UPDATE: 3 December 2011
Melatonin in Alzheimer's disease and other neurodegenerative disorders
July 2011
Rank in the TOP10 out of 3.9 M+ related articles
Updated from May 09
2004 Article, Don't Overlook There ALZ Remiders, Related NHN article This post ranks 1 of 1.23 Million about vitamins for Alzheimer's
Food and Life
HealthDay Reporter mentioned how cheap the vitamin is; the study authors "bought a year's supply for $30" and noted that it "appears to be safe." Even so, one author said that "I wouldn't advocate people rush out and eat grams of this stuff each day." (1)
The BBC quoted Rebecca Wood, Chief Executive of the UK Alzheimer's Research Trust, who said, "Until the human research was completed, people should not start taking the supplement. . . . people should be wary about changing their diet or taking supplements. In high doses vitamin B3 can be toxic." (3)
The Irish Times reiterated it: "People have been cautioned about rushing out to buy high dose vitamin B3 supplements in an attempt to prevent memory loss . . . The warnings came today one day on from the announcement . . .Vitamins in high doses can be toxic." (4)
Their choice of words is quaint but hardly accurate. There is no wild "rush;" half of the population already takes food supplements. And as for "toxic," niacin isn't. Canadian psychiatrist Abram Hoffer, M.D., asserts that it is actually remarkably safe. "There have been no deaths from niacin supplements," Dr. Hoffer says. "The LD 50 (the dosage that would kill half of those taking it) for dogs is 5,000-6,000 milligrams per kilogram body weight. That is equivalent to almost a pound of niacin per day for a human. No human takes 375,000 milligrams of niacin a day. They would be nauseous long before reaching a harmful dose." Dr. Hoffer conducted the first double-blind, placebo-controlled clinical trials of niacin. He adds, "Niacin is not liver toxic. Niacin therapy increases liver function tests. But this elevation means that the liver is active. It does not indicate an underlying liver pathology."
The medical literature repeatedly confirms niacin's safety. Indeed, for over 50 years, nutritional (orthomolecular) physicians have used vitamin B3 in doses as high as tens of thousands of milligrams per day. Cardiologists frequently give patients thousands of milligrams of niacin daily to lower cholesterol. Niacin is preferred because its safety margin is so very large. The American Association of Poison Control Centers' Toxic Exposure Surveillance System annual reports indicates there is not even one death per year due to niacin in any of its forms. (5)
One the other hand, there are 140,000 deaths annually attributable to properly prescribed prescription drugs. (6) And this figure is just for one year, and just for the USA. Furthermore, when overdoses, incorrect prescription, and adverse drug interactions are figured in, total drug fatalities number over a quarter of a million dead. Each year.
The BBC's curious mention that we should even be "wary about changing our diets" is especially odd. More and more scientists think our much-in-need-of-improvement diets are what contribute more than anything to developing Alzheimer's. "There appears to be a statistically significant link between a low dietary intake of niacin and a high risk of developing Alzheimer's disease. A study of the niacin intake of 6158 Chicago residents 65 years of age or older established that the lower the daily intake of niacin, the greater the risk of becoming an Alzheimer's disease patient." The group with the highest daily intake of niacin had a 70 percent decrease in incidence of this disease compared to the lowest group. "The most compelling evidence to date is that early memory loss can be reversed by the ascorbate (vitamin C) minerals. Greater Alzheimer's disease risk also has been linked to low dietary intake of vitamin E and of fish." (7)
Nutrient deficiency of long standing may create a nutrient dependency. A nutrient dependency is an exaggerated need for the missing nutrient, a need not met by dietary intakes or even by low-dose supplementation. Robert P. Heaney, M.D., uses the term "long latency deficiency diseases" to describe illnesses that fit this description. He writes: "Inadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. . . Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible." (8) Where pathology already exists, unusually large quantities of vitamins may be needed to repair damaged tissue. Thirty-five years ago, in another paper, Hoffer wrote: "The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure." (9)
As there is no recognized cure for Alzheimer's, prevention is vital. In their article, the Irish Times does admit that "Healthy mice fed the vitamins also outperformed mice on a normal diet" and quoted study co-author Frank LaFerla saying that "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve." (4) And study author Green added, "If we combine this with other things already out there, we'd probably see a large effect."
The US Alzheimer's Association's Dr. Ralph Nixon has said that previous research has suggested that vitamins such as vitamin E, vitamin C and vitamin B12 may help people lower their risk of developing Alzheimer's disease. At their website (although you have to search for it), the Alzheimer's Association says, "Vitamins may be helpful. There is some indication that vitamins, such as vitamin E, or vitamins E and C together, vitamin B12 and folate may be important in lowering your risk of developing Alzheimer's. . . One large federally funded study (10) showed that vitamin E slightly delayed loss of ability to carry out daily activities and placement in residential care."
But overall, at their website http://www.alz.org/index.asp the Alzheimer's Association has strikingly little to say about vitamins, and they hasten to tell people that "No one should use vitamin E to treat Alzheimer's disease except under the supervision of a physician." ( http://www.alz.org/alzheimers_disease_10428.asp ) "They write as if these safe vitamins are dangerous drugs, not be used without a doctor's consent," comments Dr. Hoffer. "I have been using them for decades."
Niacin and nerves go together. Orthomolecular physicians have found niacin and other nutrients to be an effective treatment for obsessive compulsive disorder, anxiety, bipolar disorder, depression, psychotic behavior, and schizophrenia. New research confirms that niacinamide (the same form of B3 used in the Alzheimer's research) "profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits" in animals with an illness very similar to multiple sclerosis. (11)
A measure of journalistic caution is understandable, especially with ever-new promises for pharmaceutical products. Drugs routinely used to treat Alzheimer's Disease have had a disappointing, even dismal success rate. So when nutrition may be the better answer, foot-dragging is inexplicable, even inexcusable. Nutrients are vastly safer than drugs. Unjustified, needlessly negative opinionating is out of place. Over 5 million Americans now have Alzheimer's disease, and the number is estimated to reach 14 million by 2050. Potentially, 9 million people would benefit later from niacin now.
"Man is a food-dependent creature," wrote University of Alabama professor of medicine Emanuel Cheraskin, M.D.. "If you don't feed him, he will die. If you feed him improperly, part of him will die."
When that part is the brain, it is dangerous to delay the use of optimum nutrition.
Vitamin D may help prevent Alzheimer's
Melatonin in Alzheimer's disease and other neurodegenerative disorders
Abstract
Increased oxidative stress and mitochondrial dysfunction have been identified as common pathophysiological phenomena associated with neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD). As the age-related decline in the production of melatonin may contribute to increased levels of oxidative stress in the elderly, the role of this neuroprotective agent is attracting increasing attention. Melatonin has multiple actions as a regulator of antioxidant and prooxidant enzymes, radical scavenger and antagonist of mitochondrial radical formation. The ability of melatonin and its kynuramine metabolites to interact directly with the electron transport chain by increasing the electron flow and reducing electron leakage are unique features by which melatonin is able to increase the survival of neurons under enhanced oxidative stress. Moreover, antifibrillogenic actions have been demonstrated in vitro, also in the presence of profibrillogenic apoE4 or apoE3, and in vivo, in a transgenic mouse model. Amyloid-β toxicity is antagonized by melatonin and one of its kynuramine metabolites. Cytoskeletal disorganization and protein hyperphosphorylation, as induced in several cell-line models, have been attenuated by melatonin, effects comprising stress kinase downregulation and extending to neurotrophin expression. Various experimental models of AD, PD and HD indicate the usefulness of melatonin in antagonizing disease progression and/or mitigating some of the symptoms. Melatonin secretion has been found to be altered in AD and PD. Attempts to compensate for age- and disease-dependent melatonin deficiency have shown that administration of this compound can improve sleep efficiency in AD and PD and, to some extent, cognitive function in AD patients. Exogenous melatonin has also been reported to alleviate behavioral symptoms such as sundowning. Taken together, these findings suggest that melatonin, its analogues and kynuric metabolites may have potential value in prevention and treatment of AD and other neurodegenerative disorders. Complete articleJuly 2011
Rank in the TOP10 out of 3.9 M+ related articles
Access the May 2007 issue of herbalYODA Says! that focuses on vitamin B12 with a donation to help us continue this work.
2004 Article, Don't Overlook There ALZ Remiders, Related NHN article This post ranks 1 of 1.23 Million about vitamins for Alzheimer's
Food and Life
for information on how to use B3 therapeutically, contact us for our fact sheet
UPDATE: 4 May, 2009
No wonder vitamin E works, it is antioxidant and carries O2 across the cell wall membrane as well as offering a myriad of other remarkable healing attributes.
Another FAT soluble vitamin to the rescue!
Use the search window to learn more about vitamin E on Natural Health News
Vitamin E may slow Alzheimer's disease By Megan Rauscher
NEW YORK (Reuters Health) – An analysis of "real-world" clinical data indicates that vitamin E, and drugs that reduce generalized inflammation, may slow the decline of mental and physical abilities in people with Alzheimer's disease (AD) over the long term.
"Our results are consistent for a potential benefit of vitamin E on slowing functional decline and a smaller possible benefit of anti-inflammatory medications on slowing cognitive decline in patients suffering from Alzheimer's disease," Dr. Alireza Atri told Reuters Health.
Atri, at Massachusetts General Hospital (MGH), the VA Bedford Medical Center, and Harvard Medical School, Boston, led the National Institutes of Health-sponsored research. The findings, reported at the annual meeting of the American Geriatrics Society in Chicago, stem from data on 540 patients treated at the MGH Memory Disorders Unit.
All of the patients were receiving standard-of-care treatment with a drug intended to help patients with Alzheimer's. As part of their clinical care, 208 patients also took vitamin E but no anti-inflammatory, 49 took an anti-inflammatory but no vitamin E, 177 took both vitamin E and an anti-inflammatory, and 106 took neither.
While the daily dose of vitamin E ranged from 200 to 2000 units, the majority of patients were given high doses that ranged from 800 units daily to 1000 units twice daily.
Each patient's performance on cognitive tests and their ability to carry out daily functions such as dressing and personal care were assessed every 6 months. After an average of 3 years, "there was a modest slowing of decline in function in those patients taking vitamin E," study investigator Michael R. Flaherty noted in a telephone interview with Reuters Health.
Flaherty, a second-year student at the University of New England College of Osteopathic Medicine in Biddeford, Maine, presented the findings at the meeting. He added that the treatment benefit from vitamin E was "small to medium" but increased with time.
Taking an anti-inflammatory medication was associated with "very consistent but generally only small effects on slowing long-term decline in cognitive functioning," Atri told Reuters Health.
However, in patients who took both vitamin E and anti-inflammatory medications, there appeared to be an additive effect in terms of slowing overall decline.
Given that past studies have produced equivocal results, the investigators conclude that further studies are needed to assess the long-term balance of risks versus benefits for people with Alzheimer's disease from taking vitamin E and anti-inflammatory drugs.
Copyright © 2009 Reuters Limited.
-------------------------
UPDATE: 23 MARCH, 2009
Niacin Protects against Alzheimer's Disease and Age-related Cognitive Decline
Niacin (vitamin B3) is already known to lower cholesterol. Now, research published in the August 2004 issue of the Journal of Neurology, Neurosurgery and Psychiatry indicates regular consumption of niacin-rich foods also provides protection against Alzheimer's disease and age-related cognitive decline.
Researchers from the Chicago Health and Aging Project interviewed 3,718 Chicago residents aged 65 or older about their diet, then tested their cognitive abilities over the following six years.
Those getting the most niacin from foods (22 mg per day) were 70% less likely to have developed Alzheimer's disease than those consuming the least (about 13 mg daily), and their rate of age-related cognitive decline was significantly less. In addition to eating the niacin-rich foods, another way to boost your body's niacin levels is to eat more foods rich in the amino acid tryptophan. Your body can convert tryptophan to niacin, with a little help from other B vitamins, iron and vitamin C. Foods high in tryptophan include shrimp, crimini mushrooms, yellowfin tuna, halibut, chicken breast, scallops, salmon, turkey and tofu. As you can see, several foods rich in tryptophan provide two ways to increase niacin levels as they are also rich in the B vitamin.(August 23, 2004)
UPDATE: 12 March, 2009
Another supplement to help Alzheimer's: "One of the newer drugs developed in Europe apparently 'works' by protecting brain cells from damage by over-production of glutamate, one of the well known actions of lithium.
Other research findings strongly suggest that lithium may protect against Alzheimer's disease and slow the progression of the disease. Lithium inhibits beta-amaloid secretion and protects against damage caused by beta-amyloid protein after it has formed.
Over-activation of tau protein in the brain also contributes to neuronal degeneration in Alzheimer's disease, as does the formation of neurofibrilary tangles. Lithium inhibits both of these.
People with Alzheimer's have excess aluminum accumulation in brain cells. Lithium can help protect against aluminum accumulation through chelation and easier removal from the body."
See also a related B3 article I posted in November - xref: Fetal Alcohol Syndrome.
-----------------------------
While we are on this thread of natural help for dis-ease isn't it timely that I just received this article about how "High Doses of Vitamins Fight Alzheimer's Disease".
And now I am sharing it with you, for your education, and then you can ask your doctor why they aren't recommending them.
Vitamin B3 is also used successfully for schizophrenia, rheumatoid arthritis, arthritis, reducing plaque of arteriosclerosis and cholesterol reduction. It has an excellent anti-inflammatory action.
(OMNS, December 9, 2008) The news media recently reported that "huge doses of an ordinary vitamin appeared to eliminate memory problems in mice with the rodent equivalent of Alzheimer's disease." They then quickly added that "scientists aren't ready to recommend that people try the vitamin on their own outside of normal doses." (1)Specifically, the study employed large amounts of nicotinamide, the vitamin B3 widely found in foods such as meat, poultry, fish, nuts and seeds. Nicotinamide is also the form of niacin found, in far greater quantity, in dietary supplements. It is more commonly known as niacinamide. It is inexpensive and its safety is long established. The most common side effect of niacinamide in very high doses is nausea. This can be eliminated by taking less, by using regular niacin instead, which may cause a warm flush, or choosing inositol hexaniacinate, which does not. They are all vitamin B3.
In other words, extra-large amounts of a vitamin are helpful, so don't you take them!
That does not even pass the straight-faced test. So what's the story?
Researchers at the University of California at Irvine gave the human dose equivalent of 2,000 to 3,000 mg of vitamin B3 to mice with Alzheimer's. (2) It worked. Kim Green, one of the researchers, is quoted as saying, "Cognitively, they were cured. They performed as if they'd never developed the disease."
for information on how to use B3 therapeutically, contact us for our fact sheet
HealthDay Reporter mentioned how cheap the vitamin is; the study authors "bought a year's supply for $30" and noted that it "appears to be safe." Even so, one author said that "I wouldn't advocate people rush out and eat grams of this stuff each day." (1)
The BBC quoted Rebecca Wood, Chief Executive of the UK Alzheimer's Research Trust, who said, "Until the human research was completed, people should not start taking the supplement. . . . people should be wary about changing their diet or taking supplements. In high doses vitamin B3 can be toxic." (3)
The Irish Times reiterated it: "People have been cautioned about rushing out to buy high dose vitamin B3 supplements in an attempt to prevent memory loss . . . The warnings came today one day on from the announcement . . .Vitamins in high doses can be toxic." (4)
Their choice of words is quaint but hardly accurate. There is no wild "rush;" half of the population already takes food supplements. And as for "toxic," niacin isn't. Canadian psychiatrist Abram Hoffer, M.D., asserts that it is actually remarkably safe. "There have been no deaths from niacin supplements," Dr. Hoffer says. "The LD 50 (the dosage that would kill half of those taking it) for dogs is 5,000-6,000 milligrams per kilogram body weight. That is equivalent to almost a pound of niacin per day for a human. No human takes 375,000 milligrams of niacin a day. They would be nauseous long before reaching a harmful dose." Dr. Hoffer conducted the first double-blind, placebo-controlled clinical trials of niacin. He adds, "Niacin is not liver toxic. Niacin therapy increases liver function tests. But this elevation means that the liver is active. It does not indicate an underlying liver pathology."
The medical literature repeatedly confirms niacin's safety. Indeed, for over 50 years, nutritional (orthomolecular) physicians have used vitamin B3 in doses as high as tens of thousands of milligrams per day. Cardiologists frequently give patients thousands of milligrams of niacin daily to lower cholesterol. Niacin is preferred because its safety margin is so very large. The American Association of Poison Control Centers' Toxic Exposure Surveillance System annual reports indicates there is not even one death per year due to niacin in any of its forms. (5)
One the other hand, there are 140,000 deaths annually attributable to properly prescribed prescription drugs. (6) And this figure is just for one year, and just for the USA. Furthermore, when overdoses, incorrect prescription, and adverse drug interactions are figured in, total drug fatalities number over a quarter of a million dead. Each year.
The BBC's curious mention that we should even be "wary about changing our diets" is especially odd. More and more scientists think our much-in-need-of-improvement diets are what contribute more than anything to developing Alzheimer's. "There appears to be a statistically significant link between a low dietary intake of niacin and a high risk of developing Alzheimer's disease. A study of the niacin intake of 6158 Chicago residents 65 years of age or older established that the lower the daily intake of niacin, the greater the risk of becoming an Alzheimer's disease patient." The group with the highest daily intake of niacin had a 70 percent decrease in incidence of this disease compared to the lowest group. "The most compelling evidence to date is that early memory loss can be reversed by the ascorbate (vitamin C) minerals. Greater Alzheimer's disease risk also has been linked to low dietary intake of vitamin E and of fish." (7)
Nutrient deficiency of long standing may create a nutrient dependency. A nutrient dependency is an exaggerated need for the missing nutrient, a need not met by dietary intakes or even by low-dose supplementation. Robert P. Heaney, M.D., uses the term "long latency deficiency diseases" to describe illnesses that fit this description. He writes: "Inadequate intakes of many nutrients are now recognized as contributing to several of the major chronic diseases that affect the populations of the industrialized nations. Often taking many years to manifest themselves, these disease outcomes should be thought of as long-latency deficiency diseases. . . Because the intakes required to prevent many of the long-latency disorders are higher than those required to prevent the respective index diseases, recommendations based solely on preventing the index diseases are no longer biologically defensible." (8) Where pathology already exists, unusually large quantities of vitamins may be needed to repair damaged tissue. Thirty-five years ago, in another paper, Hoffer wrote: "The borderline between vitamin deficiency and vitamin-dependency conditions is merely a quantitative one when one considers prevention and cure." (9)
As there is no recognized cure for Alzheimer's, prevention is vital. In their article, the Irish Times does admit that "Healthy mice fed the vitamins also outperformed mice on a normal diet" and quoted study co-author Frank LaFerla saying that "This suggests that not only is it good for Alzheimer's disease, but if normal people take it, some aspects of their memory might improve." (4) And study author Green added, "If we combine this with other things already out there, we'd probably see a large effect."
The US Alzheimer's Association's Dr. Ralph Nixon has said that previous research has suggested that vitamins such as vitamin E, vitamin C and vitamin B12 may help people lower their risk of developing Alzheimer's disease. At their website (although you have to search for it), the Alzheimer's Association says, "Vitamins may be helpful. There is some indication that vitamins, such as vitamin E, or vitamins E and C together, vitamin B12 and folate may be important in lowering your risk of developing Alzheimer's. . . One large federally funded study (10) showed that vitamin E slightly delayed loss of ability to carry out daily activities and placement in residential care."
But overall, at their website http://www.alz.org/index.asp the Alzheimer's Association has strikingly little to say about vitamins, and they hasten to tell people that "No one should use vitamin E to treat Alzheimer's disease except under the supervision of a physician." ( http://www.alz.org/alzheimers_disease_10428.asp ) "They write as if these safe vitamins are dangerous drugs, not be used without a doctor's consent," comments Dr. Hoffer. "I have been using them for decades."
Niacin and nerves go together. Orthomolecular physicians have found niacin and other nutrients to be an effective treatment for obsessive compulsive disorder, anxiety, bipolar disorder, depression, psychotic behavior, and schizophrenia. New research confirms that niacinamide (the same form of B3 used in the Alzheimer's research) "profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits" in animals with an illness very similar to multiple sclerosis. (11)
A measure of journalistic caution is understandable, especially with ever-new promises for pharmaceutical products. Drugs routinely used to treat Alzheimer's Disease have had a disappointing, even dismal success rate. So when nutrition may be the better answer, foot-dragging is inexplicable, even inexcusable. Nutrients are vastly safer than drugs. Unjustified, needlessly negative opinionating is out of place. Over 5 million Americans now have Alzheimer's disease, and the number is estimated to reach 14 million by 2050. Potentially, 9 million people would benefit later from niacin now.
"Man is a food-dependent creature," wrote University of Alabama professor of medicine Emanuel Cheraskin, M.D.. "If you don't feed him, he will die. If you feed him improperly, part of him will die."
When that part is the brain, it is dangerous to delay the use of optimum nutrition.
References:(1) Vitamin Holds Promise for Alzheimer's Disease. Randy Dotinga, HealthDay Reporter, Nov 5, 2008.http://www.washingtonpost.com/wp-dyn/content/article/2008/11/05/AR2008110502796.html and also http://health.yahoo.com/news/healthday/vitaminholdspromiseforalzheimersdisease.html
(2) Green KN, Steffan JS, Martinez-Coria H, Sun X, Schreiber SS, Thompson LM, LaFerla FM. Nicotinamide restores cognition in Alzheimer's disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. J Neurosci. 2008 Nov 5;28(45):11500-10.
(3) BBC, 5 Nov 2008. http://news.bbc.co.uk/2/hi/health/7710365.stm
(4) Donnellan E. Caution urged over using vitamin B3 to treat Alzheimer's. Wed, Nov 05, 2008. http://www.irishtimes.com/newspaper/breaking/2008/1105/breaking91.htm
(5) Annual Reports of the American Association of Poison Control Centers' National Poisoning and Exposure Database (formerly known as the Toxic Exposure Surveillance System). AAPCC, 3201 New Mexico Avenue, Ste. 330, Washington, DC 20016. Download any report from1983-2006 at http://www.aapcc.org/dnn/NPDS/AnnualReports/tabid/125/Default.aspx free of charge. The "Vitamin" category is usually near the end of the report.(6) Classen DC, Pestotnik SL, Evans RS, Lloyd JF, Burke JP. Adverse drug events in hospitalized patients. Excess length of stay, extra costs, and attributable mortality. JAMA. 1997 Jan 22-29;277(4):301-6.(7) 21. Hoffer A and Foster HD. Feel Better, Live Longer With Vitamin B-3: Nutrient Deficiency and Dependency. CCNM Press, 2007. ISBN-10: 1897025246; ISBN-13: 978-1897025246. Also: Foster HD. What Really Causes Alzheimer's Disease. Trafford, 2004. ISBN 1-4120-4921-0.(8) Heaney RP: Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003; Nov; 78(5):912-9.(9) Hoffer A. Mechanism of action of nicotinic acid and nicotinamide in the treatment of schizophrenia. In: Hawkins D and Pauling L: Orthomolecular Psychiatry: Treatment of Schizophrenia. San Francisco: W.H. Freeman. 1973; p. 202-262.(10) Sano M, Ernesto C, Thomas RG et al. A controlled trial of selegiline, alpha-tocopherol, or both as treatment for Alzheimer's disease. The Alzheimer's Disease Cooperative Study. N Engl J Med. 1997 Apr 24;336(17):1216-22(11) Kaneko S, Wang J, Kaneko M, Yiu G, Hurrell JM, Chitnis T, Khoury SJ, He Z. Protecting axonal degeneration by increasing nicotinamide adenine dinucleotide levels in experimental autoimmune encephalomyelitis models. J Neurosci. 2006 Sep 20;26(38):9794-804. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed See also: Vitamins fight multiple sclerosis. Orthomolecular Medicine News Service, October 4, 2006.For More Information:A complete copy of Dr. Harold D. Foster's What Really Causes Alzheimer's Disease is available in PDF format, free of charge: http://www.hdfoster.com/Foster_Alzheimers.pdfTo access a free archive of peer-reviewed medical journal papers on the safety and efficacy of vitamin therapy: http://orthomolecular.org/library/jom/Review of nutritional approaches to Alzheimer's Disease: http://www.doctoryourself.com/alzheimer.htmlAdditional Reading:Klenner FR. Response of peripheral and central nerve pathology to mega-doses of the vitamin B-complex and other metabolites. Journal of Applied Nutrition, 1973. http://www.tldp.com/issue/11_00/klenner.htmMorris MC, Evans DA, Bienias JL, Tangney CC, Bennett DA, Aggarwal N, Wilson RS, and Scherr PA. Dietary intake of antioxidant nutrients and the risk of incident Alzheimer's disease in a biracial community study. Journal of the American Medical Association, 2002. 287(24), 3230-3237.Morris MC, Evans DA, Bienias PA, Scherr A, Tangney CC, Hebert LE, Bennett DA, Wilson RS, and Aggarwal N. Dietary Niacin and the Risk of Incident Alzheimer's Disease and of Cognitive Decline. J Neurology, Psychiatry 2004; 75: 1093-1099.Bobkova NV. The impact of mineral ascorbates on memory loss. Paper presented at the III World Congress on Vitamin C, 2001, Committee for World Health, Victoria, BC, Canada.Galeev A, Kazakova A, Zherebker E, Dana E, and Dana R. Mineral ascorbates improve memory and cognitive functions in older individuals with pre-Alzheimer's symptoms. Copy of paper given to authors by R. Dana and E. Dana, Committee for World Health, 20331 Lake Forest Drive, Suite C-15, Lake Forest, California 92630, USA.Bobkova NV, Nesterova IV, Dana E, Nesterov VI, Aleksandrova IIu, Medvinskaia NI, and Samokhia AN (2003). Morpho-functional changes of neurons in temporal cortex in comparison with spatial memory in bulbectomized mice after treatment with minerals and ascorbates. Morfologiia, 123(3), 27-31. [In Russian]Engelhart MJ, Geerlings MI, Ruitenberg A, van Swieten JC, Hofman A, and Witteman JC (2002). Dietary intake of antioxidants and risk of Alzheimer's disease: Food for thought. Journal of the American Medical Association, 287(24), 3223-3229.Grant WB. Dietary links to Alzheimer's disease: 1999 update. Journal of Alzheimer's disease, 1999, 1(4,5), 197-201.Barberger-Gateau P, Letenneur L, Deschamps V, Pérès K, Jean-François Dartigues JF, and Renaud S (2002). Fish, meat, and risk of dementia: Cohort study. British Medical Journal, 325, 932-933.
Vogiatzoglou A, Refsum H, Johnston C, Smith SM, Bradley KM, de Jager C, Budge MM, Smith AD. Vitamin B12 status and rate of brain volume loss in community-dwelling elderly. Neurology. 2008 Sep 9;71(11):826-32.
September 2010 Good News for B Vitamins and Your Brain
Vitamin D may help prevent Alzheimer's
SENDAI, Japan, July 12 (UPI) -- Low levels of vitamin D may be involved in age-related decline in memory and cognition as well as Alzheimer's disease, researchers in Japan say.
Tetsuya Terasaki of Tohoku University in Japan found vitamin D injections improved the removal of amyloid beta -- the build-up of the peptide amyloid beta in the brain is linked to Alzheimer's disease -- from the brain of mice.
"Vitamin D appears [to] increase transport of amyloid beta across the blood brain barrier by regulating protein expression, via the vitamin D receptor and also by regulating cell signaling," Terasaki says.
These findings, published in the journal Fluids and Barriers of the CNS, lead the way toward new therapeutic targets in the search for prevention of Alzheimer's disease.
Tetsuya Terasaki of Tohoku University in Japan found vitamin D injections improved the removal of amyloid beta -- the build-up of the peptide amyloid beta in the brain is linked to Alzheimer's disease -- from the brain of mice.
"Vitamin D appears [to] increase transport of amyloid beta across the blood brain barrier by regulating protein expression, via the vitamin D receptor and also by regulating cell signaling," Terasaki says.
These findings, published in the journal Fluids and Barriers of the CNS, lead the way toward new therapeutic targets in the search for prevention of Alzheimer's disease.
© 2011 United Press International, Inc
