Vitamin D Acts as Protective Agent Against the Advance of Colon Cancer
Study by VHIO researchers confirms lack of vitamin D increases the aggressiveness of colon cancer
Aug. 16, 2011 – Vitamin D, the current star of the vitamin supplement world and frequent hero of clinical studies for
fighting cancers, is back in the news today with research results indicating it plays a role in slowing the growth of colon cancer cells.
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.
Review of 28 studies finds the vitamin associated
with a substantial decrease in cardiovascular disease, type 2 diabetes
and metabolic syndrome for seniors and middle aged
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 tumor 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 tumor 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 tumor 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 tumors than mice with the VDR", explains Dr. Palmer, and concludes:
"The number of tumors is not influenced by the absence of VDR, which would indicate that this factor does not protect
against the appearance of the tumor but does intervene in its growth phase, reducing its aggressiveness".
The researchers then analyzed 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 tumors 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 tumor. 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 tumors. 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-tumor medicines based on the structure of vitamin D, although their use in
patients will require further research in the next few years.
How to obtain Vitamin D
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.
Vitamins and Minerals: About Vitamin D
Vitamins are organic
substances (made by plants or animals), minerals are inorganic
elements that come from the earth; soil and water and are
absorbed by plants. Animals and humans absorb minerals from the
plants they eat. Vitamins and minerals are nutrients that your
body needs to grow and develop normally.
Vitamins and minerals have a
unique role to play in maintaining your health. For example
Vitamin D helps your body absorb the amount of calcium (a
mineral) it needs to form strong bones. A deficiency in vitamin
D can result in a disease called rickets (softening of the bones
caused by the bodies inability to absorb the mineral calcium.)
The body cannot produce calcium; therefore, it must be absorbed
through our food.
Other minerals like
chromium, copper, iodine, iron, selenium, and zinc are called
trace minerals because you only need very small amounts of them
each day. The best way to get enough vitamins is to eat a
balanced diet with a variety of foods. You can usually get all
your vitamins from the foods you eat.
About Vitamin D
Vitamin D is a fat-soluble
vitamin that is naturally present in very few foods, added to
others, and available as a dietary supplement. It is also
produced endogenously when ultraviolet rays from sunlight strike
the skin and trigger vitamin D synthesis. Vitamin D obtained
from sun exposure, food, and supplements is biologically inert
and must undergo two hydroxylations in the body for activation.
The first occurs in the
liver and converts vitamin D to 25-hydroxyvitamin D [25(OH)D],
also known as calcidiol. The second occurs primarily in the
kidney and forms the physiologically active
1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol.
Vitamin D is essential for
promoting calcium absorption in the gut and maintaining adequate
serum calcium and phosphate concentrations to enable normal
mineralization of bone and prevent hypocalcemic tetany.
It is also needed for bone
growth and bone remodeling by osteoblasts and osteoclasts.
Without sufficient vitamin D, bones can become thin, brittle, or
misshapen. Vitamin D sufficiency prevents rickets in children
and osteomalacia in adults.
Together with calcium,
vitamin D also helps protect older adults from osteoporosis.
Vitamin D has other roles in
human health, including modulation of neuromuscular and immune
function and reduction of inflammation. Many genes encoding
proteins that regulate cell proliferation, differentiation, and
apoptosis are modulated in part by vitamin D. Many
laboratory-cultured human cells have vitamin D receptors and
some convert 25(OH)D to 1,25(OH)2D. It remains to be determined
whether cells with vitamin D receptors in the intact human carry
out this conversion.
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