all things vitamin D

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Re: all things vitamin D

Postby jimmylegs » Fri Feb 24, 2017 12:03 pm

this is the next study that comes up with the search terms i'm using:

Mailhot, G. (2012). Vitamin D bioavailability in cystic fibrosis: a cause for concern?. Nutrition reviews, 70(5), 280-293.
https://academic.oup.com/nutritionrevie ... fibrosis-a
"Despite the inclusion of extra vitamin D in their regimen of fat-soluble vitamin supplementation, cystic fibrosis patients remain chronically depleted of vitamin D. The persistence of suboptimal vitamin D status is often blamed on the maldigestion and malabsorption of fat. However, the mitigated success of recent clinical trials with high-dose vitamin D supplementation suggests that vitamin D bioavailability might be impaired in these patients."

hmmm what *could* be going on there.

Magnesium in cystic fibrosis—Systematic review of the literature (2016)
http://onlinelibrary.wiley.com/doi/10.1 ... 23356/full
"The first comprehensive review of the literature confirms that, despite being one of the most prevalent minerals in the body, the importance of magnesium in cystic fibrosis is largely overlooked. In these patients, hypomagnesemia should be sought once a year. Furthermore, the potential of supplementation with this cation deserves more attention."

i think we can assume the authors do not mean hypomagnesemia should be inflicted on patients annually...
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Re: all things vitamin D

Postby jimmylegs » Fri Feb 24, 2017 12:39 pm

back on track with hypercalcemia. not playing in the same ballpark at all with dialysis, but interesting anyway

Zitt, E., Sprenger-Mähr, H., Mündle, M., & Lhotta, K. (2015). Efficacy and safety of body weight-adapted oral cholecalciferol substitution in dialysis patients with vitamin D deficiency. BMC nephrology, 16(1), 128.
http://citeseerx.ist.psu.edu/viewdoc/do ... 1&type=pdf
"Patients received a mean weekly cholecalciferol dose of 7603 ±1855 IU. After six months of substitution 25OHD3 increased to 26.1 ± 8.8 ng/mL (P < 0.01) with a mean increase of 16.2 ± 7.8 ng/mL. At the end of the study 14 (27 %) patients had a 25OHD3 level >30 ng/mL, and all 37 (73 %) other patients a level >20 ng/mL. Serum calcium and phosphorous remained constant. Figure 2 shows the course of monthly serum calcium and phosphorous levels during the whole study period. We observed six hypercalcemic episodes (serum calcium >2.55 mmol/L) representing 1.9 % of all monthly measurements (n = 306). Hypercalcemia was noted in four patients (three patients with one
episode, one patients with three episodes)."

would be interesting if we could see better detail of the individuals who experienced hypercalcemia on one or more occasions.

different kind of mag connection in this kind of study. recall this poor fellow however (orig pdf link no longer works but you can still easily get a snippet of the article via pdiconnect, and i had also posted excerpts as follows)

Gabapentin for intractable hiccups in a patient undergoing peritoneal dialysis
http://www.pdiconnect.com/content/28/6/667.extract
"Hiccups are involuntary, rhythmic, spasmodic contractions of the diaphragm. ... hiccups became frequent and severe enough to produce insomnia, anorexia, and weight loss. His other medical problems included hypertension, ischemic heart disease, gout and anemia secondary to ESRF. ... Laboratory investigations were as follows: .... magnesium 0.66 mmol/L ... gabapentin was further increased to 600 mg nightly, leading to the hiccups disappearing over a 3 month follow up period"

frustrating that the docs would allow apparently symptomatic mag deficit to persist, and try to treat the symptoms with a pharma product, without even giving essential mag a chance at the issue, apparently for fear of mag excess in dialysis.

related:
Magnesium in chronic kidney disease Stages 3 and 4 and in dialysis (2012)
https://academic.oup.com/ckj/article/5/ ... es-3-and-4
"However, in more advanced CKD (as creatinine clearance falls <30 mL/min), this compensatory mechanism becomes inadequate such that overt hypermagnesaemia develops frequently in patients with creatinine clearances <10 mL/min."

Magnesium in dialysis patients: serum levels and clinical implications (1998)
https://www.ncbi.nlm.nih.gov/pubmed/9696434
"Hypermagnesemia in these patients is frequent, usually mild (serum magnesium lower than 1.5 mmol/l) and asymptomatic, but severe and symptomatic hypermagnesemia can be induced by exogenous magnesium administration." (recall se mg level was 0.66 mmol/l for gentleman with the chronic hiccups)

they're working their way around to it more recently, looks like:

Magnesium and outcomes in patients with chronic kidney disease: focus on vascular calcification, atherosclerosis and survival (2012)
https://academic.oup.com/ckj/article/5/ ... th-chronic
"Patients with chronic kidney disease (CKD) have a high prevalence of vascular calcification, and cardiovascular disease is the leading cause of death in this population. ... Magnesium is a natural calcium antagonist and both human and animal studies have shown that low circulating magnesium levels are associated with vascular calcification. Clinical evidence from observational studies of dialysis patients has shown that low-magnesium levels occur concurrently with mitral annular calcification, peripheral arterial calcification and increased carotid intima–media thickness. Few interventional studies have been performed. Two interventional studies suggest that there may be benefits such as retardation of arterial calcification and/or reductions in carotid intima–media thickness in response to magnesium supplementation in CKD patients, though both studies have limitations. ... observational studies have shown that low serum magnesium may be an independent risk factor for premature death in CKD patients, and patients with mildly elevated serum magnesium levels could have a survival advantage over those with lower magnesium levels."

imagine that - add mag to help combat vascular calcification *and* low vit d3.
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Re: all things vitamin D

Postby jimmylegs » Thu Mar 02, 2017 8:49 am

it will be nice when there are large studies looking at this interaction explicitly. for the meantime:

Kampmann, U., Mosekilde, L., Juhl, C., Moller, N., Christensen, B., Rejnmark, L., ... & Orskov, L. (2014). Effects of 12weeks high dose vitamin D3 treatment on insulin sensitivity, beta cell function, and metabolic markers in patients with type 2 diabetes and vitamin D insufficiency–a double-blind, randomized, placebo-controlled trial. Metabolism, 63(9), 1115-1124.
http://www.sciencedirect.com/science/ar ... 9514001759

regimen: oral cholecalciferol (11,200 IU (280 μg) daily for 2 weeks, followed by 5600 IU (140 μg) daily for 10 weeks)

...............................Baseline values ............................... Changes from baseline after 3 months
...............................Vitamin D group ..... Placebo group ....... Vitamin D group ..... Placebo group
Serum 25(OH)vitD2D3....31.0 ± 4.9...............34.8 ± 3.8...............+73.9 ± 20.6...........−2.6 ± 3.2
(nmol/L)
Serum magnesium.........0.91 ± 0.05..............0.91 ± 0.03.............−0.06 ± 0.04...........−0.024 ± 0.03
(mmol)

so 2.5 x greater impact on se mag from d3 supplementation compared to placebo. the starting point for both groups is not ideal, consistent with their diabetes dx and exclusion of participants with serum d3 levels above 50 nmol/L. serum mag levels are just barely into the top half of commonly used reference ranges for serum magnesium. placebo group's follow up mean mag status drops to .886 while d3 group mean drops to 0.85 mmol/L. better to be at least 0.95 mmol/L.

slight reductions in mag and d3 in the placebo group after three months are consistent with what we know about positive correlations between se mag and se d3 status.

for comparison, in this study healthy control mean serum mag converts to 0.904 (again just barely into the top half of the normal range though) while mean serum mag for ms patients converts to 0.77.
http://ijpbs.mazums.ac.ir/article-1-139-en.pdf

so from the first study above, straight d3 supplementation takes individuals towards a healthier level for serum d3 but at the same time pushes recipients in the direction of an ms patient profile for serum magnesium.

as mentioned above, need more and larger studies looking at this dynamic, but just looking at these two small studies together for now, in 3 months of d3 treatment subjects apparently lost 40% of their healthy control magnesium advantage over a typical mean serum mag level for an average ms patient.

looking at this it makes sense that i experienced serious issues with low mag after a couple years on 4000 IU per day, with two short term megadoses along the way (1st 50K/d x 10 days, 2nd 50K/d x 8 days)
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Re: all things vitamin D

Postby jimmylegs » Sun Mar 05, 2017 7:21 am

Effects of a dietary magnesium deficiency and excess vitamin D3 on swine coronary arteries
https://www.ncbi.nlm.nih.gov/pubmed/2159962
"The effect of a moderate magnesium (Mg) deficiency on coronary arteries of 61 swine, fed various levels of vitamin D3, was studied by light and electron microscopy.
The effect of subnormal Mg intake on vitamin D3-induced intimal lesions of the arteries showed a trend towards increased damage.
The degree of cell degeneration and intimal thickening, which was induced by high vitamin D intakes, was as great in swine whose diet was low in Mg and moderately high in vitamin D, as it was in those on twice as much vitamin D.
Also, the degree of arterial calcification was intensified by inadequate Mg intake at the two higher vitamin D intakes
.
Present findings indicate that suboptimal dietary Mg, in combination with an excess of vitamin D, has an additive effect in the initiation of ultrastructural changes in the coronary arteries. Extension of the study is indicated to ascertain the extent to which further reduction of Mg intake can potentiate vitamin-D-induced coronary lesions."


how about further extension of the study to ascertain the extent to which correcting the imbalance can repair the damage...
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Re: all things vitamin D

Postby jimmylegs » Sun Mar 05, 2017 8:57 am

wonder if the full text unpacks anything to do with magnesium eg the possibly of low d3 being perhaps in part an indicator of an underlying magnesium situation.
Role of Vitamin D in Uremic Vascular Calcification
https://www.hindawi.com/journals/bmri/2017/2803579/abs/
The risk of cardiovascular death is 10 times higher in patients with CKD (chronic kidney disease) than in those without CKD. Vascular calcification, common in patients with CKD, is a predictor of cardiovascular mortality. Vitamin D deficiency, another complication of CKD, is associated with vascular calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial injury, and the therapeutic dose of active form vitamin D aggravate vitamin D deficiency and reduce its pleiotropic effect on the cardiovascular system. Vitamin D supplement for CKD patients provides a protective role in vascular calcification on the endothelium by (1) renin-angiotensin-aldosterone system inactivation, (2) alleviating insulin resistance, (3) reduction of cholesterol and inhibition of foam cell and cholesterol efflux in macrophages, and (4) modulating vascular regeneration. For the arterial calcification, vitamin D supplement provides adjunctive role in regressing proteinuria, reverse renal osteodystrophy, and restoring calcification inhibitors. Recently, adventitial progenitor cell has been linked to be involved in the vascular calcification. Vitamin D may provide a role in modulating adventitial progenitor cells. In summary, vitamin D supplement may provide an ancillary role for ameliorating uremic vascular calcification.
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Re: all things vitamin D

Postby jimmylegs » Mon Mar 06, 2017 9:20 pm

Serum 25‐hydroxyvitamin D 3 levels are elevated in South Indian patients with ischemic heart disease
http://bit.ly/2mQ4YmT

Code: Select all
Table 1. Comparison of selected variables in cases and controls
Variable..........Cases (%)............Controls (%)
..................N = 143...............N = 70

25-hydroxyvitamin D3, mmol/l (ng/ml)
<222.5 (<89)......40.6.................77.9
>222.5 (>89)......59.4.................22.1

Calcium, mmol/l (mg/dl)
<2.9 (<11.5)......80.6.................93.9
>2.9 (>11.5)......19.4..................6.1

Magnesium, mmol/l (mg/dl)
>0.85 (>1.7)......63.0.................73.5
<0.85 (61.7)......37.0.................26.5


would be very interesting to check out the raw data for this one.
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Re: all things vitamin D

Postby jimmylegs » Tue Mar 07, 2017 5:32 pm

would also be nice to get my supposed access working on this one - curious if they bother to touch on magnesium... (august 2017 update - they don't)

Vitamin D, Calcium, and Cardiovascular Disease: A“D”vantageous or “D”etrimental? An Era of Uncertainty
https://link.springer.com/article/10.10 ... 017-0637-2

While the function of vitamin D in regulating calcium homeostasis is well established, there has been growing interest in its role in the prevention of numerous chronic diseases, including cardiovascular disease (CVD). There is mounting epidemiological evidence suggesting that vitamin D deficiency is linked to increased CVD risk. However, the results of previous vitamin D supplementation trials have yielded mixed results in regards to cardiovascular health, and the results of ongoing large-scale randomized controlled trials are not yet available. Further complicating the issue, calcium supplementation, which is often prescribed concurrently with vitamin D, has been associated with increased CVD risk in some (but not all) studies. Thus, it is currently unclear whether vitamin D supplements, particularly for those that are deficient, can help prevent the development of CVD. In addition, there has not been uniform consensus regarding the threshold of 25-hydroxyvitamin D levels that constitutes “sufficiency” across organizational guidelines. This review will provide an update on the most recent evidence regarding the effects of vitamin D and calcium supplements on CVD clinical outcomes, summarize ongoing vitamin D trials, and discuss the current but remarkably disparate recommendations regarding vitamin D deficiency screening and supplementation.

might crop up to some extent in the (but not all) studies mentioned. will have to come back to this one.
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Re: all things vitamin D

Postby jimmylegs » Tue Mar 07, 2017 5:35 pm

just a case study, and it's not one with normal serum calcium by any means. however. kidney stones have come up recently on the forum, and not for the first time:

Reversible vascular calcifications associated with hypervitaminosis D
https://link.springer.com/article/10.10 ... 015-0228-7

A 64-year-old man was hospitalized in 2002 with symptoms of stupor, weakness, and renal colic. The clinical examination indicated borderline hypertension, small masses in the glutei, and polyuria. Laboratory tests evidenced high serum concentrations of creatinine, calcium, and phosphate. Imaging assessments disclosed widespread vascular calcifications, gluteal calcifications, and pelvic ectasia. Subsequent lab tests indicated suppressed serum parathyroid hormone, extremely high serum 25-hydroxy vitamin D, and normal serum 1,25-dihydroxy vitamin D. Treatment was started with intravenous infusion of saline and furosemide due to the evidence of hypercalcemia. Prednisone and omeprazole were added given the evidence of hypervitaminosis D. The treatment improved serum calcium, kidney function, and consciousness. The medical history disclosed recent treatment with exceptionally high doses of slow-release intra-muscular cholecalciferol and the recent excretion of urinary stones. The patient was discharged when it was possible to stop the intravenous treatment. The post-discharge treatment included oral hydration, furosemide, prednisone and omeprazole for approximately 6 months up to complete resolution of the hypercalcemia. The patient came back 12 years later because of microhematuria. Lab tests were normal for calcium/phosphorus homeostasis and kidney function. Imaging tests indicated only minor vascular calcifications. This is the first evidence of reversible vascular calcifications secondary to hypervitaminosis D.
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Re: all things vitamin D

Postby jimmylegs » Sun Aug 27, 2017 8:45 am

again, would be nice if there were even a whisper of analysis where serum magnesium is concerned... particularly among those who failed to achieve serum level increases at daily supplemental d3 intakes above 4000 IU. talk about a blind spot. smh

Evaluation of vitamin D3 intakes up to 15,000 international units/day and serum 25-hydroxyvitamin D concentrations up to 300 nmol/L on calcium metabolism in a community setting
https://pdfs.semanticscholar.org/30ce/e ... e164fc.pdf
Supplementation by the general public with vitamin D at doses above the Tolerable Upper Level of Intake (UL) is becoming quite common. The objective of the current analysis was to characterize the effect of vitamin D supplementation at doses up to 15,000 IU/d in a community-based program on vitamin D status, calcium homeostasis as well as on kidney, liver and immune function. We evaluated data collected for 3,882 participants in a community program for whom there were blood measurements at program entry and at follow-up within 6–18 months between 2013 and 2015. Participants were supplemented with a wide range of vitamin D doses (1,000 – 15,000 IU/d) aimed at achieving serum 25-hydroxyvitamin D [25(OH)D] levels of at least 100 nmol/L. Serum 25(OH)D concentrations up to 300 nmol/L were achieved without perturbation of calcium homeostasis or incidence of toxicity. Hypercalcemia and hypercalciuria were not related to an increase in 25(OH)D concentrations nor vitamin D dose. To achieve serum 25(OH)D levels >100 nmol/L on average, required vitamin D intakes of 6,000 IU/d for normal Body Mass Index (BMI), 7,000 IU/d for overweight and 8,000 IU/d for obese. Doses of vitamin D in excess of 6,000 IU/d were required to achieve serum 25(OH)D concentrations above 100 nmol/L, especially in individuals who were overweight or obese without any evidence of toxicity. Serum 25(OH)D concentrations up to 300 nmol/L were found to be safe.
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Re: all things vitamin D

Postby jimmylegs » Thu Feb 01, 2018 2:11 pm

older lit, but until now only documented elsewhere on the site:

Vitamin D3 Receptor (VDR) Gene rs2228570 (Fok1) and rs731236 (Taq1) Variants Are Not Associated with the Risk for Multiple Sclerosis: Results of a New Study and a Meta-Analysis
http://journals.plos.org/plosone/articl ... ne.0065487

Abstract
Background
Some epidemiological, genetic, and experimental data suggest a possible role of vitamin D in the pathogenesis of multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis. Data on the possible contribution of several single nucleotide polymorphisms (SNP) in the vitamin D receptor (VDR) gene to the risk for MS are controversial. Several studies suggested an interaction between some SNPs in the VDR gene and HLADRB1*1501 in the risk for MS.

Objectives
The aim of this study was to investigate a possible influence of the SNPs rs2228570 and rs731236 in the VDR gene in the risk for MS. A secondary objective was to address the possible interactions between VDR genes and HLADRB1*1501.

Methods
We analyzed the allelic and genotype frequency of VDR rs2228570, rs731236, and HLADRB1*1501 (rs3135388) in 303 patients with MS and 310 healthy controls, using TaqMan Assays. We also conducted a meta-analysis, that was carried out by using the software Meta-Disc 1.1.1 (http://www.hrc.es/investigacion/metadisc.html; Unit of Clinical Statistics, Hospital Ramón y Cajal, Madrid, Spain). Heterogeneity between studies in terms of degree of association was tested using the Q-statistic.

Results
VDR rs2228570 and rs731236 allelic and genotype frequencies did not differ significantly between MS patients and controls, and were unrelated with the age of onset of MS, gender, and course of MS. HLADRB1*1501 showed a high association with the risk of developing MS 4.76(95% C.I.  = 3.14–7.27; p<0.0001). The meta-analysis, after excluding data of one study that was responsible of heterogeneity for rs731236 polymorphism, showed lack of relation of both SNPs with the risk for MS. HLADRB1*1501 showed lack of interaction with VDR rs2228570 and rs731236 in increasing MS risk.

Conclusions
These results suggest that VDR rs2228570 and rs731236 polymorphisms are not related with the risk for MS, and did not confirm interaction between these VDR SNPs and HLADRB1 in the risk for MS.
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Re: all things vitamin D

Postby jimmylegs » Sat Apr 07, 2018 7:33 am

noting, i think, that this old article is not included specifically in this thread i'll include it here. unsurprisingly (especially for 2007), serum magnesium is not analyzed wrt serum dose response to natural d3 exposure. cmon science, you can do this - i know you can!!

Low Vitamin D Status despite Abundant Sun Exposure (2007)
fft: https://academic.oup.com/jcem/article/92/6/2130/2597445

Abstract
Context:
Lack of sun exposure is widely accepted as the primary cause of epidemic low vitamin D status worldwide. However, some individuals with seemingly adequate UV exposure have been reported to have low serum 25-hydroxyvitamin D [25(OH)D] concentration, results that might have been confounded by imprecision of the assays used.

Objective: The aim was to document the 25(OH)D status of healthy individuals with habitually high sun exposure.

Setting: This study was conducted in a convenience sample of adults in Honolulu, Hawaii (latitude 21°).

Participants: The study population consisted of 93 adults (30 women and 63 men) with a mean (SEM) age and body mass index of 24.0 yr (0.7) and 23.6 kg/m2 (0.4), respectively. Their self-reported sun exposure was 28.9 (1.5) h/wk, yielding a calculated sun exposure index of 11.1 (0.7).

Main Outcome Measures: Serum 25(OH)D concentration was measured using a precise HPLC assay. Low vitamin D status was defined as a circulating 25(OH)D concentration less than 30 ng/ml.

Results: Mean serum 25(OH)D concentration was 31.6 ng/ml. Using a cutpoint of 30 ng/ml, 51% of this population had low vitamin D status. The highest 25(OH)D concentration was 62 ng/ml.

Conclusions: These data suggest that variable responsiveness to UVB radiation is evident among individuals, causing some to have low vitamin D status despite abundant sun exposure. In addition, because the maximal 25(OH)D concentration produced by natural UV exposure appears to be approximately 60 ng/ml, it seems prudent to use this value as an upper limit when prescribing vitamin D supplementation.

interesting. it would be nice if i could find the articles i'd read ages ago on somewhat higher natural levels (maybe as high as 160 ng/ml ONLY if distant memory serves) and refresh my memory on the details as well as the calibre of the academic work or works in question. in a perfect world we'd be able to compare vit d3 cofactor status between subjects from those older works and this relatively recent hawaiian study.
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Re: all things vitamin D

Postby jimmylegs » Mon May 21, 2018 10:40 am

ooh maybe *this* one looked at the influence of magnesium status...

Major inter-personal variation in the increase and maximal level of 25-hydroxy vitamin D induced by UVB (2013)
https://www.ncbi.nlm.nih.gov/pubmed/27001558
Vitamin D influences skeletal health as well as other aspects of human health. Even when the most obvious sources of variation such as solar UVB exposure, latitude, season, clothing habits, skin pigmentations and ethnicity are selected for, variation in the serum 25-hydroxy vitamin D (25(OH)D) response to VB remains extensive and unexplained. Our study assessed the inter-personal variation in 25(OH)D response to UVR and the maximal obtainable 25(OH)D level in 22 healthy participants (220 samples) with similar skin pigmentation during winter with negligible ambient UVB. Participants received identical UVB doses on identical body areas until a maximal level of 25(OH)D was reached. Major inter-personal variation in both the maximal obtainable UVB-induced 25(OH)D level (range 85–216 nmol/l, mean 134 nmol/l) and the total increase in 25(OH)D (range 3–139 nmol/l, mean 48 nmol/l) was found. A linear model including measured 25(OH)D baselines as personal intercepts explained 54.9% of the variation. By further including personal slopes in the model, as much as 90.8% of the variation could be explained. The explained variation constituted by personal differences in slopes thus represented 35.9%.
Age, vitamin D receptor gene polymorphisms, height and constitutive skin pigmentation (a skin area not exposed to UVB) explained 15.1% of this variation. Despite elimination of most known external sources of variation, our study demonstrated inter-personal variation corresponding to an observed maximal difference of 136 nmol/l in the total increase of 25(OH)D and 131 nmol/l in the maximal level of 25(OH)D.

interesting, but nope. # times magnesium mentioned in full text: 0
le sigh! cmon science let's git er done.
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Re: all things vitamin D

Postby jimmylegs » Tue Jul 03, 2018 6:01 am

The Role of Vitamin D in Multiple Sclerosis: Biology and Biochemistry, Epidemiology and Potential Roles in Treatment (2018)
https://www.ncbi.nlm.nih.gov/pubmed/28933265

BACKGROUND:
Multiple sclerosis (MS) is a progressive, demyelinating condition of the central nervous system, manifesting in loss or alterations in function of sensory, motor and cognitive function. Of the various environmental and behavioural risk factors identified as playing a role in MS onset and progression, perhaps none has been as consistent as vitamin D.

OBJECTIVE:
In this review, we will endeavour to present a general background on the role of vitamin D in human health and particularly in MS, as well as the substantial epidemiological evidence in support of vitamin D's role in MS.

RESULTS:
Initially identified via the oft-noted latitudinal gradient in MS prevalence and incidence, vitamin D has since been demonstrated to have a strong and consistent inverse association with MS risk and clinical course. Cases have much lower levels of the diagnostic metabolite of vitamin D, 25- hydroxyvitamin D (25(OH)D) compared to healthy controls, while those with more active disease have lower levels of 25(OH)D than other cases with less active disease. These case-control and crosssectional study results led the way to cohort studies which indicated significant inverse associations between serum 25(OH)D and clinical activity in MS. The combined weight of indirect and direct observational evidence have been the impetus for completed and ongoing randomised trials of vitamin D supplementation, alone or in addition to standard immunomodulatory medications, as an intervention in MS onset and clinical course. Moreover, in addition to being a distinct factor in MS aetiology, vitamin D has been demonstrated to interact with a variety of other risk factors, from genetic predictors like HLA-DR1 genotype to behavioural factors like smoking.

CONCLUSION:
There is an abundance of epidemiological evidence, both direct and indirect, as well as significant biological plausibility substantiating a role for vitamin D in the onset and progression of multiple sclerosis.

no full text for me as yet. and not even hinting at vit d3 cofactors in the abstract :S le sigh
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Re: all things vitamin D

Postby jimmylegs » Thu Jul 26, 2018 1:36 pm

Evidence for a U-Shaped Relationship Between Prehospital Vitamin D Status and Mortality: A Cohort Study
https://academic.oup.com/jcem/article/99/4/1461/2537578
Objective:
The objective of the study was to examine the association between prehospital serum 25-hydroxyvitamin D [25(OH)D]and the risk of mortality after hospital admission.

Design:
We performed a retrospective cohort study of adults hospitalized for acute care between 1993 and 2011.

Setting:
The study was conducted at two Boston teaching hospitals.

Patients:
A total of 24 094 adult inpatients participated in the study.

Intervention:
There was no intervention.

Measurements:
All patients had serum 25(OH)D measured before hospitalization. The exposure of interest was 25(OH)D categorized as less than 10 ng/mL, 10–19.9 ng/mL, 20–29.9 ng/mL, 30–49.9 ng/mL, 50–59.9 ng/mL, 60–69.9 ng/mL, and 70 ng/mL or greater. The main outcome measure was 90-day mortality. Adjusted odds ratios (ORs) were estimated by multivariable logistic regression with inclusion of potential confounders.

Results:
After adjustment for age, gender, race (white vs nonwhite), patient type (surgical vs medical), season of 25(OH)D draw, and the Deyo-Charlson index, patients with 25(OH)D levels less than 30 ng/mL or 60 ng/mL or greater had higher odds of 90-day mortality compared with patients with levels of 30–49.9 ng/mL [adjusted OR (95% confidence interval) for 25(OH)D <10 ng/mL, 10–19.9 ng/mL, 20–29.9 ng/mL, 50–59.9 ng/mL, 60–69.9 ng/mL, and ≥70 ng/mL was 2.01 (1.68–2.40), 1.89 (1.64–2.18), 1.34 (1.16–1.56), 0.94 (0.69–1.26), 1.52 (1.03–2.25), and 1.69 (1.09–2.61), respectively, compared with patients with 25(OH)D levels 30–49.9 ng/mL].

Limitations:
A causal relationship between either low or high 25(OH)D levels and increased mortality can not necessarily be inferred from this observational study.

Conclusions:
Analysis of 24 094 adult patients showed that 25(OH)D levels less than 20 ng/mL and 60 ng/mL or greater before hospitalization were associated with an increased odds of 90-day mortality. Although previous reports have suggested an association between low vitamin D status and mortality, these data raise the issue of potential harm from high serum 25(OH)D levels, provide a rationale for an upper limit to supplementation, and emphasize the need for caution in the use of extremely high doses of vitamin D among patients.
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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Re: all things vitamin D

Postby jimmylegs » Thu Sep 06, 2018 7:32 am

my friend who is fighting advanced breast cancer recently went against her medical team's advice, which was to take 4000 IU per day of D3, to address her low serum level (under 50 nmol/l ie less than 20 ng/ml, and mine was only a little better)
together she and i completed a 10 day, 50K IU per day regimen. this is a protocol that is meant to boost serum levels by 50 nmol/l but personally having been around this block a couple times i know my own dose response has been much higher. triple the expected dose response was okay by me, because i'd still be at 150 nmol/l, which i'm fine with as long as i have all my cofactors in order.

i have not yet had a chance to request follow-up bloodwork for my own recent megadose, but her results came in yesterday.
her levels climbed just 30 nmol/l. she has just barely squeaked into the range of sufficiency in terms of protection against osteoporosis, never mind anything more serious.
but that lab paperwork is god. it says >75 nmol = desirable. so who cares if her level isn't even 80, never mind that the next level in the rubric is >250 = excess
circling the drain is, apparently, 'desirable'.

one of her applicable risk factors for breast cancer, aside from the obvious, is obesity.
while the literature does not seem to show a clear relationship between d3 status and risk of her cancer in particular, this research is relevant:

The Importance of Body Weight for the Dose Response Relationship of Oral Vitamin D Supplementation and Serum 25-Hydroxyvitamin D in Healthy Volunteers (2014)
https://journals.plos.org/plosone/artic ... ne.0111265
Unlike vitamin D recommendations by the Institute of Medicine, the Clinical Practice Guidelines by the Endocrine Society acknowledge body weight differentials and recommend obese subjects be given two to three times more vitamin D to satisfy their body's vitamin D requirement. However, the Endocrine Society also acknowledges that there are no good studies that clearly justify this. In this study we examined the combined effect of vitamin D supplementation and body weight on serum 25-hydroxyvitamin (25(OH)D) and serum calcium in healthy volunteers. We analyzed 22,214 recordings of vitamin D supplement use and serum 25(OH)D from 17,614 healthy adult volunteers participating in a preventive health program. This program encourages the use of vitamin D supplementation and monitors its use and serum 25(OH)D and serum calcium levels. Participants reported vitamin D supplementation ranging from 0 to 55,000 IU per day and had serum 25(OH)D levels ranging from 10.1 to 394 nmol/L. The dose response relationship between vitamin D supplementation and serum 25(OH)D followed an exponential curve. On average, serum 25(OH)D increased by 12.0 nmol/L per 1,000 IU in the supplementation interval of 0 to 1,000 IU per day and by 1.1 nmol/L per 1,000 IU in the supplementation interval of 15,000 to 20,000 IU per day. BMI, relative to absolute body weight, was found to be the better determinant of 25(OH)D. Relative to normal weight subjects, obese and overweight participants had serum 25(OH)D that were on average 19.8 nmol/L and 8.0 nmol/L lower, respectively (P<0.001). We did not observe any increase in the risk for hypercalcemia with increasing vitamin D supplementation.
We recommend vitamin D supplementation be 2 to 3 times higher for obese subjects and 1.5 times higher for overweight subjects relative to normal weight subjects. This observational study provides body weight specific recommendations to achieve 25(OH)D targets.

comments:

first, for clarity results describe a *negative* exponential curve, ie a plateau
https://journals.plos.org/plosone/artic ... 11265.g001

a clear "diminishing returns" scenario.

also, re "12.0 nmol/L per 1,000 IU in the supplementation interval of 0 to 1,000 IU per day",
if you check out the figure, the y axis seems to indicate on average subjects went from say 63 nmol/l taking no daily d3, to 85 nmol/l if taking 1000 IU/day
also looks like 5000 IU per day puts the group mean serum level above 100 nmol/l - with typically large dose response variation around the line of best fit (... and as usual no analysis of or discussion about any cofactor other than calcium.. :? )

i note with interest one of the outliers, with 150 nmol/l serum d3 level at around 2000 IU/d supplemental intake. wonder what else that person has going on in their day to day routine and/or gene pool!

anyway. i hope my friend has let her docs know about the 10 day megadose, and that her team is not under the mistaken impression that her recent 30 nmol/l gains were made as a result of their 4000 IU per day instruction. she definitely has gotten nowhere near the 100 nmol/l level that the above study's chart suggests for a 4000 IU/day intake, even *with* the megadose in the mix.

i'll be very interested to see my own results, so that we can compare notes on dose-response!!
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!
User avatar
jimmylegs
Volunteer Moderator
 
Posts: 11696
Joined: Sat Mar 11, 2006 4:00 pm

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