6/19/2016 ~ An interesting thing in the Guccifer 2.0 papers hacked from the Democratic National Committee said, “make patients into consumers.” It was under, Campaign 2016, so I’m guessing it’s aimed at tangible thanks to Pharma donors.
Since 1 in 10 Americans over the age of 65 may be affected by Alzheimer’s, the profit potential is huge as long as people don’t stymie it by using vitamin B12. Yes, I’m skeptical of pharma, the DNC and a 2015 study that mainstream media widely reported as saying B12 can’t prevent Alzheimer’s.
Alzheimer’s is a disease that impacts cognition. Loss of intellectual skills, as well as memory, tends to be associated with aging far more frequently than with low vitamin B12 levels. There is, in fact, almost an expectation of some dementia with advancing years.
The expectation of dementia is dangerous. If you accept memory loss without question, you may lose your best chance to reverse memory loss.
One large study publicized that participants with established Alzheimer’s did not respond to vitamin B12, while participants who had memory loss but not identifiable Alzheimer’s improved with vitamin B12. Effects of homocysteine lowering with B vitamins on cognitive aging: meta-analysis of 11 trials with cognitive data on 22,000 individuals, Am J Clin Nutr, 2014 Aug. Clarke, Bennett, et al.
The study was criticized in a letter to the editor of Am J Clin Nutr, by Peter Garrard and Robin Jacoby of the Neuroscience Research Centre, St. George’s, University of London, for lumping different trials together as if they evaluated cognition equally.
Most notably, Garrard and Jacoby questioned the “highly tendentious statement” that the study’s findings showed taking vitamin B12 “is sadly not going to prevent Alzheimer’s disease,’’ a quotation that was picked up by mainstream media. Garrard pointed out that there is first-rate scientific evidence that homocysteine lowering with the use of B vitamins confers both biological and neuropsychological benefits on individuals with clinical mild cognitive impairment.
For myself, having experienced getting lost while driving once familiar streets and losing memory so quickly that I felt as if a black tunnel had attached itself to me, gobbling up moments one step behind me, I am well aware that my declining cognition affected my physical health. And, just to be clear, at the time I was having regular B12 shots.
I became less and less active. I’d sit at my desk forgetting to make lunch, and yet I gained weight because all I was doing was sitting. If I thought of something I wanted to do, by the time I’d stood up, I’d forgotten what that was.
Luckily the state paid for me to see a therapist, due to my brain injury and the need for “vocational rehabilitation”. Focusing on my website gave me my first bit of improvement: In those days if I put a product link on a page it showed up on the live page differently from its placement on my editing page. I had to keep switching between the two views. And, in either view, I could not remember the other view. All I knew was that the image link wasn’t where I wanted it. So, it would take me hours to nudge the html box around till the live page looked the way I wanted.
At night, I would have no memory of the image I was trying to get into a particular position. Then, one day I worked on this one, single, simple task from 7 a.m. to 11 p.m. and that night before I fell asleep, I could see in my mind’s eye the Sharper Image logo I’d been trying all day to position. To have that tiny bit of memory was the most wonderful thing. It proved that I could build new pathways in my brain.
Today, a decade later, I’ve discovered that two years of eating Swiss Cheese with its B12 making bacteria has helped in an impressive way. Now I can do something like make coffee, and leave the kitchen with a memory of making the coffee. Previously all I had when I left the kitchen was the mug of coffee.
Playing computer games and doing puzzles exercises your brain in much the same way I exercised mine when I was working on my web pages. The point is, B12 alone will not restore your cognitive function. B12 helps, but you have to do something to rebuild pathways.
Genetic Predisposition to Alzheimers
The coalesced study of 22,000 individuals that concluded, to the joy of media/pharma and the dismay of other researchers, that vitamin B12 can not prevent Alzheimer’s in those with a genetically smaller hippocampus (memory area within the brain) is in sharp contrast to the following earlier study:
Low Vitamin B12 Associated with Poor Memory in Older People at Risk For Alzheimer’s
by David Bunce, PhD, a psychologist at Goldsmith’s College, University of London; Miia Kivipelto, PhD, MD, of the Aging Research Center at the Karolinska Institute in Stockholm and the Stockholm Gerontology Research Center; and Wahlin, PhD, a psychologist at University of Stockholm.
Among healthy people over the age of 75 who have the genotype associated with higher risk for Alzheimer’s, low levels of vitamin B12 are associated with significantly worse performance on memory tests.
A gene which moves cholesterol in the body has a version called the 4 allele. Carried by perhaps 15% of the population, it is a risk factor for dementia. Data collected over a six-year period suggests that one out of four carriers with one copy of this allele and half carrying two copies will develop Alzheimer’s. Non-carriers also can get Alzheimer’s.
Carriers of the 4 allele have smaller hippocampi, brain areas associated with memory, so the researchers wanted to measure how an additional physiological shortfall such as low Vitamin B, affected this group, given that reduced B12 has been linked with diminished memory and increased risk for Alzheimer’s.
The researchers studied 167 healthy older people, averaging nearly 83 years old. Among carriers of the 4 allele, people with normal B12 levels recalled a greater number of words.
A significant difference showed up in the experiment’s most demanding condition, when participants had just two seconds to encode words. In that situation, the high-risk genotype plus low B12 levels was significantly associated with poorer memory.
The findings endorse a complex model of vulnerability in which genetic and non-genetic factors interact. According to the authors, “4 ApoE allele carriers may derive relatively greater cognitive benefits from B12 and folate supplements. Supplement treatment is relatively inexpensive and may be required as part of preventive health regimes for older persons.” American Psychological Association, 5 April 2004
Alzheimer’s and Plaque
A known factor in Alzheimer’s Disease as well as Parkinson’s Disease is plaque buildup in the brain. Research shows that vitamin B12 reduces plaque in the brain.
I am convinced of the truth of this because in my experience plaque around my teeth was significantly reduced by vitamin B12 replacement.
Keep your teeth ~ Read more.
Prevent Memory Loss
BBC News report September 9, 2008 ~ Vitamin ‘may prevent memory loss’
Older people with lower than average vitamin B12 levels were more than six times more likely to experience brain shrinkage, researchers concluded.
The University of Oxford study, published in Neurology, tested 107 apparently healthy volunteers, aged 61 to 87, over a five-year period. The group was split into thirds depending on participants’ vitamin B12 levels.
The third with the lowest B12 levels were above a threshold used by some scientists to define vitamin B12 deficiency. Despite this they showed more signs of brain shrinkage over the five-year period.
Professor David Smith, who directs the Oxford Project to Investigate Memory and Ageing, said: “This study adds another dimension to our understanding of the effects of B vitamins on the brain – the rate of shrinkage of the brain as we age may be partly influenced by what we eat.”
Shrinkage has been strongly linked with a higher risk of developing dementia and Rebecca Wood, chief executive of the Alzheimer’s Research Trust, said: “This study suggests that consuming more vitamin B12 through eating meat, fish, fortified cereals or milk as part of a balanced diet might help protect the brain. Liver and shellfish are particularly rich sources of B12.”
Dr Susanne Sorensen, from the Alzheimer’s Society said, “Shrinkage is usually associated with the development of dementia.”
Foods containing B12 ~ Read more.
A combination of high levels of homocysteine and low levels of vitamin B12 is a significant risk factor for Alzheimer’s disease among African Americans, according to a paper presented at the International Conference on Alzheimer’s Disease and Related Disorders in Stockholm, Sweden.
Floyd Willis and colleagues at the Mayo Clinic in Florida conducted a study to evaluate the association between homocysteine, B12 and folic acid levels in African Americans with Alzheimer’s disease.
The researchers collected blood samples from 256 African Americans who showed no signs of cognitive impairment and 58 African Americans who had a clinical diagnosis of Alzheimer’s disease. All study participants were over the age of 50.
The researchers found homocysteine levels were significantly higher in the individuals with Alzheimer’s disease and levels of B12 were significantly lower.
It is interesting to consider what proportion of Alzheimer’s Dementia (AD) may result from under-nutrition, (1) especially when it seems that there may be an easy, low-cost, perfectly safe, nutritional way that may allow people to avoid a miserable illness that many people consider worse than death. Some people might say, “That’s too good to be true!” In fact, an at-home nutritional program, using a lot of vitamin B12 may indeed prevent and virtually eliminate AD. An early launch of the treatment soon after first warning symptoms start could even turn off the process.
Confusion, difficulty concentrating, loss of memory, marked changes in personality that can lead to outbursts of violence, hallucinations, wandering away, and early death all characterize Alzheimer’s dementia. An estimated 2.3 million Americans now have AD. Prevalence doubles every five years after the age of 60, increasing from one percent among those 60 to 64 up to 40% among those aged 85 years and older.
Let’s start with a little background. Mammals, including humans, are born with serum levels of vitamin B12 at about 2,000 pg/ml. The level declines throughout human life owing to practices common in Western societies. Below 550 to 600 pg/ml, deficiencies start to appear in the cerebrospinal fluid. US clinical laboratories regard 200 pg/ml as the lower range of normal.
“Most cases of Alzheimer’s dementia are actually missed B12 deficiency cases, because of the too-low normal range for B12,” wrote John V. Dommisse, MD in 1991 in Medical Hypotheses. Dommisse, who practices medicine in Tucson, Arizona, has confirmed that Alzheimer’s disease appears to result from too-low serum vitamin B12, and repletion of the vitamin succeeds despite other risk factors. Repleting B12 can reverse 75% of B12 deficiency dementias when the condition is discovered early enough.
Other aspects of the therapy should be noted: The neurological and cerebral manifestations of B12 deficiency require dosages larger, and extending over a longer time, than to those needed to reverse hematologic effects. B12 therapy appears to be perfectly safe; in other words, the risk of overdose is virtually nil. Patients of Dr. H.L. Newbold in New York City injected themselves three times daily with triple-strength doses of B12 (9,000 ug/micrograms/per day) indefinitely. Their serum B12 levels reached 200,000 pg/ml (100 times the normal level found in newborn babies and higher), but none had any significant side effects.
Functional vitamin B12 deficiency and Alzheimer disease
A. McCaddon, MRCGP, B. Regland, MD PhD, P. Hudson, MSc and G. Davies, MSc — From the University of Wales College of Medicine
Moderately elevated total serum homocysteine is associated with an increased risk of atherothrombotic vascular events. Accordingly, serum homocysteine is increased in patients with vascular dementia but is also increased in clinically diagnosed and histologically confirmed AD.
It is generally considered that homocysteine potentiates endothelial and neuronal oxidative injury in these diseases.
A complementary model of oxidative stress induced hyperhomocystinemia is proposed by the authors. The hypothesis accounts for several unusual features relating to single-carbon metabolism and AD, including the absence of macrocytic anemia in these patients. It is suggested that cerebral oxidative stress augments the oxidation of an intermediate form of vitamin B12 generated in the methionine synthase reaction, thereby impairing the metabolism of homocysteine. Oxidative stress also compromises the intraneuronal reduction of the vitamin to its metabolically active state. Neurology, 2002
High Homocysteine ~ Read more.
Alzheimer disease: protective factors.
Nourhashemi F, Gillette-Guyonnet S, Andrieu S, et al.
Individuals with Alzheimer’s disease often have low blood levels of vitamin B12. Lower vitamin B12 levels are found in the cerebrospinal fluid of patients with Alzheimer’s disease than in patients with other types of dementia, though blood levels of vitamin B12 did not differ.
Am J Clin Nutr. 2000
Low vitamin B-12 status in confirmed Alzheimer’s disease as revealed by serum holotranscobalamin
H Refsum, A D Smith — Department of Pharmacology, University of Oxford, Oxford, UK
51 patients with pathologically confirmed Alzheimer’s disease and 65 cognitively screened elderly controls were studied. Serum holotranscobalamin was measured by a new solid phase radioimmunoassay.
Geometric mean levels showed no significant differences for serum total cobalamin, but lower levels of holotranscobalamin in Alzheimer’s disease (41.1 pmol/l) than in controls (57.1 pmol/l) (p < 0.001). The odds ratio of Alzheimer’s disease was significant for low holotranscobalamin but not for low total cobalamin.
Conclusion: Disturbed cobalamin status is common in Alzheimer’s disease and accordingly measurement of holotranscobalamin should be considered in the assessment of cognitively impaired patients. Journal of Neurology Neurosurgery and Psychiatry; 2003
Alzheimer’s linked to low vitamin levels
People with low levels of the vitamins B12 or folate may have a higher risk of developing Alzheimer’s disease; scientists found that 46 out of 78 Alzheimer’s patients they examined had low levels of both vitamins and they believe a lack of the two vitamins may influence levels of chemicals that play a vital role in transmitting signals around the brain.
Researcher Dr Hui-Xin Wang said, “In our study, we found that low levels of either of these two vitamins were related to an increased Alzheimer’s disease risk.”
Professor David Smith, of the Alzheimer’s Research Trust, said the research confirmed previous studies which suggested a similar link. He also said that the deficiencies may increase levels of a chemical called homocysteine that is known to poison nerve cells.
Vitamin B12 is naturally found in animal foods including fish, milk and milk products, eggs, meat, and poultry.
Leafy greens such as spinach and turnip greens, dry beans and peas, fortified cereals and grain products, and some fruits and vegetables are rich food sources of folate – a form of water-soluble vitamin B. Neurology, the scientific journal of the American Academy of Neurology. 2001
Ageing and aberrant assimilation of vitamin B12 in Alzheimer’s disease.
McCaddon, A; Hudson, P.; Abrahamsson, L.; Olofsson, H.; Regland, B.
Vitamin B12 assimilation might be disrupted in patients with Alzheimer’s disease. Twenty-three patients, aged 60 or over, with features compatible with degenerative dementia of the Alzheimer type were recruited together with 18 cognitively intact age-matched control subjects. Total vitamin B12 was measured in serum. Alzheimer patients had significantly lower active corrinoid and the analogue/corrinoid ratio was significantly higher in the Alzheimer group. Two disparate mechanisms might exist for the development of cerebral B12 deficiency in Alzheimer’s disease, although both imply a disruption of selective B12 assimilation and analogue elimination in such patients. Dement-Geriatr-Cogn-Disord. 2001
B12 Malabsorption ~ Read more.