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My grandmother told me to eat my fish, "brain food." Most likely her grandmother told her for the same reasons. This common knowledge handed down over the centuries has some foundation in ritual, symbolism, metaphor and medical understanding. People who ate fish as part of their staple diet probably kept their sharp intellect into old age.


The sages and bible have numerous 'fish' stories and the "head" of the fish refers to the intellect and controlling headquarters of the person. Each holy New year we put fish on the table as "The Head Of The Year." We want to feed our brain and so we eat fish. Today, we have learned about the fatty acids, omega-3 and the part that plays in keep our brain well-oiled like the rotating gears in a mechanical wheel.


It surprises me when I read a headline such as, "A New Take on What Causes Alzheimer’s: A Ray of Hope" when I consider this old news, old hat. I suppose people continue to feel the need to confirm their understanding about good nutrition and the way it enhances the body and organs. 


Everyone needs to know how things work and find reasons to do the right thing, build their nutrition and eat properly in an age cluttered with processed foods that have no value anymore. Maybe that's why we have empty heads and blank brains that misfire from all the built up blockages. We haven't been oiling our brains. And, don't get me started on eating farm raised fish, because they don't contain the same natural ingredients that free swimming ocean fish in unpolluted waters can contribute to our health.

The latest theory upturns a hypothesis about the plaque build up of protein beta-amyloid that clogs the brain leading to Alzheimer's Disease (AD).


Instead of thinking that people with AD were producing more beta-amyloid, they now think the AD patients simply couldn't flush them from the brain and that's why on postmortem examinations they find 30% more of these proteins. The researchers surmise it takes 10 years for this build up to occur. So, suddenly we have the directive to eat our brain food - fish, which contains omega-3 to clear the plaque.

Omega-3-Rich Diet May Protect Against Alzheimer's Disease and protect people from memory loss. In this study researchers recorded the dietary habits of 1,219 people over age 65 for more than a year and did a check of their blood for the beta-amyloid. This differs from the previous studies on brains of deceased persons.

Mercury Levels In Fish | Mercury is a contaminant found in fish that can affect brain development and the nervous system. The FDA has released guidelines for children, women who are pregnant and women who are trying to become pregnant. These guidelines state that no more than 12 oz of low mercury fish should be consumed weekly. "Highest" mercury fish should be avoided and "high" mercury fish should be kept to only three 6-oz servings per month.


  • March 2014 News
    Two advocacy organizations sued the Food and Drug Administration  demanding that the agency require canned and packaged fish to carry labels informing consumers of the mercury content, and that federal officials force grocery stores and fish markets to display information if they sell fish high in mercury.


  • Some Facts and Figures
  • Aluminum as an adjuvant

It appears those with less amyloid in their blood samples ate more omega-3 rich diets and had a 40% reduced risk of AD. I'm not sure whether the people were taking fish oil capsules or eating more fish or other foods containing high amounts of omega-3 like walnuts. Remember, omega-6 oil does not have the same effects and may not be healthy.


The 2010 study, published in the medical journal of the American Academy of Neurology, also evaluated beta-carotene, vitamin D, vitamin B12, vitamin E, omega-6, saturated fatty acids, and non-unsaturated fatty acids in the participants diets.

  • Foods rich in omega-3 fatty acids include: mackerel, trout, herring, tuna or salmon, kale, tofu, soybeans, walnuts and flaxseed.


Photo credit: State Archives of NC: Shad fishing Wanchese- Manns Harbor
Photo credit: Dwight Sipler Photofarmer: Our most popular kale, Ripbor. Similar to Winterbor.

Rhode Island Hospital Study Finds Link Between Brain Insulin Resistance and Neuronal Stress in Worsening Alzheimer’s Disease

Rhode Island Hospital researcher Suzanne de la Monte, M.D., has found a link between brain insulin resistance (diabetes) and two other key mediators of neuronal injury that help Alzheimer’s disease (AD) to propagate. The research found that once AD is established, therapeutic efforts must also work to reduce toxin production in the brain. The study, Dysfunctional Pro-Ceramide, ER Stress, and Insulin/IGF Signaling Networks with Progression of Alzheimer’s Disease, is published in the June 22, 2012, supplement of the Journal of Alzheimer’s Disease.

This study proposes that with future research into the insulin and insulin-like growth factor IGF resistance brain link, new diabetes-like drugs can be developed to combat this disease. With the similarities between insulin resistance to diabetes, the study authors even call Alzheimer's Type III diabetes.


The Explanation of This Theory

If insulin-resistance dysregulates lipid metabolism and promotes ceramide accumulation, thereby increasing inflammation and lipid metabolism which causes toxic ceramides to accumulate in the brain. The end result is increased stress that threatens the survival and function of neurons in the brain. We're talking about the nervous system of the brain, which reminds me of the toxicity of vaccinations and the neurological damage caused by their ingredients. 


Source Rhode Island Hospital

Vitamin E and Alzheimer's Disease (AD) |  In a study at Mount Sinai School of Medicine in New York of more than 600 older veterans, high doses of vitamin E without taking any other medications delayed the decline in daily living skills, such as making meals, getting dressed and holding a conversation, by about six months over a two-year period.


About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. There is no cure and current medicines just temporarily ease symptoms.





Our Plastic Brains
Resource links

Video Can't Stop Breathing

Alzheimer's and Dementia Discussion

Avocado The Perfect Food

Improve Your Memory

Ailments of Senior Citizens

Falling In The Aged

Schizophrenia Disease

When Bees Lose Their Way Pesticides

Doctor Moulden On Neurologic Disease

A Look At Lachesis

Turmeric for Brain Health | Just imagine 1/4 teaspoon a day could help your brain.

Benefits of Vitamin B for Dementia and Alzheimer's

Dementia and Responsible Care-giving


Alzheimer's Reading Room


Turning On Lights to Stop Neurodegeneration: 
The Potential of Near Infrared Light Therapy in Alzheimer's and Parkinson's Disease Alzheimer's and Parkinson's disease are the two most common neurodegenerative disorders. They develop after a progressive death of many neurons in the brain. Although therapies are available to treat the signs and symptoms of both diseases, the progression of neuronal death remains relentless, and it has proved difficult to slow or stop. Hence, there is a need to develop neuroprotective or disease-modifying treatments that stabilize this degeneration. Red to infrared light therapy (λ = 600–1070 nm), and in particular light in the near infrared (NIr) range, is emerging as a safe and effective therapy that is capable of arresting neuronal death. Previous studies have used NIr to treat tissue stressed by hypoxia, toxic insult, genetic mutation and mitochondrial dysfunction with much success. Here we propose NIr therapy as a neuroprotective or disease-modifying treatment for Alzheimer's and Parkinson's patients.

Alzheimer's — No More! by Andreas Moritz

Discover the True Causes and Empowering Steps You Can Take Now

Alzheimer's disease is one of the world's most feared diseases, and its numbers are only growing. Just about everyone has watched a friend or loved one seem to slip away before their eyes, or knows someone who has. 

While it currently afflicts 36 million people worldwide, Alzheimer's disease is expected to triple in the projections are mirrored globally, the growing incidence of Alzheimer's is staggering, bordering on epidemic proportions. 

It's a widely held myth that this downward cognitive spiral is "just part of the aging process." But this is patently false. And while mainstream medicine and Big Pharma will have you believe that you are powerless to prevent mental decline, this is simply not true. 

In this book, respected Ayurvedic physician and best selling author in the field of mind/body medicine and natural wellness, Andreas Moritz discusses the real root causes of Alzheimer's disease, both physical and spiritual. In his indomitable style, Andreas deftly lays out cutting edge research combined with centuries-old natural health wisdom giving you the powerful tools and inspiration to take control of your health for years to come.

Homöopathischer Sonntag - Das grosse Vergessen (Alzheimer) Andreas Krüger 3 CD's

Der Herausgeber schreibt:

Das große Vergessen - Alzheimer und andere demenzielle Syndrome
über die Homöotherapie der Sklerose, Vergesslichkeit und Lernschwäche

Die Homöopathischen Sonntage sind eine seit vielen Jahren regelmäßig jeden Monat an der Samuel-Hahnemann-Schule in Berlin stattfindende Veranstaltung, in denen ein halber Tag (fünf Stunden) einem einzigen Arzneimittel, einem theoretischen oder praktischen Thema umfassend gewidmet ist. Diese Veranstaltung besteht zumeist aus einer zum Thema passenden Meditation und Trance, Fallbeispielen, einer Übersicht über das Mittel/Thema und einem abschließenden - ebenfalls zum Thema passenden - Märchen. Diese Sonntage sind berühmt, nicht zuletzt weil an ihnen die besten der Krügerschen Seelenreisen stattfanden, die Sie auch großenteils in unseren Büchern und auf den Trancen-CDs wiederfinden.

Die Aufzeichnungen wurden vom Symbolon-Verlag (Frankfurt) bearbeitet und herausgegeben, geschmückt mit passenden Motiven und Bildern aus dem Symbolon-Verlag.

74. Homöopathischer Sonntag, Samuel-Hahnemann-Schule Berlin, 3. September 2000

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Of those with Alzheimer’s disease, an estimated 4 percent are under age 65, 6 percent are 65 to 74, 44 percent are 75 to 84, and 46 percent are 85 or older.

Recently I had a case of an old man who has dementia. I told his son that it is a case of Alzheimers's disease. Immediately, to my surprise, the old man said in mono syllabus words: No doctor, I have Frontotemporal dementia.

I had studied Frontotemporal dementia (Pick’s disease) in final year. but forgotten. Now tell me who needs medicine? Doctor or patient :)

You just demonstrated what we hear on the news quite often today; that the general public self diagnose and read all the health sites to learn about their symptoms. 

Prion Detection Method Shows Promise as Alzheimer’s Test Researchers aim to detect Alzheimer symptoms long before they appear by tweaking an existing medical tool to sleuth out misfolded proteins linked with the illness March 20, 2014 By Dina Fine Maron 

New methods for picking up on Alzheimer’s disease warning signs years before patients develop irreversible symptoms are becoming a fast-growing target for brain researchers around the world. The disease is expected to afflict 115 million people by 2050 but still remains the only leading cause of death where there is no effective way to prevent or even stall its progression. A key challenge continues to be successfully predicting if the disorder will develop before it becomes symptomatic. In the absence of effective treatment for Alzheimer’s, efforts to diagnose the disease earlier could help to get the right people into clinical trials for therapies.


Loss of smell function may predict early onset of Alzheimer's disease Date: January 13, 2010 Source: NYU Langone Medical Center / New York University School of Medicine Summary: A new study links a loss of smell function in Alzheimer's disease model animals with amyloid (protein) accumulation in the brain, a distinguishing hallmark of Alzheimer's disease. New research suggests that olfactory dysfunction, a common symptom of AD, may serve as an early diagnostic tool for the disease.

A study published in the January 13, 2010 issue of the Journal of Neuroscience links a loss of smell function in Alzheimer's disease (AD) model animals with amyloid  (protein) accumulation in the brain, a distinguishing hallmark of Alzheimer's disease. Research conducted by NYU Langone Medical Center suggests that olfactory dysfunction, a common symptom of AD, may serve as an early diagnostic tool for the disease.

The formation of amyloid plaques and neurofibrillary tangles are believed to contribute to the degradation of the neurons in the brain and the subsequent symptoms of AD. In this newly published study, NYU Langone scientists used genetically engineered mice, which developed amyloids in their brains, reflecting a progressive Alzheimer's disease pathology similar to humans.

They found that Alzheimer's disease amyloid pathology occurs first in a region of the mouse brain responsible for smelling -- which is directly above their noses. This pathology also coincided with the animals having abnormal abilities to smell. The mice with a high concentration of amyloid in their brains had to sniff odors longer to "learn" them than mice with less amyloid. They also had problems differentiating between odors.

As the article in the Journal of Neuroscience suggests, since the behavioral symptoms of AD often occur early in life, it is possible that this new olfactory method, looking at olfactory perception across multiple presentations of the same odor, may be advantageous in early detection of Alzheimer's -- prior to substantial degeneration of the brain. "What was striking in our study, was that performance of the mouse in the olfactory behavior test was sensitive to even the smallest amount of amyloid presence in the brain as early as three months of age (equivalent to a young adult).

This is a revealing finding because unlike a brain scan, a laboratory-designed olfactory test may be an inexpensive alternative to early diagnosis of Alzheimer's," noted co-author of the project, Daniel W. Wesson, PhD, of the NYU School of Medicine and the Nathan S. Kline Institute for Psychiatric Research in Orangeburg, New York. Presently, much scientific interest exists in establishing methods to diagnose Alzheimer's prior to the irreversible deterioration of the brain characteristic of the disease. "These novel results provide a two-fold benefit, not only in confirming that olfactory problems may serve as an early indicator of Alzheimer's, but that further validation in humans could facilitate testing of new therapies for the disease," remarked study co-author Ralph A. Nixon, MD, PhD, Director of the Center of Excellence on Brain Aging at NYU Langone Medical Center and professor in the Departments of Psychiatry and Cell Biology.

The study was also co-authored by Donald A. Wilson, PhD, professor in the Department of Child and Adolescent Psychiatry and Efrat Levy, PhD, associate professor in the Departments of Psychiatry and Pharmacology at NYU Langone Medical Center. All researchers are affiliated with the Center of Excellence on Brain Aging at NYU Langone and the Nathan S. Kline Institute for Psychiatric Research, a facility of the New York State Office of Mental Health. Funding for the study was provided by grants from the National Institutes of Health in Bethesda, Maryland and the Alzheimer's Association.


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