The DOI matches its Crossref record; 95 of the 95 references it cites were found in a registry or an index.
Maternal adiposity—a determinant of perinatal and offspring outcomes?
Abstract
Experimental and animal data suggest that maternal obesity during pregnancy adversely affects offspring health in the short-term and the long-term. Whether these effects occur in humans and influence population health is less clear. This Review explores evidence from intervention studies and observational studies that have used designs (such as family-based comparisons and Mendelian randomization) that might help improve understanding of the causal effects of maternal obesity in humans. Collectively, human studies provide evidence that maternal overweight and obesity is causally related to pregnancy complications, increased offspring weight and adiposity at birth, and the difficulties associated with delivery of large-for-gestational-age infants. The underlying mechanisms for these effects probably involve maternal and fetal dysregulation of glucose, insulin, lipid and amino acid metabolism. Some evidence exists that extreme maternal obesity (BMI ≥40 kg/m(2)) is causally related to a long-term increase in offspring adiposity, but further exploration of this relationship is needed. High gestational weight gain may result in a long-term increase in offspring adiposity if women are already overweight or have obesity at the start of pregnancy. To date, little high-quality human evidence exists that any of these effects are mediated by epigenetic mechanisms, but approaches to appropriately test this possibility are being developed.
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“Maternal obesity has additionally been linked to cognitive dysfunction, immune alterations, and elevated cancer-related mortality in the offspring.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [75]
In the citing paper
“Increased adiposity in offspring can explain the relationship between high maternal BMI and increased risk of cardiometabolic diseases [73,74,75].”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [75]
In the citing paper
“Maternal obesity can have an adverse impact on newborn body composition and adiposity, which are related to adverse cardiometabolic outcomes, higher cancer morbidity and an increased mortality ratio in general.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [75]
In the citing paper
“It is well established that maternal obesity is associated with adverse outcomes for offspring long-term health.”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [75]
In the citing paper
“The ‘developmental overnutrition hypothesis’ suggests that greater maternal adiposity, and associated greater maternal circulating glucose and other nutrients, overfeed the developing fetus resulting in greater birthweight and adiposity throughout life.23,24”
From A structured approach to hypotheses involving continuous exposures over the life course (2016) · cites this paper as [23]
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- Wen, X. et al. Components of gestational weight gain and postpartum weight retention [abstract 60-LB-P]. In The 29th Annual Scientific Meeting of The Obesity Society. Late-Breaking Abstracts (online) . (2011).
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Mechanisms and disease consequences of nonalcoholic fatty liver disease
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ASMBS pediatric metabolic and bariatric surgery guidelines, 2018
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Oury, F., Khrimian, L., Denny, C. A., Gardin, A., Chamouni, A., Goeden, N., Huang, Y.-Y., Lee, H., Srinivas, P., Gao, X.-B., et al. (2013) · Cell · doi:10.1016/j.cell.2013.08.042 · Cited by 484
Metadata
- Authors
- Lawlor, D. A., Relton, C., Sattar, N., & Nelson, S. M.
- Affiliations
- University of Bristol (GB)
- Centre for Life (GB)
- University of Glasgow (GB)
- Western Infirmary (GB)
- Corresponding author
- Lawlor, Debbie A.
- Venue
- Nature Reviews Endocrinology
- Published
- 2012-09-25
- Volume
- 8
- Issue
- 11
- Pages
- 679-688
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- OpenAlex
- W1976542144
- Cited by
- 192
- References
- 95
- Citations by year
- 2026: 6 · 2025: 2 · 2024: 11 · 2023: 26 · 2022: 11 · 2021: 7 · 2020: 10 · 2019: 18 · 2018: 13 · 2017: 19 · 2016: 23 · 2015: 16 · 2014: 21 · 2013: 9
- FWCI
- 2.40
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Explore Bristol Research (publishedVersion)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
- Keywords
- maternal obesity, maternal adiposity, gestational weight gain, perinatal outcomes, offspring adiposity, offspring weight, large for gestational age, pregnancy complications, epigenetic mechanisms, fetal metabolism, Mendelian randomization, causal effects
- MeSH terms
- Female, Humans, Infant, Newborn, Maternal Welfare, Obesity, Pregnancy, Pregnancy Complications, Pregnancy Outcome, Risk Factors, Body Mass Index, Perinatal Care, Adiposity
About these checks
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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