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Zur Biochemie bei Vitamin D nach Prof. Dr. Bruce Hollis finden Sie den aktuellen Stand der Diskussion mit meinen email Partnern hier:
http://d.mp3vhs.de/C1/Hollis/Diskussion.docx

Biochemie von Vitamin D:
http://d.mp3vhs.de/C1/Hollis/Hollis.jpg

Biochemie von Vitamin D 3


Der Vitamin D- Stoffwechsel und seine Bedeutung für den
Menschen unter dem Gesichtspunkt eines Paradigmenwechsels
und der Ergebnisse einer 25-0H-Vitamin D Bestimmung von 185
Patienten

http://www.gaertner-servatius.de/downloads/Vitamin-D-Praevention-strauven_hausarbeit.pdf


http://d.mp3vhs.de/C1/pdfs/pdf2.pdf

 

Vitamin D Auszug aus dem Buch „Eumetabolik“

http://www.fatigue-ambulanz.de/files/medium50.pdf


http://d.mp3vhs.de/C1/pdfs/pdf3.

 

Biochemie und Pathobiochemie: Vitamin D-Stoffwechsel


http://de.wikibooks.org/wiki/Biochemie_und_Pathobiochemie:_Vitamin_D-Stoffwechsel


Vitamin D-Status [25(OH)D - und Mortalität von
Hämodialysepatienten


http://www.diss.fu-berlin.de/diss/servlets/MCRFileNodeServlet/FUDISS_derivate_000000008452/SchoberDiss_ohne_CV.pdf

http://d.mp3vhs.de/C1/pdfs/pdf4.pdf

 

Vitamin D - und entzündliche Erkrankung

 

http://edoc.sub.uni-hamburg.de/haw/volltexte/2013/2020/pdf/lsab13_48_BA_VT.pdf

 

http://d.mp3vhs.de/C1/pdfs/pdf5.pdf

 

_________________________________________________________________

Send me an email, if you can answer the following questions?


True or false? – The research of. Prof Hollis  and Prof. Heaney  invalidates all studies about Vitamin D (RCT or not) since and including the Women’s Health Study of 1992 with the consequence, that all the findings in these invalid studies are merely statistical artefacts

True or false? – The biochemical research of Prof. Hollis destroys the relevance of all studies with a weekly or longer dosing interval aiming at non bone-health effects, i.e.preventing or healing chronic diseases like cancer, arthritis, Diabetes, cardiovascular illnesses, MS or infections etc. etc.. Prof. Hollis has proven, that only a daily dosis is  a valid study-parameter in any given Vitamin – D – nutrient study. The consequence thereof is, that all studies, negating this, produce nothing but statistical artefacts.

True or false? –The biometrical finding of Prof. Heaney destroys the relevance of all studies not in compliance with the mandatory necessities for any given scientific-nutrient study of non bone-health effects, i.e.preventing or healing chronic diseases like cancer, arthritis, Diabetes, cardiovascular illnesses, MS or infections etc. etc.. The consequence thereof  is, that all studies, negating this, produce nothing but statistical artefacts.

True or false? – The mandatory requirements (Heaney) for any given nutrient study have a legal consequence. – Any RCT is from the outset unethical.

True or false? – Considering the mandatory requirement für any nutrient study, that the co-nutrients, all of them, have to be in an optimal range, before the study starts, has financial consequences. In nearly all cases, the money necessary for a valid nutrient study is a prohibiting factor for valid research in the nutrient-field.

 

Reference: Design Components of Interventions/Studies of Vitamin D - 15.01.2015 - Prof.Hollis / Prof. Heaney


https://www.youtube.com/watch?v=JGLTD9D2Yxw


http://d.mp3vhs.de/vonabisw/Vitamind3/Wi/Wi19.mp4

______________________________________________

 

25(OH)D  -  Calcidiol
25-hydroxyvitamin D
1,25(OH)2D  -  Calcitriol
1,25-dihydroxyvitamin D
RCT
randomized controlled trial
VDBP
vitamin D binding protein.

VDR – Vitamin D Rezeptor


Biochemische und biometrische Vorbedingungen für valide prospektive Interventionsstudien mit Vitamin D:


Bezug:

Prof. Dr. med. Bruce W. Hollis and Carol L. Wagner
Division of Neonatology, Medical University of South Carolina Children's Hospital, Department of Pediatrics, Charleston, South Carolina -
Vitamin D Dosing Interval -  The Role of the Parent Compound Vitamin D with Respect to Metabolism and Function: Why Clinical Dose Intervals Can Affect Clinical Outcomes 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849670/?report=classichttp://press.endocrine.org/doi/abs/10.1210/jc.2013-2653
http://d.mp3vhs.de/C1/Hollis/1.docx

Die Literatur zur Vitamin D Forschung geht davon aus, daß dem Blutwert 25(OH)D  -  Calcidiol  -  25-hydroxyvitamin D eine zentrale Rolle auch außerhalb des Knochenstoffwechsels zukommt. Dies führt dann auch zu Empfehlungen, daß es ausreiche, Vitamin D einmal wöchentlich oder sogar nur einmal monatlich zu supplementieren.

Die in Bezug genommene Arbeit von Prof. Hollis /Wagner stellt das grundsätzlich in Frage. Danach sind Interventionsstudien zum Scheitern verurteilt und erzeugen nur statistische Artefakte, wenn nicht ein täglicher Dosisintervall eingehalten wird. Begründet wird dies damit, daß Colecalciferol und nicht Calcidiol der wirksame Parameter z.B. in der Krebsprävention ist.

Zitat Hollis/Wagner:

„Control of Circulating Concentrations of Vitamin D, 25(OH)D, and 1,25(OH)2D and Tissue Delivery


The control of circulating concentrations of vitamin D, 25(OH)D, and 1,25(OH)2D is a complex matter, affected by many disease states such as malabsorption syndromes, aberrant vitamin D metabolism as in sarcoidosis and/or disruptions in the calcium homeostatic system, etc (2830). Although these are all important, they are beyond the scope of this short review and are not considered further; consideration is given only to what happens to these compounds under normal conditions when vitamin D is obtained through the diet or UV light induction and how they enter normal cells.
In humans, vitamin D3 is naturally obtained when sunlight in the UVB range strikes the skin and causes 7-dehydrocholesterol to be converted into vitamin D3, which then diffuses into the circulation through the capillary bed (31). Vitamin D also is obtained orally through the diet as either vitamin D2 or D3. As far as can be determined from the literature, this absorption process is primarily diffusion-based, is dependent on bile acid solubilization, and is not saturable (32, 33). When vitamin D3 enters the circulation after UV exposure, it is primarily associated with VDBP. In contrast, after intestinal absorption, it is coupled with both VDBP and lipoproteins (34). Vitamin D from either route is delivered primarily to the liver, where 25(OH)D is produced, becomes associated with VDBP, and is discharged into the circulation (35). However, vitamin D is circulated not only to the liver but also to all tissues in the body; many of these tissues are now known to contain not only the activating hydroxylase but also the vitamin D 25-hydroxylase that converts vitamin D into 25(OH)D, thus achieving autocrine production of 25(OH)D in those tissues (3640) (Figure 1). We believe this to be an underappreciated and very important event that has not yet been adequately considered or investigated.
On reaching the circulation, the primary determinant of how long a vitamin D metabolite will stay in circulation is its affinity for VDBP (1012). Vitamin D, 25(OH)D, and 1,25(OH)2D have vastly different dissociation constants with regard to VDBP: for 25(OH)D, it is approximately 10−9 m, and for vitamin D and 1,25(OH)2D, it is approximately 10−7 m (1012); in addition, for vitamin D, it is probably reduced to approximately 10−8 m by its relative insolubility in vitro (41). These dissociation constants also contribute to the circulating half-lives of these compounds, where for 25(OH)D, it is weeks; for vitamin D, 1 day; and for 1,25(OH)2D, a few hours (42). These dissociation constants also dictate the “free” concentration of compound that is available to diffuse across a cell membrane into cells to be metabolized or to modulate cell activity (see Figure 1). In the case of these three compounds, the “free” circulating concentrations are greater for 1,25(OH)2D than for intact vitamin D, which in turn are larger than that of 25(OH)D, matching their relative circulating half-lives.
Besides simple cellular diffusion of free compound, there exists another important tissue transport mechanism for these steroids—the megalin-cubilin endocytotic system (9). This system is key in the delivery of 25(OH)D to the 25-hydroxyvitamin D-1-α-hydroxylase in the kidney (9), and it also exists in the parathyroid glands, so that its important role in the endocrine function of vitamin D is self-evident (43). The megalin-cubilin system also functions in the placenta (43), which we will revisit later. However, where tissues lack this endocytotic system, diffusion of vitamin D compounds in relation to free circulating concentrations becomes inherently important. Interestingly, VDBP-knockout animal models show normal survival when given dietary vitamin D on a daily basis (44, 45); because vitamin D metabolite cellular access could only be by diffusion in these animals, this shows that the parent compound vitamin D is normally transferred in wild-type animals through simple membrane diffusion.


Dosing with Vitamin D and Relative Sustainability of the Compounds in the Circulation


Vitamin D is introduced into the human body in two ways, orally or by UV exposure. UV exposure is the natural way by which humans receive their vitamin D, but now, due to a variety of lifestyle changes, it is mostly obtained from oral sources. Adams et al (46) first described the magnitude and time course by which vitamin D3 is produced and released into the circulation. This work clearly demonstrated that the human body could produce and release thousands of IU of vitamin D3 into the circulation within 24 hours of modest UV exposure (46), whereas orally ingested vitamin D3 appears in the circulation at a more rapid pace, with a 12-hour peak rather than a 24-hour peak (34, 46, 47). Furthermore, there is a different plasma distribution of vitamin D in oral vs UV-stimulated release (34); yet, the circulating half-life of the compound by either route is of the order of 12–24 hours (34). Because of this short half-life, even large bolus vitamin D doses of 50 000 to 100 000 IU are cleared from the circulation within a week, making vitamin D basically undetectable in the circulation (4649). It was largely assumed that after a large bolus dose or UV exposure the rapidly disappearing vitamin D was stored in adipose tissue to be released at a later time. This has recently been shown not to occur, however, because it does not reappear in the systemic circulation at detectable concentrations (49). Early work has demonstrated vitamin D to be excreted in bile, feces, and urine (50). Thus, the only known way to sustain constant circulating vitamin D concentrations is by daily supplementation and/or chronic UV exposure (51, 52).
From a supplementation standpoint, one would have to supply an adult with a dose that would achieve increases in circulating vitamin D. For instance, a 400 IU/d dose for several months will achieve little or no detectable effect on the circulating concentration of vitamin D (51, 53). However, if one supplements adults for extended periods with 2000–6000 IU/d vitamin D3, stable circulating concentrations of vitamin D are maintained in the range of 10–40 ng/mL in a linear fashion (51, 53), although what constitutes a minimal dosage of vitamin D for achieving an optimal circulating vitamin D concentration remains to be determined.
What is the time course for the systemic appearance of 25(OH)D after acute or chronic dosing of vitamin D3? 25(OH)D does not appreciably increase in the systemic circulation until about 24 hours after oral supplementation with 100 000 IU vitamin D2, and then by only 1–4 ng/mL (54). Chronic daily dosing of vitamin D will result in a slow, sustained rise in circulating 25(OH)D that will reach a steady state at 3–4 months (55, 56), whereas acute, interval, or large bolus dosing with vitamin D results in a variety of appearance and disappearance rates (15, 49, 5760).
Given the pharmacokinetics of vitamin D and 25(OH)D, investigators considering performing a clinical trial with vitamin D should consider the above information and what the circulating profiles of vitamin D and 25(OH)D might be on dosing of 400, 1000, 2000, or 4000 IU/d; 28 000 IU/wk; 120 000 IU/mo; 360 000 IU every 3–4 months; or some higher annual dose. All of these schedules have been utilized in various clinical trials (1527, 51, 53, 5777). All of these dosing schedules appear to be well tolerated in normal adults from a toxicity standpoint because none results in hypercalcemia or hypercalciuria (1527, 51, 53, 5777). However, these doses will differ greatly in their impact on circulating concentrations of vitamin D and 25(OH)D; daily doses of vitamin D result in stable circulating concentrations of both compounds (51), whereas weekly or longer interval dosing will result in large fluctuations….”

Die Messung des Blutwerts 25(OH)D  -  Calcidiol  -  25-hydroxyvitamin D kann demnach keine Information zum Präventionsstatus liefern. Dieser Wert ist dann für den Knochenstoffwechsel weiterhin relevant, nicht aber für die übrigen Gewebearten. Allenfalls kann man daraus Resorptionswerte von Colecalciferol ableiten.
Wegen der Kurzlebigkeit von Colecalciferol im Blut wird dann die Dosisempfehlung pro Tag zu präventiven Zwecken jedenfalls z.Zt. schwierig. Da fast alle neuen Interventionstudien unterhalb von 10.000 I.E. angelegt sind, bleibt für eine Tagesdosis von 10.000 IE oder mehr nur mehr die Schätzung.

Vitamin D Biochemie nach Prof. Hollis – Stellungnahmen:

1.)
Vitamin D sollte tatsächlich täglich eigenommen werden. Die Dosierungen pro Tag liegen bei Erwachsenen bei 5000 bis 15.000 IE / Tag. 
Mit freundlichen Grüßen,
Dr. med. Rainer Didier - Praxis für ganzheitliche individuelle Medizin
Facharzt für Allgemeinmedizin - Klassische Homöopathie - Ernährungsmedizin, Naturheilverfahren - Neuraltherapie, Medizinische und Psychologische Hypnose – Umweltmedizin _ Nordhofstr. 173 - 32130 Enger - Tel. : 05224-994677 - www.dieSanfteMedizin.de - Facebook: DieSanfteMedizin - Facebook: OhneSchadstoffe