Chronic GI Inflammation and Changes in the Brain

Chronic GI Inflammation and Changes in the Brain

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Chronic intestinal inflammation alters hippocampal neurogenesis written by Svetlana Zonis and published in the Journal of Neuroinflammation in April of 2015…

Edited by David Riley, MD, AIHM Journal Club.


Memory, learning and the ability of the brain to change itself (neuroplasticity) are dependent on new neurons (neurogenesis). Chronic inflammation in the gut decreases neurogenesis in the hippocampus, which is related to depression, Alzheimer’s disease and schizophrenia. (Cannabadiol has been shown to enhance neurogenesis while delta9-tetrahydocannabinol—THC—reduces learning capacity.)…

We have some control over this process. Diet, adequate sleep, exercise and stress management reduce chronic inflammation and enhance neurogenesis….

The limited effectiveness of pharmaceuticals to enhance mental health, memory and learning by regulating neurotransmitters may shift to a range of systems-based approaches honoring the interconnected nature of life. These might include the management of inflammation, support of the microbiome, healthy diet and an enhancing lifestyle.



This study demonstrates a link between induced chronic intestinal inflammation and neurogenesis in the hippocampus. The investigators in this study evaluated the relationship between alterations in the gastrointestinal (GI) tract (induced inflammation) and hippocampus function (neurogenesis). Mice were fed dextran sodium sulfate for 7 or 29 days to induce acute or chronic inflammatory intestinal changes.

After 7 days the hippocampus of the mice exhibited increased levels of inflammatory markers (IL-6 and TNF-alpha). After 29 days, the brains of the mice not only showed elevation of inflammatory markers in the hippocampal region but also induced abnormalities. Three markers for neurogenesis (nestin, doublecortin and brain lipid binding protein) were down regulated—staining of the hippocampus also revealed significantly reduced neurogenesis. These changes were not noted in the hippocampus of control mice.



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