"You get a significant reduction in tumor growth, decrease in tumor size, and significant extension of life when the therapeutic ketosis achieved through the ketogenic diet is combined with hyperbaric oxygen," he says.
"Tumors thrive in a low-oxygen environment. As a tumor grows, it exceeds its ability to supply oxygen to the center of the tumor. That low level of oxygen, called hypoxia, further activates the oncogenes; cancer promoting genes. It activates things like HIF-1-alpha and VEGF. IGF-1 signaling goes up. Hyperbaric oxygen can reverse tumor hypoxia intermittently. In doing that, it can actually turn off the oncogenes. There are published reports on this.
... [T]he tumor thrives in a low-oxygen environment, and it's adapted to that low-oxygen environment. When you saturate a tumor with oxygen, because the mitochondria are damaged, it overproduces oxygen free radicals in the form of superoxide anion. This oxygen-induced increase in free radicals can actually cause the tumor to kill itself."
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Abnormal cancer metabolism creates a glycolytic-dependency which can be exploited by lowering glucose availability to the tumor. The ketogenic diet (KD) is a low carbohydrate, high fat diet which decreases blood glucose and elevates blood ketones and has been shown to slow cancer progression in animals and humans. Abnormal tumor vasculature creates hypoxic pockets which promote cancer progression and further increase the glycolytic-dependency of cancers. Hyperbaric oxygen therapy (HBO2T) saturates tumors with oxygen, reversing the cancer promoting effects of tumor hypoxia. Since these non-toxic therapies exploit overlapping metabolic deficiencies of cancer, we tested their combined effects on cancer progression in a natural model of metastatic disease.
We used the firefly luciferase-tagged VM-M3 mouse model of metastatic cancer to compare tumor progression and survival in mice fed standard or KD ad libitum with or without HBO2T (2.5 ATM absolute, 90 min, 3x/week). Tumor growth was monitored by in vivo bioluminescent imaging.
KD alone significantly decreased blood glucose, slowed tumor growth, and increased mean survival time by 56.7% in mice with systemic metastatic cancer. While HBO2T alone did not influence cancer progression, combining the KD with HBO2T elicited a significant decrease in blood glucose, tumor growth rate, and 77.9% increase in mean survival time compared to controls.
KD and HBO2T produce significant anti-cancer effects when combined in a natural model of systemic metastatic cancer. Our evidence suggests that these therapies should be further investigated as potential non-toxic treatments or adjuvant therapies to standard care for patients with systemic metastatic disease.