Evidence of Oxygen Model of Insulin Toxicity

Majid Ali, M.D.

Facts, Facts, and a Thought Experiment

In this article in my library of articles on insulin toxicity and oxygen model of insulin toxicity, I present some compelling facts about insulin toxicity. To make my case with simple words, I invite you to consider a thought experiment. We will conduct two large trials to investigate the incidence of death caused by insulin used to treat diabetes. 


In the first randomized trial, we take 5,000 patients with a median A1c level of 8.1% and assign them to receive intensive therapy for a target A1c value below 6.0%.. Next, we take another 5,000 patients and give them standard therapy with a target A1c level from 7.0 to 7.9%.

Needless to point out, the first group will receive more diabetes drugs to lower A1c level with higher insulin activity, since all diabetes drugs increase insulin activity. Question: Which group will have a higher death rate, the more drugs/more insulin group or the less drugs/less insulin group?


For the second randomized trial, we take 6,000 patients admitted to ICUs in various countries. We treat 3,000 of these patients with insulin by intravenous infusions to lower the blood glucose level and reach a target of 81 to 108 mg /dL. We treat the remaining 3,000 patients without insulin drips and allow the blood glucose level to reach 180 mg/dL.


Question: Which group will have a higher death rate, the group with intravenous insulin infusion or the group without it?

If insulin in excess is toxic—I strongly assert it is—then there will be more deaths in patients given larger doses of insulin in both trials. That indeed is the case. Both insulin trials of my thought experiment have been done and published in The New England Journal of Medicine. The first was called the ACCORD trial and included 10,251 patients. The second, called the NICE-SUGAR Study, included 6,104 patients. Both trials proved that higher insulin activity was associated with higher death rates. 

Below are the conclusions (verbatum) of the two trials that speak for themselves:

As compared with standard therapy, the use of intensive therapy to target normal glycated hemoglobin levels for 3.5 years increased mortality and did not significantly reduce major cardiovascular events. These findings identify a previously unrecognized harm of intensive glucose lowering in high-risk patients with type 2 diabetes (N Eng J Med. 2008;358:2560-2572. June 12, 2008 ). 

In this large, international, randomized trial, we found that intensive glucose control increased mortality among adults in the ICU: a blood glucose target of 180 mg or less per deciliter resulted in lower mortality than did a target of 81 to 108 mg per deciliter. 
(N Eng J Med. 2009;360:1283-1297 March 26, 2009)

It is hard to teach old dogs new tricks. So, I was not surprised to find the following words in an editorial on the subject in The New England Journal of Medicine (360:1346-1349 March 26, 2009): 

Clinicians, particularly those involved in critical care, are now left in something of a quandary. Until further evidence becomes available, it would seem reasonable to continue our attempts to optimize the management of blood glucose in our hospitalized patients. 

The Journal has never shown interest in the problem of grease buildup on cell membranes caused by unhealthy foods, polluted environment, and chronic anger. None of the writers of the Journal seem to understand that grease on cell membrane—composed of rancid fats, sticky sugars, pulped proteins, metabolic waste, and debris—immobilizes and incapacitates insulin receptors. They are unable to learn that insulin receptor activity can be restored by grease-removing oxygen therapies. This is how the need for insulin can be reduced—even eliminated on many occasions—for superior clinical results. This is where the real potential of de-diabetization and better care of people with diabetes can be found. Of course, there are no drugs that remove cellular grease, hence theJournal’s disdain for nondrug oxystatic therapies.


My Oxygen Model of Insulin Toxicity Is the Flip-face of  my Oxygen Model of Diabetes

My Oxygen Model of Insulin Toxicity is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of insulin toxicity—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are: (1) oxygen signaling; (2) oxygen’s ATP energy generation; (3) oxygen’s detergent functions; (4) oxygen’s cellular detox functions; (5) oxygen-regulated cell membrane and matrix functions; (6) oxygen’s cellular repair roles.

The Oxygen Model of Insulin Toxicity provides a simple model that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity.

This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of insulin toxicity.

The crucial importance of the Unifying Oxygen Model of Disease is that it:

* Explains the scientific basis of primary aging processes in the body;

* Sheds light how health can be preserved by addressing all oxygen-related issues;

* Elucidates how toxicities of foods, environments, and thoughts cause tissue injury and disease;

* Reveals the mechanisms by which various detox therapies work (Oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely).

* Allows the formulation of rational and effective designs for reversing chronic diseases; and

* Provides explanations of mechanisms by which time-honored natural remedies work.

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