The recent discoveries surrounding Alzheimer’s suggest that one day getting this disease could become optional. In understanding the progression of this disease better, researchers are finding ways to catch it earlier and identify contributing factors so that we can prevent, stop, and reverse this devastating condition.
Two of these important developments came from studying how similar diabetes and Alzheimer’s and in toxin bioaccumulation. Let’s take a closer look.
Alzheimer’s Disease is Type 3 Diabetes in Some Cases
Diabetes and Alzheimer’s disease are both top 10 leading causes of death in the United States. These two major illnesses are also on the rise across our country, and are proving to more alike than we once realized. At first glance, these two conditions might not seem too similar but both diseases are largely caused by changes in our diets and environmental exposure.
It’s well documented that diabetes and dementia are strongly associated. In fact, diabetics have a significantly higher risk of developing Alzheimer’s disease than the rest of the population. In the past few years, we’ve come to find that these two diseases share so many common pathologies, it’s led to some calling Alzheimer’s disease – type 3 diabetes.
Research has found that increased insulin resistance of the body (which is how you develop type 2 diabetes), leads to a cascade of factors that cause cognitive decline, which results in Alzheimer’s disease. These shared factors include:
- Brain insulin resistance
- Oxidative stress
- Cognitive impairment
- Disturbances in acetylcholine homeostasis
- Disturbances in insulin-like growth factor
Cognitive decline is the precursor to dementia. Up until recently, the connection between signs of prediabetes and early cognitive decline hadn’t been linked. With both these diseases on the rise in our country, the question becomes – How can we identify onset earlier so as to prevent further regression? And do these two conditions share a common biomarker?
When it comes to diabetes, we hear a lot about blood sugar levels and maintenance. However, HbA1C is a more reliable measurement because it reflects about three months of fluctuating glucose levels. As a result, HbA1C levels are a better indicator for diagnosing diabetes and identifying those at risk of developing diabetes.
Is HbA1C the Key to Catching Alzheimer’s Early?
What is HbA1C exactly? It stands for hemoglobin A1C or glycated hemoglobin. This is a type of protein found in red blood cells, which is responsible for transporting oxygen. In a diabetic, HbA1C levels are higher due to poor control of blood sugar. In addition to diabetes, higher HbA1C levels are also associated with higher risk of heart disease. Interestingly, this important marker has recently been linked to cognitive decline, which has added to the case for calling Alzheimer’s disease, Type 3 diabetes.
In a 2018 study, researchers found that not only were high HbA1C levels (as seen in diabetics) associated with cognitive decline, but this marker could be used as a predictor of early stages of cognitive decline.
This is fascinating new information!
Because it indicates we might be able to test for cognitive decline before there are even symptoms. Furthermore, this study found that there is a “linear correlation between circulating HbA1C levels and cognitive decline, regardless of diabetic status.” Meaning, you don’t have to be diabetic to have diabetically high HbA1C levels or the cognitive decline it causes.
Imagine you could get a simple blood test that could tell you if you were experiencing predementia, before you even noticed the signs. Between this promising indicator and other new understandings in the pathogenesis of Alzheimer’s disease, we are coming upon a time where early detection is going to make prevention, arresting, and reversing the development of Alzheimer’s a possibility.
If you want to learn more about how to keep yourself from becoming insulin resistance, check out the 5 Incredible Benefits of Insulin Sensitivity – Plus, 11 Ways to Reverse Insulin Resistance. This article shows you exactly how to avoid this mess in the first place.
Alzheimer’s Disease as a Protective Response
For a long time it was believed that the development of the trademark amyloid beta oligomers and plaque build ups in the brain were due to damage and degradation. However, recent research indicates there appears to be no response by the brain to the increase in oxidative stress associated with Alzheimer’s development. Additionally, the brain appears to downregulate energy metabolism, which suggests this whole process is actually the brain trying to protect itself.
So, what exactly is the brain trying to protect itself from?
It appears there are a couple of different factors the brain could be trying to protect itself from, which has resulted in the six subtypes of Alzheimer’s disease. There are definitely overlapping characteristics, but in general these breakdown as follows:
- Type 1 is characterized by systemic inflammation and thought to be a reaction to widespread, chronic inflammation.
- Type 1.5 has both inflammatory and atrophic factors.
- Type 2 Alzheimer’s is characterized by atrophic activity of certain molecules including insulin, other hormones, which is accompanied by insulin resistance.
- Type 3 appears to develop as a protective effect against toxins, such as heavy metals and mycotoxins from mold.
- Type 4 this form occurs due vascular impairment or as a reaction to blood vessel damage.
- Type 5 is associated with head trauma.
**Please note: It’s important not to confuse the term “type 3 diabetes” with “type 3 Alzheimer’s.” Type 3 diabetes is a way to explain insulin resistance in the brain and relate it to how diabetes occurs in the body. Type 3 diabetes also a helpful term because it indicates poor diet and other lifestyle factors as a major cause, which is turning out to be more true that we’ve ever realized with Alzheimer’s. On the other hand, type 3 Alzheimer’s is also called inhalational Alzheimer’s and mostly caused by toxin exposure. Though, there can be overlap in all the causes, symptoms, and pathogenesis of each type of Alzheimer’s – Shew! In case we weren’t confused enough already!
Of these, type 3 Alzheimer’s disease is of particular interest to me because the pathogenesis reveals how the brain responds in a protective manner against environmental toxins, such as mold mycotoxins. Identifying whether cognitive decline is caused by mold or other pathogens is extremely important because any treatment without removal of the assaulting microorganism or toxin l isn’t going to do anyone any good.
Research has found certain pathogens are associated with type 3 Alzheimer’s, including:
- P. gingivalis – an oral bacteria
- C. glabratus – fungi
- Herpes simplex – virus
- Borrelia burgdorferi – Lyme disease
- Mycotoxins from water-damaged buildings:
The brain is about 60 percent fat, which makes it more susceptible to persistent bioaccumulation of toxins. Science continues to unravel the mysteries of Alzheimer’s disease by finding new ways to catch cognitive decline earlier and identify contributing factors so we can eliminate them once and for all.
Most people still think an Alzheimer’s diagnosis is a death sentence but this is no longer the case. Everyday new developments are revealing that Alzheimer’s disease is a direct result of the changes in our diet and environment, which have only occurred in the past few decades. Furthermore, we are finding Alzheimer’s is not only preventable, it’s also reversible in some cases.
It’s an exciting time for Alzheimer’s research – share this article with a friend or family who would love to hear the good news!
Introducing the International Society of Environmentally Acquired Illness
As a prominent educator about environmental toxicity and mold-related illness and board-member of the organization, I am delighted to introduce the NEW professional society International Society of Environmentally Acquired Illness (ISEAI) whose mission is to “raise awareness of the environmental causes of inflammatory illnesses and to support the optimal health of individuals affected by these illnesses through the integration of clinical practice, education, and research.”