all things vitamin D

[jimmylegs]

great start napay

d

[notasperfectasyou]

great start napay

d

Thanks Jimmy. I'm hoping that by providing links others might read the basic research and post conclusions here. It honestly takes me too long to do posts the way I have in the past. I need the folks here to help synthesis the info.

My search on Vitamin D Multiple Sclerosis came up with over 2000 hits on Journal articles. I spent an hour typing out the above post.........

napay

[jimmylegs]

ya it is sure a ton of work. your time spent is well worth it and just having the links available are a great big help

[Nick]

Risk assessment for vitamin D

John N Hathcock, Andrew Shao, Reinhold Vieth, and Robert Heaney

ABSTRACT

The objective of this review was to apply the risk assessment methodology
used by the Food and Nutrition Board (FNB) to derive a revised safe Tolerable Upper Intake Level (UL) for vitamin D.

New data continue to emerge regarding the health benefits of vitamin Dbeyond its role in bone. The intakes associated with those benefits suggest a need for levels of supplementation, food fortification, or both that are higher than current levels. A prevailing concern exists, however, regarding the potential for toxicity related to excessive vitaminD intakes. The UL established by the FNB for vitaminD(50 microg, or 2000 IU) is not based on current evidence and is viewed by many as being too restrictive, thus curtailing research, commercial development, and optimization of nutritional policy. Human clinical trial data published subsequent to the establishment of the FNB vitamin D UL published in 1997 support a significantly higher UL.

We present a risk assessment based on relevant, well-designed human
clinical trials of vitamin D. Collectively, the absence of toxicity in trials conducted in healthy adults that used vitamin D dose gt/=250 microg/d (10,000 IU vitamin D3) supports the confident selection of this value as the UL.

Am J Clin Nutr 2007;85:6 –18.

This article is available for reading here.

Cheers
Nick

[JFH]

Glad you posted that Nick, thankyou.

[Nick]

Another study that promotes the virtues of vitamin D. I believe these results to be consistent with studies involving MS prevention and vitamin D. (ie. Harvard's Ascherio and the nurses)

Vitamin D Backed For Cancer Prevention In Two New Studies

Science Daily — Two new vitamin D studies using a sophisticated form of analysis called meta-analysis, in which data from multiple reports is combined, have revealed new prescriptions for possibly preventing up to half of the cases of breast cancer and two-thirds of the cases of colorectal cancer in the United States. The work was conducted by a core team of cancer prevention specialists at the Moores Cancer Center at University of California, San Diego (UCSD), and colleagues from both coasts.

The breast cancer study, published online in the current issue of the Journal of Steroid Biochemistry and Molecular Biology, pooled dose-response data from two earlier studies - the Harvard Nurses Health Study and the St. George's Hospital Study - and found that individuals with the highest blood levels of 25-hydroxyvitamin D, or 25(OH)D, had the lowest risk of breast cancer.

The researchers divided the 1,760 records of individuals in the two studies into five equal groups, from the lowest blood levels of 25(OH)D (less than 13 nanograms per milliliter, or 13 ng/ml) to the highest (approximately 52 ng/ml). The data also included whether or not the individual had developed cancer.

"The data were very clear, showing that individuals in the group with the lowest blood levels had the highest rates of breast cancer, and the breast cancer rates dropped as the blood levels of 25-hydroxyvitamin D increased," said study co-author Cedric Garland, Dr.P.H. "The serum level associated with a 50 percent reduction in risk could be maintained by taking 2,000 international units of vitamin D3 daily plus, when the weather permits, spending 10 to 15 minutes a day in the sun."
The colorectal cancer study, published online February 6 in the American Journal of Preventive Medicine, is a meta-analysis of five studies that explored the association of blood levels of 25(OH)D with risk of colon cancer. All of the studies involved blood collected and tested for 25 (OH)D levels from healthy volunteer donors who were then followed for up to 25 years for development of colorectal cancer.

As with the breast cancer study, the dose-response data on a total of 1,448 individuals were put into order by serum 25(OH)D level and then divided into five equal groups, from the lowest blood levels to the highest.

"Through this meta-analysis we found that raising the serum level of 25-hydroxyvitamin D to 34 ng/ml would reduce the incidence rates of colorectal cancer by half," said co-author Edward D. Gorham, Ph.D. "We project a two-thirds reduction in incidence with serum levels of 46ng/ml, which corresponds to a daily intake of 2,000 IU of vitamin D3. This would be best achieved with a combination of diet, supplements and 10 to 15 minutes per day in the sun."

Vitamin D3 is available through diet, supplements and exposure of the skin to sunlight, or ultraviolet B (UVB). In the paper, the researchers underscored the importance of limiting sun exposure such that the skin does not change color (tan) or burn. For a typical fair-skinned Caucasian individual, adequate vitamin D could be photosynthesized safely by spending 10 to 15 minutes in the noontime sun on a clear day with 50 percent of skin area exposed to the sun. Darker skinned individuals may require more time in the sun, such as 25 minutes. For people with photosensitivity disorders, or anyone with a personal or family history of nonmelanoma skin cancer, any amount of extra sun exposure would be inadvisable.

The meta-analysis on colorectal cancer includes data from the Women's Health Initiative, which had shown in 2006 that a low dose of vitamin D did not protect against colorectal cancer within seven years of follow-up. However, the researchers wrote, the meta-analysis indicates that a higher dose may reduce its incidence.

"Meta-analysis is an important tool for revealing trends that may not be apparent in a single study," said co-author Sharif B. Mohr, M.P.H. "Pooling of independent but similar studies increases precision, and therefore the confidence level of the findings."
The authors recommend further research to study individuals for the effect of vitamin D from sunlight, diet and supplements on the risk of cancer.

Co-authors on both the breast cancer and colorectal meta-analysis papers are Edward D. Gorham, MPH, Ph.D., Cedric F. Garland, Dr.P.H.; Frank C. Garland, Ph.D.; Sharif B. Mohr, MPH; William B. Grant, Ph.D; Martin Lipkin, M.D.; Harold L. Newmark, ScD; Edward Giovannucci, M.D., ScD; and Michael F. Holick, M.D., Ph.D. Co-author on the colorectal meta-analysis paper only was Melissa Wei, B.S. Authors' institutional affiliations are UCSD Department of Family and Preventive Medicine and Moores UCSD Cancer Center (Gorham, Garland, Garland); Naval Health Research Center, San Diego (Gorham, F.C. Garland, Mohr); SUNARC-Sunlight, Nutrition and Health Research Center, San Francisco (Grant); Strang Cancer Prevention Center of Rockefeller University, New York, NY (Lipkin); Rutgers--The State University of New Jersey and Cancer Institute of New Jersey (Newmark); Harvard Schools of Public Health and Medicine (Giovannucci, Wei); and Boston University School of Medicine (Holick). Funding for this research was provided by a Congressional allocation to the Hollings Cancer Center of the Medical University of South Carolina through the Department of the Navy.
Note: This story has been adapted from a news release issued by University of California - San Diego.

http://www.sciencedaily.com/releases/20 ... 100608.htm

Cheers
Nick

[dreddk]

Hi,
I'm curious as to whether anyone is giving a Vitamin D3 supplement to their children. Given that the research indicates that there is a probibility that Vitamin D3 reduces the likelihood of developing MS I have been wondering about giving my daughters a supplement (My wife as RRMS).
If so, what product do you use?

[Loobie]

I have an 11 year old daughter that I give 800 IU per day of Solgar D (colicalciferol(SP?)).

I am the one with MS and I take 2400 IU of Carlson D3.

My daughter shows no ill effects from taking that quantity. I have had her on 1000 IU also since that was the only size they had at the vitamin store. Before I learned of the potential benefits of D for MS prevention, I still had her on it after I listened to a radio show talk about giving your children that much in the winter to help stave off the flu as opposed to giving them the flu shot.

[dreddk]

That's interesting thanks - I see in the large study of nurses that 400IU seemed to offer some benefit but then several other studies I have read suggest that around the 800IU or greater is needed to have any real effect on the body's vitamin d levels. My eldest daughter is 2 1/2 so I'm thinking I will talk to her GP about options as the supplements available in nz with a decent amount of vitamin d also have large amounts of vitamin a and are not suitable for young children.

[JFH]

I encourage my daugters to take at least 10ug a day.

[Nick]

I have three children, ages 10,8 and 2 years old. I give the older two, 2,000 IU/d and the younger one, 1,000 IU/d. I usually give the older kids two pure D3 tablets and the younger one flavoured cod liver oil or flavoured liquid D3.

DIRECT-MS, of which I am a participant, has materials which address the issue of prevention.

Protect Your Family from Multiple Sclerosis]
This booklet emphasizes the high risk for contracting MS of first-degree relatives of persons with MS. It discusses the causal factors of MS with special emphasis on vitamin D deficiency as a primary cause. Finally it demonstrates that adequate vitamin D can likely prevent MS in most cases and provides a recommended supplementation regime.

Preventing Multiple Sclerosis and is a web cast regarding nutrition and Multiple Sclerosis. The focus of the Prevention presentation is how MS can be easily, safely and inexpensively prevented by focusing on protective factors. This is a must see for those people with MS who have children.

Cheers
Nick

[dreddk]

Hi Nick,
If you don't mind me asking, what cod liver oil are you giving your youngest? I've ordered the carlsons cod liver oil lemon flavored. The recommended dosage I have seen works out at 1 teaspoon for a 2 year old which is 400IU. Are you giving a higher dosage? I reluctant to give her more due to the high vitamin A content of cod liver oils.

Like you, once she's a bit older i'm going to switch her to the straight pills.
thanks
Dreddk

[Nick]

Hey Dredd

The CLO I give is the Arctic brand. I'm not too stringent because we don't give him cow milk nor too much gluten, thus the most likely instigators are absent or very reduced. Once he ages and is accepting of the pill form I'll try to convert him.

Of course whenever the oppotunity presents itself he gets exposed to UVR in appropriate amounts.

Cheers
Nick

[Nick]

Hi Dredd

I didn't addressyour question of how much vitamin D I give to my two yr old youngster. Ideally I would like him to have 1000 to 2000 IU/d. There's not too much credible info out there which documents how much D a toddler should have. I believe a European Commission study concluded 1000 IU/d is safe for children under two.

Cheers
Nick

[NHE]

I don't know if these have been discussed before, but I recently came across a couple interesting papers on vitamin D's role in MS. The first paper is available for free while I have only read the abstract for the second one.

Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis.
Physiol Genomics. 2004 Jul 8;18(2):141-51.

• Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] might regulate gene expression patterns in a manner that would resolve inflammation. To test this hypothesis, experimental autoimmune encephalomyelitis (EAE) was induced in mice, 1,25-(OH)2D3 or a placebo was administered, and 6 h later, DNA microarray hybridization was performed with spinal cord RNA to analyze the gene expression patterns. At this time, clinical, histopathological, and biological studies showed that the two groups did not differ in EAE disease, but changes in several 1,25-(OH)2D3-responsive genes indicated that the 1,25-(OH)2D3 had reached the CNS. Compared with normal mice, placebo-treated mice with EAE showed increased expression of many immune system genes, confirming the acute inflammation. When 1,25-(OH)2D3 was administered, several genes like glial fibrillary acidic protein and eukaryotic initiation factor 2alpha kinase 4, whose expression increased or decreased with EAE, returned to homeostatic levels. Also, two genes with pro-apoptotic functions, calpain-2 and caspase-8-associated protein, increased significantly. A terminal deoxynucleotidyl transferase-mediated dUTP nicked end labeling study detected increased nuclear fragmentation in the 1,25-(OH)2D3-treated samples, confirming increased apoptosis. Together, these results suggest that sensitization of inflammatory cells to apoptotic signals may be one mechanism by which the 1,25-(OH)2D3 resolved EAE.

IL-10 signaling is essential for 1,25-dihydroxyvitamin D3-mediated inhibition of experimental autoimmune encephalomyelitis.
J Immunol. 2006 Nov 1;177(9):6030-7.

• Multiple sclerosis (MS) results from an aberrant, neuroantigen-specific, T cell-mediated autoimmune response. Because MS prevalence and severity decrease sharply with increasing sunlight exposure, and sunlight supports vitamin D(3) synthesis, we proposed that vitamin D(3) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) may protect against MS. In support of this hypothesis, 1,25-(OH)(2)D(3) strongly inhibited experimental autoimmune encephalomyelitis (EAE). This inhibition required lymphocytes other than the encephalitogenic T cells. In this study, we tested the hypothesis that 1,25-(OH)(2)D(3) might inhibit EAE through the action of IL-10-producing regulatory lymphocytes. We report that vitamin D(3) and 1,25-(OH)(2)D(3) strongly inhibited myelin oligodendrocyte peptide (MOG(35-55))-induced EAE in C57BL/6 mice, but completely failed to inhibit EAE in mice with a disrupted IL-10 or IL-10R gene. Thus, a functional IL-10-IL-10R pathway was essential for 1,25-(OH)(2)D(3) to inhibit EAE. The 1,25-(OH)(2)D(3) also failed to inhibit EAE in reciprocal, mixed bone marrow chimeras constructed by transferring IL-10-deficient bone marrow into irradiated wild-type mice and vice versa. Thus, 1,25-(OH)(2)D(3) may be enhancing an anti-inflammatory loop involving hemopoietic cell-produced IL-10 acting on brain parenchymal cells and vice versa. If this interpretation is correct, and humans have a similar bidirectional IL-10-dependent loop, then an IL-10-IL-10R pathway defect could abrogate the anti-inflammatory and neuro-protective functions of sunlight and vitamin D(3). In this way, a genetic IL-10-IL-10R pathway defect could interact with an environmental risk factor, vitamin D(3) insufficiency, to increase MS risk and severity.

NHE