This Is MS Multiple Sclerosis Knowledge & Support Community

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. nagpal_sunil@lilly.com

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. mxc69@psu.edu

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.

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!
Lori

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

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!

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.

For the rest of the article:
http://www.latimes.com/features/health/ ... ck=tothtml

A Dose/Safety Study of Vitamin D for Persons with Multiple Sclerosis

Introduction – Beginning in 2000, Direct-MS has strongly advocated the use of adequate vitamin D supplementation for the prevention and treatment of multiple sclerosis. Since that time we have also actively promoted the need for clinical research to test the effectiveness of vitamin D for preventing and treating MS. Before clinical trials to test the efficacy of vitamin D for MS can be done, it is necessary to determine the optimal dosage of vitamin D to use in such a trial. Direct-MS chose to fund this preliminary “Dose/Safety” study for vitamin D to ensure that the necessary clinical research on the efficacy of vitamin D for MS happens as soon as possible.

Leaders – The chief investigator of the clinical research is Dr Paul O’Connor, Clinical and Research Neurologist, Chief, Division of Neurology and Director of the MS Centre at St Michael’s Hospital in Toronto. Dr O’Connor has assembled a large and impressive team of researchers for this trial. They include Dr Jodie Burton, Co-investigator, MS Clinical Fellow, St. Michael’s Hospital, University of Toronto; Dr Melanie Ursell, Co-investigator, Staff, Division of Neurology, St. Michael’s Hospital; Dr Reinhold Vieth, Co-investigator. Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto; Samantha Kimball, Co-investigator. Master of Science Student, Department of
Nutritional Sciences, University of Toronto; Dr. Louise Thibault Professor, School of Dietetics and Human Nutrition, McGill University, Montreal; Sally Kilborn, Master of Science Student, School of Dietetics and Human Nutrition, McGill University; Dr. H. Michael Dosch, Co-investigator. Professor of Immunology, University of Toronto and the Hospital for Sick Children, Toronto; Dr Amit Bar-Or, Co-investigator. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal; Dr Cheryl D’Souza, Centre for Research in Neurodegenerative Diseases, University of Toronto. .


Ethics – The study has been approved by the Ethics Boards of St Michael’s Hospital and McGill University.

Goals – The main goal of the study is to determine the optimal dose of vitamin D to use in a subsequent clinical trial which will test the efficacy of vitamin D for affecting disease activity in MS. Such an optimal dose will be the maximum dose which is well tolerated without any adverse side effects and which also has a significant effect on immune activity.
A second objective is to determine if there are any positive effects of higher doses of vitamin D3 on bone health in people with MS.
A third objective is to examine the relationship between diet and MS especially vitamin D intake from food sources.
A fourth objective is to examine the effect of vitamin D on mood and feelings of well-being of the participants.

Methods – The study will involve 30 participants, all of whom have MS (RRMS, SPMS or PPMS) and will last one year. Each participant will be given an increasing dose of vitamin D3 starting at 28,000 IU per week (4000 IU/d). The dose of vitamin D3 will be gradually increased every 2 to 6 weeks to the highest dose of 280,000 IU per week (40,000 IU per day). After the highest dose is taken for 6 weeks, the dose of vitamin D3 will be lowered to a maintenance dose of 70,000 IU per week (10,000 IU per day) that will be taken for 12 weeks. The dose of vitamin D3 will then be lowered again to 28,000 IU per week (4000 IU per day) taken for another 8 weeks. 1200 mg of calcium will be taken daily during the entire study.
Blood and urine samples will be obtained every month and analyzed to determine if any anomalous calcium or creatinine/calcium ratios are present in any of the participants. The blood samples will also be analyzed for immunological markers of inflammation and blood brain barrier integrity (cytokine profiles, lymphocyte response measures and matrix metalloproteinases) and the proportion of change in bone turnover markers. Measures of well being will be assessed using the Hospital Anxiety and Depression Scale questionnaire.

To examine dietary habits and amounts of nutrients participants get in the diet, particularly vitamin D, they will be asked to complete a “Food Frequency Questionnaire”. In addition, a “24-hour recall” food questionnaire will be given.

Results – The blood tests will determine if high doses of vitamin D3 have any adverse effects on calcium levels in the body. Such adverse effects include the elevation of serum calcium levels above normalized ranges (range 2.1-2.6 millimoles per liter) or urinary calcium:creatinine ratios above 1.0. The measurement of immunological markers will allow the determination of the effects of the various doses of vitamin D3 on immune activity. These two data sets will allow an optimal dose of vitamin D to be determined. Such a dose will be used in subsequent clinical trials for MS and possibly other diseases related to vitamin D deficiency (e.g. prostate cancer).
The other studies mentioned above will provide insight into the value of higher doses of vitamin D for preventing and treating osteoporosis and for treating depression.

Discussion – This clinical trial is basically a “Phase I” trial meaning it is designed to determine the metabolism and pharmacologic action of vitamin D3 in humans, the side effects associated with increasing doses, and evidence of effectiveness for treating immune reactions related to MS disease activity.

Such a trial must be done before any proper clinical trial on the effectiveness of optimal doses of vitamin D for treating MS can be initiated.

Cheers
Nick

Nick, I thought someone here had already posted an abstract about such a completed study (done over 7 months, I think).

This sounds as if it is proposed for the future. When is it scheduled tentatively to begin? Has this study completed the enrollment of participants? Do you (Direct-MS) have any input on this project since you have "strongly promoted the need for clinical research...."? Could you suggest that, among objectives, researchers determine if there are any effects of high doses of vitamin D3 (positive or otherwise) on insulin levels?

Hi Lynda

lyndacarol wrote:Nick, I thought someone here had already posted an abstract about such a completed study (done over 7 months, I think).?

You are partially correct. Part 1 of this trial has been completed but over a shorter duration than 7 months. We are funding the second segment for a longer duration which should provide evidence of a significant effect on immune activity.

lyndacarol wrote:This sounds as if it is proposed for the future. When is it scheduled tentatively to begin?

It is already underway to my knowledge.

lyndacarol wrote: Could you suggest that, among objectives, researchers determine if there are any effects of high doses of vitamin D3 (positive or otherwise) on insulin levels?

These are the items to be tested for:

Physical and neurological exam
(including EDSS and AI scores)
Routine blood work:
-calcium, albumin
-creatinine, urea, liver enzymes
-parathyroid hormone, vitamin D3
Urine samples:
-calcium, creatinine, +/- blood
Urine kit home collection of 2 urine samples for you to bring to next visit
Matrix Metalloproteinases
Lymphocyte response assay
Cytokine profiling
Bone marker testing:
Bone Alkaline Phosphatase (in blood)
N-Telopeptide (in urine)
Hospital Anxiety and Depression Questionnaire
Electrocardiogram (ECG)
Renal (kidney) ultrasound
Food Frequency Questionnaire
24-Hour Food Recall Questionnaire

I don't have influence over what is being measured. you would have to contact the researchers directly to test your theory. I suspect though you would be too late.

Cheers
Nick

Interesting study on vit D and latitude in the U.S.



Location and Vitamin D synthesis: Is the hypothesis validated by geophysical data?

J Photochem Photobiol B. 2006 Dec 1;
Kimlin MG, Olds WJ, Moore MR.
Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Kelvin Grove, Qld, 4059 Brisbane, Australia.

The literature reports strong correlations between UV exposure and latitude gradients of diseases. Evidence is emerging about the protective effects of UV exposure for cancer (breast, colo-rectal, prostate), autoimmune diseases (multiple sclerosis, type II diabetes) and even mental disorders, such as schizophrenia. For the first time, the available levels of vitamin D producing UV or "vitamin D UV" (determined from the previtamin D action spectrum) and erythemal (sunburning) UV from throughout the USA are measured and compared, using measurements from seven locations in the USA are measured and compared, using measurements from seven locations in the US EPA's high accuracy Brewer Spectrophotometer network.

The data contest longstanding beliefs on the location-dependence and latitude gradients of vitamin D UV. During eight months of the year centered around summer (March-October), for all sites (from 18 degrees N to 44 degrees N latitude) the level of vitamin D UV relative to erythemal UV was equal (within the 95% confidence interval of the mean level). Therefore, there was no measured latitude gradient of vitamin D UV during the majority of the year across the USA. During the four cooler months (November-February), latitude strongly determines vitamin D UV. As latitude increases, the amount of vitamin D UV decreases dramatically, which may inhibit vitamin D synthesis in humans. Therefore, a larger dose of UV relative to erythemal UV is required to produce the same amount of vitamin D in a high latitude location. However, the data shows that at lower latitude locations (<25 degrees N), wintertime vitamin D UV levels are equal to summertime levels, and the message of increasing UV exposure during winter is irrelevant and may lead to excessive exposure.

All results were confirmed by computer modeling, which was also used to generalize the conclusions for latitudes from 0 degrees to 70 degrees N. The results of this paper will impact on research into latitudinal gradients of diseases. In particular, it may no longer be correct to assume vitamin D levels in populations follow significant latitude gradients for a large proportion of the year.

Pubmed reference

I saw this one too, and it was interesting. I couldn't figure out a couple of things from the abstract though, that is, when they talked about vitamin D UV (I presume this is UVB) and erythemal UV (I presume this is UVA). I don't know if this presumption is correct without seeing the whole paper, but I'll use it as shorthand. They state that the ratio of UVB and UVA are the same over a gradient of latitude during all but winter months. I doubt though that the even if the ratios of the two wavelengths are equal, that the absolute UV radiation strength is equal across all latitudes. It can't be. I burn very easily, and the farther south I go in the US, the less time it takes me to burn in the sun. Even within the state of Florida, I can tell a difference between the northern and central/southern sections of the state. Conversely, I visited St. Petersburg, Russia, in the summer and was able to walk around in sunlight 2-3 hours with no sunscreen on and not burn. Admittedly, I was much further north than the continental US, but the same is true in San Francisco vs. Florida - I could spend maybe 30-45 minutes in the sun in San Francisco (if there is sun in the summer!) - that length of time would literally cook me in south Florida sunlight in the summer.

The abstract seems to suggest that people stay out in the sun, wherever they are, as long as they can without burning, so that overall, their UV dose would be equal. But this isn't true, because it presumes people would stay outside longer up in Vermont than Florida. If my UVA dose to start to burn in Miami is five minutes, I can also get an appreciable UVB dose in five minutes but just walking across a parking lot. If I am in Vermont, it might take me, say 30-45 minutes to get the same dose. If the only time I am outside in Vermont is walking to and from my car, I'll only get a fraction of the Miami dose of both UVA and UVB.

The real measure of vitamin D synthesis from sunlight would be to collect both blood levels in people in different latitudes and measure their UV dose while they wear some kind of personal monitor or badge. This has actually been done in some studies. There would still have to be some sort of adjustment for the amount of skin actually exposed to sunlight and skin pigmentation (dark skin less efficient) and age (elders less efficient).

Or maybe someone could get the whole paper and read it for me - I just can't figure it all out from the abstract.....

LisaBee, you know I am no scientist. And I can't claim to understand the posted abstract concerning Vitamin D, but I will hope to understand more after going over it a few more times.

From other sources I have read that UVB is responsible for sunburn as well as the source for Vitamin D manufactured in the skin. UVA is the culprit in aging and wrinkles.

It seems to me there must be distinct subcategories within UVB (or the researchers are trying to link the two effects of UVB, since one is obvious and indicates the level of the other, not-obvious-without-testing).

See if this helps...I haven't read it yet...

http://www.niwascience.co.nz/rc/atmos/u ... 6/Olds.pdf

Thanks, lyndacarol and dignan! You both cleared up some confusion for me. lyndacarol, I actually am a scientist of sorts, but that doesn't mean I'm right

lyndacarol, you are right that UVB radiation, the kind associated with vitamin D production in the skin, is also primarily the wavelength of UV that promotes skin burning. Some burning capability though, extends into the UVA range. UVA is less effective than at causing sunburn, but it can still happen with a long enough exposure. I used the terms incorrectly and when I have more time I'll try to correct my initial posted response. What the Olds and Kimlin paper that dignan showed is that the vitamin D production, even within the UVB range of 280-320 nm, falls off more quickly than the erythemal response as the wavelength of UV increases. It is easier to see on Figure 1 of the paper dignan linked to than it is to describe.

Given the clarification in Olds and Kimlin paper, I think I understand the Olds et al. 2006 abstract a little better now, but stil not completely. They are saying, I think, that there may be circumstances where the dose of erythemal UV may be high, but still not trigger significant vitamin D production, and therefore a standard "UV index" may not be good enough for indicating the potential for Vitamin D production.

I agree with them on that. I still don't think their findings argues against a gradient. I suspect, if you took two populations, one at high latitude, one at low, with similar diet and skin coloration, and similar time spent in sunlight, the group at the lower latitude (closet to equator) will have, on average, higher serum vitamin D levels than those further from the equator. If you were able to control for amount of skin exposed (hard to do in cold weather!) between the two groups that would elminate another confounder, at least as far as correlating strength of vitamin D producing UV with latitude.

However, people at lower latitudes in the US don't necessarily have a lot of sun exposure and may be vitamin D deficient due to their clothing and lifestyle. In the Olds and Kimlin conference paper, the authors note that 8% of Queensland Australia residents were deficient in vitamin D, yet that area of Australia has the highest incidence of skin cancer. The question I have is whether the 8% Queensland residents that were deficient in Vitamin D have evidence of concurrent significant sun exposure. I sort of doubt that would occur, but if it did it would be interesting (and puzzling).

Lisa

Vitamin D protects against MS, large study suggests

An abundance of vitamin D seems to help prevent multiple sclerosis, according to a study in more than seven million people that offers some of the strongest evidence yet of the power of the "sunshine vitamin" against MS. The research found that white members of the U.S. military with the highest blood levels of vitamin D were 62 per cent less likely to develop multiple sclerosis than people with low levels.

There was no such connection in blacks or Hispanics, possibly because there were so few in the group studied. Also, the body makes vitamin D from sunlight, and the pigmented skin of blacks and other dark-skinned ethnic groups doesn't absorb sunlight as easily as pale skin.
The new research echoes findings in smaller studies that examined why the nerve-damaging disease historically has been more common in people who live in regions farther from the equator where there is less intense year-round sunlight.

"This is the first large prospective study where blood levels are measured in young adults and compared to their future risk. It's definitely different and much stronger evidence," said Dr. Alberto Ascherio, the senior author and an associate professor of nutrition at Harvard's School of Public Health.The study appears in Wednesday's Journal of the American Medical Association.

"If confirmed, this finding suggests that many cases of MS could be prevented by increasing vitamin D levels," Ascherio said. Still, he said the findings don't prove that a lack of vitamin D can cause MS, so it's too preliminary to recommend that people take vitamin D pills to avoid the disease.

Vitamin D is also found in fortified milk and oily fish, but it's hard to get enough just from diet. Sunlight is the biggest source of vitamin D, which is needed for strong bones. Other studies have linked high levels of vitamin D in the blood to lower risks of a variety of cancers. The MS researchers worked with the U.S. army and navy in analyzing blood samples of military personnel stored by the Department of Defence.

Vitamin deficiency in young people

Military databases showed that 257 service men and women were diagnosed with MS between 1992 and 2004. The increased MS risk was especially strong in people who were younger than 20 when they entered the study. The researchers said that finding suggests that vitamin D exposure before adulthood could be particularly important.
Using blood samples to measure vitamin D levels "tends to nail it down in a much more reliable way" than studies that have relied on people's memories of vitamin D exposure, said Dr. Nicholas LaRocca of the National Multiple Sclerosis Society.

MS is among the most common nerve disorders affecting young adults, mostly women. Canada has the highest incidence in the world at 240 cases among every 100,000 people, according to a study by a University of Calgary team published in the journal Multiple Sclerosis in 2005.
Around two million people worldwide have MS, a chronic autoimmune disease in which the body attacks the fatty insulation that surrounds nerve fibres.

Ascherio said there's some evidence that its incidence is increasing in sunny regions including the South and West, possibly because people are avoiding the sun or using sunscreen to protect against skin cancer. Some doctors think those practices also have contributed to vitamin D deficiencies in adolescents and young adults.

"There's no question that vitamin D deficiency is an epidemic in the United States," said Dr. William Finn, a vitamin D expert at the University of North Carolina at Chapel Hill. The MS study "is just one more reason to pay attention to it."

MS symptoms vary but can be disabling and can include tingling pain in the arms and legs, fatigue and vision problems. Doctors believe it is genetic and perhaps triggered in susceptible people by environmental causes, including possibly some viruses. Vitamin D deficiency could be another trigger.

It's unclear how lack of vitamin D might contribute. In mouse experiments, the vitamin stimulated production of chemicals that fight an MS-like disease.

Cheers
Nick

I thought I’d start a list of links to Vitamin D articles that might help folks assimilate this information faster. It’s not a new topic. You can tell from the dates on some of these articles that it’s been around a while.

The Role of Vitamin D in Multiple Sclerosis

Vitamin D intake and incidence of multiple sclerosis

Vitamin D and multiple sclerosis

Genetic analysis of vitamin D related genes in Canadian multiple sclerosis patients

Vitamin D and Autoimmunity: Is Vitamin D Status an Environmental Factor Affecting Autoimmune Disease Prevalence?

A pilot study of oral calcitriol (1,25-dihydroxyvitamin D3) for relapsing–remitting multiple sclerosis

Mounting Evidence for Vitamin D as an Environmental Factor Affecting Autoimmune Disease Prevalence

That’s just a few. There are a lot more. Infact in some of these pages you can get cites of other artciles that cited that article. If you want me to post more links like this I will.

My gut tells me that Vitamin D is more so linked to prevention and likely does a lot less once you have MS. But, we’re still taking 4000 IU’s of D3 daily. D3 is one of the cheaper supplements that’s on the MS list. napay