all things vitamin D

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more d info

Postby jimmylegs » Fri May 12, 2006 11:12 am

Mult Scler. 2005 Jun;11(3):266-71.
25-Hydroxyvitamin D levels in serum at the onset of multiple sclerosis.
Soilu-Hanninen M, Airas L, Mononen I, Heikkila A, Viljanen M, Hanninen A.
Medicity Research Laboratory, University of Turku, Tykistokatu 6, FIN-20520 Turku, Finland.

Past sun exposure and vitamin D supplementation have been associated with a reduction in the risk of MS. We measured the serum concentration of 25-hydroxyvitamin D (25[OH]D) at the time of MS diagnosis in 40 MS patients and 40 controls. We found no difference in the serum levels of 25(OH)D between MS patients and controls when all samples or samples obtained during winter months were compared, but MS patients had significantly lower serum 25(OH)D concentrations in June to September than the controls. The vitamin D stores were adequate for bone metabolism (> 37 nmol/L) in 70% of MS patients throughout the year and within the hypovitaminosis level (< 37 nmol/L) in 30% of MS patients at some time of the year. During MS-relapses, 25(OH)D levels were lower than in remission, but mostly within the reference range observed in relation with normal bone metabolism. We conclude that the vitamin D stores in most MS patients are adequate for their normal bone metabolism. However, lower vitamin D levels during MS relapses than in remission suggest that vitamin D could be involved in the regulation of the clinical disease activity of MS. The optimal serum levels of vitamin D for the regulation of immune responses remain to be determined.

J Am Diet Assoc. 2006 Mar;106(3):418-24.
Vitamin D and autoimmune disease--implications for practice from the multiple sclerosis literature.
Mark BL, Carson JA.
Department of Clinical Nutrition, University of Texas Southwestern Medical Center at Dallas 75390-8877, USA.

Recent studies and commentaries link vitamin D with several autoimmune diseases, including multiple sclerosis (MS). Adequate vitamin D intake reduces inflammatory cytokines through control of gene expression, thus inadequate vitamin D intake is suggested as a mechanism that could contribute to inflammation and, consequently, development of MS. Poor vitamin D status has been associated with increased risk for development of MS, and patients with MS may suffer consequences of vitamin D deficiency, such as bone loss. Animal studies and very limited human data suggest possible benefit from vitamin D supplementation in patients with MS. Based on the current state of research, a key principle for practicing dietetics professionals is to include vitamin D status in nutritional assessment. For those at risk for poor vitamin D status, intake can be enhanced by food-based advice and, when indicated, vitamin D supplementation.

Ann Pharmacother. 2006 May 9; [Epub ahead of print]
The Role of Vitamin D in Multiple Sclerosis (June).
Brown SJ.
Drug Information Service, Skaggs School of Pharmacy, College of Health Professions and Biomedical Sciences, The University of Montana, 32 Campus Dr. Skaggs, Bldg 217, Missoula, MT
59812-1522, fax 406/243-4353,

OBJECTIVE: To evaluate the literature about the role of vitamin D in the prevention and treatment of multiple sclerosis (MS). DATA SOURCES: MEDLINE (1966-April 2006) and International Pharmaceutical Abstracts (1970-April 2006) searches were performed. In addition, pertinent references from identified articles were obtained. Key search terms included vitamin D, 25-hydroxyvitamin D, vitamin D deficiency, and multiple sclerosis. DATA SYNTHESIS: Vitamin D supplementation prevented the development and progression of experimental autoimmune encephalitis, an animal model of MS, in mice. A large, prospective, cohort study found that vitamin D supplementation was associated with a 40% reduction in the risk of developing MS. Four small, noncontrolled studies suggested that vitamin D supplementation may decrease exacerbation of MS symptoms. CONCLUSIONS: Vitamin D supplementation may help prevent the development of MS and may be a useful addition to therapy. However, current studies are in small populations and are confounded by other variables, such as additional vitamin and mineral supplementation.
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still more d info

Postby jimmylegs » Fri May 12, 2006 11:13 am

Prog Biophys Mol Biol. 2006 Feb 28; [Epub ahead of print]
Epidemiology of disease risks in relation to vitamin D insufficiency.
Grant WB.
Sunlight, Nutrition and Health Research Center (SUNARC), 2107 Van Ness Avenue, Suite 403B, San Francisco, CA 94109-2529, USA.

Vitamin D from ultraviolet-B (UVB) irradiance, food, and supplements is receiving increased attention lately for its role in maintaining optimal health. Although the calcemic effects of vitamin D
have been known for about a century, the non-calcemic effects have been studied intently only during the past two-three decades. The strongest links to the beneficial roles of UVB and vitamin D to date are for bone and muscle conditions and diseases. There is also a preponderance of evidence from a variety of studies that vitamin D reduces the risk of colon cancer, with 1000 IU/day of vitamin D or serum 25-hydroxyvitamin D levels >33ng/mL (82nmol/L) associated with a 50% lower incidence of colorectal cancer. There is also reasonable evidence that vitamin D reduces the risk of breast, lung, ovarian, and prostate cancer and non-Hodgkin's lymphoma. There is weaker, primarily ecologic, evidence for the role of vitamin D in reducing the risk of an additional dozen types of cancer. There is reasonably strong ecologic and case-control evidence that vitamin D reduces the risk of autoimmune diseases including such as multiple sclerosis and type 1 diabetes mellitus, and weaker evidence for rheumatoid arthritis, osteoarthritis, type 2 diabetes mellitus, hypertension and stroke. It is noted that mechanisms whereby vitamin D exerts its effect are generally well understood for the various conditions and diseases discussed here.

Srp Arh Celok Lek. 2005 Dec;133 Suppl 2:124-8.
[Effects of alfacalcidol therapy on serum cytokine levels in patients with multiple sclerosis]
[Article in Serbian]
[No authors listed]

Multiple sclerosis (MS) is a consequence of genetic and environmental factors. Geographic, genetic, and biological evidence suggests that an important immunopathogenic factor might be the insufficiency of vitamin D. The aim of our study was to investigate the immunomodulatory effect of alfacalcidol, a vitamin D analogue, on cytokine levels in RRMS patients in relapse. We investigated 15 patients suffering from RRMS relapse (an RRMS group) and two control groups: one control group of healthy subjects (n=10) and a NIND group, consisting of patients with non-inflammatory neurological diseases (n=10). All of the MS patients were treated with 5 microgr/day of oral alfacalcidol for a period of five days. The serum cytokine levels of TNF-alpha, IL-10, IL-4, and IL-12 were measured in all the MS patients one day prior to and one day after therapy, and in all the control subjects (ELISA, Quantikine human immunoassay, R&D Systems, UK). Our results showed significantly lower IL-4 and IL-12 levels in the RRMS patients group compared to the N group and the NIND group (p<0.001 Mann-Whitney U-test). No significant differences in TNF-alpha and IL-10 levels were found between the groups, and there was no influence of alfacalcidol on these cytokines in RRMS patients. High doses of oral alfacalcidol induced significant increases in IL-4 and IL-12 levels in RRMS patients (p<0.001, Wilcoxon rank signed test). Therefore, there were no differences in IL-4 and IL-12 levels compared to the N group and the NIND group. Alfacalcidol therapy in RRMS patients did not provoke any side effects. Vitamin D and its analogues, such as alfacalcidol, act as immunomodulatory agents, with potential therapeutic effects for patients with multiple sclerosis.

Prog Biophys Mol Biol. 2006 Feb 28; [Epub ahead of print]
Vitamin D and its role in immunology: Multiple sclerosis, and inflammatory bowel disease.
Cantorna MT.
Department of Veterinary and Biomedical Sciences, Center for Molecular Immunology and Infectious Diseases, The Pennsylvania State University, 115 Henning Bldg., University Park, PA 16802, USA.

Autoimmune diseases like multiple sclerosis (MS) and inflammatory bowel disease (IBD) occur because of an inappropriate immune-mediated attack against self-tissue. Analyses of genetically identical twins shows that besides genetics there are important environmental factors that contribute to MS and IBD development. Vitamin D availability due to sunshine exposure or diet may play a role in the development of MS and IBD. Compelling data in mice show that vitamin D and signaling through the vitamin D receptor dictate the outcome of experimental MS and IBD.

Furthermore, the evidence points to the direct and indirect regulation of T cell development and function by vitamin D. In the absence of vitamin D and signals delivered through the vitamin D receptor, auto reactive T cells develop and in the presence of active vitamin D (1,25(OH)(2)D(3) ) and a functional vitamin D receptor the balance in the T cell response is restored and autoimmunity avoided.
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guess what - info on d

Postby jimmylegs » Fri May 12, 2006 11:14 am

Tidsskr Nor Laegeforen. 2006 Apr 6;126(8):1048-52.
[The photobiology of vitamin D--a topic of renewed focus]
[Article in Norwegian]
Moan J, Porojnicu AC.
Avdeling for stralingsbiologi, Rikshospitalet-Radiumhospitalet, 0310 Oslo.

The sun is our most important source of vitamin D. Exposure to solaria, in sub-erythemogenic doses, also gives large amounts of this vitamin. The ultraviolet radiation in these sources converts 7-dihydrocholesterol to previtamin D3 in the skin. Furthermore, heat isomerization to vitamin D3 takes place, then transport to the liver and hydroxylation to calcidiol, which is transported to the kidneys and hydroxylated to the active hormone calcitriol. The vitamin D3 status of the body is supposed to be reliably imaged by calcidiol measurements. Calcidiol levels above 12.5 nmol/l prevent rickets and osteomalacia, but optimal levels are probably higher, in the range 100-250 nmol/l. A daily food intake of 100-200 microg vitamin D3 (50-100 g cod-liver oil), or a weekly exposure to two minimal erythemal doses of ultraviolet radiation (20 to 40 minutes whole body exposure to midday midsummer sun in Oslo, Norway), will give this level. An adequate supply of vitamin D3 seems to reduce the incidence rates or improve the prognosis of several cancer forms, including prostate, breast and colon cancer, as well as of lymphomas. Several other diseases are related to a low vitamin D3 status: heart diseases, multiple sclerosis, diabetes, and arthritis. The action mechanisms of vitamin D are thought to be mainly related to its known cell-differentiating and immuno-modulating effects. Even though most of the 250 annual death cases from skin cancer in Norway are caused by sun exposure, we should, in view of the health effects of ultraviolet radiation, consider modifying our restrictive attitude towards sun exposure and use of solaria.

J Rheumatol Suppl. 2005 Sep;76:11-20.
D-hormone and the immune system.
Cantorna MT, Mahon BD.
Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania 16802, USA.

D-hormone [1,25(OH)2 D3] is an important immune system regulator that has been shown to inhibit development of autoimmune diseases including experimental inflammatory bowel disease (IBD), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes. Paradoxically, other immune mediated diseases (experimental asthma) and immunity to infectious organisms were not found to be affected by D-hormone treatment. The effectiveness of D-hormone treatment of autoimmune diseases is due to inhibition of the development and function of Th1 cells and the induction of other Th cells including Th2 cells. We report results of microarray analysis of colons from D-hormone treated mice with experimental IBD. Two hundred thirty-nine genes were inhibited and 298 genes were upregulated in the colon by D-hormone treatment of mice with IBD. Of interest was the D-hormone mediated inhibition of 3 tumor necrosis factor-alpha (TNF-alpha, lipopolysaccharide-induced TNF-alpha factor, and TNF receptor) related genes in the colon. It is likely that the effectiveness of D-hormone treatment of experimental autoimmunity is due in part to the inhibition of the TNF family of genes. D-hormone is a selective regulator of the immune system, and the outcome of D-hormone treatment depends on the nature (infectious disease, asthma, autoimmune disease, etc.) of the immune response.

J Neurol Neurosurg Psychiatry. 2005 Sep;76(9):1294-6.
A pilot study of oral calcitriol (1,25-dihydroxyvitamin D3) for relapsing-remitting multiple sclerosis.
Wingerchuk DM, Lesaux J, Rice GP, Kremenchutzky M, Ebers GC.
Mayo Clinic, Scottsdale, Arizona, USA.

BACKGROUND: Epidemiological and ecological studies suggest links between vitamin D deficiency and increased multiple sclerosis (MS) prevalence. OBJECTIVE: To evaluate the safety and tolerability of oral calcitriol therapy in an open label pilot study. METHODS: 15 ambulatory patients with relapsing-remitting MS and at least one clinical relapse within the previous 12 months received oral calcitriol (target dose: 2.5 microg/d) for 48 weeks. Dietary calcium was restricted to 800 mg/d. Patients were monitored using frequent clinical and laboratory examinations, the expanded disability status scale (EDSS), and brain magnetic resonance imaging (MRI). RESULTS:
Two patients withdrew because of symptomatic hypercalcaemia (serum calcium >3.35 mmol/l in each case) resulting from persistent dietary indiscretion. Two diet compliant patients required temporary dose adjustments for mild asymptomatic hypercalcaemia. Diet compliant patients experienced mild adverse effects. The on-study exacerbation rate (27%) was less than baseline.
Four patients experienced five clinical relapses but only one patient worsened by >1 EDSS point.
Brain MRI revealed enhancing lesions in five patients at baseline (33%) and in four (29%) at both 24 and 48 weeks. CONCLUSIONS: Oral calcitriol is safe and well tolerated for up to one year by diet compliant relapsing-remitting MS patients. Further study of vitamin D related mechanisms is warranted in MS.
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and finally, some info on vit d

Postby jimmylegs » Fri May 12, 2006 11:14 am

J Neurogenet. 2005 Jan-Mar;19(1):25-38.
Variation in the vitamin D receptor gene is associated with multiple sclerosis in an Australian population.
Tajouri L, Ovcaric M, Curtain R, Johnson MP, Griffiths LR, Csurhes P, Pender MP, Lea RA.
Genomics Research Centre, School of Health Science, Griffith University Gold Coast, Southport, Queensland, Australia.

Multiple Sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) resulting in accumulating neurological disability. The disorder is more prevalent at higher latitudes. To investigate VDR gene variation using three intragenic restriction fragment length polymorphisms (Apa I, Taq I and Fok I) in an Australian MS case-control population. One hundred and four Australian MS patients were studied with patients classified clinically as Relapsing Remitting MS (RR-MS), Secondary Progressive MS (SP-MS) or Primary Progressive MS (PP-MS). Also, 104 age-, sex-, and ethnicity-matched controls were investigated as a comparative group. Our results show a significant difference of genotype distribution frequency between the case and control groups for the functional exon 9 VDR marker Taq I (p(Gen) = 0.016) and interestingly, a stronger difference for the allelic frequency (p(All) = 0.0072). The Apa I alleles were also found to be associated with MS (p(All) = 0.04) but genotype frequencies were not significantly different from controls (p(Gen) = 0.1). The Taq and Apa variants are in very strong and significant linkage disequilibrium (D' = 0.96, P < 0.0001). The genotypic associations are strongest for the progressive forms of MS (SP-MS and PP-MS). Our results support a role for the VDR gene increasing the risk of developing multiple sclerosis, particularly the progressive clinical subtypes of MS.

Postepy Hig Med Dosw (Online). 2005 Apr 6;59:129-39.
[Biological activity of calcitriol and its new analogues -- potential therapeutic applications]
[Article in Polish]
Pelczynska K, Jaroszewicz I, Switalska M, Opolski A.
Laboratorium Doswiadczalnej Terapii Przeciwnowotworowej, Zaklad Onkologii Doswiadczalnej Instytutu Immunologii i Terapii Doswiadczalnej PAN, Wroclaw.

Calcitriol is effective not only in the regulation of calcium-phosphate homeostasis, but also in promoting the differentiation and inhibition of proliferation of various cells. Calcitriol seems to be a potent drug with various therapeutic applications, such as regulation of calcium-phosphate homeostasis and treatment of psoriasis, autoimmune diseases, and cancer. Since clinical use of calcitriol is largely limited, due to its undesirable side effect of hypercalcemia, numerous calcitriol analogues have been synthesized to obtain compounds with better therapeutic profiles. This paper summarizes the current state of knowledge concerning the cellular mechanisms of calcitriol's biological activity and their clinical implications. Such medical application includes treatment (as a single-drug or in combination) of osteoporosis, renal osteodystrophy, psoriasis (calcipotriol or tacalcitol ointment), autoimmunological diseases (including multiple sclerosis), and some cancers. The efforts to obtain new vitamin D3 analogues are also briefly reviewed. The structures and roles of vitamin D receptors in the biological effects of calcitriol and its analogues are discussed.

Endocr Rev. 2005 Aug;26(5):662-87. Epub 2005 Mar 29.
Noncalcemic actions of vitamin D receptor ligands.
Nagpal S, Na S, Rathnachalam R.
Lilly Research Laboratories, Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA.

1alpha,25-Dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)], the active metabolite of vitamin D(3), is known for the maintenance of mineral homeostasis and normal skeletal architecture. However, apart from these traditional calcium-related actions, 1,25-(OH)(2)D(3) and its synthetic analogs are being increasingly recognized for their potent antiproliferative, prodifferentiative, and immunomodulatory activities. These actions of 1,25-(OH)(2)D(3) are mediated through vitamin D receptor (VDR), which belongs to the superfamily of steroid/thyroid hormone nuclear receptors. Physiological and pharmacological actions of 1,25-(OH)(2)D(3) in various systems, along with the detection of VDR in target cells, have indicated potential therapeutic applications of VDR ligands in inflammation (rheumatoid arthritis, psoriatic arthritis), dermatological indications (psoriasis, actinic keratosis, seborrheic dermatitis, photoaging), osteoporosis (postmenopausal and steroid-induced osteoporosis), cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), secondary hyperparathyroidism, and autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis, and organ transplantation). As a result, VDR ligands have been developed for the treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism. Furthermore, encouraging results have been obtained with VDR ligands in clinical trials of prostate cancer and hepatocellular carcinoma. This review deals with the molecular aspects of noncalcemic actions of vitamin D analogs that account for the efficacy of VDR ligands in the above-mentioned indications.

Mutat Res. 2005 Apr 1;571(1-2):207-19. Epub 2005 Jan 28.
Ultraviolet radiation: effects on risks of prostate cancer and other internal cancers.
Moon SJ, Fryer AA, Strange RC.
Human Genomics Research Group, Institute of Science and Technology in Medicine and Department of Urology, Keele University School of Medicine, University Hospital of North Staffordshire, UK.

Governmental and research agencies worldwide have strongly advocated sun avoidance strategies in an attempt to counter marked increases in skin cancer incidence. Concurrently, there are reports describing widespread Vitamin D3 deficiency. Because 1,25-dihydroxyvitamin D3, through interaction with the Vitamin D receptor, exerts pleiotrophic effects, such deficiency might be expected to have clinical consequences. Indeed, various reports indicate that exposure to ultraviolet radiation (UVR) exerts a protective effect on development of some common diseases including internal cancers and multiple sclerosis. We describe studies indicating that modest exposure reduces risk of prostate cancer. The effect of UVR is mediated by skin type; at lower levels of exposure a relative inability to effect skin pigmentation is protective presumably because it allows more efficient Vitamin D3 synthesis. Polymorphic variants in genes associated with pigmentation including melanocyte stimulating hormone receptor and tyrosinase are also associated with prostate cancer risk. Overall, though preliminary and requiring cautious interpretation, these data indicate that moderate UVR exposure together with characteristics linked with less effective tanning confer reduced prostate cancer risk. Clearly, it is important to define safe levels of UVR that do not result in increased risk of skin cancers such as malignant melanoma.

Curr Drug Targets Inflamm Allergy. 2004 Dec;3(4):377-93.
Immunoregulation through 1,25-dihydroxyvitamin D3 and its analogs.
May E, Asadullah K, Zugel U.
Corporate Research Business Area Dermatology, Schering AG, Mullerstrasse 178, D-13342 Berlin, Germany.

Beyond its effects on bone metabolism, calcium and phosphorus homeostasis, 1,25-dihydroxyvitamin D3 (1,25(OH)(2)D(3), calcitriol) exerts profound effects on the immune system. We here provide an overview over the metabolism, molecular and cellular action of 1,25(OH)(2)D(3) with particular regard to its immunomodulatory function. Effects of 1,25(OH)(2)D(3) on the immune system are manyfold and include suppression of T cell activation, shaping of cytokine secretion patterns, induction of regulatory T cells, modulation of proliferation, and interference with apoptosis. 1,25(OH)(2)D(3) further influences maturation, differentiation, and migration of antigen presenting cells. Altogether, its immunomodulatory potency is comparable to other established immunosuppressants without sharing their typical adverse effects. This profile makes 1,25(OH)(2)D(3) a potential drug for the treatment of immune-mediated diseases. Yet, the

major obstacle for its clinical use, its potent calcemic activity, is not overcome to date. The identification or generation of novel vitamin D derivatives with dissociated calcemic and immunomodulatory properties is therefore a major task. Its success might eventually lead to promising drugs for future therapeutic exploitation of a wide array of immune diseases, such as psoriasis, multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, and others.

Exp Biol Med (Maywood). 2004 Dec;229(11):1136-42.
Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence.
Cantorna MT, Mahon BD.
Department of Nutritional Sciences, Pennsylvania State University, University Park, PA 16802, USA.

Low vitamin D status has been implicated in the etiology of autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease. The optimal level of vitamin D intake required to support optimal immune function is not known but is likely to be at least that required for healthy bones. Experimentally, vitamin D deficiency results in the increased incidence of autoimmune disease. Mechanistically, the data point to a role for vitamin D in the development of self-tolerance. The vitamin D hormone (1,25-dihydroxy vitamin D(3)) regulates T helper cell (Th1) and dendritic cell function while inducing regulatory T-cell function. The net result is a decrease in the Th1-driven autoimmune response and decreased severity of symptoms. This review discusses the accumulating evidence pointing to a link between vitamin D and autoimmunity. Increased vitamin D intakes might decrease the incidence and severity of autoimmune diseases and the rate of bone fracture.
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Postby Loriyas » Fri May 12, 2006 12:25 pm

Thank you for posting these studies on Vit D. I, too, am a firm believer in the benefits of Vit. D, especially from sunshine. Since we moved to Florida from Ohio I have felt much better and have not have any relapses (hope I don't jinx myself!) I have not researched Vit D studies to determine why I felt better but am glad to see the research behind it. I am just grateful to reap the benefits of it!
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sunshine for sure!

Postby jimmylegs » Fri May 12, 2006 2:56 pm

hi there L, i think sunshine is the best too, because of the calcium issues with high oral d supplementation. with my current supplement levels and intent to increase my dosage for the next 10 days or so, i am going to have to get the serum values of a few things in a couple of weeks.

perhaps i should take a month off during each canadian winter and visit a different spot on the equator each year :wink:
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vit d abstracts

Postby jimmylegs » Sat May 13, 2006 6:23 am

hi all i posted a whackload of vitamin d abstracts and one article in a different thread:
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Vitamin D-insulin connection?

Postby lyndacarol » Mon May 29, 2006 6:29 am

After poring and poring over the Vitamin D information, I find I cannot ignore it! If I KNOW my insulin level is high and discover (I will ask my doctor for the blood test this week.) my D is low, couldn't they be connected?

Maybe by binding with or breaking down D, insulin is removed from the body? If so, this could explain the lower prevalence of MS the nearer the equator. And the virtual nonexistence among Eskimos, who eat a lot of fish (dietary D AND reduced carbs which promote insulin production) I wonder if the internationally recognized expert on Vitamin D there in Canada, Reinhold Vieth, knows how insulin interacts with D. Do you have any contact with him, jimmylegs?

Time to find those sun rays!
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Postby jimmylegs » Mon May 29, 2006 2:37 pm

i know LC isn't it CRAZY?

i have no contact (as yet) with RV. i'll keep digging around for more info.

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Iron and B12 research

Postby dignan » Tue May 30, 2006 6:32 pm

Interesting bit of research on the role of iron and B12 in myelination.

Iron and the folate-vitamin B12-methylation pathway in multiple sclerosis.

Metab Brain Dis. 2006 May 26
van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT.
Chemical Pathology, National Health Laboratory Service and the University of Stellenbosch, Tygerberg Hospital, PO Box 19113, 7505, Tygerberg, South Africa,

Some subjects with multiple sclerosis (MS) present with low blood iron parameters. Anecdotal reports and a single patient study suggest that iron supplementation may be beneficial in these subjects. Myelin is regenerated continually, but prerequisites for this process are iron and a functional folate-vitamin B12-methylation pathway.

The aim of this study was to determine iron status, folate and homocysteine in MS subjects, and to evaluate the effect on MS symptoms if deficiencies were addressed.

Results: In relapsing-remitting MS subjects, serum iron concentration correlated significantly with age at diagnosis (r=0.49; p=0.008). In Caucasian female MS subjects, serum iron and ferritin concentrations were significantly lower than in matched controls. In a 6-month pilot study, 12 subjects taking a regimen of nutritional supplements designed to promote myelin regeneration, improved significantly neurologically as measured by the Kurzke EDSS (Total Score means 3.50 to 2.45, 29.9%; p=0.021). These were significantly improved (p=0.002) compared to 6 control group patients taking multivitamins (Kurzke Score increased by 13.9% from 4.83 to 5.50).

Both groups had significantly reduced homocysteine concentrations at 6 months, suggesting that methylation is necessary but not sufficient for myelin regeneration.

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i agree

Postby jimmylegs » Wed May 31, 2006 5:16 am

low iron and b12 have been one of my ongoing problems prior to diagnosis. i have been tested as deficient in each at least once over the past few years, and low the rest of the time.

i was stubborn about taking supplements back when the impacts were not having much effect. this attack certainly changed my outlook on taking pills!
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General Vitamin D article

Postby dignan » Mon Jun 12, 2006 7:44 am

Here's one from the LA Times,

Wonder pill. Really.

As D's benefits become clearer, we're urged to get more -- much more -- of it.

By Chris Woolston, Special to The Times

June 12, 2006 - EVEN the most brazen snake-oil salesman might blush at trying to sell the public on a pill to ease aches and pains, strengthen bones, slow down cancer and prevent diseases as varied as Type 1 diabetes, multiple sclerosis and schizophrenia.

But these claims aren't the frothy hyperbole of a sideshow huckster. A growing number of serious scientists are quite willing to speculate that a single compound may be able to accomplish all of these feats — and possibly more. They're not talking about a new miracle drug, but a common nutrient: vitamin D, "the sunshine vitamin."

Once seen as merely a defense against rickets, vitamin D has in recent years gained recognition as a major force that acts throughout the body. It improves absorption of calcium, controls the growth of cells (both healthy and cancerous), strengthens the immune system and seems to rein in overzealous immune system cells that cause diseases such as rheumatoid arthritis and multiple sclerosis.

Much of vitamin D's potential is still just that: potential. But at this moment, to some scientists the potential looks huge. "Even if two-thirds of these things don't pan out, it's still a blockbuster," says Dr. Robert Heaney, a professor of medicine at Creighton University in Omaha, who specializes in osteoporosis.

As excitement about vitamin D grows, so does the concern that many people may not be getting enough. In March, an article in the journal Mayo Clinic Proceedings called vitamin D deficiency "a largely unrecognized epidemic in many populations worldwide."

Heaney and many other researchers believe the Food and Drug Administration should consider radically increasing the suggested daily dietary intake of the vitamin, which is currently set at 200 international units (IU) for anyone younger than 51, 400 IU for people 51 to 70, and 600 IU for those 71 and older.

They cite studies such as one published earlier this year that found that cancer deaths were especially common in men with low levels of vitamin D, and a series of studies showing that high levels of vitamin D improved strength and prevented falls in elderly people.

"The daily allowances for vitamin D are outdated," says Anthony Norman, a professor of biochemistry at UC Riverside. "I would recommend 1,000 IU per day for all ages, with a maximum of 2,000 IU. I'm considering taking 2,000 IU myself." And, he adds, current evidence suggests that even 10,000 IU — overkill by anyone's standards — would probably be safe.

"I'm 99% sure that vitamin D deficiency is becoming more common," says Dr. Walter Willett, a professor of epidemiology and nutrition at Harvard University who has conducted several studies on the health effects of vitamin D. In one of them, he and his colleagues estimated that an extra 1,500 IU of vitamin D each day could reduce the risk of deadly cancers of the digestive system by 45%.

Willett believes that more than 1 billion people on the planet — including about two-thirds of whites and almost all blacks in America — don't have enough for optimal health. In recent years, shortages of the compound have even led to a resurgence of rickets, a childhood bone deformity, especially among dark-skinned babies who are exclusively breast-fed.

Vitamin D is the only vitamin that the human body can make on its own, with a little help from rays of ultraviolet B light. On a sunny day, a fair-skinned person can make 10,000 to 20,000 IU in 15 minutes or less. Vitamin D is also available in fatty fishes such as salmon and mackerel and in fortified foods such as milk, orange juice and cereals.

The vitamin was discovered about 80 years ago, when doctors realized that both cod liver oil and sunlight could cure the rickets plaguing many poor children in northern cities. The race was on to find the common thread. The German organic chemist Adolf Windaus won that race — and the Nobel Prize — by isolating the vitamin in 1926.

For decades, nobody suspected that vitamin D could do anything other than strengthen bones. But today it's clear that D is a powerful agent with wide-ranging effects. Unlike other vitamins, which act like cogs to aid specific enzymes in the body, vitamin D cycles through the liver and kidneys to turn into a potent steroid hormone in the same chemical class as estrogen and cortisol.

Whatever messages vitamin D carries, the whole body seems to listen. Scientists have found receptors that respond to it in just about every type of human cell, from brain to bones. The hormone can also switch at least 200 genes on and off.

Researchers aren't even close to understanding all of its effects, but what they've seen so far has them buzzing. At a vitamin D scientific workshop in April, 37 speakers from around the world talked of their work, and "everybody there was excited," Norman says.

Much of that excitement is centered around cancer research. Just like nearly all healthy cells, cancer cells have vitamin D receptors too — and when D binds, it tells those cells to stop growing, a potentially life-saving command. In fact, a 2005 article in the Southern Medical Journal called vitamin D "one of the most potent inhibitors of both normal and cancer cell growth."

This potential cancer-fighting power may help explain why cancers of the breast, colon or prostate tend to be more common, or more aggressive, in dark-skinned people, Norman says. It may also, he adds, help explain why people in northern states such as Maine or Minnesota — where summers are short and sleeves, for most of the year, are long — are more prone to these cancers than people in the sunny South.

Other quirks of geography offer compelling evidence for the importance of vitamin D, says Dr. Michael Holick, a professor of medicine, physiology and biophysics at Boston University School of Medicine and one of the most vocal proponents of the compound. People in sun-deprived regions are especially prone to schizophrenia, multiple sclerosis and Type 1 diabetes, he says.

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How Much B12 to Take???

Postby notasperfectasyou » Fri Jul 07, 2006 6:34 pm

How much B12 do you take? can anyone provide info about how much folks with MS should take? There are plenty of articles that suggest that B12 is good to take, but how much? dosage? napay

followup, now I'm seeing that there are different kinds, Methylcohalam and Cyanocobalamin. The Methylcohalam is supposed to be better, but where can you buy it? Also, does B12 not work if taken orally?
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the b thing

Postby jimmylegs » Wed Jul 12, 2006 5:23 pm

napay i know we've already discussed but for the benefit of anyone else reading this thread, ms patients are typically low in b12, b12 is absorbed best when taken with calcium and the rest of the b complex, the b-complex can be low if your b12 is low, b12 and b6 together combat depression, you can absorb b12 orally, particularly sublingually where it goes directly to the bloodstream bypassing the digestive tract, methylcobalamin is more biologically active than cyanocobalamin, and b12 only did so much for me but i noticed big improvements in an hour one evening when i megadosed b1, b2, b3, b5, and b6 along with my regular b-complex and b12. i take 1000 mcg per day. my dosages for b12 and the rest of the complex are derived from the 1970s klenner protocol for ms.
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Postby notasperfectasyou » Wed Jul 12, 2006 7:03 pm

Not that I'm trying to get the last word, but I want to make sure that it's clear that the kind of B12 you swallow is not the kind that is being discussed as useful. The kind of B12 that one would want to use is one that is made to disolve under your tongue. The B12 that is in your multi-vit doesn't count. napay
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