Globally, there is an increasing prevalence of non-communicable diseases. The morbidity and mortality from these conditions confer a greater economic societal burden. Epidemiological research associates insulin resistance in the etiology of these diseases, but there is limited evidence for the mechanism of damage. Emerging research suggests that hyperinsulinemia, a symptom of insulin resistance, may cause these pathological changes, and therefore be an independent contributor to these diseases. This review shows that hyperinsulinemia, or excessive insulin secretion, should be considered independently to insulin resistance, defined as glucose uptake rate, even though the two conditions are intertwined and will co-exist under normal conditions. Hyperinsulinemia directly and indirectly contributes to a vast array of metabolic diseases including all inflammatory conditions, all vascular diseases, gestational and type 2 diabetes, non-alcoholic fatty liver disease, obesity and certain cancers and dementias. The mechanisms include increased production of: insulin growth factor-1; reactive oxidative species and advanced glycation end-products; and triglyceride and fatty acids. Hyperinsulinemia also directly and indirectly affects many other hormones and cytokine mechanisms including leptin, adiponectin and estrogen. There is limited research standardizing the hyperinsulinemia diagnostic process. Methodological concerns and lack of standardized reference ranges preclude the use of fasting insulin. Most research has also focused on insulin resistance and it is unknown whether these methods translate to hyperinsulinemia.
Full Paper at https://doi.org/10.15562/diabesity.2015.19
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Notes:
hyperinsulinemia precedes hyperglycemia, by up to 24 years.
We contend that the under-recognition of hyperinsulinemia is an important clinical issue because there are no standard diagnostic reference values
It is known that corticosteroids, especially endogenous cortisol, cause a down regulation of GLUT-4 receptors, thus preventing glucose uptake and provoking hyperinsulinemiain the presence of hyperglycemia.
This is eye opening, I knew steroids had a impact on blood glucose levels, but now the mechanism is described!
Long-term courses of exogenous corticosteroids, such as prednisone, are known to cause ‘drug-induced’type 2 diabetes, which may resolve after the medication is discontinued.
it can be assumed that the majority of people with insulin resistance are also hyperinsulinemic.
Cancer cells have a continuously high glucose uptake, which enhances cellular growth and proliferation. hyperglycemia augments this process. Hyperglycemia allows IGF-1 to stimulate vascular smooth muscle proliferation, which is a hall-mark of both cancer and atherosclerosis
hyperinsulinemia involved with the etiology of all of the symptoms of metabolic syndrome, it is also implicated in many other conditions; some of which have previously been considered to be idiopathic,such as tinnitus
Dammit I was reading this paper all happy, until i saw the word tinnitus… and now all i hear is SCREEEEEEEEEEEEEE
I wonder if the rock industry person, who was a family friend when I was a kid in the 80s, had tinnitus. I didn’t know him well enough to hear such complaints, but he had lost quite a bit of hearing due to his job.
Meanwhile and incidentally I have had my highest blood glucose result (6.1mM/L) on a blood test on zero carb, with a first thing in the morning test a year and a half into that way of eating. Apparently there’s an effect called the dawn phenomenon where blood glucose peaks around dawn, presumably to help us get moving, but the lack of demand in fat adapted people means there’s no demand, so a bit later it’s mopped up. It nearly had me get a home glucose tester.
Yeah The Dawn phenomenon is no joke! Other things that raise blood glucose without food, stress, pain, steroids, lack of sleep (which is another form of stress)