Scientists have found why a poor diet can increase cancer risk.
- Poor diet can increase the risk of
obesity, heart disease, type 2 diabetes, and some cancers.
- Experts
have not yet found any firm causative links between individual dietary
components and cancer.
- A
new study has discovered that methylglyoxal — which is produced when glucose
is broken down in cells — may help explain the link between poor diet and
cancer.
- They suggest that a long-term poor diet leads to an increase in the
production of methylglyoxal, which switches off cancer-preventing genes,
increasing cancer risk.
Poor nutrition is associated with many health
conditions, among them obesity, heart disease, type 2 diabetes, and cancers,
including those of the breast, uterus, and large intestine. High intakes of
sodium, saturated fats, and sugars can increase the risk of chronic
conditions like heart disease and type 2 diabetes, but what links diet and
cancer is less clear.
Although many foods are
said to be associated with increased or decreased cancer risk, according to
the National Cancer Institute, no studies have yet shown that
any dietary component directly causes or protects against cancer.
Now, a study from the National University of
Singapore, published in Cell, has discovered a mechanism that
may help to explain why poor diet increases cancer risk.
In cell studies, the
researchers found that methylglyoxal, which is produced when cells break down
glucose to release energy, can inhibit genes that protect against cancer. They
suggest that poor diet leads to higher levels of methylglyoxal, increasing the
likelihood of cancer.
“This
study suggests a potential correlation between high levels of methylglyoxal, a
metabolic by-product, and a genetic mutation pattern seen in some cancers. It
is an interesting area to explore further, but we need further lab research and
clinical testing to conclusively establish if methylglyoxal levels are directly
linked to cancer risk.”— Dr. Tayyaba Jiwani, science engagement manager
at Cancer
Research UK, who was not involved in the study, speaking to Medical News Today.
Breast
cancer gene increases effect of methylglyoxal
Methylglyoxal
is a by-product of the metabolism of glucose, proteins and lipids. It
is a reactive small molecule that can disrupt cell function, so is broken down
by enzymes into less harmful substances. However, if too much methylglyoxal is
produced, the study suggests, the excess can then damage DNA.
The researchers first
investigated the effect of methylglyoxal in cells from people who had inherited
a copy of a mutated gene — BRCA2 — that increases the risk of breast and
ovarian cancers.
They discovered that methylglyoxal temporarily
disabled tumor suppression by BRCA2, which could increase the likelihood of
cancer developing.
Prof.
Ashok Venkitaraman, corresponding author, NUS Centre for Cancer Research,
National University of Singapore, told Medical
News Today:
“[M]ethylglyoxal
triggers the destruction of BRCA2 protein, reducing its levels in cells. (It
doesn’t prevent expression of the BRCA2 gene.) This effect is temporary, but
can last long enough to inhibit the tumor-preventing function of BRCA2.”
Methylglyoxal damaged
DNA in cells that had the mutated form of the BRCA2 gene. Repeated exposure to
methylglyoxal increased the level of damage to the DNA.
“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,” 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,” he added.
Similar
effects seen without gene
“The
study revealed that even individuals without a genetic predisposition might
still face an increased cancer risk if they present with elevated methylglyoxal
levels. This scenario is commonly observed in those with diabetes or
pre-diabetes, conditions often linked with obesity or suboptimal dietary and
lifestyle habits.”— Kelsey Costa, MS, RDN, registered dietitian nutritionist
and founder of Dietitian Insights, who was not involved in the study, speaking
to Medical News Today.
Costa explained how
methylglyoxal might have this effect:
“Methylglyoxal produces
a group of complex compounds known as advanced glycation end-products (AGEs), which accumulate in
the body and contribute to various health conditions, including diabetes and
obesity. These AGEs have been linked to increased oxidative
stress and inflammation, both of which are critical factors in cancer
development.”
High levels of
methylglyoxal are common in people with prediabetes and diabetes, and can also
result from obesity and eating a poor diet.
“Diabetes is a condition
where the body has trouble controlling blood sugar (glucose) levels, so people
with prediabetes/diabetes have higher than normal levels of glucose. Some of
this excess glucose is broken down by glycolysis, in turn elevating
methylglyoxal,” Venkitaraman told MNT, explaining also that:
“Poor diets rich in sugar or refined carbohydrates
are known to cause blood glucose levels to spike.”
What the
findings might mean
Venkitaraman cautioned
that, as their work was carried out in cells, not patients, it would be
premature to give specific advice to reduce cancer risk on the basis of their
findings. However, he explained how their work might influence thinking about
genes and cancer:
“Our work also revises a
longstanding theory about certain cancer-preventing genes. This theory — called
the Knudson’s ‘two-hit’ paradigm — was first formulated in
1971 and proposed that these genes must be inactivated permanently in our cells
before cancer can arise.”
“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.
Dr. Jiwani cautioned
that more research was needed to confirm the effects of methylglyoxal:
“The study shows that
exposing cancer cells in the lab to high levels of methylglyoxal can
transiently deplete the tumor-suppressor protein BRCA2, increasing the risk of
DNA damage. But this alone doesn’t prove that these cells will go on to become
cancerous. Additional research is needed to see if these same effects occur in
the more complex contexts of our tissues, organs, and bodies, where metabolic
reactions and by-products are intricately regulated.”
More
evidence that diet affects cancer risk
Costa told MNT that this
research provides another reason to try and follow a healthy diet:
“Diets rich in unhealthy
processed foods, red
meats, added sugars, and refined grains, like the typical Western
diet, may lead to an increase in methylglyoxal due to metabolic dysfunction, posing
a risk for various diseases, including obesity, cardiovascular
diseases, diabetes, and an elevated risk of cancer.”
“As is often the case, the best way to reduce
methylglyoxal production and maintain metabolic, microbiome, and overall health
is to eat a balanced, plant-forward diet that is rich in dietary fiber and
bioactive compounds, with a focus on whole and minimally processed foods,” she
advised.
One diet often advocated
for improving health is the Mediterranean diet and, Costa said, and there is
now evidence that it might reduce methylglyoxal levels.
“In fact, in a recent study,” she said, “following a Mediterranean
diet was linked to lower methylglyoxal levels in the bloodstream, which
appeared to help maintain kidney health among individuals with type 2 diabetes
and coronary heart disease.”
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