Effect of In Utero and Early-Life Conditions on Adult Health and Disease
Open accessAbstract
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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Balanced nutrition in early life is important for normal neurocognitive development, which continues until late adolescence.
“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]
The Medical and Public Health Implications section links maternal nutrition and early development with the infant’s cognitive development, supporting the importance of early-life nutrition. It does not say that neurocognitive development continues until late adolescence; no page number is available in our copy. (LLM, conf=0.81)
Experimental — accuracy not yet measuredThe incidence ratio of offspring exposed to every type of maternal diabetes was increased by 29% compared to non-exposed offspring, with increased risk observed in every age group.
“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]
The Epidemiologic and Clinical Observations section says offspring of women with diabetes are at greater risk of metabolic disorders, even during childhood. It does not give a 29% incidence increase, address every type of maternal diabetes, or establish increased risk in both the under-20 and over-20 age groups. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRecent epidemiological studies show a relationship between increased risk of cardiometabolic diseases in adulthood for offspring of women whose pregnancy was complicated by GDM.
“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]
In “Epidemiologic and Clinical Observations” (page unavailable), the paper says that offspring of women with diabetes have a greater risk of metabolic disorders, even during childhood. It does not specifically identify gestational diabetes (GDM) or establish cardiometabolic disease risk in adulthood for that group. (LLM, conf=0.86)
Experimental — accuracy not yet measuredMetabolic syndromes involve reprogramming of the epigenetic landscape in a certain time and space.
“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]
The Epigenetic Mechanisms section (page unavailable) describes cell-type-specific epigenetic changes induced during a developmental window, including changes to genes involved in carbohydrate and lipid metabolism. The Conclusions (page unavailable) suggest that epigenetics may help explain links between early-life influences and later metabolic disease. The paper does not establish that metabolic syndromes themselves involve epigenetic reprogramming; it discusses developmental changes that may affect later disease risk. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThere is growing evidence correlating prenatal stress-related situations with diseases that emerge either in early pre-gestational stages or in adulthood.
“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]
The Epidemiologic and Clinical Observations and Integrated Responses sections link prenatal conditions, including nutritional and glucocorticoid challenges, to disease risks in offspring during childhood or later life. They do not describe diseases emerging in “early pre-gestational stages”; that timing is not supported by the paper. (LLM, conf=0.84)
Experimental — accuracy not yet measured
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.
“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]
Yu Y. et al. demonstrated an association between gestational diabetes and an increased rate of early-onset cardiovascular diseases (≤40 years old) in offspring.
“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]
The Epidemiologic and Clinical Observations section links maternal diabetes to metabolic disorders in offspring and, separately, smaller birth size to later cardiovascular disease. It does not report a Yu Y. study or an association between gestational diabetes and cardiovascular disease in offspring aged 40 or younger. Searches for Yu Y., gestational diabetes, and the age-specific cardiovascular outcome found no passage addressing that claim. (LLM, conf=0.75)
Experimental — accuracy not yet measuredMIA-induced disruption may work in a manner similar in directionality to rare highly penetrant ASD mutations, and may act as 'priming' or fetal programming mechanisms that enhance risk of later developing ASD.
“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]
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.
“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]
The end result of deficient remodeling will be altered development of the fetal organs, as seen in cases of severe maternal undernutrition.
“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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- 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
- 107
- 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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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