The journal Nature Metabolism has published a recent study on breast cancer, directly stating in the title that vitamin B5 induces MYC gene-mediated breast tumors.
To fully understand this study, simply reading the title isn't enough. Besides breast cancer and vitamin B5, you should also familiarize yourself with another key term—MYC.
The MYC gene is currently one of the most thoroughly studied nuclear protein oncogenes. Its main function is to regulate cell differentiation and proliferation. The MYC gene can be divided into four types, including c-MYC and N-MYC, with c-MYC being the most common. Activation of the c-MYC gene, which can occur through gene amplification or chromosomal translocation, is frequently observed in cancer research and tumor induction.
In this study, scientists cultured tumors using cells with high and low MYC gene expression, and then transplanted human breast cancer tumor tissues into mice, creating a cancer mouse model. It is important to note that each tumor-bearing mouse received a daily dose equivalent to 0.3 milligrams of vitamin B5 (VB5).
The study yielded two significant conclusions:
MYC increased the amount of VB5 entering the cells, thereby accelerating the growth of tumor cells.
A VB5-deficient diet slowed down tumor growth in mice, while a diet with adequate VB5 accelerated it.
What about the carcinogenic potential of VC and VE?
Regarding VC's carcinogenicity, at least it hasn't been as directly accused as VB, whose role was clearly stated in the study title. Instead, research papers typically use the term "antioxidants" in their titles to refer to this issue.
But once you start reading the main text, there is no mercy given to VC and VE.
Let's take a look at this experiment. A team from Sweden and Zhengzhou University in China conducted this study. The test subjects were mice with a specific type of lung cancer and mice implanted with human lung cancer cell lines, meaning two types of "cancer" mice. The experimental design was quite similar to the VB5 study mentioned earlier.
Researchers added vitamin C, vitamin E, and N-acetylcysteine to the drinking water, administering these antioxidants to the mice daily. The results showed that as the intake of antioxidants increased, the expression of the BACH1 gene also increased in both types of cancer mice. The BACH1 gene is responsible for regulating glycolysis and angiogenesis genes.
We also took a look at the related experimental dosages. In previous mouse studies, we found that the dosage of VE was 0.5g per kilogram of food, which translates to approximately 61.5mg of VE per kilogram of mouse body weight.
Now that we've covered the conclusions of the studies, our summary is that there's absolutely no need to worry about vitamins causing cancer. Next, let's analyze why you shouldn't feel anxious or alarmed after reading these experiments.
First, transplanting human tumor cells into mice differs significantly from experiments conducted directly on humans.
While there are some similarities in gene expression, particularly concerning oncogenes like MYC, between humans and mice, there are also significant differences in expression patterns. For instance, mice express the MYC gene most prominently in tissues such as the ovaries and thymus, whereas in humans, the pattern is quite different. Therefore, even when conducting experiments with human lung cancer cell lines in mice, it's challenging to draw highly accurate conclusions.
Similarly, there are also some tumor animal models involving gene knockout. While mice, rats, or other mammals have a high degree of homology with humans in terms of genetics, over 90% of drug trials have shown success in animal testing. However, when it comes to human clinical trials, they often end in failure.
Second, there's the issue of dosage in animal experiments.
In fact, we specifically mentioned the dosage issue in the studies above. For example, a mouse needing 0.3mg of VB5 per day might not seem like much, right?
But consider this: an adult mouse typically weighs around 30g, while our body weight is around 60kg. You might suddenly realize that the dosage equivalence is simple arithmetic—we are 2000 times heavier than a mouse. So, to match the dosage a mouse receives, we would need to consume 600mg of VB5 per day. Yet, the highest doses of vitamin supplements we take daily contain at most 10mg of VB5.
Of course, a professional comparison of drug efficacy dosage between animals and humans doesn't simply involve scaling by body weight; it requires calculating surface area. For instance, if a mouse's dosage is 1, a human equivalent typically ranges from 380 to 400. However, regardless of the calculation method, the human equivalent dosage always ends up being significantly higher than what we normally consume.
Additionally, in the previous study where feeding mice inulin led to liver cancer, it was also a matter of dosage. If we were to translate the dosage for human consumption, one would need to consume several hundred grams of inulin daily for it to potentially cause liver cancer. However, in reality, the maximum amount of inulin we can typically supplement per day is around 10g. So, the idea of inulin causing liver cancer in humans is far-fetched and highly unlikely.
In conclusion
Today's article is relatively straightforward, aiming to ensure more people can understand it. It's also intended to convey the message that whether it's vitamin B (VB), vitamin C (VC), vitamin E (VE), or vitamins A (VA), D (VD), and K (VK), they are all essential nutrients for our bodies. If you can ensure an adequate intake of dietary fiber and conscientiously consume a balanced diet including fruits, vegetables, meats, eggs, and dairy products, then there's no need for excessive vitamin supplements. However, if you find it challenging to meet your nutritional needs through diet alone and experience minor health issues, moderate vitamin supplementation along with regular outdoor exercise can significantly improve your well-being.
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