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Old 11-12-2009, 02:52 PM   #1
Rich66
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Vitamin D

(potentiates chemo-formulations matter, tests matter, Eag1, w/antihistamine, immune enhancer, insulin regulator, w/resveratrol, w/cytoxan, w/AI, w/Vit K menadione, reduces AI side fx, 25OH test best, Calcitriol better?, paricalcitrol available?, phosphorus intake reduces D levels)


2/2010
ABC report on Vitamin D and breast cancer. Mentions "potent form" but doesn't specify.

http://abcnews.go.com/GMA/OnCall/stu...ory?id=9904415



Cancer J. 2010 January/February;16(1):1-9.
Vitamin D: Considerations in the Continued Development as an Agent for Cancer Prevention and Therapy.

Trump DL, Deeb KK, Johnson CS.
From the Departments of *Medicine, and daggerPharmacology and Therapeutics, The Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY.
Considerable preclinical and epidemiologic data suggest that vitamin D may play a role in the pathogenesis, progression, and therapy for cancer. Numerous epidemiologic studies support the hypothesis that individuals with lower serum vitamin D levels have a higher risk of a number of cancers. Measures of vitamin D level in such studies include both surrogate estimates of vitamin D level (residence in more northern latitudes, history of activity, and sun exposure) as well as measured serum 25(OH) cholecalciferol levels. Perhaps, the most robust of these epidemiologic studies is that of Giovannucci et al, who developed and validated an estimate of serum 25(OH) cholecalciferol level and reported that among >40,000 individuals in the Health Professionals Study, an increase in 25(OH) cholecalciferol level of 62.5 ng/mL was associated with a reduction in the risk of head/neck, esophagus, pancreas cancers, and acute leukemia by >50%. Unfortunately, very limited data are available to indicate whether or not giving vitamin D supplements reduces the risk of cancer. Many preclinical studies indicate that exposing cancer cells, as well as vascular endothelial cells derived from tumors, to high concentrations of active metabolites of vitamin D halts progression through cell cycle, induces apoptosis and will slow or stop the growth of tumors in vivo. There are no data that one type of cancer is more or less susceptible to the effects of vitamin D. Vitamin D also potentiates the antitumor activity of a number of types of cytotoxic anticancer agents in in vivo preclinical models. Vitamin D analogues initiate signaling through a number of important pathways, but the pathway(s) essential to the antitumor activities of vitamin D are unclear. Clinical studies of vitamin D as an antitumor agent have been hampered by the lack of a suitable pharmaceutical preparation for clinical study. All commercially available formulations are inadequate because of the necessity to administer large numbers of caplets and the poor "bioavailability" of calcitriol (the most carefully studied analogue) at these high doses. Preclinical data suggest that high exposures to calcitriol are necessary for the antitumor effects. Clinical data do indicate that high doses of calcitriol (>100 mcg weekly, intravenously, and 0.15 mug /kg weekly, orally) can be given safely. The maximum tolerated dose of calcitriol is unclear. While a 250-patient trial in men with castration-resistant prostate cancer comparing docetaxel (36 mg/sqm weekly) +/- calcitriol 0.15 mug/kg indicated that calcitriol was very safe may have reduced to death rate, an adequately powered (1000 patients) randomized study of weekly docetaxel + calcitriol versus q3 week docetaxel was negative. The limitations of this trial were the unequal chemotherapy arms compared in this study and the failure to use an optimal biologic dose or maximum-tolerated dose of calcitriol. In view of the substantial preclinical and epidemiologic data supporting the potential role of vitamin D in cancer, careful studies to evaluate the impact of vitamin D replacement on the frequency of cancer and the impact of an appropriate dose and schedule of calcitriol or other active vitamin D analogue on the treatment of established cancer are indicated.

PMID: 20164683 [PubMed - as supplied by publisher]


Hmmmm.
As referenced above, much of the cancer research has involved Calcitriol in a high potency form that can't be readily duplicated with available forms. The previous manufacturer simply stoppped. Existing sources (Rocaltrol) would require injesting huge numbers of pills to properly emulate. Maybe paricalcitol is a workable IV/injection alternative?:




Article on IV/injection paricalcitol, an "activated" form of D, for diabetics:
http://www.news-medical.net/news/2005/02/28/8049.aspx

Quote:
Kidney failure patient cannot utilize dietary vitamin D and must receive activated forms of the nutrient to avoid deficiency.
Quote:
In 2003 the same research group published a study finding that a particular form of activated vitamin D, paricalcitol, was associated with better survival than was calcitriol, previously the standard activated vitamin D therapy.
J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):539-43.
19-Nor-1alpha,25-dihydroxyvitamin D2 (paricalcitol) exerts anticancer activity against HL-60 cells in vitro at clinically achievable concentrations.

Molnár I, Kute T, Willingham MC, Schwartz GG.
Section on Hematology and Oncology, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
19-Nor-1alpha,25-dihydroxyvitamin D2 (paricalcitol) is an analogue of 1,25(OH)2D3 with reduced calcemic effects that is approved in the United States for the suppression of parathyroid hormone in chronic renal failure. Paricalcitol has anticancer activity in prostate cancer cells. We tested the effects of paricalcitol on the HL-60 leukemia cells, studying cellular differentiation, cell cycle changes, apoptosis and cellular proliferation. Paricalcitol at 10(-8)M concentration induced the maturation of HL-60 cells in a time-dependent manner, as shown by increased expression of CD11b differentiation surface antigen. The ability of HL-60 cells to reduce nitroblue tetrazolium (NBT) was markedly increased after exposure to paricalcitol at 10(-8)M for 72 h. Paricalcitol inhibited colony formation of HL-60 cells in a soft agar semisolid media after 10-day incubation (estimated IC50 of 5 x 10(-9) M. Exposure to 10(-8)M paricalcitol for 72 h increased the number of cells in G0/G1 phase, and decreased the number of cells in S phase, and significantly increased the number of HL-60 cells undergoing apoptosis. The concentration required to achieve inhibition of growth of HL-60 cells is comparable to clinically achievable levels. These findings support the clinical evaluation of paricalcitol as an antileukemia agent.

PMID: 15225834 [PubMed - indexed for MEDLINE]



Ann Epidemiol. 2009 Feb;19(2):96-102. Epub 2008 Jul 10.
Vitamin D and intervention trials in prostate cancer: from theory to therapy.

Schwartz GG.
Departments of Cancer Biology and Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, NC, USA. gschwart@wfubmc.edu
Studies of vitamin D and prostate cancer have advanced rapidly from the hypothesis that vitamin D deficiency increases the risk of prostate cancer to intervention trials of vitamin D administration in clinical cancer. The hormonal form of vitamin D, 1,25(OH)(2)D, exerts prodifferentiating, antiproliferative, anti-invasive, and antimetastatic effects on prostate cells. Moreover, normal prostate cells synthesize 1,25(OH)(2)D from serum levels of the prohormone, 25-hydroxyvitamin D. The autocrine synthesis of 1,25(OH)(2)D by prostatic cells provides a biochemical mechanism whereby vitamin D may prevent prostate cancer. Many prostate cancer cells have lost the ability to synthesize 1,25(OH)(2)D but still possess 1,25(OH)(2)D receptors. This suggests that whereas vitamin D (e.g., cholecalciferol) might prevent prostate cancer, existing prostate tumors likely would require treatment with 1,25(OH)(2)D and/or its analogs. The major obstacle to the use of 1,25(OH)(2)D in patients therapeutically is the risk of hypercalcemia. Several maneuvers to reduce this risk, including pulse dosing and the use of less calcemic 1,25(OH)(2)D analogs, have been explored in Phase I-III clinical trials. Once merely a promise, vitamin D-based therapies for prostate cancer may soon be medical practice.

PMID: 18619854 [PubMed - indexed for MEDLINE]



Cancer Chemother Pharmacol. 2008 Oct;62(5):787-97. Epub 2008 Jan 10.
Toxicity and antitumor activity of the vitamin D analogs PRI-1906 and PRI-1907 in combined treatment with cyclophosphamide in a mouse mammary cancer model.

Wietrzyk J, Nevozhay D, Milczarek M, Filip B, Kutner A.
Department of Experimental Oncology, Institute of Immunology and Experimental Therapy, 12 R. Weigla St., 53-114, Wroclaw, Poland, wietrzyk@iitd.pan.wroc.pl.
PURPOSE: Active and less toxic vitamin D analogs could be useful for clinical applications. In the present study, we evaluated the toxicity and antitumor effect of two new synthetic analogs of vitamin D, namely PRI-1906 [(24E)-24a-Homo-(1S)-1,25-dihydroxyergocalciferol] and its side-chain unsaturated homo analog PRI-1907. METHODS: The toxicity and calcemic activity, as well as antitumor effect of calcitriol analogs was investigated in vivo. The studies were performed in a mouse mammary 16/C cancer model. Since calcitriol and its analogs inhibited 16/C tumor growth only slightly, we applied them in the combined therapy with cyclophosphamide (CY). Moreover, cell cycle analysis and VDR and p27 expression were investigated. RESULTS: The LD50 values after five daily subcutaneous (s.c.) injections were 7.8, 10.0 and 2.4 microg/kg per day for calcitriol, PRI-1906 and PRI-1907, respectively. The serum calcium level increased to 40, 23 and 63% over the control for these compounds. We also compare the antitumor activity of the PRI-1906 with the calcitriol and previously studied PRI-2191 (1,24-dihydroxyvitamin D3, tacalcitol). Statistically significant inhibition of tumor growth by calcitriol up to the eighth day was observed in all schedules applied. PRI-1906 inhibited the tumor growth at doses 1 and 5 microg/kg per day, and PRI-2191 only at the dose 5 microg/kg per day. CONCLUSION: Addition of vitamin D analogs increased the antitumor effect of CY. PRI-1906 exhibited toxicity higher than PRI-2191 but lower than calcitriol and antitumor activity similar to both PRI-2191 and calcitriol. This new analog seems to be a good candidate for the combined treatment of mammary cancer.

PMID: 18188568 [PubMed - indexed for MEDLINE]






Back to Calcitriol studies etc:





Exp Cell Res. 2009 Nov 19. [Epub ahead of print]
Calcitriol inhibits Ether-Ã* go-go potassium channel expression and cell proliferation in human breast cancer cells.

GarcÃ*a-Becerra R, DÃ*az L, Camacho J, Barrera D, Ordaz-Rosado D, Morales A, Ortiz CS, Avila E, Bargallo E, Arrecillas M, Halhali A, Larrea F.
Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga No. 15, Tlalpan 14000 México, D.F., México.
Antiproliferative actions of calcitriol have been shown to occur in many cell types; however, little is known regarding the molecular basis of this process in breast carcinoma. Ether-Ã*-go-go (Eag1) potassium channels promote oncogenesis and are implicated in breast cancer cell proliferation. Since calcitriol displays antineoplastic effects while Eag1 promotes tumorigenesis, and both factors antagonically regulate cell cycle progression, we investigated a possible regulatory effect of calcitriol upon Eag1 as a mean to uncover new molecular events involved in the antiproliferative activity of this hormone in human breast tumor-derived cells. RT-real time PCR and immunocytochemistry showed that calcitriol suppressed Eag1 expression by a vitamin D receptor (VDR)-dependent mechanism. This effect was accompanied by inhibition of cell proliferation, which was potentiated by astemizole (antihistamine), a nonspecific Eag1 inhibitor. Immunohistochemistry and western blot demonstrated that Eag1 and VDR abundance was higher in invasive-ductal-carcinoma than in fibroadenoma, and immunoreactivity of both proteins was located in ductal epithelial cells. Our results provide evidence of a novel mechanism involved in the antiproliferative effects of calcitriol, and highlights VDR as a cancer therapeutic target for breast cancer treatment and prevention.

PMID: 19932096 [PubMed - as supplied by publisher]






Study Shows Benefits of Adding High-Dose Vitamin D to Chemotherapy for Advanced Prostate Cancer: Presented at ASCO


Calcitriol May Safely Double Effectiveness of Taxotere Treatment

ORLANDO, FL -- May 21, 2002 -- The addition of high-dose calcitriol to weekly treatment with the chemotherapy agent docetaxel (Taxotere®) appears to improve the therapeutic response in men with hormone-refractory prostate cancer without compromising safety, according to results reported at the 38th Annual Meeting of the American Society of Clinical Oncology (ASCO). Calcitriol is the active form of vitamin D.

Data from a phase II clinical trial suggest as much as twice the efficacy with the docetaxel/calcitriol combination than docetaxel alone, as measured by prostate-specific antigen (PSA) response rate. The study showed that 81 percent of patients treated with the combination regimen cut their PSA levels by more than half. Studies of docetaxel without calcitriol have reported a 42 percent PSA response rate overall. PSA is a substance produced within the prostate gland, and a high PSA level may indicate the presence of cancer. In patients with advanced prostate cancer, PSA correlates with the amount of cancer in the body.

"Because there is no standard treatment for hormone-refractory prostate cancer, new therapeutic strategies are clearly needed," said Tomasz Beer, M.D., an oncologist at the Oregon Health & Science University (OHSU) Cancer Institute in Portland, Oregon, and lead investigator of the study. "Docetaxel used alone has shown promise in treating prostate cancer, and our new data strongly indicate that the favorable results can be enhanced with the addition of high-dose vitamin D."

The study included 37 men with hormone-refractory prostate cancer, or disease that was progressive despite standard hormonal therapy, including anti-androgen withdrawal. In addition to PSA response, eight of 15 men with measurable disease responded with significant reductions of their tumors.

Patients in the study received oral calcitriol, 0.5 mcg/kg, (micrograms) on the first day of the treatment cycle, followed by an infusion of docetaxel, 36 mg/m2, on the following day. The treatment was repeated weekly for six weeks of an eight-week cycle until there was evidence of disease progression or unacceptable toxicity, or until the patient requested to be withdrawn from the study.

The results of this phase II study are now the basis for a future phase III study to be conducted at OHSU and other institutions. That randomized study will evaluate the use of weekly docetaxel versus weekly docetaxel plus calcitriol in hormone-refractory prostate cancer.



2003 American Society for Clinical Oncology

Weekly High-Dose Calcitriol and Docetaxel in Metastatic Androgen-Independent Prostate Cancer

FULL TEXT/PDF: http://jco.ascopubs.org/cgi/content/full/21/1/123

Tomasz M. Beer, Kristine M. Eilers, Mark Garzotto, Merrill J. Egorin, Bruce A. Lowe, W. David Henner
From the Oregon Health & Science University and Portland VA Medical Center, Portland, OR; and University of Pittsburgh Cancer Institute, Pittsburgh, PA.
Address reprint requests to Tomasz M. Beer, MD, Department of Medicine, Oregon Health & Science University, Mail Code L586, 3181 SW Sam Jackson Park Road, Portland, OR 97239; email: beert@ohsu.edu.
Purpose: To determine the safety and efficacy of weekly high-dose oral calcitriol (Rocaltrol, Roche Pharmaceuticals, Basel, Switzerland) and docetaxel (Taxotere, Aventis Pharmaceuticals, Bridgewater, NJ) in patients with metastatic androgen-independent prostate cancer (AIPC).
Patients and Methods: Thirty-seven patients were treated with oral calcitriol (0.5 µg/kg) on day 1 followed by docetaxel (36 mg/m2) on day 2, repeated weekly for 6 weeks of an 8-week cycle. Patients maintained a reduced calcium diet and increased oral hydration. Prostate-specific antigen (PSA) response was the primary end point, which was defined as a 50% reduction in PSA level confirmed 4 weeks later.
Results: Thirty of 37 patients (81%; 95% confidence interval [CI], 68% to 94%) achieved a PSA response. Twenty-two patients (59%; 95% CI, 43% to 75%) had a confirmed > 75% reduction in PSA. Eight of the 15 patients with measurable disease (53%; 95% CI, 27% to 79%) had a confirmed partial response. Median time to progression was 11.4 months (95% CI, 8.7 to 14 months), and median survival was 19.5 months (95% CI, 15.3 months to incalculable). Overall survival at 1 year was 89% (95% CI, 74% to 95%). Treatment-related toxicity was generally similar to that expected with single-agent docetaxel. Pharmacokinetics of either calcitriol or docetaxel were not affected by the presence of its companion drug in an exploratory substudy.
Conclusion: The combination of weekly oral high-dose calcitriol and weekly docetaxel is a well-tolerated regimen for AIPC. PSA and measurable disease response rates as well as time to progression and survival are promising when compared with contemporary phase II studies of single-agent docetaxel in AIPC. Further study of this regimen is warranted.


Weekly high-dose calcitriol and docetaxel in patients with metastatic hormone-refractory prostate cancer previously exposed to docetaxel

Correspondence to Prof Guido Francini, Medical Oncology Section, Department of Human Pathology and Oncology, University of Siena, Policlinico Le Scotte,Viale Bracci 11, 53100 Siena, Italy. e-mail: r.petrioli@ao-siena.toscana.it

Copyright © 2007 THE AUTHORS; JOURNAL COMPILATION © 2007 BJU INTERNATIONAL

OBJECTIVE
To evaluate the activity and tolerability of weekly high-dose calcitriol and docetaxel in patients with metastatic hormone-refractory prostate cancer (HRPC) previously exposed to docetaxel, as patients who progress after docetaxel treatment might be considered for second-line chemotherapy, but with no standard salvage therapy available we hypothesised that high-dose calcitriol might restore sensitivity to chemotherapy.

PATIENTS AND METHODS

The study comprised 26 patients who had progressed after first-line treatment with docetaxel-based chemotherapy had failed. Treatment cycles consisted of calcitriol (32 µg orally as 0.5 µg tablets) on day 1 and docetaxel (30 mg/m2 intravenous) on day 2, administered for six consecutive weeks followed by a 2-week rest interval for a maximum of 24 cycles.

RESULTS
There was a response in prostate-specific antigen (PSA) level in eight patients (31%); seven (27%) had a stable PSA level for ≥ 12 weeks. The median time to PSA progression was 4.2 months and the median survival was 9.3 months. The regimen was generally well tolerated; there was grade 2 hypercalcaemia, probably related to calcitriol, in one patient after six treatment cycles.

CONCLUSION

Weekly high-dose calcitriol and docetaxel seems to be an effective and well-tolerated treatment option for patients with metastatic HRPC previously exposed to docetaxel-based chemotherapy.



J Steroid Biochem Mol Biol. 2009 Feb;113(3-5):227-32. Epub 2009 Jan 20.
Antiproliferative action of menadione and 1,25(OH)2D3 on breast cancer cells.

Marchionatti AM, Picotto G, Narvaez CJ, Welsh J, Tolosa de Talamoni NG.
Laboratorio Dr. Fernando Cañas, BioquÃ*mica y BiologÃ*a Molecular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Argentina.
Calcitriol or 1,25(OH)(2)D(3) is a negative growth regulator of MCF-7 breast cancer cells. The growth arrest is due to apoptosis activation, which involves mitochondrial disruption. This effect is blunted in vitamin D resistant cells (MCF-7(DRes) cells). Menadione (MEN), a glutathione (GSH)-depleting compound, may potentiate antitumoral effects of anticancer drugs. The aim of this study was to investigate whether MEN enhances cellular responsiveness of MCF-7 cells to 1,25(OH)(2)D(3). Cells were cultured and treated with different concentrations of 1,25(OH)(2)D(3)+/-MEN or vehicle for 96 h. GSH levels and the activity of antioxidant enzymes were determined by spectrophotometry and ROS production by flow cytometry. Both drugs decreased growth and enhanced ROS in MCF-7 cells, obtaining the maximal effects when 1,25(OH)(2)D(3) was combined with MEN (P<0.01 vs. Control and vs. each compound alone). MCF-7(DRes) cells were not responsive to 1,25(OH)(2)D(3), but the cell proliferation was slightly inhibited by the combined treatment. Calcitriol and MEN separately enhanced antioxidant enzyme activities, but when they were used in combination, the effect was more pronounced (P<0.05 vs. Control and vs. each compound alone). MEN, calcitriol and the combined treatment decreased GSH levels (P<0.05 vs. Control). The data indicate that MEN potentiates the effect of 1,25(OH)(2)D(3) on growth arrest in MCF-7 cells by oxidative stress and increases the activities of antioxidant enzymes, probably as a compensatory mechanism.

PMID: 19429426 [PubMed - indexed for MEDLINE]





Might want to stay away from those colas...


J Clin Invest. 1986 Jan;77(1):7-12.
Oral intake of phosphorus can determine the serum concentration of 1,25-dihydroxyvitamin D by determining its production rate in humans.

Portale AA, Halloran BP, Murphy MM, Morris RC Jr.
Changes in the oral intake of phosphorus could induce the reported changes in the serum concentration of 1,25-dihydroxyvitamin D (1,25-(OH)2D) by inducing changes in its production rate (PR) or metabolic clearance rate (MCR), or both. To investigate these possibilities, we employed the constant infusion equilibrium technique to measure the PR and MCR of 1,25-(OH)2D in six healthy men in whom the oral intake of phosphorus was initially maintained at 1,500 mg/70 kg body weight per d for 9 d, then restricted to 500 mg/d (coupled with oral administration of aluminum hydroxide) for 10 d, and then supplemented to 3,000 mg/d for 10 d. With phosphorus restriction, the serum concentration of 1,25-(OH)2D increased by 80% from a mean of 38 +/- 3 to 68 +/- 6 pg/ml, P less than 0.001; the PR increased from 1.8 +/- 0.2 to 3.8 +/- 0.6 micrograms/d, P less than 0.005; the MCR did not change significantly. The fasting serum concentration of phosphorus decreased from 3.5 +/- 0.2 to 2.6 +/- 0.2 mg/dl, P less than 0.01. With phosphorus supplementation, the serum concentration of 1,25-(OH)2D decreased abruptly, reaching a nadir within 2 to 4 d; after 10 d of supplementation, the mean concentration of 27 +/- 4 pg/ml was lower by 29%, P less than 0.01, than the value measured when phosphorus intake was normal. The PR decreased to 1.3 +/- 0.2 micrograms/d, P less than 0.05; the MCR did not change significantly. The fasting serum concentration of phosphorus increased significantly, but only initially. These data demonstrate that in healthy men, reductions and increases in the oral intake of phosphorus can induce rapidly occurring, large, inverse, and persisting changes in the serum concentration of 1,25-(OH)2D. Changes in the PR of 1,25-(OH)2D account entirely for the phosphorus-induced changes in serum concentration of this hormone.

PMID: 3753709 [PubMed - indexed for MEDLINE]


Lower Phosphorus Foods (PDF, 3.2MB)
A one-page handout (double-sided) that contains pictures of selected lower phosphorus foods and information on the phosphorus content of each one.
Higher Phosphorus Foods (PDF, 2.9MB)
A one-page handout (double-sided) that contains pictures of selected higher
phosphorus foods and information on the phosphorus content of each one.
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Old 11-13-2009, 02:44 AM   #2
Rich66
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Re: Vitamin D

Clin Cancer Res. 2009 Jan 1;15(1):190-200.
RRR-alpha-vitamin E succinate potentiates the antitumor effect of calcitriol in prostate cancer without overt side effects.


Yin Y, Ni J, Chen M, Guo Y, Yeh S.
Department of Urology and Pathology, University of Rochester Medical Center, Rochester, New York, USA.
Shuyuan Yeh, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642. Phone: 585-273-2750; Fax: 585-756-4133; E-mail: shuyuan_yeh@urmc.rochester.edu.



Abstract


PURPOSE: To determine the antitumor efficacy of using calcitriol combined with RRR-alpha-vitamin E succinate (VES) on prostate cancer. EXPERIMENTAL DESIGN: The effects of VES or VES in combination with calcitriol on the calcitriol target genes were evaluated by Western blot and real-time PCR. The antiproliferation effect of the combination in prostate cancer cells was evaluated by the combination index method. The role of the vitamin D(3) receptor (VDR) in the enhanced antitumor effects of the combination was confirmed by small interfering RNA knockdown strategy. Xenograft-bearing mice were used to reaffirm the antitumor efficacy of this combination. Pathohistology analyses and expressions of VDR and its target genes were analyzed in untreated and treated tumors. RESULTS: VES selectively increased VDR protein in different prostate cancer cells. Low doses of calcitriol combined with VES were significantly superior to the additive effect of individual treatments against prostate cancer cell proliferation. The expression of VDR target genes involved in antiproliferation were further sensitized in the presence of VES. Knockdown of VDR expression abolished the combination benefits in LNCaP and PC3 cells. Consistently, in prostate cancer xenograft models, VES enhanced the therapeutic efficacy of a tolerated dose of calcitriol yet without overt evidence of systemic toxicity and hypercalcemia. This notable in vivo effect was also accompanied by up-regulation of VDR target genes. CONCLUSIONS: Low-dose calcitriol combined with vitamin E analogue could be a solution to the calcemic side effect. The demonstration of superior antitumor activity of low-dose calcitriol plus VES provides the preclinical basis for developing a useful therapeutic strategy for prostate cancer.

PMID: 19118046 [PubMed - indexed for MEDLINE]Free Article
Quote:
Translational Relevance

Because vitamin E succinate and calcitriol have been applied in different clinical trials in combination with other agents for prostate cancer therapy, it is a relatively small and close step to initiate clinical trials of vitamin E succinate plus calcitriol to treat prostate cancer. What is important is showing persuasive evidence to prove that combined vitamin E succinate and calcitriol to treat prostate cancer is effective. Our data indeed provide solid and supportive evidence both in prostate cancer cells and in preclinical animal cancer models. Thus, the potential impact of this study could be profound for developing an alternative and improved strategy to treat prostate cancer.




calcitriol(Vitamin D)not only synergistic w AI, but anti-prostaglandin,bone-conserving


Endocrinology. 2009 Nov 11. [Epub ahead of print]
Tissue-Selective Regulation of Aromatase Expression by Calcitriol: Implications for Breast Cancer Therapy.
Krishnan AV, Swami S, Peng L, Wang J, Moreno J, Feldman D.

Departments of Medicine, Division of Endocrinology, Stanford University School of Medicine, Stanford, California 94305.

Aromatase, the enzyme that catalyzes estrogen synthesis, is critical for the progression of estrogen receptor-positive breast cancer (BCa) in postmenopausal women. We show that calcitriol, the hormonally active form of vitamin D, regulates the expression of aromatase in a tissue-selective manner. Calcitriol significantly decreased aromatase expression in human BCa cells and adipocytes and caused substantial increases in human osteosarcoma cells (a bone cell model exhibiting osteoblast phenotype in culture) and modest increases in ovarian cancer cells. Calcitriol administration to immunocompromised mice bearing human BCa xenografts decreased aromatase mRNA levels in the tumors and the surrounding mammary adipose tissue but did not alter ovarian aromatase expression. In BCa cells, calcitriol also reduced the levels of prostaglandins (PGs), major stimulators of aromatase transcription, by suppressing the expression of cyclooxygenase-2 (which catalyzes PG synthesis) and increasing that of 15-hydroxyprostaglandin dehydrogenase (which catalyzes PG degradation). The mechanism of aromatase down-regulation by calcitriol in BCa cells is therefore 2-fold: a direct repression of aromatase transcription via promoter II through the vitamin D-response elements identified in this promoter and an indirect suppression by reducing the levels of PGs. Combinations of calcitriol with three different aromatase inhibitors (AIs) caused enhanced inhibition of BCa cell growth. The combination of calcitriol and an AI may have potential benefits for BCa therapy. In addition to augmenting the ability of AIs to inhibit BCa growth, calcitriol acting as a selective aromatase modulator that increases aromatase expression in bone would reduce the estrogen deprivation in bone caused by the AIs, thus ameliorating the AI-induced side effect of osteoporosis.

PMID: 19906814


Nutr Rev. 2007 Aug;65(8 Pt 2):S121-3.
Potentiation of the growth-inhibitory effects of vitamin D in prostate cancer by genistein.

Krishnan AV, Swami S, Moreno J, Bhattacharyya RB, Peehl DM, Feldman D.
Department of Medicine, Division of Endocrinology, Stanford University School of Medicine, 300 Pasteur Drive, Grant Building, S-025, Stanford, CA 94305, USA. krishnan@cmgm.stanford.edu
PMID: 17867387 [PubMed - indexed for MEDLINE]
LINK



Potentiation of the Growth Inhibitory Effects of Vitamin D in Prostate Cancer
By Genistein
Aruna V. Krishnan1, Srilatha Swami1, Jacqueline Moreno1, Rumi B. Bhattacharyya1, Donna M. Peehl2, and David Feldman1
1Department of Medicine, Division of Endocrinology, Stanford University School of Medicine2Department of Urology, Stanford University School of Medicine

Quote:
Calcitriol, the hormonally active form of vitamin D, inhibits the growth and progression of several cancers. Inflammation has been postulated to play a role in the carcinogenic process of many cancers, including prostate cancer (PCa). Our recent research indicates that calcitriol exhibits anti-inflammatory actions that may contribute to its anti-cancer effects in PCa. Calcitriol inhibits the synthesis and actions of pro-inflammatory prostaglandins (PG) by three mechanisms:
(i) inhibition of the expression of cyclooxygenase-2 (COX-2), the enzyme that synthesizes PGs, (ii) induction of the expression of 15-prostaglandin dehydrogenase (15-PGDH), the enzyme that inactivates PGs and (iii) decreasing the expression of EP and FP PG receptors, the mediators of PG actions. Our research also shows that genistein, an active component in soy is a potent inhibitor of vitamin D-24-hydroxylase, the enzyme that initiates the catabolism of calcitriol,
thereby increasing its biologically activity.
In addition, genistein also exerts independent regulatory effects on the PG pathway in PCa cells. Like calcitriol, genistein inhibits COX-2 expression in PCa cells leading to decreased synthesis of PGE2. Genistein also decreases EP and FP PG receptor expression thereby reducing the biological effects of PGE2. The combination of calcitriol and genistein acts in a cooperative way to inhibit the PG pathway as well as retard PCa cell growth. Both calcitriol and genistein are relatively safe with little toxicity associated with their intake. We therefore postulate that the combination of calcitriol and genistein is an attractive therapeutic option for the treatment and/or prevention of PCa.


J Steroid Biochem Mol Biol. 2004 May;89-90(1-5):519-26.
Anti-tumor activity of calcitriol: pre-clinical and clinical studies.

Trump DL, Hershberger PA, Bernardi RJ, Ahmed S, Muindi J, Fakih M, Yu WD, Johnson CS.
Department of Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. donald.trump@roswellpark.org
1,25-Dihydroxycholecalciferol (calcitriol) is recognized widely for its effects on bone and mineral metabolism. Epidemiological data suggest that low Vitamin D levels may play a role in the genesis of prostate cancer and perhaps other tumors. Calcitriol is a potent anti-proliferative agent in a wide variety of malignant cell types. In prostate, breast, colorectal, head/neck and lung cancer as well as lymphoma, leukemia and myeloma model systems calcitriol has significant anti-tumor activity in vitro and in vivo. Calcitriol effects are associated with an increase in G0/G1 arrest, induction of apoptosis and differentiation, modulation of expression of growth factor receptors. Glucocorticoids potentiate the anti-tumor effect of calcitriol and decrease calcitriol-induced hypercalcemia. Calcitriol potentiates the antitumor effects of many cytotoxic agents and inhibits motility and invasiveness of tumor cells and formation of new blood vessels. Phase I and II trials of calcitriol either alone or in combination with carboplatin, taxanes or dexamethasone have been initiated in patients with androgen dependent and independent prostate cancer and advanced cancer. Data indicate that high-dose calcitriol is feasible on an intermittent schedule, no dose-limiting toxicity has been encountered and optimal dose and schedule are being delineated. Clinical responses have been seen with the combination of high dose calcitriol+dexamethasone in androgen independent prostate cancer (AIPC) and apparent potentiation of the antitumor effects of docetaxel have been seen in AIPC. These results demonstrate that high intermittent doses of calcitriol can be administered to patients without toxicity, that the MTD is yet to be determined and that calcitriol has potential as an anti-cancer agent.

PMID: 15225831 [PubMed - indexed for MEDLINE]

Researcher in the study above says "No evidence for disease specificity ..effects are seen across all tumor histotypes"
Roswell Park is a comprehensive Cancer Center http://www.roswellpark.org/


Vitamin D3 better than metformin for insulin sensitivity

http://www.tulsaworld.com/Scene/arti...4_DearPh185644

"a 2004 study published in the American Journal of Clinical Nutrition which found that raising a person's blood levels of vitamin D (from 25 to 75 nmol/l) could improve insulin sensitivity by a whopping 60 percent. "

"Compare that to metformin, one of our pharmaceutical gold-standards, which can dispose of blood sugar by a meager 13 percent "

"I suggest you ask your doctor if he minds you supplementing with about 5,000 IU "cholecalciferol" or vitamin D3 every morning."



Int J Endocrinol. 2010;2010:351385.
Role of vitamin d in insulin secretion and insulin sensitivity for glucose homeostasis.

Alvarez JA, Ashraf A.
Department of Nutrition Sciences, University of Alabama at Birmingham, AL 35233, USA.
Vitamin D functions are not limited to skeletal health benefits and may extend to preservation of insulin secretion and insulin sensitivity. This review summarizes the literature related to potential vitamin D influences on glucose homeostasis and insulin sensitivity. Cross-sectional data provide some evidence that circulating 25-hydroxyvitamin D (25(OH)D) is inversely associated with insulin resistance, although direct measurements of insulin sensitivity are required for confirmation. Reported associations with insulin secretion, however, are contradictory. Available prospective studies support a protective influence of high 25(OH)D concentrations on type 2 diabetes mellitus risk. There is a general lack of consistency in vitamin D intervention outcomes on insulin secretion and sensitivity, likely due to differences in subject populations, length of interventions, and forms of vitamin D supplementation. Vitamin D receptor gene polymorphisms and vitamin D interactions with the insulin like growth factor system may further influence glucose homeostasis. The ambiguity of optimal vitamin D dosing regimens and optimal therapeutic concentrations of serum 25(OH)D limit available intervention studies. Future studies, including cross-sectional and prospective, should be performed in populations at high risk for both vitamin D deficiency and type 2 diabetes mellitus. Well-designed, placebo-controlled, randomized intervention studies are required to establish a true protective influence of vitamin D on glucose homeostasis.

PMID: 20011094 [PubMed - in process]




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Vitamin D Good for Breast Cancer Patients

FRIDAY, Oct. 9 (HealthDay News) -- Many breast cancer patients have low levels of vitamin D, which could lead to weaker bones and increased risk of fractures, say U.S. researchers who recommend high doses of vitamin D for them.
"Vitamin D is essential to maintaining bone health, and women with breast cancer have accelerated bone loss due to the nature of hormone therapy and chemotherapy. It's important for women and their doctors to work together to boost their vitamin D intake," Luke Peppone, a research assistant professor of radiation oncology at the University of Rochester Medical Center, said in a news release from the medical cwnter.
Peppone and colleagues studied 166 women undergoing treatment for breast cancer and found that nearly 70 percent had low levels of vitamin D in their blood. The average level among the women was 27 nanograms of vitamin D per milliliter of blood. Levels of 32 nanograms per milliliter are adequate, according to the U.S. Institute of Medicine.
The lowest levels of vitamin D were in non-whites and those with late-stage breast cancer.
The researchers found that weekly supplementation with high doses of vitamin D (50,000 IU or more) boosted the levels of the vitamin among all the women.
The study was to be presented Oct. 8 at the American Society of Clinical Oncology's breast cancer symposium in San Francisco.
Previous studies have shown that nearly half of all women and men have vitamin D levels below 32 nanograms per milliliter. Along with strengthening bones, vitamin D plays an important role in cell growth and keeping the immune system strong. People obtain Vitamin D through exposure to sunlight and from foods such as milk and fortified cereals.


Video: Dr. Feldman at Stanford: Vitamin D: Not just for bones
http://med.stanford.edu/medcast/2008/vitamind.html

David Feldman, MD, professor of medicine, explores the biological action of Vitamin D beyond its widely understood role in the formation and maintenance of bone. Emerging therapeutic uses of the vitamin cover a range of conditions, including breast and prostate cancer, chronic kidney disease and arthritis.


Immunol Invest. 2009;38(5):365-82.
Dietary vitamin D3 restriction influences tumor growth, but not the ability to generate an antigen-specific immune response in OTII transgenic mice.

Goldstein BD, Kurt RA.
Department of Biology, Lafayette College, Easton, Pennsylvania 18042, USA.
Initially, we wanted to know whether dietary vitamin D(3) restriction would influence growth and metastasis of the 4T1 murine mammary carcinoma. We confirmed serum 25(OH)D levels were modulated by dietary vitamin D(3) restriction, mice were healthy, and when challenged with the 4T1 tumor alterations in tumor growth, but not metastasis were evident. Tumors grew more rapidly in mice on the vitamin D(3) restricted diet. To delineate whether dietary vitamin D(3) restriction influenced the ability to generate an antigen-specific immune response we used OTII transgenic mice which express a T cell receptor specific for ovalbumin. We found that dietary vitamin D(3) restriction did not influence the health of OTII mice, the number of circulating CD3/CD4(+), CD3/CD8(+), CD4/CD25(+) T cells, nor the ability to generate CD11c(+) bone-marrow derived dendritic cells. T cells from OTII mice maintained on the vitamin D(3) restricted diet also exhibited no significant alterations in proliferative capacity or ability to secrete IFN-gamma or IL-4 in an antigen-specific manner. Yet, EL-4 tumors grew more rapidly in OTII mice on the vitamin D(3) restricted diet. These data show that dietary vitamin D(3) restriction impacts tumor growth, but not the ability to generate an antigen-specific immune response.

PMID: 19811414 [PubMed - in process]




J Steroid Biochem Mol Biol. 2003 Feb;84(2-3):149-57.
Phytoestrogen regulation of a Vitamin D3 receptor promoter and 1,25-dihydroxyvitamin D3 actions in human breast cancer cells.

Wietzke JA, Welsh J.
Department of Biological Sciences, University of Notre Dame, IN 46556, USA.
1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), a steroid hormone derived from Vitamin D(3), is a negative growth regulator of breast cancer cells, and Vitamin D(3) analogs represent a novel treatment approach for human cancer. Elucidation of Vitamin D(3) receptor (VDR) regulation may reveal strategies to sensitize cancer cells to the effects of 1,25-dihydroxyvitamin D(3) and Vitamin D(3) analogs. We have previously characterized an estrogen responsive promoter region (800 bp upstream of exon 1c) in the human VDR gene, and the present studies examined regulation of this VDR promoter region by two phytoestrogens, resveratrol (present in red wine) and genistein (present in soy). We transiently transfected a VDR promoter luciferase construct into the estrogen receptor (ER) positive human breast cancer cell lines T47D and MCF-7, and treated with 0.4-4 microM resveratrol or 5-500 nM genistein. Both phytoestrogens up-regulated the transcription of the VDR promoter, as measured by reporter gene activity, approximately two-fold compared to vehicle treated cells. Co-treatment with the anti-estrogen tamoxifen (TAM) in T47D cells and transfection in an estrogen receptor negative breast cancer cell line demonstrated that the effects of phytoestrogens on the VDR promoter are dependent on estrogen receptor. Resveratrol and genistein also increased VDR protein expression as detected by Western blotting. Treatment with resveratrol had no effect on cell number or cell cycle profile, while treatment with genistein increased cell number. Because resveratrol could up-regulate VDR without increasing breast cancer cell growth, we hypothesized that resveratrol mediated increase in VDR expression would sensitize breast cancer cells to the effects of 1,25-dihydroxyvitamin D(3) and Vitamin D(3) analogs. In support of this hypothesis, both T47D and MCF-7 cells pre-treated with resveratrol exhibited increased VDR mediated transactivation of a Vitamin D(3) responsive promoter compared to cells pre-treated with vehicle. In addition, co-treatment with resveratrol enhanced the growth inhibitory effects of 1,25-dihydroxyvitamin D(3) and the Vitamin D(3) analog EB1089. These data support the concept that dietary factors, such as phytoestrogens, may impact on breast cancer cell sensitivity to Vitamin D(3) analogs through regulation of the VDR promoter.

PMID: 12710998 [PubMed - indexed for MEDLINE]



Cancer Nurs. 2009 Mar-Apr;32(2):143-50.
Vitamin D insufficiency and musculoskeletal symptoms in breast cancer survivors on aromatase inhibitor therapy.

Waltman NL, Ott CD, Twiss JJ, Gross GJ, Lindsey AM.
College of Nursing, University of Nebraska Medical Center, Lincoln, NE, USA.
Breast cancer survivors (BCSs) on aromatase inhibitor (AI) therapy often experience musculoskeletal symptoms (joint pain and stiffness, bone and muscle pain, and muscle weakness), and these musculoskeletal symptoms may be related to low serum levels of vitamin D. The primary purpose of this pilot exploratory study was to determine whether serum levels of 25-hydroxyvitamin D (25[OH]D) concentration were below normal (<30 ng/mL) in 29 BCSs on AI therapy and if musculoskeletal symptoms were related to these low vitamin D levels. The mean (SD) serum 25(OH)D level was 25.62 (4.93) ng/mL; 86% (n = 25) had levels below 30 ng/mL. Patients reported muscle pain in the neck and back, and there was a significant inverse correlation between pain intensity and serum 25(OH)D levels (r = -0.422; P < .05 [2 tailed]). This sample of BCSs taking AIs had below normal levels of serum 25(OH)D despite vitamin D supplements. This is one of the few studies to document a significant relationship between vitamin D levels and muscle pain in BCSs on AI therapy. Findings from this pilot study can be used to inform future studies examining musculoskeletal symptoms in BCSs on AI therapy and relationships with low serum levels of vitamin D.

PMID: 19125120 [PubMed - indexed for MEDLINE]



Cancer Cell. 2010 Mar 16;17(3):273-285.
Modulation of the Vitamin D3 Response by Cancer-Associated Mutant p53.

Stambolsky P, Tabach Y, Fontemaggi G, Weisz L, Maor-Aloni R, Sigfried Z, Shiff I, Kogan I, Shay M, Kalo E, Blandino G, Simon I, Oren M, Rotter V.
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel.
The p53 gene is mutated in many human tumors. Cells of such tumors often contain abundant mutant p53 (mutp53) protein, which may contribute actively to tumor progression via a gain-of-function mechanism. We applied ChIP-on-chip analysis and identified the vitamin D receptor (VDR) response element as overrepresented in promoter sequences bound by mutp53. We report that mutp53 can interact functionally and physically with VDR. Mutp53 is recruited to VDR-regulated genes and modulates their expression, augmenting the transactivation of some genes and relieving the repression of others. Furthermore, mutp53 increases the nuclear accumulation of VDR. Importantly, mutp53 converts vitamin D into an antiapoptotic agent. Thus, p53 status can determine the biological impact of vitamin D on tumor cells. Copyright © 2010 Elsevier Inc. All rights reserved.

PMID: 20227041 [PubMed - as supplied by publisher]






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Old 11-13-2009, 10:09 AM   #3
Rich66
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Re: Vitamin D

On best test for D level (found in a LDN discussion):

There are two vitamin D tests--1,25(OH)D and 25(OH)D: 25(OH)D is the better marker of overall D status. It is this marker that is most strongly associated with overall health. The correct test is 25(OH)D, also called 25-hydroxyvitamin D.

According to the Vitamin D council:
Unfortunately, about 20% of United States doctors order the wrong test. They order a 1,25-dihydroxy-vitamin D, thinking that by measuring the most potent steroid in the human body, calcitriol, they are getting useful information. They are not. 1,25-dihydroxy-vitamin D is an adaptive hormone; it goes up and down with calcium intake. So these doctors see the 1,25-dihydroxy-vitamin D is normal or high and tell their patients that they are ok when really, they are vitamin D deficient""
http://www.vitamindcouncil.org/health/deficiency/am-i-vitamin-d-deficient.shtml

Here is a good article:
http://www.aacc.org/publications/cln/2009/july/Pages/CovStory1July09.aspx

The out-of-kilter 1,25 (OH)2 D volume is no surprise to lab directors who are finding that not all physicians know which test —25-OH-D or 1,25 (OH)2 D—is correct for determining overall vitamin D status. “
Fifty percent of physicians are still confused about what is the appropriate test. Some clients order both and one comes back normal and the other’s not. Then they call me and ask, ‘what should I believe?’ and I have to explain the difference,” observed L.V. Rao, PhD, director of core laboratories and associate professor of pathology at

Various:
The 25-OH Vitamin D test is the correct one.

Vitamin D, 25-Hydroxy

Synonyms:

  • 25-Hydroxycalciferol
  • 25-OH-D
  • Cholecalciferol Metabolite
  • Vitamin D
  • Vitamin D3 Metabolite
In the past year, ARUP Laboratories has experienced an increase in test volume for vitamin D testing. There has been some confusion regarding which test to order.
More at
http://www.labtestsonline.org/understanding/analytes/vitamin_d/test.html




Prostate cancer researchers say it's important that the type of vitamin D used in beneficial studies is Calcitriol. Most over the counter or prescription D are other forms.

Info on Rocaltrol brand of Calcitriol: http://rocaltrol.net/

Can't vouch for company, but generic Rocaltrol/Calcitriol available here:
http://trustedpharmacyworld.com/prod...item=Rocaltrol


from the PCa study:
"vCalcitriol (Rocaltrol 0.5 µg capsules, Roche Pharmaceuticals, Basel, Switzerland) 0.5 µg/kg was given orally in four divided doses over 4 hours on day 1 followed by docetaxel (Taxotere, Aventis Pharmaceuticals, Bridgewater, NJ) 36 mg/m2 intravenously over 15 to 30 minutes on day 2 of each treatment week."



Home test available: http://www.zrtlab.com/vitamindcouncil/



Vitamin D toxicity issues discussed:
http://www.vitamindcouncil.org/vitaminDToxicity.shtml



CMSC-ACTRIMS: Content of OTC Vitamin D Low, Unpredictable


This report is part of a 12-month Clinical Context series.
By Richard Robinson, Contributing Writer, MedPage Today
Published: June 07, 2010
Reviewed by Ari Green, MD; Assistant Professor, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Action Points
  • Explain to interested patients that in one small but carefully done study, the actual dose of OTC vitamin D was below the listed dose in all brands tested.
  • Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

SAN ANTONIO -- Multiple sclerosis (MS) patients taking over-the-counter vitamin D aren't getting what they're paying for, or what their neurologists recommend, according to a study presented here. The mean vitamin D content from 10 OTC brands was only 33% of what the label claimed, with the actual content ranging from less than 1% to 82% of the advertised level. The study was presented at the meeting of the Joint Consortium of Multiple Sclerosis Centers and America's Committee on Treatment and Research in Multiple Sclerosis.
Vitamin D supplements are increasingly being recommended to MS patients, both for osteoporosis, which is common in the disease, and for presumed immunomodulatory actions as well, according to senior author Peter Calabresi, MD, of the Department of Neurology at Johns Hopkins University in Baltimore. "As the role of vitamin D in immune regulation in MS gains increasing focus, oral supplementation is growing," he said.
The level of recommended supplementation depends on the patient's individual deficiency, although 4000 IU daily is a common dose.
However, given the wide variety of vitamin D3 (cholecalciferol) supplements available and "limited regulation within the nutritional supplement industry, the true vitamin D3 content of over-the-counter supplements is a concern," Calabresi said.
To test levels in commonly purchased supplements, his group collected 10 bottles of OTC supplements from local and on-line retail pharmacies. Vitamin D3 was extracted by standard techniques and samples were analyzed by liquid chromatography and mass spectrometry.
The labeled doses ranged from 400 IU to 10,000 IU, but the mean actual dose was only 33.5% of the labeled dose, with a range from 0.24% to 81.7%.
Lower-dose products tended to be closer to their labeled dose than higher-dose products, with the three 400-IU products averaging 51.5%, the two 1000-IU products averaging 34%, and the three 10,000-IU products averaging 29.9%.
On the other hand, the single worst sample -- the one with only 0.24% of what it claimed -- was a 400-IU sample.
Neither national in-store retail brands nor online brands were more true to their labels.
The discrepancy between the advertised and actual vitamin D content "may contribute to the difficulty for some patients to reach adequate serum vitamin D levels despite supplementation," Calabresi said.
"This reflects the need for increased regulation of the vitamin industry." Because their lab is not certified to do drug testing, Calabresi declined to name the products tested in this study. Patients taking vitamin D supplements should have serum measurements made after starting therapy to determine whether they are reaching target levels, he said.


Primary source: Consortium of Multiple Sclerosis Centers
Source reference:
Eckstein C, et al "Vitamin D3 content in commercially available oral supplements" CMSC-ACTRIMS 2010; P. 33-34.






Arch Biochem Biophys. 2007 Apr 15;460(2):202-5. Epub 2007 Jan 8.
Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function.

Przybelski RJ, Binkley NC.
School of Medicine and Public Health, University of Wisconsin-Madison, 2870 University Avenue, Suite 100, Madison, WI 53705, USA. rjprzybe@facstaff.wisc.edu
Abstract

This study investigates the association of vitamin D status with cognitive function and discusses potential mechanisms for such an effect. The relationship of vitamin B12 with cognition was also assessed. A retrospective review of older adults presenting to a university-affiliated clinic providing consultative assessments for memory problems was performed. Charts of all patients (n=80) presenting for initial visits were reviewed to identify those who had serum 25-hydroxyvitamin D (25(OH)D), vitamin B12, and mini-mental state examination score (MMSE) all obtained on their first visit (n=32). Correlation analyses between MMSE and 25(OH)D and vitamin B12 levels were performed. Serum 25(OH)D concentration and MMSE showed a (p=0.006) positive correlation; no (p=0.875) correlation was observed between serum B12 concentration and MMSE. In conclusion, the positive, significant correlation between serum 25(OH)D concentration and MMSE in these patients suggests a potential role for vitamin D in cognitive function of older adults.

PMID: 17258168 [PubMed - indexed for MEDLINE]

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Old 04-08-2010, 02:44 PM   #4
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Re: Vitamin D - which test?

Rich -
Thanks for posting that there is more than one test available to order to check our vitamin D level.

I am wondering if I did not have 2 different tests for my last checks.

My GP ordered my vitamin D checked when I had my last fasting lipid profile in January. My result was 41 after the 12-hour+ fast. Don't know which test was used.

The very next day I was at my cancer center for regular blood draw which happened to also include my vitamin D level. On my result they say that the 25 Hydroxy test was used. Result was 50.4. I had taken my multivitamin and calcium/D supplement that morning.

Curious what anyone thinks about this discrepancy or if that would be a normal variation in a 24-hour period?
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MY STORY SO FAR ~~~~
Found suspicious lump 9/2000
Lumpectomy, then node dissection and port placement
Stage IIB, 8 pos nodes of 18, Grade 3, ER & PR -
Adriamycin 12 weekly, taxotere 4 rounds
36 rads - very little burning
3 mos after rads liver full of tumors, Stage IV Jan 2002, one spot on sternum
Weekly Taxol, Navelbine, Herceptin for 27 rounds to NED!
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All clear until treated cerebellum spot showing activity on Jan 2006 brain MRI & brain PET
Brain surgery on Feb 9, 2006 - no cancer, 100% radiation necrosis - tumor was still dying
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Fall-2006 - off Zometa - watching one small brain spot (scar?)
2007 - spot/scar in brain stable - finished anticoagulation therapy for clot along my port-a-catheter - 3 angioplasties to unblock vena cava
2008 - Brain and body still NED! Port removed and scans in Dec.
Dec 2008 - stop Herceptin - Vaccine Trial at U of W begun in Oct. of 2011
STILL NED everywhere in Feb 2014 - on wing & prayer
7/14 - Started twice yearly Zometa for my bones
Jan. 2015 checkup still shows NED
2015 Neuropathy in feet - otherwise all OK - still NED.
Same news for 2016 and all of 2017.
Nov of 2017 - had small skin cancer removed from my face. Will have Zometa end of Jan. 2018.
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