Long-term effects of different diets on the central nervous system

Introduction

The food we consume does not only provide our body with the necessary energy for anabolic processes and to perform daily tasks. Its nutritious factors have complex biochemical interactions with the molecular mechanisms in each cell, tissue and organ. The central nervous system is strongly affected by diet. The lack or abundance of certain nutrients can alter cognition, and cause or worsen neurological disorders. Most importantly, certain diets can improve brain health and prevent the development of neurological disorders. We will discuss common diets such as the Standard American (Western) diet, the Mediterranean diet, the Plant-Based diet and the Pescatarian diet, as well as less widespread diets, such as the Ketogenic and Palaeolithic diets.

Standard American Diet

The standard American diet (SAD) is high in refined carbohydrates/sugars and animal-based products such as meats, dairy and eggs. It lacks in whole grains, fruits and vegetables while being high in saturated fat, processed/convenience foods and sodium (Grotto and Zied, 2010). The diet is also high in omega-6 fatty acids and low in omega-3 fatty acids. (Cordain et al, 2005). SADs are correlated to obesity, diabetes type II and hypercholesterolemia (Okręglicka, 2015).

The SAD has been linked to changes in appetite and behaviour. High-calorie foods induce behavioural changes due to the release of dopamine upon consumption. As dopamine is a “feel good” neurotransmitter this can cause addiction-like behaviour and affect the hippocampus and the hypothalamus which have roles in memory and food intake. Once these foods are not consumed, the individual may experience changes in their dopamine levels, receptors, mood and the dopamine-mediated reward system (Johnson and Kenny, 2010; Edward et al, 2011; Reichelt and Rank, 2017). The disturbance of the hypothalamus due to the SAD causes increased appetite (Kanoski et al, 2010; Stevenson et al, 2020). This cycle repeats leading to decreased cognition and a further increase in food intake (Kanoski and Davidson, 2011), as shown in figure 1.

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