Alzheimer’s disease (AD) may be a type of diabetes that primarily damages brain nerve cells, according to a theory that has emerged relatively lately. Nowadays, a lot of medical professionals and researchers refer to AD as Type 3 Diabetes, or T3D.
Alzheimer’s disease
Alzheimer’s disease is a type of dementia marked by speech difficulty, disorientation, forgetfulness, and short-term memory loss. Delusional thinking, repeated actions, loss of long-term memory, occasionally abrupt mood swings, and incontinence are characteristics of later phases. The only way to get a firm diagnosis is to perform an autopsy and a microscopic examination of the brain when significant levels of tau and beta amyloid protein appear as tangled “threads” in the nerve cells. There is currently no test to diagnose AD, not even a blood test.
It is estimated that 20% of those over 65 have Alzheimer’s disease, albeit to differing degrees. The likelihood that a person may exhibit AD symptoms increases to 50% by the time they are in their 80s.
Similar to T1D and T2D, AD progresses gradually and is influenced by both hereditary and environmental factors. Research has shown that those with T2D are 50–65% more likely to develop AD. Additionally, there is evidence of comparable forms of oxidative cell damage in both AD and T2D, two chronic inflammatory disorders.
Most notably, new research suggests that insulin resistance as well as resistance to another hormone, insulin-like growth factor, or IGF, are present in brain nerve cells. It is thought that insulin and IGF resistance indicate prediabetes. Since blood sugar, or glucose, is the brain cells’ main energy source, it is believed that growing levels of insulin and IGF resistance effectively starve the brain cells of their most vital energy supply. Chronic “starvation” has the potential to cause oxidative damage, protein “tangles” observed during biopsy, and AD signs and symptoms in the long run.
Treatment for AD with insulin or a class of diabetic medications called PPAR (Peroxisome Proliferator-Activated Receptor) agonists has showed potential in clinical trials on people with early AD. Examples of PPAR agonists are the glitazones (pioglitazone, Actos), and rosiglitazone, Avendia, which can help stabilize blood lipid (fat) and blood glucose levels. Fibriates, a different class of medications, also function in part as PPAR agonists. Among these medications are gemfibrozil (Lopid) and fenofibrate (Tricor). Currently, glitazones and fibrates are being researched as AD treatments.
Alzheimer’s Disease and Nutrition
There were dietary correlations with AD, similar to those found with diabetes and heart disease, according to early research that was mainly ignored. Laboratory animals that were fed a diet rich in nutrients and supplemented with particular antioxidant elements, such vitamin C and vitamin E, demonstrated improved learning capabilities and reduced memory impairments. Healthy diets richer in antioxidants, especially vitamin E, may offer substantial protection against the usual symptoms of dementia, according to a small number of human studies.
A diet rich in saturated fats has also been linked to an increased risk of AD and T2D. The risk of AD was doubled or tripled by high intakes of saturated fats and even modest intakes of trans fats, which are primarily present in fast food. Conversely, increased consumption of polyunsaturated fats (PUFAs), namely omega-3 fats, provided protection against type 2 diabetes and Alzheimer’s disease. It is well established that omega-3 fats have anti-inflammatory properties, lessen protein aggregation (as demonstrated by brain biopsies from AD patients), and lower blood clotting (which helps avoid strokes from blood clots).
“Alzheimer’s could be the most catastrophic impact of junk food,” says a recent headline.Food for thought: Eat your way to dementia” is the headline of another article in The New Scientist. Junk food and fast food have high levels of saturated and trans fats, low levels of antioxidant and anti-inflammatory substances, and comparatively low levels of other nutrients. Therefore, it is thought that eating a healthy diet high in essential nutrients, avoiding processed and fast food, and consuming an abundance of unprocessed whole foods and fruits, vegetables, beans, legumes, nuts, seeds, and whole grains can either prevent AD and diabetes, especially T2D, or lessen its effects.
Sugar as a Persistent Brain Toxin
Many studies believe that sugar is a dangerous substance.Although sugar cane has been grown for more than 8000 years, almost everyone on the earth has only lately been able to obtain sugar in the form of table sugar, or sucrose. Increased sugar intake—either from table sugar or, more recently, from high fructose corn syrup (HFCS), which is added (in enormous amounts) to many processed foods—has been linked to diabetes, obesity, heart disease, and now Alzheimer’s disease. Parts of HFCS are glucose and fructose, two sugars with comparable molecular structures. Only the liver is capable of converting fructose to glucose, which puts a great deal of stress on the liver. Insulin resistance, obesity, T2D, and high HFCS consumption have all been linked to fatty liver disease. It is currently believed that high blood sugar levels are the fundamental cause of nerve and vascular damage in both diabetes and Alzheimer’s disease. All of these facts are used to support the theory that sugar behaves like a slowly acting poison when ingested in large quantities.
The comparison of brain scans (MRI and PET) between the brains of obese people (referred to as “sugar addicts”) and cocaine addicts is one of the lines of evidence used to demonstrate how sugar operates on the brain like a drug; the results are remarkably comparable. The same brain regions that are “lit up” when cocaine addicts use cocaine are also activated when fat people consume sugar.
Summary
We are aware that diabetes, heart disease, obesity, and now Alzheimer’s disease can all be predisposed by eating a bad diet heavy in processed foods and rich in sugar. It is well known that insulin resistance is linked to both diabetes and Alzheimer’s disease, and medications that treat diabetes are being researched as possible Alzheimer’s disease treatments. It is well known that people with diabetes are more likely to develop AD. We also know that sugar is thought to be the primary cause of damage to blood vessels and nerves, and that some studies classify sugar as a medicine in addition to a poison. Even if further study is required, it is becoming increasingly evident that Alzheimer’s disease can legitimately be linked to brain insulin resistance and a type of diabetes that predominantly impairs the brain’s functionality.
Citations
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769828/
- 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.
- http://blogs.scientificamerican.com/brainwaves/is-sugar-really-toxic-sifting-through-the-evidence/
- http://www.webmd.com/food-recipes/your-brain-on-sugar