Department of Child and Adolescent Mental Health, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg (FAU), Schwabachanlage 6, 91054, Erlangen, Germany.
Department of Psychology I - Developmental Psychology, Otto-Friedrich-University Bamberg, Bamberg, Germany.
Eur Arch Psychiatry Clin Neurosci. 2024 Mar;274(2):343-352. doi: 10.1007/s00406-023-01657-z. Epub 2023 Aug 2.
Prenatal alcohol exposure (PAE) has been linked to severe, adverse child outcomes. However, little is known regarding subclinical outcomes of low/moderate PAE and its longitudinal consequences, especially regarding neurophysiological and neurocognitive development. A newborn biomarker of PAE, meconium ethyl glucuronide (EtG), has been shown to predict cognitive impairments in primary-school-aged children. The current study investigated the ongoing effects of subclinical PAE in adolescence.
A sample of n = 96 mother-child dyads of the FRAMES/FRANCES cohort were classified into PAE/no PAE using EtG with a 10 ng/g cutoff. Mothers were recruited during pregnancy and children were assessed during primary-school age (M = 7.57, SD = 0.65, range: 6.00-9.92 years) and adolescence (M = 13.26, SD = 0.31, range: 12.79-14.20 years) on three levels: clinical (ADHD rating), neuropsychological (IQ score and performance in a go/nogo task), and neurophysiological (analysis of P3 event-related potentials (ERP) during said go/nogo task). Developmental outcomes and courses following PAE were assessed using rmANCOVAs, controlling for relevant confounders (socioeconomic status (SES), birth weight, and maternal psychopathology).
Neurophysiological impairments emerged for exposed children in the form of diminished attentional resource recruiting in childhood and adolescence (reduced go-P3 amplitudes) with no differences in performance. Neuropsychological testing showed a reduced IQ score for both time points with dose-dependent effects in childhood. Clinical ADHD symptoms were not significantly affected.
Subclinical PAE, as determined by meconium EtG, has negative developmental consequences on cognitive function that persist from childhood to adolescence. These findings suggest that there is no safe limit for alcohol consumption during pregnancy and that more thorough screening of alcohol consumption during pregnancy is necessary for early identification and treatment of at-risk children.
产前酒精暴露（PAE）与严重的不良儿童结局有关。然而，对于低/中度 PAE 的亚临床结局及其纵向后果，特别是关于神经生理和神经认知发育的情况，人们知之甚少。胎粪乙基葡糖苷酸（EtG）作为一种 PAE 的新生儿生物标志物，已被证明可预测小学生认知障碍。本研究调查了青春期亚临床 PAE 的持续影响。
使用 10ng/g 截止值的 EtG，对 FRAMES/FRANCES 队列的 96 名母婴对子样本进行 PAE/非 PAE 分类。母亲在怀孕期间招募，孩子在小学年龄（M=7.57，SD=0.65，范围：6.00-9.92 岁）和青春期（M=13.26，SD=0.31，范围：12.79-14.20 岁）进行三次评估：临床（ADHD 评分）、神经心理学（智商得分和 go/nogo 任务中的表现）和神经生理学（在所述 go/nogo 任务中分析 P3 事件相关电位（ERP））。使用 rmANCOVA 评估 PAE 后的发育结果和过程，控制相关混杂因素（社会经济地位（SES）、出生体重和产妇精神病理学）。
暴露儿童的神经生理学损伤表现为儿童期和青春期注意力资源募集减少（go-P3 振幅降低），但表现无差异。神经心理学测试显示两个时间点的智商得分均降低，且儿童期存在剂量依赖性效应。临床 ADHD 症状无显著影响。
胎粪 EtG 确定的亚临床 PAE 对认知功能有负面影响，从儿童期持续到青春期。这些发现表明，怀孕期间饮酒没有安全限制，需要更彻底地筛查怀孕期间的饮酒情况，以便及早发现和治疗高危儿童。
