Alzheimer's disease is a chronic disease frequently associated with age.  It is the most common dementing illness and affects 50% of those who reach age 85. Type II diabetes, insulin resistance and the Metabolic Syndrome are all considered risk factors for this disorder because they double or triple the chances of developing it and may also accelerate disease progression.  Based on this observation, it is reasonable to conclude that abnormalities of either blood sugar or insulin metabolism play a pivotal role.  If that is true, then it is likely that refined and other rapidly digested carbohydrates are important factors as well.

The characteristic brain tissue findings associated with Alzheimer's disease, senile plaques and neurofibrillary tangles , were identified by Alois Alzheimer about 100 years ago.  The 1990s were called the "Decade of the Brain" and with this designation research on Alzheimer's disease was put in the cross hairs of neurological investigators.  While this helped, what really was instrumental in facilitating an improved understanding of what caused the disease was the recognition that aberrations of glucose and insulin metabolism were associated with increased incidence. 

Among the vanguard of scientists pursuing this approach is Dr. Suzanne Craft at the University of Washington.  She has documented numerous abnormalities of glucose and insulin metabolism in Alzheimer's disease and has observed associations between these metabolic changes and the physiology of the beta-amyloid peptide found in the senile plaques that accumulate in the brains of afflicted patients.  Additional investigators pursuing this lead have found aberrations in the insulin signaling pathway in the brain,  while other neuroscientists have identified a link between the degradation of beta-amyloid and IDE (Insulin Degrading Enzyme-the enzyme responsible for recycling the hormone insulin).  When researchers inject a compound into the brains of mice that blocks the insulin receptor in the brain, or separately blocks the insulin signaling pathway, the animals develop plaque-like deposits and become demented.  Doctors from Brown University Medical School have coined the phrase "Type III Diabetes" to refer to the inability of the brain to properly use glucose in Alzheimer patients, akin to what happens in the bodies of diabetics.

To evaluate whether such findings have clinical merit, Dr. Craft conducted a study in patients suffering from Alzheimer's disease.  There are pharmaceutical compounds on the market that are able to improve the body's sensitivity to insulin.  She asked the question, if insulin resistance (the metabolic abnormality linked with diabetes and the Metabolic Syndrome) truly does play a seminal role in this form of dementia, then a drug that is able to improve insulin sensitivity should be a beneficial treatment.   That is exactly what she found!  Such observations serve to open the door for new pharmaceutical approaches.

The most exciting news is that factors other than drugs can improve insulin sensitivity.  They are diet and lifestyle choices including good nutrition, weight maintenance and exercise-all easily within our purview.  The new book Good Calories, Bad Calories by Gary Taubes provides novel nutritional recommendations to help in this regard. 

Just remember, the time to get started on such a brain-healthy program is now.

The prognosis for most patients with malignant brain tumors is poor.  Surgical resection followed by radiation therapy is the standard therapy.  Chemotherapy is often used in an adjuvant fashion.  Of potential interest in this area are several papers that have appeared in the medical literature over the past 10-15 years evaluating potential dietary approaches to these devastating, and frequently poorly responsive, neoplasms.  Interestingly, they didn't seem to make the radar screen of most oncologists and other physicians treating these patients.  Recently there has been renewed interest in the possible beneficial effects of a nutritional program to assist in the treatment of various cancers. 

The basis for such an approach arises from the metabolic inflexibility shown by brain tumor cells.  Having arisen from the same basic cell type, brain tumor cells share many common traits with normal brain cells.  However one of the key differences, and one that is shared by many other types of cancer cells, is that as they make the normal to cancerous transition they lose some of the properties of the normal brain cells.  In the case at hand, we will contrast how normal and cancer cells produce the large amount of energy that allows them to proliferate.  Brain cells depend almost exclusively on glucose they receive from the blood stream as the ultimate fuel source they generate their energy from.  Somewhere during their evolutionary history they learned a neat trick.  Famine and starvation were common occurrences and were usually associated with a fall in glucose availability.  This was because the body can only store enough glucose (mostly in the liver) to last about 24 hours.  After this reserve is exhausted, protein is broken down and converted to glucose to provide a continuing fuel supply for the brain cells.  It is not surprising that if this continues unabated our lean tissues including the heart and muscles would eventually start to malfunction.  In order to prevent this from occurring, we tap into our fat stores.  Yet, the brain can't burn fat so how does this help?  The fats in the blood are transported to the liver where they are partially burned.  The remaining partially burned fats are called ketone bodies, or ketones.  They are released into the blood and carried to the brain where they may be used as an alternative fuel source by the brain cells.  This preserves our lean tissue and gives the brain an additional source of energy.

Thus, normal brain cells can burn a mixture of glucose and ketone bodies and are very happy to do so.  They actually feel no difference because the energy is all they require whatever the source.  Stick with me, this is where it gets interesting.  Brain cancer cells usually lose the sophisticated metabolic machinery required to burn both glucose and ketones.  They still depend solely on glucose.  When they are faced with less glucose and more ketone bodies, they can only use the former.  Hence they react as if they were being starved.  When this happens, they can't produce the energy required to sustain their rapid growth rate, at least this is what should happen theoretically.  But does it really occur this way.  That is what several fascinating studies suggest.

In an article published in the Journal of the American College of Nutrition (1995;14:202-208) the impact of a diet that decreased serum glucose levels and increased ketone levels in two patients with advanced malignant astrocytomas (brain tumors) was studied.  To determine the effect on the metabolic rate of the tumors a special type of scanning technique was used.  It is called positron emission tomography, or PET.  Since tumors can't burn ketones, their metabolic rate is determined by how much glucose they burn.  That is precisely what PET scans measure.  After only one week on the diet these patients had their PET scans.  Amazingly, the metabolic rate of the tumors was cut by 20%.  This was the end of the study. 

What we really want to know is what effect this type of diet will have on the growth of the tumor.  This information can only be provided by controlled clinical trials.  To make sure they are comparing apples with apples, scientists need to perform the experiment in identical animals with identical tumor types.  When this was done they observed a 35-65% decrease in tumor growth and a marked increase in function and survival.  If confirmed in humans, this would be extraordinary indeed.      

The type of diet used was a calorically-restricted ketogenic diet.  One version of the diet was enhanced by the provision of MCT oil (medium chain triglyceride) which is rapidly converted to ketones in the body.  For information in how the diet was configured you can see the published results in the Journal of the American Dietetic Association (1995;95:693-697).