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Neurodevelopmental Pathways from Maternal Obesity to Offspring Outcomes: An Umbrella Review of Cognitive and
Evgenia Gkintoni1,2, Eleni Papachatzi1,3, Erifili Efthymiadou4
1Laboratory of Public Health, Department of Medicine, University of Patras, 26504 Patras, Greece.
Insights
Maternal obesity is linked to poorer child neurodevelopment, including lower IQ and more ADHD symptoms. Interventions targeting inflammatory, metabolic, and epigenetic pathways before and after conception may improve outcomes.
Area of Science:
- Neuroscience
- Developmental Biology
- Public Health
Background:
- Maternal obesity affects 20-25% of global pregnancies.
- Linked to adverse offspring neurodevelopmental outcomes.
- Umbrella review to synthesize evidence on neurodevelopmental pathways.
Purpose of the Study:
- Synthesize evidence on neurodevelopmental pathways linking maternal obesity to offspring cognitive, executive, and behavioral outcomes.
- Identify mechanistic pathways involved.
- Assess the strength of evidence.
Main Methods:
- Systematic umbrella review following PRISMA 2020 guidelines.
- Searched six databases for studies published 2008-2024.
- Included prospective cohorts, animal experiments, systematic reviews, neuroimaging, and RCTs.
Main Results:
- 78 studies (650,000+ mother-child pairs) showed significant associations.
- Maternal obesity linked to reduced cognitive abilities, impaired executive function, increased ADHD symptoms, and emotional dysregulation.
- Identified inflammatory, metabolic, epigenetic, and neurotransmitter pathways; dose-response effects noted.
Conclusions:
- Maternal obesity is a modifiable risk factor for offspring neurodevelopmental impairment.
- Evidence from human observational and animal studies supports this link.
- Multimodal interventions targeting identified pathways during critical windows warrant investigation.
Abstract:
Background: Maternal obesity affects 20-25% of pregnancies globally and has been associated with adverse offspring neurodevelopmental outcomes. This umbrella review synthesized evidence on neurodevelopmental pathways linking maternal obesity to offspring cognitive, executive, and behavioral outcomes. Methods: Following PRISMA 2020 guidelines, we systematically searched six databases (PubMed/MEDLINE, Scopus, Web of Science, PsycINFO, EMBASE, CINAHL) for studies published 2008-2024. We included original peer-reviewed studies examining maternal pre-pregnancy obesity (BMI ≥ 30 kg/m2) and offspring neurodevelopmental outcomes using prospective cohort, experimental, neuroimaging, or systematic review designs with validated assessments. Risk of bias was assessed using Newcastle-Ottawa Scale, Cochrane RoB 2.0, and SYRCLE guidelines. Results: Analysis of 78 studies encompassing 650,000+ mother-child pairs from 17 countries revealed significant associations. Study designs included prospective cohorts (59%), animal experiments (22%), systematic reviews/meta-analyses (13%), neuroimaging studies (4%), and randomized trials (3%). Maternal obesity (BMI ≥ 30 kg/m2) was associated with reduced cognitive abilities (IQ differences: -2.5 to -5.8 points), impaired executive function (OR 1.4-2.3), and increased ADHD symptoms (OR 1.4-2.8) and emotional dysregulation (OR 1.5-2.2). Dose-response relationships revealed threshold effects at BMI ≥ 30 kg/m2, accelerating at BMI ≥ 35 kg/m2. Four primary mechanistic pathways were identified: inflammatory, metabolic, epigenetic, and neurotransmitter alterations. Only 57.7% of studies used prospectively measured pre-pregnancy BMI. Conclusions: Observational and experimental evidence indicates maternal obesity represents a modifiable risk factor for offspring neurodevelopmental impairment. The primarily observational human evidence, supported by mechanistic animal studies, suggests multimodal interventions targeting identified pathways during critical windows (pre-conception through early postnatal period) warrant investigation.
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