The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
The developmental origins of chronic adult disease
Abstract
Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin-dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. Coronary heart disease and the disorders related to it arise through a series of interactions between environmental influences and the pathways of development that preceded them. These diseases are the product of branching pathways of development in which the branchings are triggered by the environment before and after birth.
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WEIGHT IN INFANCY AND DEATH FROM ISCHAEMIC HEART DISEASE
Barker, D. J. P., Osmond, C., Winter, P. D., Margetts, B., & Simmonds, S. J. (1989) · The Lancet · doi:10.1016/s0140-6736(89)90710-1 · Cited by 3,574
Fetal origins of coronary heart disease
Barker, D. J. P. (1995) · BMJ · doi:10.1136/bmj.311.6998.171 · Cited by 3,570
Self-citationFetal and infant growth and impaired glucose tolerance at age 64
Hales, C. N., Barker, D. J., Clark, P. M., Cox, L. J., Fall, C., Osmond, C., & Winter, P. D. (1991) · BMJ · doi:10.1136/bmj.303.6809.1019 · Cited by 2,708
Phenotypic Plasticity and the Origins of Diversity
West-Eberhard, M. J. (1989) · Annual Review of Ecology and Systematics · doi:10.1146/annurev.es.20.110189.001341 · Cited by 2,110
Fetal origins of adult disease: strength of effects and biological basis
Barker, D., Eriksson, J., Forsén, T., & Osmond, C. (2002) · International Journal of Epidemiology · doi:10.1093/ije/31.6.1235 · Cited by 2,024
Compensation for a bad start: grow now, pay later?
Metcalfe, N. B., & Monaghan, P. (2001) · Trends in Ecology & Evolution · doi:10.1016/s0169-5347(01)02124-3 · Cited by 1,948
Health consequences of obesity
Reilly, J. J. (2003) · Archives of Disease in Childhood · doi:10.1136/adc.88.9.748 · Cited by 1,652
Calvert, H., Horwich, A., Newlands, E. S., Beǵent, R. H. J., Rustin, G. J. S., Kaye, S. B., Harris, A. L., Williams, C. J., & Slevin, M. L. (1988) · The Lancet · doi:10.1016/s0140-6736(88)92709-2 · Cited by 1,183
Nephron Number in Patients with Primary Hypertension
Keller, G., Zimmer, G., Mall, G., Ritz, E., & Amann, K. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa020549 · Cited by 1,102
The role of size at birth and postnatal catch-up growth in determining systolic blood pressure
Huxley, R., Shiell, A. W., & Law, C. (2000) · Journal of Hypertension · doi:10.1097/00004872-200018070-00002 · Cited by 1,046
Research works printed but not linked: 1
- Bateson P, 1999, Design for a life: how behaviour develops
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Environmental epigenomics and disease susceptibility
Jirtle, R. L., & Skinner, M. K. (2007) · Nature Reviews Genetics · doi:10.1038/nrg2045 · Cited by 2,492
Franceschi, C., Capri, M., Monti, D., Giunta, S., Olivieri, F., Sevini, F., Panourgia, M. P., Invidia, L., Celani, L., Scurti, M., et al. (2007) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2006.11.016 · Cited by 2,087
Every Newborn: progress, priorities, and potential beyond survival
Lawn, J. E., Blencowe, H., Oza, S., You, D., Lee, A. C., Waiswa, P., Lalli, M., Bhutta, Z., Barros, A. J., Christian, P., et al. (2014) · The Lancet · doi:10.1016/s0140-6736(14)60496-7 · Cited by 1,929
Van den Bergh, B. R. H., van den Heuvel, M. I., Lahti, M., Braeken, M., de Rooij, S. R., Entringer, S., Hoyer, D., Roseboom, T., Räikkönen, K., King, S., et al. (2020) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.07.003 · Cited by 1,181
“The ‘fetal programming hypothesis’ (Seckl and Holmes, 2007), the ‘developmental programming hypothesis’ (Barker, 2004; Langley-Evans, 2006; Langley-Evans, 2015), and the ‘Developmental Origins of Health and Disease (DOHaD) hypothesis’ (Barker, 2004; Barker,”
BackgroundMore than a feeling: A unified view of stress measurement for population science
Epel, E. S., Crosswell, A. D., Mayer, S. E., Prather, A. A., Slavich, G. M., Puterman, E., & Mendes, W. B. (2018) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2018.03.001 · Cited by 1,077
Metadata
- Authors
- Barker, D.
- Affiliations
- Southampton General Hospital (GB)
- Corresponding author
- Barker, DJP
- Venue
- Acta Paediatrica
- Publisher
- Wiley
- Published
- 2004-11
- Volume
- 93
- Issue
- s446
- Pages
- 26-33
- ISSN
- 0365-1436 (ISSN-L)
- 0803-5253
- 1651-2227
- OpenAlex
- W2143230895
- Cited by
- 790
- References
- 53
- Citations by year
- 2026: 19 · 2025: 38 · 2024: 49 · 2023: 42 · 2022: 36 · 2021: 63 · 2020: 55 · 2019: 42 · 2018: 39 · 2017: 37 · 2016: 33 · 2015: 40 · 2014: 37 · 2013: 40 · 2012: 45
- FWCI
- 17.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Paediatrica (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- developmental origins of health and disease, low birth weight, coronary artery disease, stroke, hypertension, type 2 diabetes, developmental plasticity, fetal growth restriction, gestational age, child weight gain, environmental influences on development
- MeSH terms
- Adult, Birth Weight, Cardiovascular Diseases, Child, Child Development, Child, Preschool, Chronic Disease, Diabetes Mellitus, Type 2, Female, Humans, Infant, Infant, Newborn, Male
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