Coconut Oil, Ketones and Alzheimer's

Tuesday, September 26, 2017


Awakening From Alzheimer's Series

This is a very helpful and informative FREE web series currently in progress with a new episode each 24 hours. The entire series will be repeated on October 6 through 9. I am one of the speakers. Other featured speakers are Dr. Dale Bredesen, who has a studied protocol for Alzheimer's that has put some people in the earlier stages back to work, Dr. David Perlmutter, a neurologist whose neurosurgeon father suffered from Alzheimer's, and has written excellent books on the microbiome and effect of gluten on Alzheimer's and other disorders.  Dr. Dominic D'Agostino and Dr. Angela Poff, who study many aspect of ketones including cancer, and many more...

Watch as the world’s leading experts in Alzheimer’s and dementia share their most effective breakthroughs and discoveries after decades of grueling research in this groundbreaking series.
Join hundreds of thousands of people and watch the series trailer here ► https://wr374.isrefer.com/go/trailerfba/marynewport

https://membership.awakeningfromalzheimers.com/wp-content/uploads/2017/08/AFA2017Trailer-AdImage-1.jpg

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Tuesday, May 22, 2012

Fourth Anniversary of Steve's Ketone Rebirth (May 21, 2012)


Yesterday, May 21, 2012, was the fourth anniversary of the day Steve started taking coconut oil to provide ketones as an alternative fuel to glucose for his brain, with very positive results.  He is now 62 years old and in his eleventh years of symptoms related to early onset Alzheimer's disease.  Much has happened in these four years, both setbacks and recoveries. Fortunately, we are in a recovery phase.  We have surprises all of the time that lead me to believe that everything he was is still in there, but he has a problem getting access to it.
I will post a point by point update in the near future.
In the meantime, here is a little bit of my funny old Steve coming out to visit yesterday:

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Monday, August 1, 2011

Some YouTube testimonials - Alzheimer's and Coconut Oil

There are two very interesting videos posted on www.youtube.com by people with Alzheimer's who have had dramatic responses to coconut oil, as well as a video from a man whose "brain fog" lifted with coconut oil. If you go to YouTube and do a search for Alzheimer's and coconut oil they will pop up. One is titled: Our Story: Alzheimer's and coconut oil; Ian Blair Hamilton and Cassie Bond; the second is called "Bruce is overcoming dementia..." and the third "Brain Fog and Coconut Oil".

We are having a good summer. Steve seems to be very stable for the past six months after recovering from his setback during the holidays that seemed to be related to taking prednisone for a gout flare-up, and he is about the same as he was a year ago. He is still taking a mixture of MCT and coconut oil 3 tablespoons three times a day and also a fourth dose at bedtime of 2 tablespoons, which was added when he was having some difficulty sleeping and seemed a bit more confused in the morning. He is now sleeping well and back to baseline in the morning.

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Friday, February 4, 2011

Dr. Veech needs an angel

Coconut oil and MCT oil provide relatively low levels of ketosis, however, the ketone ester made and studied in the lab of Dr. Richard Veech can provide levels at least 10 times as high. As noted in the article that is the subject of my previous post, the amount of energy provided to the brain is directly proportional to the level of ketones in the blood. Thus his ketone ester could provide as much as 60% of the brain's energy requirement compared to perhaps 5-10% by MCT oil/coconut oil.

There have been more than 700,000 hits on my website www.coconutketones.com. I am pleased that very many people now know that ketones may provide an alternative fuel to glucose in the brain for people with Alzheimer's and other neurodegenerative diseases. There must be someone out there who can help provide funding for continuation of Dr. Veech's very important work. He has only enough funding from the NIH to continue the research in his lab and production of the ketone ester until June 2011. He is in need of a charitable or government source of funding to continue just this basic work. He wishes to perform a pilot study of Parkinson's and the ketone ester. This would be a 28 day study. He lacks funding to even begin this short term study. Thereafter, he wishes to study Alzheimer's and this would require $10 to 15 million to manufacture enough ketone ester and fund the clinical trial. Alzheimer's is so complex and symptoms so variable from person to person, as compared to Parkinson's, that a two year study would be required to determine that the ester is effective.

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New brain metabolism and ketone review article

I recently received this new article that discusses in great detail what is known about brain metabolism as we age and the potential for alternative fuels to glucose to prevent or stabilize the progression of Alzheimer's disease:

"Brain fuel metabolism, aging, and Alzheimer’s disease",
Stephen Cunnane Ph.D., Scott Nugent B.Sc., Maggie Roy M.Sc., and others, Nutrition, January 2011

Here are some important excerpts from this article:

"The recent development of 11C-acetoacetate as a ketone tracer for PET studies opens a new window to compare brain metabolism of glucose and ketones in the same individual. If brain
ketone metabolism is not lower in AD or is less affected than glucose metabolism, one potential strategy to improve brain fuel availability and reduce the risk of AD that has already been targeted in clinical studies would be to develop a way to safely and reliably provide the brain with ketones as an alternative fuel to glucose..."

"Whether or not mitochondrial dysfunction reflects genetic or metabolic disturbances,
clinical trials attempting to redress the energy deficit in the AD brain suggest that cognitive function can be at least transiently improved if more fuel (glucose or ketones) can be
supplied to the brain."

"In carriers of apo E4, small areas of lower brain glucose metabolism are observed at an age
as young as 30 y old, e.g., 30-40 y before clinical onset. Indeed, we see an inverse relationship between CMRg in several brain regions and fasting plasma insulin, so brain metabolism
seems to be sensitive to even mild disturbances in systemic insulin control even if no clinical symptoms of cognitive decline are observed. Compared to non-carriers of apo E4, carriers have altered u3 [omega-3] fatty acid metabolism and higher measures of oxidative stress in the brain, both of which may contribute to a higher risk of early onset of brain hypometabolism. If brain hypometabolism can be present before clinical symptoms are apparent, this does not prove that hypometabolism is the earliest event in AD. However, to the best of our knowledge, hypometabolism is currently the earliest measurable abnormality in the brain that is connected to AD so its features and the reasons for it should shed light on the etiology of AD."

"The cerebral metabolic rate of ketones (CMRk) varies directlywith their blood concentration, starting at very low ketone concentrations...Hence, at a plasma b-hydroxybutyrate [one of the primary ketone bodies] concentration of 0.3-0.5 mM, such as can be achieved during 12-24 h fasting, b-hydroxybutyrate supplies 3-5% of whole brain energy requirements. As plasma ketones rise, CMRk also rises such that at a b-hydroxybutyrate of about 1.5mM, ketones provide about 18%, and at 6 mM, they provide about 60% of brain fuel." [Dr. Richard Veech's ketone ester can provide levels this high].

"Acute, controlled human experiments show that ketone infusion or ketogenesis inhibits the cognitive and behavioral sequelae of acute, experimental hypoglycemia, both in healthy
adults and in type 1 diabetes. It is generally assumed that the cognitive effects of hypoglycemia can be prevented by ketones because they seamlessly replace glucose to meet the brain’s energy requirements. However, acutely raising plasma ketones also increases cerebral blood flow in humans, an effect that may contribute to their beneficial impact on cognition during hypoglycemia. Studies in humans and animal models suggest further protective effects of ketones in the brain after ischemic insult [lack of oxygen/stroke] and other treatments damaging neuronal function."

"More recent controlled clinical trials confirm that short-term improvement can occur in cognitive tests when individuals with mild to moderate AD are provided with an exogenous source of glucose, ketones, insulin, or insulin sensitizers. These clinical studies show that the
affected brain regions in AD are at least partially viable and that cognition can improve when exogenous fuel supply to the brain is increased. In two of these studies, ketogenic supplements
based on medium chain triglycerides were used, thereby permitting a relatively normal choice of meals. Medium chain triglycerides have long been known to be ketogenic because they contain medium chain fatty acids (octanoic [8:0] and decanoic [10:0] acids), which do not require activation by CoA to enter mitochondria. The mild beneficial effects on cognition and relatively good tolerance to the doses of medium chain triglyceride used are promising, notwithstanding the possibility that carriers of apo E4 with AD derive little benefit from this treatment [Dr. Newport's comment: per one of the authors of the MCT oil studies, many of the ApoE4+ individuals did experience improvement, as a group when data was combined on the average they did not]. The explanation for the beneficial effect of mild, experimental ketonemia on cognition in AD may be as simple as exchanging one brain fuel for another as occurs in
fasting or starvation. It may also be due to the observation that although glycolysis may be impaired in the AD brain, CMRk and metabolic capacity to use a fuel other than glucose may
both be relatively normal in AD."

"...two observations in particular support the notion that the neurons affected in AD are still functional: (1) in AD, brain ketone uptake is apparently normal or at least less impaired than is glucose, and (2) there is a functional response to nutritional supplements that increase brain fuel
availability, particularly ketones. Hence, if brain fuel metabolism could be optimized or even partially returned toward normal, the risk of further cognitive decline may diminish. Raising plasma ketones to 0.4-0.5 mM would contribute to 5-10% of the brain’s energy requirements, which is equivalent to the early cortical glucose deficit in those genetically at risk AD. Such a mild, safe level of ketonemia is achievable with ketogenic supplements, so if implemented before symptoms develop, it seems plausible that they could diminish the risk of further metabolic deterioration and clinical onset of cognitive decline."

Regarding Omega-3 fatty acids:

"The u3 [omega-3] polyunsaturated fatty acid, DHA, is now widely understood to have an important role in mammalian brain development...Insufficient dietary intake of DHA and low levels of DHA in the hippocampus may have a role in cognitive decline in the elderly and/or AD. Hence, the low intake of DHA now widely but not universally reported in AD may contribute to the evolution of cognitive decline because of its role in brain glucose transport and in other aspects of brain function and structure. This emerging role of DHA in brain energy metabolism could be linked to the early presymptomatic onset of brain glucose hypometabolism in AD, at least in carriers of the e4 allele of apoE4. Nevertheless, such an effect probably involves relatively subtle changes in DHA metabolism because plasma DHA appears to be higher in the healthy elderly and is widely variable in AD."

Dr. Newport's comments:

The bottom line here, to try to prevent or stabilize AD, include medium chain fatty acids (coconut oil, palm kernel oil and MCT oil are the richest sources) in the diet to provide ketones as an alternative fuel to glucose AND eat fish (especially salmon) and/or take a supplement of marine based omega-3 oil (fish oil for most of us; algae based oil for vegans found in brands that are marketed to pregnant women).

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Mirrors and Windows - Temporary solutions

This post has nothing to do with coconut oil!

Many people with Alzheimer's have an interesting interaction with mirrors, windows and other reflective surfaces, sometimes pleasant and other times not so pleasant. This may be more prominent in the evening when dark windows may present disturbing images. We have seen some of this in Steve with glass doors and windows facing our courtyard that were not covered with curtains. He feels like there are a lot of people/strangers in the room when he sees reflections in a dark window.

In our kitchen, we put up sheer cafe curtains with a spring rod that can easily be readjusted to any height. The curtains are positioned so that the top is just above his eye level. For the glass doors I also put up sheers that are positioned to allow light to come in above and below, but again reach to just above eye level to eliminate the reflection.

There is also privacy film that can be placed on mirrors or windows as an easier solution than taking down the mirrors. We used some of this on the sidelights to our doors. I have found this at stores such as Home Depot, and Bed Bath and Beyond. There are two types - one is very much like holiday window decorations, that sticks easily to the surface and peels right off. There is another type, much harder to install, that requires spraying the surfaces with water then burnishing out the bubbles with a squeegy; this is much more difficult to use and would probably be a nightmare to remove as well. Both types have a number of different patterns available.

In restaurants, the person may be more comfortable if facing away from any dark reflective windows, if at all possible. If you are in a restaurant and your loved one becomes unsettled, consider the possibility that window reflections could be the issue.

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Saturday, December 11, 2010

More on herpes simplex virus and Alzheimer's

On a previous post, I discussed the research conducted by Dr. Ruth Itzhaki in England providing very strong evidence that recurrent infection with herpes simplex in the brain may be the cause of Alzheimer's in certain people, those who are ApoeE4+. Please look back for the details.

Nearly all of us acquire herpes simplex virus at some point and then carry it. When we are young most of us can apparently control these infections more so than when we age. Some people, though, have recurrent outbreaks, usually as fever blisters, or for some, genital lesions. Some people with active virus show no outward symptoms at all. Reactivation of the virus produces inflammation in the brain. Most of the episodes are mild, but over time the effects could be cumulative. An infection such as this could explain why Alzheimer's begins in certain parts of the brain and eventually spreads to other areas. It could also explain the fluctuations that we often see in symptoms - when the virus is latent the person may do a little better, when there is a reactivation and greater inflammation, the person may get worse, a sort of two steps forward (worsening) and one step back (improvement) kind of process.

Steve has a long time history of lengthy outbreaks of fever blisters on his mouth, and had an outbreak around his eye and was quite sick at age 29. I strongly believe that, at least in his case, herpes simplex may be the cause of his Alzheimer's disease and this particularly bad episode could explain why he became symptomatic so early.

Now another group led by Dr. Nancy Sawtell at Cincinnati Children's Medical Center is providing more proof that herpes simplex may be the culprit for some people. She was inspired to do this work after Dr. Ruth Itzhaki visited her lab a few years ago. They have been working with mice in which the Apoe4 allele has been "knocked in" and infected them with the virus. They found that a lot more virus got into the brains of the Apoe4 mice than the non-Apoe4 mice. They are now trying to learn what makes some people more susceptible to the virus. She has found that the viral protein VP 16 is essential in triggering the virus's reactivation. So now they are trying to find substances that may inhibit VP 16 and therefore keep the virus from reactivating.

Dr. Itzhaki, in the meantime, is having difficulty getting funding for continuing her vital research. One skeptic on a review board can keep the board from approving a grant. I believe she and Dr. Sawtell are on the right path - their work needs to continue.

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Thursday, October 21, 2010

2nd Ketone Conference in Edinburgh, Scotland

Steve, our daughter Joanna, and I travelled to Edinburgh, Scotland in early October 2010 to attend the 2nd symposium on ketones called “Dietary Interventions for Epilepsy and Other Neurologic Diseases,” where I presented two abstracts on posters. One was Steve’s case study and the other was caregiver reports of responses of persons with dementia to medium chain fatty acids. I hope to get the chart up on the website very soon. Dr. Veech’s work and/or his ketone ester were discussed in several of the presentations. About 150 people attended, mostly pediatric neurologists, PhD researchers, and dieticians, who are interested in and involved in ketogenic diet and other ketone research. Several of the presenters were from John Hopkins University, where the ketogenic diet has been used for many decades for childhood epilepsy. This diet is used primarily in children who do not respond to anti-convulsant medication, but recently has been used in adults as well. We met a man named Mike from England who had resistant epilepsy who became seizure free on this diet and has remained so for about three years ago. The diet has even been tried as a first line (before medication) at John Hopkins with success in some infants with infantile spasms. About 18-20% of children with drug resistant epilepsy become seizure free and another 35-40% have a reduction in their seizures by at least 50%. They do not know exactly why it works and also why it works in some people and not in others. This is the same thing that we see in our friends with Alzheimer's that some respond to the ketones from coconut oil and/or MCT oil and some do not.
The strictest form of the diet calls for about 75-80% of the total calories to be consumed as fat and the rest as a combination of carbohydrate and protein. The protein is calculated to allow the child to grow, or the adult to maintain lean body mass. Some of the presenters have done research showing that less strict forms of the diet may work for some people. There is an MCT oil modification of the diet, using 60% of the calories as MCT oil, a modified Atkins diet, and the Low Glycemic Index Diet. Any of these diets could be tried with the help of a dietician in someone with Alzheimer’s, Parkinson’s, ALS, traumatic brain injury and potentially some other neurologic diseases. There are some small studies and case studies suggesting that this could be beneficial. One study showed that following stroke, the ketogenic diet can help preserve brain volume.
Another section of the conference focused on cancer and the ketogenic diet with caloric restriction (20-40% less than maintenance calories). Dr. Tom Seyfried presented his research showing that glioblastomas shrink by as much as 80% in response to this type of diet. He believes that at least 80% of cancerous tumors would shrink with this approach, since most cancers can use only glucose as fuel and cannot use ketones. On this type of diet as the blood sugar becomes low, the blood supply and energy to the tumor dwindles as well as the tumor(s), even in the case of metastatic tumors. He has some human case studies as well as plenty of animal studies to support this.
The organizers for this conference were www.matthewsfriends.org and for the previous conference in 2008 www.charliefoundation.org. Both of these organizations were founded by parents of children with epilepsy who responded to the ketogenic diet, and either of these can provide information and dietician help with these diets. The next conference will be in 2012 and they are seriously considering including a section on Alzheimer’s disease.
We had a wonderful time in Edinburgh, although the travelling back and forth is not much fun. Steve did amazingly well, although there was some confusion when we were out after dark. The hardest part was trying to figure out the best times to give him his oil since we were five hours ahead there. It is always good to get back home - much less confusion there!

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Tuesday, August 17, 2010

New animal studies with ketones and coconut oil

I have learned of two new studies that have received funding.

One is at University of Maryland, conducted by Dr. Beverly Teter, in which she will look at whether coconut oil improves the outcome for "Alzheimer" mice. The second is a study of ketones at Univesity of South Florida, Byrd Alzheimer Institute.

They will be looking at ketogenic diet, ketone ester, caloric deprivation and their effect on abnormal amyloid and tau production compared to the "normal" diet in mice.

If these studies have the outcome we hope for, this may spur further human research.

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Bad news for Eli Lilly Drug Trial/ More thought about beta-amyloid and infection

The Eli Lilly drug that has been in phase III trials has been stopped due to increased risk of skin cancer and, even worse, an acceleration of deterioration of AD compared to the placebo, the opposite of what was hoped for. This is yet another sad turn of events. Steve was in this study but we stopped in the winter due to several side effects; I believe he was on the actual drug for only about a month at that point. His hair started to grow out a very light gold color (one of the known effects that didn't bother us)and when we stopped it, the darker hair grew in again. He had a half inch white stripe work its way out to the tips of his hair! I no longer have any regrets that we pulled him out of the study.

I believe the worsening of AD in people who were on this drug supports infection as at least one important cause of Alzheimer's disease. One group has found that beta-amyloid kills microbes; they tested a number of bacteria, all of which were killed by beta-amyloid, and this group is now looking at viruses, such as herpes simplex, and other microbes (Soscia "The Alzheimer’s Disease-Associated Amyloid b-Protein Isan Antimicrobial Peptide" PLOS March 2010,Volume 5, Issue 3, e9505: www.plosone.org). If a drug is used to suppress the production of beta-amyloid and it normally is part of the brain's defense against infection, then infection could spread more readily and potentially cause more extensive damage to brain tissue. Beta-amyloid may be more prevalent in people with AD because they have chronic, recurrent infections that are provoking this response. So the increase in amyloid may be the aftermath, no the cause of, the process that does cause AD.

Drs. Ruth Itzhaki and Mark Wozniak in the UK have done extensive work looking at the herpes simplex virus as a cause of AD (they have numerous papers on this from 2005 through 2009.) This virus causes fever blisters, can cause shingles (along with the chickenpox virus, a close relative), and also genital herpes. Herpes simplex lives within nerves and the nerves to the face around the mouth orignate deep in the brain. Most people carry this and other viruses by the time they reach old age, but they have found that people who are ApoE4+ are particularly likely to suffer recurrent episodes of fever blisters. these researchers have found this virus within about 90% of the beta-amyloid plaques in the autopsied brains they have looked at, which strongly suggests that beta-amyloid is there to defend the brain against it. They have also found in animals that the herpes virus increases production of beta-amyloid and also induces AD-like tau phosphorylation (production of tangles). They want to study whether suppression of herpes virus with anti-viral medication would be beneficial to people with AD, but have had trouble getting funding for this.

Acyclovir, for example, is taken daily orally by many people to suppress the genital variety of herpes simplex, including woman who are pregnant, to try to prevent spread of the nfection to the newborn. Perhaps such a treatment could decrease the number and severity of outbreaks in the brain as well. Lysine (available OTC) is used to suppress herpes infections and the lauric acid (C:12) and capric acid (C:10)found in coconut oil kill herpes family of viruses by dissolving the lipid capsule around the virus.

It could also be that, even though beta-amyloid is there to fight infection, it causes some of the damage as well; if you think about it, whenever there is inflammation, part of the body's defensive reaction to infection, there can be damage/scarring to the nearby tissue from the inflammation. The infectious agent is the cause of the whole process, but the body's defenses can also cause some collateral damage, in order to preserve the whole person.

I hope work by Itzhaki and others studying infection will be taken more seriously so that they can get the funding they need.

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Tuesday, June 22, 2010

Steve's MRI - Two years later

Steve had an MRI at the end of April 2010. His previous MRI was nearly two years ago, just about the time we started using the coconut oil, in June 2008. I am very pleased to report that Steve's MRI was reported as "stable" compared to the previous study. In contrast, his MRI went from normal in 2004 to having significant atrophy by 2008. Normally with Alzheimer's disease, the brain would continue to atrophy over such a two year period. This is quite encouraging, to think that medium chain triglycerides might be responsible for heading off the process of brain atrophy.

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Saturday, May 1, 2010

Great New Book for Caregivers

I want to recommend a wonderful new book for caregivers of people who have AD or other forms of dementia. The book is called Staying Afloat in a Sea of Forgetfulness: Common Sense Caregiving. It is written by Gary LeBlanc who lived with and cared for his father 24/7 for more than 3000 days until he finally passed away. Gary writes a column with tips for caregivers that appears in the Hernando Today section of the Tampa Tribune. This is a very practical book, written from caregiver to caregiver in a very down to earth style and injected with humor when appropriate. He addresses a variety of problems that arise on a day to day basis and ways that he found to deal with them. This is very helpful in that people who are newer to caregiving won't have to reinvent the wheel. I can totally relate to so many of the issues he discusses in this book and find his advice very useful. Between each section there is a short piece called "Dear Caregiver," usually a meaningful or humorous quote from a famous person that we will all appreciate.

If you want to learn more about this wonderful new book the website is: www.stayingafloatbook.com .

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Update about Steve, Greece, the ketone ester, IVIG

I have been delinquent in keeping up with this blog the past few months and must apologize. There are not enough hours in the day!

Our trip to Greece was quite an adventure - our younger 24 year old daughter Joanna came with us to stay with Steve while I attended some of the meetings at the conference. My presentation went very well and was well received. There were researchers and doctors from around the world, so I am hopeful this will get the message out to many more. Steve held up amazingly well. I took him by the hand when getting off and on public transportation to make sure we didn't lose each other. We got to see some wonderful sites in Athens, London and NYC, but in the end we were all very happy to be home.

This May 21 will mark two years since Steve started taking coconut oil. He had many improvements, some immediate and others more gradual that became obvious over several months or even longer. In many respects he is still doing better than two or even three years ago. None of the physical symptoms or visual disturbance have returned. His has retained many memories of events that have taken place in the last year or longer. He continues to volunteer in the warehouse at the hospital where I work, putting stickers on supplies and moving boxes. He has also gotten his riding lawn mower out recently several times to cut the grass and had no trouble working it. For those who don't know, there are several controls that need to be operated simultaneously to get it running. There is no need to cut grass in our area from November to March, so I was biting my nails wondering whether he would remember how to operate the tractor this year and, alas, he does. On the other hand, we have seen some new problems since the last update. He has had setbacks when he has an illness, with more confusion. This has been most obvious to me when he has a fever blister. I always worry that "this is it," but he manages to bounce back, although not always completely. He has developed a problem in recent months at times with understanding the relationship of where we live to where the rest of his family lives. Usually after I explain this to him, he gets it. I do believe that overall, the use of coconut oil/MCT oil has taken us back in time at least two years and in many respects even longer. I don't know if we will beat it, but we have at least gotten a reprieve from this disease.

A pilot study for Parkinson's disease, using Dr. Veech's ketone ester, will soon begin. since the symptoms of this disease are more consistent from person to person and many are measurable physicla symptoms, he believes they will be able to know within one month if the ketone ester is effective. Clinical trials for Alzheimer's typically last 12-18 months or longer, due to the nature of the disease. We can be hopeful that if the results of the Parkinson's study are positive that more funding will be forthcoming for producing and studying the ketone ester.

Another promising treatment is IVIG (Gammagard and other brands). A pilot study for Gammagard was recently completed showing that there was no worsening of brain scans and there was improved mental function in people with AD over an 18 month period. IVIG has been used for people with immune deficiency for decades. It is pooled antibodies to many different types of infection from 100s of people and is given intravenously usually every two weeks. The company believes that it works by removing beta-amyloid plaque. Another possibility is that it controls a chronic or recurrent infection in the brain, such as the herpes simplex virus type 1 that causes fever blisters - work has been done by Dr. Ruth Itzhaki and others in England showing that this virus is present in the brains, and even within all of the beta-amyloid plaques they have looked at, of people with Alzheimer's who are APOE4+. The virus has also been shown to cause this plaque and also the classic tangles to form. For those who want to screen for the study look at www.clinicaltrials.gov and so a search for Alzheimer's and IVIG. There will be a list of centers who are recruiting now for the IVIG clinical trials.

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Friday, December 4, 2009

ADI Conference in Greece March 2010

I am very pleased to announce that an abstract I submitted entitled "Dietary Intervention Using Coconut Oil to Produce Mild Ketosis in an APOE4 Male with Early Onset Alzheimer's Disease" has been accepted for an oral presentation at the Alzheimer's Disease International Conference to be held in Thessaloniki, Greece March 10-13, 2010. A second abstract, "Caregiver reports following dietary intevention with medium chain fatty acids in 47 persons with dementia," was also accepted as a poster presentation.

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