IDENTIFYING THE FUNDAMENTAL causes of Alzheimer’s disease (AD) is imperative. Addressing the challenge of AD at its source is the best hope for preventing, slowing the progression of, and possibly even reversing this form of neurodegeneration. The vast majority of pharmaceutical drugs targeting the condition have failed to demonstrate any beneficial effects. In fact, some initially promising drugs have actually made the signs and symptoms of AD worse.1
An examination of the scientific literature regarding the causes of AD reveals a wealth of information indicating that the condition is a result of metabolic abnormalities that start outside the brain. It affects the entire body, but health care professionals often miss the signs until damage to the brain is so deep and widespread that it begins to cause cognitive decline that interferes with everyday living. This renders formerly strong, capable people unable to care for themselves and live independently.
The research is unambiguous: AD results primarily from a failure of the brain to properly use glucose as a fuel. The connection between glucose handling, insulin signaling, and AD is so strong that many study authors now refer to AD as “diabetes of the brain” or “type 3 diabetes.”2 Although type 2 diabetes and AD are closely associated, it’s incorrect to say that type 2 diabetes causes AD. Many type 2 diabetics will never go on to develop AD, and many AD patients are not diagnosed as diabetic. The relationship between the two is more like that of physiological cousins. That is, they result from the same underlying metabolic imbalances but manifest differently depending on which parts of the body are affected. In type 2 diabetes, the way glucose is handled and insulin signaling occurs primarily affects the muscles, organs, and peripheral parts of the body. In AD, damage is mostly localized to the brain.