What is type II diabetes and prediabetes?

Type II diabetes is a disorder that is both preventable and reversible. It is caused by the gradual loss (over years) of pancreatic Beta cells. This results in an ongoing inability to produce enough insulin quickly enough to avoid the damage, principally to small blood vessels, caused by long-term raised blood glucose levels. That damage can result in the various complications of diabetes which include heart disease, stroke, kidney failure, amputation, and blindness.

Insulin is required to clear glucose from the blood by moving it into cells.

The risk factors for type II diabetes are well known. They are increasing age, genetic disposition, obesity, and inactivity. However, and this is a critical point, these are not causes of diabetes. In particular, as young adults become fatter, their Beta cell mass increases. We know this by autopsy studies of the Beta cell mass in obese and non-obese young adults.

Beta cell mass is lost as the death rate of Beta cells exceeds their replication rate. Beta cells, like other cells in the body do not live forever. They divide and they die. Excess Beta cell death is the result of overwork, and the precipitant of that overwork is not obesity. Commonly, it is insulin resistance, a much studied but poorly understood phenomenon which results in the requirement for higher doses of insulin to move the same amount of glucose from the blood into cells. Type II diabetes can be caused by a diet rich in sugar (such as fizzy drinks), presumably because such a diet requires Beta cells to work at maximum output for prolonged periods, and some fail.

Prediabetes refers to a state where so many Beta cells have been lost that the result of at least one of the test for diabetes is no longer normal, but none of the tests is diagnostic of diabetes.

The conventional medical approach to diabetes is wrongheaded. It focusses on reducing the modifiable risk factors, obesity and inactivity, when the risk has already crystallized as diabetes. The most that this approach achieves is a longer interval between diagnosis and the appearance of complications.

An alternative, and in my view superior, approach is to focus on reversing excess Beta cell death with the aim of restoring Beta cell mass and curing diabetes.



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