The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer.
Level 5 - mechanism / opinion, no new human data
Preclinical animal experiment with no human data
PubMed 17313687 · doi:10.1186/1743-7075-4-5
What was done
Adult mice were orthotopically implanted with either a mouse astrocytoma (CT-2A) or a human glioma (U87-MG) cell line. Mice received KetoCal (a high-fat, low-carbohydrate ketogenic diet) in either unrestricted or calorically restricted amounts. Tumor growth, microvessel density, survival, plasma glucose, beta-hydroxybutyrate levels, and ketone metabolic enzyme gene expression were compared against an unrestricted high-carbohydrate standard diet.
What was found
Calorically restricted KetoCal reduced intracerebral tumor growth by approximately 65% in the CT-2A model and approximately 35% in the U87-MG model compared to the standard diet control. The restricted diet decreased plasma glucose, elevated plasma beta-hydroxybutyrate, reduced tumor microvessel density, and significantly extended survival. In addition, gene expression of beta-hydroxybutyrate dehydrogenase and succinyl-CoA: 3-ketoacid CoA transferase was lower in tumors than in normal contralateral brain tissue.
Why it matters
This study provides preclinical evidence that combining a ketogenic diet with caloric restriction impairs glioma growth and angiogenesis by exploiting the tumor's reduced capacity to metabolize ketone bodies.
Limits
The study is entirely preclinical in mice, so findings cannot be directly translated to clinical efficacy or survival in human patients. The abstract does not report specific sample sizes, statistical variance, or exact survival numbers. Therapeutic efficacy depended on caloric restriction rather than the ketogenic diet alone.
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- context Feeding mice an ad libitum ketogenic diet containing non-sugar sweeteners causes insulin resistance, high blood glucose, and accelerated tumor progression in brain and colon cancer models.