Relatively recently, it has been proposed that Alzheimer’s Disease (AD) is a form of diabetes that primarily affects the nerve cells of the brain., Many researchers and physicians now refer to AD as Type3Diabetes or T3D.
Alzheimer’s Disease is a form of dementia characterized by loss of short-term memory, confusion, forgetfulness and difficulties in speech. Later stages can be characterized by delusional thinking, repetitive behaviors, loss of long-term memory, sometime rapid mood swings and incontinence. It can only be definitively diagnosed by autopsy and microscopic examination of the brain when large amounts of protein (beta amyloid, tau) show up as tangled “threads” in the nerve cells. Currently, there is no blood or other test to diagnose AD.
Alzheimer’s disease is believed to affect 20% of those over 65 to varying degrees. By the time an individual is in their 80s, the chances that they will show signs of AD reach 50%.
AD, like T1D and T2D is a slowly progressive disease with both environmental and genetic factors at play. Studies have indicated that those individuals with T2D have a 50-65% higher risk of AD. Also, both AD and T2D are chronic inflammatory diseases with evidence of similar types of damage (oxidative) to the cells of the body.
Most importantly, recent evidence indicates that the nerve cells of the brain show insulin resistance and resistance to another hormone, insulin-like growth factor or IGF. Insulin resistance and IGF resistance is considered a sign of prediabetes. Since glucose (blood sugar) is the primary source of energy for brain cells, it is thought likely that the increasing degree of insulin and IGF resistance essentially starves the brain cells of its most importance energy source. Over the long term, this chronic “starvation” may lead to oxidative damage, the protein “tangles” seen at biopsy and the signs and symptoms of AD.
Clinical studies on individuals with early AD have shown promise treating AD with insulin or a class of diabetes drugs, the PPAR (Peroxisome Proliferator-Activated Receptor) agonists. Examples of the PPAR agonists, which can help stabilize blood glucose and blood lipid (fat) levels include the glitazones (pioglitazone (Actos) and rosiglitazone (Avandia)). Another class of drugs, the fibrates, also act in part as PPAR agonists. These drugs include fenofibrate (Tricor) and Gemfibrozil (Lopid). Fibrates and glitazones are currently being investigated as treatment for AD.
Alzheimer’s Disease and Diet
Early evidence that was largely forgotten indicated that there were dietary associations with AD, much as there are with heart disease and diabetes. Laboratory animals fed a diet high in nutrients along with specific anti-oxidant nutrients such as Vitamin C and Vitamin E had better abilities to learn new tasks and had fewer problems with memory. A relatively small number of human studies have also indicated that healthy diets higher in anti-oxidants, particularly Vitamin E, could provide significant protection against the common signs of dementia.
There is also an association with a diet high in saturated fats for both T2D and AD. High intakes of saturated fats and even moderate intakes of trans fats (found most commonly in fast foods) doubled or tripled the risk of AD. On the other hand, high intakes of polyunsaturated fats (PUFAs) such as omega-3 fats was protective for both AD and T2D. Omega-3 fats are known to be anti-inflammatory and to reduce aggregation of proteins (as seen in biopsies of brains from individuals with AD) and to reduce blood clotting (helping to prevent strokes due to blood clots).
A recent headline reads “Alzheimer’s could be the most catastrophic impact of junk food.” Another headline in The New Scientist reads “Food for thought: Eat your way to dementia”  Junk food and fast food is high in trans fats and in saturated fats, relatively low in nutrients and particularly low in anti-inflammatory and antioxidant nutrients. It is believed, therefore, that AD and diabetes, particularly T2D, can be prevented or the effects lessened by eating a healthy diet high in vital nutrients, staying away from fast foods and processed foods, and instead eating unprocessed whole foods and a diet high in fruits, vegetables, beans, legumes, nuts, seeds and whole grains.
Sugar as a Chronic Toxin for the Brain
There are many researchers who consider sugar to be toxic drug. Sugar cane has been cultivated for over 8000 years, but only recently has sugar, in the form of table sugar (sucrose) been widely available to nearly everyone on the planet. Diabetes, obesity, heart disease and now Alzheimer’s Disease have been associated with increased consumption of sugar, either in the form of table sugar or, more recently, in the form of high fructose corn syrup (HFCS), which is added (in large amounts) to many processed foods. HFCS is part glucose and part fructose, a sugar with a similar chemical structure. The liver is the only organ that can convert fructose to glucose—this can put significant strain on the liver. Fatty liver is a condition that has been associated with high intakes of HFCS, insulin resistance and with T2D and obesity. High levels of blood sugars are thought to be the underlying cause of nerve and vessel damage in diabetes, and now in Alzheimer’s disease. All this data is used as evidence that sugar, when consumed in high amounts, acts like a slowly acting toxin.
One of the lines of proof used to show that sugar acts like a drug on the brain is the comparison of brain scans (MRI and PET scans) comparing the brains of individuals who are obese (considered “sugar addicts”) to those of cocaine addicts—the results are strikingly similar. When obese individuals eat sugar, the areas of the brain that are “lit up” are the same areas that are “lit up” when cocaine addicts take cocaine.
We know that a poor diet high in processed foods and containing high levels of sugar can predispose an individual to diabetes, heart disease, obesity and now Alzheimer’s disease. We know that insulin resistance is associated with both diabetes and with Alzheimer’s disease and that drugs that combat diabetes are being studied as treatments for Alzheimer’s disease. We know that individuals with diabetes have a higher risk for AD. We also know that sugar is suspected to be the ultimate culprit in nerve and blood vessel damage and that at least some researchers consider sugar to be both a toxin and a drug. While more research needs to be done, it is getting clearer that indeed, Alzheimer’s disease can justifiably be considered to be caused by insulin resistance in the brain and a form of diabetes that primarily affects the brain and its function.
- Steen E, Terry BM, Rivera EJ, Cannon JL, Neely TR, Tavares R, Xu XJ, Wands JR, de la Monte SM. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease—is this type 3 diabetes? J Alzheimers Dis. 2005;7(1):63–80.
- Monbiot G. Alzheimer’s could be the most catastrophic impact of junk food. Guardian 10 Sept 2012.
- Trivedi B. Food for thought: Eat your way to dementia. New Scientist 3 Sept 2012; issue 2880.