Type II Diabetes & Nutraceutical Intervention
What Caused this Epidemic, and Why is Patient Education Important?
Non-insulin dependent Diabetes, or Type II Diabetes, is sometimes referred to as “adult-onset” diabetes. This disease has reached epidemic proportions all over the globe, with China as an “epicenter” of increased prevalence of Type II Diabetes. Diabetes is more than a disease involving just an elevation of blood sugar levels.
The CDC, in 2014, claimed that 1/3 of Americans are Pre-Diabetic, and 29 million people in the US are diagnosed with Type II Diabetes. In 2001, the established research model did not predict such a high prevalence until year 2050.
In 2012 alone, the financial deficit due to to Diabetes and Diabetes-related health problems in the United States was 245 Billion Dollars, after all health care costs and lost productivity figures were calculated. This disease and its co-morbid conditions are requiring more and more of our valuable resources.
What Is Type II Diabetes?
This type of Diabetes is not the result of insufficient insulin production; it is actually the result of too much insulin chronically produced, usually from excess dietary intake of carbohydrates (sugars). The constant overabundance of insulin levels make the body “resistant” to the signals sent by insulin acting on the receptors. The onset of Type II Diabetes, or non-insulin dependent Diabetes, begins with a cellular insensitivity to insulin, also called Insulin-Resistance.
This ineffective use of insulin allows high levels of glucose to build up in the blood rather than be transported to various tissues as a fuel source. Insulin resistance and the inability to utilize insulin essentially starves the cells within muscle, fat, and liver tissues from the primary fuel source, glucose. This cell starvation then signals the pancreas to increase its output of insulin.
Increase of weight occurs because insulin directly stimulates fat deposition. Insulin levels increase in response to blood glucose, after which fat is deposited in the belly area.
Most cases of Type II diabetes result from dysfunctional insulin receptor chemistry, and not due to actual insulin levels at all. Insulin has physiological actions other than managing blood sugar. Insulin is heavily involved in fat physiology and weight management. Insulin is designed to physiologically to push fatty acids into cells; as insulin levels increase, fat deposition increases as well.
Even if receptor sensitivity decreases in its response to insulin, the increasing concentration of insulin rises even as blood sugar levels remain within “normal” ranges. This chronic state of elevated insulin levels and receptor dysfunction will result in continued fat deposition. This is why it is difficult to lose weight to control diabetes– the diabetes may have caused the weight problem, not the other way around.
Insulin levels also modulate inflammation, so pain problems tend to worsen in those with Type II Diabetes, as well as worsen cardiovascular/peripheral vascular diseases.
Soon after the onset of Type II Diabetes, various bodily changes occur, including changes affecting the brain and cognitive function.