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Cited by 193Gestational Diabetes Research and ManagementBirth, Development, and HealthPregnancy and preeclampsia studies

Maternal adiposity—a determinant of perinatal and offspring outcomes?

Lawlor, Debbie A., Relton, Caroline, Sattar, Naveed, Nelson, Scott M.·2012·Nature Reviews Endocrinology
DOI 10.1038/nrendo.2012.176
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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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Crossref · 10.1038/nrendo.2012.176

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  • Maternal obesity is linked to cognitive dysfunction, immune alterations, and elevated cancer-related mortality in the offspring.

    “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]

  • Increased adiposity in offspring can explain the relationship between high maternal BMI and increased risk of cardiometabolic diseases.

    “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]

  • Maternal obesity can adversely impact newborn body composition and adiposity, which are related to adverse cardiometabolic outcomes, higher cancer morbidity, and an increased mortality ratio in general.

    “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]

  • Maternal obesity is associated with adverse outcomes for offspring long-term health.

    “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]

  • 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.

    “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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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.
ORCID
Venue
Nature Reviews Endocrinology
Publisher
Springer Science and Business Media LLC
Published
2012-09-25
Volume
8
Issue
11
Pages
679-688
ISSN
  • 1759-5029 (ISSN-L)
  • 1759-5037
DOI
10.1038/nrendo.2012.176
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

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