Nutrition

Seasonality of UV-radiation and vitamin D status at 69 degrees north. Brustad M, Edvardsen K, Wilsgaard T, Engelsen O, Aksnes L, Lund E. Photochem Photobiol Sci. 2007 Aug;6(8):903-8. Epub 2007 Jun 27. PMID: 17668121 The generally high dietary intakes of vitamin D, especially in winter, mask largely the effect of seasonal variation in UV-exposure, causing an atypical seasonal variation in vitamin D status. The UV-hour variable significantly predicted 25(OH)D levels in blood when adjusted for intakes and artificial UV-radiation exposure and sun holidays abroad.

The high prevalence of vitamin D insufficiency across Australian populations is only partly explained by season and latitude. van der Mei IA, Ponsonby AL, Engelsen O, Pasco JA, McGrath JJ, Eyles DW, Blizzard L, Dwyer T, Lucas R, Jones G. Environ Health Perspect. 2007 Aug;115(8):1132-9. PMID: 17687438 doi: 10.1289/ehp.9937. Conclusion Vitamin D insufficiency is common over a wide latitude range in Australia. Season appears to be more important than latitude, but both accounted for less than one-fifth of the variation in serum 25(OH)D levels, highlighting the importance of behavioral factors. Current sun exposure guidelines do not seem to fully prevent vitamin D insufficiency, and consideration should be given to their modification or to pursuing other means to achieve vitamin D adequacy.

Research has uncovered the fact that vitamin K also plays a crucial role in maintaining bone health. It was found that the amount of vitamin K required to halt bone absorption leading to osteoporosis requires much greater intakes than that required for blood clot regulation. Further, it appears that bone and vascular tissue (like coronary arteries) maintain a preference for a different form of vitamin K than that required for blood clotting regulation. Rather than vitamin K1 needed for clotting, vitamin K2 is the form preferred by bones and arteries (Schurgers LJ et al 2001). It appears that much of the information generated over the years for vitamin K focused on the K1 form, ignoring the K2 form necessary for bone and vascular health. Normal deposition of calcium occurs only in bone and in teeth. Abnormal deposition of calcium in the body occurs in three places: the inner lining of the arteries of the body (the intima) that causes atherosclerotic plaque; the muscle layer of arteries ("medial calcification"); and heart valves. K2 appears to be the form of vitamin K responsible for controlling these phenomena.

Deficiency of K2 in both mice and humans is associated with coronary calcification; low vitamin K2 levels are associated with increased activity of Gla matrix protein, an enzyme that causes calcium deposition in artery walls. People who take warfarin (Coumadin®), a potent blocker of vitamin K2, experience more arterial and heart valve calcification. The 2004 Rotterdam Heart Study was the experience that really brought this concept closer to our interests. This well-conducted study of 4800 Dutch demonstrated an association of vitamin K2 intake with 57% reduction in cardiovascular events and lesser degrees of aortic calcification (another surrogate for atherosclerosis). Benefit appeared to be associated with a daily K2 intake of 32.7 micrograms per day (Geleijnse JM et al 2004). An important corollary of this study is that it suggests that a vitamin K2-mediated reduction in coronary calcification is accompanied by reduced likelihood of heart attack and other events.

Tissue phylloquinone and menaquinones in rats are affected by age and gender. Huber AM, Davidson KW, O'Brien-Morse ME, Sadowski JA. J Nutr. 1999 May;129(5):1039-44. PMID: 10222397 The results suggest that in extrahepatic tissues, certain menaquinones may be the predominant form of vitamin K. The specific tissue distribution and the general decline of MK-4 and MK-6 in extrahepatic tissues during aging suggest a vitamin K tissue dynamic that is affected not only by diet, but also by gender, age and the specific roles of phylloquinone, MK-4 and MK-6 in metabolism. All of these factors must be taken into account in establishing the nutrient requirement for vitamin K.

Age and dietary form of vitamin K affect menaquinone-4 concentrations in male Fischer 344 rats. Booth SL, Peterson JW, Smith D, Shea MK, Chamberland J, Crivello N. J Nutr. 2008 Mar;138(3):492-6. PMID: 18287355 These data suggest that dihydrophylloquinone, which differs from phylloquinone in its side phytyl chain, is absorbed but its intake results in less MK-4 in certain tissues. Dihydrophylloquinone may be used in models for the study of tissue-specific vitamin K deficiency

Conversion of phylloquinone (Vitamin K1) into menaquinone-4 (Vitamin K2) in mice: two possible routes for menaquinone-4 accumulation in cerebra of mice.\nOkano T, Shimomura Y, Yamane M, Suhara Y, Kamao M, Sugiura M, Nakagawa K.\nJ Biol Chem. 2008 Apr 25;283(17):11270-9. Epub 2007 Dec 14. \nPMID: 18083713 \ndoi: 10.1074/jbc.M702971200 \n\nOur results suggest that cerebral menaquinone-4 originates from phylloquinone intake and that there are two routes of accumulation, one is the release of menadione from phylloquinone in the intestine followed by the prenylation of menadione into menaquinone-4 in tissues, and another is cleavage and prenylation within the cerebrum.

Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. Davidson RT, Foley AL, Engelke JA, Suttie JW. J Nutr. 1998 Feb;128(2):220-3. PMID: 9446847 These data offer conclusive proof that the tissue-specific formation of MK-4 from K is a metabolic transformation that does not require bacterial transformation to menadione as an intermediate in the process

What can high-vitamin D foods do for you? * Help prevent a growing list of chronic diseases, including type 2 diabetes, heart disease, hypertension, osteoporisis, breast cancer, colon cancer, and ovarian cancer * Help keep your bones and teeth strong and healthy * Regulate the growth and activity of your cells * Reduce inflammation What events can indicate a need for more foods rich in vitamin D? * Bone pain and/or soft bones * Frequent bone fractures * Bone deformities or growth retardation in children * Lack of exposure to sunlight for any reason, including geography, use of sunscreen, or wearing of protective clothing

Apigenin inhibits growth and motility but increases gap junctional coupling intensity in rat prostate carcinoma (MAT-LyLu) cell populations. Czernik M, Sroka J, Madeja Z, Czyz J. Cell Mol Biol Lett. 2008;13(3):327-38. Epub 2008 Feb 21. PMID: 18292973 DOI: 10.2478/s11658-008-0003-z This in vitro data indicates that apigenin may affect cancer development in general, and prostate carcinogenesis in particular, via its influence on cellular activities decisive for both cancer promotion and progression, including cell proliferation, gap junctional coupling and cell motility and invasiveness.

"NEW YORK (Reuters Health) - Women who eat greater amounts of plant-based foods and drinks with the naturally occurring flavonoid, apigenin, may have a decreased risk for ovarian cancer, study findings suggest. Apigenin, found in celery, parsley, red wine, tomato sauce, and other plant-based foods may be "particularly beneficial," said Dr. Margaret A. Gates, of Brigham and Women's Hospital and Harvard Medical School, in Boston, Massachusetts. Flavanoids are compounds with antioxidant properties that protect cells against damage by oxygen molecules. In a study that compared flavonoid intake among women with and without ovarian cancer, women reporting the highest apigenin intake had a "borderline significant decrease" in ovarian cancer risk over women reporting the lowest apigenin intake, Gates and her associates report in the International Journal of Cancer."

Zingiber officinale (ginger). Monograph. [No authors listed] Altern Med Rev. 2003 Aug;8(3):331-5. PMID: 12946242

Antioxidants and Cancer III: Quercetin Davis W. Lamson, MS, ND, and Matthew S. Brignall, ND Alternative Medicine Review ◆ Volume 5, Number 3 ◆ 2000. review

Marshall K. Therapeutic applications of whey protein. Altern Med Rev. 2004 Jun;9(2):136-56. Review. PMID: 15253675 [PubMed - indexed for MEDLINE]

Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev. 2005 Jun;10(2):94-111. Review. PMID: 15989379 [PubMed - indexed for MEDLINE]

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.56 Nodules of non-small cell lung cancer freshly removed from patients expressed a marked imbalance toward Th2, as did biopsy samples from basal cell carcinoma.57 In prostate cancer patients IL-2 was low (Th1) and IL-10 high.58 IL-10 is a confirmed Th1-suppressive cytokine, and heightened IL-10 is a common factor in cancer.55 IL-10 has a variety of suppressive effects that include inhibiting Th1 cytokine production, down-regulating APC and NK cell function, and lowering overall T-cell proliferation.57 Especially under the influence of IL-4 (Th2), tumor cells apparently up-regulate IL-10 that suppresses nearby killer cells. Tumor-derived IL-10 has been documented in lymphoma, ovarian carcinoma, melanoma, neuroblastoma, and renal cell and colon carcinoma.57 IL-12 is another cytokine that can be up-regulated by Th1 activity and inhibited by Th2.59 A low IL-12/IL-10 ratio was found in cervical cancer patients.55 Recent clinical studies suggest elevated IL-10 is predictive of a poor prognosis. 57 With both IL-4 and IL-10 being proven inhibitors of Th1 and promoters of Th2 activity, the recognized capability of cancerous tissue to suppress immunity is readily rationalized.

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Plasma selenium, manganese superoxide dismutase, and intermediate- or high-risk prostate cancer. Chan JM, Oh WK, Xie W, Regan MM, Stampfer MJ, King IB, Abe M, Kantoff PW. J Clin Oncol. 2009 Aug 1;27(22):3577-83. Epub 2009 Jun 15. PMID: 19528373 DOI: 10.1200/JCO.2008.18.8938 Conclusion: These data suggest that the relationship between circulating selenium levels at diagnosis and prognostic risk of prostate cancer is modified by SOD2 genotype and indicate caution against broad use of selenium supplementation for men with prostate cancer.

"MedWire News: High levels of selenium in the blood may worsen prostate cancer in some men who already have the disease, results of a US study suggest. In recent years, selenium supplements have been promoted as a means of preventing prostate cancer, largely based on observational studies that found higher prostate cancer incidence and mortality in geographical areas that are naturally low in selenium, compared with in those that are naturally high in the mineral. However, the current research findings suggest that "if you already have prostate cancer, it may be a bad thing to take selenium," said study researcher Dr Philip Kantoff, from the Dana-Farber Cancer Institute in Boston, Massachusetts, USA."

Natural Sphingadienes Inhibit Akt-Dependent Signaling and Prevent Intestinal Tumorigenesis. Fyrst H, Oskouian B, Bandhuvula P, Gong Y, Byun HS, Bittman R, Lee AR, Saba JD. Cancer Res. 2009 Nov 24. [Epub ahead of print] PMID: 19934323 DOI: 10.1158/0008-5472.CAN-09-2341