Scientists uncover missing link between junk food and cancer – which could explain explosion of tumors in young people

Scientists think they have discovered a missing link in how eating junk food increases the risk of cancer.

A study in Singapore looked at the effect of methylglyoxal, a substance released when the body breaks down sugary and fatty foods, on a gene that helps fight tumors.

For the first time, the academics discovered that methylglyoxal was able to temporarily disable the BRCA2 gene’s ability to protect against the formation and growth of cancer.

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 not understood.

It could explain, at least in part, why cancer is becoming so prevalent among young, apparently healthy Americans, especially tumors in the colon.

Researchers from the National University of Singapore found that methylglyoxal, more of which the body produces when eating junk food, could inhibit the function of cancer-protecting genes such as BRCA2.

The above graph shows the change in cancer rates around the world

The above graph shows the change in cancer rates around the world

The team also noted that the study contradicts a long-standing theory called Knudson’s “two-hit” paradigm, which states that genes such as BRCA2 must be completely inactive in the body to reduce the risk of cancer. to increase.

These genes are intended to help protect the body against cancer, although patients who inherit faulty copies from their parents have been shown to have an increased risk of certain cancers, such as breast and pancreatic cancer.

Dr. Ashok Venkitaraman, author of the study and director of the Center for Cancer Research at the National University of Singapore, said Medical news today: ‘[M]ethylglyoxal causes the destruction of BRCA2 protein, reducing its levels in cells.”

‘This effect is temporary, but may last long enough to inhibit the tumor preventive function of BRCA2.’

He noted that repeated exposure, for example through eating processed foods and red meat, would increase damage to genes such as 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 eliminated tumor suppression.

“It is well documented that some individuals 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 cells from such individuals are particularly sensitive to the effects of methylglyoxal, a chemical produced when our cells break down glucose to create energy.

‘We find that methylglyoxal inhibits the tumor-preventing function of BRCA2, ultimately causing errors in our DNA that are early warning signals of cancer development.’

Furthermore, Dr. Venkitaraman notes that high levels of methylglyoxal are common in people with diabetes and prediabetes.

“Our latest findings show that methylglyoxal can temporarily inactivate such cancer prevention genes, suggesting that repeated episodes of poor diet or uncontrolled diabetes can ‘add up’ over time and increase the risk of cancer,” he said.

However, the team cautioned that since the study was conducted in cells and not humans, more research on this topic is needed.

The research adds to a long list of studies suggesting that diet can have an impact on the risk of cancer, especially colorectal cancer.

For example, research from the Cleveland Clinic found that people under 50 who ate diets high 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 inhibits tumor growth.

The new study was published in the journal last week Cell.