HOW TO REVERSE DEMENTIA AND ALZHEIMER'S - DR. MARK HYMAN

FORUM DISCUSSION ON COCONUT OIL AND ALZHEIMER'S DISEASE

Here is a forum post that I found on Natural Medicine Talk.  In it, you can join in the conversation with others who are discussing the benefits of coconut oil to treat the symptoms of Alzheimer's Disease:

A few days ago I got the latest newsletter from Dr. Whitaker. It tells of a 59 yr. old accountant who began having problems at work: disorganized, error prone, depressed. He was eventually diagnosed with Alzheimer's and it rapidly progressed. His wife is an MD and she learned of a clinical trial that was going on and that half of the participants who took the medication in the pilot study showed remarkable improvements and the other half held steady compared to a placebo group that continued to decline. She did some searching and discovered that the drug's active ingredient was medium chain triglycerides (MCT's) natural fatty acids that are abundant in coconut oil.

Although he didn't qualify for the clinical trial his wife started him on coconut oil. After the very first dose, "a light switch came on." Over the next 2 months he became more alert and talkative, and his sense of humor slowly returned. His attentiion and ability to stay on task improved, and at a family reunion he remembered the names of relatives he couldn't recognize the year before. Today, a year and a half after beginning treatment, Steve volounteers in a hospital warehouse and enjoys his job and coworkers. His previously impaired gait has normalized and he is able to run, can read again with decent comprehension and his short-term memory is gradually getting better. He feels as if he "got his life back".

The reason for this is ketones. Medium chain triglycerides don't behave like the more common long chain fats. Thanks to their shorter chemical structure, they are easily absorbed and rapidly metabolized in the liver. And rather than being stored as fat, they are converted into ketones. Ketones are your body's alternative energy source.

Dr. Whitaker says that unrefined coconut oil has numerous benefits. It does not raise cholesterol or in any other way increase risk of heart disease. In fact it is cardioprotective and contains compounds that support the liver, improve immune function, and have antimicrobial properites. He is now recommending ketone therapy for all of his patients with Alzheimer's, Parkinson's disease, dementia, multiple sclerosis, ALS and other neurodegenerative disorders. There is evidence to suggest that it may also be beneficial for individuals with Down syndrome, autism, and diabetes.
The most practical and economidal way of raising ketone levels is with the MCT/coconut oil combo. Mix the 2 oils in a jar and measure out the desired amount for each meal. (Take by the spoon, add to oatmeal, cook with it, etc.) Dr. Whitaker feels that ketone therapy also has a promising role in prevention. Poor glucose tolerance precedes symptoms of neurodegenerative disorders and contributes to their progreression. Why shouldn't healthy people--especially if they're older or have a family history of any of these diseases--take a few spoonfuls of these oils every day to help stave off future problems?

The recommended dose of MCT's for neurodegenerative disorders is 20 g per meal (7 teaspoons or a scant 2 1/2 tablespoons). Dr. Newport's (it was her husband mentioned in the above story) recipe is to combine 16 ounces of MCT oil plus 12 ounces of coconut oil, store at room temperature and use as needed. To avoid diarrhea, start with 1-2 teaspoons per meal and build up gradually--and be aware that some people will only be able to tolerate lower amounts. Because coconut oil contains no omega 3 essential fatty acids, a minimum of 2 g of fish oil should also be taken daily.

This is certainly not the whole article but I hope that I have given the most important points!! I ordered some MCT oil (NOW brand) and plan to start taking a few tbsps. a day as a preventative as there is Alzheimer's Disease in my family. I've used nothing but coconut oil and butter for the last several years and love it!

To read the responses of the others on the forum, click here.

COCONUT OIL AND ALZHEIMER'S - THE NEWS IS SPREADING

I came across this article today on the website Health Impact News Daily on some of the information available on the use of coconut oil to treat Alzheimer's Disease.

by Brian Shilhavy Health Impact News

 

The Failure of the Medical System to Treat Alzheimer’s

The news about how effective coconut oil is in treating Alzheimer’s Disease is spreading fast, as news about the failure of drugs in treating Alzheimer’s continues to make headlines in 2012. Just recently, drug companies Pfizer and Medivation admitted that the new drug they were developing for Alzheimer’s, dimebon, not only did not help patients in trials, but made patients worse. The expensive drug had already reached phase III trials. (See story here on ABC News)

In May 2012 a federal judge ruled that a case against Harvard Medical School and its teaching hospitals regarding fraudulent research using public funds for Alzheimer’s disease was to proceed. (Read the story here)

So as the development of this drug has now been abandoned, and so many other potential drugs have also failed (possibly due to fraudulent research?), many are beginning to look at the role of diet in Alzheimer’s and focusing on prevention. People are also beginning to see positive results in using coconut oil to reverse the effects of Alzheimer’s.

The harm of low-fat high-carbohydrate diets in cholesterol uptake in the brain

One of the most recent studies that looked at the role of nutrition in Alzheimer’s was published in the European Journal of Internal Medicine: “Nutrition and Alzheimer’s disease: The detrimental role of a high carbohydrate diet”¹.

The authors of this study have noted how researchers have begun to direct their energies towards understanding the earlier stages of AD, since drug research in later stages has not been very successful. They note that several researchers have noticed a strong correlation between insulin resistance in the brain and early AD, suggesting that AD might be considered a neuroendocrine disorder of the brain or so-called “type 3 diabetes.” Other observations have noted an association of AD with mitochondrial dysfunction, which is also common in Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).

But the authors’ main conclusions regarding the early causes of AD center around the transport of cholesterol from the blood stream to the brain. They state that there is mounting evidence which suggests that a defect in cholesterol metabolism in the brain may play an important role in AD. They give a nice summary of the brain’s dependency on cholesterol:

The brain represents only 2% of the body’s total mass, but contains 25% of the total cholesterol. Cholesterol is required everywhere in the brain as an antioxidant, an electrical insulator (in order to prevent ion leakage), as a structural scaffold for the neural network, and a functional component of all membranes. Cholesterol is also utilized in the wrapping and synaptic delivery of the neurotransmitters. It also plays an important role in the formation and functioning of synapses in the brain.

They point to several studies that show a lack of cholesterol present in the brains of AD patients which is so vital for several functions, and also note that other studies show this cholesterol deficiency in dementia and Parkinson’s disease. In contrast, high cholesterol levels are positively correlated with longevity in people over 85 years old, and in some cases has been shown to be associated with better memory function and reduced dementia.

The authors go on to explain that the lipid theory of heart disease started by the work of Ancel Keys in the 1960s led to dietary beliefs that cholesterol was to be avoided in the diet, and with that belief came the “over-zealous prescription of cholesterol-reducing medications over the same decades in which there has been a parallel rise in AD prevalence.”

Another result of the low-fat dietary belief was the replacement of fats in the diet with refined carbohydrates, which leads to a rise in blood glucose levels and over time to insulin resistance and diabetes. They point out that the prevalence of fructose, mostly in the form of high fructose corn syrup, is ten times more reactive than glucose in inducing glycation. This impairs serum proteins, and they hypothesize that this leads to a depletion of much needed cholesterol and fat in the brain. Strong evidence in favor of their hypothesis is the fact that studies show patients with type-2 diabetes are at two to five times increased risk to AD.

Increased lipid peroxidation is also shown to be an early cause of Alzheimer’s disease. Liquid vegetable oils, the polyunsaturates, are highly prone to oxidation and rancidity, and it is now well known that in the form of trans fatty acids (through the process of hydrogenation) they are extremely toxic. (More research on polyunsaturated oils here.)

Dr. Raymond Peat has talked about the difference between polyunsaturated oils and saturated oils in their importance for brain tissue for years now:

Brain tissue is very rich in complex forms of fats. The experiment (around 1978) in which pregnant mice were given diets containing either coconut oil or unsaturated oil showed that brain development was superior in the young mice whose mothers ate coconut oil. Because coconut oil supports thyroid function, and thyroid governs brain development, including myelination, the result might simply reflect the difference between normal and hypothyroid individuals. However, in 1980, experimenters demonstrated that young rats fed milk containing soy oil incorporated the oil directly into their brain cells, and had structurally abnormal brain cells as a result. Lipid peroxidation occurs during seizures, and antioxidants such as vitamin E have some anti-seizure activity. Currently, lipid peroxidation is being found to be involved in the nerve cell degeneration of Alzheimer’s disease.²

How Coconut Oil Can Help Alzheimer’s

Coconut oil, by contrast, is highly saturated, and in its natural unrefined form has a shelf life of more than 2 years. Unlike unsaturated oils, it is not prone to oxidation.

Also, the study from the European Journal of Internal Medicine referenced above notes that Alzheimer’s, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS) all have an association with mitochondrial dysfunction. A study published in 2010 used coconut oil to show that a diet enriched in the saturated fatty acids of coconut oil offered strong advantages for the protection against oxidative stress in heart mitochondria.³

Much research is also being uncovered now on the advantages of high HDL cholesterol levels, besides the study we mentioned above in direct relation to Alzheimer’s. A study appearing in the American Journal of Cardiology in February 2011 showed that the higher men’s HDL cholesterol levels, the longer they lived and the more likely it was that they would reach the age of 85.⁴ A diet with adequate amounts of saturated fat is essential to keeping HDL high cholesterol levels. Those with deficiencies and suffering from neurological disorders need to consider a diet that is high in saturated fat, in stark contrast to the mainstream dietary advice for low-fat diets that might be causing many of these late-in-life diseases.

Another major advantage the saturated fat of coconut oil provides is its ability to provide the brain with an alternate source of energy in ketones. Ketones are high energy fuels that nourish the brain. Our body can produce ketones from stored fat while fasting or in starvation, but they can also be produced by converting medium chain fatty acids in certain foods. Coconut oil is nature’s richest source of these medium chain triglycerides (MCTs). A study done in 2004 took MCTs from coconut oil and put them into a drink that was given to Alzheimer’s patients while a control group took a placebo.⁵ They observed significant increases in levels of the ketone body beta-hydroxybutyrate (beta-OHB) 90 minutes after treatment when cognitive tests were administered. Higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects.

As coconut oil’s use becomes more accepted and widespread, and as people begin to realize the dangers of the low-fat dietary belief, we are starting to see more testimonies in relation to diseases like Alzheimer’s. One of the most widely published reports is from Dr. Mary Newport as reported by the St. Petersburg Times on October 29, 2008⁶. Dr. Newport’s husband had been diagnosed with early onset Alzheimer’s and was watching her husband quickly deteriorate. After using drugs that slowed down the effects of Alzheimer’s, she looked into clinical drug trials and found one based on MCTs that not only slowed the progression of Alzheimer’s, but offered improvement. Not being able to get her husband into one of these trials, she began to give him Virgin Coconut Oil, and saw incredible improvement in his condition.

The coconut oil he’d ingested seemed to “lift the fog.” He began taking coconut oil every day, and by the fifth day, there was a tremendous improvement. “He would face the day bubbly, more like his old self,” his wife said. More than five months later, his tremors subsided, the visual disturbances that prevented him from reading disappeared, and he became more social and interested in those around him.⁷

Click here to read the rest of the article.

DR. LARRY MCCLEARY INTERVIEWED BY HANK GARNER OF "MY LOW CARB JOURNEY"

Here is a recent podcast from Hank Garner of My Low Carb Journey.  In this 53 minute podcast, Hank interviews Dr. Larry McCleary, neurosurgeon and author of Feed Your Brain, Lose Your Belly, about the connections between eating high carb and the development of Alzheimer's Disease.

There are a few different topics discussed in this podcast, all on the topic of eating low carb to feed the brain.

Of particular interest is the research being done using an inhaled version of insulin that goes directly to the brain to enhance memory and reverse Alzheimer's symptoms!

Listen and read listeners' comments by clicking here. 


Related Posts: 
KETONE BODIES PRODUCED BY A LOW-CARB DIET ARE HIGH OCTANE BRAIN FOOD 
NEUROLOGIST DR. LARRY MCCLEARY ON HEALTHY LOW-CARB BRAIN FOODS AND TYPE III DIABETES

ALZHEIMER'S DISEASE MAY BE 'TYPE 3' DIABETES - DAILY NEWS CENTRAL

Could Alzheimer's be a form of diabetes? That's the tantalizing suggestion from a new study that finds insulin production in the brain declines as Alzheimer's disease advances. "Insulin disappears early and dramatically in Alzheimer's disease," senior researcher Suzanne M. de la Monte, a neuropathologist at Rhode Island Hospital and a professor of pathology at Brown University Medical School, said in a prepared statement.

"And many of the unexplained features of Alzheimer's, such as cell death and tangles in the brain, appear to be linked to abnormalities in insulin signaling. This demonstrates that the disease is most likely a neuroendocrine disorder, or another type of diabetes," she added.

The discovery that the brain produces insulin at all is a recent one, and de la Monte's group also found that brain insulin produced by patients with Alzheimer's disease tends to fall below normal levels.

Now her group has discovered that brain levels of insulin and its related cellular receptors fall precipitously during the early stages of Alzheimer's. Insulin levels continue to drop progressively as the disease becomes more severe -- adding to evidence that Alzheimer's might be a new form of diabetes, she said.

In addition, the Brown University team found that low levels of acetylcholine -- a hallmark of Alzheimer's -- are directly linked to this loss of insulin and insulin-like growth factor function in the brain.

The report appears in the November issue of the Journal of Alzheimer's Disease.

Insulin Receptors

In its study, de la Monte's team autopsied the brain tissue of 45 patients diagnosed with different degrees of Alzheimer's called "Braak Stages." They compared those tissues to samples taken from individuals with no history of the disease.

The team analyzed insulin and insulin receptor function in the frontal cortex of the brain, a major area affected by Alzheimer's. They found that as the severity of Alzheimer's increased, the levels of insulin receptors and the brain's ability to respond to insulin decreased.

"In the most advanced stage of Alzheimer's, insulin receptors were nearly 80 percent lower than in a normal brain," de la Monte said.

In addition, the researchers found two abnormalities related to insulin in Alzheimer's. First, levels of insulin dropped as the disease progressed. Second, insulin and its related protein -- insulin-related growth factor-I -- lose the ability to bind to cell receptors. This creates a resistance to the insulin growth factors, causing the cells to malfunction and die.

"We're able to show that insulin impairment happens early in the disease," de la Monte said. "We're able to show it's linked to major neurotransmitters responsible for cognition. We're able to show it's linked to poor energy metabolism, and it's linked to abnormalities that contribute to the tangles characteristic of advanced Alzheimer's disease. This work ties several concepts together and demonstrates that Alzheimer's disease is quite possibly a Type 3 diabetes," she said.

Clinical Potential

One expert believes declining insulin levels may be an important feature of Alzheimer's, but not the whole story.

"There is now increasing evidence primarily from observational studies that diabetes, its predecessor metabolic syndrome, and insulin resistance are implicated in increasing risk for Alzheimer's disease," said Dr. Hugh C. Hendrie. He is a professor of psychiatry and co-director of the Center for Alzheimer's Disease and Related Neuropsychiatric Disorders at Indiana University Center for Aging Research, in Indianapolis.

This study adds support to these biological hypotheses and has perhaps treatment implications for the use of certain types of anti-diabetes drugs that influence insulin resistance, Hendrie said.

"There are many other factors also implicated in Alzheimer's disease, such as hypertension and
inflammation, so I think it's a bit of a stretch at the moment to describe Alzheimer's disease as an endocrinological disorder like diabetes," he said.

Another expert thinks that insulin and insulin-like growth factors may be the key to slowing the progression of Alzheimer's.

"We have shown that insulin-like growth factors regulate learning and memory," said Douglas N. Ishii, a professor in the Department of Biomedical Sciences at Colorado State University in Fort Collins.

"We had shown that by blocking insulin-like growth factors in the brain you block learning and memory."

When Ishii's group treated rats with insulin-like growth factors, the researchers found that the intervention prevented the loss of both learning and memory. "In addition, we showed that insulin normally regulates brain weight in adults," he said.

"The clinical potential is that by injecting insulin-like growth factors into patients, one might be able to prevent the loss of learning and memory," Ishii said. "In particular, we have a paper coming out showing that insulin-like growth factors can not only prevent the loss of learning and memory, but prevent the loss of a protein in the brain. This may lead to the slowing down of the progression of Alzheimer's."

Read the full article here.

AVOID THE FATES OF RONALD REGAN AND MICHAEL J. FOX

Here is today's blog post from neurosurgeon Dr. Jack Kruse, concerning the use of a low carb paleolithic diet to prevent Alzheimer's Disease, Parkinson's Disease and other neurodegenerative diseases:

Dr. Jack Krus

READERS SUMMARY:

1. Why the presence of genes means nothing to disease risk.

2. What do people over 100 years old teach us about genetics?

3. What six pieces of evidence found in 2011 tell us about AD or PD etiology?

4. How will industry try to solve the mystery?

5. What you can do right now to obliterate your current risk of AD and PD?



If you did not know that Ronald Reagan suffered and died from end stage Alzheimer’s, you do now. Micheal J. Fox is afflicted with Parkinson’s disease and trying to solve its etiology as a fundraiser. Recently in 2011, several announcements were made that several genetic mutations seem to predispose us to Alzheimer’s disease (AD) and Parkinson’s Disease (PD). I tend to glance over these findings often because based upon my current understanding, genetic mutations are not where science seems to be headed these days. Genetic determinism has been the dogma for the last 50 years, but the most recent data suggest that we can reprogram our genes by turning on and off their function if we know how. This makes sense considering that most biologic systems don’t rely on the presence or absence of genes in disease states. In fact, in Mount Sinai’s supercentenarian group they found that the longest lived people all tend to have the “bad genes” in their cells we all worry about. The interesting part is that they are not “turned on” and appear to be of no consequence to those people.

The old dogma led us to believe that the mere presence of these genes spelled doom. If you don’t think genetic determinism is alive and wellin 2011 talk to any woman who tests positive for the BRCA 1 gene for breast cancer. Many of these women are electing for mastectomies in the face of no immediate cancer presence just because of the scare due to the BRCA 1 gene being present. I don’t advocate that kind of thinking. WHY? The Mount Sinai supercentenary group makes a great example for us to learn from. Think of an analogy of genes and their epigenetic signals to a “stick of dynamite” and “lit match”. A stick of dynamite is not dangerous to us unless it is around a lit match. It appears the same is true for genes. The mere presence means little as long as the on switch is not present at the same time. This is where genetic testing is now headed.

The recent AD announcements gained lots of attention but the thing that caught my eye about the genes found in AD patients were all tied to lipid metabolism and inflammation generation. The AD jigsaw puzzle is a long way from complete, but the pieces are emerging that suggests inflammation is the root cause of this condition. So Dr. Kruse, what exactly are those pieces of evidence? What six things have we learned about the brain and neurodegenerative disorders as of 2011?

1. The genesis cause of AD et al is caused by the presence of insoluble plaques made up of a protein called Amyloid beta (A-beta) inside neurons.

These proteins block signal transmission and molecule transfers that occur in the brain normally. This process continues for sometime and then another protein becomes more common called Tau protein. When both occur together they begin to interact and form the insoluble protein called a neurofibrillary tangle that is classically associated with many neurodegenerative diseases. (AD, Parkinson’s, and Mad Cow disease are a few.)

2. The second bit of evidence is found on the APO E gene present on chromosome 19. If it is present many researchers and clinicians believe your risk of getting AD rises. In fact, having two copies of the four we have of this gene, raises your risk of developing AD 20 fold before the age of 75! SO APO E presence sound bad does it not?

Guess what APO E gene function is for? It is to remove the build up of the A-beta and Tau proteins before they induce nerve damage and eventual cell suicide. The solubility factor is important because it is determined by how the protein folds after it is made. If it folds incorrectly it become less soluble. This is why we can see these tangles under a microscope. So this means that the presence of APO E gene is a great thing and not a bad thing that many have been led to believe the last 15 years. More proof that genetic determinism is not as important as the epigenomic effects upon those genes.

3. The third bit of evidence comes from Dr Chris Dobson’s lab in Cambridge University.

He cleverly made 17 small genetic adjustments to the A-beta protein in the lab to make it either more or less soluble. After doing this he then transferred these genetically altered proteins into the DNA of fruit flies and clearly proved that the less soluble the protein transferred the shorter lived were the flies. Their life spans clearly correlated with the percent solubility of the protein transferred to the mutant flies. So after his experiment neuroscientists began to ask why do misfolded proteins show up in elderly brains to begin with?

4. It appears that all neurons have an internal quality control mechanism that not only detects misfolded proteins, but one that also self corrects this process from happening.

Research was published in March of 2011 from Brown University that both parts of this mechanism, the detector and refolder, are functional but overwhelmed in diseased brains with neurodegenerative changes. They can not keep up with the workload of all the A- beta protein being made.

5. Then the 5th bit of evidence came in April of 2011 from Dr. Jeffrey Kelly.

Dr. Kelly is at the Scripps Research Institute, and found that a chemical formed when cholesterol reacts with ozone attaches to A-beta and makes misfolding hundreds of times more likely. Take a guess where Dr. Kelly found the ozone came from? It comes from inflammation generated within the neurons from cellular metabolism. This linked the etiology of protein misfolding directly to carbohydrate and omega six fuels in our diet and their eventual metabolism over years. Both of these pathways are known to cause the development of inflammation in human biochemistry. It also links diabetes risk to AD fairly tightly. This news is not surprising to my readers at all if you follow the Quilt’s Levees.

6. The last bit of evidence comes from the recent studies on studies on stress and the development of all neurodegenerative diseases. That is the hormone cortisol. This links another levee to the "brick in the wall".

This is a clearly a hormone most of my blog readers have become quite familiar with. Remember that cortisol rises in end stage leptin resistance to cause the generation of even more inflammatory cytokines. Remember that cortisol is made from the cholesterol backbone, pregnenolone. 2011 work done at the University of California at Irvine has pointed to the elevation of cortisol as the main generator of the inflammation in diseased neurons. This further fuels protein misfolding and overwhelms the detector and refolding mechanisms in the brain.

SUMMARY:

It appears that the brains cholesterol stores are used up to make the cortisol that fuels the inflammation that drives this pathologic process. This inflammation becomes the currency that overwhelms the internal quality assurance system of neurons to make sure proper protein folding occurs. When the system is overwhelmed the end result is the formation of neurofibrillary tangles from insoluble proteins. These insoluble proteins then block the transport of vital ingredients into the brain cells to offset the assault. One of those ingredients appears to be cholesterol itself. It appears that normal lipid metabolism repair mechanisms become so unbalanced that it induces the nerve cells to undergo apoptosis! This ties another levee to the AD and Parkinson’s disease story.

Many physicians and researchers are hoping that we can find a place in this chain of events that can be attacked or blocked by a medication to prevent the inflammation, production of ozone reactions, slow the conversion of cholesterol to cortisol, and encourage the refolding apparatus that evolution provided us to make a dent in this disease. Maybe then we can improve protein solubility and even boost the plaque removal mechanism that we were born with? I have a better idea. Why don’t we stop providing that the fuels that are known to provide the ” lit match” to the dynamite?

Maybe we should advocate a low carb paleolithic diet that decreases carbohydrates that upregulate IGF 1 and 2 and lower omega six free fatty acids? We know that will help slow the progression of the disease since we now know what drives it. Some how I bet they’d rather make a drug they could make money on then teach people what really might help now? After all, no food company makes money unless they are selling the SAD (Standard American Diet), do they? The choice is clearly yours to ponder.

To read the full article and comments, click here.

STOP ALZHEIMER'S NOW! - BRUCE FIFE - BOOK REVIEW

How to Prevent and Reverse Dementia, Parkinson's, ALS, Multiple Sclerosis, and Other Neurodegeneratvie Disorders

Review

Dr. Fife outlines a specific battle plan to combat these disorders, one that fits very nicely with what we know of these disorders and is easy to follow. I would encourage everyone faced with the possibility of encountering neurodegenerative disease, which now includes most of us, to read this book carefully. It is a treasure trove of invaluable information and practical advice. --Russell L. Blaylock, MD, Board Certified Neurosurgeon and author of Excitotoxins: The Taste That Kills

A must read for any and all health care professionals, as well as any family members or friends of those stricken by these maladies. --Jeffrey Grill, MD

Stop Alzheimer s Now! represents a major step forward in Alzheimer s disease, exposing the reality that Alzheimer s and other brain diseases are inflammation-related disorders and therefore can be effectively treated and potentially completely prevented by reversing inflammation through better nutrition and healthy lifestyles. --Catherine Shanahan, MD, author of Deep Nutrition: Why Your Genes Need Traditional Food

Stop Alzheimer's Now!...will not only be beneficial for Alzheimer's but also for a wide variety of other diseases. I strongly recommend reading this book! --Sofie Hexeberg, MD, PhD

A must read for everyone concerned with Alzheimer's disease...the author explains how diet modifications and the addition of coconut oil can drastically change the course of the disease. --Edmond Devroey, MD, The Longevity Institute

The author's dietary recommendations are a valuable aid to nutritional therapy of chronic neurodegenerative diseases. I recommend this enlightening book to both physicians and those who simply want to better understand how our brain functions. --Igor Bondarenko, MD, PhD

A must read for everyone concerned with Alzheimer's disease...the author explains how diet modifications and the addition of coconut oil can drastically change the course of the disease. --Edmond Devroey, MD, The Longevity Institute

The author's dietary recommendations are a valuable aid to nutritional therapy of chronic neurodegenerative diseases. I recommend this enlightening book to both physicians and those who simply want to better understand how our brain functions. --Igor Bondarenko, MD, PhD

Description

Dementia and other forms of neurodegeneration are not a part of the normal aging process. You should not expect to develop dementia as you grow older. The brain is fully capable of functioning normally for a lifetime, regardless of how long a person lives. While aging is a risk factor for neurodegeneration, it is not the cause! Dementia and other neurodegenerative disorders are disease processes that can be prevented and successfully treated. This book outlines a program that is backed by decades of medical and clinical research that has proven successful in restoring mental function and improving both brain and overall health. You will learn how to prevent and even reverse symptoms associated with Alzheimer's disease, Parkinson's disease, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington's disease, epilepsy, diabetes, stroke, and various forms of dementia. The information in this book is useful not only for those who are suffering from neurodegenerative disease, but for anyone who wants to be spared from encountering these devastating afflictions. These diseases don t just happen overnight. They take years, often decades, to develop. In the case of Alzheimer's disease, approximately 70 percent the brain cells responsible for memory are destroyed before symptoms become noticeable. Once symptoms surface, the brain is already in an advanced stage of degeneration. You do not want to wait until most of your brain has died before you start to do something about it. You can stop Alzheimer's and Parkinson's and other neurodegenerative diseases before they take over your life, but you must start now.

Stop Alzheimer's Now!  can be ordered by clicking here.