StemCell Therapy

Its often said that Alzheimers disease is the medical condition people fear mosteven more than cancer. This is understandable, considering the staggering statistics around Alzheimers and the fact that, at least so far as we currently know, there are no truly effective treatments and no cure. (According to the Alzheimers Association in the US, between the years 2000 and 2017, deaths from Alzheimers disease (AD) increased 145%,1 while deaths from other noncommunicable conditions, such as heart disease, actually decreased. In the US alone, approximately 5.8 million people are living with Alzheimers, and this is projected to more than double to about 13.8 million people by 2050.)

Alzheimers may seem mysterious, and the lack of progress toward treatments has been disheartening, but a robust body of scientific evidence suggests that this illness may be a metabolic condition rooted in dysregulated glucose metabolism and insulin signaling.2,3 With this in mind, lets take a closer look at the connections between type 2 diabetes and Alzheimers.

Alzheimers disease is sometimes referred to as type 3 diabetes and has also been described as brain insulin resistance.4,5 In fact, associations between metabolic syndrome (a.k.a. insulin resistance syndrome6) and cognitive impairment are so strong that researchers have coined the term metabolic cognitive syndrometo emphasize these links.7,8,9 The primary malfunction in the brain of someone afflicted with AD is that neurons in affected regions lose the capacity to metabolize glucose properly.10,11 Being unable to harness energy from glucose, these cells atrophy and wither, and the resulting breakdown in neuronal communication may be what leads to the memory loss, cognitive impairment, personality changes, and other hallmarks of the illness.12

Weve known since the research of Rosalyn Yalow in the 1960s that T2D is a disease of too much insulin (unlike type 1 diabetes in which there is not enough insulin). Many researchers believe T2D is the final stage of chronically elevated insulin. Another factor affecting proper insulin secretion and development of type 2 diabetes is the accumulation of fat in the pancreas. (Compromised liver function resulting from the buildup of fat in the liver is called non-alcoholic fatty liver disease, or NAFLD. The analogous condition in the pancreas is non-alcoholic fatty pancreas disease15, although it is not as widely recognized as NAFLD.) Abnormal accumulation of fat in the pancreas may interfere with healthy beta cell function and insulin secretion, and is associated with increased risk for type 2 diabetes and metabolic syndrome.16,17,18

In some people, chronically elevated insulin can precede a T2D diagnosis by a decade or more. Theres a parallel in Alzheimers: in people at risk for AD, reduced brain glucose metabolism is measurable when theyre in their 30s and 40s.19 At this young age, though, they are cognitively healthy and show no signs or symptoms of AD. Even though the brains energy supply from glucose is already compromised, the brain is able to compensate and overcome this fuel shortage. Its only when the damage is so severe and widespread and the brain is no longer able to compensate that problems with cognition and memory begin to manifest.

Turning back to T2D, for many people, the elevated fasting blood glucose or A1c that would trigger a diabetes or pre-diabetes diagnosis is a late developmentin the disease process. Chronically high insulin preceded this for some length of time, going undetected because measuring insulin levels is not a routine part of a checkup or standard bloodwork. In the same way, its possible that the memory problems and cognitive impairment associated with AD are late developments, becoming apparent after years or possibly decades during which the brain has suffered from a progressive decrease in energy.20

Disruptions in either the supply of fuel to the brain or the brains ability to usethis fuel can have catastrophic consequences for cognitive function. The brain accounts for just 2% of a typical adults body weight, but it consumes as much as 20-25% of the bodys glucose and oxygen:

Given the high energy requirement of the brain and its critical dependence on the delivery of a constant supply of fuel, the consequences of leaving such an energy shortfall untreated can be dire. When the brains energy supply is insufficient to meet its metabolic needs, the neurons that work hardest, especially those concerned with memory and cognition, are among the first to exhibit functional incapacity (e.g., impairment of memory and cognitive performance).21

People with type 2 diabetes have an increased risk for Alzheimers disease and other types of dementia compared to those without diabetes.22,23,24 However, even in the absence of high blood sugar, people with chronically high insulin are also at greater risk for AD. In fact, one study showed that risk for AD was highest among people with elevated insulin but who were notdiabetic.25 In a study of subjects with newly diagnosed T2D or pre-diabetes who had seemingly normal cognitive function, greater insulin resistance was associated with reduced brain glucose metabolism and subtle cognitive impairments.26 Its possible that hyperinsulinemia and a disruption in brain fuel usage are the first dominos to fall in the Alzheimers cascade, setting the stage for future cognitive decline.

An interesting point to note is that while elevated insulin in the bloodappears to be a major risk factor for AD, many AD patients havelowerthan normal insulin levels in the brain.27,28 Insulin is not required to transport glucose across the blood-brain barrier, nor for neurons to take up and use glucose. However, insulin receptors are scattered richly throughout the brain, and insulin is believed to play a role in facilitating healthy cognition and the viability and proper functioning of neurons.29,30

Chronically elevated blood glucose and/or insulin have negative impacts on nearly every organ and tissue system in the body: the eyes, the kidneys, the skin, the liver, the ovaries, the prostate gland, nerve cells, and more. The brain is no less susceptible to the detrimental effects of deranged glucose metabolism. In fact, owing to its high energy demands, it might even be moresusceptible than other parts of the body, and Alzheimers disease could be the most severe manifestation of this.

Written by Amy Berger, MS, CNS

Amy Berger, MS, CNS, is a U.S. Air Force veteran and Certified Nutrition Specialist who specializes in using low-carbohydrate and ketogenic nutrition to help people reclaim their vitality through eating delicious foods, and showing them that getting and staying well don't require starvation, deprivation, or living at the gym. Her motto is, Real people need real food! She blogs atwww.tuitnutrition.com, where she writes about a wide range of health and nutrition-related topics, such as insulin, metabolism, weight loss, thyroid function, and more. She has presented internationally on these issues and is the author ofThe Alzheimer's Antidote: Using a Low-Carb, High-Fat Diet to Fight Alzheimers Disease, Memory Loss, and Cognitive Decline.

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The Connection Between Type 2 Diabetes and Alzheimer's Disease - A Sweet Life

This entry was posted on January 26, 2020 at 4:47 am and is filed under Diabetes. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed. |