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Effect of In Utero and Early-Life Conditions on Adult Health and Disease
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Many lines of evidence, including epidemiologic data and extensive clinical and experimental studies, indicate that early life events play a powerful role in influencing later susceptibility to certain chronic diseases. This review synthesizes evidence from several disciplines to support the contention that environmental factors acting during development should be accorded greater weight in models of disease causation.
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“The importance of balanced nutrition in early life for normal neurocognitive development, a process that is not finished until late adolescence, has been widely recognized.427”
From Vascular Contributions to Cognitive Impairment and Dementia: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association (2011) · cites this paper as [427]
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“The incidence ratio of offspring exposed to every type of maternal diabetes was increased by 29% compared to non-exposed offspring, and the increase in risk was observed in every age group (<20 years old; >20 years old) [33,62,63,64,65].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [65]
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“Recent epidemiological studies show a relationship between an increased risk of cardiometabolic diseases in adulthood for offspring of women whose pregnancy has been complicated by GDM.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [65]
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“In another aspect, given that epigenetic signatures are specific to each tissue, various studies affirm that metabolic syndromes involve the reprogramming of the epigenetic landscape in a certain time and space.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [96]
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“In this case, there is a growing amount of evidence that correlates prenatal stress-related situations involved in diseases that emerge either early pre-gestational stages or in adulthood.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [96]
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“The collective evidence from epidemiological studies, clinical cohorts and animal model experiments supports the theory that environmental exposures in early life can determine the long-term health of individuals, including cardiovascular and metabolic diseases [36,37].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [36]
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“A large study conducted by Yu Y. et al. demonstrated an association between gestational diabetes and an increased rate of early-onset cardiovascular diseases (CVD; ≤40 years old) in offspring.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [65]
Experimental — accuracy not yet measuredIn the citing paper
“MIA-induced disruption may work in a manner similar in directionality to rare highly penetrant ASD mutations, and may act as ‘priming’27, 28, 29, 30 or fetal programming21, 22 mechanisms that enhance risk of later developing ASD.”
From Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder (2018) · cites this paper as [22]
In the citing paper
“Perturbation of gene expression or cell proliferation and differentiation during vulnerable periods by nutritional and other environmental influences can alter the structure and functional capacity of major organ systems for life, a process known as developmental programming.”
From Placental Origins of Chronic Disease (2016) · cites this paper as [215]
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“The end result will be altered development of the fetal organs, as seen in cases of severe maternal undernutrition (215, 374, 565).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [215]
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Metadata
- Authors
- Gluckman, P. D., Hanson, M. A., Cooper, C., & Thornburg, K. L.
- Affiliations
- University of Auckland (NZ)
- University of Southampton (GB)
- Oregon Health & Science University (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2008-07-03
- Volume
- 359
- Issue
- 1
- Pages
- 61-73
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC3923653
- OpenAlex
- W2114949397
- Cited by
- 3,898
- References
- 106
- Citations by year
- 2026: 157 · 2025: 143 · 2024: 179 · 2023: 231 · 2022: 275 · 2021: 232 · 2020: 239 · 2019: 267 · 2018: 231 · 2017: 206 · 2016: 250 · 2015: 270 · 2014: 250 · 2013: 233 · 2012: 205
- FWCI
- 23.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Funders
- British Heart Foundation
- Versus Arthritis
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P01HD034430, P01-HD-34430)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Health, Environment, Cognitive Aging
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Prenatal Substance Exposure Effects
- Keywords
- early life exposure, developmental origins of health and disease, chronic disease susceptibility, adult health outcomes
- MeSH terms
- Adaptation, Biological, Adult, Birth Weight, Disease, Female, Gene Expression Regulation, Growth, Health, Humans, Infant, Infant, Newborn, Male, Nutritional Physiological Phenomena, Pregnancy, Prenatal Exposure Delayed Effects, Prenatal Nutritional Physiological Phenomena, Epigenesis, Genetic, Fetal Development
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