Neurology Central

Prenatal diet and childhood ADHD: exploring the potential role of IGF2 methylation

Unhealthy diet during pregnancy is a risk factor for a wide range of negative health and psychiatric outcomes [1]. For example, high-sugar and fat diets associate not only with increased risk for noncommunicable diseases [2], such as diabetes and obesity, but also for neurodevelopmental disorders, such as attention-deficit hyperactivity disorder (ADHD) and conduct problems (CP) [3]. In the nutritional field, epigenetics is an important area of investigation, as nutrients and bioactive compounds can alter the expression of genes at the transcriptional level [4]. Because epigenetic modifications, such as DNA methylation, can be passed on during cell division and result in long-term phenotypic changes [5], they also provide a framework for understanding the biological mechanisms through which pre- and post-natal environmental exposures may influence disease vulnerability [6,7].
In a recent paper [8], we examined how exposure to unhealthy fats (e.g., vegetable oils in fast foods) and sugars (e.g., sweets) might associate with ADHD symptoms in children who follow an early onset (age ≤ 10 years; n = 83) versus low (n = 81) trajectory of CP, via DNA methylation of the IGF2 gene. We focused on IGF2 due to its relevance in metabolic function [9], placental and fetal growth [10] and the development of brain regions implicated in ADHD [11–13]. Data were drawn from the Accessible Resource for Integrated Epigenomics Studies [14], a subsample of the Avon Longitudinal Study of Parents and Children, which includes: firstly, maternal reports of diet (32-week gestation, age 3 and 7 years); secondly, peripheral measures of DNA methylation (Illumina 450 k) at birth and age 7 years (n = 671, 49% male) and thirdly, repeated assessments of psychiatric symptomatology, including CP (ages 4–13 years) and ADHD (ages 7–13 years). Below, we summarize our key findings before discussing limitations and future directions.
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