jimmylegs wrote:hi jen, and welcome i'm the vittymin nut here, if you tell me your nutrient results (did they do more than the standard b12?) i can most likely tell you whether they're in the good part of the normal range, or the "ms" part. or at least i could tell you some levels to aim for in a few things. you might want to ask for some mineral tests too. like zinc, and rbc magnesium. and a uric acid test.
jimmylegs wrote:your b12 looks enviable!
nope uric acid is not urine ph. you can read up on it at wikipedia:
did you get units for any of those other levels? i don't have my own file here so i can't compare. i'll be back with my files by sept 7.
besides rbc magnesium, zinc, and uric acid, d3 is a useful thing to have tested. 25hydroxyvitamind3, to be exact.
the literature to support the investigation of these things in ms cases is out there. if you need to take anything to your doc i can probably drum up a few links, but also if you search for related posts here you should get a lot of abstracts to keep you busy!
The current high life expectancy is overshadowed by neurodegenerative illnesses that lead to dementia and dependence. Alzheimer’s disease (AD) is the most common of these conditions, and is considered to be a proteinopathy, with amyloid-b42 as a key factor, leading via a cascade of events to neurodegeneration. Major factors involved are oxidative stress, perturbed Ca homeostasis and impaired energy metabolism. Protection against oxidative stress by micronutrients (including secondary bioactive substances) has been shown in transgenic Alzheimer model systems to delay AD. Epidemiological evidence is less conclusive, but the vast majority of the evidence supports a protective effect on cognitive functions in old age and AD. Thus, a diet rich in fruits and vegetables but also containing meat and fish is the most suitable to provide adequate micronutrients. The strong link between cardiovascular risk and AD may be explained by common pathogenetic mechanisms mediated, for example, by homocysteine and thus dependant on B-vitamins (folate and vitamins B12 and B6). However, micronutrients may also be harmful. The high affinity of amyloid for metals (Fe, Al and Zn) favours the generation of reactive oxygen species and triggers an inflammatory response.
Micronutrients in a balanced diet have a long-lasting, albeit low, protective impact on brain aging, hence prevention should be life long.
Alzheimer's disease-diabetes connection explained
A study published in the December 8 2004 issue of the Journal of Neuroscience reported that a shortage of a protein called insulin degrading enzyme occurs in the brains of Alzheimer's patients, and established for the first time a cause and effect relationship between insulin signaling and increased production of the protein. Insulin-degrading enzyme (IDE) is involved in eliminating amyloid peptides that form plaques in the brains afflicted with Alzheimer's disease.
The increased risk of Alzheimer's disease experienced by individuals with type 2 diabetes has generated interest in the relationship of insulin signalling to the disease. Diabetes is characterized by insulin resistance and reduced insulin secretion, leading to an elevation of blood glucose.
Lead author and professor of medicine and neurology at the David Geffen School of Medicine at UCLA, Greg M Cole, PhD, and colleagues studied fetal rat brain cultures and brain tissue from humans with Alzheimer's disease. They also examined the brains of adult mice bred to develop amyloid who were given a diet in which the source of fat was safflower oil, or a standard diet whose fat content was provided by soy and fish oil. A safflower oil based diet provides almost no omega-3 fatty acids, and has been found to speed up Alzheimer's-like conditions in the brains of laboratory animals.
The team found that insulin increased IDE protein in fetal rat brain tissue. In human brains afflicted with Alzheimer's disease, a deficiency of IDE protein was observed. And in the brains of mice whose source of dietary fat was from safflower oil rather than fish and soy, IDE levels were lower than in those from mice on the standard diet.
The findings explain the association between type 2 diabetes and Alzheimer's disease, and show that the protective IDE protein can be increased by dietary manipulation.
Two years ago researchers at the Massachusetts General Hospital reported that the antibiotic clioquinol inhibited and even reduced the build-up of amyloid plaques in the brain of mice engineered to developed Alzheimer-like deposits. Now researchers at the Harvard Medical School and the University of Melbourne are about to release the results of a phase II trial involving the use of clioquinol in human Alzheimer's patients. So far the findings are extremely promising. Clioquinol treatment slowed down the disease and significantly reduced the accumulation of beta-amyloid plaques, a cardinal feature of Alzheimer's.
Dr. Ashley Bush of the Harvard Medical School believes that Alzheimer's disease begins when iron, copper and zinc accumulates in the brain and turns beta-amyloid into a rogue enzyme that catalyses the production of hydrogen peroxide which then attacks and destroys brain cells. In the process beta-amyloid forms into the long chain of insoluble plaque so characteristic of Alzheimer's. Dr. Bush believes that clioquinol works by removing (chelating?) the metals from the brain. This, in turn, stops the formation of hydrogen peroxide and thus the destruction of brain cells and also prevents the beta-amyloid particles from clumping together. There is some concern that clioquinol depletes vitamin-B12 in the body so vitamin B12 supplementation is a must when taking clioquinol.
jimmylegs wrote:hey there, ohhh so it's about 450 in my language most people would say that that b12 result is still a pretty darned good number. well within the normal range in most places. if you trust the normal range. but you're getting pretty close to the line for CSF b12 deficiency. i try to keep my level over 500, which would be about 680 for you. once you drop under 600, that's unhappy time for the spine.
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