Vitamin D and Autoimmune Diseases: Is Vitamin D Receptor (VDR) Polymorphism the Culprit?
Isr Med Assoc J. 2017 Jul;19(7):438-443.
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Bizzaro G1, Antico A2, Fortunato A3, Bizzaro N4.
1 Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel.
2 Laboratorio Analisi, Ospedale Civile, Santorso, Italy.
3 Patologia Clinica, Area Vasta 5 ASUR Marche, Ascoli-Piceno, Italy.
4 Laboratorio di Patologia Clinica, Ospedale S. Antonio, Tolmezzo, Italy.
Vitamin D deficiency is becoming an increasing problem worldwide. It should not be underestimated, not only due to the well-known consequences vitamin D deficiency has on bone health, but primarily because recent studies have shown how the biologically active form of vitamin D - 1,25(OH)2D - is involved in many biological processes, including immune system modulation. Moreover, the presence of a vitamin D receptor was discovered in almost all immune cells and some of its polymorphisms were found to be associated with increased incidence of autoimmune diseases. This finding led to a proposed link between vitamin D deficiency and autoimmune diseases. Patients affected by various autoimmune diseases showed low levels of vitamin D. However, it is not always clear whether vitamin D deficiency is the cause or rather a consequence of the disease. Limitations of the studies, such as the small number of patients, heterogeneity of selected groups, environmental conditions, methods used to measure vitamin D serum concentration and other confounding factors do not lead to unequivocal results to demonstrate a direct link between low vitamin D levels and autoimmune disease. Therefore, randomized trials are needed to clarify conflicting results.
Table of contents
25-hydroxy vitamin D, 25(OH)D, the major circulating form of vitamin D, with an half-life of 3 weeks. Due to its long half-life, 25(OH)D is the most reliable compound to assess individual vitamin D levels. Finally, the molecule is converted in the kidney to the biologically active form, 1,25-dihydroxy vitamin D - 1,25(OH)2D - also known as calcitriol. 1,25(OH)2D enters the target cells, binds to the vitamin D receptor (VDR) and induces a conformational modification that leads to its interaction with the retinoic acid receptor (RXR). The VDR is an intracellular polypeptide part of the steroid-thyroid-retinoid acid receptor superfamily. It binds as VDR/VDR homodimers or VDR/RXR heterodimers to target cell DNA, leading to special protein syntheses. Although the most well-known function of vitamin D is the role it plays in maintaining the right balance between calcium and phosphate serum levels, thus promoting bone health, binding of 1,25(OH)2D to the intracellular VDR regulates more than 900 genes involved in many physiological processes. As such, vitamin D has recently started to be considered essential for the maintenance of physiological homeostasis, and its deficiency has been associated with a wide range of diseases and cardiovascular and metabolic disorders, including cancer, hypertension, and infectious and autoimmune diseases. Vitamin D deficiency is commonly defined as levels < 20 ng/ml [Table 1], and has been documented both in healthy and diseased populations worldwide, mainly in northern areas . This new evidence is exposing vitamin D deficiency as a pandemic increasing problem.
Binding of 1,25(OH)2D to the intracellular vitamin D receptor (vdR) regulates more than 900 genes involved in many physiological processes, including both innate and adaptive immunity
Vitamin D, commonly defined as “the sunshine vitamin" is a steroid hormone originating from cholesterol. Few foods naturally contain vitamin D, which is mostly synthesized in human skin through sun exposure. As vitamin D is absorbed by the skin after exposure to ultraviolet B light, its synthesis is influenced by latitude, season, lifestyle and skin pigmentation. Vitamin D is initially synthesized as a biologically inactive precursor, with a half-life of 12-16 hours. In the liver it is converted to
After stimulation by biologically active vitamin D, the VDR regulates the expression of genes in a variety of vitamin D responsive tissues. The discovery of VDR as well as of vitamin D-activating enzymes in cell types other than those involved in mineral and bone homeostasis strongly indicates the role of the hormone in other physiological conditions. Activation of VDR induces a wide variety of so-called non-classic effects, with modulation of cellular growth, proliferation, apoptosis, and immune cell activation .
Table 2. Mechanisms of vitamin D action on the immune system
Genetic vitamin D receptor (VDR) mutations may result in an alteration of the effects produced by the binding of the receptor with 1,25(oh)2D in the promoter regions of genes that respond to vitamin D
Awareness of a the role vitamin D takes in the regulation of immune responses was prompted by the discovery of VDR in almost all immune cells, including activated CD4+ and CD8+ T cells, B cells, neutrophils, and antigen-presenting cells (APC) such as macrophages and dendritic cells. It has been shown that resting monocytes and dendritic cells express VDR intra-cellularly, while resting T and B lymphocytes express little to no VDR. However, VDR expression in T cells is increased fivefold upon lymphocytes activation .
Allelic variations within the VDR gene have been implicated in mediating susceptibility to endocrine autoimmune disease. The most studied VDR polymorphism are TaqI, BsmI, ApaI and FokI. Autoimmune thyroid disease risk was found associated with the BsmI or TaqI polymorphism, while the BsmI and FokI polymorphism are associated with increased risk of systemic lupus erythematosus (SLE) . FokI polymorphism in the VDR gene might affect individual susceptibility to diabetic nephropathy , while the ApaI, BsmI and TaqI polymorphisms may be susceptibility risk factors for rheumatoid arthritis (RA) . Taken together, these data show that there is a link between autoimmune diseases and vitamin D, which seems to be important to maintain immune homeostasis.
Vitamin D regulates both innate and adaptive immunity [Table 2]. The innate immune response is characterized by the activation of monocytes and macrophages, which are able to recognize pathogen-associated molecular patterns (PAMPs) and thus provide a first line of defense against outside agents, increasing the anti-microbial activity of macrophages and enhancing the chemotactic and phagocytic capacity of these cells . Conversely, vitamin D deficiency impairs the ability of macrophages to mature, produce macrophage-specific surface antigens, produce the lysosomal enzyme acid phosphatase, and secrete hydrogen peroxide, which is essential to their antimicrobial function.
In addition, the upregulation of VDR on toll-like receptor activation of monocytes and macrophages leads to the induction of cathelicidins, a family of polypeptides found in lysosomes of macrophages and polymorphonuclear leukocytes that have a critical role in innate immune defense. Cathelicidin production is enhanced after Mycobacterium tuberculosis (TB) infection, when macrophages recognize TB-PAMPs and upregulate VDR expression, inducing cathelicidin gene activation, thus killing the TB . Monocytes activated in the presence of 1,25(OH)2D show a decreased production of TNF-a, IL-1a and IL-6, and an increased IL-10 production. Thus, vitamin D can modulate the immune response in a more anti-inflammatory and regulatory fashion .
Adaptive immunity is also influenced by vitamin D in many ways. Vitamin D acts on cells of the monocyte-macrophage lineage preventing differentiation into dendritic cells  and reducing the expression of surface co-stimulatory molecules CD80 and CD86, thus affecting the T cell stimulatory capacity of these APC cells . Moreover, 1,25(OH)2D suppresses dendritic cell maturation, decreasing antigen presentation and T and B cells activity [10,11]. Dendritic cell-derived cytokine and chemokine expression are modulated by vitamin D, skewing the Th1/Th2 balance to a wider Th2 response and increasing the regulatory T lymphocyte compartment . There is increasing evidence from in vitro studies and animal models that 1,25(OH)2D can suppress Th1 and Th17 responses while promoting the T regulatory cell and Th2 cell expression by enhancing the production of IL-4, IL-5 and IL-10 . Moreover, after vitamin D stimulation, dendritic cells have a reduced capacity to trigger T cell proliferation . In addition to dendritic cells, 1,25(OH)2D has direct effects on T lymphocytes, and directly alters the cytokine profile of T cells, inhibiting pro-inflammatory cytokines production such as IL-2, INF-y, IL-17 and IL-21 . The B cell population is also influenced by the vitamin D pathway. Exposing B cells to 1,25(OH)2D inhibits their proliferation, plasma cell differentiation and immunoglobulin secretion (IgG and IgM), and memory B cell generation as well as inducing B cell apoptosis .
Sustaining the link between hypovitaminosis D and increased incidence of autoimmune diseases, Mathieu et al.  demonstrated that 1,25(OH)2D supplementation alone was able to reduce incidence of insulitis and prevent diabetes when administered to 3 week old non-obese diabetic mice. At 8 weeks it was efficient only if associated with an immune suppressor and was not therapeutic if given after lesion onset. These new results led to the speculative hypothesis that in genetically predisposed subjects living at high latitudes and presenting chronic insufficient or deficient hormone concentration, early vitamin D supplementation could control and/or block disease onset. Conversely, vitamin D supplementation, even at high dosage, after the immunological reaction may be able to reduce the severity of symptoms .
Low vitamin D status and vitamin D receptor (VDR) polymorphism have been thought to be important environmental risk factors in the development of autoimmune disease
The pathogenesis factors of autoimmune diseases are a mosaic of genetic predisposition, hormonal effects and environmental factors. Low vitamin D status and VDR polymorphism have been suggested as important environmental risk factors in the development of autoimmune diseases. Growing evidence shows that VDR polymorphism (especially BsmI, Apal, TaqI, and FokI polymorphism genotypes) are related to an increased incidence of autoimmune diseases, and it has been shown that the interaction between VDR and its ligand produces an anti-inflammatory effect on innate immunity and a regulatory and immunosuppressive action on adaptive immunity.
Low vitamin D levels have been reported in several autoimmune disorders, including multiple sclerosis (MS), type 1 diabetes mellitus (T1DM), SLE, RA, inflammatory bowel disease, thyroiditis and autoimmune gastritis [1,15-17]. However it is not always clear whether vitamin D deficiency is the cause or rather a consequence of the disease.
A well-designed study  investigated the association between vitamin 25(OH)D status and development of autoimmune disease in 12,555 individuals from three population- based studies. Relative risks of autoimmune disease were estimated by Cox regression and expressed as hazard ratio (HR) with 95% confidence interval (CI). There were 525 cases of incident autoimmune disease. The HR for a value of 10 nmol/l was 0.94 (95%CI 0.90-0.98) for any autoimmune disease, 0.83 (95%CI 0.72-0.96) for thyrotoxicosis, 0.95 (95%CI 0.88-1.02) for T1DM, 0.89 (95%CI 0.74-1.07) for MS, 1.00 (95%CI 0.86-1.17) for iridocyclitis, 0.95 (95%CI 0.80-1.13) for Crohn’s disease, 0.88 (95%CI 0.75-1.04) for ulcerative colitis, 0.99 (95%CI 0.86-1.13) for psoriasis vulgaris, 0.97 (95%CI 0.89-1.07) for seropositive RA, and 0.94 (0.83-1.06) for polymyalgia rheumatica.
Zerr et al.  analyzed the role of VDR signaling in fibrosis patients with systemic sclerosis (SSc), in which the levels of vitamin D3 are decreased. They characterized VDR as a negative regulator of TGF-p/Smad signaling. Impaired VDR signaling with reduced expression of VDR and decreased levels of its ligand may thus contribute to hyperactive TGF-p signaling and aberrant fibroblast activation in SSc. Vitamin D has been proposed as an anti- fibrotic treatment option in the early onset of fibrosis in specific genotypes for VDR due to its known crosstalk with transforming growth factor (TGF)-p signaling. In primary human hepatic stellate cells vitamin D supplementation improved TGF-p- induced fibrogenesis through both VDR-dependents and VDR- independent mechanisms, while known polymorphisms of the VDR (A1012G single nucleotide polymorphisms) may influence the response to vitamin D treatment, abolishing the reduction of fibrogenic response.
Prevalence of MS in northern Europe strongly correlates with vitamin D deficiency and the risk of disease onset. It is known that vitamin D has immunomodulatory functions and suppresses an animal model of MS. Genome-wide association studies have identified more than 20 susceptible loci in MS, including the VDR gene and rs2248359. This last locus can increase MS risk by regulating the expression of nearby genes, for example CYP24A1, which encode the enzyme responsible for the degradation of 1,25(OH)2D. rs2248359-C increases CYP24A1 expression in the human brain, thus showing a genetic connection between MS and vitamin D metabolism and indicates that the physiologic active form of vitamin D is protective. Some studies conducted in Iran, Japan, Australia and United Kingdom to find the association between VDR polymorphisms (SNPs, TaqI and Apal) and MS, have shown links between allelic and genotype frequencies and the disease. No correlation was found in other studies conducted in Greece, USA and the Netherlands. This discrepancy highlights the need for randomized trials.
In patients affected with SLE a significant inverse correlation was reported between disease activity and serum vitamin D concentration , and anti-vitamin D antibodies were found in a subset of patients with SLE and antiphospholipid syndrome . The relation between VDR gene polymorphism and the risk of SLE is conflicting, A meta-analysis including 13 studies was conducted to evaluate the relationship between VDR BsmI (rs1544410), Fok1 (rs2228570), ApaI (rs7975232) and TaqI (rs731236) gene polymorphism and the risk of SLE. In this meta-analysis, the BsmI B allele and bb genotype, Fok1 f allele and ff genotype, and ApaI aa genotype were associated with the risk of SLE in the overall populations. In Asians, the BsmI B allele, BB genotype and bb genotype, Fok1 f allele and ff genotype were associated with the risk of SLE. In Africans, the BsmI B allele, BB genotype and bb genotype, Fok1 f allele and ff genotype, ApaI A allele, AA genotype and aa genotype were associated with the risk of SLE. However VDR BsmI, Fok1, ApaI and TaqI gene polymorphism were not associated with the risk of SLE in Caucasians .
Several studies suggested association between VDR polymorphisms and type 1 diabetes mellitus (T1DM) pathogenesis . The interactions of genetic background with the development of TIDM are well documented in various populations as the incidence of childhood T1DM is known to vary widely between and within countries. A study conducted to investigate the relationship between VDR gene polymorphisms (at positions Taq I and Apa I) and the incidence of T1DM in Egyptians showed a significant association in diabetic patients compared with controls . The results obtained in a study performed in an Iranian population demonstrated that genotypes frequency of the TaqI VDR polymorphism differed significantly between T1DM patients and controls . The Diabetes Autoimmunity Study in the Young (DAISY) longitudinal study  explored the association between seven vitamin D metabolism gene singlenucleotide polymorphisms (SNPs) and the risk of islet autoimmunity (IA), the preclinical phase of T1DM. Two novel intronic variants for the association with T1DM, DHCR7/NADSYN1 and CYP27B1 were found to be significantly associated with the appearance of IA. Interestingly, these two variants were not found to be associated with progression to T1DM in IA-positive children. Six of the seven SNPs were significantly associated with 25(OH)D levels. These findings may offer insights concerning the complex role of vitamin D in the etiology of T1DM.
A recent meta-analysis including 24 reports involving 3489 patients showed that RA patients had lower vitamin D levels than healthy controls and that a negative relationship exists between serum 25-hydroxyvitamin D (25OHD) levels and disease activity index .
A study conducted on a Tunisian cohort (108 patients with RA and 152 controls) to establish the associations of VDR gene polymorphisms FokI and BsmI with susceptibility to RA, demonstrated that FokI polymorphism alleles and genotype were significantly more common in the RA group than in controls (P = 0.001 and P = 0.005, respectively). In patients with RA, the FokI polymorphism was significantly associated with female gender (P = 0.003). No significant associations were found between the Bsm1 polymorphism and RA . Moreover a case-control study including 106 RA Tunisian patients and an appropriate number of healthy control subjects showed no significant association for VDR ApaI and TaqI polymorphisms with RA risk (P > 0.05) .
Another study explored the role of vitamin D in RA pathogenesis by investigating enrichment of vitamin D response elements (VDREs) in confirmed RA susceptibility loci and testing variants associated with vitamin D levels for association with RA. SNPs in the DHCR7/NADSYN1 locus showed evidence of positive association with RA (P = 0.008, OR 1.14 95%CI 1.03— 1.24). The significant enrichment of VDREs at RA-associated loci and the modest association of variants in loci controlling levels of circulating vitamin D support the hypothesis that vitamin D plays a role in the development of RA .
Some studies have suggested an influence of vitamin D receptor polymorphisms on the development of autoimmune thyroid disease (AITD). One study investigated the distribution of VDR alleles (FokI, BsmI, ApaI TaqI polymorphisms) in a group of 111 Turkish patients with Hashimotos thyroiditis and 159 healthy controls. It showed that the VDR gene TaqI TT and FokI FF genotypes were associated with increased risk of Hashimotos thyroiditis. BbAaTtFf genotype seemed to be protective to Hashimotos thyroiditis disease in the same population .
Another study tested whether the functional VDR polymorphisms (TaqI rs731236, ApaI rs7975232, FokI rs2228570 and BsmI rs1544410), group-specific component (GC) gene (rs7041 and rs4588), and CYP2R1 (rs10741657) are involved in the pathogenesis of AITD . Using polymerase chain reaction-restriction fragment length polymorphism, 139 patients with Graves’ disease, 116 HT patients and 76 control subjects were genotyped. The frequency of the TT genotype for the TaqI polymorphism was higher in Graves’ disease patients than in HT patients (P = 0-0147). The frequency of the C allele for the Apal polymorphism was higher in Graves’ disease patients than in control subjects (P = 0-0349). The frequency of the CC genotype for the FokI polymorphism was higher in HT patients than in control subjects (P = 0-0174) and Graves’ disease patients (P = 0-0149). The frequency of the GclGcl genotype for the GC polymorphism and the AG genotype for the CYP2R1 polymorphism were lower in intractable Graves’ disease than in Graves’ disease in remission (P = 0-0093 and 0-0268, respectively). This study showed how genetic differences in the VDR gene may be involved in the development of AITD and the activity of Graves’ disease. Eight studies were identified and meta-analyzed to address the association of VDR gene FokI (rs2228570), TaqI (rs731236), BsmI (rs1544410), and ApaI (rs7975232) polymorphisms with AITD risk . The result indicates that the BsmI or TaqI polymorphisms are significantly associated with AITD risk (Pz = 0.001 for B vs. b; Pz = 0.010 for t vs. T) while the ApaI or FokI polymorphism are not. In the subgroup analysis in Europeans, the decreased risk of AITD remained for the B or t variant. This gene-based analysis indicates that, based on current evidence from published studies, the cumulative effect of BsmI or TaqI polymorphisms in VDR is significantly associated with AITD.
Another recent meta-analysis investigated the association between vitamin D level and AITD through an accurate systematic literature review . After identifying hundreds of references, the authors considered 20 papers that met their inclusion criteria. Analyzing the studies, Wang and co-authors  concluded that serum 25(OH)D was lower in AITD patients compared to healthy control individuals, and AITD was more likely to develop in individuals who showed low levels of serum 25(OH)D, which suggested that vitamin D deficiency may play a role in the pathological process of AITD.
However, other studies failed to demonstrate a firm correlation. Effraimidis et al.  showed how vitamin D deficiency is not associated with early stages of thyroid autoimmunity, while an Asian Indian community-based survey found only a weak inverse correlation between serum 25(OH)D values and anti- thyroperoxidase antibody titers .
Thus, controversial opinions on the role of vitamin D in autoimmune disease onset are expressed by the scientific community . Critical observers claim that many studies show strong limitations that impede the process of getting irrefutable and clear results. Although most of the observational studies reported moderate to strong inverse associations between vitamin D and autoimmune diseases, in most trials vitamin D supplementation had no effect on the disorders studied. This discrepancy between observational and interventional studies suggests that vitamin D deficiency could be the result and not the cause of the diseases. Additional co-factors may affect the result of epidemiological studies, such as obesity, smoking, pregnancy, and sedentary lifestyle. For example, in SLE patients many factors can lead to vitamin D deficiency, including chronic steroid use, enzymatic problems due to renal involvement, anti-vitamin D antibodies and the need to avoid sun exposure . Moreover, study designs are often conducted on small patient cohorts, with only partial case-control matching, with heterogeneity of the groups selected and environmental conditions. These contradictory data are further affected by the imprecision and variability of analytical methods for the measurement of blood levels of vitamin D, denying the possibility to have unequivocal results demonstrating a direct link between low levels of vitamin D and autoimmune diseases.
The heterogeneity of analytical methods used are reflected by a lack of concordance of the measured concentrations . To make determinations of vitamin D performed in laboratories with different methodologies directly comparable, the US Office of Dietary Supplements of the National Institutes of Health launched a collaborative project among institutional organizations, scientific societies and industries in 2010, called Vitamin D Standardization Program (VDSP) . The objective of this program, besides the compatibility of results obtained by different methods, was to ensure that the measured concentrations are accurate and consistent with the actual concentration of analyte contained in the sample to produce adequate information for clinical purposes and for health policy measures.
Growing evidence proves that the increase in 25(OH)D attributable to vitamin D3 supplementation may vary according to functional common genetic differences in vitamin D 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1), and the VDR genes.
Some studies performed on representative case series found a statistically significant association between specific polymorphisms of VDR, single nucleotides, and autoimmune diseases. These mutations may result in a phenotypic change and an alteration of the biological effects produced by the binding of the receptor with 1,25(OH)2D in the promoter regions of genes that respond to vitamin D, leading to ineffectiveness of regulatory actions produced by the hormone in the cells of the innate and adaptive immune systems.
Therefore, prospective studies designed to prove the link between vitamin D deficiency and autoimmunity will need to assess genetic differences and VDR polymorphisms, since these factors appear to influence the therapeutic strategy of intervention.
Correspondence Dr. N. Bizzaro: Laboratorio di Patologia Clinica, Ospedale S. Antonio, Tolmezzo 33028, nic.bizzaro at gmail.com
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- Insulin resistance correlated with low vitamin D levels in Arab Americans – June 2010
- Vitamin D deficiency associated with many diseases – Greece April 2010
- More obese had less vitamin D, and after low calorie diet, vitamin D went up – June 2010
- Twice as likely to die of type 2 diabetes if severely vitamin D deficient - Mar 2010
- Vitamin D Improves Insulin Sensitivity and Helps Prevent Diabetes – March 2010
- People with high level of vitamin D were 40% less likely to get Type 2 diabetes – June 2010
- Disease Database - nice links for Diabetes
- Diabetes Statistics including more diabetes with darker skin – 2007
- You Can Reverse PreDiabetes – Nov 2009
- Less than 4 ng is more common in Saudis than diabetic Saudis – July 2010
- Low vitamin D levels linked to poor blood sugar control in type 2 diabetes – June 2010
- 300000 IU of vitamin D every 3 months may not have been enough – July 2010
- Possible link between osteoporosis and diabetes – July 2010
The most recent items in category Lupus
- MS vs Latitude
- Vit D and autoimmune
- Veith 2009 MS subset
- Vitamin D regulates MS gene
- Vit D evidence mountain for MS
- New hypotheses on sunlight
- Prevalence of multiple sclerosis in Denmark 1950–2005
- MS in US in WWII vs latitude
- Rheumatoid Arthritis vs latitude Nurses Study
- An estimate of the economic burden and premature deaths due to vitamin D deﬁciency in Canada
- MS increased if low UV during first trimester -April 2010
- Vitamin D and Immune system after 30 years - June 2010
- Vitamin D and Immune system – May 2010
- Review of vitamin D preventing MS - Lancet June 2010
- MS association with latitude has virtually been eliminated- Lancet chart June 2010
- The Causal Cascade to Multiple Sclerosis: A Model for MS Pathogenesis
- MS Latitude correlation - Garland smile graph
- MS mountain of evidence
- Role of vitamin D with ms - 2010
- Ways to reduce reoccurance of MS - May 2010
- T cells MS and vitamin D - Aug 2009
- Lack of UV increased offsping MS - April 2010
- MS decrease by number of hours in the sun
- wiki page:
- Vitamin D decreases incidence of disease
- Scotland and Vitamin D
- 10,000 IU vitamin D plus Calcium trial for those with MS - April 2010
- MS relapse rate for children was 34% less for every extra 10 ng/ml of vit D
- Lancet article: Vit D may provide hope for MS - June 2010
- Vitamin D and sunshine are two ways to reduce MS relapses - May 2010
- Mouse MS: UVB but not Vitamin D reduced incidence - April 2010
- Low vitamin D associated with brain atrophy in MS – April 2010
- MS onset 2 years earlier in northern latitudes – June 2010
- Vitamin D Linked to Poor Learning Performance in Patients With MS – June 2010
- Lancet concludes that Vitamin D can protect against MS, but do know know why – June 2010
- MS causes explored - vitamin D is in 2 of the 4 - 2009
- Patients like me survey found vitamin D to be number one supplement
- Overcoming Multiple Sclerosis - book 2010, 2016
- Comment about vitamin D on a MS blog – Feb 2009
- Disease Database - nice links for Multiple Sclerosis
- Assessing vitamin D in the central nervous system – July 2010
- Vitamin D deficiency probably a risk factor for MS – June 2010
- Lack of UV increased offspring MS - April 2010
- Effective Treatment for Multiple Sclerosis is Completely Free with the sun
- African-Americans and MS
- UV suppresses MS but vitamin D might not – March 2010
- MS UV and Vitamin D – 2009
- 3X increase in MS in Denmark 1950 to 2005 Vitamin D is a possible reason
- MS prevented and treated with Vitamin D – 2009
- Hypothesis - more in sunshine than vitamin D to reduce MS – Feb 2010
- MS and Vitamin D – VitD3 World Jan 2010
The most recent items in category Autoimmune
- Vit D may reduce fatigue in people with Lupus
- Review of Vitamin D, immunity and lupus
- Vit D and autoimmune
- Vit D and Lupus
- Vitamin D may not be a good marker of disease activity in Korean patients with systemic lupus
- Geoepidemiology of rheumatic diseases - June 2010
- 2000 IU vitamin D for Lupus repletion - Sept 2010
- Vitamin D in Lupus - Oct 2010.PDF
- Rheumatoid Artiritis Lupus and vitamin D - Review- Nov 2010.pdf
- wiki page:
- Lupus again found to be related to vitamin D deficiency - should supplementation start? – May 2010
- Is it time to routinely supplement Lupus patients with vitamin D? - May 2010
- Disease Database - nice links for Lupus
- Taking vitamin D reduced Lupus fatigue– Aug 2010
- Vitamin D deficiency prevalent with Lupus R-Arthritis and Diabetes – Oct 2010
- Lupus in vicious circle with vitamin D - Nov 2010
- Lupus 8X more likely to not even have 20 ng of vitamin D – May 2011
- Vitamin D patent for treating immune system diseases
- Vitamin D deficiency and diabetes – rheumatoid arthritis – lupus – Oct 2010
- Lupus increased when whites had low vitamin D (winter) – March 2012
- Lupus flares totally eliminated by loading dose then 100000 IU of vitamin D each month – Oct 2012
- Hypothesis of Autoimmunity which includes Barr Virus and Vitamin D Deficiency – 2012
- When lupus affects the kidneys vitamin D levels drop even further - Nov 2012
- Lupus flareups cut in half by just 2,000 IU of vitamin D – RCT Dec 2012
- Lupus and Vitamin D: good evidence, no conclusions – Review Jan 2013
- Vitamin D increasingly associated with inflammation such as RA, TB, Lupus, and cancer – March 2013
- Lupus biomarker ( regulatory T cell, treg) is associated with level of vitamin D – Jan 2013
- Lupus in blacks associated with low vitamin D AND short telomeres – May 2013
- Vitamin D2 did not help Lupus (no surprise, D2 was given weekly) – June 2013
- Lupus reduced with vitamin D intervention – Feb 2014
- The Antibiotic Effects of Vitamin D – 2014
- Lupus is yet again strongly associated with low vitamin D (when will supplementation be tried) -Dec 2014
- Musculoskeletal pain reduced with 4,000 IU of vitamin D – RCT April 2015
- Lupus not treated by monthly 50,000 IU vitamin D (no surprise) – RCT April 2015
- Lupus is associated with low vitamin D (research in Southern Hemisphere concurs) – April 2015
- Juvenile Lupus fatigue reduced by vitamin D ( 50,000 IU weekly for 6 months) – RCT May 2015
- 2,000 IU vitamin D recommended for pediatric rheumatology – May 2015
- Lupus – vitamin D is essential in preventing and modulating it – May 2016
- If Lupus in family – 5 times more likely to get Lupus if low vitamin D and poor CYP24A1 – June 2016
- Lupus associated with both low vitamin D and Vitamin D receptor problems – April 2016
- Connective tissue disorders (Lupus, RA, etc) treated by vitamin D – May 2016
- It is time to routinely give vitamin D to Lupus patients – Dec 2016
- Lupus in children 2.6 X more likely if they had poor Vitamin D Receptor – Jan 2017
- Omega-3 reduces Lupus, Rheumatoid Arthritis and Osteoarthritis – review Sept 2017
- Dermatologists are reminded of the importance of vitamin D in 8 diseases – Oct 2017
- Lupus reduced by Vitamin D for all trials longer than 12 weeks - review Sept 2017
- Autoimmune diseases associated with low Vitamin D and Vitamin D Receptor – July 2017
- Inflammation and immune responses to Vitamin D (perhaps need to measure active vitamin D) – July 2017
- Lupus is both prevented and treated by Vitamin D – review Dec 2017
- file gallery:
The most recent items in category Thyroid and parathyroid
- IOM Table 1 Vit D primary studies
- IOM Table 2 Primary Calcium studies
- IOM Table 3 primary Vit D and Calcium studies
- Does Vitamin D Intake During Infancy Promote the Development of Atopic Allergy?
- meta-analysis of autoimmune - 2010.pdf
- Vitamin D and Autoimmune slides wisconsin - 2010.pdf
- Gene, vitamin D, and food allergy - 2011.pdf
- wiki page:
- GlutenDoctors on D3 better than D2 and problems with Vitamin A
- Anti-bacterial action of vitamin D – March 2010
- Autoimmunity and vitamin D - several articles April 2010
- Mechanisms for hypothesis between sunshine and food allergy - July 2010
- Vitamin D may be linked to food allergies by intestinal flora – July 2010
- Review of vitamin D asthma and allergic diseases – abstract lacks details July 2010
- International patent for sublingual liquid analogue forms of vitamin D – 2007
- 2X more allergies if 11th womb week was in Spring – Vitamin D or pollen Oct 2010
- Vitamin D may reduce risk of autoimmune disease – systematic review - Oct 2010
- More childhood allergies when vitamin D is less than 15 ng – Feb 2011
- 3X more allergy to peanuts if child born with low UV – Feb 2011
- Vitamin D less than 15 ng associated with some allergies – Feb 2011
- Allergy - Overview
- Lupus 8X more likely to not even have 20 ng of vitamin D – May 2011
- Narcolepsy with Cataplexy was 5X higher if low Vitamin D – May 2011
- Huge increase in food allergies in Australia may be due to low vitamin D
- Increase food sensitization by 80 percent if vitamin D deficient with specific genotypes – Aug 2011
- Allergic diseases in the elderly – Oct 2011
- Being told you have allergies is associated with less than 10 ng vitamin D – Nov 2011
- Still unsure of association between vitamin D and asthma and allergies – review April 2012
- Solar, vitamin D, and autoimmunity – Dec 2011
- Vitamin D and Allergic Disease: Sunlight at the End of the Tunnel – Dec 2011
- Is Vitamin D Supplementation Responsible for the Allergy Pandemic – May 2012
- Vitamin D, Allergy, and genetics – June 2012
- Youths with autoimmunity disorders were 2.3 X more likely to be vitamin D deficient – July 2012
- 6X as many people with allergic rhinitis were severely vitamin D deficient – Jan 2012
- Review of Autoimmune diseases, solar radiation and vitamin D – Schwalfenberg 2012
- Hypothesis of Autoimmunity which includes Barr Virus and Vitamin D Deficiency – 2012
- High level of maternal vitamin D and infant food allergy – controversy
- 30 to 40 ng of vitamin D associated with the least peanut allergy – Nov 2012
- Autoimmunity and vitamin D – review Jan 2013
- Autoimmune disorder patients in Brazil helped by vitamin D – video and Facebook – Nov 2012
- Vitamin D reduces inflammation (heat shock protein) – Aug 2012
- Infectious burden linked to cognitive decline (both linked to low vitamin D) – March 2013
- Sjögren’s syndrome (2nd most common rheumatic disease) and vitamin D – April 2013
- Yet another meta-analysis ignores vitamin D dose and serum level – Autoimmune disease – Dec 2012
- Vitamin D, Vitamin A, or Vitamin E association with allergies and asthma – Feb 2012
- Autoimmunity, T Cells and vitamin D: A chemical network analysis – May 2013
- Vitamin D protects against many types of health problems – review May 2013
- Myasthenia gravis score improved 38 percent with just 800 IU of vitamin D daily – Dec 2012
- Vitamin D and Immune Function – Review July 2013
The most recent items in category Top news
- wiki page:
- Japanese decided that 28 ng mimimum for proper parathyroid hormone – June 2010
- Survey Shows Dogma Not Data Can Dictate Doctors' Decisions - June 2010
- Iodine deficiency might cause obesity
- PTH needs vitamin D level higher than 13 ng – Cohort June 2010
- Overview Hyperparathyroidism and vitamin D
- Review concludes that vitamin D and Calcium help after thyroid removal – Aug 2010
- Price and Masterjohn on Vitamin A Vitamin D and Vitamin K – 2010
- Patients low on vitamin D stay in hospital longer after thyroid removal – Dec 2010
- Every Thyroidectomy patient should get vitamin D and Calcium – Nov 2010
- Overview Thyroid and Vitamin D
- Vitamin D and Primary Hyperparathyroidism – 2011, 2016
- Vitamin D and autoimmune thyroid diseases. – Jan 2011
- Chronic kidney disease and PTH – Calcium – Phosphate – Vitamin D – April 2011
- Need 40 ng of vitamin D to have proper PTH levels – May 2011
- Hashimoto's Thyroiditis and Vitamin D - multiple studies
- Children have PTH problems when vitamin D is less than 15 ng – Nov 2011
- Primary Hyperparathyroidism perfectly predicted with a Vitamin D-Based nomogram – Nov 2011
- Interaction between Vitamin D and calcium – April 2012
- Vitamin D testing typically not needed, but in 9 cases it is – April 2012
- PTH boosts immune response when vitamin D levels are low – May 2012
- Variations in Parathyroid Hormone Concentrations in Patients with Low Vitamin D – June 2012
- 2X more Thyroid Cancer malignancy if less than 15 ng of vitamin D – June 2012
- Hypothesis: Primary hyperparathyroidism might increase when vitamin D levels increase – Aug 2012
- Calcium and bone disorders in pregnancy – May 2012
- PTH does not plateau with increasing vitamin D, but does decrease with patient age – Aug 2012
- African-Americans need only 20 ng of vitamin, not 30 ng, based on iPTH – Sept 2012
- 50,000 IU vitamin D weekly is safe and effective for Primary Hyperparathyroidism – Jan 2013
- Long term Hashimoto's Thyroiditis has lower level of vitamin D – Jan 2013
- Fix Thyroid then increase vitamin D - Oct 2013
- Autoimmune Thyroid Disease 2X more likely if low vitamin D – Dec 2013
- 2800 IU of vitamin D before and after parathyroid surgery helped a lot – RCT Jan 2014
- Hyperparathyroidism – still not absolutely, positively sure that vitamin D should be used to treat it – March 2014
- Diabetes after giving birth was associated with low vitamin D combined with high PTH – May 2014
- Vitamin D helps with T2 Diabetes, hyperparathyroidism, PCOS, and some other endocinological diseases – Sept 2014
- PTH reduced 3.5 pmol by vitamin D intervention which added 22 ng – meta-analysis June 2014
- Following primary hyperparathyroidism surgery 1600 IU vitamin D was not enough to help - RCT Feb 2015
- Autoimmune Thyroid Disease 3X more likely if low vitamin D – meta-analysis April 2015
- Graves Disease is 2.2X more likely with low vitamin D – meta-analysis May 2015
- Critically ill injected with 300,000 IU of vitamin D, 3X more likely to die if PTH did not respond - RCT July 2015
- Hypothesis Vitamin D receptor controls PTH without needing Vitamin D – Aug 2015
- 3000 IU of vitamin D minimum to reduce parathyroid hormone (PTH) – meta-analysis Sept 2015
- Graves' disease and Hashimoto's thyroiditis 1.5X less likely for each 2 ng more vitamin D – Sept 2015
- Lots of vitamin D supplementation by those with Primary Hyperparathyroidism – Sept 2015
- Thyroid diseases and vitamin D – review 2015
- Sunshine vitamin and thyroid - Jan 2017
- Sunshine vitamin and thyroid – Jan 2017
- Ischemic Stroke risk best predicted by Vitamin D, including PTH improves the prediction – Feb 2017
- The Role of Vitamin D in Thyroid Diseases – Sept 2017
- wiki page:
- Smoking reduces vitamin D
- Low cost cofactors for vitamin D
- Vitamin D Recommendations around the world - IU and ng
- Strong association of non alcoholic fatty liver disease and low vitamin D
- Vitamin D - roles in women's reproductive health - Nov 2011
- Reasons for low response by vitamin D level in the blood
- Percent of population with less than 20 ng of vitamin D
- 100 percent of Acute Respiratory Failure patients had low vitamin D - April 2012
- VA showed increased vitamin D testing associated with lower health costs - Lancet May 2012
- Sunlight for babies – US Govt 1933
- Vitamin D after breast cancer diagnosis
- Whites were 2X more likely to be vitamin D deficient if wear long sleeves – Jan 2012
- Yes, need more than 400 IU of vitamin D to strengthen bones
- 7 improvements in lives of veterans with chronic pain with 50,000 IU vitamin D weekly – June 2012
- 400 iu of vitamin D is like 24 seconds of sun in a swimsuit in Los Angeles
- Acute lower respiratory infection 5X more frequent with low vitamin D intake – June 2012
- Hypothesis: Sun provides more than vitamin D – June 2012
- Female Athlete health problems may be due to lack of vitamin D and Iron – July 2012
- Low vitamin D increased probability of low birth weight by 60 percent – meta-analysis June 2012
- Extra 4,000 IU daily raised the vitamin D levels of blacks to that of whites – July 2012
- Overview Schizophrenia and Vitamin D
- Survey finds that Non-Caucasians do not feel that people need sun exposure – July 2012
- Low risk Prostate Cancer decreased with 4,000 IU of vitamin D – July 2012
- Most people have major problems of milk as a source of vitamin D
- Vitamin D presentation by Dr. Holick Spring 2012
- Depression not reduced with 5700 IU vitamin D average in 6 months – July 2012
- Vitamin D from phototherapy lamps, tanning beds, and the sun – Jan 2012
- Half of the US will be people of color – wonder how many will be vitamin D deficient
- Ways to block UVA but not the UVB which makes vitamin D
- With just 200 IU vitamin D in intravenous feeds, deficiency results
- Reproduction function in males improved by vitamin D – review Aug 2012
- 3X more vitamin D from the sun if take MS drug Interferon-β – July 2012
- Pregnant blacks 50 pcnt more likely to be depressed if 3 ng less vitamin D – July 2012
- Free-range bacon has 2800 IU of vitamin D per 100 grams
- In less than 3 weeks chickens have problems if they do not have vitamin D
- Vitamin D less than 20 ng associated with 73 pct chance becoming obese in 11 years – May 2012
- Cognitive Impairment 2.4X more likely if low vitamin D – meta-analysis July 2012
- Death due to cystic fibrosis reduced about 4X due to 250000 IU of vitamin D – RCT June 2012
- European adults can take 4000 IU of vitamin D – July 2012
- Major depression associated with low vitamin D and low bone density – July 2012
- UVB produced 8X more vitamin D as solar UV – July 2012
- Several papers on Vitamin D for critically ill children in Journal of Pediatrics – Aug 2012
- Compelling evidence – Breast Cancer and vitamin D – Dissertation June 2012
- 5X increase in hip fracture rates in 65 years - 1998
- Probability of Type I diabetes reduced 29 percent with vitamin D – systematic review July 2012
- 7100 IU (50000 weekly) restored vitamin D levels for those with Chronic Kidney Disease – July 2012
- Statins associated with 14X increase in Polymyalgia Rheumatica (a new disease) – Aug 2012
- 95 new vitamin D INTERVENTION trials added during 2012
- Vitamin D from the sun thru a special window or heat shield
- NYC Vitamin D Conference Sept 21, 2012