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How sugar causes cancer

Reading time: 5 minutes

A major breakthrough in cancer research has discovered that sugar—usually from fast food—switches off our cancer-fighting genes. Bryan Hubbard reports

C stands for cancer; frustratingly, it also stands for complicated or even confusing, and that’s because understanding the processes of cancer and predicting who is likely to get it aren’t straightforward.

As we know, smoking poses one of the biggest risks for developing cancer, and around 48 percent of smokers will get the disease—which also means 52 percent won’t. The same goes for processed food. It’s another big risk factor.

Researchers from Imperial College London analyzed a database of nearly 200,000 participants and discovered that for every 10 percent increase in ultra-processed food (UPF) in a person’s diet, there was a 2 percent rise in cancer cases overall (see table, below).1

Worrying stuff, but it also means many people who eat processed food never develop cancer—even though, as a population, we are eating a lot of it. In the US, the average person is consuming around 26 kg (57 lb) of sugar every year, and in the UK it’s about 16 kg (34 lb), mainly from processed food.

Despite this vast overconsumption, researchers say they have seen only an “association” between poor diet and a host of health problems, such as obesity, heart disease, type 2 diabetes and some cancers, but they haven’t established a direct cause-and-effect relationship.

It’s in the process

Researchers at the National University of Singapore have taken a step closer to understanding how some people dodge the cancer bullet, even if they’re not living a great lifestyle, while others become its victims.2

It’s all to do with the way the body processes sugar. When the body breaks down glucose to create energy in a process known as glycolysis, it also produces the compound methylglyoxal (MGO).

MGO can be a dangerous byproduct of glycolysis because it has the ability to disrupt cell function, but enzymes usually break it down into less harmful substances before it can do its damage. When there’s too much MGO circulating, though, our bodies can’t cope. It goes on to damage our DNA, and this can be the precursor of cancer, but it also does something else that’s even worse.

The researchers started by looking at people who had inherited a faulty copy of the cancer-suppressing gene BRCA2 from their parents—the mutated gene increases the risk of breast, ovarian and prostate cancers. They discovered these people’s cells were particularly sensitive to the effects of MGO. In other words, it could switch off the protective effects of their BRCA2 gene.

But MGO affects other people, too. Diabetics and those with prediabetes can also have high levels of the chemical, and there’s a direct causal link between diabetes and a diet of UPFs and obesity.

“We started the study aiming to understand what factors elevate risk in families susceptible to cancer but ended up discovering a deeper mechanism linking an essential energy consumption pathway to cancer development. These findings raise awareness of the impact of diet and weight control in the management of cancer risks,” said lead researcher Li Ren Kong.

Don’t forget Knudson

So, higher levels of MGO increase the risk of cancer—but that’s only part of the story. To understand another piece of the puzzle, we must go back to 1971 and the discoveries of geneticist Alfred Knudson. He was one of the first to recognize that we have genes that suppress cancer, and so cancer can start only when they mutate or are damaged.

Our cancer-fighting genes also repair DNA damage, which blocks the process of cancer development. “Tumor suppressor genes act as brakes to stop cells in their tracks before they can take the road to cancer,” one science commentator explained.3

Knudson discovered that both cancer-suppressor genes in our cells must be switched off permanently for cancer to start, an observation that became known as Knudson’s “two-hit” paradigm.

It came about after he had been studying retinoblastoma, a childhood eye cancer. Usually, cells in the developing eye stop growing and dividing, and they begin differentiating into photoreceptor cells and nerve cells.

However, cells don’t differentiate but continue to divide to form tumors in the eyes of children with retinoblastoma. The thinking at the time was that the cancer developed after an infection, but Knudson established that a mutation in the cancer-suppressing RB1 gene—as it became known—was responsible.

His theory was derided by other scientists at the time but has since been accepted as the basis for understanding how cancer develops.

More sugar does it

So, what causes our cancer-preventing genes to switch off in the first place? The Singapore researchers discovered that MGO can temporarily affect them—but Knudson had observed that they must be permanently inactivated before cancer can start. What turns a temporary problem into a permanent one, the researchers say, is simply more MGO, and that requires eating ever larger amounts of UPFs, or sugar.

Physiologist Otto Warburg would have agreed. Warburg observed in the 1920s that cancer cells consume enormous amounts of glucose, which ferments to produce lactate, an acid, even when oxygen is present.

But what do Warburg’s and Knudson’s observations have in common? Quite a lot, says researcher Kjeld Engvild at the Technical University of Denmark, who regards the two as different aspects of the same single theory of cancer.4

We have five repair mechanisms that prevent cancer from developing: tetraploidization (doubling of chromosomes), cell division arrest, apoptosis (cell death), elimination of cancerous cells by the immune system and prevention of cancerous cell survival. Warburg and Knudson recognized that cancer begins when these protective mechanisms are knocked out.

They also noticed that cancer has more to do with environmental influences than genetic ones, something that became apparent when cancer developed in chimney sweeps who had been exposed to coal tar, in hospital patients who had been x-rayed, and in those who had breathed in asbestos or were smokers.

Today, we can add UPFs to the mix—and with their high levels of sugar, they may be the biggest culprits of them all. Researchers from Stony Brook University have confirmed that up to 90 percent of cancers are caused by environmental factors, such as pollutants, radiation and lifestyle choices, which includes diet. Cancer isn’t down to chance or bad luck; instead, it’s a disease that is very much within our control.5

Frustratingly, even though everyone suspects processed food is a major cause of cancer, nobody has definitively established it—probably because the studies are “lifestyle” focused and incorporate other influences as well.

But the Singapore and Imperial researchers have added nuance to the argument. They have shown that the poison is in the dose and how to prevent it.

Add more processed food to your diet, and you will increase the likelihood of developing cancer, the Imperial team has discovered. And now we also know why: too much processed food switches off our cancer fighters.

Knowing this, we also know that cancer prevention is simple, the Singapore team says. Don’t smoke, avoid environmental pollutants as much as you can, avoid x-rays, lose weight if you’re obese and, most important of all, don’t eat UPFs. If you do occasionally succumb to your sugar addiction, make it a very rare treat.

The fast-food track to cancer1

Increase in UPF consumption

 

10% 20% 30%
Increase in incidence of cancer

 

Ovarian cancer 19% 38%  

57%

 

Breast cancer  death 16% 32%  

48%

 

Ovarian cancer death 30% 60%  

90%

 

Any cancer death 6% 12%  

18%

 

 

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References
 
  1. eClinical Medicine, 2023; 56: 101840
  2. Cell, 2024; doi: 10.1016/j.cell.2024.03.006
  3. Nature Education, 2008; 1(1): 177
  4. OBM Genetics, 2019; 3(4): 100
  5. Mol Cell Oncol, 2016; 3(3): e1143079
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