Van alles m.b.t. Vitamine D

Onderwerpen met wetenschappelijke, medische of algemene gezondheidsgerelateerde informatie en discussie dat niet specifiek betrekking heeft op de ziekte van Lyme.
Berichten: 224
Lid geworden op: Za 11 Mei 2013 11:52

Re: Van alles m.b.t. Vitamine D

Berichtdoor Diesel » Ma 1 Jul 2013 15:37

Lijkt inmiddels wel gedateerde info van R. Heaney (filmpje 2010) op diverse punten o.a. zijn bewering over Vit.D intoxicatie er uit gelicht gelet op een recente publicatie in 2012.

Vitamin D: Health panacea or false prophet? ... attId=2363

However, this point of view may be excessively optimistic. There also is evidence that despite the current heavy reliance on serum 25-OHD3 concentration for the diagnosis of an individual’s vitamin D status, local tissue vitamin D intoxication may be present in individuals with much lower serum 25-OHD3 concentrations than are currently appreciated. Only rarely are the symptoms of local tissue vitamin D intoxication associated with vitamin D status or intake. An individual’s serum 25-OHD3 concentration may appear to be “low” for reasons totally independent of sunlight exposure or vitamin D intake. Serum 25-OHD3 concentration is only poorly responsive to increases in vitamin D intake, and the prolonged routine consumption of thousands of international units of vitamin D may interfere with the regulation of phosphate homeostasis by fibroblast growth factor-23 (FGF23) and the Klotho gene product, with consequences that are detrimental to human health. In light of these counterbalancing observations, curbing excessive enthusiasm for universally increasing vitamin D intake recommendations may be in order.

In addition, genetic polymorphisms, toxic insults, autoimmune disease, gradually accumulating oxidative damage, or chronic mineral imbalances may result in dysfunctional vitamin D receptors with reduced affinity for 1,25-OH2 D3 and reduced ability of 1,25-OH2 D3 to induce the activity of renal CYP24A1, allowing 1,25-OH2D3 concentration to rise while relieving some of the negative feedback inhibition of the conversion of 25-OHD3 to 1,25-OH2D3 [105,106]. When an excess of dietary vitamin D is present, elevated systemic and local concentrations of 1,25-OH2 D3 can occur. When an excess of 1,25-OH2 D3 is present within a tissue, local hypervitaminosis D can be produced. In the mildly compromised kidney, local hypervitaminosis D can produce hyperphosphatemia, triggering increased FGF23 secretion, whereas elevated 1,25-OH2D3 concentration can inhibit hepatic 25-hydroxylation of ingested vitamin D, resulting in concurrent renal hypervitaminosis D and low serum 25-OHD3 concentration[100]. A desire to establish a higher serum 25-OHD3 concentration may encourage undue clinical reliance on potentially counterproductive dietary supplementation with increasing amounts of vitamin D.

In such a scenario, local vitamin D toxicosis can occur and produce renal atrophy and calcification that may go unrecognized until clinical signs of “idiopathic” renal disease appear [107] Although Queen acknowledges that vitamin D plays important preventive and therapeutic roles in supporting human health, he cautions that renal and cardiovascular toxicity and increased mortality can be caused by covert physiologic vitamin D toxicosis [107]. For example, in the presence of age-associated reduction in Klotho expression, prolonged supplementation with large Klotho-suppressing amounts of vitamin D may produce 1,25-OH2 D3 excess and low serum 25-OHD3 concentration while increasing the risk of the expression of an aberrant FGF23 gene product that fails to regulate renal phosphate reabsorption, resulting in hyperphosphatemic tumoral calcinosis with carotid artery calcification [108,109].

Queen also expresses concerns that the current interpretation of vitamin D requirements and contributions to human health results from an excessive reliance on epidemiologic evidence (the science of association) that has become dissociated from the basic science of vitamin D and mineral homeostasis. He suggests that rather than reflecting inadequate exposure to vitamin D, a low serum 25-OHD3 concentration may reflect, in some individuals, a set of internal homeostatic attempts to correct an excess of free calcium ions and therefore, viewed from a basic science perspective, a strong argument can be made for the conclusion that in some individuals, a low serum 25-OHD3 concentration results from disease rather than produces disease.

In cautioning against excessive enthusiasm for increasing vitamin D intake recommendations, Queen emphasizes the following key points:

Despite the current heavy reliance on serum 25-OHD3 concentration for the diagnosis of an individual’s vitamin D status, local tissue vitamin D intoxication may be present in individuals with much lower serum 25-OHD3 concentrations than are currently appreciated.

• Only rarely are the symptoms of local tissue vitamin D associated with vitamin D status or intake.

• A serum 25-OHD3 concentration may appear to be “low” for reasons totally independent of sunlight exposure or vitamin D intake. Serum 25-OHD3 concentration is only poorly responsive to increases in vitamin D intake.

• The prolonged routine consumption of megadoses of vitamin D may interfere with Klotho and FGF23 regulation of phosphate homeostasis with consequences that are detrimental to health.

The recent rush to elevate serum 25-OHD3 concentrations universally may benefit from a brief pause to reflect on the actual merits (and potential pitfalls) of doing so. Despite the detailed and persuasive data presented by Holick and his colleagues, reconsideration of the paradigm that a single or even a few biochemical markers can provide meaningful insight into the health status of an individual may be appropriate. This may be an area in which the modern reductionist approach to medical nutrition can benefit from an organismal reassessment.

The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures ... b-0439.pdf

Resolution of vitamin D intoxication was associated with a rebound in bone mineral density. In the long run, the best way to reverse the condition is to bring the level of 1,25D in the body back into a range where minerals will no longer be leached from the bones and the level of inflammatory cytokines can return to normal. In the meantime, getting the RDA of calcium from foods and supplements without vitamin D can be helpful.[69] Another misconception among some clinicians is the idea that vitamin D enhances the absorption of calcium. This is not the case. 25-D is a simple steroid which does not affect the genes responsible for calcium absorption. In contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,[6] some of which do affect the metabolism of calcium.

Ter aanvulling: twee sluipmoordenaars respectievelijk botontkalking en aderverkalking (het dicht metselen van je bloedvaten) door verhoogde 1,25D gehalten zijn geen acute Vit.D intoxicatie verschijnselen. Wel lange termijn sloop effecten op je gezondheid.

''Hij is wijs, die weet, dat hij niets weet''

My weblog tells you more about Vit.B12 deficiency

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Di 2 Jul 2013 13:17

Mensen die gevoelig zijn voor gluten nemen vitamine d oraal minder goed in de darmen op:
Where does vitamin D fit into all of this? We know that persons with celiac disease have low blood levels of vitamin D. This is thought to be due their inability to absorb the vitamin D. The atrophy (cell death) that occurs in the small bowel makes it virtually impossible for patients with advanced celiac disease to absorb vitamin D.

It is also possible that low vitamin D early in life can lead to celiac disease. This has to do with vtamin D’s actions.

Berichten: 224
Lid geworden op: Za 11 Mei 2013 11:52

Re: Van alles m.b.t. Vitamine D

Berichtdoor Diesel » Wo 3 Jul 2013 18:13

bamboe schreef: Mensen die gevoelig zijn voor gluten nemen vitamine d oraal minder goed in de darmen op:

We know that persons with celiac disease have low blood levels of vitamin D. This is thought to be due their inability to absorb the vitamin D.

De hoeveelheden Vit.D in voeding voor absorptie is marginaal dan wel verwaarloosbaar te noemen om significante verschuivingen in de 25D (calcidiol) waarde te doen plaats vinden. Zowel voor een coeliakie patiënt, met een zogezegd absorptie probleem, als wel voor een persoon zonder coeliakie zonder een absorptie probleem.

Vit.D gehalten van voedingsmiddelen ... n/volledig

In dit tijdschrift spraken Blom et al. onlangs over het belang van het gebruik van ‘vitamine D bevattende voedingsbestanddelen, zoals melk, boter, kaas en eieren’.1 Hier is sprake van een wel vaker voorkomend misverstand. Blijkens recente analyses bevatten melk, roomboter (‘echte’ boter) of kaas van nature namelijk slechts verwaarloosbare hoeveelheden vitamine D.2-5

Hierbij kan nog aan toegevoegd worden dat de ‘gepasteuriseerde’ melk uit het 'schap van Ap' blijkbaar een slap aftreksel is voor je Vit.D voorziening.

Secosteroïd Vit.D en voeding: Verrijking niet verplicht, toevoeging ook niet verboden.

suggestie: lees het gehele artikel.

http://b12vitaminetekortpodium.blogspot ... jking.html

Pasteurized Milk: Killing the bad AND the Good (61)

Citaat: Vitamins A, B6, B12, C, D, and E are reduced to some degree during the pasteurization process. The amount of damage depends on the type of pasteurization.

Real milk (62)

Citaat: Pasteurization destroys not only harmful bacteria, but benificial bacteria as well. It also destroys enzymes, making digestion difficult for the human system. Pasteurization makes proteins less bioavailable, and it alters amino acids and some vitamins. Natural Vitamin D, for example, is destroyed and has to be added back artificially, to pasteurised milk

De zon wordt gezien als primaire bron voor het overgrote deel aan Vit.D voor een ieder hierin. Vandaar dat de 25D waarde bij de mens in de regel (bij blootstelling: 10 á 15 min handen en gezicht zonder sunblocker is genoeg) in de zomer periode veelal het hoogste niveau kan bereiken. Of je nu coeliaak bent of niet. Je hebt geen zogenaamd Vit.D opname probleem in je huid.

De D vorm die fotochemisch (synthese) geproduceerd wordt door de inwerking van buiten(zon)licht van de sterol precursor 7-dehydrocholesterol die aanwezig is in de epidermus in de huid is pre-D3, en nog geen (molecuul) D3. De geproduceerd pre-D3 in de huid voor gebruik, wordt naar de lever getransporteerd waar de welbekende D3 (calcidiol) wordt gemaakt. Wanneer de 25D (calcidiol) waarde in de zomer periode (zonlicht dan wel Vit.D suppletie gebruik) niet stijgt, is dit een gerede aanwijzing voor een 1,25D bepaling. Ongeacht welke aandoening dan ook.

Vitamin D is a secosteroid. It binds to the vitamin D receptor and thus regulates gene activities.

De blog schrijver maakt melding van het feit dat Vit.D een secosteroid is. Voor de duidelijkheid een seco steroid is een hormoon met steroide werking (geen nutriënt dan wel een echte vitamine).

Vitamin D: The secosteroid hormone and human reproduction

Cholecalciferol is the natural form of vitamin D in humans, although it lacks significant biological effects.

Wat betreft het binden aan de VDR (Vitamine D Receptor) en het reguleren van gene activiteit. De auteur van deze blog vermeldt er helaas niet bij dat het hier betreft om de actieve metaboliet 1,25D (calcitriol).

Vitamin D Insufficiency

Mayo clinic

Vitamin D receptor

The steroid hormone 1,25(OH)2D3, like other steroid hormones, generates biological responses by regulating gene transcription (genomic responses) and by activating a variety of signal transduction patways at or near plasma membrane (nongenomic rapid responses) (22). The genomic responses are due to stereospecific interaction of 1,25(OH)2D3 with its nuclear receptor, VDR. The primary amino acid sequence of the VDR consists, like in other steroid hormone receptors, of 6 functional domains: the variable regions, DNA binding, the hinge region, the ligand binding region, and the transcriptional activation domain (2). Formation of the ligand-receptor complex results in conformational changes in the receptor protein, which allow the ligand-receptor complex to specifically interact with many proteins from the transcriptional machinery. It is estimated that the VDR can regulate the expression of as many as 500 of the 20 488 genes in the human genome (23). The large number of VDR-regulated genes undoubtedly reflects the consequence of the distribution of both the VDR and 25(OH)D3-1a-hydroxylase to many organs.

The characteristics of 1,25(OH)2D are those of a hormone, and consequently vitamin D is a prohormone rather than a true vitamin. The structure of 1,25(OH)2D is similar to that of other steroid hormones.

blog schrijver:

Where does vitamin D fit into all of this?

We know that persons with celiac disease have low blood levels of vitamin D.

Zou dit ook gelden voor coeliakie patiënten in zonnig Afrika, Hawaï, Californie of Australië etc. die relatief meer aan zonlicht blootgesteld worden? Ik heb niet de indruk dat de coeliakie patiënten aldaar als Zorro ‘look a like’ door het leven gaan of een boerka dragen tot de standaard garderobe uitrusting behoort.

Overigens valt het mij op dat deze blog schrijver wel verhaaltjes schrijft, in dit artikel over coeliakie. Echter bronvermeldingen naar wetenschappelijk c.q. literatuurstudies zijn schaars dan wel in zijn geheel niet aanwezig. Lijkt mij niet onbelangrijk. Aangezien hij afsluit met zijn volgende gedachten gang:

Does this mean a normal person with a low vitamin D level could develop celiac disease?

This has not been studied as far as I know and will need to be the topic of a future study to answer that question.

Als er nog geen studies hebben plaats gevonden, wordt het voor deze auteur haast onmogelijk om een bronvermelding van enig gezaghoudende waarde te plaatsen.

Hierbij kan nog vermeld worden dat deze auteur (artikel 2011) vermoedelijk is uit gegaan van een ‘onbetrouwbare’ biomarker voor bepaling van de Vit.D status (is hem niet aan te rekenen op het moment van schrijven).

Hypovitaminosis D and disease; consequence rather than cause?

Published 24 August 2012 ... 6.full.pdf

Volgens deze ‘scientists’ is het serum 25OHD een ‘negatieve acute fase reactant’ en dit heeft gevolgen voor acute en chronische ziekten. Ten eerste, is serum 25OHD een ‘onbetrouwbare’ biomarker van de Vit.D status na een acute inflammatie aanval. Ten tweede, brengen wij ten berde dat hypovitaminose D mogelijk eerder het ‘gevolg’ is dan de algemeen beweerde ‘oorzaak’ van ontelbare chronische ziekten.

Serum 25OHD is a negative acute phase reactant and this has implications for acute and chronic diseases. Firstly, serum 25OHD is an unreliable biomarker of vitamin D status following an acute inflammatory insult. Secondly, we suggest that hypovitaminosis D may be the consequence rather than the widely purported cause of a myriad of chronic diseases

blog schrijver:

Celiac disease is an autoimmune disease.

Wellicht een eye-opener voor deze blog schrijver voor de toekomst: ... l=Medicine

Current studies are aimed at assessing the antigenic specificity and pathogenic relevance of the immune response to gluten, using proteomic approaches and in vitro and in vivo models. In addition, we are studying the role of immune mechanisms in the persistence of symptoms following exposure to pathogens, particularly in the context of infection with Borrelia burgdorferi in Lyme disease (Chandra et al., Clin Immunol, 2011; Jacek et al., J Neuroimmunol, 2013; Ajamian et al., JAMA, 2013).

Chronic Lyme Disease and co-infections: Differential Diagnosis ... TONEUJ.pdf

Parotid swelling, phlegmonous abcess in the neck region, septic shock, thrombocytopenic purpura, overproduction of calcitriol

Celiac and D metabolite levels

Some patients with celiac disease have low/normal 25D but elevated 1,25D apparently related to celiac. For examples, see PubMed articles 8186825 and 15310538
Quoting 15310538, “Our patient had hypocalcemia caused by celiac disease and values for serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D that were normal and elevated, respectively. Correction was demonstrated after dietary gluten withdrawal.”

Het merendeel van de gepresenteerde artikelen over Vit.D zijn gebaseerd op veelal epidemiologische studies (wetenschap van associaties). In zijn algemeenheid oude wijn in nieuwe zakken info, die in de regel geen causale uitkomst data bevatten, maar verbanden leggen tussen de bijvoorbeeld voedingstoffen en ziekte. Het artikel van deze blog schrijver als voorbeeld (herhaling van zetten).

''Hij is wijs, die weet, dat hij niets weet''

My weblog tells you more about Vit.B12 deficiency

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Zo 27 Okt 2013 13:49

Am J Clin Nutr. 2013 Oct 9. [Epub ahead of print]
Effect of vitamin D supplementation on antibiotic use: a randomized controlled trial.
Tran B, Armstrong BK, Ebeling PR, English DR, Kimlin MG, van der Pols JC, Venn A, Gebski V, Whiteman DC, Webb PM, Neale RE.

Population Health Department, Queensland Institute of Medical Research, Brisbane, Queensland, Australia (BT, DCW, PMW and REN); the Centre for Research Excellence in Sun and Health, Queensland University of Technology, Kelvin Grove, Queensland, Australia (BT, MGK, DCW and REN); the School of Population Health, University of Queensland, Brisbane, Queensland, Australia (JCvdP); the Sydney School of Public Health (BKA) and the National Health and Medical Research Council of Australia Clinical Trials Centre, Sydney Medical School (VG), University of Sydney, Camperdown, New South Wales, Australia; Northwest Academic Centre, University of Melbourne, and Western Health, Melbourne, Victoria, Australia (PRE); the School of Population Health, University of Melbourne, Parkville, Victoria, Australia (DRE); the AusSun Research Laboratory, Queensland University of Technology, Kelvin Grove, Queensland, Australia (MGK); and the Menzies Research Institute Tasmania, Hobart, Tasmania, Australia (AV).

Observational data suggested that supplementation with vitamin D could reduce risk of infection, but trial data are inconsistent.

We aimed to examine the effect of oral vitamin D supplementation on antibiotic use.

We conducted a post hoc analysis of data from pilot D-Health, which is a randomized trial carried out in a general community setting between October 2010 and February 2012. A total of 644 Australian residents aged 60-84 y were randomly assigned to receive monthly doses of a placebo (n = 214) or 30,000 (n = 215) or 60,000 (n = 215) IU oral cholecalciferol for ≤12 mo. Antibiotics prescribed during the intervention period were ascertained by linkage with pharmacy records through the national health insurance scheme (Medicare Australia).

People who were randomly assigned 60,000 IU cholecalciferol had nonsignificant 28% lower risk of having antibiotics prescribed at least once than did people in the placebo group (RR: 0.72; 95% CI: 0.48, 1.07). In analyses stratified by age, in subjects aged ≥70 y, there was a significant reduction in antibiotic use in the high-dose vitamin D compared with placebo groups (RR: 0.53; 95% CI: 0.32, 0.90), whereas there was no effect in participants <70 y old (RR: 1.07; 95% CI: 0.58, 1.97) (P-interaction = 0.1).


Although this study was a post hoc analysis and statistically nonsignificant, this trial lends some support to the hypothesis that supplementation with 60,000 IU vitamin D/mo is associated with lower risk of infection, particularly in older adults. The trial was registered at the Australian New Zealand Clinical Trials Registry ( as ACTRN12609001063202. ... t=Abstract

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Zo 27 Okt 2013 14:28

Hypovitaminosis D is associated with increased whole body fat mass and greater severity of non-alcoholic fatty liver disease.
Dasarathy J, Periyalwar P, Allampati S, Bhinder V, Hawkins C, Brandt P, Khiyami A, McCullough AJ, Dasarathy S.

Department of Family Medicine, MetroHealth Medical Center, Cleveland, OH, USA.

Hypovitaminosis D is common in obesity and insulin-resistant states. Increased fat mass in patients with non-alcoholic fatty liver disease (NAFLD) may contribute to hypovitaminosis D. To determine the relation among plasma vitamin D concentration, severity of disease and body composition in NAFLD.

Plasma vitamin D concentration was quantified in 148 consecutive biopsy-proven patients with NAFLD (non-alcoholic steatohepatitis - NASH: n = 81; and hepatic steatosis: n = 67) and healthy controls (n = 39). NAFLD was scored using the NASH CRN criteria. Body composition was quantified by bioelectrical impedance analysis and abdominal CT image analysis.

Plasma vitamin D concentration was significantly lower in NAFLD (21.2 ± 10.4 ng/ml) compared with healthy controls (35.7 ± 6.0 ng/ml). Higher NAFLD activity scores were associated with lower plasma concentration of vitamin D (r2 = 0.29; P < 0.001). Subgroup analysis among patients with NAFLD showed that patients with NASH had significantly lower (P < 0.01) vitamin D levels than those with steatosis alone (18.1 ± 8.4 vs. 25.0 ± 11.3 ng/ml). Low concentrations of vitamin D were associated with greater severity of steatosis, hepatocyte ballooning and fibrosis (P < 0.05).On multivariate regression analysis, only severity of hepatocyte ballooning was independently associated (P = 0.02) with low vitamin D concentrations. Plasma vitamin D (P = 0.004) and insulin concentrations (P = 0.03) were independent predictors of the NAFLD activity score on biopsy. Patients with NAFLD had higher fat mass that correlated with low vitamin D (r2 = 0.26; P = 0.008).

Low plasma vitamin D concentration is an independent predictor of the severity of NAFLD. Further prospective studies demonstrating the impact of vitamin D replacement in NAFLD patients are required.

© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. ... t=Abstract

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Ma 11 Nov 2013 22:20

In deze donker wordende dagen is het niet verkeerd om zoveel mogelijk zon te pakken. Vitamine D blijkt namelijk niet alleen goed voor je botten, maar ook tegen tandbederf.

‘Vooral niet te lang in de zon zitten’, zo luidt het credo tegenwoordig. Daardoor hebben de meesten van ons een tekort aan vitamine D en dat blijkt tandbederf vrijer spel te geven. Dit is aangetoond door onderzoekers aan de universiteit van Washington, in Seattle, die vaststelden dat voldoende vitamine D wel 50 procent minder kans geeft op gaatjes.

We wisten al dat vitamine D goed is voor je botten, maar ook voor je tanden? Dat laatste heeft de tandheelkundige wereld zestig jaar lang weerlegd, maar de analyse van 24 klinische onderzoeken met 3000 kinderen uit diverse landen is duidelijk: vitamine D zorgt voor sterkere tanden.

D ook voor de aderen
Een tekort aan vitamine D speelt niet zomaar een rol bij diabetes: onderzoekers stelden vast dat het bij diabetespatiënten dé oorzaak is van verstopte aderen en hartfalen. Vitamine D vertraagt namelijk het ontstekingsproces bij diabetes, waarbij immuuncellen zich binden aan bloedvaten bij het hart.

Bij een vitamine-D-tekort blijkt een bepaald soort wittebloedcellen zich eerder dan gebruikelijk te binden aan cellen in de slagaderwanden, aldus onderzoekers aan de Washington University School of Medicine in St. Louis.

Dit artikel verscheen eerder in Medisch Dossier, Wat artsen je niet vertellen, een maandelijks magazine over gezondheid, therapieën en behandelingen en de alternatieven die ervoor bestaan. ... 875EA1C8E2

Berichten: 2342
Lid geworden op: Di 19 Apr 2011 19:52

Re: Van alles m.b.t. Vitamine D

Berichtdoor Tulipano » Do 14 Nov 2013 21:42

Rosalind Peterson (een landbouwdeskundige uit de VS) vertelt tijdens een interview over cloud seeding (Geo Engineering/Weather Manipulation/ Climate control/Chemtrails) dat een groeiend aantal kinderen in de VS lijden aan de botziekte Rickets:

Rickets is a softening of bones in immature mammals due to deficiency or impaired metabolism of vitamin D,[1] phosphorus or calcium,[2] potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets (cases of severe diarrhea and vomiting may be the cause of the deficiency). Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood.

Osteomalacia is a similar condition occurring in adults, generally due to a deficiency of vitamin D.[3]

Signs and symptoms of rickets include:
Bone tenderness
dental problems
muscle weakness (rickety myopathy)
increased tendency for fractures (easily broken bones), especially greenstick fractures
Skeletal deformity
Toddlers: Bowed legs (genu varum)]
Older children: Knock-knees (genu valgum) or "windswept knees"
Cranial deformity (such as skull bossing or delayed fontanelle closure)
Pelvic deformity
Spinal deformity (such as kyphoscoliosis or lumbar lordosis)
Growth disturbance
Widening of wrist raises early suspicion, it is due to metaphyseal cartilage hyperplasia.

Cases have been reported in Britain in recent years of rickets in children of many social backgrounds caused by insufficient production in the body of vitamin D because the sun's ultraviolet light was not reaching the skin due to use of strong sunblock, too much "covering up" in sunlight, or not getting out into the sun. Other cases have been reported among the children of some ethnic groups in which mothers avoid exposure to the sun for religious or cultural reasons, leading to a maternal shortage of vitamin D; and people with darker skins need more sunlight to maintain vitamin D levels. The British Medical Journal reported in 2010 that doctors in Newcastle on Tyne saw 20 cases of rickets per year. Rickets had been a significant malaise in London, especially during the Industrial Revolution. Persistent thick fog and heavy industrial smog permeating the city blocked out significant amounts of sunlight so much so that up to 80 percent of children at one time had varying degrees of rickets in one form or the other.


Met volgende details:

Asian immigrants living in Europe have an increased risk for Vitamin D deficiency. Vitamin D insufficiency was found in 40% of non-Western immigrants in the Netherlands, and in more than 80% of Turkish and Moroccan immigrants.


Mistaken for child abuse

Infants with rickets often suffer bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation.[25] People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight.

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Do 14 Nov 2013 23:55

hoi Tulipano, zou er een relatie zijn met darmproblemen bij vitamine D-gebrek (en waar zouden die dan vandaan komen?):

Orv Hetil. 2013 Nov;154(46):1821-8. doi: 10.1556/OH.2013.29750.
[Vitamin D level in Hungarian patients with inflammatory bowel diseases].
[Article in Hungarian]
Lőrinczy K, Lakatos PL, Tóth M, Salamon A, Nemes A, Csontos AA, Fekete B, Terjék O, Herszényi L, Juhász M, Tulassay Z, Miheller P.

Semmelweis Egyetem, Általános Orvostudományi Kar II. Belgyógyászati Klinika Budapest Szentkirályi u. 46. 1088.
in English, Hungarian

Introduction: Vitamin D has an important role in the immune regulation. Vitamin D is essential for innate and adaptive immune systems and it plays a significant role in the formation of immune tolerance, as well. Aim: Vitamin D deficiency has been observed in patients with inflammatory bowel diseases in Western Europe, but there is no data available from Eastern Europe. Method: The study included 169 patients with inflammatory bowel disease. Results: The median vitamin D level was 22.7±10.6 ng/ml. Only 20% of the patients had adequate vitamin D level (>30 ng/ml), 52% had vitamin D insufficiency (15-30 ng/ml), and 28% of them had severe vitamin D deficiency (<15 ng/ml). Vitamin D concentration failed to correlate with clinical activity indexes (partial Mayo score: r = -0.143; Crohn's disease activity index: r = -0.253) and with inflammatory parameters (C-reactive protein: r = 0.008; erythrocyte sedimentation rate: r = 0.012). Conclusions: Since vitamin D deficiency can be frequently observed in Hungarian patients with inflammatory bowel disease, its level should be tested in these patients. Orv. Hetil., 154(46), 1821-1828.

Rickets (Rachitis) leidt o.a. tot tandrot.
Als je honden volkoren graan geeft, dan hebben ze sneller last van Rachitis, dan als je diezelfde honden geraffineerd graan geeft.
Graan, en helemaal volkoren graan, rooft een lichaam van vitamine d.
Ook rooft graan en nog meer: volkoren graan mensen ook van vitamine c.
Bron: Genees Tandbederf van Ramiel Nagel.

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Lid geworden op: Di 19 Apr 2011 19:52

Re: Van alles m.b.t. Vitamine D

Berichtdoor Tulipano » Vr 15 Nov 2013 0:30

Bamboe, helaas moet ik je het antwoord schuldig blijven. Als ik het artikel goed begrijp heeft onderzoek uitgewezen dat een aanzienlijk aantal Hongaarse patiënten die een vit. D tekort hebben dus ook lijden aan darmaandoeningen/-ontstekingen. En als je denkt aan het grote aantal mensen in Europa en de VS met een vit. D tekort en het grote aantal mensen met darmaandoeningen daar, dan zou je inderdaad een verband zien. Anderzijds lees ik in het Marshall Protocol ( dat een teveel aan vit. D het immuunsysteem kan onderdrukken waardoor je ook weer van alles en nog wat kan gaan mankeren. Aangezien ik last heb van darmontstekingen maar ook een hele slechte weerstand, zal ik zeker mijn vit. D waarden laten controleren, want ik wil nu toch wel eens weten welke situatie voor mij van toepassing is.

Berichten: 4028
Lid geworden op: Di 23 Dec 2008 4:30

Re: Van alles m.b.t. Vitamine D

Berichtdoor bamboe » Vr 15 Nov 2013 0:46
Bone pain and extremely low bone mineral density due to severe vitamin D deficiency in celiac disease
Arch Osteoporos. 2011 December; 6(1-2): 209–213.
Published online 2011 June 15. doi: 10.1007/s11657-011-0059-7
Noortje M. Rabelink,corresponding author1 Hans M. Westgeest,1 Nathalie Bravenboer,2 Maarten A. J. M. Jacobs,3 and Paul Lips1
Dramatic effect of vitamin D supplementation and a gluten-free diet on bone mineral density in a patient with celiac disease.
J Clin Densitom. 2012 Jan-Mar;15(1):120-3. doi: 10.1016/j.jocd.2011.07.003. Epub 2011 Aug 31.
Duerksen DR, Ali M, Leslie WD.
Department of Medicine University of Manitoba, Winnipeg, Manitoba, Canada.

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