Food for thought: how nutrition impacts cognition and emotion

Abstract

More than one-third of American adults are obese and statistics are similar worldwide. Caloric intake and diet composition have large and lasting effects on cognition and emotion, especially during critical periods in development, but the neural mechanisms for these effects are not well understood. A clear understanding of the cognitive-emotional processes underpinning desires to over-consume foods can assist more effective prevention and treatments of obesity. This review addresses recent work linking dietary fat intake and omega-3 polyunsaturated fatty acid dietary imbalance with inflammation in developing, adult, and aged brains. Thus, early-life diet and exposure to stress can lead to cognitive dysfunction throughout life and there is potential for early nutritional interventions (e.g., with essential micronutrients) for preventing these deficits. Likewise, acute consumption of a high-fat diet primes the hippocampus to produce a potentiated neuroinflammatory response to a mild immune challenge, causing memory deficits. Low dietary intake of omega-3 polyunsaturated fatty acids can also contribute to depression through its effects on endocannabinoid and inflammatory pathways in specific brain regions leading to synaptic phagocytosis by microglia in the hippocampus, contributing to memory loss. However, encouragingly, consumption of fruits and vegetables high in polyphenolics can prevent and even reverse age-related cognitive deficits by lowering oxidative stress and inflammation. Understanding relationships between diet, cognition, and emotion is necessary to uncover mechanisms involved in and strategies to prevent or attenuate comorbid neurological conditions in obese individuals.

Keywords: Neuroendocrine diseases; Obesity.

Fig. 1

Schematic depiction of how nutrition influences cognition and emotion. Overeating, obesity, acute high-fat diet consumption, poor early-life diet or early life adversity can produce an inflammatory response in peripheral immune cells and centrally as well as having impact upon the blood–brain interface and circulating factors that regulate satiety. Peripheral pro-inflammatory molecules (cytokines, chemokines, danger signals, fatty acids) can signal the immune cells of the brain (most likely microglia) via blood-borne, humoral, and/or lymphatic routes. These signals can either sensitize or activate microglia leading to de novo production of pro-inflammatory molecules such as interleukin-1beta (IL1β), IL-6, and tumor necrosis factor alpha (TNFα) within brain structures that are known to mediate cognition (hippocampus) and emotion (hypothalamus, amygdala, prefrontal cortex and others). Amplified inflammation in these regions impairs proper functioning leading to memory impairments and/or depressive-like behaviors. Polyunsaturated fatty acids (PUFA), polyphenolics, and a positive (+ve) early life environment (appropriate nutrition and absence of significant stress or adversity) can prevent these negative outcomes by regulating peripheral and central immune cell activity. Images are adapted from Servier Medical Art, which is licensed under a Creative Commons Attribution 3.0 Unported License https://creativecommons.org/licenses/by/3.0/. Salmon and hamburger images were downloaded from Bing.com with the License filter set to “free to share, and use commercially”. The blueberry image is courtesy of author Assistant Prof. Ruth Barrientos