Vitamin D nutritional policy needs a vision for the future. Exp. Biol. Med. (Maywood)

Department of Biochemistry and Division of Biomedical Sciences, University of California, Riverside, CA 92521, USA.
Experimental Biology and Medicine (Impact Factor: 2.23). 09/2010; 235(9):1034-45. DOI: 10.1258/ebm.2010.010014
Source: PubMed

ABSTRACT Historically vitamin D is known to be essential for normal bone growth and quality, and thus appropriate dietary vitamin D supplementation can eliminate vitamin D deficiency childhood rickets and adult osteomalacia. In spite of many government and medical associations' worldwide guidelines for the reference daily intake (RDI) of vitamin D, scientists and nutritionists from many countries agree that at present about half of elderly North Americans and Western Europeans and probably also of the rest of the world are not receiving enough vitamin D to maintain healthy bone. In addition, over the past decade there has been a dramatic increase in our understanding of the many biological actions that result from vitamin D acting through its daughter steroid hormone, 1alpha,25-dihydroxyvitamin D(3) [1alpha,25(OH)(2)D(3)] in collaboration with its cognate vitamin D receptor (VDR). Consequently, evidence has accumulated that beside intestine and bone, there are five additional physiological systems where the VDR with 1alpha,25(OH)(2)D generates biological responses. These include the immune system (both the innate and adaptive), pancreas and metabolic homeostasis, heart-cardiovascular, muscle and brain systems as well as the control of the cell cycle, and thus of the disease process of cancer. Acting through the VDR, 1alpha,25(OH)(2)D(3) can produce a wide array of favorable biological effects that collectively are projected to contribute to the improvement of human health. Responsible medicine demands that worldwide vitamin D nutritional guidelines reflect current scientific knowledge about vitamin D's spectrum of activities. Thus, worldwide vitamin D nutritional policy is now at a crossroads. This paper presents several proposed policy changes with regard to the amount of vitamin D daily intake that if implemented will maximize vitamin D's contribution to reducing the frequency of many diseases, which would then increase the quality and longevity of life and significantly reduce the cost of medical care worldwide.

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Available from: Anthony W Norman, Aug 12, 2015
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    • "The efficiency of vitamin D synthesis in the body depends on factors such as pigmentation of the skin, the geographic latitude where an individual lives, the amount of sunlight present, sunlight exposure, and the age of the individual [109]. The primary cause of vitamin D deficiency has been suggested to be geographical conditions, seasons, cultural features, and nutrition. "
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    ABSTRACT: Scientists have worked for over a century to uncover the basis of Alzheimer's disease (AD) with the ultimate goal of discovering a treatment. However, none of the approaches utilized have defined the exact cause of the disease or an ultimate treatment for AD. In this review, we aim to define the role of vitamin D in AD from a novel and fundamental perspective and attempt to answer the following question: Why should we seriously consider "simple" vitamin D as a "fundamental factor" in AD? To answer this question, we explain the protective effects of vitamin D in the central nervous system and how the action of vitamin D and AD-type pathology overlap. Furthermore, we suggest that the role of vitamin D in AD includes not only vitamin D deficiency and vitamin D-related genes but also the disruption of vitamin D metabolism and action. This suggestion is supported by evidence that the disruption of vitamin D pathways mimic amyloid pathology. We define the term "inefficient utilization of vitamin D" as any alteration in vitamin D-related genes, including receptors, the enzymes related to vitamin D metabolism or the transporters of vitamin D, and we discuss the potential correlation of vitamin D status with the vulnerability of neurons to aging and neurodegeneration. Finally, in addition to the current knowledge that defines AD, we suggest that AD could be the result of a long-term hormonal imbalance in which the critical hormone is vitamin D, a secosteroid that has long been misnamed.
    Journal of Alzheimer's disease: JAD 01/2014; 40(2). DOI:10.3233/JAD-131970 · 4.15 Impact Factor
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    • "In addition to high educational level, enriched social network and active engagement in mental, social and physical activities (Qiu et al., 2009; Coley et al., 2008), epidemiological data suggest that some nutrients may also have a protective role (Gillette Guyonnet et al., 2007). Some evidence exists that macronutrients have influence on cognitive decline, such as glycemic load, which has an impact on insulin resistance and glucose handling in brain (Hsu et al., 2011), omega-3 fatty acids that would promote neuronal plasticity and improve learning capacities and cognitive functions (Sinclair et al., 2007) and Vitamin D3 that could in case of deficiency to alters adult behavior and brain function by increasing risk of obesity and cardiovascular diseases, impairing insulin secretion and increasing insulin resistance (Norman and Bouillon, 2010). Other micronutrients (vitamins B6, B12 and folate) play a protective role against cognitive decline (Ortega et al., 1997; Murakami et al., 2010; Lee et al., 2009). "
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    12/2013; El Zoghbi M,et al.(xxxx):1-9. DOI:10.1016/j.gmhc.2013.04.007
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    • "Being the major circulating form of vitamin D in blood, 25(OH)D is metabolized to its active form 1,25-dihydroxyvitamin D (1,25(OH) 2 D) in kidneys and many nonrenal tissues, including bone, placenta, prostate, keratinocytes, etc. [9]. As steroid hormone, 1,25(OH) 2 D regulates calcium metabolism and bone health, a wide variety of genes in more than 30 different tissues, including brain, liver, kidney, prostate, and have important function in regulating cell growth, modulating immune system and cardiovascular health [2] [7]. "
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