Washington Study Finds That Dietary Fructose Including Corn Syrup Drives Cancer Growth

Medical News: The relationship between diet and cancer has long intrigued scientists and public health advocates alike. A groundbreaking study from Washington University in St. Louis-USA has revealed alarming evidence linking dietary fructose, including high-fructose corn syrup, to accelerated cancer growth. Researchers found that fructose consumption promotes tumor growth indirectly by fueling the liver's production of lipids, which cancer cells then use to proliferate. This finding has significant implications for dietary guidelines and potential cancer therapies.


Washington Study Finds That Dietary Fructose Including Corn Syrup Drives Cancer Growth

Fructose, a simple sugar found naturally in fruits, vegetables, and honey, has seen a dramatic rise in dietary prevalence over the past five decades, largely due to the ubiquitous use of high-fructose corn syrup in processed foods and beverages. The research focused on animal models of melanoma, breast cancer, and cervical cancer. While fructose itself does not directly nourish tumors, the liver’s metabolic processes convert it into nutrients that cancer cells readily utilize, revealing a complex interplay between diet, metabolism, and cancer growth.
 
This Medical News report dives deep into the findings, methodologies, and potential implications of this study, shedding light on how dietary fructose influences cancer progression and what it means for public health.
 
Understanding the Mechanism
The study team, led by Dr. Gary Patti, the Michael and Tana Powell Professor of Chemistry in Arts & Sciences and a professor of genetics and medicine at Washington University, explored how fructose impacts tumor growth. "The idea that you can tackle cancer with diet is intriguing," said Patti. “Our initial expectation was that tumor cells metabolize fructose directly, much like glucose, to fuel their growth. However, we found that the tumors barely metabolized fructose themselves.”
 
Instead, the researchers discovered that the liver plays a pivotal role. Fructose is metabolized almost entirely in the small intestine and liver, where it is converted into lipid molecules, including lysophosphatidylcholines (LPCs). These lipids are then secreted into the bloodstream and consumed by cancer cells, which use them to build cellular membranes necessary for rapid proliferation.
 
"We quickly learned that the tumor cells alone don’t tell the whole story," said Ronald Fowle-Grider, the study’s first author and a postdoctoral fellow in Patti’s lab. “Equally important is the liver, which transforms fructose into nutrients that the tumors can use.”
 
Fructose’s Rise in Modern Diets
The dramatic increase in dietary fructose consumption is a relatively recent phenomenon. In the early 20th century, the average person consumed about 5-10 pounds of fructose annually. Today, that number has skyrocketed to nearly 60 pounds per year for many individuals in industrialized nations. High-fructose corn syrup, a cheap and potent sweetener, has infiltrated countless food products, from soft drinks to salad dressings.
 
“If you go through your pantry, you’ll likely find high-fructose corn syrup in a surprising number of items,” Patti explained. “Unless you actively avoid it, it’s probably part of your diet.”
 
This shift in dietary habits coincides with rising rates of certain cancers, particularly among younger populations. While direct causation remains under investigation, the correlation is compelling and warrants further study.
 
Key Findings of the Study
The researchers conducted experiments on animal models, feeding them diets rich in fructose. The results were striking:
 
-Tumors in animals consuming high-fructose diets grew at significantly accelerated rates, in some cases doubling in size compared to control groups.

This tumor growth occurred without noticeable changes in body weight, fasting glucose, or insulin levels, suggesting that fructose’s effects are not merely a byproduct of general metabolic disruption.
 
-Elevated levels of LPCs were detected in the blood of fructose-fed animals, confirming the liver’s role in converting fructose into tumor-feeding nutrients.

Further in vitro experiments revealed that cancer cells do not metabolize fructose directly. Instead, they rely on liver-derived LPCs, which provide an efficient and readily available source of lipids for membrane synthesis.
 
“Cancer cells often prefer to take up lipids rather than synthesize them from scratch,” Patti noted. “LPCs may offer the most efficient way to support tumor growth.”
 
Implications for Diet and Therapy
The study’s findings raise important questions about the role of diet in cancer prevention and treatment. Avoiding high-fructose foods may be a crucial strategy for individuals at risk of or currently battling cancer. However, as Patti acknowledged, avoiding fructose entirely is challenging given its pervasive presence in processed foods.
 
“One take-home message is that if you have cancer, you should consider minimizing your fructose intake,” he said. “But this is easier said than done.”

Beyond dietary changes, the research also opens avenues for new therapeutic approaches. Targeting the liver’s metabolic pathways to prevent the conversion of fructose into LPCs could be a promising strategy. Patti and his colleagues are exploring potential drugs that could inhibit these processes, thereby starving tumors of the nutrients they need to grow.
 
Future Research and Clinical Trials
The study team is now collaborating with clinical partners at Washington University School of Medicine to design trials that examine the impact of dietary fructose on cancer patients. Additionally, Patti is part of an international consortium funded by Cancer Grand Challenges to investigate broader links between diet and cancer incidence.
 
“This research highlights the potential for targeting healthy tissues’ metabolism as a way to treat cancer,” Patti said. “It’s a shift from the traditional focus on the tumor itself, and it holds a lot of promise.”
 
Conclusions
The Washington University study underscores the complex relationship between diet and cancer. By elucidating the mechanisms through which dietary fructose indirectly fuels tumor growth, the research provides valuable insights that could inform both prevention and treatment strategies. The findings highlight the liver’s central role in converting fructose into lipids that cancer cells use to thrive, offering new targets for therapeutic intervention.
 
While the rise of high-fructose corn syrup in modern diets is a relatively recent phenomenon, its potential contribution to cancer progression cannot be ignored. This study serves as a wake-up call for consumers, healthcare providers, and policymakers alike. Reducing dietary fructose consumption, particularly in the form of high-fructose corn syrup, may be a critical step in combating the growing cancer epidemic.
 
The study’s implications extend beyond individual dietary choices. They pave the way for innovative treatments that target the metabolic interactions between the liver and tumors, offering hope for more effective cancer therapies. As research continues to unfold, the findings from Washington University represent a significant milestone in our understanding of cancer metabolism.
 
The study findings were published in the peer-reviewed journal: Nature.
https://www.nature.com/articles/s41586-024-08258-3
 
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