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"We have been bombarded over the past couple of years with scientific articles suggesting that vitamin D is the key to improving many aspects of our health, including reducing the risks of dying from cancer. An article in this week's Journal of the National Cancer Institute reminds us that perhaps we should be a bit cautious in embracing vitamin D as "the answer" before we do more research. The report, from the National Cancer Institute and the Centers for Disease Control and Prevention, concluded that vitamin D levels in the blood were not related to overall cancer mortality. However, the study did find that higher levels of vitamin D were associated with a substantial decrease in the risk of dying from colorectal cancer, and possibly with a reduction in the risk of dying from breast cancer."

Review article: vitamin D acquisition and breast cancer risk. Pérez-López FR, Chedraui P, Haya J. Reprod Sci. 2009 Jan;16(1):7-19. Review. PMID: 19144887 DOI: 10.1177/1933719108327595 Conclusions: Although there are controversial results, it seems plausible that sufficient endogenous vitamin D levels may have a protective function on mammary cells, reducing breast cancer risk.

Vitamin D related articles in "The Heart Scan Blog" by Dr. William Davis

Articles about vitamin D and cancer

Vitamin D and type 2 diabetes: are we ready for a prevention trial? Scragg R. Diabetes. 2008 Oct;57(10):2565-6. PMID: 18820212 doi: 10.2337/db08-0879 Despite evidence from the current article (3) and the Finnish study (17), doubts still remain about whether low vitamin status is a cause of type 2 diabetes. Further cohort studies are required, assessing baseline vitamin D status using blood 25(OH)D to be sure that the Ely and Finnish studies are not false-positive results. Glucose clamp studies are also required because we are still not sure of the mechanism influenced by vitamin D-whether it is insulin resistance, secretion, or both. But most importantly, given that nearly three decades have passed since the first studies linking vitamin D with insulin metabolism (6,7), well-designed clinical trials of the effect of vitamin D supplementation on glycemia status and diabetes risk are urgently required to settle this question. And they need to prevent past mistakes. In particular, the vitamin D dose given in such trials needs to be high enough-above 2,000 IU per day (19)-to raise blood 25(OH)D levels above 80 nmol/l because diabetes risk is lowest at this level (9,20). If well-designed trials are carried out and confirm a protective effect from vitamin D, it could be used by the general population as a simple and cheap solution to help prevent the diabetes epidemic.

Fatigue fractures in military conscripts : A study on risk factors, diagnostics and long-term consequences Ruohola, Juha-Petri University of Helsinki, Faculty of Medicine, Institute of Clinical Medicine, Orthopaedics and Traumatology, Helsinki University Central Hospital Centre of Military Medicine, Helsinki 2007-03-09 Doctoral dissertation (article-based) It seems likely that low vitamin D levels are related to fatigue fractures, and that an increasing trend exists between TRACP-5b bone resorption marker elevation and fatigue fracture incidence. Though seldom detected by plain radiography, fatigue fractures often underlie unclear lower leg stress-related pain occurring in the distal parts of the tibia. Femoral neck fatigue fractures, when displaced, lead to long-term morbidity in a high percentage of patients, whereas, when non-displaced, they do not predispose patients to subsequent adverse complications. Importantly, an educational intervention can diminish the incidence of fracture displacement by enhancing awareness and providing instructions for earlier diagnosis of fatigue fractures

Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)

This article discusses our experience at the one-day Institute of Medicine workshop on vitamin D and calcium. Both of us had an opportunity to make comments before the committee. Here are Paul's comments and slides and here are Amy's comments and slides. Note that our 2009 paper in Autoimmunity Reviews[1] discusses some of the science we allude to in further detail.

A recent Wall Street Journal article "Defending Against Disease -- With Vitamin D New Studies Suggest It Isn't Just Bones That Might Benefit" by the wonderful Melinda Beck highlights benefits of Vitamin D3. In TYP, we've known the benefits for years :) but it's nice to see the rest of the world catching up. The benefits of Vitamin D3 are potent, powerful immunomodulation -- to the point where autoimmune diseases, viral and bacterial infections and cancer are effectively reduced. What is the value for heart disease and diabetes prevention? In hemodialysis patients, great lessons are can be learned. Nephrologists often describe patients with severe (stage 5) chronic kidney disease (CKD) patients on hemodialysis as having 'hearts of stone, blood vessels of glass.' Unfortunately over 70% of chronic hemodialysis patients have coronary artery disease (and Lp(a)). What medical science shows is that Agatston coronary calcification scores can be dramatically reduced when vitamin D is replenished and calcium is restricted. Sevelamer (Renagel) is a calcium-free, metal-free polymer phosphate binder. In 52-weeks, calcium restriction, a phosphate-binder and vitamin D resulted in one individual in a 21% reduction in Agatston CAC score (from 968 to 756; see Figure 2).

I have been inundated with letters asking about Professor Marshall's recent "discovery." Some have written that to say they have stopped their vitamin D and are going to avoid the sun in order to begin the "Marshall protocol." The immediate cause of this angst is two publications, a press article in Science Daily about Professor Marshall's "study" (which is no study but simply an opinion) in BioEssays. Dr. Trevor Marshall has two degrees, both in electrical engineering

Amsterdam, The Netherlands, May 26, 2009 - There are several risk factors for the development of Alzheimer's disease and vascular dementia. Based on an increasing number of studies linking these risk factors with Vitamin D deficiency, an article in the current issue of the Journal of Alzheimer's Disease (May 2009) by William B. Grant, PhD of the Sunlight, Nutrition, and Health Research Center (SUNARC) suggests that further investigation of possible direct or indirect linkages between Vitamin D and these dementias is needed. Low serum levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased risk for cardiovascular diseases, diabetes mellitus, depression, dental caries, osteoporosis, and periodontal disease, all of which are either considered risk factors for dementia or have preceded incidence of dementia. In 2008, a number of studies reported that those with higher serum 25(OH)D levels had greatly reduced risk of incidence or death from cardiovascular diseases

In the July 2005 FASEB Journal, Adrian F. Gombart of the University of California, Los Angeles (UCLA) and his colleagues reported that vitamin D boosts production in white blood cells of one of the antimicrobial compounds that defends the body against germs.\n\nImmediately, Cannell says, the proverbial lightbulb went on in his head: Maybe the high doses of vitamin D that he had been prescribing to virtually all the men on his ward had boosted their natural arsenal of the antimicrobial, called cathelicidin, and protected them from flu. Cannell had been administering the vitamin D because his patients, like many other people in the industrial world, had shown a deficiency:

Cancer incidence and mortality and vitamin d in black and white male health professionals.

PLYMOUTH medical researchers have discovered a link between lack of the 'sunshine vitamin' and the onset of dementia.\n\nTeams from the city's Peninsula Medical School and the universities of Cambridge and Michigan have for the first time found a relationship between lower Vitamin D levels and cognitive impairment in older people.\n\nThe results of their large-scale study are to be published in the Journal of Geriatric Psychology and Neurology.

"Last Wednesday night I gave a lecture to my clients on hunter-gatherer diets. The turnout was great and the information was well-received. I had it professionally video-recorded and will probably offer this as a DVD for sale (with the handout included). Watch for it in the future. Part of what I discussed was vitamin D3 supplementation. Since I have been supplementing with 4,000-10,000 Units of D3 per day I have noted enhanced recovery and size response from my training. Apparently, skeletal muscle has both surface receptors and nuclear receptors for D3 that augment calcium flux during contraction (from surface receptors) and have steroid-like effects at the nuclear level WRT protein synthesis. This D3 supplementation is not really "supplementation" but is instead "augmentation" to levels that would be normal if we got normal sun exposure as we did in our evolutionary past. Check out www.vitamindcouncil.org for more information. Also, check out this abstract below for your consideration. Also, check out this article."

"Summer vs Winter Mode: Explaining AMPK Last year I read an article which made a statement that has not left my mind. The statement went as follows: "You are only good as your mitochondria." In fact, the more a dwell into the details of human metabolism, the more I sense that this is true - especially with the metabolic syndrome. For those who are not familiar with the concept of mitochondria, they are the tiny energy factories within the cells that produce cellular energy through aerobic means (meaning oxygen). Mitochondria utilize oxygen to ultimately produce Adenosine Triphosphate or simply ATP. ATP relays energy by donating a phosphate bond resulting in Adenosine Diphosphate (ADP). Another phosphate release would entail Adenosine Monophosphate or AMP. ATP is one of the main sources of cellular energy in the body