Alzheimer’s: Type 3 Diabetes?
by Chris D. Meletis, N.D.
When you’re eating that piece of cake or pie at your favorite restaurant or family gathering, you fully expect it to have an effect on your blood sugar and waistline. But what you probably don’t expect is for it to have an effect on your brain, too.
Researchers are establishing a strong link between blood sugar and brain health to the point where they’re calling Alzheimer’s disease “type 3 diabetes.” There’s also a link between diabetes and other forms of memory problems, including vascular dementia and mild cognitive impairment.
Studies consistently show a two to 3.4-fold increased risk of vascular dementia and a 1.8 to two-fold increased risk of Alzheimer’s disease in older people with diabetes.1 Many studies also show that you’re 1.5 times more likely to develop mild cognitive impairment—a condition known as predementia—if you have diabetes.1
Diabetes is thought to account for six to eight percent of all cases of dementia in older people.2 Additionally, people who have diabetes are 50 to 75 percent more likely to develop Alzheimer’s disease, and people with Alzheimer’s disease have a higher than normal tendency to develop type 2 diabetes or impaired fasting glucose.3
Scientists looked at 15 studies that investigated the link between type 2 diabetes and Alzheimer’s. Fourteen of those studies found that the two conditions were related, and in nine of those studies, the link between the two conditions was statistically significant. Smoking and hypertension—when they existed along with diabetes—increased the risk of Alzheimer’s even more.4
As fascinating as these statistics are, what’s really eye-opening is the many reasons why impaired blood sugar is so damaging to your brain.
This Is Your Brain on Sugar
When researchers first began to suspect there was a link between diabetes and Alzheimer’s, they wanted to know why this connection existed. Their search led them to two peptides—chains of amino acids that form proteins.
One type of peptide, known as amyloid beta, is found in Alzheimer plaques in neurons of the brain—and in the pancreas of diabetic patients. The other peptide, amylin, is found in both the pancreas and the brain.5
In one study, researchers found that same hallmark of Alzheimer’s disease—amyloid beta—in both the brains and the retinas (which is considered an extension of the brain) of diabetic patients. Specifically, the researchers looked at brain-cell-damaging toxins—known as oligomers—produced by amyloid beta.6 Oligomers are responsible for causing Alzheimer’s-related memory loss.
Insulin plays an important role in the formation of memories. And when oligomers attach to neurons, they knock out the insulin receptors from the neuron’s surfaces, which causes insulin resistance in the brain.6
Normally, after eating, an increase in sugar in the bloodstream signals the pancreas to boost levels of insulin, which in turn signals cells to remove sugar from the bloodstream so that the cells can use the sugar for energy. Insulin resistance occurs when cells fail to respond to insulin’s signal to allow glucose into the cells. This causes the pancreas to secrete even more insulin. Over time, the elevated insulin levels aren’t enough to compensate for the higher blood sugars, and the result is high blood sugar or diabetes since glucose can’t get into the cells.
Diabetes causes even more oligomers to build up in the brain and retina, which makes neurons even more insulin resistant.6
If glucose can’t get into the cells, the brain is starved of the fuel it needs to function. Without glucose, your brain would work about as effectively as your car when it runs out of gas. The brain composes only about two percent of the entire human body mass. Yet, 50 percent of glucose use in the body occurs in the brain.7-8 The majority of the brain glucose is converted to ATP energy,9 so that your brain cells can work properly and your memory remains in top shape.
The brain needs a balanced amount of glucose to function effectively. The problem occurs when the body is subjected to too much glucose and other forms of sugar such as sucrose and fructose. Too much of these sugars and it overwhelms your body to the extent that your body keeps producing more and more insulin, which ultimately loses its effectiveness, and results in the insulin resistance mentioned above. This is why, when mice with Alzheimer’s disease are fed excessive quantities of glucose, amyloid beta levels increase.10
Tau proteins are another culprit to blame for the connection between diabetes and Alzheimer’s. When tau proteins clump together, they form neurofibrillary tangles, one of the hallmarks of Alzheimer’s disease. Researchers don’t know for sure whether these tangles actually cause Alzheimer’s, but they definitely play an important role in the development of the disease.
Hyperglycemia (high blood sugar) modifies these tau proteins in the brain in such a way that they begin clumping together, causing them to form neurofibrillary tangles.3
The Inflammation Link
Inflammation is another link between Alzheimer’s and diabetes. Inflammation triggers the production of amyloid beta and increases the risk of the vascular disease associated with dementia.
Low-grade, systemic inflammation also is linked to diabetes as well as the cognitive decline that occurs in diabetics. One study reported that higher levels of inflammation markers such as C-reactive protein were associated with lower cognitive performance.1
Not the Brain You Were Born With
Diabetes results in changes to the brain’s structure—including more frequent brain lesions, and wasting away of an important area of the brain—compared to people who don’t have diabetes.1
And it’s not only the structure of the brain that changes during diabetes. The blood-brain barrier becomes more permeable as well.11 The blood-brain barrier separates circulating blood from the extracellular fluid of the central nervous system. This is because the brain is very choosy about what it allows inside of it. The blood-brain barrier keeps bacteria and other large molecules that don’t belong from entering the brain while allowing in glucose, hormones and other substances the brain needs to function.
When the blood-brain barrier isn’t working properly, it allows amyloid beta to slip through into the brain.11
The ability to allow amyloid beta proteins into your brain is controlled, in part, by a receptor for advanced glycation end products—better known as AGEs—which are produced in excess in diabetes and prediabetes.12 AGEs form as a result of a protein or fat molecule combining with a sugar molecule.
AGEs are easiest to understand when you think of them in relation to the browning of food. When you toast a slice of bread, the browning of the bread is the result of AGE formation in the food. This same process occurs in your body during blood sugar spikes. The more diabetes or insulin resistance disrupts your blood sugar, the more AGEs that form in your body. And, therefore, the more amyloid beta that can get into your brain and damage your neurons.12
Starving the Brain
Some research shows that during diabetes and insulin resistance, the brain is being starved of the insulin it needs to function. Yet, even while high levels of insulin are saturating the body during prediabetes, the brain becomes deficient in insulin because overproduction of this hormone weakens insulin receptors at the blood–brain barrier. This results in reduced amounts of insulin transported to the brain.1
This spells disaster for brain function, since insulin enhances memory and learning. Insulin deficiency in the brain also is involved in cerebral vascular dysfunction, inflammation, oxidative stress and the inability of neurons in the brain to repair themselves.1
Are Genetics to Blame?
Researchers have discovered a gene that may explain the link between Alzheimer’s and diabetes. They found that the gene, present in many Alzheimer’s disease cases, affects the insulin pathway.13
Yet, of the two types of Alzheimer’s disease—type 1 and type 2—only type 1, which accounts for five to 10 percent of Alzheimer’s cases, is genetic. This type of Alzheimer’s often develops at an earlier age. The rest of the cases, 90 to 95 percent, are type 2 and aren’t connected to genetics.
Interestingly, this sounds a lot like diabetes as well, doesn’t it? Of the two types of diabetes—type 1 and type 2—type 1 accounts for five percent of all diabetes cases, with 95 percent of diabetes falling under the type 2 classification.
Improve Your Diet, Boost Your Memory
The research linking Alzheimer’s and diabetes means that the key to having a good memory resides in your stomach. Commit to eating a healthy diet free of sugary foods and sodas. Choose whole wheat bread and pasta over white, refined products. Stick with healthy sweeteners such as xylitol and stevia that don’t raise your blood sugar levels.
And get moving! Exercise not only supports healthy blood sugar levels, it also enhances cognitive health, too.
Chromium, cinnamon and Gymnema sylvestre are good choices for supplemental blood-sugar support. An analysis of the medical literature found that chromium reduced glycosylated hemoglobin (HbA1c), which is a measure of blood sugar control, as well as fasting blood glucose levels.14 Gymnema sylvestre also reduced HbA1c levels in two small trials, while other studies showed cinnamon improved fasting blood glucose.14
In my practice, I often call chromium “will power in a bottle.” That’s because by balancing blood sugar, it also helps reduce the cravings for sweets that occur when your blood sugar is low.
You’ll want to consider supplementing with 1-6 grams of cinnamon, 600 mcg of chromium and 200-800 mg of Gymnema sylvestre per day.
Put the above strategies into practice and you’ll not only reap all the rewards of having balanced blood sugar—you’ll keep your memory sharp, too.
1. Samaras K, et al. Ther Adv Endocrinol Metab. 2012 Dec;3(6):189-96.
2. Kloppenborg R, et al. Eur J Pharmacol. 2008;585:97-108.
3. Kim B, et al. J Alzheimers Dis. 2012 Dec 19. [Epub ahead of print.]
4. Vagelatos NT, et al. Epidemiol Rev. 2013 Jan 21. [Epub ahead of print.]
6. Bitel CL, et al. Journal of Alzheimer’s Disease. October 2012;32(2):291-305.
7. Fehm HL, et al. Prog. Brain Res. 2006;153:129-40.
8. Liu F, et al. Brain. 2009;132:1820-32.
9. Shah K, et al. Int J Mol Sci. 2012 Oct 3;13(10):12629-55.
10. Takeda S. Nihon Shinkei Seishin Yakurigaku Zasshi. 2012 Nov;32(5-6):239-44.
11. Acharya NK, et al. J Alzheimers Dis. 2013 Feb 6. [Epub ahead of print.]
12. Kuwahara H, et al. Brain Nerve. 2013 Feb;65(2):145-51.
13. Ewald CY, et al. Genetics. June 1, 2012;191(2);493-507.
14. Nahas R. Canadian Family Physician. June 2009;55(6):591-6.