Prevention and Reversal of Dementia: What Role Does Insulin Play?

by Krista Russ

As many providers can attest, Alzheimer’s Dementia (AD) is a complex brain disease that slowly destroys a person’s memory and thinking abilities until sufferers become so debilitated that they cannot carry out the simplest of tasks (1). Over six million Americans over the age of 65 suffer from dementia  (1). Even grimmer, as the condition progresses, it can become fatal within as little as 3-10 years (1). Few providers would disagree with these statements. Where the tables turn is the consensus on the causes of dementia, who will get it, and whether or not dementia is a destined part of aging. Dementia is debilitating, life-altering, and ultimately, life-ending. The question is, does it have to be? Can dementia be prevented or even reversed?

Correlation does not Equate to Causation in AD

Alzheimer’s Dementia is characterized by a buildup of beta amyloid plaques and neurofibrillary tangles comprised of a protein called tau that builds up in the brain (2). In fact, one of the main features of the disease is the harmful buildup of these plaques and tangles, but are they really the main issue?

At first glance, it seems reasonable to infer that if we observe plaques and tangles building up in the brains of people who have Alzheimer’s Dementia, then surely that must have something to do with what is causing dementia, but the reality is far more complex. Correlation does not equate to causation. Just because these features are observed in AD does not automatically mean that they are the cause of dementia. It could very well be the end result and not the cause similar to the chicken and the egg theory. Which came first? Did the plaques and tangles cause the dementia or did whatever caused the dementia result in the plaques and tangles? Observational studies show the presence of certain changes in the brains of people with AD, but when it comes to proving what caused something, more than observation is needed. By focusing solely on observations without identifying the true cause, we may inadvertently draw conclusions that lead to harm or at the very least are ineffective. To discover causation, interventional studies must be conducted. 

A good example of this point can be seen with another common illness, type two diabetes. Type two diabetics have trouble controlling their blood sugar, and the illness is characterized by high blood sugar. On the surface, it seems that there must be a deficiency of insulin because we know that insulin lowers blood sugar; thus, we prescribe insulin to treat severe diabetes and it works…sort of. It works in the interim, but the disease continues to progress. Blood sugar levels climb higher and higher even as more insulin is administered. So, what is really going on? In reality, type two diabetics do not have a deficiency of endogenous insulin. In fact, they produce plenty of it, even too much of it, and yet their blood sugars continue to rise to no avail. This observation had puzzled scientists for decades until we realized that insulin resistance–not insulin deficiency–was the true cause of type two diabetes. 

Something quite similar may be said for AD, especially because not everyone with beta amyloid plaques has dementia. Indeed, as many as 20% of people with beta amyloid plaques have NO signs of the disease (2). If the plaques themselves were responsible for the symptoms of dementia, we’d expect nearly everyone with these plaques to have dementia, but that is simply not the case. So if not, then what is the cause?

Multifactorial Origins in Dementia

There are countless abnormalities observed in dementia, which is why experts consider it to be a multifactorial illness as opposed to having one single cause. Biochemical, molecular, hormonal, and cellular abnormalities all typify AD (2). Everything from metal buildup (aluminum) to free radical damage to mitochondrial dysfunction has been linked to AD. In this article, we will briefly discuss one well-documented hypothesis that is believed to be a major cause of dementia and/or allow for its progression—Type Three Diabetes.

Type Three Diabetes

Alzheimer’s Dementia may well be a variant of diabetes; hence, the term  “Type 3 Diabetes.” This is because AD shares many features in common with both Type One (T1D) and Type Two Diabetes (T2D), yet it differs in some critical ways (2). Like the other forms of diabetes, AD is characterized by insulin resistance; however, this insulin resistance exclusively involves the brain, rather than the peripheral insulin resistance seen in T2D (2). 

Indicators of the “brain-specific” insulin resistance observed in AD include the following:

• Brain deficiencies in IGF-1, IGF-2, and insulin, along with their corresponding receptors (2). 
• Tau protein gene expression and phosphorylation are both regulated by insulin and IGF signaling (2). 
• Lab experiments show that much of the Central Nervous System degeneration that occurs in AD is impacted by impaired insulin signaling (2). 

But just how does insulin resistance contribute to the development of Alzheimer’s Dementia? And if we learn how insulin resistance contributes to AD, what can we do to help sufferers? Fortunately, there is promising research in this area. We will discuss the research and support on the Type Three Diabetes pathway and what you can do to help your patients who are suffering from AD or at risk for it in our exciting 7th Annual Academic Summit: Breakthroughs in Brain Health, CVD, and Autoimmunity.