Scientists believe they have discovered a missing link between how eating junk food increases cancer risk.
A study from Singapore examined the effect of methylglyoxal, a compound released when the body breaks down sugary and fatty foods, on a gene that helps fight tumors.
In a first, the academics found that methylglyoxal was able to temporarily disable the ability of the BRCA2 gene to protect against cancer formation and growth.
Doctors have known for decades that junk food consumption is linked to a much higher risk of cancer, even if the person is not obese, but the exact mechanism remains to be understood.
This could, at least in part, explain why cancers among young, seemingly healthy Americans are becoming so prevalent, particularly colon tumors.
Researchers at the National University of Singapore found that methylglyoxal, which the body produces more of when eating junk food, could inhibit the function of cancer-protective genes like BRCA2.
The graph above shows the evolution of cancer case rates around the world
The team also noted that the study contradicts a long-standing theory called Knudson’s “two strikes” paradigm, which states that genes like BRCA2 must be completely inactive in the body to increase cancer risk.
These genes are thought to help protect the body against cancer, although patients who inherit defective copies from their parents have been shown to have an increased risk of certain cancers, such as breast and pancreatic cancer.
Dr Ashok Venkitaraman, study author and director of the Cancer Research Center at the National University of Singapore, told Medical News Today: “(M)ethylglyoxal triggers the destruction of the BRCA2 protein, thereby reducing its levels in cells. »
“This effect is temporary, but may last long enough to inhibit the tumor-preventing function of BRCA2.”
He noted that repeated exposure, for example by eating processed foods and red meat, among others, would increase the extent of damage to genes like BRCA2.
The team looked at the effect of methylglyoxal on cells from people who had inherited a defective copy of BRCA2 and were therefore more likely to develop cancer.
They found that exposure to methylglyoxal disabled tumor suppression.
“It is well established that some people are at high risk of developing breast, ovarian, pancreatic or other cancers because they inherit a defective copy of the cancer prevention gene – BRCA2 – from their parents,” said Dr Venkitaraman.
“Our recent findings show that the cells of these individuals are particularly sensitive to the effects of methylglyoxal, a chemical produced when our cells break down glucose to create energy.”
“We found that methylglyoxal inhibits the tumor-preventing function of BRCA2, ultimately causing defects in our DNA that are warning signs of cancer development.”
Additionally, Dr. Venkitaraman noted that high levels of methylglyoxal are common in people with diabetes and prediabetes.
“Our latest findings show that methylglyoxal can temporarily inactivate these cancer prevention genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can “add up” over time and increase cancer risk,” said Dr. he declared.
However, the team cautioned that since the study was conducted on cells rather than people, more research is needed on the topic.
This research adds to a long list of studies suggesting that diet may impact cancer risk, particularly colorectal cancer.
Research from the Cleveland Clinic, for example, found that people under 50 who ate diets high in red meat and sugar had lower levels of citrate, a compound created when the body converts food into energy. and which inhibits the growth of tumors.
The new study was published last week in the journal Cell.
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