Research suggests that there is hyperinsulinemia and insulin resistance in approximately 75 percent of Type-2 diabetics in the initial phases. The elevated levels of insulin happen because insulin signaling is not being heard.54 Later on, there is more of a para-inflammatory burn- out and actual cell dysfunction and death of the overworked pancreatic beta cells—hence insulin production goes down. The inability of Type-2 diabetic cell membranes to process insulin is not necessarily a result only of insulin and glucagon influences but, as I pointed out earlier, is due to leptin and insulin resistance that results in high concentrations of insulin, which because of its biphasic nature, can actually turn off receptor function at high concentrations. I remind the reader that this supports my theory that the diabetic onset of Type-2 may be associated in some way with cell membrane abnormalities. One study comparing 575 diabetics with 319 nondiabetics showed there was a problem incorporating polyunsaturated fatty acids into the cell membrane for the diabetics. All the diabetic red blood cell membranes were lower in polyunsaturated fatty acids. Plasma phospholipids, triglycerides, and cholesterol esters were also affected, suggesting there is an impairment of polyunsaturated fatty acid metabolism in diabetes. This suggests that in NIDDM impaired insulin activity may be both a cause and an effect of membrane polyunsaturated fatty acid composition. Gabriel Cousens, MD There Is a Cure for Diabetes - Revised Edition Dr. Cousens Diabetes Recovery Program - A Holistic Approach begins October 23rd! ow.ly/AsTOZ
Posted on: Mon, 01 Sep 2014 07:30:24 +0000
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