The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women
Abstract
Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. These programmed changes may be the origins of a number of diseases in later life, including coronary heart disease, hypertension, and noninsulin- dependent diabetes. We review epidemiologic studies in which the incidence of these diseases has been related to the recorded, early growth of individuals, while considering factors in the adult lifestyle, such as obesity and socioeconomic status. We discuss possible mechanisms. For hypertension these mechanisms include placentation, maternal blood pressure, fetal undernutrition; childhood growth, activation of the renin-angiotensin system, renal structure, programming of the hypothalamic-pituitary-adrenal axis, vascular structure, and sympathetic nervous activity. For noninsulin-dependent diabetes we discuss mechanisms concerning both insulin resistance and insulin deficiency. We include a review of evidence for the programming of serum cholesterol and clotting factor concentrations. We address the timing of critical windows for coronary heart disease, reviewing studies that allow assessment of the relative importance of fetal, infant, and childhood growth. We argue for a research strategy that combines clinical, animal, and epidemiological studies.
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“Moreover, it is well documented that, in comparison with children born at term, those born prematurely are more likely to present cerebral palsy, sensory deficits, learning disabilities, and respiratory illnesses [5,6,7,8,9,10,11,12,13].”
From A Comprehensive Review on Social Inequalities and Pregnancy Outcome—Identification of Relevant Pathways and Mechanisms (2022) · cites this paper as [10]
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Cites
Levy, D., Garrison, R. J., Savage, D. D., Kannel, W. B., & Castelli, W. P. (1990) · New England Journal of Medicine · doi:10.1056/nejm199005313222203 · Cited by 5,699
Sick individuals and sick populations
Rose, G. (2001) · International Journal of Epidemiology · doi:10.1093/ije/30.3.427 · Cited by 3,736
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 nutrition and cardiovascular disease in adult life
Barker, D. J. P., Godfrey, K. M., Gluckman, P. D., Harding, J. E., Owens, J. A., & Robinson, J. S. (1993) · The Lancet · doi:10.1016/0140-6736(93)91224-a · Cited by 2,753
Self-citationSick individuals and sick populations
ROSE, G. (1985) · International Journal of Epidemiology · doi:10.1093/ije/14.1.32 · Cited by 2,701
Barker, D. J. P., Hales, C. N., Fall, C. H. D., Osmond, C., Phipps, K., & Clark, P. M. S. (1993) · Diabetologia · doi:10.1007/bf00399095 · Cited by 2,468
Self-citationThe Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM
DeFronzo, R. A. (1988) · Diabetes · doi:10.2337/diab.37.6.667 · Cited by 2,456
Fetal and placental size and risk of hypertension in adult life.
Barker, D. J., Bull, A. R., Osmond, C., & Simmonds, S. J. (1990) · BMJ · doi:10.1136/bmj.301.6746.259 · Cited by 1,728
Self-citationGlucose tolerance in adults after prenatal exposure to famine
Ravelli, A., van der Meulen, J., Michels, R., Osmond, C., Barker, D., Hales, C., & Bleker, O. (1998) · The Lancet · doi:10.1016/s0140-6736(97)07244-9 · Cited by 1,606
Self-citationMartyn, C., Barker, D., & Osmond, C. (1996) · The Lancet · doi:10.1016/s0140-6736(96)04257-2 · Cited by 381
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Cited by
Health Disparities Beginning in Childhood: A Life-Course Perspective
Braveman, P., & Barclay, C. (2009) · Pediatrics · doi:10.1542/peds.2009-1100d · Cited by 653
Witchel, S. F., Oberfield, S. E., & Peña, A. S. (2019) · Journal of the Endocrine Society · doi:10.1210/js.2019-00078 · Cited by 653
Developmental origins of disease paradigm: A mechanistic and evolutionary perspective
Gluckman, P. D., & Hanson, M. A. (2004) · Pediatric Research · doi:10.1203/01.pdr.0000135998.08025.fb · Cited by 607
Jansson, T., & Powell, T. L. (2007) · Clinical Science · doi:10.1042/cs20060339 · Cited by 542
The developmental origins of adult disease
Gluckman, P. D., Hanson, M. A., & Pinal, C. (2005) · Maternal & Child Nutrition · doi:10.1111/j.1740-8709.2005.00020.x · Cited by 473
Metadata
- Authors
- Osmond, C., & Barker, D. J.
- Affiliations
- MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton, United Kingdom. co@mrc.soton.ac.uk
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2000-06-01
- Volume
- 108
- Issue
- suppl 3
- Pages
- 545-553
- ISSN
- 0091-6765
- 1552-9924
- Cited by
- 307
- References
- 12
- Language
- en
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- CoChat. (2026). Citation check: Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women. https://app.cochat.ai/papers/10.1289/ehp.00108s3545
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- Osmond, C., & Barker, D. J. (2000). Fetal, Infant, and Childhood Growth Are Predictors of Coronary Heart Disease, Diabetes, and Hypertension in Adult Men and Women. Environmental Health Perspectives. https://doi.org/10.1289/ehp.00108s3545
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
