The Interplay between Maternal Smoking and Genes in Offspring Birth Weight

Pereira, Rita Dias; Rietveld, Cornelius A.; Kippersluis, Hans van

doi:10.3368/jhr.1020-11266r2

Cited by 7 publications

(6 citation statements)

References 69 publications

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“…Despite not being able to detect a meaningful genetically moderated exposure effect, overall our results suggest that smoking before pregnancy or smoking in the first three months of pregnancy results in a lower birth weight compared to not smoking. This is in line with previous publications [26, 19, 8].…”

Section: Applied Examplesupporting

confidence: 94%

“…Instances of genetically driven effect heterogeneity do exist in main stream epidemiological investigations of non-pharmaceutical interventions. For example, smoking in pregnancy has been shown to have measurable consequences on offspring b irth w eight, w hich i s a n i mportant m arker o f l ong-term h ealth [8]. Specifically, Freathy et al [9] show that single-nucleotide polymorphism (SNP) rs1051730 on chromosome 15 is associated with smoking cessation during pregnancy as well as smoking quantity.…”

Section: Introductionmentioning

confidence: 99%

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Exploring and accounting for genetically driven effect heterogeneity in Mendelian Randomization

Jaitner,

Tsaneva-Atanasova,

Freathy

et al. 2024

Preprint

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Mendelian randomization uses genetic variants as instrumental variables to estimate the causal effect of a modifiable health exposure or drug target on a downstream outcome. A crucial assumption for accurate estimation of the average causal effect in MR, termed Homogeneity, is that the causal effect does not vary across levels of any instrument used in the analysis. In contrast, the science of pharmacogenetics seeks to actively uncover and exploit genetically driven effect heterogeneity for precision medicine. In this paper we consider a recently proposed method for performing pharmacogenetic analysis on bservational data (The Triangulation WIthin a STudy (TWIST) framework), and explore how it can be combined with traditional MR approaches to properly characterise average and causal effects and genetically driven effect heterogeneity. We propose two new methods which not only estimate the genetically driven effect heterogeneity but also enable the estimation of a causal effect in the genetic group with and without the risk allele separately. Both methods utilise homogeneity-respecting and homogeneity-violating genetic variants and rely on a different set of assumptions. Using data from the ALSPAC study, we apply our new method to estimate the causal effect of smoking before and during pregnancy on offspring birth weight in mothers whose genetics mean they find it (relatively) easier or harder to quit.

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Section: Applied Examplesupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Exploring and accounting for genetically driven effect heterogeneity in Mendelian Randomization

Jaitner,

Tsaneva-Atanasova,

Freathy

et al. 2024

Preprint

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“…Causal evidence on genetic heterogeneities relating to smoking behaviours is sparse since this area of research is still relatively young. Pereira et al (2022) examine whether the causal effects of maternal smoking on birth weight differ by genetic ‘predisposition’ for smoking, but find no evidence of such gene-environment interactions.…”

Section: Discussionmentioning

confidence: 99%

“…These associations were robust to controlling for a range of confounders such as maternal age, parity and social circumstances (Lowe, 1959). Since then, many subsequent studies have shown the adverse impacts of in utero exposure to tobacco and cigarette smoke on outcomes around birth (e.g., birth weight; Rantakallio, 1978b; Walker et al, 2009; Yang et al, 2020; Pereira et al, 2022) but also the impacts of prenatal smoking on outcomes in the longer run (e.g., hospital admissions, childhood height, educational outcomes, child behaviour; Butler and Goldstein, 1973; Rantakallio, 1978a; Dolan et al, 2016). 1 While the harmful effects of smoking during pregnancy are well-known today and maternal smoking rates are lower than decades ago (see e.g.…”

Section: Introductionmentioning

confidence: 99%

The prevalence, trends and heterogeneity in maternal smoking around birth between the 1930s and 1970s

von Hinke,

James,

Sorensen

et al. 2023

Preprint

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This paper shows the prevalence, trends and heterogeneity in maternal smoking around birth in the United Kingdom, focusing on the war and post-war reconstruction period in which there exists surprisingly little systematic data on (maternal) smoking behaviours. Within this context, we highlight relevant events, the release of new information about the harms of smoking, and changes in (government) policy aimed at reducing smoking prevalence. We show stark changes in smoking prevalence over a 30-year period, highlight the onset of the social gradient in smoking, as well as genetic heterogeneities in smoking trends.

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“…In the UK, the NHS digital service provides statistics indicating that approximately 8.6 % of mothers were known smokers at the time of delivery in the first half of 2023 2 . Mendelian Randomization studies between smoking during pregnancy and offspring birth weight suggest a causal relationship between smoking during pregnancy and lower birth weight [3][4][5][6] . However, the underlying mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Smoking during pregnancy and its effect on placental weight: A Mendelian randomization study

Jaitner,

Vaudel,

Tsaneva-Atanasova

et al. 2023

Preprint

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Background: The causal relationship between maternal smoking in pregnancy and reduced offspring birth weight is well established and is likely due to impaired placental function. However, observational studies have given conflicting results on the association between smoking and placental weight. We aimed to estimate the causal effect of newly pregnant mothers quitting smoking on their placental weight at the time of delivery. Methods: We used one-sample Mendelian randomization, drawing data from the Avon Longitudinal Study of Parents and Children (ALSPAC) (up to N = 805) and the Norwegian Mother, Father and Child Cohort Study (MoBa) (up to N = 4475). The analysis was performed in pre-pregnancy smokers only, due to the specific role of the genetic instrument SNP rs1051730 (CHRNA5-CHRNA3-CHRNB4) in affecting smoking cessation but not initiation. Results: Fixed effect meta-analysis showed a 175 g [95%CI: 16, 334] higher placental weight for pre-pregnancy smoking mothers who continued smoking at the beginning of pregnancy, compared with those who stopped smoking. Using the number of cigarettes smoked per day in the first trimester as the exposure, the causal estimate was a 12 g [95%CI: 2,22] higher placental weight per cigarette per day. Results were similar when the smoking exposures were measured at the end of pregnancy. Using the residuals of birth weight regressed on placental weight as the outcome, we showed weak evidence of lower offspring birth weight relative to the placental weight for continuing smoking. Conclusion: Our results suggest that continued smoking during pregnancy causes higher placental weights.

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The Interplay between Maternal Smoking and Genes in Offspring Birth Weight

Cited by 7 publications

References 69 publications

Exploring and accounting for genetically driven effect heterogeneity in Mendelian Randomization

Exploring and accounting for genetically driven effect heterogeneity in Mendelian Randomization

The prevalence, trends and heterogeneity in maternal smoking around birth between the 1930s and 1970s

Smoking during pregnancy and its effect on placental weight: A Mendelian randomization study

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