Recent evidence has linked excessive intake of the so-called western diet (rich in saturated fat and refined carbohydrates) with cognitive deficits in adolescents as well as adults. We have shown in rats that both high fat, and high sugar diets can impair hippocampal dependent behaviours, even after short-term exposure. Potential mechanisms underlying the cognitive deficits include neuroinflammation and reductions in brain neurotrophic factors, in addition to diet-related changes in gut microbiota.
When animals consumed liquid sugar for 2 weeks, we observed hippocampal inflammation, assessed as increased expression of proinflammatory cytokines, along with hippocampal selective memory deficits (place recognition). Cytokine mRNA expression correlated with blood glucose concentrations.
Next we examined the effect of 2 weeks exposure to purified isocaloric diets which varied only in the amount of sugar, saturated fat or polyunsaturated fat. Both sugar and saturated fat diets were associated with cognitive deficits, and macronutrient-specific gut microbiota changes were observed that correlated with memory. No differences in energy intake or weight gain were observed. In addition, Distance based linear models found relationships between memory, a cluster of hippocampal inflammation related genes, and gut microbiota composition.
Finally, we have shown that even intermittent exposure to an energy-dense, western diet is sufficient to shift the biota towards that seen in obese rats, with reduced microbial diversity. We are currently examining the impact of probiotic treatment on the behavioral and gut biota responses to unhealthy diets in rats, and will explore the gene expression changes induced in the brain. Examining key underlying processes is an essential step to enable testing of novel interventions in humans to combat diet-related cognitive deficits.