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Dysglycemia

 

DYSGLYCEMIA

 

Dysglycemia: an imbalance in the sugar metabolism/energy production mechanisms of the body. Because of the long term exposure to refined carbohydrates (sugars), a state of insulin insensitivity can occur. Because of the huge demand on the pancreas to produce enough insulin to deal with the vast amount of sugar in the bloodstream, over the course of many years the cell receptor sites for insulin have become insensitive, or unresponsive, to insulin. The result is that the body requires more and more insulin to get the job done. Along with insulin resistance, we also see a corresponding problem with fatty acid metabolism. This results in a shift toward pro-inflammatory rather than anti-inflammatory conditions. Increased body fat accumulation is also associated with altered insulin sensitivity.

 

Insulin: a hormone produced by the pancreas in response to glucose (a sugar) in the bloodstream. Its purpose is to take sugar out of the bloodstream and put it into the cells. Insulin is also a signaling molecule. It controls many cellular processes, including modulation of gene expression, which influences cellular processes such as mitochondrial function (energy production), cytokine synthesis (inflammation), adrenal and sex hormone metabolism, and much more.

 

Physiological effects: The physiological control of insulin/glucose is of paramount importance to good health and long life. Increased levels of insulin have many damaging effects on the body. These may include lipid abnormalities, blood pressure elevation, hormonal alterations, increased risk for diabetes and, in general, accelerated biological aging at the cellular level. Dysglycemia is also associated with increased risk of vascular disease. Insulin resistance, which is a precursor to type II (adult-onset) diabetes, may contribute not only to dysglycemia, but also to increased risk of coronary heart disease. Research clearly shows a relationship between insulin resistance/hyperinsulinemia (Syndrome X) and non-insulin dependent diabetes mellitus, hypertension, and coronary heart disease.

 

Control: Glycemic index plays a very important role in restoring proper glucose regulation and insulin sensitivity. It is more complex, however, than simply adhering to the numbers listed on a GI chart. The type and amount of carbs, the relationship with dietary fiber, and the type and amount of fat all participate in establishing the overall GI of the diet.

Increased levels of resistant starch and lower levels of simple sugars are the preferable forms of carbohydrate. Increased consumption of (good) poly- unsaturated fatty acids (especially CLA and EPA/DHA) increases membrane fluidity, thereby improving insulin binding and activity. Alternately, (bad) saturated fats and trans-fatty acids decrease membrane fluidity with a corresponding decrease in insulin binding.

 

Important note: There appears to be a genetic link between immune hypersensitivity reactions and the destruction of specific cell types (such as the beta cells of the pancreas, resulting in diabetes, or the colonic cells of the gut, resulting in celiac disease). In fact, it has recently been shown that a polypeptide sequence exists in a bovine (cow) milk protein that can cross-react with the immune system in humans and potentially initiate autoimmune hypersensitivity. Evidence further exists that suggests that the cow's milk protein, beta-lactoglobulin may, in certain children, trigger non-specific upregulation of the production of antibodies that react with cell surface receptors. This activity could then trigger the autoimmune process found in insulin-dependent diabetes mellitus.

 

 

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