Type 2 diabetes results when cells in the body becomes resistant to insulin, no longer allowing it to deliver glucose into cells. As a result, the cells starve. This is the reason that diabetes sufferers lose weight and feel very tired early on in the disease.

Even though the blood sugar rises to very high levels, it cannot enter the cells unless insulin is working.

With Type 1 diabetes, there is a deficiency of insulin itself and replacement of the insulin corrects the problem. In both cases, the cell is starving — as if there was no glucose in the body.

Several studies have shown that diabetics have a significantly higher risk of developing Alzheimer’s dementia, and Alzheimer’s patients are more likely to develop diabetes.

In experimental animals made diabetic with special chemicals, researchers saw some of the characteristics of Alzheimer’s.

However, the animals did not suffer from dementia. So diabetes itself does not cause Alzheimer’s dementia.

Studies have now shown that a person can develop insulin resistance localized to specific organs. For instance, you can have a Type 2 diabetes of the liver, the kidneys, or the muscles while the rest of the body processes insulin normally.

The brain is not immune to this condition, and a growing number of studies indicate that isolated insulin resistance can occur in the brain.

Animal models of isolated brain insulin resistance show all of the changes that occur with Alzheimer’s disease — and the animals suffered dementia. This would explain the loss of brain energy years before the onset of Alzheimer’s symptoms.

Researchers refer to this as Type 3 brain diabetes, which differs from Type 2 diabetes in several ways.

For one thing, instead of having very high levels of insulin in the brain, one sees very low levels — which may result from a transport problem.

Insulin, as it turns out, can be very beneficial to the brain. It reduces inflammation, improves brain energy levels, corrects some of the chemical changes seen in Alzheimer’s disease, and reduces microglial activation.