Vitamin supplements have long been touted as a way to enhance overall health and well-being, but recent research has unveiled a potentially alarming connection between vitamin C supplements and the promotion of cancerous tumor growth.
Scientists at the Karolinska Institutet, a prominent research-led medical university in Solna, Sweden, have been investigating the impact of vitamin and mineral supplementation, particularly antioxidants like vitamin C, on cancerous tumors.
While antioxidants derived from natural food sources are generally considered safe, the excessive intake of these compounds through supplements has raised eyebrows due to its association with the formation of new blood vessels within tumors.
Professor Martin Bergö, from the Department of Biosciences and Nutrition, Karolinska Institutet, articulated the surprising findings of his research team.
“We’ve found that antioxidants activate a mechanism that causes cancer tumors to form new blood vessels, which is surprising since it was previously thought that antioxidants have a protective effect,” Professor Bergö explained.
“The new blood vessels nourish the tumors and can help them grow and spread. There’s no need to fear antioxidants in normal food, but most people don’t need additional amounts of them.
In fact, it can be harmful for cancer patients and people with an elevated cancer risk.”
The study’s findings center around the impact of antioxidants on free oxygen radicals in the body.
While antioxidants are effective at reducing these harmful radicals, the introduction of excessive amounts through supplements triggers a drop in free radicals, activating a protein known as BACH1.
This protein, in turn, induces the formation of new blood vessels, a process called angiogenesis.
The study identified that vitamin A, vitamin C, selenium, and zinc, commonly found in supplements, all stimulate the formation of new blood vessels within lung cancer tumors.
The implications of this research are profound, potentially affecting all types of cancers and their progression.
Ting Wang, a doctoral student in Professor Bergö’s team, emphasized the significance of these findings: “Our study opens the door to more effective ways of preventing angiogenesis in tumors.
For example, patients whose tumors exhibit high levels of BACH1 might benefit more from anti-angiogenesis therapy than patients with low BACH1 levels.”