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Review
. 2017 Jan;37(1):95-110.
doi: 10.1002/pd.4932. Epub 2016 Nov 7.

Maternal obesity and neurodevelopmental and psychiatric disorders in offspring

Andrea G Edlow  1   2
Affiliations
Review

Maternal obesity and neurodevelopmental and psychiatric disorders in offspring

Andrea G Edlow. Prenat Diagn. 2017 Jan.

Abstract

There is a growing body of evidence from both human epidemiologic and animal studies that prenatal and lactational exposure to maternal obesity and high-fat diet are associated with neurodevelopmental and psychiatric disorders in offspring. These disorders include cognitive impairment, autism spectrum disorders, attention deficit hyperactivity disorder, cerebral palsy, anxiety and depression, schizophrenia, and eating disorders. This review synthesizes human and animal data linking maternal obesity and high-fat diet consumption to abnormal fetal brain development and neurodevelopmental and psychiatric morbidity in offspring. In addition, it highlights key mechanisms by which maternal obesity and maternal diet might impact fetal and offspring neurodevelopment, including neuroinflammation; increased oxidative stress, dysregulated insulin, glucose, and leptin signaling; dysregulated serotonergic and dopaminergic signaling; and perturbations in synaptic plasticity. Finally, the review summarizes available evidence regarding investigational therapeutic approaches to mitigate the harmful effects of maternal obesity on fetal and offspring neurodevelopment. © 2016 John Wiley & Sons, Ltd.

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Conflict of interest statement

Conflicts of interest: None declared

Figures

Figure 1
Figure 1
Mechanisms by which maternal obesity may result in offspring neurodevelopmental and psychiatric morbidity. Altered maternal physiology results in increased inflammation, lipotoxicity, and oxidative stress in the fetoplacental unit. These changes in the in utero environment contribute to malprogramming of the fetal brain, pancreas, skeletal muscle, and adipose tissue, among other organs. Peripheral inflammation and insulin resistance contribute to central insulin resistance and aberrant central glucose metabolism and transport. Only organ malprogramming known to influence fetal and offspring neurodevelopment is depicted here. In utero malprogramming results in an increased risk for offspring neurodevelopmental and psychiatric morbidity. CRP, C-reactive protein; DA, dopamine; FFA, free fatty acid; IL, interleukin; TG, triglyceride; TNF, tumor necrosis factor; VLDL, very low-density lipoprotein; 5-HT, serotonin
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