Hunger feeds a healthy brain

  • January 21, 2013
Hunger feeds a healthy brain

The unprecedented rise in obesity is now a global epidemic. It is widely known that the accumulation of excess body fat increases the risk of chronic illnesses, such as Type 2 diabetes, heart disease, and certain forms of cancer; however, recently there has been growing consensus that obesity also has detrimental effects on the brain. For example, obesity is associated with a greater risk of cognitive dysfunction and increases the likelihood of developing a neurodegenerative disorder, such as Alzheimer’s disease (AD) or another type of dementia. In fact, because insulin deficiency and insulin resistance appear to act as mediators of Alzheimer’s-type neurodegeneration, some researchers even claim that AD is “type 3 diabetes”, which selectively involves the brain. Identifying this important link between metabolism and cognition is not new. For years, researchers have recognised the benefits of reducing daily food intake on overall health, longevity, and cognition. Reducing the number of calories consumed each day has been shown to reduce age-related cognitive decline in humans and several animal models, while also augmenting the production of new brain cells. The mechanisms underlying this relationship are not well understood; however, there is evidence that the gut hormone, ghrelin, may be responsible. Ghrelin is a chemical-signalling molecule synthesised and released from the stomach in the absence of food. This important hormone is responsible for mealtime hunger, and regulating body weight and adiposity [human body fat]. Although ghrelin is not produced in the brain, it is released into the bloodstream where it then circulates throughout the body and can then act on particular areas of the brain. Whilst seen predominately as a potential target for anti-obesity treatments, this potent appetite stimulant also appears to have cognitive-enhancing properties. Ghrelin treatments provided to normal and aged rats and mice have consistently been shown to improve performance on tasks measuring a variety of cognitive processes, including spatial memory. In addition to improving cognition, ghrelin appears to cause positive physical changes in the brain, such as increasing the production of new brain cells in structures critically important for memory. This creation of new brain cells is called ‘neurogenesis’, and is thought to underlie some of the cognitive benefits of restricting calorie consumption. Because reducing daily food intake and fasting naturally elevates ghrelin levels, some researchers believe that this rise in ghrelin may underlie the increased neurogenesis associated with low-calorie diets. Together, this suggests that ghrelin may be one mechanism connecting nutritional status with cognitive function. Importantly, there is a growing body of literature suggesting that a disruption of the normal modulation of ghrelin secretion may contribute to both the metabolic changes and cognitive impairments associated with AD. Involuntary weight loss and nutritional deficiencies are common in individuals diagnosed with AD, and these metabolic changes appear to precede cognitive impairments. Identification of modifiable risk factors to delay or prevent the progression of AD could have a dramatic impact on the prevalence of this devastating disease. Because ghrelin is an important regulator of appetite, as well as cognition, it may be a potential target for early detection and prevention of AD. The aforementioned research further establishes the important relationship between nutritional status and cognitive function. Knowing this, along with the old adage, “prevention is the best medicine”, suggests that keeping ghrelin high by reducing daily food intake may be a powerful way to protect your brain. Not only does maintaining a healthy weight avoid the deleterious effects of obesity, but the higher levels of ghrelin may be protective against age-related neurodegeneration. *Brianne Kent is doing a PhD in Experimental Psychology. Picture credit: and Ohmega1982.

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