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Blood Sugar, Insulin, and the Brain – Could Alzheimer’s Disease Be “Type 3 Diabetes?”

Brain Function

We know that the brain is especially sensitive to blood sugar levels, and that our moods track right behind our blood sugar. Case in point: when your blood sugar is low, you’re more likely to be irritable and impatient.

 

But some doctors now believe that problems with blood sugar and insulin are major factors in the development of Alzheimer’s disease. Just like the rest of the body, the brain can develop its own form of diabetes, a condition that has been dubbed “type 3 diabetes” by Suzanne de la Monte, M.D., Ph.D., a neuropathologist at the Brown Medical School, in Providence, Rhode Island. The reason is that Alzheimer’s disease has characteristics that resemble both type 1 and type 2 diabetes. Specifically, insulin levels become low (a trait of type 1 diabetes) and insulin resistance increases (a trait of type 2 diabetes) in the brain.

 

The Role of Blood Sugar and Insulin in the Brain

Glucose, or blood sugar, is the primary fuel of brain cells. We make it from dietary carbohydrates, sugars, and to some extent from protein. As in all other cells, the hormone insulin helps bring glucose into cells, where the fuel is burned for energy.

 

But, according to recent studies, insulin plays many other roles in the brain. For example, insulin is an anabolic hormone, meaning that it stimulates the growth of cells. In the body as a whole, the hormone can trigger the production of muscle or fat cells. In the brain, insulin stimulates the growth of neurons, brain cells that process and store information.

 

Neurons transmit information to each other via synapses, which are sort of like microscopic telephone network hubs. These synapses contain receptors—docking ports—for insulin molecules. Researchers now understand that the docking of insulin to synapses is essential for forming memories. Without insulin, new memories can’t form. The loss of memory is one of the key traits of Alzheimer’s disease, and the latest research indicates that the catastrophic loss of memory is related to problems with insulin.[i]

 

This link between insulin dysfunction and memory loss might sound interesting in theory, but what proof do we have? It turns out that insulin injections improve the memory of people with Alzheimer’s disease. A better memory probably reflects both a temporary improvement in glucose tolerance and enhanced insulin function in the brain. But as a treatment, insulin injections will increase insulin resistance and likely worsen memory in the long run.

 

When Insulin Turns Bad

Insulin injectionsInsulin resistance, one of the hallmarks of prediabetes and type 2 diabetes, occurs when the body makes lots of insulin (typically in response to a high-glycemic diet) while cells ignore insulin’s glucose-managing properties. Studies have found that both insulin resistance and type 2 diabetes are strongly associated with Alzheimer’s disease.

 

In a 32-year study of 2,322 men in Sweden, poor insulin function was related to a 33 percent increase in the risk of Alzheimer’s disease. Indeed, simple glucose intolerance, a form of prediabetes, was also associated with Alzheimer’s.[ii] And in a separate study, Dutch researchers reported that type 2 diabetes increased the risk of Alzheimer’s and more dementia by almost two times. The researchers also found that using insulin injections in the treatment of type 2 diabetes increased the risk of Alzheimer’s disease by four times![iii]

 

No wonder some people believe that Alzheimer’s disease is type 3 diabetes. But there’s more to the story.

 

Connecting the Dots

For years, researchers have believed that clumps of amyloid beta protein in the brain are the cause of memory loss in Alzheimer’s disease. But the real culprit might actually be close chemical relatives called amyloid beta-derived diffusible ligands (ADDLs).[iv] ADDLs are known neurotoxins. Eerily, ADDLs have a similar structure to prions, an insidious type of malformed protein that causes another brain disease, Creutzfeldt-Jakob disease (CJD). CJD, the human version of “mad cow disease,” results in a rapid deterioration of the brain, sort of like a fast-track form of Alzheimer’s.

 

Recently, William Klein, Ph.D., of Northwestern University, Chicago, discovered a link between ADDLs and insulin resistance in the brain. ADDLs damage synapses so that insulin molecules cannot attach and create new memories. In this way, ADDLs make brain cells insulin resistant, and they also leave a trail of free radical damage.[v]

 

In separate research, Brown University’s de la Monte and her colleagues analyzed brain tissue from 45 patients who had died from Alzheimer’s. Insulin activity was inversely related to the progression of Alzheimer’s disease in the tissues, meaning that the more advanced cases of Alzheimer’s had the least insulin activity. Other researchers have reported that the brains of Alzheimer’s patients have fewer insulin receptors and less insulin, compared with healthy brains.

 

Eating to Reduce Diabetes and Alzheimer’s Risk

The role of blood sugarSo if Alzheimer’s disease is a type of diabetes, or is at least related to poor glucose tolerance, what steps can you take to lower your risk? The answer lies in more than just following a low-glycemic diet—after all, ice cream and M&M Peanuts are low-glycemic but not healthy foods.

 

My dietary recommendations sidestep the hassle of counting calories or carbs or memorizing the glycemic index of foods. I emphasize freshly prepared foods over most foods sold in a box, can, jar, bottle, tub, or bag. The difference points to wholesome, unadulterated foods versus packaged, convenience, and processed foods. Whole natural foods almost always are low carb and low glycemic. In contrast, packaging typically reflects some measure of food processing, and processing usually involves a decrease in a food’s original nutritional value.

 

Of course, my recommendations mean either making the time to cook most of your foods from scratch or eating at restaurants that use mostly fresh and wholesome ingredients. It’s actually easier than you might think. If you usually eat lunch in a restaurant, order a chicken Caesar salad sans the croutons. At home, it doesn’t take a lot of time to prepare a simple meal, such as pan frying a salmon filet in olive oil, with steamed vegetables and brown rice on the side.

 

Protein. It’s important to think in terms of quality protein sources, such as fish, chicken, or grass-fed beef. Protein helps maintain normal blood sugar levels, which will in turn aids normal insulin function.[vi] [vii] Protein prompts the liver’s release of glucagon, a hormone that counteracts insulin in the body and therefore reduces the risk of insulin resistance. Although legumes are considered a source of protein, they also contain a large amount of carbohydrate. Still the occasional consumption of black beans is fine.

 

High-Fiber Vegetables. Like protein, fiber also improves blood sugar and insulin levels, and studies have found that high-veggie eating habits—like the traditional Mediterranean diet—lead to a lower risk of Alzheimer’s disease. Just about all veggies are fine, with the exception of potatoes.

 

Heathy Carbs. For most people, veggies provide plenty of complex carbohydrates for energy. If you exercise strenuously, you may need to add sweet potatoes, yams, and legumes to your diet. Large amounts of grain-based carbs, such as wheat and corn, can be problematic because they tend to be highly processed and contain a high ratio of carbohydrate to vitamins, minerals, and protein.

 

Supplements That Can Aid Memory

Several supplements can play vital roles in memory and brain health.

 

Niacinamide. The late nutritionally oriented psychiatrist, Abram Hoffer, M.D., Ph.D., often recommended the B-vitamin niacinamide for ensuring a good memory. It certainly worked for him—Hoffer lived until 92 and kept his marbles until the very end. Studies support the role of niacinamide in protecting against Alzheimer’s disease.[viii]

 

Alpha-Lipoic Acid and Acetyl-L-Carnitine. In animal studies, this combination of supplements reversed many of the signs of aging, leading to higher energy levels and improved memory. A study with people showed promising results.

 

B-Complex. Several B vitamins can help lower blood levels of homocysteine, a risk factor for strokes. Elevated homocysteine damages blood vessels and increases the risk of dementia.

 

Omega-3 Fish Oils. The omega-3s help brain cells communicate with each other. They also have anti-inflammatory benefits in the brain and throughout the body.

 

Phosphatidyl Serine. Phosphatidylserine is incorporated into the membranes (walls) of brain cells, where it helps maintain a youthful flexibility and enable communication between brain cells.

 

Supplements Than Can Aid Blood Sugar and Insulin

These are my favorite supplements for improving blood sugar and insulin levels.

 

Silymarin. This remarkable extract of the herb milk thistle is one of the best supplements for lowering blood sugar and improving insulin function. Silymarin enhances liver function, which works in tandem with the pancrease to regulate blood sugar.[ix] [x] [xi]

 

Chromium. This essential mineral enhances insulin function and helps regulate blood sugar.[xii]

 

Biotin. This B vitamin regulates genes involved in glucose metabolism, and it has insulin-like effects.[xiii] [xiv] Biotin works especially well when taken with chromium. It is extraordinarily safe and can be taken in large amounts.

 

Vitamin D. Good for your bones, vitamin D also plays a big role in regulating blood sugar and insulin levels. People who take vitamin D supplements, sometimes in combination with calcium, do a better job of maintaining normal blood sugar levels.[xv] [xvi]

 

Words to the Wise

There are certainly many factors that influence the risk of Alzheimer’s disease. They include runaway inflammation and neuro-inflammation; obesity, which increases the risk of type 2 diabetes by 80 times; free radical damage to brain cells; and a reduction in mitochondrial energy output. Insulin also seems to interfere with how the body normally processes dopamine, one of our stimulating neurotransmitters. Parkinson disease, which often precedes Alzheimer’s, is characterized by the inability to make sufficient dopamine. All of these other factors are intertwined to one extent or another, with poor glucose tolerance and decreases in insulin function.

 

Whether or not the term type 3 diabetes becomes part of our standard medical lexicon, one thing remains certain: Problems with blood sugar and insulin do increase the risk of Alzheimer’s disease. Because Alzheimer’s symptoms take decades to develop, it only makes sense to take steps to eat right and manage your blood sugar and insulin now.


[i] Kroner Z. The relationship between Alzheimer’s disease and diabetes: Type 3

diabetes? Alternative Medicine Review, 2009;14:373-379.

[ii] Rönnemaa E, Zethelius B, Sundelöf J, Sundström J, Degerman-Gunnarsson M, Berne

C, Lannfelt L, Kilander L. Impaired insulin secretion increases the risk of

Alzheimer disease. Neurology, 2008;71:1065-1071.

[iii] Ott A, Stolk RP, van Harskamp F, Pols HA, Hofman A, Breteler MM. Diabetes

mellitus and the risk of dementia: The Rotterdam Study. Neurology, 1999;53:1937-1942.

[iv] Catalano SM, Dodson EC, Henze DA, Joyce JG, Krafft GA, Kinney GG. The role of

amyloid-beta derived diffusible ligands (ADDLs) in Alzheimer’s disease. Curr Top

Med Chem, 2006;6:597-608.

[v] Viola KL, Velasco PT, Klein WL. Why Alzheimer’s is a disease of memory: the

attack on synapses by A beta oligomers (ADDLs). J Nutr Health Aging, 2008;12:51S-7S.

[vi]Gannon MC, Nutthall JA, Damberg G, et al. Effect of protein ingestion on the glucose appearance rate in people with type 2 diabetes. Journal of Clinical Endocrinology & Metabolism. 2001;96:1040-1047.

[vii] Layman DK, Baum JI. Dietary protein impact on glycemic control during weight loss. Journal of Nutrition, 2004;134:968S-973S.

[viii] Morris MC, Evans DA, Bienias JL, et al. Dietary niacin and the risk of incident Alzheimer’s disease and of cognitive decline. J Neurol Neurosurg Psychiatry, 2004;75:1093-1099.

[ix]Huseini HF, Larijani B, Heshmat R, et al. The efficacy of Silybum marianum (L.) Gaertn. (Silymarin) in the treatment of type II diabetes: a randomized, double-blind, placebo-controlled, clinical trial. Phytotherapy Research, 2006;20:1036-1039.

[x] Hussain SAR. Silymarin as an adjunct to glibenclamide therapy improves long-term and postprandial glycemic control and body mass index in type 2 diabetes. Journal of Medicinal Food, 2007;10:543-547.

[xi] Velussi M, Cernigoi AM, De Monte AD, et al., Long-term (12 months) treatment with an antioxidant drug (silymarin) is effective on hyperinsulinemia, exogenous insulin need and malondialdehyde levels in cirrhotic diabetic patients. Journal of Hepatology, 1997;26:871-879.

[xii] Anderson RA, Chen N, Bryden NA, et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with type 2 diabetes. Diabetes, 1997;46:1786-1791.

[xiii] Rodriguez-Melendez R, Zempleni. Regulation of gene expression by biotin. Journal of Nutritional Biochemistry, 2003;14:680-690.

[xiv] Fernandez-Mejia C. Pharmacological effects of biotin. Journal of Nutritional Biochemistry, 2005;16:424-427.

[xv] Pittas AG, Harris SS, Stark PC, et al. The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults. Diabetes Care, 2007;30:980-986.

[xvi] Pittas AG, Dawson-Hughes B, Li T, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care, 2006;29:650-656.

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