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| Medicalnewstoday.com |
During a study of rickets in children, vitamin D was initially identified as an important player in bone health. We now know that vitamin D has an array of duties in the body beyond that of bone health.
For instance, vitamin D is thought to impact the workings of muscles and blood vessels. And, even more recently, evidence has been gathering that the vitamin might have a protective effect on heart health. Specifically, studies have linked low levels of vitamin D to coronary artery disease and heart failure.
Heart failure is a serious, potentially life-threatening condition, wherein the heart is unable to pump sufficient blood and oxygen to nourish the tissues of the body. In 2009, around 1 in 9 deaths in the United States "included heart failure as contributing cause."
And because heart failure is so common, understanding exactly what is involved physiologically is important. Due to the recent evidence that vitamin D might protect against heart failure, scientists are keen to get a clearer understanding of the relationship.
Although the benefits of vitamin D for heart health are becoming well-established, the mechanisms at work are not understood. Recently, a team of researchers from Westmead Institute for Medical Research in Australia decided to take a closer look.
To dig into this problem, the scientists used a mouse model and a form of vitamin D called 1,25-dihydroxyvitamin D3 (1,25D), which "interacts with hormones." They wanted to understand how 1,25D affected an important set of heart cells.
The cells of interest to the team are known as cardiac colony-forming unit fibroblasts (cCFU-Fs), and they are responsible for forming scar tissue following a heart attack.
A heart attack occurs when the supply of blood to the heart is stopped. And, because no oxygen is reaching sections of the tissue, they become damaged, which triggers inflammation in the region. In the inflamed tissue, cCFU-Fs begin to replace damaged cells with "collagen-based scar tissue."
As Chong explains, "This is a problem because scarring of heart tissue can reduce the heart's ability to pump blood effectively, which can lead to heart failure."
The team found that vitamin D was able to block the action of cCFU-Fs, thereby preventing the buildup of scar tissue and potentially stopping a blockage from developing.
Their results are published this week in the journal Heart Lung and Circulation.
On the importance of the results, Chong explains, "Cardiovascular diseases, including heart attacks and heart failure, are the leading cause of death worldwide."
"To change this, we need to research heart conditions from every possible angle. This study is the first to demonstrate the role of 1,25D in regulating cardiac progenitor cells, and the findings are encouraging. With further study, vitamin D could prove to be an exciting, low-cost addition to current treatments, and we hope to progress these findings into clinical trials for humans."
So, although research into vitamin D and its cardioprotective powers is in its infancy, the results are encouraging. Finding any intervention that improves the chances of battling heart disease is good news, and finding one that is readily available is an added bonus.
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