Hyperinsulinemia is an endocrine disorder characterized by a failure of our Blood Sugar Control System (BSCS) to work properly. It manifests when insulin progressively loses its effectiveness in sweeping the blood glucose from the blood stream into the sixty seven trillion or so cells that constitute our bodies. The insulin level in the bloodstream then rapidly rises to damaging levels and, together with the resulting elevated glucose levels, account for much of the damage to our arteries and vascular system. When insulin loses its effectiveness this loss is not due to any change in the insulin produced by the pancreas. It is due to a change in the cellular metabolism of almost every cell in our body. Although our insulin has not changed, our cell metabolism has changed. Our cells no longer respond to blood borne insulin signaling as they should.

Our BSCS works like any negative feedback system to maintain our blood sugar at a predetermined setpoint. This setpoint is below the threshold where excess glucose can cause vascular damage. And the insulin required to do this is normally below the threshold where it will cause arterial or vascular damage. When the BSCS is working right, it automatically, without our conscious knowledge, maintains correct blood sugar with a minimum amount of insulin whether we have just eaten a meal or been fasting and exercising for a week.

When our system starts to exhibit hyperinsulinemia, our pancreatic beta cells simply increase insulin production and for a time this maintains our ability to swiftly lower post prandial (after eating) blood glucose. For a time this maintains normal glucose levels, albeit by the secretion of these abnormally high insulin levels.

At some point during the progressive loss of effectiveness of insulin, our pancreatic beta cells may no longer produce enough insulin to manage normal post prandial and fasting glucose. This may occur because our pancreas becomes exhausted by trying to maintain abnormally high insulin levels needed. It may occur because the progressive failure of our cellular metabolism has created a chronic demand for insulin beyond what even a healthy pancreas can supply. In either event, when this happens Type 2 diabetes is diagnosed. Of course, hyperinsulinemia has been around for some while, often for a long while, by the time this diagnosis is made.

As these elevated levels of insulin and glucose in the body continue they set in motion two damaging sequences of events that rapidly lead to atherosclerosis and heart failure.

The insulin sequence is:

Elevated insulin---increased delta desaturase enzymes---increased conversion of omega 6 fatty acids to arachidonic acid--increased prostaglandin 2's--increased production of cytokines--increased inflammatory
response throughout the entire body.

The glucose sequence is:

Elevated serum glucose--increased intestinal candida--migration of candida to upper intestine--root formation of candida in duodenum--migration of candida spores throughout the bloodstream--candida infection throughout the body.

A naturopathic doctor, with access to a dark field microscope, can readily show you the candida spores that appear in large numbers in the bloodstream. This is an  inexpensive test and one well worth the few  dollars that  it costs.

This candida source of infection is not the only source of infection. Because of the increased availability of cytokines, he body becomes subject to infection from many other sources. This is one reason that diabetics experience poor wound healing. One of the most important sites of infection is the coronary artery.  This is located in the high pressure, sugar rich side of the blood supply. When the infection that occurs here is noticed by the immune system, the body attempts to patch the damage with cholesterol, Lp(a), free calcium and a few other things. This patching process is known as atherosclerosis. As the patching process continues, the interior of the artery becomes narrowed. As the artery narrows, we become more susceptible to ischemic events.  These are events where a clot forms in the artery and blocks the artery at a narrow atherosclerotic point. When this occurs in the coronary artery, the blood supply to the heart muscles is stopped and a heart attack ensues. This whole process is exacerbated by  the fact that without adequate omega 3 fatty acids in the diet the blood thickens and the platelets become sticky and prone to form clots. Our book, Insulin: Our Silent Killer discusses this phenomenon more  fully.

Notice the role of omega 6 fatty acids in making the entire body subject to the inflammatory response mediated by the prostaglandin 2 family of prostaglandins.  The body would, if it could, manufacture the antagonists to these prostaglandin 2's to prevent setting up this whole body inflammatory response. These antagonists are the prostaglandin 1's and 3's. Our bodies, typically, cannot manufacture these anti-inflammatory  prostaglandins because they lack the basic raw materials. These are the omega 3 fatty acids. We typically need and do not have, any omega 3 fatty acids in our diet at all. We have an over abundance of omega 6's and transfats in our diet. The separate damaging role of transfat substitution for omega 3 fatty acids has been discussed elsewhere in connection with the glucose transport system.

Epidemiologically, the fat and oils connection to Hyperinsulinemia, and thus to all of the diseases mentioned on our home page, clearly parallels the rise of the Hydrogenated and Refined fats and oils business. Although not well known outside of research circles, (for reasons that are probably economic), the connection between artificial fats and oils and the Hyperinsulinemic destruction of vital functions is now well established. Recent advances in the study of appropriate cellular biochemical pathways have been most revealing.

To stop and reverse the progress of Hyperinsulinemia the following is mandatory:

Do not eat any hydrogenated oils or any prepared foods that contain them as ingredients.
Add to the daily diet a therapeutic amount of beneficial oils containing omega 3 fatty acids.

This one thing will, in conjunction with the rest of the program, greatly delay the onset of and in many cases prevent entirely these terrible diseases. This one simple dietary change is a part of a complete program thoroughly discussed in our special report, Insulin: Our Silent Killer. By making this change we are forcing the body to begin the healing process on every cell in the body. This is a drastic step and cannot be maintained for ever. When the body begins to heal, it then becomes necessary to restore the other fats and oils that it needs to accelerate the healing process. The timing on  this is critical to the  success of the program. To maintain such a drastic change in the fats and oils balance for the body forces every cell in the body to adjust. This is a therapeutic protocol and is not a protocol that can be maintained for ever. To use it safely, requires care and knowledge of what is going on so as to be able to decide when to move on to the next step. At some point it is  necessary, in order to continue the healing process, to add back into the diet the other fats and oils that we need. In our book, Insulin: Our Silent Killer we are able to expand, explain and elaborate upon this protocol and present useful tricks and techniques to assure its speedy success in the vast majority of cases.

However, there is another problem that must be faced when curing this disease. It is this: during that part of the cure cycle when elevated blood glucose and insulin levels are manifest, the body is being slowly destroyed by these agents. This period may last for many weeks or months dependent upon how long the disease has been allowed to run rampant before a cure is attempted. During this period of time it is of the utmost importance to use all measures available to keep blood sugar and insulin levels as low as possible so as to minimize the damage.  This is the focus of the drug treatment available from the medical community.  While this is an  important  step in minimizing vascular damage to the body during  the cure process, it itself is not a cure for anything. In our book we fully discuss a number of proven effective ways to minimize blood sugar and insulin levels without drugs and their damaging side effects.

Our program will, relatively quickly, reverse hyperinsulinemia, type 2 diabetes and some of the other symptomatic diseases caused by hyperinsulinemia. In my case, my type 2 diabetes was reversed in 103 days from start to finish. At the start my fasting blood sugar was 368  mg/dl. At the end of the program it varied between 75 and 85 mg/dl.

This program will remove much stress from the components of the BSCS; over a period of time they too will be restored to youthful function. This includes the liver, pancreas, adrenals, thyroid and the interior transport agents in every cell of our body.

This program will slow and in some cases reverse vascular damage and gangrenous damage to our extremities. There are faster ways to reverse this sort of damage which is thoroughly discussed in our Special Report.

This program will, over time, revcrse much of the neuropathic damage to the nervous system.

It will reverse atherosclerosis too, but may take years to do it. But here too, there are faster and better ways to reverse atherosclerosis which we cover in our Special Report.

Although this brief discussion of hyperinsulinemia has been designed to provide the basic information needed to understand the condition, a great deal more information is available, in our Special Report. This is for those who prefer to have a reference book handy, that is more focused on reversing the condition. This is because more detail, beyond this elementary explanation, is needed to assure a safe, effective and comfortable reversal of this disease than is practical to include in a web page.


  1. Lepsanovic L. et al, "[Hyperinsulinemia as a key factor in the development of many metabolic disorders]. Med Pregl 1997 Nov;50(11-12):469-472
  2. Nagasaki K, et al, "Relationship between hyperinsulinemia and risk factors of atherosclerosis.", Jpn J Med 1986 Aug;25(3):270-277
  3. Sheu WH, et al, "Insulin resistance, glucose intolerance,and hyperinsulinemia. Hypertriglyceridemia vs hyperlemia.", Arterioscler Thromb 1993 Mar;13(3):367-370
  4. Reaven GM, et al, "Diabetic hypertriglyceridemia.", Am J Med Sci 1975 May;269(3):382-389
  5. Folsom AR, et al, "Relation between plasma phospholipid saturated fatty acids and hyperinsulinemia.", Metabolism 1996 Feb;45(2):223-228

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