birth, abnormal fetal size, and birth defects. It is clear that epigenetic modifications may begin as early as pre-pregnancy. These differences are likely not attributable to one factor in the IVF process. Each variable likely plays a subtle role in the epigenetic manipulation of the embryo. Thus, moving forward, physicians should practice with heightened determination to follow the long-term outcomes of the offspring of ART in an effort to further modify and perfect the field.

 
  • References

  • 1 Deans C, Maggert KA. What do you mean, “epigenetic”?. Genetics 2015; 199 (04) 887-896
  • 2 Jin B, Li Y, Robertson KD. DNA methylation: superior or subordinate in the epigenetic hierarchy?. Genes Cancer 2011; 2 (06) 607-617
  • 3 Barker DJ. The fetal and infant origins of adult disease. BMJ 1990; 301 (6761): 1111
  • 4 Kaplan GA, Salonen JT. Socioeconomic conditions in childhood and ischaemic heart disease during middle age. BMJ 1990; 301 (6761): 1121-1123
  • 5 Coggon D, Margetts B, Barker DJ. , et al. Childhood risk factors for ischaemic heart disease and stroke. Paediatr Perinat Epidemiol 1990; 4 (04) 464-469
  • 6 Burr ML, Sweetnam PM. Family size and paternal unemployment in relation to myocardial infarction. J Epidemiol Community Health 1980; 34 (02) 93-95
  • 7 Barker DJ, Winter PD, Osmond C, Margetts B, Simmonds SJ. Weight in infancy and death from ischaemic heart disease. Lancet 1989; 2 (8663): 577-580
  • 8 Barker DJ, Bull AR, Osmond C, Simmonds SJ. Fetal and placental size and risk of hypertension in adult life. BMJ 1990; 301 (6746): 259-262
  • 9 Leddy MA, Power ML, Schulkin J. The impact of maternal obesity on maternal and fetal health. Rev Obstet Gynecol 2008; 1 (04) 170-178
  • 10 Gillman MW, Rifas-Shiman S, Berkey CS, Field AE, Colditz GA. Maternal gestational diabetes, birth weight, and adolescent obesity. Pediatrics 2003; 111 (03) e221-e226
  • 11 Whitaker RC. Predicting preschooler obesity at birth: the role of maternal obesity in early pregnancy. Pediatrics 2004; 114 (01) e29-e36
  • 12 Thornburg KL, Shannon J, Thuillier P, Turker MS. In utero life and epigenetic predisposition for disease. Adv Genet 2010; 71: 57-78
  • 13 Gluckman PD, Buklijas T, Hanson MA. The Developmental Origins of Health and Disease (DOHaD) concept: past, present, and future. In: Cheryl R. , ed. The Epigenome and Developmental Origins of Health and Disease. Boston, MA: Academic Press; 2016: 1-15
  • 14 Barker DJ, Gluckman PD, Robinson JS. Conference report: fetal origins of adult disease--report of the First International Study Group, Sydney, 29-30 October 1994. Placenta 1995; 16 (03) 317-320
  • 15 DOHaD Society. About the Society. Available at: https://dohadsoc.org/about/ . Accessed June 28, 2018
  • 16 Lumey LH. Decreased birthweights in infants after maternal in utero exposure to the Dutch famine of 1944-1945. Paediatr Perinat Epidemiol 1992; 6 (02) 240-253
  • 17 Roseboom T, de Rooij S, Painter R. The Dutch famine and its long-term consequences for adult health. Early Hum Dev 2006; 82 (08) 485-491
  • 18 Thorn SR, Rozance PJ, Brown LD, Hay Jr WW. The intrauterine growth restriction phenotype: fetal adaptations and potential implications for later life insulin resistance and diabetes. Semin Reprod Med 2011; 29 (03) 225-236
  • 19 Roseboom TJ. Developmental plasticity and its relevance to assisted human reproduction. Hum Reprod 2018; 33 (04) 546-552
  • 20 Mazumder B, Almond D, Park K, Crimmins EM, Finch CE. Lingering prenatal effects of the 1918 influenza pandemic on cardiovascular disease. J Dev Orig Health Dis 2010; 1 (01) 26-34
  • 21 Wadhwa PD, Buss C, Entringer S, Swanson JM. Developmental origins of health and disease: brief history of the approach and current focus on epigenetic mechanisms. Semin Reprod Med 2009; 27 (05) 358-368
  • 22 National Children's Study (NCS). Available at: https://www.nichd.nih.gov/research/supported/NCS . Accessed June 24, 2018
  • 23 Fleming TP, Lucas ES, Watkins AJ, Eckert JJ. Adaptive responses of the embryo to maternal diet and consequences for post-implantation development. Reprod Fertil Dev 2011; 24 (01) 35-44
  • 24 Watkins AJ, Ursell E, Panton R. , et al. Adaptive responses by mouse early embryos to maternal diet protect fetal growth but predispose to adult onset disease. Biol Reprod 2008; 78 (02) 299-306
  • 25 Cavoretto P, Candiani M, Giorgione V. , et al. Risk of spontaneous preterm birth in singleton pregnancies conceived after IVF/ICSI treatment: meta-analysis of cohort studies. Ultrasound Obstet Gynecol 2018; 51 (01) 43-53
  • 26 Carpinello OJ, Casson PR, Kuo CL, Raj RS, Sills ES, Jones CA. Cost implications for subsequent perinatal outcomes after IVF stratified by number of embryos transferred: a five year analysis of Vermont data. Appl Health Econ Health Policy 2016; 14 (03) 387-395
  • 27 Wennerholm UB, Henningsen AK, Romundstad LB. , et al. Perinatal outcomes of children born after frozen-thawed embryo transfer: a Nordic cohort study from the CoNARTaS group. Hum Reprod 2013; 28 (09) 2545-2553
  • 28 Sun LM, Lanes A. , Kingdom, et al. Intrapartum interventions for singleton pregnancies arising from assisted reproductive technologies. J Obstet Gynaecol Can 2014; 36 (09) 795-802
  • 29 Davies MJ, Moore VM, Willson KJ. , et al. Reproductive technologies and the risk of birth defects. N Engl J Med 2012; 366 (19) 1803-1813
  • 30 Vermeiden JP, Bernardus RE. Are imprinting disorders more prevalent after human in vitro fertilization or intracytoplasmic sperm injection?. Fertil Steril 2013; 99 (03) 642-651
  • 31 Uk A, Collardeau-Frachon S, Scanvion Q, Michon L, Amar E. Assisted reproductive technologies and imprinting disorders: results of a study from a French congenital malformations registry. Eur J Med Genet 2018; 61 (09) 518-523
  • 32 Johnson JP, Beischel L, Schwanke C. , et al. Overrepresentation of pregnancies conceived by artificial reproductive technology in prenatally identified fetuses with Beckwith-Wiedemann syndrome. J Assist Reprod Genet 2018; 35: 985-992
  • 33 Beckwith-Wiedemann syndrome. Available at: https://ghr.nlm.nih.gov/condition/beckwith-wiedemann-syndrome#resources . Accessed July 5, 2018
  • 34 Guo XY, Liu XM, Jin L. , et al. Cardiovascular and metabolic profiles of offspring conceived by assisted reproductive technologies: a systematic review and meta-analysis. Fertil Steril 2017; 107 (03) 622-631.e5