Excessive Vitamin C Supplements Linked to Increased Cancer Risk, New Study Finds
New research from the Karolinska Institutet in Sweden suggests that excessive intake of antioxidants, such as Vitamin C, can increase the risk of cancer by stimulating the growth of tumors. The study emphasizes the potential harm of antioxidant supplements, particularly for cancer patients and those at risk. Future research aims to delve deeper into the regulation of antioxidants and their clinical implications.
New research from the Karolinska Institutet in Sweden has found that taking excessive amounts of antioxidants, such as Vitamin C, through dietary supplements may increase the risk of cancer. The study, published in The Journal of Clinical Investigation, revealed that antioxidants can stimulate the formation of new blood vessels in lung cancer tumors, thereby promoting the growth and spread of cancer cells. Antioxidants are commonly found in dietary supplements and are known to neutralize free oxygen radicals that can damage the body.
However, the study suggests that while antioxidants in normal food are generally safe, additional amounts through supplements can be harmful, especially for cancer patients and those at an elevated risk of cancer. Previous research conducted by the same group of scientists demonstrated that antioxidants like Vitamin C and E actually accelerate the growth and spread of lung cancer by stabilizing a protein called BACH1. The activation of BACH1 was found to induce the formation of new blood vessels, a process known as angiogenesis, not only under low oxygen levels but also in the presence of normal oxygen levels.
The study also uncovered that BACH1 is regulated in a similar manner as the HIF-1alpha protein, which received the 2019 Nobel Prize in Physiology or Medicine for its role in cellular response to changes in oxygen levels. The findings of this study have important implications for the efficacy of angiogenesis inhibitors, which are often used in cancer treatment. The researchers suggest that patients with tumors exhibiting high levels of BACH1 may benefit more from anti-angiogenesis therapy than those with low BACH1 levels.
The study utilized various cell-biological methods and focused primarily on lung cancer tumors through the analysis of organoids, small cultivated micro tumors from patients. Additionally, mice and samples of human breast and kidney tumors were also examined. The next step for the research team is to further investigate how oxygen and free radicals regulate the BACH1 protein, as well as determine the clinical relevance of their findings. Future studies will also explore similar mechanisms in other types of cancer, including breast, kidney, and skin cancer.