Is cancer really a genetic disease — or a metabolic one? 🧬
In this episode, Dr. Thomas Seyfried, professor of biology at Boston College and author of Cancer as a Metabolic Disease, breaks down why glucose and glutamine fuel cancer growth and how nutritional ketosis and metabolic therapy can help prevent and manage cancer more effectively.

Discover how tracking the Glucose-Ketone Index (GKI), exercising regularly, and targeting cellular metabolism can transform the way we understand cancer treatment. 🚀

If you care about metabolic health, cancer prevention, or functional medicine, this is a must-watch episode.

💡 Key Takeaways
✅Cancer is primarily a metabolic disease, not a genetic one.
✅Glucose and glutamine are the main fuels for cancer cells.
✅A ketogenic diet and GKI monitoring can support cancer management.
✅The press-pulse strategy targets cancer cells through metabolic control.
✅Exercise and mitochondrial health are vital in prevention.
✅Philanthropy fuels innovation in cancer research.

👨‍🔬 About Dr. Thomas Seyfried
Dr. Thomas N. Seyfried is a Professor of Biology at Boston College and one of the world’s leading experts on metabolic therapy for cancer. His groundbreaking research challenges the conventional genetic theory of cancer and focuses on how metabolic dysfunction drives tumor growth.
He is the author of “Cancer as a Metabolic Disease” — a book that’s changing how the world thinks about cancer treatment and prevention.

Connect with Dr. Thomas Seyfried:
Website: http://bit.ly/4hwsttS
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Based on the provided transcript, here is a structured version including chapter titles with timestamps and a clean, uploadable transcript format.

🔗Links to Dr. Thomas Seyfried for further readings

Press-pulse: a novel therapeutic strategy for
the metabolic management of cancer: http://bit.ly/3LyWMDY

Clinical research framework proposal
for ketogenic metabolic therapy in glioblastoma: http://bit.ly/43E0pP9

The Warburg hypothesis and the emergence of the mitochondrial
metabolic theory of cancer: http://bit.ly/4oj9EwG

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