Taking vitamin or mineral supplements could feed tumors and allow them to grow, new research suggests.
Common antioxidants, such as vitamins A, C, selenium, and zinc, when taken in addition, can cause blood vessels to grow in cancer.
The discovery has come as a surprise as antioxidants were believed to have a protective effect.
The researchers said the natural levels in food were fine, but if people also take supplements that contain antioxidants, the extra amount can fuel tumor growth.
The study, published in the Clinical Research JournalIt was carried out by the Karolinska Institute of Sweden.
He concluded that vitamin C and other antioxidants stimulate the formation of new blood vessels in lung cancer tumors.
They say this could be applied to all cancers and their spread.
Study leader Martin Bergö, Professor at the Department of Biosciences and Nutrition, said: “We have found that antioxidants activate a mechanism that causes cancerous tumors to form new blood vessels, which is surprising as it was previously thought that antioxidants had a protective effect. effect.
“The new blood vessels nourish tumors and can help them grow and spread.”
Antioxidants neutralize oxygen free radicals, which can damage the body, and for this reason they are commonly found in dietary supplements. But too high doses can be harmful.
Professor Bergö added: “Antioxidants in normal foods are not to be feared, but most people don’t need extra amounts of them.
“In fact, it may be harmful to cancer patients and people at high risk of cancer.”
The team found that antioxidants reduce levels of oxygen free radicals, but when additional amounts are introduced, the free radical knockdown activates a protein called BACH1.
This then induces the formation of new blood vessels, known as angiogenesis.
Ting Wang, a PhD student in Professor Bergö’s group, said: “Many clinical trials have evaluated the efficacy of angiogenesis inhibitors, but the results have not been as successful as expected.
“Our study opens the door to more effective ways to prevent angiogenesis in tumors; for example, patients whose tumors have elevated BACH1 levels might benefit more from antiangiogenic therapy than patients with low BACH1 levels.”
Using lung, breast, and kidney tumors, they found that when BACH1 was activated, either by ingesting antioxidants or by overexpressing the BACH1 gene, it produced more new blood vessels, but was highly sensitive to angiogenesis inhibitors.
Ms Wang added: “The next step is to examine in detail how oxygen levels and free radicals can regulate the BACH1 protein, and we will continue to determine the clinical relevance of our results.
“We will also do similar studies in other forms of cancer, such as breast, kidney, and skin.”