Ispectrum Magazine Ispectrum Magazine #06 - Page 36

Sleep Deprivation and the Shrinking Brain Indeed, in Scotland, a group of endocrinology and metabolic scientists are using retinal impairment as a model for dementia associated with diabetes – retinopathy. Here again the problem is that they consider type 2 diabetes as a major risk factor for retinopathy, and not that incipient dementia of the brain is the initiating and driving causative influence. They seem to miss the correct sequence of events – from chronic cerebral and retinal glucose deprivation (hunger) to increased consumption of more high-energy carbohydrate foods, in a repeating cycle. One of the most universal and pernicious influences on modern metabolic impairment is that driven by the myth that sleep is a low energy protocol. This has led to the notion, promoted by diet gurus and not opposed by the health professions, that it is unhealthy to eat late. The impact of this on metabolic health has been profoundly negative – it means that after an early evening meal we retire to bed with a depleted liver, with insufficient reserve energy supply (liver glycogen) to provision the brain overnight. This does not activate quality sleep and recovery physiology, but rather chronic nocturnal metabolic stress and increased risk of metabolic syndromes – dementias/obesity/ diabetes and heart disease; note the seminal paper by Turek and Bass in 2005: “ ... However, while there is a growing awareness among some sleep, metabolic, cardiovascular, and diabetes researchers that insufficient sleep could lead to a cascade of disorders, few in the general medical profession or in the lay public have yet made the connection ...”: Sleepless in America: A Pathway to Obesity and Metabolic Syndrome. 35