all things vitamin D

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jimmylegs
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d3 magnesium epigenetics, interactions

Post by jimmylegs » Thu Oct 10, 2019 1:18 pm

Does the environment influence multiple sclerosis pathogenesis via UVB light and/or induction of vitamin D? (2019)
https://www.sciencedirect.com/science/a ... 2817304782

Highlights
• Low Vitamin D levels are associated with MS susceptibility and –progression.
• UVB light is involved in MS etiology and progression independent from Vitamin D.
• Clinical aspects of UVB light and Vitamin D in epidemiological and clinical studies.
• α-MSH as an environmental mimetic for the development of novel MS therapeutics.

"Interestingly, genetic variation in Vit D binding protein (SNP rs4588 or its proxy rs2282679) has further been found to result in a smaller serum Vit D increase after vitamin D3 supplementation as compared to individuals without the SNP (Nimitphong et al., 2013), demonstrating some pharmacokinetic implications in potential supplementation regimens. In this line, the responsiveness to Vit D supplementation seems to also be impaired in MS patients: a recent study investigating whether Vit D supplementation results in similar increase in serum Vit D levels in healthy controls and MS patients showed that people with MS had a lower increase in Vit D levels following oral vitamin D supplementation as compared to healthy controls (Bhargava et al., 2016). These findings might support assumptions that are the basis of the so-called “Coimbra protocol” claiming that MS patients (and other autoimmune diseases) need higher doses of Vit D to reach adequate levels due to a genetically caused hypovitaminosis D (Finamor et al., 2013). As there are no peer reviewed study results available for the effects of the “Coimbra protocol” (doses of Vit D up to 400.000 IU!), it is currently unclear if ultrahigh doses of Vit D really have the desired disease-modifying effect, nor if the higher risk of side effects from ultra-high doses is worth the benefit"

oh genetics, you say? and what might fire up SNP rs4588, i wonder??

Therapeutic perspectives of epigenetically active nutrients (2015)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439873/
"So far, only magnesium has been linked to epigenetics (Takaya et al., 2011)."

all right we'll wait and see. in the meantime, recalling this one posted a year ago and recently revisited above:

Role of Magnesium in Vitamin D Activation and Function (2018)
https://www.ncbi.nlm.nih.gov/pubmed/29480918

"Vitamin D is transported in blood bound to the carrier proteins, and the major carrier is vitamin D–binding protein. Importantly, the activity of vitamin D–binding protein is also a magnesium-dependent process (Figure 2).62,63"

test day tomorrow - doing d3 and mag together, followed by any corrective action that may be needed, then a retest. can somebody please arrange to scale this solo effort up...!?!
take control of your own health
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jimmylegs
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adding perspective to safe d3 claims

Post by jimmylegs » Fri Oct 11, 2019 3:45 am

and returning to the recently-discussed d3 study using psychiatric inpatients and their caregivers, which provided low quality / anecdotal support for megadose d3 safety in terms of calcium interactions only, i am pleased to see this contribution to the literature:
  • Serum Vitamin D and Magnesium levels in a psychiatric cohort (2019)
    https://www.ncbi.nlm.nih.gov/pubmed/31488730

    ...
    SUBJECTS AND METHODS:
    A single site audit of serum Vitamin D and magnesium levels in patients at an Acute Day Treatment Unit was carried out. Blood tests were performed on admission and analysed in house. Data were collected between April - June 2019 and was analysed subsequently, as described below (n=73).

    RESULTS:
    Our data show that our psychiatric day treatment unit cohort (n=73) had a higher proportion of vitamin D deficiency (52%) than the general population (40%), although due to the limited sample size this was not significant (p=0.22, Chi-squared test). The percentage of patients who were magnesium deficient was 78.6% (n=22/28). However, the F60 subgroup of patients with personality disorders showed a high prevalence of vit D deficiency (p=0.07), highlighting a trend towards significance despite the limited size of this subgroup.
    ...
note that levels were only obtained for 28 individuals. more data needed!

i'm amazed to see the relatively high cutoff used to define magnesium deficiency. i would have liked to see more on the case made for that number in particular.
  • "Overall, 78.6% (n=22/28) of patients were magnesium deficient (<0.9 mmol/L) as defined by serum magnesium. The median serum magnesium level was 0.85 mmol/L."
i'm still curious to see what the stats would have been if they'd established some insufficiency and sufficiency numbers, 0.95 or 1.0 or 1.1 mmol/l say. or, for that matter, if they'd used a more typical deficiency cutoff like 0.7 or 0.65 mmol/l ... :S i'd also like to see studies more frequently clarifying what real serum magnesium excess looks like, so people can be clear on how far we are from that point when we talk about this tight range of more 'usual' numbers.
  • "We recommend larger studies to gain better understanding of numerous factors that interact (from the molecular to clinical level) to show somewhat consistent link between low Vitamin D and magnesium levels and various psychiatric disorders."
agree :)
take control of your own health
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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jimmylegs
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the 60s called...

Post by jimmylegs » Sun Oct 13, 2019 7:32 am

then the 70s called... with a case study...
  • Magnesium-Induced Reversal Of Vitamin-D Resistance In Hypoparathyroidism (1973)
    https://www.thelancet.com/journals/lanc ... 8/fulltext

    A 13-year-old girl had hypoparathyroidism which was refractory to therapy with high doses of vitamin D2 (given orally and intramuscularly), dihydrotachysterol (' A.T. 10 ') treatment, and up to 8 g. per day of calcium-salt supplement. The patient responded convincingly when 25 meq. of magnesium per day was given in addition to moderate oral doses of vitamin D2.
boo. i only have full text access from 1995 onward. i want to know which mag form was used, starting and ending serum mag levels, starting and ending d3 levels.

science? got any replication? anything scaled up? i'll keep looking....
take control of your own health
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jimmylegs
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the 70s called...

Post by jimmylegs » Fri Oct 25, 2019 2:30 pm

about cows, but still interesting..
  • Influence of Mg supply on toxicity of cholecalciferol in cattle (1970)
    Einfluss der Magnesiumversorgung auf die Toxizitat von Vitamin D3 beim Rind.
    https://www.cabdirect.org/cabdirect/abs ... 9711406943

    Abstract : Groups of 5 yearlings or cattle 2 years old were fed in stalls on a diet poor in Mg, 0.22 g per kg, of potato starch, casein, molasses, cellulose and urea with mineral and vitamin mixture; it was given without or with 1.8 or 17 g MgO per 100 kg liveweight until mean serum Mg values were 0.70, 2.04 and 3.00 mg%.
    At that time each animal was given an injection of cholecalciferol, 4 million IU per 100 kg (6 million for 2 cattle); the diet supplied 5000 IU per kg feed.
    Ten days after the injection serum Mg had fallen by on average 0.07, 0.30 and 0.66 mg% and Ca had risen by 1.4, 1.8 and 2.5 mg%. About 12 days after the injection the Mg-deficient diet was replaced by an ordinary diet of hay and concentrates, the Mg supplements being continued until the cattle were killed 25 to 30 days after the injection.
    There were calcified lesions in the aorta in all groups and in all cattle except one in the group given most Mg. In cattle given insufficient Mg the lesions were more extensive and occurred also in other major arteries and veins, lungs and heart. In the group given no Mg supplement 4 cattle had subepicardial calcification in one or both auricles and all had lesions of endocardium and valves
    It was concluded that in hypomagnesaemia treatment with vitamin D is contraindicated.
genau! mehr Humanstudien bitte..
take control of your own health
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ask for referrals to preventive health care specialists eg dietitians
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jimmylegs
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the 80s called..

Post by jimmylegs » Sat Oct 26, 2019 7:16 am

The effect of zinc on vitamin D3-induced cardiac necrosis (1985)
https://www.sciencedirect.com/science/a ... 2885800146

Multifocal heart muscle necrotic lesions in rats were induced with high oral doses of vitamin D3 (300,000 iu/rat in three daily doses 100 000 iu each). The calcium content increased over 100 fold in the hearts of rats receiving vitamin D3. Parenteral pre-treatment with zinc sulphate (50 or 200 mg/rat in ten daily doses) resulted either in a reduction or in the total prevention of myocardial lesions on macroscopic, light and electron microscopic examination. The effect of zinc was dose-dependent. The administration of various doses of zinc sulphate resulted in a gradual normalisation of heart calcium content.
take control of your own health
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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jimmylegs
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2020: proposed paradigm shift

Post by jimmylegs » Tue Oct 29, 2019 10:26 am

Randomized clinical trials of oral vitamin D supplementation in need of a paradigm change: The vitamin D autacoid paradigm (2020)
https://www.sciencedirect.com/science/a ... 7719309715

Epidemiological studies highlight the negative correlation between vitamin D levels and the incidence of many non-skeletal diseases including inflammatory diseases, cancer, and metabolic and neurological disorders. However, most randomized controlled trials (RCTs) with oral vitamin D supplementation give mixed results or are inconclusive. It has been said that “discovery commences with the awareness of anomaly”. The “anomaly” between our preclinical and clinical data provides the opportunity to propose an alternative paradigm to the vitamin D endocrine system: the vitamin D autacoid paradigm. In the vitamin D autacoid paradigm, the extra-skeletal effects of vitamin D depend on the tissue reserves of vitamin D metabolites. These vitamin D autacoid systems are inducible oscillatory ecosystems in which 1,25D is produced, acts and is inactivated locally. In the vitamin D autacoid paradigm, attaining adequacy of vitamin D in the systemic circulation is necessary but not sufficient; we must also ensure the repletion of the tissue stores. The co-existence of two different vitamin D systems, endocrine and autacoid, with different functions and regulations leads to “significant shifts in the criteria determining the legitimacy both of problems and of proposed solutions”. With respect to our clinical trials of vitamin D supplementation for unconventional effects, the proposed solution is administering and quantifying vitamin D metabolites directly to the target tissue.
take control of your own health
pursue optimal self care at least as actively as a diagnosis
ask for referrals to preventive health care specialists eg dietitians
don't let suboptimal self care muddy any underlying diagnostic picture!

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Petr75
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Location: Czech Republic

Re: all things vitamin D

Post by Petr75 » Sat Nov 16, 2019 2:21 am

2019 Nov 12
From the Department of Neurology (R.H., J.S.,), Zuyderland Medical Centre Sittard, Maastricht University Medical Centre; Department of Neurology (J.S.), Canisius Wilhelmina Ziekenhuis, Nijmegen, the Netherlands
Randomized trial of daily high-dose vitamin D3 in patients with RRMS receiving subcutaneous interferon β-1a
https://www.ncbi.nlm.nih.gov/pubmed/31594857

Abstract
OBJECTIVE:
In the phase II, randomized, double-blind, placebo-controlled Supplementation of Vigantol Oil versus Placebo Add-on in Patients with Relapsing-Remitting Multiple Sclerosis (RRMS) Receiving Rebif Treatment (SOLAR) study (NCT01285401), we assessed the efficacy and safety of add-on vitamin D3 in patients with RRMS.
METHODS:
Eligible patients with RRMS treated with SC interferon-β-1a (IFN-β-1a) 44 μg 3 times weekly and serum 25(OH)D levels <150 nmol/L were included. From February 15, 2011, to May 11, 2015, 229 patients were included and randomized 1:1 to receive SC IFN-β-1a plus placebo (n = 116) or SC IFN-β-1a plus oral high-dose vitamin D3 14,007 IU/d (n = 113). The revised primary outcome was the proportion of patients with no evidence of disease activity (NEDA-3) at week 48.
RESULTS:
At 48 weeks, 36.3% of patients who received high-dose vitamin D3 had NEDA-3, without a statistically significant difference in NEDA-3 status between groups (placebo 35.3%; odds ratio 0.93; 95% confidence interval [CI] 0.53-1.63; p = 0.80). Compared with placebo, the high-dose vitamin D3 group had better MRI outcomes for combined unique active lesions (incidence rate ratio 0.68; 95% CI 0.52-0.89; p = 0.0045) and change from baseline in total volume of T2 lesions (difference in mean ranks: -0.074; p = 0.035).
CONCLUSIONS:
SOLAR did not establish a benefit for high-dose vitamin D3 as add-on to IFN-β-1a, based on the primary outcome of NEDA-3, but findings from exploratory outcomes suggest protective effects on development of new MRI lesions in patients with RRMS.
CLINICALTRIALSGOV IDENTIFIER:
NCT01285401.
CLASSIFICATION OF EVIDENCE:
This study provides Class II evidence that for patients with RRMS treated with SC IFN-β-1a, 48 weeks of cholecalciferol supplementation did not promote NEDA-3 status.

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