Einfluss des mütterlichen Alkoholkonsums während der Schwangerschaft auf die Entwicklung von ADHS beim Kind

Zusammenfassung

In der Ursachenforschung zur Entwicklung des Aufmerksamkeits-Defizit-(Hyperaktivität)-Syndroms (AD[H]S) bei Kindern können erbliche Prädisposition, Umweltfaktoren und Verhalten der Mutter in der Schwangerschaft, wie z. B. pränataler Alkoholkonsum, eine Rolle spielen. Tiermodelle zeigen strukturelle Schäden der Gehirnentwicklung durch pränatale Alkoholwirkung mit schwerwiegenden Verhaltensauffälligkeiten, äquivalent zu einem Aufmerksamkeitsdefizit als Folge. Dies tritt bei kleinen Säugetieren wie auch bei Menschenaffen auf und kann bereits durch moderate Alkoholzufuhr verursacht werden. Bei fetalem Alkoholsyndrom (FAS) und fetaler Alkoholspektrumserkrankung (FASD) zeigt sich ein Symptombild aus Hyperaktivität und impulsivem Verhalten bei schlechterer Aufmerksamkeit und langsameren Reaktionszeiten. Dies entspricht Befunden bei ADHS, weswegen bei Kindern mit FAS/FASD häufig diese Diagnose parallel gestellt wird. Aber nicht nur bei kontinuierlich großen, sondern bereits bei geringeren Alkoholmengen konnten bleibende, auf den Alkohol zurückzuführende Schädigungen (Intelligenzminderungen) nachgewiesen werden. Bis zu 50 % der erwachsenen ADHS-Patienten weisen Alkoholmissbrauch oder -abhängigkeit und/oder andere Suchterkrankungen auf, daher erscheint eine Exposition gegenüber Suchtstoffen bei Kindern von hinsichtlich ADHS genetisch vorbelasteten Müttern als wahrscheinlicher. Eine suffiziente, objektivierte Datenlage zum ADHS- und Suchtstatus der Mütter existiert jedoch nicht, wodurch die Beurteilung der Auswirkung von genetischer Komponente und Umwelteinflüssen zusätzlich erschwert wird. Ein Zusammenhang zwischen moderater, pränataler Alkoholbelastung und der Entwicklung von ADHS beim Kind konnte bisher nicht untermauert werden. Allerdings ist die Aussagekraft der bisherigen, rein fragebogengestützt erhobenen Daten mit Vorbehalt zu betrachten. Die Frage nach Alkoholmissbrauch der Mutter wird in den meisten Fällen im Sinne der sozialen Erwünschtheit beantwortet. Die fragebogengestützt/im Interview ermittelten Daten können hierdurch nicht als reliabel angesehen werden. Studien, in welchen eine Evaluierung anhand objektiver Alkoholabbauparameter wie Fettsäureethylester oder Ethylglucuronid durchgeführt wurde, zeigten dramatisch höhere Raten von Alkoholkonsum bei Schwangeren, als aus den Angaben zu schließen gewesen wäre. Weitere Studien unter Miteinbeziehung objektiver Alkoholparameter sind notwendig, um Zusammenhänge zwischen schwangerschaftsbezogenem Alkoholmissbrauch und ADHS beim Kind besser klären zu können.

Abstract

Besides genetic susceptibility, environmental factors and gene-environment interactions are of central interest in research on attention deficit/hyperactivity disorder in children. Focusing on maternal behaviour during pregnancy, prenatal maternal alcohol consumption is associated with behavioural disorders in children. In animal models, developmental disorders of brain structures as well as subsequent behavioural disorders – similar to findings in attention deficit disorder – were caused by prenatal alcohol exposure. These findings occur in small rodents (mice, rats) as well as in primates and can be caused by even moderate alcohol exposure. In foetal alcohol syndrome (FAS) and foetal alcohol spectrum disease (FASD) in humans, symptoms like hyperactivity, disruptive or impulsive behaviour along with reduced attention and slower reaction time are observed. These findings resemble the symptoms of ADHD. For that reason, children diagnosed with FAS/FASD are frequently diagnosed with ADHD in parallel. Even small amounts of alcohol during pregnancy are responsible for cognitive and behavioural impairments like a significantly decreased IQ. About 50 % of adult ADHD patients show alcohol abuse or dependency and/or other substance disorders. Due to this, a higher rate of prenatal exposition to psychoactive substances for children of mothers affected with ADHD seems probable. However, there are no sufficient data on ADHD and its association to substance abuse in pregnancy, which makes it difficult to quantify the impact of genetic and environmental causes for the development of childhood ADHD. So far, no link could be proven with a high level of evidence between moderate prenatal alcohol consumption and the development of childhood ADHD. It has to be recognised that all present studies are based on self-reported alcohol consumption. Data collected by this methodology are usually severely biased to an underestimation of alcohol abuse. Objective tests for alcohol abuse in pregnancy, such as the analysis of fatty acid ethyl esters or ethyl glucuronide in foetal feces after birth, show rates of alcohol consumption in pregnant women which are dramatically higher than reported. Therefore, studies investigating the association between prenatal alcohol exposure and ADHD should incorporate the analysis and validation of more objective methods, such as parameters for alcohol degradation.

Aufmerksamkeit - Defizit - Alkohol - pränatal - Fettsäureethylester - Ethylglucuronid

attention - deficit - alcohol - prenatal - FAEE - ethyl glucuronide

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