Evidence map›Paper›PMID 35073992›Full record

SynthesisClinical epigenetics2022

Association of prenatal alcohol exposure with offspring DNA methylation in mammals: a systematic review of the evidence.

Mitchell Bestry, Martyn Symons, Alexander Larcombe, Evelyne Muggli, Jeffrey M Craig, Delyse Hutchinson, Jane Halliday, David Martino

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
7.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Mitchell BestryTelethon Kids Institute, The University of Western Australia, Perth, WA, Australia.
Martyn SymonsTelethon Kids Institute, The University of Western Australia, Perth, WA, Australia.
Alexander LarcombeWal-yan Respiratory Research Centre, Telethon Kids Institute, Perth, Australia.
Evelyne MuggliVictorian Infant Brain Studies, Murdoch Children's Research Institute, Parkville, VIC, Australia.
Jeffrey M CraigDepartment of Paediatrics, The University of Melbourne, Parkville, VIC, Australia.
Delyse HutchinsonDepartment of Paediatrics, The University of Melbourne, Parkville, VIC, Australia.
Jane HallidayDepartment of Paediatrics, The University of Melbourne, Parkville, VIC, Australia.
David MartinoWal-yan Respiratory Research Centre, Telethon Kids Institute, Perth, Australia. david.martino@telethonkids.org.au.ORCID 0000-0001-6823-4696
The Kids Research Institute Australia · AUThe University of Melbourne · AUDeakin University · AURoyal Children's Hospital · AU

Funding

National Health and Medical Research Council 1110341National Health and Medical Research Council 1141601
6 · The paper itself

Abstract

backgroundPrenatal alcohol exposure (PAE) is associated with a range of adverse offspring neurodevelopmental outcomes. Several studies suggest that PAE modifies DNA methylation in offspring cells and tissues, providing evidence for a potential mechanistic link to Fetal Alcohol Spectrum Disorder (FASD). We systematically reviewed existing evidence on the extent to which maternal alcohol use during pregnancy is associated with offspring DNA methylation.

methodsA systematic literature search was conducted across five online databases according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed, Web of Science, EMBASE, Google Scholar and CINAHL Databases were searched for articles relating to PAE in placental mammals. Data were extracted from each study and the Risk of Bias in Non-Randomized Studies of Interventions (ROBINS-I) was used to assess the potential for bias in human studies.

resultsForty-three articles were identified for inclusion. Twenty-six animal studies and 16 human studies measured offspring DNA methylation in various tissues using candidate gene analysis, methylome-wide association studies (MWAS), or total nuclear DNA methylation content. PAE dose and timing varied between studies. Risk of bias was deemed high in nearly all human studies. There was insufficient evidence in human and animal studies to support global disruption of DNA methylation from PAE. Inconclusive evidence was found for hypomethylation at IGF2/H19 regions within somatic tissues. MWAS assessing PAE effects on offspring DNA methylation showed inconsistent evidence. There was some consistency in the relatively small number of MWAS conducted in populations with FASD. Meta-analyses could not be conducted due to significant heterogeneity between studies.

conclusionConsidering heterogeneity in study design and potential for bias, evidence for an association between PAE and offspring DNA methylation was inconclusive. Some reproducible associations were observed in populations with FASD although the limited number of these studies warrants further research. Trail Registration: This review is registered with PROSPERO (registration number: CRD42020167686).

Indexed as

Alcohol DrinkingAnimalsDNA MethylationFemaleMammalsPregnancyPrenatal Exposure Delayed EffectsDNA methylationEpigeneticsFetal alcohol spectrum disorderPregnancyPrenatal alcohol exposure

Identifiers

PMID35073992
PMCPMC8785586
OpenAlexW4206897040

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.