Hostname: page-component-cd9895bd7-jn8rn Total loading time: 0 Render date: 2024-12-23T06:56:05.119Z Has data issue: false hasContentIssue false
  • English
  • Français

Beyond birthweight: the maternal and placental origins of chronic disease

Published online by Cambridge University Press:  10 June 2010

D. J. P. Barker ,
K. L. Thornburg ,
C. Osmond ,
E. Kajantie  and
J. G. Eriksson
D. J. P. Barker*
Affiliation:
MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, UK Heart Research Center, Oregon Health and Science University, Portland, OR, USA Fetal Programming Research Chair, King Saud University, Saudi Arabia
K. L. Thornburg
Affiliation:
Heart Research Center, Oregon Health and Science University, Portland, OR, USA
C. Osmond
Affiliation:
MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, UK
E. Kajantie
Affiliation:
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland Hospital for Children and Adolescents, Helsinki University Central Hospital, Helsinki, Finland
J. G. Eriksson
Affiliation:
Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland Department of General Practice and Primary Health Care, University of Helsinki, Helsinginyliopisto, Finland Vasa Central Hospital, Sandviksgatan 2–4, Vasa, Finland Folkhälsan Research Centre, Helsinki, Helsingfors Universitet, Finland Unit of General Practice, Helsinki University Central Hospital, Finland
*
*Address for correspondence: Prof. D. J. P. Barker, MRC Epidemiology Resource Centre, Southampton General Hospital, University of Southampton, Southampton, SO16 6YD, UK. (Email [email protected])
Get access Rights & Permissions [Opens in a new window]

Abstract

New findings on the maternal and placental programming of chronic disease lead to four conclusions: (1) Growth of the placental surface is polarized from the time of implantation, so that growth along the major axis, the length, is qualitatively different from growth along the minor axis, the breadth. (2) The human fetus may attempt to compensate for undernutrition by expansion of the placental surface along its minor axis. This only occurs if the mother was well nourished before conception, and may have long-term costs that include hypertension. (3) The effects of placental size on long-term health are conditioned by the mother’s nutritional state, as indicated by her socio-economic status, height and body mass index. (4) The maternal–placental programming of chronic disease differs in boys and girls. Boys invest less than girls in placental growth but more readily expand the placental surface if they become undernourished in mid-late gestation. Boys are more responsive to their mothers’ current diets while girls respond more to their mothers’ lifetime nutrition and metabolism.

Keywords

placental sizematernal body sizechronic disease
Type
Reviews
Information
Journal of Developmental Origins of Health and Disease , Volume 1 , Issue 6 , December 2010 , pp. 360 - 364
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Harding, JE. The nutritional basis of the fetal origins of adult disease. Int J Epidemiol. 2001; 30, 15–23.CrossRefGoogle ScholarPubMed
2. Jackson, AA. All that glitters. British Nutrition Foundation Annual Lecture. Nutr Bull. 2000; 25, 11–24.CrossRefGoogle Scholar
3. Barker, DJP, Osmond, C, Kajantie, E, Eriksson, JG. Growth and chronic disease: findings in the Helsinki Birth Cohort. Ann Hum Biol. 2009; 36, 445–458.CrossRefGoogle ScholarPubMed
4. Eriksson, J, Forsen, T, Toumilheto, J, Osmond, C, Barker, D. Fetal and childhood growth and hypertension in adult life. Hypertension. 2000; 36, 790–794.CrossRefGoogle ScholarPubMed
5. Forsén, T, Eriksson, JG, Tuomilehto, J, et al. ‘Mother’s weight in pregnancy and coronary heart disease in a cohort of Finnish men: follow up study’. BMJ. 1997; 315, 837–840.CrossRefGoogle Scholar
6. Anderson, MC. Lessons in Midwifery for Nurses and Midwifes, 1930. A & C Black: London.Google Scholar
7. Hinselmann, H. Biologie und Pathologie des Weibes, 1925. Urban & Schwarzenberg: Berlin.Google Scholar
8. Barker, DJP, Thornburg, KL, Osmond, C, Kajantie, E, Eriksson, JG. The surface area of the placenta and hypertension in the offspring in later life. Int J Dev Biol. 2010; 54, 525–530.CrossRefGoogle ScholarPubMed
9. Roberts, JM, Cooper, DW. Pathogenesis and genetics of preeclampsia. Lancet. 2001; 357, 53–56.CrossRefGoogle Scholar
10. Kajantie, E, Barker, DJP, Osmond, C, Kajantie, E, Eriksson, JG. In pre-eclampsia the placenta grows slowly along its minor axis. Int J Dev Biol. 2010; 54, 469–473.CrossRefGoogle Scholar
11. Sibley, CP. The pregnant woman. In Human Physiology: Age, Stress, and the Environment (eds. Case RM, Waterhouse JM), 1994; pp. 3–27. Oxford University Press: Oxford.Google Scholar
12. Barker, DJP, Bull, AR, Osmond, C, Simmonds, S. Fetal and placental size and risk of hypertension in adult life. BMJ. 1990; 301, 259–262.CrossRefGoogle ScholarPubMed
13. Martyn, CN, Barker, DJP, Osmond, C. Mothers pelvic size, fetal growth and death from stroke in men. Lancet. 1996; 348, 1264–1268.CrossRefGoogle ScholarPubMed
14. McCrabb, GJ, Egan, AR, Hosking, BJ. Maternal undernutrition during mid-pregnancy in sheep. Placental size and its relationship to calcium transfer during late pregnancy. Br J Nutr. 1991; 65, 157–168.CrossRefGoogle ScholarPubMed
15. McCrabb, GJ, Egan, AR, Hosking, BJ. Maternal undernutrition during mid-pregnancy in sheep: variable effects on placental growth. J Agric Sci. 1992; 118, 127–132.CrossRefGoogle Scholar
16. Tanner, JM. Fetus into Man, 2nd edn, 1989. Castlemead, Ware.Google Scholar
17. Duggleby, SL, Jackson, AA. Relationship of maternal protein turnover and lean body mass during pregnancy and birth length. Clin Sci (Lond). 2001; 101, 65–72.CrossRefGoogle ScholarPubMed
18. Pesonen, AK, Raikkonen, K, Heinonen, K, et al. Depressive symptoms in adults separated from their parents as children: a natural experiment during World War II. Am J Epidemiol. 2007; 166, 1126–1133.CrossRefGoogle ScholarPubMed
19. Barker, DJP, Bagby, S, Hanson, MA. Mechanisms of disease: in utero programming in the pathogenesis of hypertension. Nature Clin Pract Nephrol. 2006; 2, 700–707.CrossRefGoogle ScholarPubMed
20. Eriksson, JG, Thornburg, KL, Osmond, C, Kajantie, E, Barker, DJP. The prenatal origins of lung cancer: I. The fetus. Am J Hum Biol 2010; doi:10.1002/ajhb.21041.CrossRefGoogle Scholar
21. Barker, DJP, Thornburg, KL, Osmond, C, Kajantie, E, Eriksson, JG . The prenatal origins of lung cancer: II. The placenta. Am J Hum Biol 2010; doi:10.1002/ajhb.21041.CrossRefGoogle Scholar
22. Pedersen, JF. Ultrasound evidence of sexual difference in fetal size in first trimester. BMJ. 1980; 281, 1253.CrossRefGoogle ScholarPubMed
23. Forsén, T, Eriksson, JG, Tuomilehto, J, Osmond, C, Barker, DJP. Growth in utero and during childhood among women who develop coronary heart disease: longitudinal study. BMJ. 1999; 319, 1403–1407.CrossRefGoogle ScholarPubMed
24. Eriksson, JG, Kajantie, E, Osmond, C, Thornburg, K, Barker, DJP. Boys live dangerously in the womb. Am J Hum Biol. 2010; doi:10.1002/ajhb.20995.CrossRefGoogle ScholarPubMed
25. Ounsted, M, Scott, A, Ounsted, C. Transmission through the female line of a mechanism constraining human fetal growth. Ann Hum Biol. 1986; 13, 143–151.CrossRefGoogle ScholarPubMed
26. Ravelli, AC, van der Meulen, JHP, Osmond, C, Barker, DJP, Bleker, OP. Obesity at the age of 50 y in men and women exposed to famine prenatally. Am J Clin Nutr. 1999; 70, 811–816.CrossRefGoogle ScholarPubMed
27. Ozaki, T, Nishina, H, Hanson, MA, Poston, L. Dietary restriction in pregnant rats causes gender-related hypertension and vascular dysfunction in offspring. J Physiol. 2001; 530, 141–152.CrossRefGoogle ScholarPubMed
28. Woods, LL, Ingelfinger, JR, Rasch, R. Modest maternal protein restriction fails to program adult hypertension in female rats. Am J Physiol Regul Integr Comp Physiol. 2005; 289, R1131–R1136.CrossRefGoogle ScholarPubMed
29. Grigore, D, Ojeda, NB, Alexander, BT. Sex differences in the fetal programming of hypertension. Gend Med. 2008; 5(Suppl. A), S121–S132.CrossRefGoogle ScholarPubMed
30. Coall, DA, Charles, AK, Salafia, CM. Gross placental structure in a low-risk population of singleton, term, first born infants. Ped Develop Path. 2009; 12, 200–210.CrossRefGoogle Scholar