קטגוריה: ויטמין D
אינדקס UV בישראל
שמש מונעת סרטן
How strong is the evidence that solar ultraviolet B and vitamin D reduce the risk of cancer?
An examination using Hill’s criteria for causality William B. Grant Dermato-Endocrinology 1:1, 17-24; January/February 2009; ©2009 Landes Bioscience Summary and Conclusion
The solar UVB—vitamin D—cancer theory now satisfies most, if not all, of the criteria for causality in a biological system as initially postulated by Robert Koch and expanded by A. Bradford Hill.
Thus, from a scientific point of view, vitamin D reduces the risk of developing many types of cancer and increases survival once cancer reaches the detectable stage.
Unfortunately, health policy often lags scientific discoveries by years to decades. An example from the mid-19th century was the discovery by Ignaz Semmelweis that doctors carried germs from autopsies to women giving birth and infected them, resulting in puerperal sepsis.
A more recent example is the announcement by Barry Marshall and Robin Warren that Helicobacter pylori caused stomach ulcers. Although Marshall infected himself with H. pylori in 1981 and developed an ulcer,126 he concluded by 1995 that Koch’s postulates were not well satisfied.
However, in 2005, Marshall and Warren were awarded the Nobel Prize in Medicine. It is hoped that the acceptance of the beneficial role of vitamin D in reducing the risk of cancer and many other diseases will not have to wait much longer.
It is encouraging that the National Academy of Sciences’ Institute of Medicine (http:// www.iom.edu) is embarking on a 2-year study of vitamin D dietary requirements and is expected to issue a report in October 2010.
ביצועים ספורטיבים וויטמין D
Athletic Performance and Vitamin D JOHN J. CANNELL1, BRUCE W. HOLLIS2, MARC B. SORENSON3, TIMOTHY N. TAFT4, and JOHN J. B. ANDERSON5
1Atascadero State Hospital, Atascadero, CA; 2Departments of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC; 3sunlightandhealth.org, Saint George, UT; 4Departments of Orthopedics and Sports Medicine, University of North Carolina, Chapel Hill, NC; and 5Departments of Public Health and Nutrition, University of North Carolina, Chapel Hill, NC
ABSTRACT
CANNELL, J. J., B. W. HOLLIS, M. B. SORENSON, T. N. TAFT, and J. J. ANDERSON.
Athletic Performance and Vitamin D. Med.Sci. Sports Exerc., Vol. 41, No. 5, pp. 1102–1110, 2009.
Purpose: Activated vitamin D calcitriol) is a pluripotent pleiotropic secosteroid hormone. As a steroid hormone, which regulates more than 1000 vitamin D–responsive human genes, calcitriol may influence athletic performance. Recent research indicates that intracellular calcitriol levels in numerous human tissues, including nerve and muscle tissue, are increased when inputs of its substrate, the prehormone vitamin D, are increased.
Methods: We reviewed the world’s literature for evidence that vitamin D affects physical and athletic performance.
Results: Numerous studies, particularly in the German literature in the 1950s, show vitamin D–producing ultraviolet light improves athletic performance. Furthermore, a consistent literature indicates physical and athletic performance is seasonal; it peaks when 25-hydroxy-vitamin D [25(OH)D] levels peak, declines as they decline, and reaches its nadir when 25(OH)D levels are at their lowest. Vitamin D also increases the size and number of Type II (fast twitch) muscle fibers. Most cross-sectional studies show that 25(OH)D levels are directly associated with musculoskeletal performance in older individuals. Most randomized controlled trials, again mostly in older individuals, show that vitamin D improves physical performance.
Conclusions: Vitamin D may improve athletic performance in vitamin D–deficient athletes. Peak athletic performance may occur when 25(OH)D levels approach those obtained by natural, full-body, summer sun exposure, which is at least 50 ngImLj1. Such 25(OH)D levels may also protect the athlete from several acute and chronic medical conditions.
Key Words: PHYSICAL PERFORMANCE, PEAK ATHLETIC PERFORMANCE, ACTIVATED VITAMIN D, CALCITRIOL, 1, 25-DIHYDROXY-VITAMIN D, 25(OH)D
ויטמין D תלוי במגנזיום
- הגברה מלאכותית של סידן במזון עקב הדעה המוטעית שמחסור בסידן הוא הגורם לאוסטאופורוזיס (בעוד שהגורם לכך הוא מחסור בויטמין D)
- מחסור במגנזיום באדמות גירניות בישראל ובמים בישראל
- התפלת מי ים וערבוב המים המותפלים במי שתיה
Abstract
Background: Magnesium plays an essential role in the synthesis and metabolism of vitamin D and magnesium supplementation substantially reversed the resistance to vitamin D treatment in patients with magnesium-dependent vitamin-D-resistant rickets. We hypothesized that dietary magnesium alone, particularly its interaction with vitamin D intake, contributes to serum 25 hydroxyvitamin D (25(OH)D) levels, and the associations between serum 25(OH)D and risk of mortality may be modified by magnesium intake level.
Methods: We tested these novel hypotheses utilizing data from the National Health and Nutrition Examination Survey (NHANES) 2001 to 2006, a population-based cross-sectional study, and the NHANES III cohort, a populationbased cohort study. Serum 25(OH)D was used to define vitamin D status. Mortality outcomes in the NHANES III cohort were determined by using probabilistic linkage with the National Death Index (NDI).
Results: High intake of total, dietary or supplemental magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively. Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency. Additionally, the inverse association between total magnesium intake and vitamin D insufficiency primarily appeared among populations at high risk of vitamin D insufficiency. Furthermore, the associations of serum 25(OH)D with mortality, particularly due to cardiovascular disease (CVD) and colorectal cancer, were modified by magnesium intake, and the inverse associations were primarily present among those with magnesium intake above the median.
Conclusions: Our preliminary findings indicate it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status. The associations between serum 25(OH)D and risk of mortality may be modified by the intake level of magnesium. Future studies, including cohort studies and clinical trials, are necessary to confirm the findings.
Keywords: Magnesium intake, Serum 25-hydroxyvitamin D levels, Vitamin D insufficiency, Vitamin D deficiency, Parathyroid hormone, Mortality, Colorectal cancer, Cardiovascular diseases.