Diagnosis 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.

Scientists are looking at a biomaker that may possibly aid in the identification of individuals with mild memory problems who will eventually develop Alzheimer’s disease. The finding, which was published in the online version of Neurology, the journal of the American Academy of Neurology. It is believed that the new biomarker may prove to be more accurate compared to already established biomarkers.

According to the study author Robert Perneczky, MD, of the Technical University Munich in Germany, identifying individuals who will have Alzheimer’s disease earlier will be an important development. Once treatments that can be used for the prevention of the disease are available, it will become easier to treat and even prevent memory loss.

Fifty eight people with mild cognitive impairment (MCI) participated in the study. It is estimated that as many as 15% of the people who have MCI will develop Alzheimer’s every year.

Cerebrospinal fluid was taken from each participant and tested for certain proteins. Participants were then studied for about three years. Of the participants, 21 developed Alzheimer’s, 27 remained with MCI while 8 people regained normal cognitive skills. Researchers discovered that participants who later developed Alzheimer’s had significantly high levels of sAPPβ or soluble amyloid precursor protein beta in their cerebrospinal fluid.

Based on their findings, the researchers discovered that the person’s age, a protein called tau, and sAPPβ were excellent predictors of future cases of Alzheimer’s. Using these factors as a basis, it was easier to predict if an individual ran the risk of developing the disease. The accuracy for this prediction is pegged at about 80%.

A protein amyloid known as Aβ1-42 or amyloid beta1-42 was once considered one of the biomarkers significant to Alzheimer’s disease. However, it was not used as one of the predictive factors in the study.

The results, Perneczky said, suggest that sAPPβ could be useful as a biomarker and that it may even be better than Aβ1-42 for use in diagnosing Alzheimer’s earlier. The reason for this may be that Aβ1-42 can only indicate events at a later stage – events that already point to the accumulation of amyloid plaques in the brain. Since sAPPβ can be used as a critical initial step in determining if the disease will develop, it is likely to provide a more accurate indication on important pathological events.

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Researchers at the Research Institute of the McGill University Health Centre (MUHC) have discovered a new blood test to diagnose Alzheimer’s disease (AD) which was published in the May issue of the Journal of Alzheimer’s Disease.  They have found a distinctive biochemical diagnosis in AD patients according to senior author Dr. Vassilios Papadopoulos.

Papadopoulos reports that post-mortem analysis of brain tissue has been the only definitive tool for AD. Now this clinical study shows that a non-invasive blood test based on a chemical process may be able to diagnose Alzheimer’s disease at an early stage and could be differentiated from other types of dementia.

This blood test is based on the production of a brain hormone called dehydroepiandrosterone (DHEA) which is present at high levels and has a wide range of biological effects. The researchers used a chemical process called oxidation to promote the production of DHEA in blood taken from non-Alzheimer’s patients. However, blood from AD patients did not produce an increase of DHEA.

The researchers were able to accurately and repetitively detect AD with small samples of blood. Although there are many possible therapies in clinical trials, there must first be an accurate diagnosis. Together with clinical findings, the blood test could be used to diagnose AD at a very early stage and the appropriate therapies could be monitored.

Source: MUHC Newsroom

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According to an article published in Translational Neuroscience, a study done at the Mount Sinai School of Medicine found that patients with Alzheimer’s disease (AD) have lower glucose utilization in the brain than those with normal cognitive function. The decreased levels could possibly be detected 20 years prior to the first symptoms of AD. With this knowledge comes the possibility of developing new therapies of preventing the start of Alzheimer’s.

In the article reported at NeuroScienceNews.com (http://tinyurl.com/3ompjp6), the study used mice modified to develop Alzheimer’s disease. The research team found that when β-amyloid, an abnormal protein linked to Alzheimer’s disease, starts to become detectable in the brain in its soluble toxic form, the mitochondria, or “power plants” of the cell where glucose is converted into energy, became impaired. Within the equivalent of about 20 human years, mice with decreased energy metabolism developed signs of Alzheimer’s disease such as cognitive defects and impairment of the synaptic terminal, the area of brain cells important in memory formation.

“This evidence in mice validates that the diagnosis of probable Alzheimer’s disease may be the end result of impairment in brain cell energy production,” said the study’s lead author, Giulio M. Pasinetti, MD, PhD, The Saunder Family Professor in Neurology, and Professor of Psychiatry, Geriatrics, and Adult Development at Mount Sinai School of Medicine. “Identifying that mitochondrial impairment is evident years earlier than cognitive defects is a major breakthrough.”

“This new evidence could revolutionize the way we design interventions,” said Merina T. Varghese, MD, co-author of the study and Postdoctoral Fellow in Neurology at Mount Sinai School of Medicine. “This study sets the stage for the development of potential novel preventions or therapies to apply in humans, even when they have normal cognitive function, to prevent the eventual onset of Alzheimer’s disease.”

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Genes Linked to Alzheimer’s Disease

The Miami Herald reported on Sunday that research institutions, including the University of Miami  have identified four genes implicated in causing Alzheimer’s disease (AD). There may be up to 100 genes linked to AD, but only a half dozen or so of them are known at this time. This is the biggest such study to date and marks a monumental breakthrough that could lead to identifying almost all of the suspect genes in three to five years, according to Dr. Margaret Pericak-Vance, director of the John P. Hussman Institute for Human Genomics and who led the analysis of the genes.

Pericak-Vance was instrumental in finding the first genetic evidence for Alzheimer’s in the 1990s. She discovered another gene last year and now is in on the discovery of four more. Although it used to be slow, with new technology it should speed up the search.

The University of Miami has a  $1-million-plus “Illumina Platform,” which uses computer chips to compare, contrast and analyze genetic-factor samples from thousands of test subjects. Such advanced equipment made it possible to process evidence from 11,000 people with Alzheimer’s and a nearly equal number of those without it.

The new methods also are enabling an even larger gene study now starting by UM’s new International Genomics of Alzheimer’s Project, along with other U.S. and French researchers. According to Pericak-Vance, one major value of identifying more genes implicated in Alzheimer’s is that it will help pharmaceutical companies create “designer drugs” aimed specifically at the faulty genes. It also will help with earlier predictions of who is at risk, so they can make lifestyle changes to try to slow its progress,

The current study results appear in this month’s issue of Nature Genetics. It’s a collaboration of investigators from 44 universities and research institutions led by Gerard Schellenberg at University of Pennsylvania School of Medicine, Lindsay Farrer of the Boston University School of Medicine and UM’s Pericak-Vance.


Last week the Alzheimer’s Association released its new 2011 Alzheimer’s Disease Facts and Figures report. The statistics are grim. It is the sixth leading cause of death and of the top 10, it’s the only one where we do not know exactly how it can be prevented, cured, or slowed. Yes, we do have many research studies going on, but there has not been anything definitive. Most of the studies are just the tip of the iceberg and require further research. Some have produced disappointments. Highlights from the report include the following:

  • An estimated 5.4 million American’s have Alzheimer’s disease. Another American develops Alzheimer’s disease every 69 seconds.
  • In 2010, 14.9 million family and friends provided 17 billion hours of unpaid care to those with Alzheimer’s and other dementias.
  • The cost of caring for those with Alzheimer’s to American society will total $183 billion in 2011.
  • Deaths from Alzheimer’s increased 66 percent between 2000 and 2008, and Alzheimer’s is the only cause of death among the top 10 in America without a way to prevent, cure, or even slow its progression.

The complete 2011 Alzheimer’s Disease Facts and Figures report allows you to get information specific to your state. Let’s hope we will have a major breakthrough this year and the 2012 report will be a lot more promising.

The Alzheimer’s Association produced a video capturing these statistics.

Meditation is often associated with words such as relaxation, peacefulness, and calm. Researchers and scientists have for some time now endorsed the value of meditation. Not only do people who practice meditation feel calm and happy, they also report enhanced cognition and memory abilities. Although researchers at the Massachusetts General Hospital did not include those with Alzheimer’s Disease (AD), they sought to study the benefits of mindfulness meditation training and in my opinion, this can certainly apply to the AD population.

A recent study that was supported by the Institutes of Health, The Mind and Life Institute and the British Broadcasting Company studied the changes in the brain after an 8-week mindfulness meditation program. The findings from the study have been published in the Psychiatry Research: Neuroimaging, January 30 issue. It reports that this is the first time that changes in the brain and related improvements have been documented due to meditation over a period of time.

Magnetic Resonance Images (MRI) were taken two weeks before and after the Mindfulness-Based Stress Reduction Program Program was conducted, for both the control group and the group that practiced mindfulness meditation. This form of mediation focuses on the feelings, emotions and state of mind in a non judgmental manner. The study group conducted meditation exercises for about 27 minutes daily. Their responses to a mindfulness questionnaire showed a marked improvement when compared with those made before the study began.

MRI after the mindfulness meditation program focused on parts of the brain that have shown improvement in earlier studies. The images showed an increase in the grey matter density of the hippocampus, a part of the brain that affects memory and learning. Similarly, brain parts that are related with compassion, self understanding and introspection also increased in size.

The participants reported reduced stress and this was correlated with the reduction in density at the amygdala, the part of the brain that affects the stress and anxiety that an individual experiences. However the insula, which is believed to be associated with self awareness, did not show any changes. More research in this direction may be required.  The MRI of the control group showed no changes in the same period of time.

There is no known cure for Alzheimer’s disease, but mindfulness meditation may aid Alzheimer’s disease patients in dealing with AD more effectively. Britta Hölzel, PhD, is first author of the paper and a research fellow at Massachusetts General Hospital and Giessen University in Germany. James Carmody, PhD, of the Center for Mindfulness at University of Massachusetts Medical School is the co-author.

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Researchers at the University of South Florida’s Department of Psychiatry and the Center of Excellence for Aging and Brain Repair have discovered that the CD45 molecule, a receptor on the surface of the brain’s microglia cells (cells that support the brain’s neurons and also participate in brain immune responses) is a new focus for the prevention of detrimental immune responses which are determined as elements in the development of Alzheimer’s disease (AD). Their findings were reported in the Journal of Neuroscience.

Previous studies by the USF researchers demonstrated that triggering CD45 was advantageous because it blocked a very early step in the development of Alzheimer’s disease. In the current study, the researchers showed in Alzheimer’s mouse models that a loss of CD45 led to dramatically increased microglial inflammation.

Although the brain’s immune response is associated with Alzheimer’s disease pathology, “this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation,” said study senior author Jun Tan, MD, PhD, a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran’s Hospital.

The investigators also found a raised level of harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.

“In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer’s mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons,” Dr. Tan said. “These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor.”

The next step is to apply these findings to develop new Alzheimer’s disease treatments, said Paula Bickford, PhD, a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran’s Hospital. “We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain’s immune cells,” Dr. Bickford said.

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Last week Reuters reported that international experts on Alzheimer’s disease (AD) are recommending that a new criteria for diagnosing Alzheimer’s should be used considering the recent scientific discoveries which includes the use of biomarkers (biological signals) which can determine if a person is at risk for developing the disease well before there are any symptoms. Hence, even as many as 10 years before any symptoms begin to show, it would be best to intervene. Recent studies have shown that brain scans, spinal fluid analyses, and other tests can possibly predict who will develop AD. With this knowledge, researchers and pharmaceutical companies can develop new drugs.

According to caring.com, the new criteria for diagnosing Alzheimer’s is much more accurate. It requires:

  • An early and significant episodic memory impairment
  • Gradual and progressive change of memory for more than 6 months
  • Objective evidence of recall memory that does not improve or does not normalize with adequate cueing or recognition testing

PLUS one or more of the following supportive features (the new early markers for increasing the specificity of a patient having AD):

  • Medial temporal atrophy on MRI
  • Abnormal spinal fluid concentrations of (1) amyloid, (2) total tau or (3) phospho-tau
  • Specific patterns of PET scanning producing hypometabolism of bitemporal parietal regions or Pittsburgh compound B
  • Proven AD autosomal dominant mutation within the immediate family

The criteria currently being used was adopted in 1984. In light of what the current research is showing, we are headed in the right direction to try to intervene as early as possible.