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Benefits of Vitamin D Supplementation Joel M. Kauffman, Ph.D. Journal of American Physicians and Surgeons Volume 14 Number 2 - Summer 2009 Clinical trials show that vitamin D supplementation at higher levels than previously recommended is beneficial for many conditions. It decreases the frequency of falls and fractures, helps prevent cardiovascular disease, and reduces symptoms of colds or influenza. Benefits are also seen in diabetes mellitus, multiple sclerosis, Crohn disease, pain, depression, and possibly autism. Sunlight does not cause an overdose of vitamin D production, and toxicity from supplementation is rare. Dose recommendations are increasing, but appear to be lagging the favorable trial results. A number of common drugs deplete vitamin D levels, and others may limit its biosynthesis from sunlight. People with adequate levels from sun exposure will not benefit from supplementation. While dietary intake is helpful, supplementation is better able to raise serum 25-hydroxyvitamin D , the major circulating metabolite, to the level now thought adequate, 30-50 ng/mL. Where there is inadequate daily sun exposure, oral doses of 1,000-2,000 IU/d are now considered routine, with much higher doses (up to 50,000 IU) for rapid repletion now considered safe.

(NaturalNews) Levels of the beneficial, cancer-fighting compound sulforaphane in broccoli are reduced by 90 percent when the vegetable is cooked, according to a study conducted by researchers from TNO Quality of Life in the Netherlands, and published in the Journal of Agricultural and Food Chemistry. "Consumption of raw broccoli resulted in faster absorption, higher bioavailability, and higher peak plasma amounts of sulforaphane, compared to cooked broccoli," the researchers wrote.

Relationship between low ultraviolet B irradiance and higher breast cancer risk in 107 countries. Mohr SB, Garland CF, Gorham ED, Grant WB, Garland FC. Breast J. 2008 May-Jun;14(3):255-60. Epub 2008 Apr 17. PMID: 18422861 DOI: 10.1111/j.1524-4741.2008.00571.x There was a protective effect of UVB irradiance on risk of breast cancer that was independent of fertility rate, proportion of the population overweight, alcohol intake, animal energy intake, and other covariates.

Calcium Associated With Lower Risk Of Cancer In Women\nScienceDaily (Feb. 24, 2009) - Women with higher intake of calcium appear to have a lower risk of cancer overall, and both men and women with high calcium intakes have lower risks of colorectal cancer and other cancers of the digestive system, according to a report in the February 23 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.

Vitamin D may not just be good for you, it may help save your life. Recent research from Johns Hopkins University suggests that higher amounts of vitamin D in your diet decreases your likelihood of dying. Studies found that a vitamin D deficiency increases your risk of death by 26 percent, and vitamin D decreases the mortality rate from almost every type of cancer including breast, colon and prostate. Research also suggests that vitamin D helps prevent diabetes, kidney disease and cardiovascular disease.

"HOUSTON - A diet that incorporates a daily dose of pistachios may help reduce the risk of lung and other cancers, according to data presented at the American Association for Cancer Research Frontiers in Cancer Prevention Research Conference, held Dec. 6-9. "It is known that vitamin E provides a degree of protection against certain forms of cancer. Higher intakes of gamma-tocopherol, which is a form of vitamin E, may reduce the risk of lung cancer," said Ladia M. Hernandez, M.S., R.D., L.D., senior research dietitian in the Department of Epidemiology at the University of Texas M. D. Anderson Cancer Center, and doctoral candidate at Texas Woman's University - Houston Center. "Pistachios are a good source of gamma-tocopherol. Eating them increases intake of gamma-tocopherol so pistachios may help to decrease lung cancer risk," she said. Pistachios are known to provide a heart-healthy benefit by producing a cholesterol-lowering effect and providing the antioxidants that are typically found in food products of plant origin. Hernandez and colleagues conducted a six-week, controlled clinical trial to evaluate if the consumption of pistachios would increase dietary intake and serum levels of gamma-tocopherol. A pistachio-rich diet could potentially help reduce the risk of other cancers from developing as well, according to Hernandez. "Because epidemiologic studies suggest gamma-tocopherol is protective against prostate cancer, pistachio intake may help," she said. "Other food sources that are a rich source of gamma-tocopherol include nuts such as peanuts, pecans, walnuts, soybean and corn oils.""

"CHICAGO (Reuters) - Post-menopausal women who have three to four alcoholic beverages a week of any sort have a significantly higher risk that their breast cancer will come back, U.S. researchers said Thursday."

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

T-helper/T-regulator lymphocyte ratio as a new immunobiological index to quantify the anticancer immune status in cancer patients. Brivio F, Fumagalli L, Parolini D, Messina G, Rovelli F, Rescaldani R, Vigore L, Vezzo R, Vaghi M, Di Bella S, Lissoni P. In Vivo. 2008 Sep-Oct;22(5):647-50. PMID: 18853761 RESULTS: The mean TH/TR ratio observed in patients with metasytases was significantly lower with respect to that found in both patients without metastases and controls. On the contrary, the absolute mean number of T-reg cells was higher in patients with metastases than in those without, but the difference was not statistically significant. CONCLUSION: The evaluation of T-reg cells in terms of their proportion with respect to T-helper cell total number seems to be more appropriate than the simple measurement of their absolute count, in order to quantify cancer-related immunosuppression. Thus, the TH/TR ratio could represent a useful biological marker to explore the immune status of cancer patients.

Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease. Kidd P. Altern Med Rev. 2003 Aug;8(3):223-46. Review. PMID: 12946237 Th1 pathways typically produce activation of cytotoxic T lymphocytes (Tc), NK cells, macrophages, and monocytes, all of which can attack cancer cells and generally defend against tumors.55 IFN-gamma and other Th1 cytokines are typically lower in advanced cancer patients, while the Th2 marker IL-4 can be higher or unchanged

Higher blood levels of selenium may reduce the incidence of skin cancer by about 60 per cent, according to a new study from Dutch and Australian researchers. Writing in Cancer Epidemiology, Biomarkers & Prevention, the researchers report that the mineral was associated with reduced risks of both basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). On the other hand, blood levels of carotenoids and alpha-tocopherol (vitamin E) were not associated with any influence on skin cancer risks, report the researchers from Queensland Institute of Medical Research, the University of Queensland, and Maastricht University.

Safety Study of Seneca Valley Virus in Patients With Solid Tumors With Neuroendocrine Features This study is currently recruiting participants. Verified by Neotropix, September 2008 This is the first study in man of Seneca Valley Virus, a virus which seeks and kills certain tumors in non-human model systems. Subjects in this trial will be patients with advanced cancer displaying certain specified neuroendocrine features, pathologically; they will have exhausted standard methods of treatment for their tumor. The primary purpose of the trial is to determine if the virus may be administered safely. Additional purposes are to learn about the distribution of the virus in the body, the elimination of the virus from the body, the immune response to the virus and whether the virus might have some beneficial effects upon the tumors which the patients have. The first patients will be treated with low amounts of virus and subsequent patients may receive higher amounts. At the end of the trial, it is intended to select a dose for further study.

Watercress was declared the latest super food yesterday for being packed with a higher than usual amount of nutrients found in vegetables. Research has shown that eating a packet of raw watercress a day, or a bowl full, for eight weeks increased the ability of cells to resist damage to their DNA, helping to protect against the cell changes that lead to cancer.

Mice injected with cancer cells experienced significantly elevated levels of C-reactive protein, white blood cells, and lipid peroxidation compared with control mice. These levels were reduced in animals that received cisplatin and/or DHA. While treatment with 125 mg/kg DHA inhibited tumor growth by 38 percent compared to untreated animals, 250 mg/kg suppressed tumor growth by 79 percent, which was a greater effect than that of cisplatin alone (which was associated with a 55 percent reduction). The combination of DHA and cisplatin resulted in an 81 percent inhibition of growth, while reducing elevated white blood cell levels (leukocytosis) to normal levels. Treatment with the higher dose of DHA alone was associated with a similar reduction in white blood cells, which, when elevated, are associated with tumor growth. A strong relationship was observed between tumor growth and white blood cell levels as well as C-reactive protein levels. In another experiment with rats treated with cisplatin, the addition of 250 mg/kg DHA prevented lethal kidney toxicity in 88 percent of the animals that received it, while none of the rats that received cisplatin alone survived.

Vitamin D status and the risk of lung cancer: a cohort study in Finland. Kilkkinen A, Knekt P, Heliövaara M, Rissanen H, Marniemi J, Hakulinen T, Aromaa A. Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3274-8. PMID: 18990771v In conclusion, although there was no overall association between vitamin D and lung cancer risk, women and young participants with a higher level of vitamin D were observed to have a lower lung cancer risk. Although experimental data support the suppressing effect of vitamin D on the development of lung cancer, large epidemiologic studies from different populations with repeated measurements of vitamin D are warranted to confirm this finding. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3274-8)

Circulating 25-hydroxyvitamin d levels and survival in patients with colorectal cancer. Ng K, Meyerhardt JA, Wu K, Feskanich D, Hollis BW, Giovannucci EL, Fuchs CS. J Clin Oncol. 2008 Jun 20;26(18):2984-91. PMID: 18565885 DOI: 10.1200/JCO.2007.15.1027 Conclusion Among patients with colorectal cancer, higher prediagnosis plasma 25(OH)D levels were associated with a significant improvement in overall survival. Further study of the vitamin D pathway and its influence on colorectal carcinogenesis and cancer progression is warranted.

Israeli 'cancer shift' over heart disease mortality may be led by greater risk in women with high intake of n-6 fatty acids. Shapira N. Eur J Cancer Prev. 2007 Oct;16(5):486-94. PMID: 17923822 doi: 10.1097/CEJ.0b013e3280145b6d Population studies of Israeli Jews, Arabs, and women support the association of high n-6 polyunsaturated fatty acid intake with increased cancer risk and higher female sensitivity. Research findings suggest that gender and sex hormones may influence n-6 polyunsaturated fatty acid metabolism and carcinogenesis. This appears to be the first time gender has been proposed to modulate national cancer epidemiology, suggesting implications for differential nutritional prevention, warranting further research.

Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions. Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ. J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17. PMID: 17704354 doi: 10.1124/jpet.107.128017 The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.

Berberine inhibits growth, induces G1 arrest and apoptosis in human epidermoid carcinoma A431 cells by regulating Cdki-Cdk-cyclin cascade, disruption of mitochondrial membrane potential and cleavage of caspase 3 and PARP. Mantena SK, Sharma SD, Katiyar SK. Carcinogenesis. 2006 Oct;27(10):2018-27. Epub 2006 Apr 18. PMID: 16621886 doi:10.1093/carcin/bgl043 In the present investigation, we show that berberine, which is present abundantly in Berberis plant species, significantly inhibits the viability, proliferation and induces cell death in human epidermoid carcinoma A431 cells (Figure 1), but this effect was not found in normal human epidermal keratinocytes under the identical conditions, except for a non-significant reduction in cell viability at higher concentrations of berberine (50 and 75 µM) and treatment of cells for a longer period of time (72 h). These data suggested that berberine may be examined as an effective chemotherapeutic agent against non-melanoma skin cancers. In conclusion, our study indicates that berberine inhibits growth, induces G1 arrest and apoptotic cell death of human epidermoid carcinoma A431 cells. We also provide mechanistic evidences that berberine-induced apoptosis in human epidermoid carcinoma cells is mediated through disruption of mitochondrial membrane potential and activation of caspase 3 pathway, although other pathways may have a role and that require further investigation. Moreover, further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the prevention of non-melanoma skin cancers.

Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells. Mantena SK, Sharma SD, Katiyar SK. Mol Cancer Ther. 2006 Feb;5(2):296-308. PMID: 16505103 doi: 10.1158/1535-7163.MCT-05-0448 The effectiveness of berberine in checking the growth of androgen-insensitive, as well as androgen-sensitive, prostate cancer cells without affecting the growth of normal prostate epithelial cells indicates that it may be a promising candidate for prostate cancer therapy. The evaluation of ancient herbal medicines may indicate novel strategies for the treatment of prostate cancer, which remains the leading cause of cancer-related deaths in American men (1). In our present investigation, we show that a naturally occurring isoquinoline alkaloid, berberine, significantly inhibits the proliferation and reduces the viability of DU145 and PC-3 as well as LNCaP cells (Fig. 1), which suggests that berberine may be an effective chemotherapeutic agent against both androgen-sensitive and androgen-insensitive prostate cancer cells. Importantly, we found that berberine did not exhibit toxicity to nonneoplastic human prostate epithelial cells under the conditions used, except for a moderate reduction in cell viability at higher concentrations when cells were treated in vitro for an extended period of time. In conclusion, the results of the present study indicate that berberine inhibits proliferation and induces G1-phase arrest and apoptosis in human prostate cancer cells but not in normal human prostate epithelial cells. In addition, we provide mechanistic evidence that berberine-induced apoptosis in prostate carcinoma cells, particularly hormone-refractory prostate carcinoma cells, is mediated through enhanced expression of Bax, disruption of the mitochondrial membrane potential, and activation of caspase-3.