High Calorie Diet and the Human Brain by Akhlaq A. Farooqui

Author:Akhlaq A. Farooqui
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

5.11 Consumption of Sugar-Sweetened and Low-Calorie Sodas and Neurological Disorders

According to US Department of Agriculture per capita soft-drink consumption has increased by almost 500 % in the past 50 years (Putnam and Allshouse 1999). Large studies of US men and women have indicated that greater consumption of sugar-sweetened and artificial sweeteners containing sodas may contribute to insulin resistance and obesity, which is caused by an imbalance between energy intake and energy expenditure. Obesity is an important risk-factor for the development of type II diabetes and metabolic syndrome (Fig. 5.9). Indeed, the incidences of stroke increase many folds in metabolic syndrome patients with cardiovascular diseases. Thus, patients with heart disease have ninefold high risk of cerebral infarction compared to the general population. Induction of neuroinflammation, increased production of free radicals, alterations in neurotrophic factors, and reduction of insulin transport into the brain has been reported in the patients with metabolic syndrome (Farooqui 2013). Similarly, long-term presence of hyperglycemia and insulin resistance may result in cerebrovascular disease, which may accelerate cognitive decline and promote dementia and AD. Furthermore, insulin and insulin-signaling mechanisms are important for neuronal survival. Insulin place an important role in regulating memory therefore long-term disturbance in insulin signaling may have a negative impact on memory formation and may promote the initiation of AD (Bernstein et al. 2012; Farooqui et al. 2012; Farooqui 2013). It is also reported that type II diabetes and depression are linked with each other through stress, which impairs the ability of brain to regulate corticosteroid release. This may lead to hypercortisolemia. Excessive stimulation of corticosteroid receptors in hippocampus may cause hippocampal atrophy, which may lead to depression and dementia (Farooqui et al. 2012; Farooqui 2013). Collective evidence suggests that cellular and biochemical alterations observed in metabolic syndrome like elevation in lipid mediators, impairment of endothelial cell function, abnormality in essential fatty acid metabolism along with abnormal insulin/leptin signaling may represent a pathological bridge between metabolic syndrome and neurological disorders such as stroke, Alzheimer’s disease (AD), and depression (Farooqui et al. 2012; Farooqui 2013).

Fig. 5.9Effects of artificial sweeteners and high fructose corn syrup on the pathogenesis of neurological disorders

Download

Copyright Disclaimer:
This site does not store any files on its server. We only index and link to content provided by other sites. Please contact the content providers to delete copyright contents if any and email us, we'll remove relevant links or contents immediately.