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"Retinol-induced Intestinal Tumorigenesis in Min/+ Mice and Importance of Vitamin D Status. Hetland RB, Alexander J, Berg JP, Svendsen C, Paulsen JE. Anticancer Res. 2009 Nov;29(11):4353-60. PMID: 20032378 The effects of life-long dietary exposure, starting in utero, to high retinol, low vitamin D, or high retinol in combination with low vitamin D on intestinal tumorigenesis in Min/+ mice were investigated. In males, high retinol alone significantly increased the number (2.6-fold) and size (1.3-fold) of small intestinal tumours; in females no significant increase in tumour number or size was seen. In both genders, low vitamin D intake alone did not affect intestinal tumorigenesis. In males, intake of the combined high retinol/low vitamin D diet did not further increase the effects caused by high retinol alone. In females, however, the high retinol/low vitamin D-induced increase in tumour number (3.1-fold) and tumour size (1.5-fold) exceeded that of high retinol alone. In conclusion, a high dietary intake of retinol stimulated intestinal tumorigenesis in Min/+ mice. Furthermore, the results indicate a combined effect of high retinol and low vitamin D on tumorigenesis in females"

Low vitamin D status, high bone turnover, and bone fractures in centenarians. Passeri G, Pini G, Troiano L, Vescovini R, Sansoni P, Passeri M, Gueresi P, Delsignore R, Pedrazzoni M, Franceschi C. J Clin Endocrinol Metab. 2003 Nov;88(11):5109-15. PMID: 14602735 We conclude that the extreme decades of life are characterized by a pathophysiological sequence of events linking vitamin D deficiency, low serum calcium, and secondary hyperparathyroidism with an increase in bone resorption and severe osteopenia. These data offer a rationale for the possible prevention of elevated bone turnover, bone loss, and consequently the reduction of osteoporotic fractures and fracture-induced disability in the oldest olds through the supplementation with calcium and vitamin D.

After much consideration into this blog's new name in the light of my new direction, the decision has been made. "Free the Animal" Why? First, if you read that post linked above, you know that my health and fitness approach is perfectly in harmony with my philosophical approach; and hence, my approach to politics and all that. In other words, a big part of the reason I have discovered something that truly works; and moreover, is the simplest, most natural, downright fun way of living: that gets you lean and fit; gets you feeling and sleeping great; and gets you looking years and years younger is precisely because I don't believe in the gods of heaven or earth, we evolved over millions of years and are conditioned by survival pressures that in no way include all vegetable diets, gorging on bottled water all day, eating ground grass seeds (grains and derivatives) running on a treadmill or elliptical, or involving ourselves in social schemes and cons that leave us powerless, with no influence, and at the mercy of the crowd and collective (the cannibal pot). Some have a lot of the pieces and do good work. I have all of the major pieces, though acquiring all of the specifics is a lifelong and never-ending journey of discovery. I will focus on essentials and specifics that really matter to me and others living a normal life in pursuit of survival, prosperity and happiness. I will point to other sources that provide more depth in specific areas that are of interest to only some

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

"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."

There are numerous means and ways to treat diabetes. The triplet formula of life with diabetes is 'Diet, Medicine, and Exercise'. A few individuals take consistently medication for handling diabetes. There likewise persons who give careful consideration on exercise routine for getting alleviation from diabetes complications.

The panel selected to analyze the health claims is being criticized for not including the medical researchers whose work prompted intense scientific interest in the nutrient in the first place. "If you were publicly in favour of vitamin D, you were not included, and I find that outrageous," said Reinhold Vieth, a professor in the department of nutritional sciences at the University of Toronto, and one of Canada's leading experts on the nutrient.

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. Vitamin D More Effective Than Previously Known 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.

This critical nutrient builds bones, helps fight infection and may protect against some cancers. Do we get enough?

African Americans, 25-hydroxyvitamin D, and osteoporosis: a paradox. Aloia JF. Am J Clin Nutr. 2008 Aug;88(2):545S-550S. Review. PMID: 18689399

"(NaturalNews) People still don't get it: Vitamin D is the "miracle nutrient" that activates your immune system to defend you against invading microorganisms -- including seasonal flu and swine flu. Two months ago, an important study was published by researchers at Oregon State University. This study reveals something startling: Vitamin D is so crucial to the functioning of your immune system that the ability of vitamin D to boost immune function and destroy invading microorganisms has been conserved in the genome for over 60 million years of evolution. As this press release from Oregon State University (http://www.eurekalert.org/pub_relea...) explains: The fact that this vitamin-D mediated immune response has been retained through millions of years of evolutionary selection, and is still found in species ranging from squirrel monkeys to baboons and humans, suggests that it must be critical to their survival, researchers say. "The existence and importance of this part of our immune response makes it clear that humans and other primates need to maintain sufficient levels of vitamin D," said Adrian Gombart, an associate professor of biochemistry and a principal investigator with the Linus Pauling Institute at Oregon State University."

Defining Adequate Vitamin D Intake : Cross-sectional and Intervention Studies Viljakainen, Heli Tuulikki University of Helsinki 2008-05-23 Doctoral dissertation (article-based) Vitamin D is required for normal bone growth and maintenance of the skeleton throughout life. In Finland, like in many other Western countries, the population suffers from inadequate or deficient vitamin D status, especially during winter, which is thought to increase the risk of osteoporosis. New strategies to prevent osteoporosis are actively being sought. The main objective of this thesis was to determine whether vitamin D is feasible in the primary prevention of osteoporosis; does it affect bone mineral accrual during the growth period? A second goal was to ascertain whether seasonal variation in calcitropic hormones affects bone remodelling, and to elucidate the vitamin D intake needed to overcome this variation in different age groups. In summary, vitamin D intake remains inadequate among the target groups of this thesis, as reflected by seasonal variation in calcitropic hormones and bone metabolism. Dietary intake of vitamin D should be increased to achieve at least an adequate vitamin D status (S-25-OHD>50 nmol/l) and possibly an optimal vitamin D status (S-25-OHD>80 nmol/l) throughout the year. This could be accomplished by introducing new vitamin D-fortified foods to the market."

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