http://link.springer.com/article/10.100 ... 015-0966-2
They used 980 IU/kg daily for 4 weeks and 490 iu/kg daily for another 4 weeks.
Drs denied her dialysis and appropriate treatment for her MPA and forced her into hospice.
She is in heaven and free from pain.
mrtmeo wrote:Anyone see this study?
http://link.springer.com/article/10.100 ... 015-0966-2
They used 980 IU/kg daily for 4 weeks and 490 iu/kg daily for another 4 weeks.
I did not know.
Thanks mrtmeo for post this study.
The Three Sisters of Fate in Multiple Sclerosis: Klotho (Clotho), Fibroblast Growth Factor-23 (Lachesis), and Vitamin D (Atropos).
The klotho (Klt)-fibroblast growth factor-23 (FGF-23)-vitamin D axis is the main component of calcium (Ca) and phosphorus (P) metabolisms; on the contrary, it is also secreted from the choroid plexus (CP).
This study is aimed at evaluating serum soluble Klt (sKlt), FGF-23, and 25-(OH)-vitamin D levels in multiple sclerosis (MS) patients.
Thirty-two relapsing-remitting MS patients (11 males and 21 females; mean age 38.3 years) and 31 age-sex matched healthy controls (12 males and 19 females; median age 38.5 years) were included in this study. All patients were diagnosed with MS according to the criteria of McDonald.
Serum sKlt, FGF-23, and P levels were significantly higher in MS patients compared to the control group (p < 0.01, p < 0.01, and p = 0.02, respectively). Serum 25-(OH)-vitamin D and Ca levels were significantly lower in MS patients (p < 0.01 and p = 0.04, respectively).
Klt, which is secreted from CP, could be a response to the inflammatory condition in MS. Elevated FGF-23 levels suppress 1α-hydroxylase and upregulates 24α-hydroxylase, which results in a decrease in 1,25-(OH)2D3 levels. Thus, the neuroprotective and immunomodulatory effects of vitamin D might not be seen in MS patients.
Vitamin D3 for the Treatment of Epilepsy: Basic Mechanisms, Animal Models, and Clinical Trials.
There is increasing evidence supporting dietary and alternative therapies for epilepsy, including the ketogenic diet, modified Atkins diet, and omega-3 fatty acids. Vitamin D3 is actively under investigation as a potential intervention for epilepsy. Vitamin D3 is fat-soluble steroid, which shows promise in animal models of epilepsy. Basic research has shed light on the possible mechanisms by which Vitamin D3 may reduce seizures, and animal data support the efficacy of Vitamin D3 in rat and mouse models of epilepsy. Very little clinical data exist to support the treatment of human epilepsy with Vitamin D3, but positive findings from preliminary clinical trials warrant larger Phase I and II clinical trials in order to more rigorously determine the potential therapeutic value of Vitamin D3 as a treatment for human epilepsy.
Core Symptoms of Autism Improved After Vitamin D Supplementation
Autism spectrum disorder (ASD) is a common neurodevelopmental disorder caused by a complex interaction between genetic and environmental risk factors. Among the environmental factors, vitamin D3 (cholecaliferol) seems to play a significant role in the etiology of ASD because this vitamin is important for brain development. Lower concentrations of vitamin D3 may lead to increased brain size, altered brain shape, and enlarged ventricles, which have been observed in patients with ASD. Vitamin D3 is converted into 25-hydroxyvitamin D3 in the liver. Higher serum concentrations of this steroid may reduce the risk of autism. Importantly, children with ASD are at an increased risk of vitamin D deficiency, possibly due to environmental factors. It has also been suggested that vitamin D3 deficiency may cause ASD symptoms. Here, we report on a 32-month-old boy with ASD and vitamin D3 deficiency. His core symptoms of autism improved significantly after vitamin D3 supplementation. This case suggests that vitamin D3 may play an important role in the etiology of ASD, stressing the importance of clinical assessment of vitamin D3 deficiency and the need for vitamin D3 supplementation in case of deficiency.
http://pediatrics.aappublications.org/c ... e196.short
High dose Vitamin D intake and quality of life in relapsing-remitting multiple sclerosis: a randomized, double-blind, placebo-controlled clinical trial
Background: Low level of vitamin D is associated with a more severe course and low quality of life in relapsing-remitting multiple sclerosis (RRMS). Low dose vitamin D intake has improved quality of life in RRMS patients.
Objective: This study explored the effect of high dose vitamin D intake on quality of life in RRMS patients in a double blind randomized clinical trial.
Methods: 94 RRMS patients were randomized to two groups. One group received 50,000 IU vitamin D3 every five days for 3 months. The other group received placebo. Interferon-β (IFN-β) continued as the main treatment in both groups. Quality of life was assessed using MSQOL-54 Persian version at the beginning and at the end of the study.
Results: After 3 months, the vitamin D group had a significant difference in mental health composite with placebo group, 62.41 ± 13.99 vs. 60.99 ± 17.99 (p-value = 0.041). Change in health was 75.74 ± 25.73 and 70.59 ± 26.45 in vitamin D and placebo group, respectively (p-value = 0.036).
Conclusions: Mental QOL improved significantly after taking high dose vitamin D for 3 months in vitamin D group relative to placebo.
Results of daily oral dosing with up to 60,000 international units (iu) of vitamin D3 for 2 to 6 years in 3 adult males.
In the 1930's and 1940's, vitamin D was reported to be an effective treatment for a number of diseases, including asthma, psoriasis, rheumatoid arthritis, rickets and tuberculosis. High doses were used, 60,000 to 300,000 IU a day for asthma, and 200,000 to 600,000 IU a day for rheumatoid arthritis. Toxicity from hypercalcemia occurred after prolonged oral dosing with these supraphysiologic doses. Assays for measuring vitamin D in the blood were not available, and blood levels of vitamin D associated with hypercalcemia were unknown. A 2011 report on vitamin D toxicity showed that hypercalcemia resolved when 25-hydroxyvitamin D (25OHD) blood levels dropped below 400ng/ml in 2 patients with blood levels ranging from 645ng/ml to 1220ng/ml after accidental ingestion of massive doses of vitamin D. We now know that vitamin D is made in the skin in amounts ranging up to 25,000 IU a day with exposure to UVB radiation. There is little data on the safety and blood levels of 25OHD and calcium after prolonged daily intake of amounts of vitamin D in this range. In this report, one subject took increasing daily doses of vitamin D3 for 6 years starting in April 2009: 6500 IU for 6 months; increasing to 10,000 IU for 13 months; 20,000 IU for 24 months; 40,000 IU for 12 months; 50,000 IU for 10 months, and 60,000 IU since October 2014. 25OHD blood levels were 28, 81, 204, 216, 225, 166, and 218ng/ml. Subject 2 began 10,000 IU in Nov 2011, increased to 20,000 IU in Feb 2014, 25,000 IU in June 2014, and 30,000 IU in Oct 2014, and then decreased to 20,000 IU in June 2015. 25OHD blood levels were 96.6, 161.1 and 106.9ng/ml. He reported marked clinical improvement in his asthma. Subject 3 started on daily 10,000 IU in Sept 2013, increasing to 20,000 IU on Nov 2013. 25OHD blood levels were 31.4, 102, 164, 148, and 143ng/ml. No one developed hypercalcemia or any adverse events. The major finding of this case series is prolonged daily dosing of vitamin D3 with doses of 10,000 to 60,000 IU was safely tolerated.
A high fat diet alone cannot trigger a metabolic syndrome, a cluster of conditions associated with an increased risk of heart disease and diabetes. Researchers of a new study published in Physiology said that vitamin D deficiency is needed for this syndrome to progress. Authors reached this conclusion after observing mice and their gut bacteria. Their research found that vitamin D supplementation decreased the risk of developing a metabolic syndrome. If these findings prove to be similar among humans, it could imply more affordable prevention options.
“Based on this study, we believe that keeping vitamin D levels high, either through sun exposure, diet or supplementation, is beneficial for prevention and treatment of metabolic syndrome,” said Professor Stephen Pandol on ScienceDaily.com. Professor Pandol was a co-author of the study. He went on to state, “A sufficient dietary vitamin D supplement can partially but significantly antagonize metabolic syndrome caused by high fat diet in mice. These are amounts equivalent to the dietary recommendations for humans.”
The marriage of diet and sunlight
It is well-known that a high fat diet significantly increases the risk of developing a metabolic syndrome, characterized by obesity, insulin resistance, and most notably, a fatty liver. The diet affects the balance between good and bad bacteria in the gut. However, researchers noted that an insufficient supply of vitamin D further aggravated the balance, and acted as a catalyst for the full onset of a metabolic disease. Vitamin D deficiency reduced the amount of the antimicrobial molecules that promote healthy gut bacteria. When these vitamin D levels were balanced, blood sugar levels improved and livers became less fatty.
In conclusion, authors of the study stated that a high fat diet alone is not enough to trigger metabolic syndrome. A vitamin D deficiency is needed in combination for people to develop a metabolic condition. Yuan-Ping Han, the other co-author of the study said, “Few studies have indicated that vitamin D supplementation may not improve metabolic disorders in humans. However, these studies are largely based on long-term surveys, which may be hampered by poor compliance and insufficient dosage.”
Both Han and Pandol are optimistic that the results of their study will prove true among humans. “We are planning a clinical study to confirm the link of vitamin D deficiency with gut bacteria disruption, and its association with metabolic syndrome,” said Han.
How do I know if I am deficient in vitamin D?
Health professionals suggest that nearly half of the world’s population are deficient in Vitamin D. Known as the “sunshine vitamin,” vitamin D is essential for calcium absorption in the body and promotes bone and cell growth. While vitamin D can be found in certain foods, the main source of vitamin D is sunlight exposure. An article on AuthorityNutrition.com has listed some of the more common symptoms of a vitamin D deficiency. (Related: Learn how to improve your health with the articles on Prevention.news.)
Being sickly: Vitamin D fights the bacteria and viruses that cause illness.
Fatigue and tiredness: Case studies suggest a relationship between Vitamin D deficiency and severe fatigue.
Bone and back pain: Vitamin D is necessary for bone health.
Depression: Researchers note a link between depression and low levels of Vitamin D.
Impaired wound healing: Vitamin D increases the production of the compounds that are crucial for wound healing.
Bone loss: An observational study concluded that middle-aged postmenopausal women with low bone mineral density showed low Vitamin D levels as well.
Hair loss: Hair loss in women has been linked to insufficient Vitamin D levels.
Muscle pain: New evidence suggests a Vitamin D deficiency can lead to muscle pain.
These symptoms can be easily alleviated with proper diet and vitamin D supplementation.
http://www.naturalnews.com/2017-05-07-v ... ments.html
Influence of Diet in Multiple Sclerosis: A Systematic Review
Nutrition is considered to be a possible factor in the pathogenesis of the neurological disease multiple sclerosis (MS). Nutrition intervention studies suggest that diet may be considered as a complementary treatment to control the progression of the disease; a systematic review of the literature on the influence of diet on MS was therefore conducted. The literature search was conducted by using Medlars Online International Literature (MEDLINE) via PubMed and Scopus. Forty-seven articles met the inclusion criteria. The reviewed articles assessed the relations between macro- and micronutrient intakes and MS incidence. The patients involved used alternative therapies (homeopathy), protocolized diets that included particular foods (herbal products such as grape seed extract, ginseng, blueberries, green tea, etc.), or dietary supplements such as vitamin D, carnitine, melatonin, or coenzyme Q10. Current studies suggest that high serum concentrations of vitamin D, a potent immunomodulator, may decrease the risk of MS and the risk of relapse and new lesions, while improving brain lesions and timed tandem walking. Experimental evidence suggests that serum vitamin D concentration is lower during MS relapses than in remission and is associated with a greater degree of disability [Expanded Disability Status Scale (EDSS) score >3]. The findings suggest that circulating vitamin D concentrations can be considered a biomarker of MS and supplemental vitamin D can be used therapeutically. Other studies point to a negative correlation between serum vitamin B-12 concentrations and EDSS score. Vitamin B-12 has fundamental roles in central nervous system function, especially in the methionine synthase-mediated conversion of homocysteine to methionine, which is essential for DNA and RNA synthesis. Therefore, vitamin B-12 deficiency may lead to an increase in the concentration of homocysteine. Further research is clearly necessary to determine whether treatment with vitamin B-12 supplements delays MS progression.
High dose vitamin D supplementation does not affect biochemical bone markers in multiple sclerosis – a randomized controlled trial
People with multiple sclerosis have high risk of osteoporosis and fractures. A poor vitamin D status is a risk factor for MS, and vitamin D supplementation has been recommended both to prevent MS progression and to maintain bone health.
We assessed the effect of 20,000 IU vitamin D3 weekly compared to placebo on biochemical markers of bone metabolism in 68 persons with relapsing remitting multiple sclerosis.
Serum levels of 25-hydroxyvitamin D more than doubled in the vitamin D group, and parathyroid hormone decreased in the vitamin D group compared to the placebo group at week 48 and week 96. There was however no effect on bone formation as measured by procollagen type I N propeptide (PINP), or on bone resorption as measured by C-terminal cross-linking telopeptide of type I collagen (CTX1). Neither PINP nor CTX1 predicted bone loss from baseline to week 96.
These findings corroborate the previously reported lack of effect of weekly high dose vitamin D supplementation on bone mass density in the same patients, and suggest that such vitamin D supplementation does not prevent bone loss in persons with MS who are not vitamin D deficient.
https://bmcneurol.biomedcentral.com/art ... 017-0851-0
The Expression of VDR mRNA but not NF-κB surprisingly Decreased after Vitamin D Treatment in Multiple Sclerosis Patients.
BACKGROUND AND PURPOSE:
The aim of this study was to investigate the expression levels of vitamin D receptor (VDR) and NF-κB mRNAs in vitamin D (VD) supplemented multiple sclerosis (MS) patients.
RRMS patients received 50,000 IU vitamin D3/week as an intra-muscular injection for 2 months. Blood samples were obtained from 30 MS patients before and after VD supplementation and 32 healthy individuals, and then VDR and NF-κB mRNA levels were measured by real time PCR method and analyzed with independent and paired t tests. Moreover, some correlations were performed between the expression levels of selected genes and some clinical features of MS and control groups.
Surprisingly, the expression level of VDR mRNA significantly decreased after 2 months supplementation with VD in our selected patients and in contrast, the level of serum 25(OH) D increased after supplementation. Although, we didn't find any significant difference in the expression level of NF-κB gene before and after treatment with VD, its expression significantly decreased in untreated MS cases compared with healthy controls.
In conclusion, we found some new evidences from the molecular mechanism of vitamin D effectiveness in MS treatment. Also, we need more functional studies to find the effect of VD on the expression level of VDR mRNA.
Vitamin D Deficiency in Axial Spondyloarthritis is Associated With Higher Disease Activity
Objectives: This study aims to assess whether vitamin D deficiency is associated with increased disease activity and functional impairment in axial
spondyloarthritis (axSpA), with control for its seasonal variation.
Patients and methods: Serum 25-hydroxyvitamin D [25(OH)D] levels were measured in 235 consecutive axSpA patients (176 males, 59 females;
mean age 46.3 years; range 18 to 85 years) attending a specialist spondyloarthritis service in the United Kingdom. Disease activity and functional
status were assessed using Bath Ankylosing Spondylitis indices, C-reactive protein, and erythrocyte sedimentation rates. Vitamin D deficiency was
defined as 25(OH)D <30 nmol/L. Associations between vitamin D deficiency and: (i) disease activity (Bath Ankylosing Spondylitis Disease Activity
Index), (ii) spinal pain, (iii) functional impairment (Bath Ankylosing Spondylitis Functional Index), and (iv) inflammatory markers were explored using
multivariable logistic regression models (adjusted for age, sex, vitamin D supplementation, and seasonal variation).
Results: Median symptom duration was 17 years (inter-quartile range 8.5 to 28.6 years). Median 25(OH)D was 54.5 nmol/L (inter-quartile range
34 to 77 nmol/L) and 52 patients (22%) were deficient for vitamin D. Increasing Bath Ankylosing Spondylitis Disease Activity Index (adjusted odds
ratio 1.23; 95% confidence interval 1.06-1.41), spinal pain visual analog scale (adjusted odds ratio 1.21; 95% confidence interval 1.07-1.38), and
C-reactive protein (adjusted odds ratio 1.02; 95% confidence interval 1.01-1.04) were each significantly associated with 25(OH)D deficiency.
Conclusion: This cross-sectional study demonstrated associations between vitamin D deficiency and both higher disease activity and functional
impairment in axSpA. Whilst this may reflect reduced ultra-violet exposure in functionally impaired patients, it supports the hypothesis that vitamin
D may have an immunomodulatory role. Interventional studies are needed to evaluate evaluate a potential causal relationship, as optimizing vitamin D may
be a cost-effective adjunctive intervention to modify disease activity in axSpA.
https://drive.google.com/file/d/0B9UGWV ... gyNEE/view
A recent animal study suggests that vitamin D may provide a treatment and prevention method for degenerative changes of the intervertebral disc among diabetic patients. Intervertebral discs act as cushions between each of the small bones forming the backbone, known as the vertebrae.
Overall, the study provided a new and exciting perspective on vitamin D for the treatment and prevention of disc degeneration. Although, the research on this topic remains in its infancy.
https://www.vitamindcouncil.org/vitamin ... eneration/
A low vitamin D status at diagnosis is associated with an early conversion to secondary progressive multiple sclerosis.
Low circulating 25-hydroxyvitamin D (25(OH)D) levels have been associated with an increased risk of relapses in relapsing remitting multiple sclerosis (RRMS), but an association with disability progression is uncertain. Lower 25(OH)D levels are found in secondary progressive MS (SPMS) when compared to RRMS. We hypothesized that a poor vitamin D status in RRMS is associated with an increased risk of conversion to SPMS. In a retrospective longitudinal study we measured 25(OH)D levels at the start of a 3-year follow-up, and analyzed whether these levels predict the risk of RRMS to SPMS conversion. In 338 RRMS patients, vitamin D status did not predict the 3-year risk of conversion to SPMS (n=51; OR 0.970; p=0.65). However, in diagnostic blood samples of SPMS patients with a relatively short RRMS duration (n=19) 25(OH)D levels were significantly lower (38nmol/L; Q1-Q3: 24-50) than in diagnostic samples of matched RRMS patients with no progression to SPMS ((n=38; 55nmol/L; Q1-Q3: 40-70) (p<0.01). These data indicate an association between a low vitamin D status at the start of RRMS and the early conversion to SPMS. Therefore, time to SPMS conversion is of interest as clinical measure in (follow-up of) clinical vitamin D supplementation studies.
Vitamin D and multiple sclerosis: An update.
The most recent findings linking exposure to sun and vitamin D insufficiency to multiple sclerosis (MS) are reviewed. Due to insufficient sunshine and changing lifestyles, hypovitaminosis D is widespread in temperate countries. Numerous epidemiological studies have strongly suggested that sunshine and vitamin D insufficiency contributes to MS risk in these countries. Moreover, several large genetic studies in MS patients have recently stated unequivocally that diverse abnormalities involving vitamin D metabolism are related to the risk of the disease. The important implications of such results are discussed here. Then, the interactions of hypovitaminosis D with the other genetic and environmental protective and risk factors, such as the allele HLA DRB1*1501, Epstein-Barr virus infection, obesity, smoking and sexual hormones, are summarized. Vitamin D insufficiency and sufficiency could be a risk and a protective factor, respectively, among many other factors possibly continuously modulating the global MS risk from the mother's pregnancy to the triggering of MS in adulthood. However, many interactions between these different factors occur more particularly between conception and the end of adolescence, which corresponds to the period of maturation of the immune system and thymus and may be related to the dysimmune nature of the disease. The main mechanisms of action of vitamin D in MS appear to be immunomodulatory, involving the various categories of T and B lymphocytes in the general immune system, but neuroprotector and neurotrophic mechanisms could also be exerted at the central nervous system level. Furthermore, several controlled immunological studies performed in MS patients have recently confirmed that vitamin D supplementation has multiple beneficial immunomodulatory effects. However, there is still an enduring absence of major conclusive randomized clinical trials testing vitamin D supplementation in MS patients because of the quasi-insurmountable practical difficulties that exist nowadays in conducting and completing over several years such studies involving the use of a vitamin. Nevertheless, it should be noted that similar robust statistical models used in five different association studies have already predicted a favorable vitamin D effect reducing relapses by 50-70%. If there is now little doubt that vitamin D exerts a beneficial action on the inflammatory component of MS, the results are as yet much less clear for the progressive degenerative component. Lastly, until more information becomes available, vitamin D supplementation of MS patients, using a moderate physiological dose essentially correcting their vitamin insufficiency, is recommended.
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