Fetal origins of adult disease: strength of effects and biological basis
Abstract
BACKGROUND: Low birthweight has been consistently shown to be associated with coronary heart disease (CHD) and its biological risk factors. The effects of low birthweight are increased by slow infant growth and rapid weight gain in childhood. To quantify the importance of developmental processes in the genesis of CHD it is necessary to establish the impact of fetal, infant and childhood growth on major pathological events in later life-death, hospital treatment and the need for medication. METHODS: Longitudinal study of 13 517 men and women who were born in Helsinki University Hospital during 1924-1944, whose body sizes at birth and during childhood were recorded, and in whom deaths, hospital admissions, and prescription of medication for chronic disease are documented. RESULTS: The combination of small size at birth and during infancy, followed by accelerated weight gain from age 3 to 11 years, predicts large differences in the cumulative incidence of CHD, type 2 diabetes and hypertension. CONCLUSIONS: Coronary heart disease and type 2 diabetes may originate through two widespread biological phenomena-developmental plasticity and compensatory growth.
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The relationship between poor growth in the womb and the risk of adult disease has been confirmed in many other countries, including Finland, Sweden, China, India, and the USA.
“This relationship between poor growth in the womb and the risk of adult disease has since been confirmed in many other countries, including Finland (26), Sweden (332), China (183), India (517), and the USA (464).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [26]
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- Authors
- Barker, D., Eriksson, J., Forsén, T., & Osmond, C.
- Affiliations
- Medical Research Council (GB)
- University of Helsinki (FI)
- Corresponding author
- Barker, DJP
- ORCID
- Osmond, C
- Venue
- International Journal of Epidemiology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-12
- Volume
- 31
- Issue
- 6
- Pages
- 1235-1239
- ISSN
- 0300-5771 (ISSN-L)
- 1464-3685
- OpenAlex
- W2101153618
- Cited by
- 2,024
- References
- 31
- Citations by year
- 2026: 34 · 2025: 63 · 2024: 68 · 2023: 69 · 2022: 73 · 2021: 78 · 2020: 86 · 2019: 120 · 2018: 97 · 2017: 95 · 2016: 94 · 2015: 121 · 2014: 104 · 2013: 121 · 2012: 111
- FWCI
- 41.70
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Epidemiology (publishedVersion)
- PubMed (publishedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (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 › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- fetal origins of adult disease, low birth weight, coronary artery disease, type 2 diabetes, hypertension, developmental plasticity, compensatory growth, infant growth, child weight gain, cumulative incidence, chronic disease, medication use, hospitalization
- MeSH terms
- Aged, Anthropometry, Birth Weight, Cardiovascular Diseases, Coronary Disease, Diabetes Mellitus, Type 2, Female, Embryonic and Fetal Development, Finland, Growth, Humans, Hypertension, Infant, Low Birth Weight, Infant, Newborn, Longitudinal Studies, Male, Middle Aged, Pregnancy, Prenatal Exposure Delayed Effects, Weight Gain, Body Mass Index, Incidence, Odds Ratio
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