Medications Archives

Coconut Oil and Alzheimer’s Disease

Back in July 2008, Dr. Mary Newport wrote a case study, “What if there was a Cure for Alzheimer’s Disease and no one Knew?” However, last month it was brought to our attention again when cbn.com did an interview with Dr. Newport (see video below). In her case study, she writes about ketone bodies which serve as fuel for your brain that your body makes when you ingest coconut oil. This may prove to be highly beneficial in fighting Alzheimer’s disease (AD).

Several people sent me e-mail about this interview and since then I’ve been researching various Web sites as well as checking out local retail outlets for coconut oil. Health food stores and specialty supermarkets carry coconut oil in capsule form, although you may be able to find some health food stores carrying the actual oil (I was pleased to find it in a health food store in my area). However, with experts recommending between two and three tablespoons of coconut oil daily for prevention of AD and up to five tablespoons for AD and with each capsule having only about 500 to 1000 mg of oil (each tablespoon is equal to about 15 grams), you would need at least 15 capsules to get one tablespoon. Taking 45 to 75 capsules a day would be quite costly and ill advised.

One of the top producers of coconut oil is the Philippines so I visited a local Filipino market in southern California that was recommended by a Filipino acquaintance who uses coconut oil. It is recommended that you start slowly, and thus far I’ve used about a teaspoon in my morning oatmeal. (I’m trying to get used to greasy oatmeal). I’ve also tried substituting the olive oil in my salad with the coconut oil (the taste did not agree with me). Finally, I substituted one tablespoon of coconut oil for butter and syrup on my pancakes and that was by far the tastiest option. But since I don’t eat pancakes every day, I continued to experiment and now I find that adding coconut oil to a small amount of coffee or tea works well.

Bruce Fife, ND, author of Stop Alzheimer’s Now!: How to Prevent & Reverse Dementia, Parkinson’s, ALS, Multiple Sclerosis & Other Neurodegenerative Disorders cautions that proper diet is also a necessary component. Simply adding coconut oil to the diet will produce disappointing results. He says that the fundamental problem associated with Alzheimer’s disease is the inability of the brain to effectively utilize glucose, or blood sugar, to produce energy. The brain then needs another source of energy and this comes in the form of ketone bodies produced in the liver. Medium chain triglycerides (MCTs) like coconut oil are converted into ketones in the body.

There are different methods of producing coconut oil. According to Tropical Traditions, a producer of coconut oil, “Virgin Coconut Oil can only be achieved by using fresh coconut meat or what is called non-copra. Chemicals and high heating are not used in further refining, since the natural, pure coconut oil is very stable with a shelf life of several years. There are currently two main processes of manufacturing Virgin Coconut Oil:

1. Quick drying of fresh coconut meat which is then used to press out the oil. Using this method, the coconut meat is quick dried, and the oil is then pressed out via mechanical means. This is the most common type of “Virgin” or “Extra Virgin” (see below) coconut oil sold in the market today that you will find in stores. It is mass-produced.

2. Wet-milling. With this method the oil is extracted from fresh coconut meat without drying first. “Coconut milk” is expressed first by pressing. The oil is then further separated from the water. Methods which can be used to separate the oil from the water include boiling, fermentation, refrigeration, enzymes and mechanical centrifuge.

Currently there is no known medication to prevent or stop Alzheimer’s disease. Coconut oil offers hope for this disease affecting 5.4 million Americans. Should you decide to try it, let me know how you’re ingesting it.

Possible New Drug for Alzheimer’s Disease

Taken orally, E64d, a type of cysteine pro-tease inhibitor, has shown to reduce the buildup of β-amyloid (Aβ) present in animal model brains used in Alzheimer’s disease studies. This action resulted in significant improvement in memory loss. The findings were discovered by a group of researchers from the American Life Science Pharmaceuticals-San Diego, University of California-San Diego and the Medical University of South Carolina. Their findings will be published in the Journal of Alzheimer’s Disease in the September issue.

Dr. Vivian Y.H. Hook praises the discovery since according to her, E64d has been proven safe for human consumption and that the results of the research has excellent potential for use in the treatment of Alzheimer’s disease.

It is known that there is a co-relation in the increase in the levels of Aβ peptides, amyloid plaques and the onset of loss of memory. Aβ peptides are separated from the APP or amyloid precursor protein by the β-secretase. The peptides later develop plaques in the regions of the brain associated with memory.

E64d reduces the level of Aβ by blocking the β-secretase from taking apart the amyloid precursor chain. However, researchers also discovered that it also increases BACE1 activity, a protease known as the principal β-secretase. E64d seems to decrease Aβ in the lower brain by blocking the β-secretase activities of Cathepsin B, another protease.

According to Hook, the study shows that Cathepsin B may be used for the inhibition of the production of Aβ and the resulting improvement of memory function. The finding is important since inhibition of β-secretase and Cathepsin-B is possible without the inhibition of BACE1.

The research involved the use of young and old mice with transgenic Alzheimer’s. Young mice fed with E64d avoided memory loss while old mice showed improved memory.

The study is not new — it actually used a previous work where Cathepsin B was also utilized for memory enhancement. In that study published in 2008, though, Cathepsin B inhibitors were directly administered into brains of mice with AD. The recent study shows that oral administration was effective and could pave the way for future human clinical trials.

The study is co-authored by Dr. Gregory Hook of San Diego’s American Life Science Pharmaceuticals and Dr. Mark Kindy of the Medical University of South Carolina, the Ralph H. Johnson VA Medical Center, and Applied Neurotechnology, Inc. in Charleston, SD. The recent study also received some support from the National Institutes of Health and the Alzheimer’s Drug Development Foundation’s National Institute on Aging.

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Statins for Treatment of Alzheimer’s Disease

Alzheimer’s disease (AD) is a disease of the brain and the most common form of dementia that causes problems with daily living, memory, thinking, and behavior.  While statistics vary, as many as 5.1 million Americans suffer from Alzheimer’s.  This estimate counts for as many as 70 percent of dementia cases in adults 60 or older.  While there are several recommendations for AD prevention, including reducing cholesterol, researchers have yet to find a cure for this form of dementia.  Although cholesterol lowering drugs such as statins can slow down the process of Alzheimer’s development, there is a large debate on whether these drugs are effective for reducing damage in patients with Alzheimer’s. How do statins work and how are they used in the treatment of Alzheimer’s disease?

Statins are prescription drugs that are used to lower blood cholesterol levels by blocking chemicals in the liver that produce cholesterol.  While many may ask how a cholesterol lowering medication could treat Alzheimer’s, many studies have proven that statins have a positive effect in the body for those who suffer from the disease.  High cholesterol levels are recognized as one of the common risk factors that leads to the development of Alzheimer’s.  By lowering these levels early, Alzheimer’s development can be slowed.

In addition to eliminating one of the most common risk factors, statins are known to protect nerve cells against damage in the brain.  The nerve cell damage that is caused by Alzheimer’s is what leads to memory loss and difficulty comprehending.  By reducing cell damage in the brain, studies published by the Journal of Alzheimer’s Disease, have proven that Lovastatin prevents the death of cells in the brain to keep the brain responsive.  Laboratory studies at the University of Groningen have shown that the neuroprotective mechanism slows the progression of the disease.

While there is skepticism relating to Alzheimer’s and statins, studies have shown that if statins are administered in the early stages of Alzheimer’s, patients will not advance through the disease as quickly.  While statins are not a cure or a way to prevent the disease entirely, they are a protective measure that could have a beneficial effect.

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Hope for Alzheimer’s Disease

I know it’s difficult for families with an Alzheimer’s disease patient. What looks like so much promise for those of us who are candidates down the road, will not be a solution for those currently experiencing this dreadful disease. What’s available today are only five medications discussed previously here. These may slow down the progression of the disease, but they also have side effects (like most prescription medications) and are not permanent solutions. There are also many clinical trials going on. The Alzheimer’s Association is an excellent place to start your research.

This year there has also been a greater focus on caregivers because of organizations like the Alzheimer’s Foundation of America and celebrity involvement. Earlier this month, Al Roker of the Today show, hosted the first telethon, Together for Care, for the foundation. See video below.

Occasionally, we hear good news such as “New Piece of Alzheimer’s Puzzle Identified” which is very encouraging. Sometimes encouraging news turns out to be disappointing, but there’s always hope. In this new study, researchers from the Mayo Clinic in Rochester, Minnesota found that endothelial dysfunction increases production of proteins that provide the raw material for the amyloid plaques seen in the brains of people with Alzheimer’s disease. Simply put, endothelial dysfunction is a problem with the lining of the blood vessels. Read the full news release here.

So, as we turn the page to a new calendar year, let us keep the hope in our hearts. I wish all of you and your families a heart-warming new year.

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Most people did not believe Columbus when he said the world is round. Now in the world of Alzheimer’s disease research, Sam Gandy, M.D., Ph.D., Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer’s Disease Research Center, Mount Sinai School of Medicine, has created quite a stir. He states, “The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer’s pathology. But there has been a longstanding debate over whether plaques are toxic, protective, or inert.”

So instead of the belief that brain cells are being destroyed by the sticky plaques, Gandy and his researchers think that there are free-floating clumps of protein that may be the culprit and that the sticky plaques may actually be protecting the body against these toxic clumps.

According to the Mount Sinai School of Medicine:

Several research groups had previously proposed that rather than plaques, floating clumps of amyloid (called oligomers) are the key components that impede brain cell function in Alzheimer’s patients. To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.

The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers. Moreover, when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before.

This will take research in a new direction. Drugs that target plaques may not be of any help and could even make the disease worse.  Gandy works with specially engineered mice and William Thies, Chief Medical Officer, Alzheimer’s Association, warns us that the leap from mice to men is a long one and until Gandy’s experiments can be duplicated, drug companies will not be investing billios of dollars into creating new medication.

When Andrew Dillin, Ph.D., of the Salk Institute for Biological Studies started pursuing the oligomer theory several years ago, he said the the idea was so controversial that some scientists would walk out of the room when he made his presentations at conferences. Now, many top researchers are convinced.

More about oligomers and plaques in the next post.

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In September 2008, the International Journal of Geriatric Psychiatry published an interesting article: Smell test predicts performance on delayed recall memory test in elderly with depression. Who would’ve thought that a smell test might be a tool to forecast cognitive impairment. But it turns out that the elderly, particularly those diagnosed with depression, have an increased risk for cognitive dysfunction and dementia.

According to sensonics.com, Sensonics, Inc. tests can be used to detect smell loss but cannot be used alone to diagnose disease. Smell and taste monitor the intake into the body of all nutrients and airborne chemicals required for life.

Here is an abstract of the study that was done.

Purpose

To assess the validity of the CC-SIT (Cross-Cultural Smell Identification Test) as a screening test for cognitive impairment in elderly with depression.

Methods

Forty-one patients, aged 60 and over, were assessed with the CC-SIT and CVLT (California Verbal Learning Test) after three months of treatment of a Major Depressive Episode (DSM-IV) at the Day Hospital for Depression, Baycrest. Patients already diagnosed with dementia, or other psychiatric and neurological disorders, were excluded. Receiver Operating Characteristics (ROC) analysis was applied to assess the CC-SIT’s accuracy in identifying individuals with impairment (2 SD below the mean for age and education or less) on CVLT delayed recall trials.

Results

Forty-one patients (33 women and eight men) were assessed. Mean age was 76.8 (SD: 6.5), mean HRSD scores before treatment was 22.0 (SD: 5.1). Nine patients had impairment on CVLT delayed recall measures. The area under the ROC curve was 0.776 (95% CI = 0.617-0.936).

Conclusions

Our results support the use of the CC-SIT as a screening tool for cognitive impairment among elderly with depression as an indicator for the need of a comprehensive neuropsychological evaluation. Replication with larger samples is necessary. Copyright © 2008 John Wiley & Sons, Ltd.

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