Diabetes of the brain

Zoomer | May 22nd, 2011

Alzheimer’s disease (AD) is one of the best known and most-dreaded of all degenerative diseases. An initial diagnosis is based on people making too frequent mistakes on simple and straightforward memory recall. The firm diagnosis of AD is based on agnosia (established memory impairment), with the presence of at least one of these cognitive deficits: apraxia (trouble with certain movements); aphasia (language impairment); or diminished executive capacity (an impaired ability to plan, sequence, organize, and reason abstractly).

Standard tests done on people who are suspected of having AD include a wide range of systems because so many factors can create cognitive impairment. Our brains are highly sensitive, and are affected quickly by almost everything that we drink, eat, say, believe, do, and are exposed to. Some AD tests are for thyroid, liver, or kidney dysfunction. Others involve blood counts to look for infections — including syphilis and HIV. While still others are checks of electrolyte, glucose, homocysteine, and vitamin B12 levels.

To date, no contagious microbe, pathogen, or parasite has stood up as either the probable cause or a major contributor — except that one study has found a potential association with Chlamydia bacteria. The ultimate cause may well be a combination of lifestyle, environment, and genetic susceptibility — which I believe to be the case with most degenerative diseases.

Brain changes for the worse

At autopsy, the brains of people with AD exhibit characteristic changes in the cerebral cortex, basal forebrain, and other areas. The characteristic plaques and tangles of proteins may be the result of scarring from altered proteins and abnormal cellular deposits.

The parts of the brain that are most affected are those that are largely stimulated by the neurotransmitter acetylcholine (AC) and there is a correlation between AD and a lower-than-normal AC level. Trying to correct this deficiency is one of the primary approaches of both natural and pharmaceutical medicine with varying degrees of success. The drug approach has been less than stellar, with a host (of course) of adverse effects.

Some enlightening research at the Rhode Island Hospital and Brown University Medical School has uncovered the fact that, in the early stages of AD, the brain’s insulin levels and the number of insulin receptors both diminish considerably. The insulin levels continue to plummet as AD advances into late stages by up to 80 percent. These findings are significant because previous work by the same senior researcher, Dr. Suzanne DeLaMonte, showed that insulin and other proteins are made inside the brain. This new evidence points in the direction of AD being in large part a neuroendocrine disorder.

Regulating the brain

Alzheimer’s disease disrupts the brain’s metabolism, setting it up for inflammation and cell death, which leads to cognitive malfunctions. Insulin resistance occurs when insulin and growth factor proteins (such as insulin growth factor-1, or IGF-1) have a diminished ability to bind to receptors. Without their influence, brain cells will fail and eventually die.

For the first time, the researchers at Brown University showed the clear connection that insulin and IGF-1 have to dementia. The two substances regulate the genetic expression for producing choline acetyltransferase — the enzyme pathway that is directly responsible for making AC. Higher levels increase AC production, but lower levels decrease it, which is exactly what we see in Alzheimer’s. The more severe the disease, the more the patients are deficient of and resistant to insulin.

Essentially, it appears that AD may be a form of diabetes — a diabetes of the brain that is caused by an imbalanced metabolism. The imbalance creates insulin alterations and resistance that lead to growth factor deprivation, raging inflammation from poor brain energy production, and brain lesions and neuronal death from metabolic starvation.

Fixing the fuzz

The feeling of being tired or mentally fuzzy after a meal could be a red flag that your blood sugar is too high. Research at the University of Virginia Health System showed that higher blood sugar levels are more likely to be associated with more mistakes on tests of mental function including reaction times and number subtraction. If this sounds like you, now would be the perfect time to turn the tide before fuzziness advances to full-out dementia. Stabilizing your glucose level and insulin function, and correcting your body’s imbalances, will naturally decrease inflammation. And dietary intervention is the perfect place to start.

By now, you certainly know the dangers of fast food, but recent research pointed out the effect of even the occasional burger and shake. In a 15-year study of over 3,000 people between ages 18 and 30, the folks who ate at fast-food establishments more than twice a week were twice as likely to develop insulin resistance. If you find that you’re constantly on the go and don’t have time to stop for a proper meal, then make it a habit to take along energy bars or meal-replacement shakes and a bottle or two of water. There are several tasty bars out there, but watch out for added sugar — some of them are loaded with the stuff. Of course, bars that contain a lot of fruit may list a lot of sugar on the nutrition facts panel, but fruit sugar is okay. Watch for added sugar (and artificial sweeteners) in the list of ingredients.

Finally, exercise is another key to balancing your glucose regulation. A study published in the Annals of Internal Medicine tracked over 1,700 dementia-free people over age 65 for up to nine years. By the study’s end, those who had exercised three or more times a week had a significantly lower risk of developing dementia. Intensity isn’t as important as consistency. Something as simple as walking regularly is enough to help your brain.

Mental exercise is another requirement for keeping your marbles. To emphasize how much effect using your brain power actually has on improving your mind; a study in NeuroReport showed that test subjects increased the levels of brain biomarkers in their hippocampus after only five weeks of using memory-based exercises. The changes were exactly the opposite of what is seen in patients with AD.

A more recent article by the same researcher, Dr. Michael Valenzuela in Australia, combined the data from 22 worldwide studies involving almost 30,000 people. He found that those people who had high mental stimulation had a 46 percent decreased risk of dementia. The protective effect was present even in later life as long as mentally stimulating activities were undertaken.

I mentioned earlier that there is also a genetic component to AD. Research out of Johns Hopkins University reveals that people who have a gene form called APO-E2 are somewhat protected against AD, while those who have the APO-E4 form are at higher risk. However, as I’ve said before, your genes are not your destiny they’re only the stage on which your choices act. Studies following 500 identical twins showed that AD is not a directly inherited disease. For instance, one twin might get Alzheimer’s while the other twin does not. In the end, it’s all about the diet and lifestyle choices you make.

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The content and opinions expressed in this article are the professional and/or personal view or opinion of the author only. Opinions expressed should not be construed as medical advice, and the article’s content is not a substitute for direct, personal, professional medical care and diagnosis. Individuals should always consult with their health care provider before beginning or changing any treatment program.