The indication that vitamin D and its derivatives have a protective effect against various types of cancer is not new. In the field of colon cancer, numerous experimental and epidemiological studies show that vitamin D3 (or cholecalciferol) and some of its derivatives inhibit the growth of cancerous cells. Researchers at the Vall d’Hebron Institute of Oncology (VHIO), in collaboration with the Alberto Sols Institute of Biomedical Research (CSIC-UAB), have confirmed the pivotal role of vitamin D, specifically its receptor (VDR), in slowing down the action of a key protein in the carcinogenic transformation process of colon cancer cells. These results are being published in the journal PLoS One.

This protein, known as beta-catenin, which is normally found in intestinal epithelial cells where it facilitates their cohesion, builds up in large quantities in other areas of the cells when the tumour transformation begins. As a result of these changes, the protein is retained in the cell nucleus, where it facilitate the carcinogenic process, and this is the point at which vitamin D intervenes, or rather, the vitamin D receptor (VDR). “Our study has confirmed the pivotal role of the VDR in controlling the anomalous signal that sparks off the growth and uncontrolled proliferation of colon cells which, in the final instance, ends up causing a tumour to emerge”, says Héctor Palmer, the coordinator of this study and head of the VHIO’s Stem Cells and Cancer laboratory. He continues, “The stimulation of this receptor suppresses the action of the beta-catenin protein, intercepting the series of events that change the intestinal cell into a malignant tumour cell”.

The study was conducted on mice and human colon cancer cells. The mice were used as a model to replicate the initial phases of colon cancer. “These findings show that mice of this kind, which also lack the VDR and hence do not respond to vitamin D, present larger and more aggressive tumours than mice with the VDR”, explains Dr. Palmer, and concludes: “The number of tumours is not influenced by the absence of VDR, which would indicate that this factor does not protect against the appearance of the tumour but does intervene in its growth phase, reducing its aggressiveness”.

The researchers then analysed the effect of the VDR on human colon cancer cell cultures and observed that the concentration of the altered protein, beta-catenin, increased in cells without the VDR. These findings were repeated in the three types of colon cancer cells studied, and confirmed the results observed in the mice.

In two-thirds of advanced colon cancer tumours there was a lack of VDR in the cancer cells, and this circumstance leads us to believe that this loss may contribute to speeding up the growth of the tumour. The findings of this study confirm this supposition.

Vitamin D: essential in the initial phases of colon cancer

In light of these findings, chronic vitamin D deficiency represents a risk factor in the development of more aggressive colon tumours. Patients in the initial stages of colon cancer, the time when the VDR still has a substantial presence in the cells, could benefit from being treated with vitamin D3. However, this would not be useful in the advanced stages of the disease when the presence of the VDR is very much reduced.

The study data support the development of anti-tumour medicines based on the structure of vitamin D, although their use in patients will require further research in the next few years.

The body not only obtains vitamin D from food, especially milk and fish oils, but also manufactures it from exposure to sunlight. Prolonged exposure is not necessary; just 10 minutes in the sun every day when it is not at its peak is sufficient to stimulate its production. During the summer, when we are more likely to sunbathe, it is important to use the appropriate protective measures against sunburn to avoid future sun damage. Use high-factor solar protection products and do not expose the skin to the sun in the middle of the day to protect against skin cancers.

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Here is a list of references that I referred to in my TEDx Memphis Talk on May 21, 2011.

Psychological stress— both perceived stress and chronicity of stress—is significantly associated with higher oxidative stress, lower telomerase activity, and shorter telomere length, which are known determinants of cell senescence and longevity, in peripheral blood mononuclear cells from healthy premenopausal women. Women with the highest levels of perceived stress have telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low stress women. These findings have implications for understanding how, at the cellular level, stress may promote earlier onset of age-related diseases. People who are stressed over long periods tend to look haggard, and it is commonly thought that psychological stress leads to premature aging and the earlier onset of diseases of aging. Numerous studies demonstrate links between chronic stress and indices of poor health, including risk factors for cardiovascular disease and poorer immune function. Nevertheless, the exact mechanisms of how such stress exerts these effects are not well known, including whether stress accelerates aging at a cellular level and how cellular aging translates to organismal aging. Recent research points to the crucial roles of telomeres and telomerase in cellular aging and potentially in disease. Telomeres are DNA–protein complexes that cap chromosomal ends, promoting chromosomal stability. When cells divide, the telomere is not fully replicated because of limitations of the DNA polymerases in completing the replication of the ends of the linear molecules, leading to telomere shortening with every replication (3). In vitro, when telomeres shorten sufficiently, the cell is arrested into senescence. In people, telomeres shorten with age in all replicating somatic cells that have been examined, including fibroblasts and leukocytes (4). Thus, telomere length can serve as a biomarker of a cell’s biological (versus chronological) “age” or potential for further cell division.

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New research published in the Journal of Nutrition shows that pecans are good for the heart and may help stave off diseases. Pecans are very high in vitamin E (particularly gamma tocopherols) and in polyphenols, which are both very potent antioxidants. The study showed that after eating a meal consisting of pecans the levels of oxidized bad cholesterol (LDL) were dramatically reduced. This is important for cardiovascular health because oxidized cholesterol leads to inflammation in the arteries which contributes to atherosclerosis. The findings also demonstrated that the levels of vitamin E in in the blood doubled and the antioxidant activity increased by as much as 12% 2 hours after a meal of pecans. There is one last thing that I want to mention and that is that most of the vitamin E that we consume is the alpha tocopherol because gamma tocopherol is hard to find. Bottom line is eat your pecans!

Coconut oil has made a return to its previous place of glory as a health food with a multitude of uses. One of the most popular uses has been a total reversal of its presumed role in weight gain. Though coconut oil is a saturated fat, it is a very special one known as a medium chain fatty acid. Medium chain fatty acids are not able to be metabolized in the same ways as ordinary fats. Consequently, when you ingest coconut oil it actually boosts your metabolism.

Coconut oil also has the highest content of lauric acid among any products currently out there — aside from breastmilk. Lauric acid is a special compound that harbors anti-microbial properties that have been demonstrated in vitro to kill bacteria called propionibacterium acnes. These are the bacteria responsible for causing the acne that plagues so many teenagers around the world.

Lauric acid is said to be a cox1 and cox2 inhibitor by some sources. If correct, this means that lauric acid may play a role in reducing inflammation which is the cause of a very large number of diseases that plague the modern world such as atherosclerosis.

Are you a health fanatic? You should spread the word. Use the new good news about coconut oil not being a bad fat, and in fact, being a fat that is healthy as a way to connect with others. If more people knew about the health benefits of coconut oil then it is likely that we would not have such a severe obesity problem here in the United States, as well as in the other developed nations of the world.

A snow day postponed our last scheduled meetup on alpha lipoic acid and aging. This meetup has been re-scheduled for February 10th from 7:00-8:00 we will be having the meetup at Republic Coffee. We will be discussing alpha-lipoic acid and its role in the aging process with focus on antioxidant recycling, skin aging and blood sugar.

The facebook event can be found at:
http://www.facebook.com/event.php?eid=184062998290949

The address for Republic Coffee is…
2924 Walnut Grove Rd
Memphis, Tennessee 38111

We will be in the back room.

Questions? (901) 451-9506

The title says it all. Tomorrow at 7PM Rhonda will be giving a presentation on Alpha Lipoic Acid and Aging. Read more on the meetup page at meetup.com/foundmyfitness.

The address for Republic Coffee is…
2924 Walnut Grove Rd
Memphis, Tennessee 38111

We will be in the back room.

Questions? (901) 451-9506

Just when you thought eating a diet high in fruits would give your body super human powers, bursting with anti-oxidants to stave off reactive oxygen species and inflammation; you find out that fruit is a double-edged sword. Fructose found naturally in fruits and artificially in syrups like high fructose corn syrup produce something in our bodies called advanced glycation end products or AGE’s for short. AGE’s crosslink proteins in our bodies, resulting in non-functional proteins, ultimately, damaging all our organs and tissues. The worst part, as we age we accumulate more and more of them, subsequently, accelerating the aging process. Among other things, AGE’s made from fructose wreak havoc on collagen, decreasing collagen’s elasticity and causing the formation wrinkles (J Nutr. 1998 Sep;128(9):1442-9).

A happy accident may hold the key to healing muscle diseases and granting humans incredible physiques. Researchers at the University of Colorado at Boulder and the University of Washington discovered that stem cells injected into mouse muscles led to increased growth for the rest of the mouse’s life. Young mice with injured legs were given donor muscle stem cells from other young mice. Those injuries not only healed, but muscle mass increased 50% and muscle volume increased by an incredible 170%! Performance tests show the muscles were twice as strong as normal, and still above average when you control for size. (via: 1, 2.)