Food and Behaviour Research

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Enduring consequences of maternal obesity for brain inflammation and behavior of offspring.

Bilbo SD, Tsang V. (2010) FASEB J.  24 2104-2115. Epub Feb 2 

Web URL: View this and related abstracts via PubMed here

Abstract:

Obesity is well characterized as a systemic inflammatory condition, and is also associated with cognitive disruption, suggesting a link between the two.

We assessed whether peripheral inflammation in maternal obesity may be transferred to the offspring brain, in particular, the hippocampus, and thereby result in cognitive dysfunction. Rat dams were fed a high-saturated-fat diet (SFD), a high-trans-fat diet (TFD), or a low-fat diet (LFD) for 4 wk prior to mating, and remained on the diet throughout pregnancy and lactation.

SFD/TFD exposure significantly increased body weight in both dams and pups compared to controls. Microglial activation markers were increased in the hippocampus of SFD/TFD pups at birth.

At weaning and in adulthood, proinflammatory cytokine expression was strikingly increased in the periphery and hippocampus following a bacterial challenge (lipopolysaccharide (LPS)) in the SFD/TFD groups compared to controls. Microglial activation within the hippocampus was also increased basally in SFD rats, suggesting a chronic priming of the cells. Finally, there were marked changes in anxiety and spatial learning in SFD/TFD groups.

These effects were all observed in adulthood, even after the pups were placed on standard chow at weaning, suggesting these outcomes were programmed early in life.

FAB RESEARCH COMMENT:

This animal study found that diet-induced obesity in mothers before pregnancy increased inflammation and impaired brain development and function in the offspring, permanently increasing their anxiety and reducing their spatial learning ability.

In humans, associations between pre-pregnancy maternal obesity and neurodevelopmental disorders such as ADHD have already been well documented. See for example:

 
Clearly, similar controlled studies in humans are simply not possible for ethical reasons, but these findings provide clear evidence of causality. They further suggest that public health policies to reduce the high prevalence of obesity in women of childbearing age could also help to combat the apparent increases in ADHD, autism and related childhood neurodevelopmental disorders.

See also: