Evidence map›Paper›PMID 42125938›Full record

ArticleAlcohol, clinical & experimental research2026

Dysmorphological and Neuropsychological Phenotypes of Prenatally Alcohol-Exposed 6-Year-Old Children: A Prospective Longitudinal Birth Cohort Study.

M Jolma, E Wallén, E Saure, K Rämö, H Kahila, N Kaminen-Ahola

Abstract read
In one paragraph

Article in Alcohol, clinical & experimental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

6 authors.

M JolmaDivision of Child Neurology, Päijät-Häme Central Hospital, Lahti, Finland.ORCID https://orcid.org/0000-0002-6760-0495
E WallénEnvironmental Epigenetics Laboratory, Department of Medical and Clinical Genetics, Medicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-9926-0106
E SaureBABA Center, Pediatric Research Center, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-4061-554X
K RämöEnvironmental Epigenetics Laboratory, Department of Medical and Clinical Genetics, Medicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0001-8070-4785
H KahilaDepartment of Obstetrics and Gynecology, Helsinki University Hospital and University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0001-9658-1193
N Kaminen-AholaEnvironmental Epigenetics Laboratory, Department of Medical and Clinical Genetics, Medicum, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0003-1255-4716

Funding

Academy of Finland 332212AlkoholitutkimussäätiöInstrumentariumin TiedesäätiöJane ja Aatos Erkon Säätiö 230032Lastentautien TutkimussäätiöMärta and Peter Klaus FoundationMedicinska Understödsföreningen Liv och Hälsa
6 · The paper itself

Abstract

backgroundPrenatal alcohol exposure (PAE) disrupts embryonic development, resulting in variable fetal alcohol spectrum disorder (FASD) phenotypes characterized by dysmorphological and neurodevelopmental abnormalities. To elucidate the etiology of FASD, we established a prenatally recruited prospective birth cohort collecting biological samples at birth and longitudinal data from alcohol-exposed and unexposed control children.

methodsDysmorphological, neuropediatric, and neuropsychological assessments were performed at 6 years of age in 28 children with substantial PAE and 52 control children.

resultsAmong the PAE group, 76% (19/25) of the children who completed the full evaluation met the diagnostic criteria for FASD, including five with fetal alcohol syndrome (FAS), six with partial FAS, seven with alcohol-related neurodevelopmental disorder, and one with alcohol-related birth defect. None of the tested children had a prior FASD diagnosis. In addition to the characteristic features of FAS, including short palpebral fissures, smooth philtrum, and thin vermilion border, several additional anomalies, such as mild midface hypoplasia, were significantly associated with PAE (p < 0.001). Also, PAE was associated with both underweight and overweight at 6 years of age, particularly among boys. Neurocognitive assessments revealed lower performance scores and a high prevalence of ADHD symptoms in PAE children compared with controls. Furthermore, PAE children exhibited additional phenotypic features not captured by the diagnostic FASD criteria, including impairments in adaptive and social functioning, somatic health problems, and reduced postural stability. Moreover, 11 children with early-only PAE limited to the first seven gestational weeks showed dysmorphic features and cognitive outcomes comparable to those of children with longer exposure.

conclusionsThe high proportion of affected children demonstrates the need for systematic follow-up of those with PAE and comprehensive phenotypic characterization to improve FASD identification. Importantly, these findings indicate that substantial PAE limited to very early pregnancy is sufficient to result in FASD with clinically significant neurocognitive impairment.

Indexed as

Fetal Alcohol Spectrum DisordersPrenatal Exposure Delayed EffectsBirth CohortChildFemaleHumansLongitudinal StudiesMaleNeuropsychological TestsPhenotypePregnancyProspective Studiesbalancecognitiondysmorphismearly exposurefetal alcohol spectrum disorderprenatal alcohol exposure

Identifiers

PMID42125938
PMCPMC13169235

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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.