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Short Summary: How dietary fructose affects the growth rate of cancer.

About the guest: Gary Patti, PhD is a professor at Washington University in St. Louis, holding appointments in chemistry, medicine, and genetics

Note: Podcast episodes are fully available to paid subscribers on the M&M Substack and everyone on YouTube. Partial versions are available elsewhere. Full transcript and other information on Substack.

Episode Summary: Nick Jikomes talks to Dr. Patti, exploring how cancer cells metabolize sugars like glucose and fructose, focusing on a recent study showing fructose indirectly boosts tumor growth in mice via liver-produced lipids called LPCs. The discussion covers cancer biology basics, Warburg effect, tumor microenvironments, and systemic metabolic impacts of cancer, while also touching on dietary implications, fasting, and the complexities of nutrient use in cancer progression.

Key Takeaways:

• Cancer cells often rely heavily on glucose, excreting it as lactate even when oxygen is available (Warburg effect), but take up more than their mitochondria can handle.
• In a study, high fructose diets accelerated tumor growth in mice by 4x, not because cancer cells use fructose directly, but because the liver converts it to LPCs, which tumors use to build membranes.
• Tumors are not just cancer cells; they recruit healthy cells in their microenvironment, and their metabolic effects ripple across the entire body, altering distant tissues.
• Excessive fructose consumption may worsen tumor growth, but cutting it poses little risk and could benefit cancer patients, pending human studies.
• Fasting may reduce cancer initiation risk in animals, but its effect on existing tumors is less clear and could worsen wasting (cachexia) in late stages.
• The body tightly regulates blood glucose via the liver, so simply cutting dietary glucose won’t starve tumors, highlighting cancer’s metabolic adaptability.

Related episode:

• M&M #200: Dietary Fats & Seed Oils in Inflammation, Colon Cancer

*Not medical advice.

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