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of aging itself. When a diet is high in fat some of the receptor sites for insulin
become coated with an impermeable layer of fat thereby rendering insulin less
effective. In this way fat people become insensitive to their own insulin and so
they secrete abnormally high levels. Blood sugar levels then accumulate leading
to hyperglycemia or diabetes. Hyperglycemic fasting-levels of blood glucose are
around 126 mg/dL and hypoglycemic levels are at 70 mg/dL. After years of excess
carbohydrate intake, blood glucose levels tend to increase as insulin becomes less
and less effective at bringing them down. This insulin resistance is evident in
hyperglycemic, pre-diabetic symptoms, and is so prevalent in our culture that it
is taken as a “normal” sign of aging, however, insulin resistance is not found in
cultures eating little starch and sugar.
Insulin resistance includes the production of antibodies against insulin
that lead to reduce glucose below norm and decreased sensitivity of the insulin
receptors, so that sugar remains in the blood for a longer period of time. During
advanced hyperglycemia pancreatic B-cells are unable to produce adequate insulin
to maintain normal blood sugar levels. Blood sugar spiking with high glycemic
carbohydrates can severely damage tissues and turn the body toward insulin
resistance and down-regulate other receptors as well. Excess calcium inside the cells
and depleted magnesium is associated with insulin resistance. Fiber consumption
is inversely correlated to insulin resistance; to counter the aging effect of insulin
resistance our fiber intake needs to be at least 25 gr. each day. Blood sugar spiking
must be avoided with the maintenance of a low glycemic diet and exercise leads to a
more efficient use of insulin. N-acetylcysteine and taurine prevent hyperglycemia-
induced insulin resistance possibly through preventing oxidative stress.
Insulin resistance occurs as cells become less responsive to insulin, and this
results in higher blood sugar. Thus the pancreas is forced to over produce insulin in
an effort to lower the blood sugar and get the glucose into the cells. This condition
of excess insulin coupled with insulin resistance leads to increased storage of body
fat or obesity. Damage to receptors and cell membranes occurs from the increased
oxidation by the high blood sugar condition and high transfats. Transfats have
the same chemical signature as omega 3 & 6, so the body uses them for the same
purpose. But because they are structurally straight rather than bent they make the
cell membrane rigid rather than porous. This contributes to many health problems
including insulin resistance and type 2-diabetes. It also decreases osmosis, excytosis
and endocytosis and reduces cell signaling and cell recognition. Increased levels of
insulin are very inflammatory to blood vessel endothelium. Also, higher levels of
insulin reduce the livers ability to keep cholesterol from becoming oxidized.
Besides being covered by fatty plaque, insulin receptor desensitization also
occurs through damage to the endothelial cell membranes by silent inflammation
(oxidation). Confirming this idea, studies show that insulin resistance can
be markedly dropped by consuming DHA-omega 3 (fish oil). Raised levels of
insulin from eating too many high glycemic carbohydrates stimulates the enzyme
that changes the fatty acids to the inflammatory agent, arachidonic acid (AA).
The arachidonic acid pathway constitutes one of the main mechanisms for the