This diet can damage your DNA and increase cancer risk 🧬

A recent study reveals how a diet high in fats and sugars can damage DNA, thereby increasing the risk of liver cancer in patients with fatty liver disease. These findings could pave the way for new therapeutic strategies.


Researchers at the University of California, San Diego, have explored the underlying mechanisms of the progression from fatty liver disease to cancer. Their work, published in Nature, highlights the crucial role of DNA damage in this process. This research also underscores the significant impact of diet on cellular health and cancer risk.

Over the past two decades, the incidence of hepatocellular carcinoma (HCC), the most common form of liver cancer, has increased by 25 to 30%. This rise is partly attributed to the growing prevalence of fatty liver disease, affecting a quarter of American adults. Approximately 20% of these patients develop a more severe form, metabolic steatohepatitis (MASH), which significantly increases the risk of HCC.

The scientists used mouse models and human tissue samples to demonstrate that diets high in fats and sugars cause DNA damage in liver cells. These cells then enter senescence, a state where they can no longer divide but remain metabolically active. This senescence is normally a protective response, but in the case of the liver, it can paradoxically promote cancer development.

The results suggest that damaged liver cells sometimes survive senescence and can become proliferative again, thereby increasing the risk of cancer. This discovery opens up prospects for the development of new treatments aimed at preventing or repairing DNA damage, offering hope for patients with MASH.


In addition to these therapeutic implications, the study sheds new light on the relationship between aging and cancer. It reveals how similar molecular mechanisms could be at play in various types of cancer, highlighting the importance of research on cellular senescence.

Finally, this research emphasizes the detrimental effects of a poor diet on cellular metabolism. It could thus help strengthen public health messages regarding the risks associated with fatty liver disease and obesity, showing that dietary choices have a profound impact on our long-term health.

What is cellular senescence?

Cellular senescence is a state in which cells stop dividing in response to damage or stress. This mechanism is generally considered a protection against cancer, preventing damaged cells from proliferating.

However, in some cases, such as in the liver cells studied, senescence may not be sufficient to prevent cancer development. Senescent cells remain metabolically active and can sometimes escape this control mechanism, leading to cancerous proliferation.

This discovery underscores the complexity of cellular defense mechanisms and opens up prospects for new therapeutic approaches aimed at reinforcing or bypassing senescence in cancer treatment.

How does diet influence cancer risk?

Diet plays a crucial role in cellular health and cancer risk. A diet high in fats and sugars can cause DNA damage, thereby increasing the risk of cancerous mutations.

In the case of fatty liver disease, this damage can lead to inflammation and liver fibrosis, further increasing the risk of cancer. Researchers have shown that these diets can lead to senescence of liver cells, which, although intended to protect, can paradoxically promote cancer.

These results highlight the importance of a balanced diet to preserve cellular health and reduce the risk of chronic diseases, including cancer.