Does sugar directly feed cancers, boosting their growth? The answer
seems to be ‘Yes’ at least in mice according to a study led by
researchers at Baylor College of Medicine and Weill Cornell Medicine.
Their study, published in Science, showed that consuming a daily modest
amount of high-fructose corn syrup—the equivalent of people drinking
about 12 ounces of a sugar-sweetened beverage daily—accelerates the
growth of intestinal tumors in mouse models of the disease,
independently of obesity. The team also discovered the mechanism by
which the consumption of sugary drinks can directly feed cancer growth,
suggesting potential novel therapeutic strategies.
“An increasing number of observational studies have raised awareness of
the association between consuming sugary drinks, obesity and the risk of
colorectal cancer,” said co-corresponding author Dr. Jihye Yun,
assistant professor of molecular and human genetics at Baylor. “The
current thought is that sugar is harmful to our health mainly because
consuming too much can lead to obesity. We know that obesity increases
the risk of many types of cancer including colorectal cancer; however,
we were uncertain whether a direct and causal link existed between sugar
consumption and cancer. Therefore, I decided to address this important
question when I was a postdoc in the Dr. Lewis Cantley lab at Weill
Cornell Medicine.”
First, Yun and her colleagues generated a mouse model of early-stage
colon cancer where APC gene is deleted. “APC is a gatekeeper in
colorectal cancer. Deleting this protein is like removing the breaks of a
car. Without it, normal intestinal cells neither stop growing nor die,
forming early stage tumors called polyps. More than 90% of colorectal
cancer patients have this type of APC mutation”, Yun said.
Using this mouse model of the disease, the team tested the effect of
consuming sugar-sweetened water on tumor development. The sweetened
water was 25% high-fructose corn syrup, which is the main sweetener of
sugary drinks people consume. High-fructose corn syrup consists of
glucose and fructose at a 45:55 ratio.
When the researchers provided the sugary drink in the water bottle for
the APC-model mice to drink at their will, mice rapidly gained weight in
a month. To prevent the mice from being obese and mimic humans’ daily
consumption of one can of soda, the researchers gave the mice a moderate
amount of sugary water orally with a special syringe once a day. After
two months, the APC-model mice receiving sugary water did not become
obese, but developed tumors that were larger and of higher-grade than
those in model mice treated with regular water.
“These results suggest that when the animals have early stage of tumors
in the intestines—which can occur in many young adult humans by chance
and without notice— consuming even modest amounts of high-fructose corn
syrup in liquid form can boost tumor growth and progression
independently of obesity,” Yun said. “Further research is needed to
translate this discovery to people; however, our findings in animal
models suggest that chronic consumption of sugary drinks can shorten the
time it takes cancer to develop. In humans, it usually takes 20 to 30
years for colorectal cancer to grow from early stage benign tumors to
aggressive cancers.”
“This observation in animal models might explain why increased
consumption of sweet drinks and other foods with high sugar content over
the past 30 years is correlating with an increase in colorectal cancers
in 25 to 50-year-olds in the United States,” said Cantley,
co-corresponding author, former mentor of Yun and professor of cancer
biology in medicine and director of the Sandra and Edward Meyer Cancer
Center at Weill Cornell Medicine.
The team then investigated the mechanism by which this sugar promoted
tumor growth. They discovered that the APC-model mice receiving modest
high-fructose corn syrup had high amounts of fructose in their colons.
“We observed that sugary drinks increased the levels of fructose and
glucose in the colon and blood, respectively and that tumors could
efficiently take up both fructose and glucose via different routes.”
Using cutting-edge technologies to trace the fate of glucose and
fructose in tumor tissues, the team showed that fructose was first
chemically changed and this process then enabled it to efficiently
promote the production of fatty acids, which ultimately contribute to
tumor growth.
“Most previous studies used either glucose or fructose alone to study
the effect of sugar in animals or cell lines. We thought that this
approach did not reflect how people actually consume sugary drinks
because neither drinks nor foods have only glucose or fructose. They
have both glucose and fructose together in similar amounts,” Yun said.
“Our findings suggest that the role of fructose in tumors is to enhance
glucose’s role of directing fatty acids synthesis. The resulting
abundance of fatty acids can be potentially used by cancer cells to form
cellular membranes and signaling molecules, to grow or to influence
inflammation.”
To determine whether fructose metabolism or increased fatty acid
production was responsible for sugar-induced tumor growth, the
researchers modified APC-model mice to lack genes coding for enzymes
involved in either fructose metabolism or fatty acid synthesis. One
group of APC-model mice lacked an enzyme KHK, which is involved in
fructose metabolism, and another group lacked enzyme FASN, which
participates in fatty acid synthesis. They found that mice lacking
either of these genes did not develop larger tumors, unlike APC-model
mice, when fed the same modest amounts of high-fructose corn syrup.
“This study revealed the surprising result that colorectal cancers
utilize high-fructose corn syrup, the major ingredient in most sugary
sodas and many other processed foods, as a fuel to increase rates of
tumor growth,” Cantley said. “While many studies have correlated
increased rates of colorectal cancer with diet, this study shows a
direct molecular mechanism for the correlation between consumption of
sugar and colorectal cancer.”
“Our findings also open new possibilities for treatment,” Yun said.
“Unlike glucose, fructose is not essential for the survival and growth
of normal cells, which suggests that therapies targeting fructose
metabolism are worth exploring. Alternatively, avoiding consuming sugary
drinks as much as possible instead of relying on drugs would
significantly reduce the availability of sugar in the colon.”
While further studies in humans are necessary, Yun and colleagues hope
this research will help to raise public awareness about the potentially
harmful consequences consuming sugary drinks has on human health and
contribute to reducing the risk and mortality of colorectal cancer
worldwide.
Other contributors to this work include Drs. Sukjin Yang, Yumei Wang and
Justin Van Riper with Baylor, Marcus Goncalves (lead author), Changyuan
Lu, Jordan Trautner, Travis Hartman, Seo-Kyoung Hwang, Charles Murphy,
Roxanne Morris, Sam Taylor, Quiying Chen, Steven Gross and Kyu Rhee, all
with Weill Cornell Medicine, Chantal Pauli with the University Hospital
Zurich, Kaitlyn Bosch with the Icahn School of Medicine at Mount Sinai,
H Carl Lekaye with Memorial Sloan Kettering Cancer Center, Jatin Roper
with Duke University and Young Kim with Chonnam National University.
This study was supported by the National Institutes of Health, Stand Up 2
Cancer, the Cancer Prevention and Research Institute of Texas and the
National Cancer Institute.
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