Originally published November 28 2014
Vitamin D inhibits prostate cancer by activating inflammation-regulating gene, study suggests
by David Gutierrez, staff writer
(NaturalNews) Vitamin D may reduce prostate cancer risk by acting on a gene that lowers inflammation, according to a study conducted by researchers from the University of Colorado Cancer Center and published in the journal Prostate.
Back in 1990, scientists first suggested that vitamin D might be the common variable linking a number of known prostate cancer risk factors, including older age (associated with reduced vitamin D synthesis), living at a northern latitude (where people are more likely to be vitamin D-deficient due to lower levels of the sunlight that stimulates synthesis of the vitamin) and African descent (because darker skin leads to reduced vitamin D synthesis). In addition, studies had shown that prostate cancers diagnosed in the summer or autumn, when vitamin D levels in the body tend to be highest, were less deadly than those diagnosed in the winter or spring.
Prostate cancer levels are also known to be low in Japan, where people tend to consume high levels of soy and fatty fish rich in vitamin D and omega-3 fatty acids. Omega-3s make vitamin D more stable in the body, while soy makes it remain active longer.
More recently, researchers have found that vitamin D supplementation might slow the progression of prostate cancer, and that many prostate cancer cells contain receptors for vitamin D.
Inflammation is the keyThe new study sought to clarify the role of vitamin D by understanding exactly how it affects prostate cancer cells.
"When you take Vitamin D and put it on prostate cancer cells, it inhibits their growth," researcher James R. Lambert, PhD, said. "But it hasn't been proven as an anti-cancer agent. We wanted to understand what genes Vitamin D is turning on or off in prostate cancer to offer new targets."
Prior research had indicated that vitamin D increases the expression of a gene known as GDF-15, which codes for a specific protein. Yet, when the researchers looked more closely at GDF-15 expression, it seemed to have no connection with prostate cancer.
"We thought there might be high levels of GDF-15 in normal tissue and low levels in prostate cancer," Lambert said, "but we found that in a large cohort of human prostate tissue samples, expression of GDF-15 did not track with either normal or cancerous prostate tissue."
When the researchers added in the variable of inflammation, however, the picture changed radically. They found that GDF-15 levels were lowest in prostate cells with the most inflammation.
"Inflammation is thought to drive many cancers including prostate, gastric and colon," Lambert said. "Therefore, GDF-15 may be a good thing in keeping prostate tissue healthy -- it suppresses inflammation, which is a bad actor potentially driving prostate cancer."
The solution to drug ineffectiveness?The researchers also found that GDF-15 expression inhibited another gene, called NFkB. This gene has been shown in other studies to increase inflammation and to contribute to tumor formation and growth. Yet all efforts to dampen the activity of NFkB with drug treatments have been unsuccessful so far.
The new study suggests that upregulating GDF-15 -- perhaps by a mechanism as simple as increased sunlight exposure -- could be a better strategy.
"There's been a lot of work on inhibiting NFkB," said Lambert. "Now from this starting point of Vitamin D in prostate cancer, we've come a long way toward understanding how we might use GDF-15 to target NFkB, which may have implications in cancer types far beyond prostate."
Research is increasingly linking vitamin D to a lower risk of cancer, autoimmune disease and other chronic diseases. Doctors recommend that light-skinned people get at least 15 minutes of unprotected sun exposure on their face and hands daily; people with darker skin and those living far from the equator may need two to three times as much exposure.
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