i wonder what the mice in the above study had for dietary calcium
Dietary Calcium Is a Major Factor in 1,25-Dihydroxycholecalciferol Suppression of Experimental Autoimmune Encephalomyelitis in Mice1
http://jn.nutrition.org/content/129/11/1966.fullThe active form of vitamin D (1,25-dihydroxycholecalciferol) is a potent immune system regulator. Treating mice with 1,25-dihydroxycholecalciferol and feeding them diets high in calcium can completely suppress the induction of experimental autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). Experiments described here were carried out on mice in which development of EAE was induced. Mice were fed diets containing various amounts of calcium and 1,25-dihydroxychole-calciferol. Variables measured were as follows: 1) incidence and severity of EAE; 2) serum calcium concentrations; 3) body weight; 4) total number of cells in the lymph nodes; and 5) interleukin-4 (IL-4) and transforming growth factor-ß1 (TGF-ß1) mRNA levels. When calcium was removed from the diet, the incidence of EAE was reduced 20% in both males and females. Further, the lower the dietary level of calcium, the higher was the dose of 1,25-dihydroxycholecalciferol required to prevent the symptoms. Thus, 1,25-dihydroxycholecalciferol was found most effective in mice fed a diet adequate or high in calcium. 1,25-Dihydroxycholecalciferol treatment of mice fed high dietary calcium resulted in a decreased number of lymphocytes in the lymph nodes and increased IL-4 and TGF-ß1 mRNA levels. When calcium was omitted from the diet, 1,25-dihydroxycholecalciferol supplementation increased TGF-ß1 mRNA. Increased IL-4 mRNA and decreased lymphocytes in the lymph nodes in response to 1,25-dihydroxycholecalciferol occurred only when dietary calcium was adequate or high. Our results suggest that dietary calcium and 1,25-dihydroxycholecalciferol are both involved in the prevention of symptomatic EAE.
in humans, we know about the calcium magnesium and zinc requirements but as a fat soluble vitamin, absorption is also fat-dependent. last night i ran across the relevant study but i'm not using the right search terms to find it again. for the nonce, a study on another fat soluble vit:
The absorption of vitamin E is influenced by the amount of fat in a meal and the food matrix.
http://www.ncbi.nlm.nih.gov/pubmed/15522126Abstract
Vitamin E absorption requires the presence of fat; however, limited information exists on the influence of fat quantity on optimal absorption. In the present study we compared the absorption of stable-isotope-labelled vitamin E following meals of varying fat content and source. In a randomised four-way cross-over study, eight healthy individuals consumed a capsule containing 150 mg (2)H-labelled RRR-alpha-tocopheryl acetate with a test meal of toast with butter (17.5 g fat), cereal with full-fat milk (17.5 g fat), cereal with semi-skimmed milk (2.7 g fat) and water (0 g fat). Blood was taken at 0, 0.5, 1, 1.5, 2, 3, 6 and 9 h following ingestion, chylomicrons were isolated, and (2)H-labelled alpha-tocopherol was analysed in the chylomicron and plasma samples. There was a significant time (P<0.001) and treatment effect (P<0.001) in (2)H-labelled alpha-tocopherol concentration in both chylomicrons and plasma between the test meals. (2)H-labelled alpha-tocopherol concentration was significantly greater with the higher-fat toast and butter meal compared with the low-fat cereal meal or water (P<0.001), and a trend towards greater concentration compared with the high-fat cereal meal (P=0.065). There was significantly greater (2)H-labelled alpha-tocopherol concentration with the high-fat cereal meal compared with the low-fat cereal meal (P<0.05). The (2)H-labelled alpha-tocopherol concentration following either the low-fat cereal meal or water was low. These results demonstrate that both the amount of fat and the food matrix influence vitamin E absorption. These factors should be considered by consumers and for future vitamin E intervention studies.
it's key to separate the influence of light period, from the influence of vitamin d3. what the uv light is doing for symptoms is possibly related moreso to melatonin and hippocampal neurogenesis than straight vit d3.
http://wolfweb.unr.edu/homepage/vpravos ... memory.htm ms patients have characteristic hippocampal atrophy, and the eae virus attacks and kills murine hippocampal pyramidal neurons.
dietary tryptophan is a key ingredient for melatonin production.
Biological Synthesis and Metabolism of Melatonin
http://www.ch.ic.ac.uk/local/projects/s ... synth.htmlso now the question is, does the wavelength matter. thought back to some chats we had about 5 yrs ago, found this tidbit:
post15775.html?hilit=murine d3#p15775
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kasuku, i just ran across something related to zinc and thought of your comment some time back:
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also would like to attract your attention to the paper on vit. D in the latest posts. The paper described that people with depression did better if they were located in the side of the hospital with sun exposure as well as people recovering from surgery. I assume that the exposure is mostly sunlight filtered by windows so in theory no UVB exposure. Light itself stimulates the pituitary gland resulting in hormone secretions and that could explain quicker recovery from depression as opposed to people kept in darker rooms. Perhaps light itself plays a role in addition to vit D. from UVB exposure. I guess my understanding is that UVB are filtered by glass. Am I right on this? What do you think Jimmylegs?
K
(i didn't answer that question about filtering originally, but the answer is yes..)
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i have the feeling i have made this connection before but in case i didn't post it:
i was just reading these bits and pieces which reminded me of the light exposure sans D3 production element:
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Med Hypotheses. 2000 Sep;55(3):239-41.
The possible role of gradual accumulation of copper, cadmium, lead and iron and gradual depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis.
Johnson S.
Multiple sclerosis (MS) has a much higher incidence among caucasians that in any other race. Furthermore: females are much more susceptible than males and white females living in colder, wetter areas are much more susceptible than those living in warmer areas. On the other hand, menstruating women have increased copper (Cu) absorption and half-life, so they tend to accumulate more Cu than males. Moreover, rapidly growing girls have an increased demand for zinc (Zn), but their rapidly decreasing production of melatonin results in impaired Zn absorption, which is exacerbated by the high Cu levels. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide. Menstruating females also often present with low magnesium (Mg) and vitamin B6 levels. Vitamin B6 moderates intracellular nitric oxide (NO) production and extracellular Mg is required for NO release from the cell, so that a deficiency of these nutrients results in increased NO production in the cell and reduced release from the cell. The trapped NO combines with superoxide to form peroxinitrite, an extremely powerful free radical that leads to the myelin damage of MS. Iron (Fe), molybdenum (Mo) and cadmium (Cd) accumulation also increase superoxide production. Which explains MS in males, who tend to accumulate Fe much faster and Cu much less rapidly than females. Since vitamin D is paramount for Mg absorption, the much reduced exposure to sunlight in the higher latitudes may account for the higher incidence in these areas. Moreover, vitamin B2 is a cofactor for xanthine oxidase, and its deficiency exacerbates the low levels of uric acid caused by high Cu levels, resulting in myelin degeneration. Finally Selenium (Se) and vitamin E prevent lipid peroxidation and EPA and DHA upregulate CuZnSOD. Therefore, supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 microg Se, 180 mg EPA and 120 mg DHA per day between 14 and 16 years of age may prevent MS.
also found this...
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Melatonin: Where It Comes From
Melatonin is a naturally occuring hormone that is synthesized from the neurotransmitter serotonin which in turn is synthesized from the amino acid tryptophan. This synthesis or production occurs primarily in a gland located at the center of the brain called the pineal gland. The pineal gland is light-activated, i.e., it is controlled by the amount of light seen by the eyes each day. This light activation gives rise to the belief that the pineal gland functions as the body's internal clock, regulating functions that are time-related such as sleep and the ageing process. Melatonin production via serotonin synthesis occurs at its peak during the dark hours around 2:00 a.m. Inversely, during daylight hours, melatonin production is low. It is for this reason that melatonin is believed to aid in regulating our sleep cycle and help stimulate sleep. Also, evidence exists that the pineal gland not only controls our 24 hour clock but our "life clock", meaning that it appears to be a major controller regarding our ageig process. As we age, several things happen to our pineal gland that result in it producing less melatonin. Since the pineal gland is derived from nerve tissue, the gland's cells do not replicate when damaged or lost. This loss of pineal gland cells may result from chemical or biological injury to the gland, or for a myriad of other reasons. Therefore, as we age, the pineal gland literally decreases in size or atrophies which has a direct effect on the amount of melatonin it is capable of synthesizing. Additionally, the gland itself is susceptible to the ageing processes that occur, such as calcium deposits and a decreased blood supply due to atherosclerosis. These in conjunction with other ageing processes interfere with the pineal gland’s melatonin-producing activities.
i am working on finding some info on pineal gland nutrition and support, i found one 2001 rat study but will keep looking
Hi Jimmylegs,
Very interesting! Do you recall the work coming out of Stanford where they found that tryptophan giving to mice in the EAE model not only stopped the progression of the disease, but also improved the clinical signs. The connection between tryptophan, melatonin and light is definitely interesting. I wonder if there are ways to stimulate the pineal gland other than with light. Taking melatonin may have the opposite effect due to biofeedback. What do you think?
K
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