Vitamin D: Scientific Studies & News

[RufusG]

Some doctors in Brazil have been treating MS patients with very, very high doses of Vitamin D

Read more about this at: http://www.vitamindwiki.com/Overview+MS+and+vitamin+D

Much of the high strength Vitamin D used in medical trials is made by:
http://www.biotechpharmacal.com/catalog ... vitamin-d/

Here is where you can find their products:
http://greenvits.eu/pages/where-to-buy

.

[shadowfax]

If calcium is crucial why the non-dairy diet to reduce calcium intake when on high doses of vitamin D?

[lyndacarol]

Is hypovitaminosis D one of the environmental risk factors for multiple sclerosis?
Brain 2010 Jul;133(Pt 7):1869-88. doi: 10.1093/brain/awq147

Abstract
The role of hypovitaminosis D as a possible risk factor for multiple sclerosis is reviewed. First, it is emphasized that hypovitaminosis D could be only one of the risk factors for multiple sclerosis and that numerous other environmental and genetic risk factors appear to interact and combine to trigger the disease. Secondly, the classical physiological notions about vitamin D have recently been challenged and the main new findings are summarized. This vitamin could have an important immunological role involving a number of organs and pathologies, including autoimmune diseases and multiple sclerosis. Furthermore, human requirements for this vitamin are much higher than previously thought, and in medium- or high-latitude countries, they might not be met in the majority of the general population due to a lack of sunshine and an increasingly urbanized lifestyle. Thereafter, the different types of studies that have helped to implicate hypovitaminosis D as a risk factor for multiple sclerosis are reviewed. In experimental autoimmune encephalomyelitis, vitamin D has been shown to play a significant immunological role. Diverse epidemiological studies suggest that a direct chain of causality exists in the general population between latitude, exposure to the sun, vitamin D status and the risk of multiple sclerosis. New epidemiological analyses from France support the existence of this chain of links. Recently reported immunological findings in patients with multiple sclerosis have consistently shown that vitamin D significantly influences regulatory T lymphocyte cells, whose role is well known in the pathogenesis of the disease. Lastly, in a number of studies on serum levels of vitamin D in multiple sclerosis, an insufficiency was observed in the great majority of patients, including at the earliest stages of the disease. The questionable specificity and significance of such results is detailed here. Based on a final global analysis of the cumulative significance of these different types of findings, it would appear likely that hypovitaminosis D is one of the risk factors for multiple sclerosis.


Source:
http://www.ncbi.nlm.nih.gov/pubmed/?term=20584945

[PointsNorth]

Could High-Dose Vitamin D Help Fight Multiple Sclerosis? - US News

@EB et al I will increase my dosage in the coming weeks to 100Kiu+ adding K2 to my regimen which already includes several other vitamin D cofactors, zinc and magnesium among them. Hopefully this will prevent soreness in my ribs that I get at night with high levels of vitamin D. After 16 months on high dose of vitamin D my bloodwork looks normal. It looks as if I do not respond to lower amounts. But it looks like you can start low and then move higher. Coimbra/Holick are using 1Kiu of D per 1kg as a reference point.

http://health.usnews.com/health-news/ar ... -sclerosis

[AntonioBR]

Safety and immunologic effects of high- vs low-dose cholecalciferol in multiple sclerosis


December 30, 2015

Elias S. Sotirchos, MD*, Pavan Bhargava, MD*, Christopher Eckstein, MD, Keith Van Haren, MD, Moira Baynes, RN, Achilles Ntranos, MD, Anne Gocke, PhD, Lawrence Steinman, MD, Ellen M. Mowry, MD, MCR and Peter A. Calabresi, MD

ABSTRACT


Objective: To study the safety profile and characterize the immunologic effects of high- vs low-dose cholecalciferol supplementation in patients with multiple sclerosis (MS).

Methods: In this double-blind, single-center randomized pilot study, 40 patients with relapsing-remitting MS were randomized to receive 10,400 IU or 800 IU cholecalciferol daily for 6 months. Assessments were performed at baseline and 3 and 6 months.

Results: Mean increase of 25-hydroxyvitamin D levels from baseline to final visit was larger in the high-dose group (34.9 ng/mL; 95% confidence interval [CI] 25.0–44.7 ng/mL) than in the low-dose group (6.9 ng/mL; 95% CI 1.0–13.7 ng/mL). Adverse events were minor and did not differ between the 2 groups. Two relapses occurred, one in each treatment arm. In the high-dose group, we found a reduction in the proportion of interleukin-17+CD4+ T cells (p = 0.016), CD161+CD4+ T cells (p = 0.03), and effector memory CD4+ T cells (p = 0.021) with a concomitant increase in the proportion of central memory CD4+ T cells (p = 0.018) and naive CD4+ T cells (p = 0.04). These effects were not observed in the low-dose group.

Conclusions: Cholecalciferol supplementation with 10,400 IU daily is safe and tolerable in patients with MS and exhibits in vivo pleiotropic immunomodulatory effects in MS, which include reduction of interleukin-17 production by CD4+ T cells and decreased proportion of effector memory CD4+ T cells with concomitant increase in central memory CD4+ T cells and naive CD4+ T cells.

Classification of evidence: This study provides Class I evidence that cholecalciferol supplementation with 10,400 IU daily is safe and well-tolerated in patients with MS and exhibits in vivo pleiotropic immunomodulatory effects.



Source: http://www.ncbi.nlm.nih.gov/pubmed/26718578

[AntonioBR]

Taking vitamin D with the largest meal improves absorption and results in higher serum levels of 25-hydroxyvitamin D.

1Department of Endocrinology, Diabetes, and Metabolism, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Abstract
Many patients treated for vitamin D deficiency fail to achieve an adequate serum level of 25-hydroxyvitamin D [25(OH)D] despite high doses of ergo- or cholecalciferol. The objective of this study was to determine whether administration of vitamin D supplement with the largest meal of the day would improve absorption and increase serum levels of 25(OH)D. This was a prospective cohort study in an ambulatory tertiary-care referral center. Patients seen at the Cleveland Clinic Foundation Bone Clinic for the treatment of vitamin D deficiency who were not responding to treatment make up the study group. Subjects were instructed to take their usual vitamin D supplement with the largest meal of the day. The main outcome measure was the serum 259(OH)D level after 2 to 3 months. Seventeen patients were analyzed. The mean age (+/-SD) and sex (F/M) ratio were 64.5 +/- 11.0 years and 13 females and 4 males, respectively. The dose of 25(OH)D ranged from 1000 to 50,000 IU daily. The mean baseline serum 25(OH)D level (+/-SD) was 30.5 +/- 4.7 ng/mL (range 21.6 to 38.8 ng/mL). The mean serum 25(OH)D level after diet modification (+/-SD) was 47.2 +/- 10.9 ng/mL (range 34.7 to 74.0 ng/mL, p < .01). Overall, the average serum 25(OH)D level increased by 56.7% +/- 36.7%. A subgroup analysis based on the weekly dose of vitamin D was performed, and a similar trend was observed.Thus it is concluded that taking vitamin D with the largest meal improves absorption and results in about a 50% increase in serum levels of 25(OH)D levels achieved. Similar increases were observed in a wide range of vitamin D doses taken for a variety of medical conditions.

Copyright 2010 American Society for Bone and Mineral Research.


Source: http://www.ncbi.nlm.nih.gov/pubmed/20200983

[AntonioBR]

Effect of high-dose vitamin D3 intake on ambulation, muscular pain and bone mineral density in a woman with multiple sclerosis: a 10-year longitudinal case report.


Abstract
Mounting evidence correlate vitamin D3 (cholecalciferol) supplementation or higher serum levels of vitamin D (25(OH)D) with a lower risk of developing multiple sclerosis (MS), reduced relapse rate, slower progression or fewer new brain lesions. We present here the case of a woman who was diagnosed with MS in 1990. From 1980 to 2000, her ability to walk decreased from ~20 to 1 km per day. Since January 2001, a vitamin D3 supplement was ingested daily. The starting dose was 20 mcg (800 IU)/day and escalated to 100 mcg (4000 IU)/day in September 2004 and then to 150 mcg (6000 IU)/day in December 2005. Vitamin D3 intake reduced muscular pain and improved ambulation from 1 (February 2000) to 14 km/day (February 2008). Vitamin D intake over 10 years caused no adverse effects: no hypercalcaemia, nephrolithiasis or hypercalciuria were observed. Bowel problems in MS may need to be addressed as they can cause malabsorption including calcium, which may increase serum PTH and 1,25(OH)2D levels, as well as bone loss. We suggest that periodic assessment of vitamin D3, calcium and magnesium intake, bowel problems and the measurement of serum 25(OH)D, PTH, Ca levels, UCa/Cr and bone health become part of the integral management of persons with MS.


Source: http://www.ncbi.nlm.nih.gov/pubmed/23202962

Full text: http://www.ncbi.nlm.nih.gov/pmc/article ... -13461.pdf



---------------------------------------------------------------------------------------------------------------------

A 10-Year Case Study of One - Using Vitamin D3 to Improve MS

Effect of High-Dose Vitamin D3 Intake on Ambulation, Muscular Pain and Bone Mineral Density in a Woman with Multiple Sclerosis: A 10-Year Longitudinal Case Report
Barbara M. van Amerongen and François Feron
VU University Medical Center, Amsterdam, The Netherlands
October 2012


About Barbara M. van Amerongen, DDS, PhD.

Dr. Barbara M. van Amerongen received her dental degree from the University of Amsterdam in 1974 and earned her PhD in 1985. At the University of Amsterdam, she was working at the Department of Preventive Dentistry; in addition she had her own part-time dental practice. In 1990 she was diagnosed with multiple sclerosis (MS), the symptoms having started around 1975. In 1997 she closed her dental practice, due to MS-related fatigue. She joined the Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, part of the MS Center, to study MS and Vitamin D. This resulted in two papers (van Amerongen et al., 2004 and Kragt et al., 2009). These papers led her to test her hypothesis (that vitamin D aids MS) on herself.

About Dr. van Amerongen's Case Study


In January 2001 Dr. van Amerongen started with vitamin D3 800 IU/day, resulting in serum levels between 33-40 ng/ml (84-102 nmol/L). September 2004 she increased to 4000 IU/day, which seemed to keep the serum level around 40 ng/ml (100 nmol/L). In December 2005 she increased again to 6000 IU/day, and serum levels rose to above 55 ng/ml (135 nmol/L). Although there were rises and falls in the serum level throughout the 10 year period, her vitamin D level was always within a "safe" physiological range of 30-80 ng/ml (75-200 nmol/L). She found it took her about 8 months at a new dosage level to reach a steady state 25(OH)D level. Calcium was also taken daily - initially 240 mg/day, and only from March to July 2009 increased to 1332 mg/day.

She used patient related outcome measures - ambulation (walking distance in km/day) and muscular pain (pain killers yes/no) - to keep track of her progress. In addition bone mineral density (BMD) and serum levels were monitored.

Results

Ambulation was the key patient related outcome measure. The walking distance increased, as vitamin D levels increased, from 1 km/day to 14 km/day.


(Chart note: for vitamin D3, 1 mcg/day = 40 IU/day)


Muscular pain decreased, as vitamin D levels increased. She stopped using a painkiller (Paracetamol). Even after a long walk, she no longer suffered from muscular pain, whether calf muscle pain or nocturnal leg cramps.

Unfortunately, her PTH level did not reach the lower limit of its normal (reference) range and her BMD decreased. She was diagnosed with osteopenia in 2009.

Adverse Effects

Adverse events including hypercalcaemia, nephrolithiasis or fracture, were not observed. Serum calcium levels remained within the normal range. In January 2009, a scan with a sonographer revealed no renal calculus (kidney stones) after eight years of vitamin D supplementation. Additionally, no hypercalciuria was observed.

Discussion

This paper discusses the blunted parathyroid hormone (PTH) response, vitamin D resistance, and ways to reduce PTH level as found in the literature.

Conclusion

The authors recommend that periodic assessment of vitamin D3, calcium and magnesium intake, bowel problems and the measurement of serum 25(OH)D, PTH, Ca levels, UCa/Cr and bone health become part of the integral management of persons with MS.

While a clinical trial of one will not make headlines, it is a very interesting, detailed case-study of one person with MS who took vitamin D3, in increasing dosages, calcium and magnesium and improved her quality of life. She can walk for exercise and enjoyment and she is no longer in pain.

More information

Van Amerongen publishes a website (Vitamin D and MS - http://www.vitamindandms.org/) where she collects news on Vitamin D and MS, gives an overview of the ongoing clinical trials with Vitamin D in MS, and presents a growing number of researchers, including neurologists, interested in vitamin D and MS. There is also an outreach to Dutch people with MS.

[CureOrBust]

In January 2001 Dr. van Amerongen started with vitamin D3 800 IU/day, resulting in serum levels between 33-40 ng/ml (84-102 nmol/L). September 2004 she increased to 4000 IU/day, which seemed to keep the serum level around 40 ng/ml (100 nmol/L). In December 2005 she increased again to 6000 IU/day, and serum levels rose to above 55 ng/ml (135 nmol/L). Although there were rises and falls in the serum level throughout the 10 year period, her vitamin D level was always within a "safe" physiological range of 30-80 ng/ml (75-200 nmol/L).

This is NOT Coimbria Protocol. It even explicitly speaks of a "safe physiological range of 30-80 ng/ml", which i think would be safe to say is below what someone actually on Coimbria Protocol would reach. There is also no mention of measuring her PTH to adjust the dose, and she even included Calcium supplementation. If anything, it shows that results with D3 can be achieved without the use of the high doses of Coimbria Protocol.

[PointsNorth]

#CMSC16: MS Experts Agree on Benefits of Vitamin D Supplements, Despite Mostly Circumstantial Evidence

http://multiplesclerosisnewstoday.com/2 ... 7-71579141

[Lionel]

Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract.


Abstract
PURPOSE:
Vitamin D is well known for its effects on bone mineralisation but has also been attributed immunomodulatory properties. It positively influences human health, but in vivo data describing vitamin D effects on the human gut microbiome are missing. We aimed to investigate the effects of oral vitamin D3 supplementation on the human mucosa-associated and stool microbiome as well as CD8+ T cells in healthy volunteers.

METHODS:
This was an interventional, open-label, pilot study. Sixteen healthy volunteers (7 females, 9 males) were endoscopically examined to access a total of 7 sites. We sampled stomach, small bowel, colon, and stools before and after 8 weeks of vitamin D3 supplementation. Bacterial composition was assessed by pyrosequencing the 16S rRNA gene (V1-2), and CD8+ T cell counts were determined by flow cytometry.

RESULTS:
Vitamin D3 supplementation changed the gut microbiome in the upper GI tract (gastric corpus, antrum, and duodenum). We found a decreased relative abundance of Gammaproteobacteria including Pseudomonas spp. and Escherichia/Shigella spp. and increased bacterial richness. No major changes occurred in the terminal ileum, appendiceal orifice, ascending colon, and sigmoid colon or in stools, but the CD8+ T cell fraction was significantly increased in the terminal ileum.

CONCLUSION:
Vitamin D3 modulates the gut microbiome of the upper GI tract which might explain its positive influence on gastrointestinal diseases, such as inflammatory bowel disease or bacterial infections. The local effects of vitamin D demonstrate pronounced regional differences in the response of the GI microbiome to external factors, which should be considered in future studies investigating the human microbiome.

http://www.ncbi.nlm.nih.gov/pubmed/26130323

[Lionel]

VITAMIN D AND THE GUT’S INTESTINAL MUCOSAL BARRIER



Did you know that the debilitating childhood disease rickets is making a comeback in the world? Especially in western countries like England and the U.S.? Or that our children are suffering from more and more autoimmune diseases at earlier and earlier ages? Do you know why? It isn’t because pollution, it isn’t because of poverty, it isn’t really even due a lack of lack of vitamin D in the diet. Its a lack of sun exposure. For the most part, our children aren’t being forced into dark factories like in previous generations, those factories aren’t spewing out black soot blocking the sun, there isn’t rampant disease causing parents to keep children off the streets. The cause is a largely unfounded and irrational fear of skin cancer. Often times the disease shows up in infants because the babies mother is Vitamin D deficient and the baby is breastfed (PubMed #PMC3012634). Vitamin D deficiency and insufficiency are increasingly common in western cultures.

It is clear from the studies (below) that Vitamin D insufficiency is directly related to inflammation and poor mucosal barrier function. Both of these have a direct impact on the gut and gut related diseases such as SIBO. Vitamin D is so important to the immune system that some bacteria actually inhibit our body’s ability to absorb and utilize Vitamin D, doing this for their own survival.

“Over the past decade, numerous studies have shown that many Americans have low vitamin D levels and as a result, vitamin D supplement use has climbed in recent years. Vitamin D has been shown to boost bone health and it may play a role in preventing diabetes, cancer, cardiovascular disease and other illnesses. In light of the increased use of vitamin D supplements, Mayo Clinic researchers set out to learn more about the health of those with high vitamin D levels. They found that toxic levels are actually rare…We found that even in those with high levels of vitamin D over 50 ng/mL, there was not an increased risk of hypercalcemia, or elevated serum calcium, with increasing levels of vitamin D” — Mayo Clinic Proceedings, summary (full text)

“VDR (Vitamin D Receptor) signaling on immune function has been the focus of many recent studies as a link between 1,25(OH)2D3 and susceptibility to various infections and to development of a variety of inflammatory diseases has been suggested. It is also becoming increasingly clear that microbes slow down immune reactivity by dysregulating the VDR ultimately to increase their chance of survival.” — PubMed #PMC3684798

Besides getting enough Vitamin D, it is also important to be able to utilize it. A very small minority of people are born with a defective in the CYP27B1 gene that codes for VDR (Vitamin D Receptor). In the elderly mitochondrial dysfunction can cause CYP27B1 to not function properly. But what is most fascinating is the thought that some microbes may have the ability to interfere with vitamin D utilization by dysregulating VDR. This would not only protect the microorganism but cause additional diseases to take hold, even making someone much more susceptible to the flu. However, it may be possible to overcome VDR dysregulation in some cases by increasing Vitamin D intake (PubMed #PMC2553887) to compensate.

“VDR plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the healing capacity of the colonic epithelium. Therefore, vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD…D3 markedly enhanced tight junctions formed by Caco-2 monolayers by increasing junction protein expression and TER and preserved the structural integrity of tight junctions” — PubMed #17962355

“Our recent studies unveil a regulatory circuit that centers gut epithelial VDR as a key molecule in the control of mucosal inflammation and colitis development. On the one hand, intestinal epithelial VDR signaling protects the integrity of the mucosal barrier by inhibiting inflammation-induced epithelial cell apoptosis. This barrier-protecting, anti-colitic activity is independent of the non-epithelial immune VDR actions. A healthy and intact mucosal barrier prevents bacterial invasion and thus reduces mucosal inflammation. On the other hand, inflammation in turn down-regulates epithelial VDR expression by inducing VDR-targeting microRNA-346, thus compromising mucosal barrier functions. Consistently, colonic epithelial VDR levels are markedly reduced in patients with inflammatory bowel diseases or in experimental colitis models, whereas vitamin D analog therapy that ameliorates colitis up-regulates epithelial VDR. Thus, gut epithelial VDR signaling appears to play an essential role in controlling mucosal inflammation and thus could be a useful therapeutic target in the management of inflammatory bowel diseases.” — PubMed #25603468

If the bacteria are preventing Vitamin D utilization we won’t be able to repair the mucosal barrier, thus allowing for a worsening of the infection and perhaps secondary infections. All of this leads to mucosal inflammation and leaky gut. As the following study indicates poor Vitamin D levels also affects the Tight Junctions, which prevent bacteria and proteins from crossing through the small intestine into the bloodstream (leaky gut).

“The anti-inflammation and anti-infection functions for Vitamin D are newly identified and highly significant activities. Vitamin D/VDR have multiple critical functions in regulating the response to intestinal homeostasis, tight junctions, pathogen invasion, commensal bacterial colonization, antimicrobe peptide secretion, and mucosal defense. Interestingly, microorganisms modulate the VDR (Vitamin D Receptor) signaling pathway.” — PubMed #PMC2955835

“Many studies have implicated Vitamin D and VDR in inflammatory bowel disease (IBD). Low Vitamin D levels have been reported in patients with IBD. The VDR protein is significantly lower in IBD and colitis-associated colon cancer patients… It has also been shown that VDR stabilizes cell tight junction structures in the intestinal epithelial cells; hence, proper functioning of VDR is needed to control intestinal homeostasis…Consistent with its anti-inflammatory role, 1,25(OH)2D3 downregulates the expression of many proinflammatory cytokines…. Cells of the gastrointestinal tract, including epithelial cells and lamina propria macrophages, are constantly exposed to lumenal bacteria, which play key roles in normal intestinal development and innate immunity. The intestinal Paneth cells are known to secrete antimicrobial peptides, which are regulated by VDR signaling.” — PubMed #PMC2955835

“The involvement of Vitamin D/VDR in anti-inflammation and anti-infection represents a newly identified and highly significant activity for VDR. Studies have indicated that the dysregulation of VDR may lead to exaggerated inflammatory responses, raising the possibility that defects in Vitamin D and VDR signaling transduction may be linked to bacterial infection and chronic inflammation.” — PubMed #20639756

Have you ever wondered why the cold and flu are more common in the winter? It isn’t because we congregate together more in the winter, most of us now work indoors all year round.

“In 1981, R. Edgar Hope-Simpson proposed that a ‘seasonal stimulus’ intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter… 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the ‘oxidative burst’ potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection… An interventional study showed that vitamin D reduces the incidence of respiratory infections in children. We conclude that vitamin D, or lack of it, may be Hope-Simpson’s ‘seasonal stimulus’.” — PubMed #16959053

“The data support the hypothesis that a high vitamin D level, as that found in the summer, acts in a protective manner with respect to influenza as well as pneumonia.: — PubMed #PMC3092571

“Deficiency in vitamin D is associated with increased autoimmunity as well as an increased susceptibility to infection. As immune cells in autoimmune diseases are responsive to the ameliorative effects of vitamin D, the beneficial effects of supplementing vitamin D deficient individuals with autoimmune disease may extend beyond the effects on bone and calcium homeostasis…The implications of vitamin D deficiency on the immune system have become clearer in recent years and in the context of vitamin D deficiency, there appears to be an increased susceptibility to infection and a diathesis, in a genetically susceptible host to autoimmunity” — PubMed #PMC3166406

“One report studied almost 19,000 subjects between 1988 and 1994. Individuals with lower vitamin D levels (<30 ng/ml) were more likely to self-report a recent upper respiratory tract infection than those with sufficient levels” — PubMed #PMC3166406

“type 1 diabetes mellitus, rheumatoid arthritis, multiple sclerosis (MS), and inflammatory bowel disease has been linked to geographic location with a higher incidence of these diseases at higher degrees of latitude. One explanation of this geographical distribution is low exposure to sunlight and hence lower levels of vitamin D” — PubMed #PMC3684798

“Recently, important progress has been made in understanding how the noncanonical activities of Vitamin D influence the pathogenesis and prevention of human disease. Vitamin D and VDR are directly involved in T cell antigen receptor signaling. The involvement of Vitamin D/VDR in anti-inflammation and anti-infection represents a newly identified and highly significant activity for VDR. Studies have indicated that the dysregulation of VDR may lead to exaggerated inflammatory responses, raising the possibility that defects in Vitamin D and VDR signaling transduction may be linked to bacterial infection and chronic inflammation.” — PubMed #PMC2955835

“low 25(OH)D concentrations were associated with serum markers of inflammation that are indicators of cardiac risk.” — PubMed #PMC3012634

“A number of studies have suggested that patients with autoimmune diagnoses are deficient in 25-hydroxyvitamin D (25-D) and that consuming greater quantities of vitamin D, which further elevates 25 D levels, alleviates autoimmune disease symptoms… the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes…symptomatic improvements among those administered vitamin D is the result of 25-D’s ability to temper bacterial-induced inflammation” — Pubmed #19393200

“The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system… The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors… Vitamin D deficiency in humans is associated with increased prevalence of diseases… ” — PubMed #PMC2583388

Lower Mortality Rates:

“In a prospective observational study of adults older than 65 years participating in NHANES III, the risk of death was 45% lower in those with 25(OH)D values greater than 40 ng/mL compared with those with values less than 10 ng/mL” — PubMed #PMC3012634

“In noninstitutionalized older adults, a group at high risk for all-cause mortality, serum 25(OH)D levels had an independent, inverse association with CVD and all-cause mortality. Randomized controlled trials of vitamin D supplementation in older adults are warranted to determine whether this association is causal and reversible.” — PubMed #19549021

“Low 25(OH)D levels are associated with all-cause mortality and even more pronounced with cardiovascular mortality” — PubMed #19226272

“Ecological and observational studies suggest that low vitamin D status could be associated with higher mortality from life-threatening conditions including cancer, cardiovascular disease, and diabetes mellitus that account for 60% to 70% of total mortality in high-income countries. We examined the risk of dying from any cause in subjects who participated in randomized trials testing the impact of vitamin D supplementation… Intake of ordinary doses of vitamin D supplements seems to be associated with decreases in total mortality rates.” — PubMed #17846391

Now that they’ve shown that it is very difficult to overdose on Vitamin D and that even among people with high blood levels (up to 80ng/ml) hypercalcemia, and other side effects, are very rare — Mayo Clinic News Release there really is no reason not to supplement to get your blood levels up to the optimal 50ng/ml.

The sun is the preferred source of Vitamin D. If you burn easily you can greatly enhance your ability to avoid sunburn (and enjoy more time outdoors!) by doing the following:

-Avoid polyunsaturated fats (PUFA) as much as possible, replace with unsaturated (olive oil) and saturated fats (coconut oil, palm oil, butter and other animal fats)

-Improve your Omega 6:Omega 3 ratio. Largely accomplished by reducing PUFAs. Consuming fish, fish oil tablets, and a DHA supplement will also help.

-Take a astaxanthin supplement daily, at least 4mg / day, 8mg is better, especially in the summer months.

-Supplement with 8-10 grams of glycine per day and/or consume bone broths daily. Glycine is very protective of UV radiation damage and inflammation.

-Take a Vitamin D supplement. Vitamin D is protective of UV damage.

-Caucasians – Tan. Once you’ve added the above to your diet you should be able to get a tan quite easily. Start off slowly. 30 minutes the first day. Waits 48 hours and see what happens. If all is well try an hour the next time. Increase as desired. (non-caucasians with dark skin need more sun than light skinned people. The good news is that it’s harder for your to burn)


http://www.theguthealthprotocol.com/wp/ ... l-barrier/

[ElliotB]

"Its a lack of sun exposure."

Then why aren't the Eskimos sick? Consider that there is ZERO incidence of MS among them (native Eskimos) and they have the least amount of sun exposure than possibly any group of people on the planet.

[jackD]

This is simple to explain.

DIET - DIET - DIET

They eat LOTS of fish and therefore get LOTS of Vitamin D3.

jackD

p.s. Of course those Eskimos who do not eat a native fish diet are at risk for health problems related to low Vitamin D3 levels. Also there are some concerns of excess Vitamin A toxicity if one tries to get their Vitamin D3 level up by taking fish liver oil.

[AntonioBR]

"Its a lack of sun exposure."

Then why aren't the Eskimos sick? Consider that there is ZERO incidence of MS among them (native Eskimos) and they have the least amount of sun exposure than possibly any group of people on the planet.

Hi ElliotB,

Eskimos evolved to get and limit Vitamin D from food. In regards to the Inuit and Eskimo their diet of whale, seal, and walrus blubber (vitamin D saturated fat), along with eggs and char (trout) are all rich in vitamin D.

There is an interesting article from vitamindwiki.com explaining about it with evidences: http://www.vitamindwiki.com/Eskimos+evo ... +from+food

[AntonioBR]

-
Short-Term Effect of High-Dose Vitamin D
on the Level of Interleukin 10 in Patients with Multiple Sclerosis:
A Randomized, Double-Blind, Placebo-Controlled Clinical Trial

Ashtari F.a · Toghianifar N.b · Zarkesh-Esfahani S.H.d · Mansourian M.c
aDepartment of Neurology, bIsfahan Neuroscience Research Centre, and cDepartment of Biostatistics and Epidemiology, Health School, Isfahan University of Medical Sciences, and dDepartment of Biology, University of Isfahan, Isfahan, Iran


BACKGROUND:
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. Vitamin D has been related to the prevention of MS and to modulating its course. Recent studies have shown the safety of high-dose vitamin D in MS.
OBJECTIVE:
This study compared the effects of high-dose vitamin D on interleukin 10 (IL-10) levels in MS patients in a double-blind, randomized clinical trial.
METHODS:
Ninety-four patients with relapsing remitting MS (RRMS) were randomized into a treatment and a placebo group. Both groups received conventional MS treatment. The intervention group received 50,000 IU of vitamin D every 5 days for 3 months. IL-10 was measured at baseline and after 3 months.
RESULTS:
Serum levels of IL-10 were (median ± IQR): 12.58 ± 11.97 and 10.97 ± 9.97 pg/ml in the intervention and placebo groups, respectively, at baseline (p = 0.161); after 3 months, these levels were 13.76 ± 18.95 and 11.31 ± 19.63 pg/ml, respectively (p = 0.158). The IL-10 level increased significantly after receiving high-dose vitamin D for 3 months (β = 0.737, p = 0.015 and R2 = 0.91).
CONCLUSION:
IL-10 levels increased significantly in RRMS patients after taking high-dose vitamin D3 for 3 months. High-dose vitamin D might be useful in promoting an anti-inflammatory state in RRMS patients.


https://www.ncbi.nlm.nih.gov/pubmed/26401986