The common pathogenesis of Alzheimer’s disease and diabetes.
By Renata Trister DO
Recent studies show new evidence that Alzheimer’s disease and type 2 diabetes share common features in their pathophysiology. Insulin resistance is a characteristic feature of both diseases. Glucose metabolic disorders, related to Alzheimer’s disease, are type 2 diabetes, and pre-diabetes/metabolic syndrome. Based on the common pathophysiology of these two diseases, Alzheimer’s disease is by some called type 3 diabetes. This is yet another example of chronic illnesses that caused by modern diets and lifestyle habits. Diets high in refined carbohydrates lack of sleep and physical activity all contribute to insulin resistance. In the research on dementias, insulin resistance has much documented harmful effects on cognitive function. Insulin-like growth factor also influences cognitive functions. Insulin resistance causes glycation and oxidative stress on the brain. In Alzheimer’s brains, amyloid deposition, hyper-phosphorylation of tau proteins and neurofibrillary tangles, are characteristic features. Amyloid ß is co-secreted in the ß-cells of the pancreas with insulin. Amyloid ß and hyper-phosphorylated tau protein can be found in the Langerhans islets (in autopsy). Amyloid deposits, found in the pancreas and brain are similar. As a result of hyperglycemia, glycation end products cause the development of amyloid plaques, neurofibrillary tangles; these are all typical in Alzheimer’s disease. Hyperglycemia leads to oxidative stress, which plays significant role in the development of both illnesses. Low-grade inflammation is also a significant pathophysiological factor in both disorders. The sources of this inflammation are inflammatory adipo-cytokines, dysbiosis, and metabolic endotoxemia, caused by lipopolysaccharides. Cerebral glucose metabolism is also impaired in Alzheimer’s disease. A reduced presence of insulin and resulting decrease in cerebral glucose metabolism creates an energy crisis in the brain. Neurons are unable to harvest energy and basically starve. In order to conserve energy, these affected neurons degrade axons and dendrites. The retraction of these projections results in damaged synapses and cell communication loss. Symptomatically, this presents as cognitive impairment. Another possible etiology of this glucose deficit is reactive hypoglycemia. Reactive hypoglycemia is low blood glucose that occurs within four hours after eating, especially high glycemic foods. After eating sugary foods, blood glucose levels spike rapidly and become very high. In response insulin is produced. Reactive hypoglycemia results from having too much insulin produced in response to eating, leading to low blood glucose levels. This happens chronically and can be very damaging. During waking hours the symptoms are quickly ameliorated by having another snack. However, consuming sweets at night, this hypoglycemia goes unnoticed and not corrected. This hypoglycemic state continues until you wake up and eat. Consequently cells in the body have an energy deficit. Alzheimer’s disease is a heterogeneous disorder, and as yet there is no effective therapy. Encouraging results have emerged by using intranasal insulin spray. Insulin sensitizers like metformin, have shown some improvements in cognitive functions, mainly in animal experiments. The real breakthrough comes from prevention of both chronic diseases via a healthier life-style. Reducing refined carbohydrates in diet appears essential.