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Weight and Obesity Behavior Diet GI-Digestive

Diet Determines Behavior

7 years, 8 months ago

35326  0
Posted on Nov 03, 2016, 6 a.m.

A high-fat diet prompts brain inflammation, in a lab animal model.

High-fat diets have long been known to increase the risk for medical problems, including heart disease and stroke, but there is growing concern that diets high in fat might also increase the risk for depression and other psychiatric disorders. Annadora J. Bruce-Keller, from Louisiana State University (Louisiana, USA), and colleagues employed a mouse model to assess the changes to the gut microbiome – the bacteria that resides in the GI tract, which thereby may trigger susceptibility to neuropsychiatric disorders. Non-obese adult mice were conventionally housed and maintained on a normal diet, but received a transplant of gut microbiota from donor mice that had been fed either a high-fat diet or control diet. The recipient mice were then evaluated for changes in behavior and cognition. The animals who received the microbiota shaped by a high-fat diet showed multiple disruptions in behavior, including increased anxiety, impaired memory, and repetitive behaviors. Further, the animals fed the high-fat diet showed many detrimental effects in the body, including increased intestinal permeability and markers of inflammation. Signs of inflammation in the brain were also evident and may have contributed to the behavioral changes. Observing that: “The mice given [high-fat diet] microbiota had significant and selective disruptions in exploratory, cognitive, and stereotypical behavior,” the study authors conclude that: “these data reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or pharmacologic manipulation of gut microbiota could attenuate the neurologic complications of obesity.”

Annadora J. Bruce-Keller, J. Michael Salbaum, Meng Luo, Eugene Blanchard, Christopher M. Taylor, David A. Welsh, Hans-Rudolf Berthoud.  “Obese-type Gut Microbiota Induce Neurobehavioral Changes in the Absence of Obesity.”  Biological Psychiatry, Vol. 77, Issue 7, p607–615.

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