Influence of Maternal Obesity on the Long-Term Health of Offspring
Open accessAbstract
In addition to immediate implications for pregnancy complications, increasing evidence implicates maternal obesity as a major determinant of offspring health during childhood and later adult life. Observational studies provide evidence for effects of maternal obesity on her offspring's risks of obesity, coronary heart disease, stroke, type 2 diabetes, and asthma. Maternal obesity could also lead to poorer cognitive performance and increased risk of neurodevelopmental disorders, including cerebral palsy. Preliminary evidence suggests potential implications for immune and infectious-disease-related outcomes. Insights from experimental studies support causal effects of maternal obesity on offspring outcomes, which are mediated at least partly through changes in epigenetic processes, such as alterations in DNA methylation, and perhaps through alterations in the gut microbiome. Although the offspring of obese women who lose weight before pregnancy have a reduced risk of obesity, few controlled intervention studies have been done in which maternal obesity is reversed and the consequences for offspring have been examined. Because the long-term effects of maternal obesity could have profound public health implications, there is an urgent need for studies on causality, underlying mechanisms, and effective interventions to reverse the epidemic of obesity in women of childbearing age and to mitigate consequences for offspring.
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Both undernutrition and overnutrition affect fetal metabolism, predisposing offspring to obesity and cardiometabolic disorders in adulthood.
“Both undernutrition and overnutrition affect fetal metabolism, predisposing offspring to obesity and cardiometabolic disorders in adulthood.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [3]
The Introduction and Body composition and cardiometabolic outcomes section describe fetal metabolic changes associated with maternal obesity and increased obesity and cardiovascular risks in adult offspring. The Conclusion mentions fetal undernutrition as an earlier focus of research on later-life disease, but does not establish that undernutrition alters fetal metabolism or predisposes offspring specifically to adult obesity and cardiometabolic disorders. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe fetus exhibits plasticity enabling physiological adaptations to adverse intrauterine conditions such as nutrient deprivation or hormonal imbalances.
“The fetus exhibits a remarkable degree of plasticity, enabling physiological adaptations to adverse intrauterine conditions, such as nutrient deprivation or hormonal imbalances.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [3]
The Introduction reports that maternal obesity can alter fetal metabolic processes, including the response to leptin, and the neurocognitive outcomes section describes effects of elevated nutrients and hormones on fetal development. These passages support fetal responses to the intrauterine environment, but they do not establish a general capacity for adaptive plasticity or address nutrient deprivation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredFetal adaptations to adverse intrauterine conditions may predispose the individual to metabolic, cardiovascular, and neurodevelopmental disorders later in life.
“However, such adaptations—while advantageous for short-term survival—may predispose the individual to metabolic, cardiovascular, and neurodevelopmental disorders later in life, a phenomenon often referred to as “fetal programming” [3,4].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [3]
The Introduction reports that maternal obesity can permanently alter fetal metabolic processes, and the Conclusion links it to later metabolic, cardiovascular, and possible neurodevelopmental outcomes. The paper does not establish that these fetal changes are advantageous for short-term survival, and its evidence centers on maternal obesity rather than adverse intrauterine conditions generally. Page numbers are not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredObesity predisposes newborns to an increased risk of obesity and cardiometabolic diseases in adulthood, such as hypertension, type II diabetes, and dyslipidemia.
“Obesity, in addition to increasing the risk of adverse pregnancy outcomes, mainly represented by obstetric complications caused by excessive fetal growth, also has the capacity to predispose newborns to an increased risk of obesity and cardiometabolic diseases in adulthood, such as hypertension, type II diabetes, and dyslipidemia [3,72].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [3]
The Body composition and cardiometabolic outcomes section links maternal obesity with higher offspring BMI in adulthood and reports more cardiovascular disease and type 2 diabetes among adult offspring of obese mothers. It associates higher blood pressure and adverse lipid profiles with offspring in childhood, but says associations with other cardiovascular risk factors were not consistent in adults. Thus, the specific claims about adult hypertension and dyslipidemia go beyond the evidence presented. (LLM, conf=0.87)
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- Authors
- Godfrey, K. M., Reynolds, R. M., Prescott, S. L., Nyirenda, M., Jaddoe, V. W. V., Eriksson, J. G., & Broekman, B. F. P.
- Affiliations
- University Hospital Southampton NHS Foundation Trust (GB)
- The Queen's Medical Research Institute (GB)
- The Kids Research Institute Australia (AU)
- University of Malawi (MW)
- Erasmus MC (NL)
- University of Helsinki (FI)
- Agency for Science, Technology and Research (SG)
- Corresponding author
- Godfrey, Keith M
- ORCID
- Venue
- The Lancet Diabetes & Endocrinology
- Publisher
- Elsevier BV
- Published
- 2017-01
- Volume
- 5
- Issue
- 1
- Pages
- 53-64
- ISSN
- 2213-8587 (ISSN-L)
- PMC
- PMC5245733
- OpenAlex
- W2531320855
- Cited by
- 1,059
- References
- 30
- Citations by year
- 2026: 129 · 2025: 138 · 2024: 107 · 2023: 101 · 2022: 137 · 2021: 121 · 2020: 119 · 2019: 94 · 2018: 66 · 2017: 37 · 2016: 6
- FWCI
- 10.48
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Diabetes & Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (acceptedVersion, other-oa)
- LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- National Institute for Health and Care Research (NF-SI-0515-10042)
- British Heart Foundation (RG/15/17/31749)
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (016.136.361)
- Medical Research Council (MC_UU_12011/4)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Obesity, Physical Activity, Diet
- Keywords
- maternal obesity, offspring health, childhood obesity, type 2 diabetes, coronary artery disease, stroke, asthma, cognitive performance, neurodevelopmental disorders, cerebral palsy, epigenetics, DNA methylation, gut microbiota, maternal weight loss, pregnancy, obesity prevention
- MeSH terms
- Asthma, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Female, Health Status, Humans, Obesity, Pregnancy, Pregnancy Complications, Time Factors, Adult Children, Observational Studies as Topic, Neurodevelopmental Disorders
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