Maternal effects for preterm birth: a genetic epidemiologic study of 630,000 families.
Abstract
This study was undertaken to disentangle the maternal genetic from the fetal genetic effects for preterm birth and to study the possibility of these effects being explained by known risk factors. By cross-linking of the population-based Swedish Multigeneration and Medical Birth registers, 989,027 births between 1992 and 2004 were identified. Alternating logistic regression was applied to model the familial clustering with pairwise odds ratios (PORs), and covariates were included to evaluate if the familial aggregation was explained by exposure to shared risk factors. Generalized linear mixed models were used to estimate the contribution of genetic and environmental effects. Sisters of women who had a preterm delivery had themselves an increased odds of having a preterm delivery (POR = 1.8, 95% confidence interval: 1.5, 2.1), while there was no corresponding increase in odds in families joined by brothers (POR = 1.1, 95% confidence interval: 0.9, 1.4). Twenty-five percent of the variation in preterm birth was explained by maternal genetic factors, whereas fetal genetic factors only marginally influenced the variation in liability. The increased odds ratio between offspring of sisters was independent of maternal risk factors for preterm birth, suggesting that the relative importance of maternal effects is not explained by these well-known risk factors.
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The present estimates align with those from recent population cohorts and a twin-study meta-analysis that reported heritability between 64% and 91%.
“These results are similar to those of recent population-based cohorts 4,9,10 as well as a recent metaanalysis of twin studies, 8 which estimated heritability in the range of 64% to 91%.”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
Because ASD begins prenatally, maternal effects are a plausible source of these noninherited genetic influences.
“Given the prenatal origins of ASD, an important source of such genetic influences could be maternal effects.4”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
Three recent Swedish population studies reported ASD heritability estimates of 83%, 80%, and 66%.
“and 3 population-based studies from Sweden recently estimated the heritability of ASD to be 83%, 9 80%, 4 and 66%. 10”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
The observed pattern of results supports the hypothesis that severity corresponds to the load of liability factors.
“We believe that these patterns of results add support to the hypothesis that severity maps onto the load of liability factors.4”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
Reported shared-environment contributions to ASD vary from 7% to 35%, although several studies find zero.
“Estimates of the contribution of shared environment range from 7% to 35%, 8 but multiple studies estimate the contribution to be zero.4,9,11,12”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
Of the earlier twin and family heritability studies, only one estimated maternal effects and found at most a modest ASD contribution.
“Among those earlier heritability calculations from twin and family studies (eTable 1 in the Supplement), a single study has estimated maternal effects, 4 reporting modest, if any, contribution to ASD.”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
The absence of a maternal effect in this study agrees with an earlier analysis of Swedish data.
“This corroborates a previous analysis of the data from Sweden.”
From Association of Genetic and Environmental Factors With Autism in a 5-Country Cohort (2019) · cites this paper as [4]
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- Authors
- Svensson, A. C., Sandin, S., Cnattingius, S., Reilly, M., Pawitan, Y., Hultman, C. M., & Lichtenstein, P.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Svensson, Anna C.
- ORCID
- Venue
- American Journal of Epidemiology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-10-23
- Volume
- 170
- Issue
- 11
- Pages
- 1365-1372
- ISSN
- 0002-9262 (ISSN-L)
- 1476-6256
- OpenAlex
- W2137514719
- Cited by
- 150
- References
- 39
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 11 · 2023: 13 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 10 · 2018: 10 · 2017: 14 · 2016: 10 · 2015: 9 · 2014: 7 · 2013: 13 · 2012: 10
- FWCI
- 4.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Epidemiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Preterm Birth and Chorioamnionitis
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Infant Development and Preterm Care
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Assisted Reproductive Technology and Twin Pregnancy
- Keywords
- preterm birth, maternal genetic effects, familial aggregation, shared risk factors, sisters, brothers, genetic epidemiology, environmental effects
- MeSH terms
- Birth Certificates, Female, Humans, Mothers, Pedigree, Pregnancy, Registries, Risk Factors, Sweden, Prevalence, Confidence Intervals, Logistic Models, Odds Ratio, Siblings, Premature Birth
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