all things vitamin D

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Petr75
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Re: all things vitamin D

Post by Petr75 » Wed May 29, 2019 8:44 am

2019 Apr 27
Department of Neurology, Inselspital Bern, University Hospital, University of Bern, Bern, Switzerland
Vitamin D increases glucocorticoid efficacy via inhibition of mTORC1 in experimental models of multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/31030237

Abstract
The limited efficacy of glucocorticoids (GCs) during therapy of acute relapses in multiple sclerosis (MS) leads to long-term disability. We investigated the potential of vitamin D (VD) to enhance GC efficacy and the mechanisms underlying this VD/GC interaction. In vitro, GC receptor (GR) expression levels were quantified by ELISA and induction of T cell apoptosis served as a functional readout to assess synergistic 1,25(OH)2D3 (1,25D)/GC effects. Experimental autoimmune encephalomyelitis (MOG35-55 EAE) was induced in mice with T cell-specific GR or mTORc1 deficiency. 25(OH)D (25D) levels were determined in two independent cohorts of MS patients with stable disease or relapses either responsive or resistant to GC treatment (initial cohort: n = 110; validation cohort: n = 85). Gene expression of human CD8+ T cells was analyzed by microarray (n = 112) and correlated with 25D serum levels. In vitro, 1,25D upregulated GR protein levels, leading to increased GC-induced T cell apoptosis. 1,25D/GC combination therapy ameliorated clinical EAE course more efficiently than respective monotherapies, which was dependent on GR expression in T cells. In MS patients from two independent cohorts, 25D deficiency was associated with GC-resistant relapses. Mechanistic studies revealed that synergistic 1,25D/GC effects on apoptosis induction were mediated by the mTOR but not JNK pathway. In line, 1,25D inhibited mTORc1 activity in murine T cells, and low 25D levels in humans were associated with a reduced expression of mTORc1 inhibiting tuberous sclerosis complex 1 in CD8+ T cells. GR upregulation by 1,25D and 1,25D/GC synergism in vitro and therapeutic efficacy in vivo were abolished in animals with a T cell-specific mTORc1 deficiency. Specific inhibition of mTORc1 by everolimus increased the efficacy of GC in EAE. 1,25D augments GC-mediated effects in vitro and in vivo in a T cell-specific, GR-dependent manner via mTORc1 inhibition. These data may have implications for improvement of anti-inflammatory GC therapy.

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Petr75
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Re: all things vitamin D

Post by Petr75 » Thu May 30, 2019 8:39 am

2019 Apr 12
Myelin Maintenance and Peripheral Neuropathies, Faculties of Medicine and Pharmacy, University of Limoges, Limoges, France
Focus on 1,25-Dihydroxyvitamin D3 in the Peripheral Nervous System.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6474301/

Abstract
In this review, we draw attention to the roles of calcitriol (1,25-dihydroxyvitamin D3) in the trophicity of the peripheral nervous system. Calcitriol has long been known to be crucial in phosphocalcium homeostasis. However, recent discoveries concerning its involvement in the immune system, anti-cancer defenses, and central nervous system development suggest a more pleiotropic role than previously thought. Several studies have highlighted the impact of calcitriol deficiency as a promoting factor of various central neurological diseases, such as multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease, and Alzheimer's disease. Based on these findings and recent publications, a greater role for calcitriol may be envisioned in the peripheral nervous system. Indeed, calcitriol is involved in myelination, axonal homogeneity of peripheral nerves, and neuronal-cell differentiation. This may have useful clinical consequences, as calcitriol supplementation may be a simple means to avoid the onset and/or development of peripheral nervous-system disorders.

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vitamind d3 excess, toxicity

Post by jimmylegs » Fri Sep 13, 2019 10:53 am

Vitamin D toxicity resulting from overzealous correction of vitamin D deficiency (2015)
https://onlinelibrary.wiley.com/doi/abs ... /cen.12836

Our data demonstrate an emergence of vitamin D toxicity as an increasingly common cause of symptomatic hypercalcaemia. Irrational use of vitamin D in mega‐doses resulted in vitamin D toxicity in all cases. Awareness among healthcare providers regarding the toxic potential of high doses of vitamin D and cautious use of vitamin D supplements is the key to prevent this condition.
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d3 deficiency overcorrection, toxicity

Post by jimmylegs » Fri Sep 13, 2019 10:57 am

Development of Vitamin D Toxicity from Overcorrection of Vitamin D Deficiency: A Review of Case Reports (2018)
https://www.mdpi.com/2072-6643/10/8/953/htm

Over the past two decades, vitamin D level measurements have become some of the most frequently ordered tests in the laboratory. This increase is due to a growing awareness of widespread vitamin D deficiency and scientific data suggesting the beneficial effects of vitamin D in various diseases. A literature search was carried out in PubMed for cases reporting vitamin D intoxication and overdose. Thirteen articles were included in this review. Intoxication was severe in the reported cases. Patients presented with serum vitamin D concentrations ranging between 150 and 1220 ng/mL and serum calcium concentrations between 11.1 and 23.1 mg/dL. Most of the reported patients showed symptoms of vitamin D toxicity such as vomiting, dehydration, pain, and loss of appetite. The underlying causes included manufacturing errors, overdosing by patients or prescribers, and combinations of these factors. Our literature search highlights the fact that even though vitamin D intoxication is rare, it does occur and therefore patients and prescribers should be more cognizant of the potential dangers of vitamin D overdose
take control of your own health
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vitamin d3 intoxication

Post by jimmylegs » Fri Sep 13, 2019 11:09 am

Vitamin D exposures reported to US poison centers 2000–2014: Temporal trends and outcomes (2016)
https://www.ncbi.nlm.nih.gov/pubmed/26519481
fft is out there and easy to find if you want it

...Significant injury after vitamin D intoxication has been reported in individual cases and in small case series from manufacturing errors, dosing errors, and misuse of OTC vitamin D supplementation. Severe clinical effects after vitamin D intoxication have occurred in children and adults, and have included confusion, seizures, coma, renal failure, cardiac arrhythmias, and psychiatric disturbances. Severe events appear to be uncommon however, despite the massive increase in the use of vitamin D both by prescription and as a widely available OTC vitamin supplement.
...
because the nature of follow up by poison centers is short term and the half-life of 25(OH)D is 2–3 weeks, the onset of clinical effects renal stones or renal failure may have been delayed and therefore not recorded in these cases.

Conclusion
The NPDS provides a large, accessible database conducive to characterizing toxicity and demographic trends after vitamin D ingestion. From 2000 to 2014, the number of patients reported to US poison centers of vitamin D ingestion increased to 1600%, from a mean of 196 patients per year by >4500 patient per year. Approximately 10% of these patients were seen in an HCF. The incidence of severe cases remains remarkably low, without a notable increase in morbidity and no mortality. Rare severe outcomes may occur.
take control of your own health
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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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Re: all things vitamin D

Post by Zyklon » Fri Sep 13, 2019 12:21 pm

D3 misuse is very very common. Whenever I know a friend using D3, I ask dosage and other supplements. Even with monthly megadoses of 50k, none of my friends use magnesium. They all say stiff muscles, fatigue, and cramps...
Pain! You made me a, you made me a believer, believer
Pain! You break me down, you build me up, believer, believer
Pain! Oh let the bullets fly, oh let them rain
My life, my love, my drive, it came from... Pain!

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jimmylegs
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Re: all things vitamin D

Post by jimmylegs » Fri Sep 13, 2019 12:47 pm

me too! it's frustrating that so many pros do not have the issue on the radar, but comforting when you encounter the occasional person whose doc gave them the heads up. if only those individuals weren't so rare. i just met up with a friend yesterday who takes d3 alone on doc's orders, and that's after all the mag depletion from chemo too. le sigh...
take control of your own health
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ask for referrals to preventive health care specialists eg dietitians
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Re: all things vitamin D

Post by tzootsi » Sat Sep 14, 2019 12:02 pm

The study below just published states that even 50,000 a day is safe.
https://www.ncbi.nlm.nih.gov/pubmed/30611908

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Re: all things vitamin D

Post by jimmylegs » Sun Sep 15, 2019 7:47 am

ah yes, yet another study with zero attention to d3 impacts on magnesium status.

the only place magnesium appears in the full text: #84 of 100 references in the literature cited.

specifically:
Dietary Reference Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride, National Academies Press (US), Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Washington
(DC), 1997.

in contrast, 43 hits in the full text on 'hypercalc' in reference to 'hypercalcemic' or 'hypercalcemia'.

authors repeatedly state that no adverse effects including hypercalcemia or other signs or symptoms of vit d excess occurred. the signs and symptoms are not specified but where mentioned it is usually something like: "there were no patients who exhibited any signs or symptoms associated with hypercalcemia in either group"

i note also that the highest doses over the longest periods covered in this study comes down to three individuals: "The first is a patient who has been on 50,000 IU/d of vitamin D2 for over 2 years for treatment of psoriasis. The second is a staff member who has been on 25,000 IU/d for several years for treatment of asthma (author JA), and the third is a staff member who has been on 60,000 IU/d of vitamin D3 for the past 4 years for the treatment of an ulcerated skin lesion (author PM).'

i will underscore here the difference between D2 and D3.

i note also that nowhere in this article do the words 'limitations' or 'bias' appear. nor do the words 'strength' or 'weakness' in application to authors' self-assessment of their study's quality.

overall, single individuals' experiences should not be taken as blanket safety evidence for all, even if the anecdote has been published in a refereed journal.

i also note zero mention of specific d3 goals, targets or optimal status for the authors themselves or for the balance of the study subjects ie the authoring doctors' psychiatric inpatients.

final aside, i also checked the full text for mention of d3 excretion into wastewater and the environment in general. nothing. zero hits on bile. the four mentions of excretion have only to do with calcium excretion in urine. no reference to downstream waterwater vit d3 contamination and wildlife impacts whatsoever. luckily, that last issue is at least making it into the literature elsewhere. i hope at a bare minimum people start paying attention to excretion so that they're not wasting their own money not to mention potentially messing up wildlife.

good find though, it's worth having the publication represented in the collection here

i'm so glad that some other researchers at least are starting to clue in that it's not all about calcium.

Personalized magnesium intervention to improve vitamin D metabolism: applying a systems approach for precision nutrition in large randomized trials of diverse populations (2018)
https://academic.oup.com/ajcn/article-a ... 59/5239922

'... some observations have been well recognized, including high prevalence of vitamin D and magnesium insufficiency in westernized populations (9, 10) and the large interpersonal variations of vitamin D and magnesium metabolisms in the general population (11). Studies have shown that magnesium plays a critically important role in the synthesis and metabolism of vitamin D, raising the possibility that magnesium should be included in any vitamin D regimen'

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

comment on ^ :
Investigating the Influence of Vitamin D Replacement Therapy on Magnesium Status (2018)
https://jaoa.org/article.aspx?articleid=2716916
'periodic assessment of serum magnesium levels among these patients is necessary because with continued cholecalciferol supplementation as maintenance therapy, further depletion of magnesium with possible clinical consequences could result. The depletion of magnesium is expected to be serious among patients who take vitamin D supplements and have coexisting conditions that increase the risk of magnesium deficiency, including insufficient dietary magnesium intake, hypoalbuminemia, chronic alcoholism, type 2 diabetes mellitus, gastrointestinal diseases (eg, celiac disease, chronic diarrhea, Crohn disease), and use of drugs (eg, insulin, loop and thiazide diuretics, aminoglycosides, proton pump inhibitors, and certain chemotherapies).'

from response to comment ^
Response (2018)
https://jaoa.org/article.aspx?articleid=2716917
'As vitamin D supplement-induced hyperphosphatemia may appear even before changes in serum calcium levels, it would be clinically important to monitor the serum phosphorus levels in these patients. Of significance, phosphorus dysregulation induced by exogenous vitamin D supplementation may lead to tissue and organ damage even without the development of hypervitaminosis D. Again, by consuming the optimal amount of magnesium, it might be possible to reduce the dependency on vitamin D supplements, which is not always risk-free, particularly when consumed in higher doses or used for prolonged periods.'

meh, why bother checking though, right?

lastly to be crystal clear, over the last decade and a half i have taken d3 @ 50,000 IU per day on 4 occasions.
the first time was for 10 days while malnourished and my serum d3 levels increased by about 80 nmol/l. i was comfortable with the resulting level based on the related literature on d3 levels in chronic disease and ms in particular.
later, after working on nutrition for i think a couple of years, based on an unsatisfactory d3 lab result i wanted definitely a 50 and not an 80 nmol/. increase so i decreased the duration of the regimen. that time, 50K IU/d over just 8 days resulted in a 170 nmol/l increase. that took me above 250 nmol/l and i had no case for wanting my levels that high.
then, within the last couple of years when my d3 starting point was the lowest i have ever seen it, the 10 day x 50K regimen gave me a mere 40 nmol/l boost. by this time i knew about magnesium and cofactors right from the start, so for me that was pretty bad.
the fourth and last session to date was because of dissatisfaction with the 40 nmol/l boost. my levels had not reached my personal target. having been working much harder on nutrient status in general, i did one more 50K IU per day regimen, again for 10 days, which increased my d3 levels by another 70 nmol/l in serum. that result was higher than my personal target, so i have backed off to more reasonable maintenance intakes thereafter.

i have never directly felt any effect, positive or negative, from these short term efforts but i had had a crap mri in early 2018 following a rough spell symptom-wise, concurrent with the bad d3 result, and after a year of hard work on self care including these judicious rounds of d3, my last mri showed no evidence of disease activity, with evidence of a pre-exising old lesion being smaller.

contrast the disaster caused by a modest daily 4K IU of d3. i suffered for years before i learned about magnesium. as with the info above, that story is thoroughly documented elsewhere on the forum but i did think i was going to die before that one pharmacist finally helped me figure it out.
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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High dose vitamin D exacerbates CNS autoimmunity

Post by jimmylegs » Mon Sep 30, 2019 5:41 pm

thx to petr for finding this one. be safe ppl!
  • High dose vitamin D exacerbates central nervous system autoimmunity by raising T-cell excitatory calcium (2019).
    https://www.ncbi.nlm.nih.gov/pubmed/31302671

    Poor vitamin D status is associated with a higher relapse rate and earlier disability in multiple sclerosis. Based on these associations, patients with multiple sclerosis are frequently supplemented with the vitamin D precursor cholecalciferol, although it is unclear whether this regimen is of therapeutic benefit. To model consequences of this common practice, mice were fed for more than 3 months with a low, medium or high dose of cholecalciferol, representative of vitamin D deficiency, modest and disproportionally high supplementation, respectively, in patients with multiple sclerosis. Compared to vitamin D-deprived mice, its moderate supplementation reduced the severity of subsequent experimental autoimmune encephalomyelitis, which was associated with an expansion of regulatory T cells. Direct exposure of murine or human T cells to vitamin D metabolites inhibited their activation. In contrast, mice with 25-(OH) vitamin D levels above 200 nmol/l developed fulminant experimental autoimmune encephalomyelitis with massive CNS infiltration of activated myeloid cells, Th1 and Th17 cells. When dissecting this unexpected outcome, we observed that high, but not medium dose vitamin D had caused mild hypercalcaemia, which rendered T cells more prone to pro-inflammatory activation. Exposing murine or human T cells to equivalent calcium concentrations in vitro enhanced its influx, triggering activation, upregulation of pro-inflammatory gene products and enhanced transmigration across a blood-brain barrier model. These findings suggest that vitamin D at moderate levels may exert a direct regulatory effect, while continuous high dose vitamin D treatment could trigger multiple sclerosis disease activity by raising mean levels of T-cell excitatory calcium.
    ...
    Mice were fed with a diet containing either low (<5 IU/kg food), standard (1500 IU/kg food) or high (75 000 IU/kg food) vitamin D3 concentrations (ssniff Spezialdiaeten) for at least 8 weeks. These doses were chosen after a dose titration, as they generated serum vitamin D levels reflective of vitamin D deficiency (<30 nmol/l), physiological vitamin D levels (100 nmol/l) and continuous high-dose supplementation (250 nmol/l) in patients (Vieth, 1999; Burton et al., 2010; Smolders et al., 2010). All three diets contained identical calcium (1%) and phosphate (0.7%) concentrations (Supplementary Fig. 1). Hypercalcaemia in mice was induced by daily intraperitoneal injection of calcium gluconate (2000 mg/kg/day; Sigma-Aldrich) starting 3 days before immunization
    ...
    recent clinical trials revealed enhanced immune cell activation in patients with multiple sclerosis supplemented with 50 000 IU of vitamin D3 every 5 days (Naghavi Gargari et al., 2015), whereas the functionally opposite outcome occurred at moderate vitamin D levels (Muris et al., 2016; Sotirchos et al., 2016). In conjunction with these observations, our novel findings highlight excessive vitamin D supplementation and resulting hypercalcaemia as novel risk factors promoting worsening of CNS demyelinating disease. Our data caution that in light of the currently limited information on a direct beneficial effect of vitamin D in multiple sclerosis, patients with multiple sclerosis may be at danger of experiencing untoward immunological and/or clinical effects when vitamin D is supplemented excessively.
from muris et al (trying to figure out the 'functionally opposite outcome' sentence)
  • patients received either IFNβ-1a and placebo or IFNβ-1a and vitamin D3 (cholecalciferol, Vigantol® Oil, Merck KGaA, Darmstadt, Germany) 7000 IU daily for 4 weeks, followed by 14,000 IU daily up to week 48.
    ...
    Serum 25(OH)D levels in the placebo group were rather stable (54 (43–63) nmol/L at wk0 and 60 (36–85) nmol/L at wk48, p = 0.38), while they increased significantly from 60 (38–85) nmol/L at wk0 to 231 (162–250) nmol/L at wk48 in the vitamin D3 group (p b 0.001). These differences were significant between the groups (p b 0.001). None of the patients in the placebo group and 11 of the patients in the vitamin D3 group reached the upper limit of a 25(OH)D level of 250 nmol/L (Fig. 3)
    ...
(ok so i guess 14K every day is 'moderate' now... although the authors themselves do describe it as high-dose... anyway yikes, that one patient in the d3 group with levels flat at 40 nmol/l while taking 14K IU/d for close to a year... can you say cofactors wow. what a waste!)
  • The results of our current study reveal only minor effects of vitamin D3 supplementation on immune regulation, in contrast with many other previous studies, including our own pilot study, which suggested clearer effects of vitamin D on immune parameters. The added value of the SOLARIUM study is, however that it is a placebo controlled RCT in a homogeneous population with a long-term follow-up investigating the Th cell compartment as a whole
    ...
    In summary, 48-weeks of high dose vitamin D3 supplementation in IFNβ treated RRMS patients does not have substantial beneficial effects on the circulating regulatory immune cell compartment. However, our data point towards a role in the prevention of gradual worsening or (immunological) imbalance.
and now to unpack sotirchos et al... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4776090/
  • This study provides Class I evidence that cholecalciferol supplementation with 10,400 IU daily is safe and well-tolerated in patients with MS and exhibits in vivo pleiotropic immunomodulatory effects.

    Forty patients were randomized to receive 10,000 IU or 400 IU of cholecalciferol (Continental Vitamin Company, Vernon, CA) daily for 6 months. In addition, all study participants received a daily multivitamin (LuckyVitamin, Conshohocken, PA) including 400 IU cholecalciferol and 1,000 mg calcium.

    it has been proposed that 25(OH)D levels between 40 and 60 ng/mL may be the optimal target for patients with MS.23 In our study, supplementation with 800 IU daily was inadequate to achieve this goal, whereas supplementation with 10,400 IU daily achieved the desired levels, with no difference in safety outcomes. Randomized controlled trials are currently underway to examine the effects of vitamin D supplementation on clinical and radiologic outcomes, with dosages of 5,000 to 10,000 IU daily.23,–25
ok, this luckyvitamin multivit product let's see... lol magnesium content: 10mg mag oxide. 3% daily value (which, i might add, applies to anyone age 4 and up, as distinct from dris which vary by age and gender based on a reference 'average' weight - too bad if that's not you) *while* dosing with 10.4K IU d3 daily. good one.

without a super close look at the details, i have my suspicions as to the back story (cofactor depletion, anyone? other unknown unknowns?) on that serum d3 decline end of study in the higher dose d3 group, compared to the mid study numbers.


and not forgetting, study magnesium assessment/mention: 0. so let's just clarify: 'safe in the context of the specific assessments we bothered to conduct'.

i am right on board with the proposed optimal target range for d3 but not at the expense of my body's magnesium stores. never again will i subject my system to supplemental d3 without careful attention to its impact on my mag status!!

now for some finer-grained info than 100-250 nmol/l...
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2019 case:pediatric Gummy Vitamin OD

Post by jimmylegs » Thu Oct 03, 2019 11:44 am

a study with possible value even for attentive and well-meaning parents:
  • Subacute Gummy Vitamin Overdose as a Rare Manifestation of Child Neglect (2019)
    https://europepmc.org/abstract/med/30624424

    We present a case of a 20-month-old girl who presented to the emergency department with anorexia, progressive weakness, and lethargy who was found to have severe hypercalcemia (20.7 mg/dL) and vitamin D hypervitaminosis. Further questioning revealed that this was secondary to a subacute toxic ingestion of "L'il Critters" calcium and vitamin D3 gummy vitamins that were being administered by the patient's mother multiple times a day for several weeks or even months. This occurred in the setting of child neglect due to the mother's mental illness. The patient required intensive care unit admission and had a prolonged hospital course complicated by hypomagnesemia, hyperphosphatemia, weight loss, and persistent weakness. Her hypercalcemia was initially refractory to standard treatment of intravenous fluids, prednisone, multiple trials of calcitonin, and zoledronic acid. Our patient had the highest calcium level we are aware of in a toddler and is the only case we know of that occurred as a result of a prolonged, intentional exposure in the setting of child neglect and a complex social situation. This case reviews the causes and management of hypercalcemia and vitamin D intoxication. It also highlights the need for a comprehensive social history and exposes the vulnerabilities of children living in homes afflicted by parental depression and severe mental illness.
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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Re: 2019 case study:pediatric Gummy Vitamin OD

Post by NHE » Thu Oct 03, 2019 2:19 pm

jimmylegs wrote:
Thu Oct 03, 2019 11:44 am
Subacute Gummy Vitamin Overdose as a Rare Manifestation of Child Neglect (2019)
https://europepmc.org/abstract/med/30624424
That's because there's a half teaspoon of sugar in each serving. They look like candy. They taste like candy. They come in a jar with smiling children and a cute bear. Gummy vitamins and supplements are just another way to push more sugar on consumers.

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2019 case: D3 kidney failure

Post by jimmylegs » Fri Oct 04, 2019 5:36 pm

  • Use of vitamin D drops leading to kidney failure in a 54-year-old man (2019)
    http://www.natap.org/2019/HIV/E390.full.pdf

    ... On more detailed questioning, the patient mentioned that he was seeing a naturopathic specialist who had prescribed high doses of vitamin D, advising him to take 8 drops of a specific brand daily. He did not have a history of a fragility fracture or documented vitamin D deficiency. The recommended brand contained 500 IU per drop. Unknowingly, the patient obtained another vitamin D preparation that contained 1000 IU per drop. The patient was not counselled about toxicity risks and, over a period of 2.5 years, he took 8–12 drops of vitamin D daily, for a total daily dose of 8000–12 000 IU.
    ...
    KEY POINTS
    • Vitamin D toxicity is rare, but clinicians must be aware of the risks of vitamin D use to limit complications related to hypercalcemia.
    • Calcium levels may get worse before getting better in patients even after cessation of supplements, as vitamin D is fat soluble.
    • Observational data and expert opinion suggest that glucocorticoids, ketoconazole and hydroxychloroquine are reasonable options to treat hypercalcemia related to vitamin D toxicity by decreasing the “active” 1, 25 dihydroxyvitamin D3 levels.
recalling also that previously posted older case documenting effective hypercalcemia treatment with iv magnesium... anyway, to continue:
  • Misconception about the cause of vitamin D toxicity (2019)
    https://search.proquest.com/openview/7d ... 7333aeca8/
    In the case reported by Auguste and colleagues,1 we believe that the patient experienced vitamin D intoxication because of an underlying pathologic condition that the authors failed to recognize ... they did not appreciate the patient’s previous history of urothelial carcinoma, which has been reported to be associated with vitamin D toxicity associated with unregulated extrarenal conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. This was the likely cause of the patient’s vitamin D intoxication and renal failure, not the dosage of vitamin D.
  • RE: Misconception for the cause of vitamin D toxicity (2019)
    http://www.cmaj.ca/content/re-re-miscon ... d-toxicity
    It is difficult to accept that a locally noninvasive bladder carcinoma resulted in the burden of hypercalcemia that our patient experienced, which left him with permanent kidney damage ... Charoenngam and colleagues propose esoteric differential diagnoses for our patient’s hypercalcemia, failing to acknowledge the potential risks of vitamin D toxicity associated with chronic misuse. The purpose of our case study was not to minimize the importance of vitamin D, but rather to raise awareness that chronic misuse can result in permanent renal damage.
this kind of general idiocy may well be the end of over the counter vitamin d3 as we know it. i'm still using up a freaking dangerously high dose product but at least i know what i'm doing and how cautiously to use it to get just the dose i need (now) even if i did have to negotiate the prescription working back and forth between my doc and the pharmacy originally. once it's gone (and it is taking a LOOOONG time) i'll never bother with this product again.

update: just found this. will have to unpack details another time:
"RE: Hypercalcemia and a No Observed Adverse Effect Level (NOAEL) Intake of Vitamin D" (2019)
http://www.cmaj.ca/content/re-hypercalc ... -vitamin-d
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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case:toxic/'undetectable' D3

Post by jimmylegs » Sat Oct 05, 2019 3:17 pm

come on, people...
  • Vitamin D Toxicity & Undetectable Serum Levels - A Conundrum (2017)
    https://www.endocrine-abstracts.org/ea/0050/ea0050ep033

    59 year old woman with relapsing remitting multiple sclerosis (MS), not under Neurology follow-up was privately consulting a nutritionist based in Ireland and following the Coimbra protocol since December 2016. This included cholecalciferol (1000-170,000 IU/day), vitamin B-complex and trace elements. Dose adjustments were advised during weekly skype consultations based on blood tests (via General Practitioner) and symptoms.
    Fluid intake was 2 litres/day (‘prescribed’ 3-4) for a week when hospital admission was advised for hypercalcaemia (corrected calcium level was 3.76 [2.20-2.60]) and acute kidney injury (AKI) stage1. She was getting thirstier and constipated. Serum 25-hydroxy vitamin D (25-OHD) was reportedly <15 nmol/L, and parathyroid hormone (PTH) was unsuppressed (4.7 pmol/L [1.6-7.5]). Vitamin D metabolites were requested and sample sent to another laboratory to confirm results by liquid chromatography-mass spectrometry (LC-MS). In view of undetectable 25-OHD computed tomography of chest, abdomen and pelvis was done (adrenal incidentaloma). Rehydration with intravenous normal saline, stopping supplements, led to corrected calcium settling to 2.68 and resolution of AKI.

    We advised discontinuation of high dose vitamin D but she attributed significant improvement in her MS symptoms to it. After patient’s discharge, it emerged that there was a reporting error (information and technology issue) and the true 25-OHD level in-house was >374 nmol/L by immunoassay, and 862 nmol/L (99.6% vitamin D3) by LC-MS.

    Learning points:
    • Hypercalcaemia secondary to hypervitaminosis D is not widely recognised or reported.
    • PTH may be normal in ‘gradual’ cholecalciferol toxicity, even in presence of hypercalcaemia, unlike in 1,25 dihydroxy Vitamin D toxicity e.g. alfacalcidiol which happens rapidly
    • Patients’ faith in their alternative ‘treatment’, details of which must be sought, may be undeterred despite severe adverse effects.
    • Close liaison with chemical pathology colleagues can help solve an apparent clinical conundrum.
yes, very generally a little of something in the right situation can result in a subjective improvement. such improvements are not automatically transferable to other people in other settings. and they don't necessarily mean that more, or the same amount over a longer time period, will also be safe. far from it. i look forward, with some misgivings, to the day when clinical care and public health get it together.
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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2019 'great idea'

Post by jimmylegs » Sat Oct 05, 2019 3:55 pm

seriously... we're still glossing over cofactors? 'oh hey it's not working, let's throw MORE of what's not working into the broken machine'. makes all the sense. flat tires? cool, let's get that gas tank topped right up for ya. (would be a better analogy if adding fuel also let air out of the tires, but we can't have everything i guess)
  • Comorbidities in multiple sclerosis—a plea for interdisciplinary collaboration to improve the quality of life of MS patients (2019)
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584285/
    ...Future aspects of vitamin D supplementation
    Carlberg et al developed the concept of the “personal VD response index“ and were able to classify persons receiving a VD supplementation as high, medium and low respondents. The “personal VD response index” describes the effectiveness of the molecular response to supplementation with VD. For example, persons with a low VD response index should aim for a high VD status in order to derive maximum benefit from VD’s protective role. This suggests that the dose of daily VD supplementation should be adjusted to the VD response index of the individual and not only to VD status.115 Measuring “vitamin D sensitive molecular parameters” would facilitate the controversial discussion about the recommended VD dose, although the determination in practice is still in the distant future...
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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