…hyperinsulinemia (high levels of insulin), a compensatory response caused by insulin resistance, is the foundation for most chronic health conditions?
One of insulin's functions is to move glucose from the blood into the cells to be used as energy. Moving glucose into cells becomes more difficult as one becomes insulin resistant.
The current belief of many experts to explain insulin resistance is the "lock and key" theory. Insulin is the key, and the cell receptor is the lock. The receptor unlocks when insulin is inserted to allow glucose to pass through the cell wall. While insulin resistant, the receptor no longer opens easily to allow glucose into the cell, causing blood glucose levels to rise. The pancreas responds by producing more insulin (keys) to lower increasing blood glucose levels. Too bad this is not based in reality.
The key (insulin) and lock (the receptor) model sound impressive and makes sense. However, insulin or the receptor has never been proven to be the problem. When comparing patients with type 2 diabetes and normal patients, there is no difference between their insulin or receptors if both insulin and the receptor appear unchanged, what causes insulin resistance.
There is another possibility to explain insulin’s inability to get glucose in the cell. Maybe the cell is denying entry of glucose because it is stuffed to its limit with glucose. This would explain why there is no difference between insulin or the receptors of patients with type 2 diabetes and normal patients.
The receptor/insulin model has been the foundation for treating type two diabetes for more than half a century, which has been an utter disaster. Despite using exogenous insulin (by injection) or other medications used to combat excessive blood glucose levels, diabetics only get worse (Buse et al., 2007; Green et al., 2015). Sure, a diabetic’s blood glucose levels decrease due to more insulin. However, their diabetes will still progress along with many complications, e.g., neuropathy, heart disease, weight gain, hypertension, blindness, kidney disease, amputation, and stroke.
If hyperinsulinemia occurs because of the overflow of glucose, prescribing more insulin or eating carbohydrates couldn’t be a worse remedy. And if left unchecked, hyperinsulinemia brings with it a whole host of risk factors which may include (Carnethon et al., 2003):
Weight gain (Abdominal or visceral obesity)
Hypertension
Kidney disease
blindness
Dyslipidemia (High cholesterol and triglycerides)
Type 2 diabetes
Increased inflammation
Neuropathy
Cardiovascular disease
Elevated uric acid levels
Although one may not realize they have hyperinsulinemia because there is often no clear indicator (Crofts et al., 2016), hyperinsulinemia symptoms may include:
Food cravings especially sugar
Increased hunger
Weight gain
Lack of focus or motivation
Feeling anxious
Fatigue
So how does one reverse hyperinsulinemia? The root cause can be targeted by diet, exercise, and other lifestyle changes. The sooner hyperinsulinemia is diagnosed, which may come with pre-diabetes or type two diabetes, the sooner one can mitigate the risk factors. A low-carbohydrate diet and fasting are the only ways to treat and reverse insulin resistance, reduce insulin levels, and in the process, lose body fat.
Are you interested in intermittent fasting? You should be. It’s one of the most effective changes to your lifestyle to improve your health. Best of all, fasting doesn’t cost you a dime. Watch for the next article, The Foundation of Optimal Health – What and When to Eat. Part I
References
Buse, J.B., et al. (2007). Action to Control Cardiovascular Risk in Diabetes (ACCORD) Trial: Design and methods. American Journal of Cardiology, 99(12A), 21i-33i. Received from https://www.ajconline.org/action/showPdf?pii=S0002-9149%2807%2900438-9
Carnethon, M. R., Fortmann, S. P., Palaniappan, L., Duncan, B. B., Schmidt, M. J., & Chambless, L. E. (2003). Risk factors for progression to incident hyperinsulinemia: The atherosclerosis risk in communities study, 1987–1998. American Journal of Epidemiology, 158(11), 1058–1067. https://doi.org/10.1093/aje/kwg260
Crofts, C., Schofield, G., Zinn, C., Wheldon, M., & Kraft, j (2016). Identifying hyperinsulinemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Research and Clinical Practice, 118, 50-57. DOI: 10.1016/j.diabres.2016.06.007
Green, B. J. et al. (2015). Effect of Sitagliptin on cardiovascular outcomes in type 2 diabetes. New England Journal Medicine, 373, 232-242. DOI: 10.1056/NEJMoa1501352
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