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"We are fond of grumbling about Britain's grey skies, but there may be a good medical reason for doing so. It seems the dreary weather is bad for our hearts - worse, even, than raised cholesterol and an unhealthy diet. That's the controversial claim being made by Dr David Grimes, a gastroenterologist from Blackburn. He's been gazing at the sky for 20 years for clues about why his patients get more sick than those in the south of the country. And what he's found turns key assumptions about heart disease on their head. 'It's not diet or cholesterol levels that raise your risk of heart disease,' he claims. 'It's where you live. People in the north are more likely to be ill because they get less sunshine Basically they are suffering from 'latitude' sickness. The link is vitamin D. While we get some from our diet, the main source is the sun - sunlight converts a compound in the skin into vitamin D, so the amount you make is directly related to the amount of sunshine you get. In a new book Dr Grimes argues the higher the level of vitamin D in your blood, the lower your risk of heart disease and a range of other illnesses. If he's right, what we need is not diet and lifestyle advice, but food fortified with vitamin D. For years the vitamin was thought to be useful only for preventing rickets. So how does he treat them? 'You can do it with diet,' he says 'One Bangladeshi woman eats oily fish every day and now has a vitamin D blood level of 40. 'We give supplements of 1,000 international units (IU) a day or we can give an injection of 300,000 IU that lasts for a year. 'The patients respond well,' says Grimes 'but what's needed is a proper controlled, long-term trial and who is going to fund that? Not a drug company.'"

"Do Your Vitamin D Research Here Links to all the Latest Research Studies Welcome to the Vitamin D Research Library. Here you'll find links to all of the latest Vitamin D Facts and Research studies, clinical trials and other scholarly Vitamin D Facts. The Research Library is Open 24/7 and is always growing. I'll be adding more and more links all of the time. Can't find what you are looking for or just don't want to spend the time doing the research yourself? Chances are, I've already done the Vitamin D Research myself and can answer your question. Read Frequently Asked Questions about Vitamin D OR Ask Your Question About Vitamin D Here and I'll answer your Question about Vitamin D Personally based on the best available Vitamin D Research."

One hour public information video lecture about vitamin D by professor Reinhold Vieth, Toronto University, Canada.Also a video lecture about nutritional interventions in multiple sclerosis,

Multiple Sclerosis Blog By Julie Stachowiak, Ph.D.,

In the last post, we talked about the new report on vitamin D and cancer from the International Agency for Research into Cancer (IARC). In this one, we'll summarise what the report has to say on the balance between getting enough vitamin D through sun exposure and reducing the risk of skin cancer by being SunSmart. IARC calls for more trials to really pin down the effects of vitamin D supplements - either positive or negative - depending on how much vitamin D people already have in their system. Until then, they feel that there is no solid basis for changing any existing recommendations about vitamin D.

The Vitamin D Cure (Paperback) by James Dowd MD (Author), Diane Stafford Diane Stafford (Author) › Visit Amazon's Diane Stafford Page Find all the books, read about the author, and more. See search results for this author Are you an author? Learn about Author Central (Author)

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

What is VITAL? The VITamin D and OmegA-3 TriaL (VITAL) is a research study in 20,000 U.S. men and women investigating whether taking daily dietary supplements of vitamin D (about 2000 IU) or fish oil (about 1 gram of omega-3 fatty acids) reduces the risk of developing cancer, heart disease, and stroke in people who do not have a prior history of these illnesses. Recruitment for the study will begin in January 2010.

Vitamin D and cancer mini-symposium: the risk of additional vitamin D. Vieth R. Ann Epidemiol. 2009 Jul;19(7):441-5. Epub 2009 Apr 11. Review. PMID: 19364661 Conclusion The results of well-conducted trials of vitamin D lead to the conclusion that the current U.S. National Academy of Sciences-Institute of Medicine upper limit for vitamin D intake of 2000IU per day 1, 37 is excessively conservative. That intake would raise serum 25(OH)D by an average of about 50 nmol/L (20 ng/mL), well within the safe range of serum 25(OH)D concentrations that extends to 500 nmol/L (200 ng/mL). Intake of 4,000IU per day would raise serum 25(OH)D by an average of about 100 nmol/L (40 ng/mL). Even prolonged physiologic-replacement intake of 10,000IU per day of vitamin D3 would pose no known risk of adverse effects in virtually all adults.

What causes coronary heart disease or coronary atherosclerotic plaque, this thing that we track with heart scans? Well, here are a few little-publicized facts about heart disease that you are unlikely to hear from your When's-the-next-stent? cardiologist or the What is there besides statins? primary care doctor. (Since everybody knows that smoking is a modifiable risk for heart disease that can be readily identified, let's focus on the blood tests that reveal heart disease causes.)

True to form, Dr. John Cannell has published yet another wonderfully insightful Vitamin D Newsletter. One item caught my eye, a response to a question about the Marshall Protocol. I, like Dr. Cannell, was inundated with questions about this so-called protocol, which amounts to little more than the unfounded speculations of a non-physician, actually someone not even involved in health care. In all honesty, I blew the whole issue off after I read Dr. Marshall's rants. They smack of pure quackery, though from somebody who clearly has a command of scientific lingo. To Dr. Cannell's credit, he took the time and effort to construct a rational response in the latest issue of the newsletter. I reproduce his response here:

"Had enough about reading/hearing about Vitamin D? Well, it keeps on coming. And for my lack of surprise, the medical community in general is not catching on like wild fire. I really don't understand it. A recent study from the Heart Institute at Intermountain Medical Center in Salt Lake City (click) followed 27,686 patients greater than 50 years of age with no prior history of cardiovascular disease. The Vitamin D levels were checked and classified as such: * normal - greater than 30 ng/ml * low - 15 to 30 * very low - less than 15 The results of the study showed that patients with very low Vitamin D levels in comparison to normal had: * 77% greater risk of death * 45% increased risk of coronary artery disease * 78% increased risk of stroke * twice the risk of developing heart failure"

"I discussed in my last post how Dr Vieth has a model of tissue 1,25(OH)2D synthesis and degradation in which the level of active substance is pretty well independent of blood vitamin D level, provided the level is either rising or stable. I think it is also worth pointing out that he is talking, hypothetically, about tissue 1,25(OH)2D, not plasma level... As we know, almost nothing is known about tissue 1,25(OH)2D control. By Vieth's hypothesis tissue 1,25(OH)2D is OK so long as there is at least SOME vitamin D present in plasma and the level dose not vary too much. Obviously there is a level below which you can have as much of the enzyme for converting vitamin D to the active form as you like, if there is no vitamin D in your blood you can't make any 1,25(OH)2D in your tissues, or in your kidneys for export to your blood to control calcium levels. At the lower extremes we have rickets and osteomalacia. These are clear cut, unarguable markers of vitamin D deficiency, in the absence of confounding factors (there are a few)."

The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures Author: Amy Proal

My plans to take vitamin D seemed well funded (lots of positive research these days about high vitamin D levels) and then I stumbled upon this article that promotes the views of Trevor Marshall. "The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures", by Amy Proal (a biologist), 15/09/2007 http://bacteriality.com/2007/09/15/vitamind/

Induction of ovarian cancer cell apoptosis by 1,25-dihydroxyvitamin D3 through the down-regulation of telomerase. Jiang F, Bao J, Li P, Nicosia SV, Bai W. J Biol Chem. 2004 Dec 17;279(51):53213-21. Epub 2004 Oct 12. PMID: 15485861 doi: 10.1074/jbc.M410395200 Overall, the study suggests that the down-regulation of telomerase activity by 1,25(OH)2VD3 and the resulting cell death are important components of the response of OCa cells to 1,25(OH)2VD3-induced growth suppression. Progressive shortening of telomere associated with cell divisions limits the life span of normal cells and eventually leads to senescence. To become immortal, human cancers including OCa are invariably associated with activation of mechanism that maintains telomere length. Approximately 85-90% of cancers show reactivation of telomerase. The present study shows that telomerase in OCa cells is down-regulated by 1,25(OH)2VD3. Down-regulation of telomerase is due to decreased stability of hTERT mRNA rather than VDRE-mediated transcriptional repression through the putative VDRE present in the regulatory region of the hTERT gene. It is known that the inhibition of telomerase may lead to a phenotypic lag during which cells would continue to divide until the point at which the telomeres became critically short. This phenomenon may explain why the apoptotic induction by 1,25(OH)2VD3 needs the treatment for more than 6 days. As mentioned in the results, no detectable shortening of telomeric repeats was observed in parental OVCAR3 cells after 9 days of treatment with 1,25(OH)2VD3 (Fig. 4D). This is likely due to the fact that the short telomere (about 3 kb) in OVCAR3 cells is very close to the minimal length required for survival and that cells with detectably shorter telomere may have been selected against apoptosis. It has been shown that transformed human cells enter crisis once the terminal restriction fragment of the telomere reaches a length of about 4 kb. This is insufficient to protect chro

The Author The author of this site is the British writer, John Davidson. Please note that the author is neither a doctor, nor a qualified health practitioner. Every cancer patient should always consult his or her medical practitioner with regard to the use of complementary remedies or treatments, and nothing on this site should be construed in any way as medical or therapeutic advice. It is simply the result of one person's search for solutions. Please read our disclaimer. About This Site Internet searches trawl up vast amounts of information about cancer, from a broad spectrum of viewpoints. The information and internet links on this site are for those seeking to augment the treatment offered by their hospital oncology (cancer) unit. Of course, a great many other internet sites concerning cancer can be found by keying the requisite search words into any of the major search engines. The content of this site was initially prepared, at the request of medical and nursing staff and others, some weeks after I had had an emergency operation for the removal of a colon cancer, and while undergoing chemotherapy in case any cancer cells had gone AWOL. There had been some escape of cancer cells into associated lymph nodes (3 out of 17, including the most distal), but no other tumours had been picked up by a CT scan. When I returned home from hospital in September 2005, with the help of friends, I started doing some research on cancer. I was amazed to discover that despite the billions of pounds/euros/dollars etc. spent on cancer research, and the many advances in understanding the numerous variants of the disease, the standard treatment for my stage of colon cancer is still a drug (fluorouracil, also called 5FU) that has been in use for more than forty years, has uncomfortable side effects, and which only increases the chances of survival after five years by 5 to 10%.

Good Information

"For what reason I don't know, but this January 2009 editorial by William Faloon of the Life Extension Foundation is making the rounds. Perhaps it just came available on the web. It's a good read, particularly in light of the billions and trillions of dollars the thieves & thugs in DC are about to flush down the crapper on your behalf. Some notable excerpts. A large number of new vitamin D studies have appeared in the scientific literature since I wrote my plea to the federal government. These studies don't just confirm what we knew 16 months ago-they show that optimizing vitamin D intake will save even more lives than what we projected. For instance, a study published in June 2008 showed that men with low vitamin D levels suffer 2.42 times more heart attacks. Now look what this means in actual body counts. Each year, about 157,000 Americans die from coronary artery disease-related heart attacks. Based on this most recent study, if every American optimized their vitamin D status, the number of deaths prevented from this kind of heart attack would be 92,500. To put the number of lives saved in context, tens of millions of dollars are being spent to advertise that Lipitor® reduces heart attacks by 37%. This is certainly a decent number, but not when compared with how many lives could be saved by vitamin D. According to the latest study, men with the higher vitamin D levels had a 142% reduction in heart attacks."

Zittermann A, Schleithoff SS, Koerfer R. Vitamin D insufficiency in congestive heart failure: why and what to do about it? Heart Fail Rev. 2006 Mar;11(1):25-33. PMID: 16819575 [PubMed - in process]