Recent studies have raised concerns about the potential dangers of over-supplementing with vitamins. Research published in Nature reveals that excessive vitamin E can help cancer cells avoid ferroptosis, promoting tumor growth, while vitamin B5 fuels cancer metabolism, particularly in MYC-driven breast cancers. Furthermore, high doses of nicotinamide riboside (vitamin B3) have been linked to a 27% increased risk of cancer occurrence and a 3.8-fold increase in brain metastasis in mice. These findings highlight that while vitamins are essential, their excessive intake may have unintended, harmful effects on cancer progression. Moderation is key to safe supplementation.
Every morning, before starting the busy day, many people’s daily routine includes drinking a glass of water and taking a few vitamin pills. A quick scroll through social media reveals health influencers promoting this practice: some claim that “taking a few every day makes you feel more energized,” while others swear by vitamins for “antioxidant benefits, anti-aging, and improved metabolism.”
As part of the trend of health-conscious individuals, it's not uncommon for people to stock up on vitamins during the holidays, consuming them religiously every day. Some even believe that “more is better,” taking handfuls of supplements, convinced they’re doing something good for their health.
However, recent research has cast serious doubt on the safety of “blindly over-supplementing” in pursuit of ultimate health benefits. A study published in Nature by a research team from the University of Texas Southwestern Medical Center in June this year discovered that vitamin E, which is thought to combat free radicals and protect cells, can actually help cancer cells escape ferroptosis, a form of cell death.
DO1:10.1038/s41586-025-09162-0
Vitamin E Helps Cancer Cells Avoid Ferroptosis
More and more studies have shown that lipoproteins, which are primarily responsible for transporting lipids in the blood, not only deliver “nutrition” to cancer cells but also help them escape ferroptosis. Ferroptosis is characterized by the accumulation of lipid peroxides in cell membranes, which requires iron. Cancer cells, exposed to constant oxidative stress, are more prone to ferroptosis in the tumor microenvironment. To survive and expand, cancer cells need to develop strategies to resist ferroptosis.
In the study, the researchers found that when lipoproteins were present, cancer cells became less dependent on GPX4, an enzyme that protects against ferroptosis by eliminating lipid peroxides. Further analysis revealed that the most potent anti-ferroptosis component in lipoproteins was α-tocopherol (α-toc), the active form of vitamin E.
At the cellular level, α-toc effectively alleviates lipid oxidation, promoting cancer cell growth. In animal experiments, mice deficient in α-toc had a significant reduction in tumor growth, as well as a loss of the ability to resist ferroptosis.
Lipoproteins promote cancer cell resistance to ferroptosis by transporting α-toc (the main form of vitamin E).
It turns out that vitamin E not only serves as a classic fat-soluble antioxidant, but also helps cancer cells avoid ferroptosis. However, it does not enter cells alone—vitamin E “rides” along with lipoproteins like low-density lipoprotein (LDL) and high-density lipoprotein (HDL) into various tissues, including tumors.
So, should we target the transportation system to stop cancer cells from receiving vitamin E? While directly limiting vitamin E intake may not be feasible in clinical settings, the researchers found a promising approach: instead of blocking vitamin E itself, they tried blocking the lipid uptake pathway, thus depriving cancer cells of this crucial supply.
By conducting large-scale CRISPR screenings on cancer cells with active lipoprotein uptake, they discovered a long-neglected metabolic pathway related to the synthesis of glycosaminoglycans (GAGs). These GAGs form a “carpet” of sugar chains on the cell surface, which can bind proteins, metals, and lipoproteins. The researchers showed that blocking GAG synthesis significantly reduced lipid uptake by cancer cells, making them more susceptible to ferroptosis.
In summary, cancer cells use GAGs to enhance lipoprotein uptake, thus acquiring antioxidants like vitamin E to combat oxidative stress. When GAG synthesis is disrupted, cancer cells lose their protection against ferroptosis and are ultimately forced to undergo cell death.
Cancer cells require GAGs synthesis to maintain lipoprotein uptake, ferroptosis resistance, and tumor growth.
Vitamin B5 Fuels Breast Cancer Growth
But vitamin E isn’t the only culprit; B vitamins also have a “dark side” when it comes to cancer. A study published in Nature Metabolism by researchers from the Francis Crick Institute revealed that cancer cells rely on vitamin B5 (pantothenic acid) for energy and growth.
DO1:10.1038/s42255-023-00915-7
The MYC gene, which is often overexpressed in various cancers, activates a transporter protein called SLC5A6, which significantly increases cancer cells' uptake of vitamin B5. Once inside the cell, vitamin B5 is converted into coenzyme A (CoA), which boosts the activity of the tricarboxylic acid (TCA) cycle—the “power plant” of the cell that generates energy by oxidizing sugars, fats, and proteins.
By enhancing CoA levels, MYC-driven breast cancer cells essentially “fuel” their growth. The research team also found that limiting vitamin B5 intake in mice slowed tumor growth and inhibited cancer cell proliferation. They concluded that blocking vitamin B5’s role in energy metabolism could effectively reduce tumor progression.
Spatial association and functional dependence of pantothenic acid and MYC expression.
Excessive Vitamin B3 May Increase Cancer Risk and Brain Metastasis
Another recent “health trend” has been the use of vitamin B3, especially its form known as nicotinamide riboside (NR), which is often promoted for anti-aging and metabolic health. However, a study by the Swiss Federal Institute of Technology raised concerns about the potential risks of overusing NR, particularly in the context of cancer.
In a mouse model of triple-negative breast cancer, NR supplementation led to a 27% increase in tumor occurrence. More alarmingly, the mice supplemented with NR had a brain metastasis rate that was 227% higher than that of the control group. This suggests that excessive NR could not only increase the risk of developing cancer, but also accelerate its spread to the brain.
The researchers proposed that NR might increase cancer cell survival and spread by providing more energy and metabolic raw materials, and possibly by weakening the blood-brain barrier, allowing cancer cells to invade the brain.
DO1:10.1016/j.bios.2022.114826
Conclusion: Don’t Overdo It with Vitamin Supplements
This research highlights that vitamins are not always “the more, the better” solution to good health. While vitamins can play important roles in maintaining bodily functions, their excessive intake may have unintended consequences, including promoting cancer growth and metastasis. Instead of blindly following health trends or overloading on supplements, it might be wiser to adopt a more balanced, natural approach to health.
Note: These studies primarily use animal models, so their applicability to humans requires further verification.
References:
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Calhoon, D., Sang, L., Ji, F. et al. Glycosaminoglycan-driven lipoprotein uptake protects tumors from ferroptosis. Nature, 644, 799–808 (2025).
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Kreuzaler, P., Inglese, P., Ghanate, A. et al. Vitamin B5 supports MYC oncogenic metabolism and tumor progression in breast cancer. Nat Metab, 5, 1870–1886 (2023).
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Maric T., Bazhin A., Khodakivskyi P., et al. A bioluminescent-based probe for in vivo non-invasive monitoring of nicotinamide riboside uptake reveals a link between metastasis and NAD+ metabolism. Biosens Bioelectron, 2022 Oct 29;220:114826. Link