Oxygen Models of Hyperinsulinism and Diabetes Type 2

Majid Ali, M.D.

Direct Evidence for the Oxygen Model of Diabetes


On April 14, 2014, the journal PLOS One published additional direct evidence for my Oxygen Model of Diabetes. The study was conducted to investigate the effects of hypoxia (lack of oxygen) at high altitudes on Mount Everest climbers. Its core finding is that hypoxia increased blood levels of markers of inflammation and oxidative stress known to lead to insulin resistance.

During the Everest expedition in 2007, 24 people traveled to the mountain and were checked for blood sugar control, body weight changes and signs of inflammation at base camp, which was at an altitude of 5,300 meters (about 17,388 feet).

Half of the participants remained at base camp while the other half climbed Everest to a maximum altitude of 8,848 meters (29,028 feet). Measurements were taken in each group at week six and week eight of the trek.

“These results have given us useful insight into the clinical problem of insulin resistance. Fat tissue in obese people is believed to exist in a chronic state of mild hypoxia because the small blood vessels are unable to supply sufficient oxygen to fat tissue,” study leader Mike Grocott, a professor of anesthesia and critical care at the University of Southampton, said in a university news release.

Oxygen Model of Diabetes

My Oxygen Model of Diabetes is a unifying model that explains all aspects of diabetes Types 1 and 2—causes, clinical course, consequences, and control—on the basis of impaired oxygen signaling, diminished oxygen’s detergent functions, and interrupted oxygen’s cellular detox and repair functions. I put forth this model first in a series of articles in 2000 and presented it at length it in my book “Dr. Ali’s Plan for Reversing Diabetes (2006)” (available for download at http://www.aliacademy.org)

In my book, I illustrated the insulin/insulin receptor dysfunction with a crank/crank-shaft analogy.Briefly, the cell membranes become resistant to insulin when they become chemicalized—plasticized, so to speak—and hardened, immobilizing the insulin receptors embedded in the membranes. The insulin receptor is a protein that criss-crosses the cell membrane like a cord. One of the consequences of grease buildup on cell membranes is that insulin receptor becomes turned and twisted, literally and figuratively. In a previous paper, I offered the analogy of a crank and a crank-shaft to explain insulin resistance. I visualize insulin as a crank—a device that transmits rotary motion—and the insulin receptor protein as a crank-shaft embedded in the cell membrane.

Suggestred Readings

For more info, please consider:

  1. Dr. Ali’s Diabetes Course
  2. Dr. Ali’s Insulin Course
  3. Dr. Ali’s Oxygen Course




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