Vit D and Inflammation

Dr. Weeks Comment:   My mother, now thriving at 90, use to say to me when she was frustrated by life:   “I’m so mad I could squeeze a grape!”   We kids knew to be careful at these times around her!   Well, I feel that mad now.   Yet again, a wonderful young lady who has suffered greatly with inflammatory illnesses for years came to me after having to suffer bad medical care as well.  She was told years ago that she has arthritis in her knee and she was given powerful but toxic medications – methotrexate and Enbrel.  The problem?  She was given an inadequate work-up and no one determined which if any causative factors much be remedied by nutritional medicine. For example, a corrective medical doctor who wants to fix the problem and not just suppress the symptoms would ask what her vitamin D level is… the 25-OH D3.  Why?   Read below… The problem is that her vitamin D level was never even tested by her doctors!  And no doctor told her about the anti-inflammatory diet of the role of anti-inflammatory seeds or that even niacinamide or niacin (vitamin B3)  help with arthritis.  And no doctor told her about how honey bee venom is so beneficial for arthritis.  It is a predictable knee jerk reaction by medical doctors to  just prescribe symptom- suppressing patented synthetic medications regardless of toxic side-effects. 

 

 

Vitamin D Deficiency and Rheumatoid Arthritis.

Clin Rev Allergy Immunol. 2016 Aug 2. [Epub ahead of print]

Ishikawa LL et al

Vitamin D (VitD) is a hormone primarily synthesized in human skin under the stimulation of ultraviolet radiation. Beyond its endocrine role in bone metabolism, VitD is endowed with remarkable immunomodulatory properties. The effects of VitD on the immune system include the enhancement of microbicidal ability of monocytes/macrophages and the down-modulation of inflammatory cytokines produced by T lymphocytes. VitD deficiency is involved in many health problems, including immune-mediated diseases such as autoimmune disorders. Rheumatoid arthritis (RA) is a chronic inflammatory systemic autoimmune disease that compromises the joints, causing cartilage destruction and bone erosion. RA treatment usually consists of combined therapies that generally suppress the entire immune response leading to increased susceptibility to infections. This review describes the main effects of VitD on innate and adaptive immune system and also VitD status in inflammatory rheumatic diseases such as RA. Despite some controversies, the majority of reports reinforce the idea that lower VitD levels correlate with more severe clinical manifestations in RA and other rheumatic diseases. Therefore, supplementation with VitD to achieve normal serum levels is worthwhile as an aforethought. Original data concerning the potential applicability of 1,25-dihydroxyvitamin D3 (VitD3), the active form of vitamin D, as a tolerogenic adjuvant are also included. In this sense, the effect of VitD3 associated with proteoglycan (PG), which is a specific cartilage antigen, was tested in the course of experimental arthritis. This association significantly lowered clinical scores and local histopathological alterations. Even though local analysis of T cell subsets and cytokine production did not reveal any difference between the experimental groups, VitD3+PG association significantly reduced cytokine production by spleen cells. These results suggest that VitD3 played a role as a tolerogenic adjuvant by down-modulating the course of experimental RA. Considering this tolerogenic effect of VitD3+PG association, further investigations will reveal its plausible use in human RA.

 

 

Vitamin D attenuates inflammation, fatty infiltration, and cartilage loss in the knee of hyperlipidemic microswine.

Arthritis Res Ther. 2016 Sep 13;18(1):203. doi: 10.1186/s13075-016-1099-6.

Rai V et al

BACKGROUND: Osteoarthritis (OA) of the knee joint is a degenerative process resulting in cartilage loss. Recent evidence suggests that OA is not merely a disease of cartilage but a disease of the entire knee joint and that inflammation may play an important role. OA has been associated with vitamin D deficiency.

Vitamin D as an immunomodulator and anti-inflammatory agent may attenuate inflammation in the knee. The aim of this study was to assess the anti-inflammatory effect of vitamin D on inflammation in the knee.

 

METHODS: This study was conducted with 13 microswine on a high cholesterol diet categorized into three groups of vitamin D-deficient, vitamin D-sufficient, and vitamin D supplementation. After 1 year, microswine were killed, and their knee joint tissues were harvested. Histological and immunofluorescence studies were carried out on the tissue specimens to evaluate the effect of vitamin D status.

RESULTS: Histological and immunofluorescence studies of the knee joint tissues showed (1) increased inflammation in the knee joint tissues, (2) fatty infiltration in quadriceps muscle, patellar tendon, and collateral ligaments, and (3) chondrocyte clustering in the vitamin D-deficient and vitamin D-sufficient groups compared with the vitamin D supplementation group. Architectural distortion of the quadriceps muscle, patellar tendon, and collateral ligaments was also seen in the areas of inflammatory foci and fatty infiltration in the vitamin D-deficient group.

CONCLUSIONS: Decreased inflammation and fatty infiltration in the vitamin D supplementation group suggest the potential role of vitamin D in attenuating inflammation and fatty infiltration as well as in protecting the architecture of the tissue in the knee joint.

 

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Vitamin D Status in Patients with Systemic Lupus Erythematosus in Serbia:

Correlation with Disease Activity and Clinical Manifestations.

Open Access Maced J Med Sci. 2015 Jun 15;3(2):256-61. doi:

10.3889/oamjms.2015.052. Epub 2015 May 4.

Miskovic Ret al

 

BACKGROUND: Numerous studies indicate potential role of vitamin D as an important factor in the development of many autoimmune diseases including systemic lupus erythematosus (SLE). Patients with SLE are especially prone to the development of vitamin D deficiency due to the nature of their illness.

AIM: The aims of our study were to determine the prevalence of vitamin D insufficiency and deficiency in patients with SLE in Serbia, to identify clinical variables associated with vitamin D status and to examine the impact of vitamin D status on disease activity and presence of specific lupus autoantibodies.

MATERIAL AND METHODS: The study included 46 patients with SLE. Serum 25(OH)D concentration was measured by electrohemiluminiscent immunoassay.

RESULTS: The mean serum concentration of 25(OH)D was 11.9 ± 7.3 ng/ml. The prevalence of insufficiency was 32.6%, while the prevalence of deficiency was 67.4%. There was no association between vitamin D status and photosensitivity, skin lesions, arthritis and lupus nephritis. Vitamin D status was not associated with the presence of specific autoantibodies. There was no correlation between disease activity assessed by SLEDAI scale with the concentration of 25(OH)D.

Patients who used vitamin D supplements and calcium did not have a significantly higher concentration of 25(OH)D.

CONCLUSION: In conclusion, vitamin D deficiency is common in patients with SLE.

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