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Assessing Intrauterine Influences on Offspring Health Outcomes: Can Epidemiological Studies Yield Robust Findings?
Open accessAbstract
Abstract: The influence of factors acting during the intrauterine period on health outcomes of offspring is of considerable research and public health interest. There are, however, methodological challenges in establishing robust causal links, because exposures often act many decades before outcomes of interest, may act before it is evident that women are pregnant and would enter pregnancy birth cohorts, and may also be strongly related to other factors, generating considerable degrees of potential confounding. The degree of confounding can sometimes be estimated by comparing the association between exposures experienced by the mother during pregnancy and outcomes among the offspring with the association of exposures experienced by the father during the pregnancy period and offspring outcomes. If the effects are due to an intrauterine exposure, then maternal exposure during pregnancy should have a clearly greater influence than paternal exposure. A different approach is that of Mendelian randomization, which utilizes genetic variants of known functional effect that can proxy for modifiable exposures. If carried by the mother, these variants would influence the intrauterine environment experienced by her offspring. These genetic variants are stable over time and can be assessed after pregnancy is complete or even after outcomes in the offspring have been observed. The variants would also not generally be related to potential confounding factors. Other epidemiological strategies are briefly reviewed. It is concluded that the naïve acceptance of findings utilizing conventional epidemiological methods in this setting is misplaced.
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“The idea behind triangulation is that when we compare different approaches with assumed unrelated sources of bias, particularly if the expected direction of bias for some of the approaches is different, we would not expect to obtain the same estimates of the causal effect (unless all were unbiased).7,15”
From Triangulation in aetiological epidemiology (2017) · cites this paper as [7]
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Metadata
- Authors
- Smith, G. D.
- Affiliations
- University of Bristol (GB)
- Corresponding author
- Smith, George Davey
- ORCID
- Smith, George Davey
- Venue
- Basic & Clinical Pharmacology & Toxicology
- Publisher
- Wiley
- Published
- 2008-01-22
- Volume
- 102
- Issue
- 2
- Pages
- 245-256
- ISSN
- 1742-7835 (ISSN-L)
- 1742-7843
- OpenAlex
- W1564669788
- Cited by
- 257
- References
- 94
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 4 · 2023: 6 · 2022: 9 · 2021: 12 · 2020: 17 · 2019: 16 · 2018: 19 · 2017: 16 · 2016: 16 · 2015: 16 · 2014: 14 · 2013: 28 · 2012: 23
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-10-13)
- Open access
- bronze
- doi.org
- Locations
- Basic & Clinical Pharmacology & Toxicology (publishedVersion)
- PubMed (publishedVersion)
- Explore Bristol Research (submittedVersion)
- Funders
- Medical Research Council
- 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
- Physical Sciences › Mathematics › Statistics and Probability › Statistical Methods in Epidemiology
- Keywords
- prenatal exposure, offspring outcomes, paternal exposure, confounding, birth cohort studies, Mendelian randomization, causal inference, intrauterine environment
- MeSH terms
- Female, Genotype, Humans, Male, Pregnancy, Prenatal Exposure Delayed Effects, Genetic Variation, Epidemiologic Studies, Maternal Exposure, Paternal Exposure
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