Scientists believe they have uncovered a missing link between how eating junk food increases the risk of cancer.
A study in Singapore looked at the effect of methylglyoxal, a compound released when the body breaks down sugary and fatty foods, on a gene that helps fight off tumors.
In a first, the academics found that methylglyoxal was able to temporarily shut off the BRCA2 gene’s ability to protect against cancer forming and growing.
Doctors have known for decades that eating junk food is linked to a much higher risk of cancer, even if the person is not obese, but the exact mechanism is still being understood.
It could, at least in part, explain why cancers among young, ostensibly healthy Americans are becoming so prevalent, particularly tumors in the colon.
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-protecting genes like BRCA2
The above graph shows the change in cancer case rates around the world
The team also noted that the study contradicts a longstanding theory called the knudson’s ‘two-hit’ paradigm, which said that genes like BRCA2 must be completely inactive in the body to raise cancer risk.
These genes are meant to help protect the body against cancer, though patients who inherit faulty copies from their parents have been shown to have an increased risk of certain cancers, such as breast and pancreatic.
Dr Ashok Venkitaraman, study author and director of the National University of Singapore’s Centre for Cancer Research, told Medical News Today: ‘[M]ethylglyoxal triggers the destruction of BRCA2 protein, reducing its levels in cells.’
‘This effect is temporary, but can last long enough to inhibit the tumor-preventing function of BRCA2.’
He noted that repeated exposure, such as through eating processed foods and red meat, among others, would increase the amount of damage to genes like BRCA2.’
The team looked at the effect of methylglyoxal on cells from people who had inherited a faulty copy of BRCA2 and were therefore more likely to develop cancer.
They found that methylglyoxal exposure disabled tumor suppression.
‘It is well documented that some individuals are at a high risk of developing breast, ovarian, pancreatic or other cancers because they inherit a faulty copy of the cancer-preventing gene — BRCA2 — from their parents,’ Dr Venkitaraman said.
‘Our recent findings show that cells from such individuals are particularly sensitive to the effects of methylglyoxal, which is a chemical produced when our cells break down glucose to create energy.
‘We find that methylglyoxal inhibits the tumor-preventing function of BRCA2, eventually causing faults in our DNA that are early 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 such cancer-preventing genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can “add up” over time to increase cancer risk,’ he said.
However, the team cautioned that since the study was carried out in cells rather than people, more research is needed on the topic.
The research adds to a long list of studies suggesting that diet could have an impact on cancer risk, particularly colorectal cancer.
Research from the Cleveland Clinic, for example, found that people under 50 who ate diets rich in red meat and sugar had lower levels of the compound citrate, which is created when the body converts food into energy and has been shown to inhibit tumor growth.
The new study was published last week in the journal Cell.
