Possible link between unhealthy prenatal diet and ADHD

A longitudinal study examined the relationship between prenatal or postnatal high-fat, high-sugar diet and symptoms of attention-deficit/hyperactivity disorder (ADHD) in children who demonstrated either early-onset persistent conduct disorder or minimal conduct problems.

Conduct disorder and ADHD and often coexist, and, when found together, increase the likelihood for behavioral problems, academic underachievement, substance abuse, social maladjustment, and poor self-esteem.¹ Conduct disorders fall into different categories based on their developmental course (early-onset persistent [EOP], childhood limited, and adolescent onset), but are all generally characterized by repeated violation of the rights of others and lack of age-appropriate conformity to rules or societal norms.

Previous studies have linked an unhealthy prenatal maternal diet (ie, consumption of foods that are high in fat and sugar) with ADHD and other neuropsychiatric disorders in their offspring.² The putative effect of such a diet is to increase DNA methylation, which in turn influences gene expression. One gene whose methylation is known to incur persistent changes in methylation due to diet is insulin-like growth factor 2 (IGF2).³ The IGF2 gene also has developmental significance, as it has been linked to placental and fetal growth as well as to postnatal brain development.^4,5

Looking for connections

In a first-of-its-kind study, Jolien Rijlaarsdam, PhD, Leiden University Centre for Child and Family Studies, Leiden, The Netherlands, and colleagues evaluated the relationships between a high-fat/high-sugar diet (ie, an unhealthy diet) during the prenatal and postnatal periods, IGF2 DNA methylation, and ADHD symptoms. The results, published in the Journal of Child Psychology and Psychiatry,⁶ indicate that there are connections between these factors.

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The study population consisted of 164 children from the Avon Longitudinal Study of Parents and Children who were identified as having either EOP or a low conduct-problem trajectory (children with childhood limited or adolescent onset conduct disorders were not included). Prenatal and postnatal diet were determined by parental self-report; IGF2 DNA methylation was quantified using blood samples collected at birth and at age 7 years; and ADHD symptoms were evaluated using a validated instrument at ages 7, 10, and 13 years.

Among the various associations detected, investigators found that children classified as EOP had an overall greater burden of ADHD symptoms compared with low conduct-problem children. In both the EOP and low conduct-problem groups, a prenatal unhealthy diet correlated with a greater extent of IGF2 methylation at birth. In the EOP population (but not the low conduct-problem group), increased IGF2 methylation at birth was associated with a greater ADHD symptom burden. Because of the link between a prenatal unhealthy diet and IGF2 methylation at birth, an unhealthy prenatal diet indirectly correlated with ADHD symptoms in children with EOP.

Notably, IGF2 methylation was not associated with other psychiatric disorders assessed (oppositional defiant disorder, generalized anxiety disorder, and major depressive disorder) in either the EOP or low conduct-problem groups.

The researchers conclude that “Preventing ‘unhealthy diet’ in pregnancy might reduce the risk of ADHD symptoms in EOP youth via lower offspring IGF2 methylation.”

REFERENCES

1. Faraone SV, Kunwar AR. ADHD in children with comorbid conditions. Available at: http://www.medscape.org/viewarticle/555748. Accessed on October 24, 2016.

2. Sullivan EL, Riper KM, Lockard R, Valleau JC. Maternal high-fat diet programming of the neuroendocrine system and behavior. Horm Behav. 2015;76:153-161.

3. Heijmans BT, Tobi EW, Stein AD, et al. Persistent epigenetic differences associated with prenatal exposure to famine in humans. Proc Natl Acad Sci U S A. 2008;105(44):17046-17049.

4. Constância M, Hemberger M, Hughes J, et al. Placental-specific IGF-II is a major modulator of placental and fetal growth. Nature. 2002;417(6892):945-948.

5. Pidsley R, Dempster E, Troakes C, Al-Sarraj S, Mill J. Epigenetic and genetic variation at the IGF2/H19 imprinting control region on 11p15.5 is associated with cerebellum weight. Epigenetics. 2012;7(2):155-163.

6. Rijlaarsdam J, Cecil CA, Walton E, et al. Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention-deficit/hyperactivity disorder symptoms in youth with early-onset conduct problems. J Child Psychol Psychiatry. August 18, 2016. Epub ahead of print.

Dr Murcia is a medical writer in North Carolina. She has nothing to disclose in regard to affiliations with or financial interests in any organizations that may have an interest in any part of this article.