Then, several weeks ago, in my daily researches, I came across a reference to the use of the ketogenic diet in brain cancers and immediately did a search on PubMed. Sure enough, up popped a whole bunch of references, and what I discovered is that cancer cells cannot use ketones for fuel. Starving them of their one source of fuel - glucose - may definitely help keep tumors from regrowing. (...)
I pulled a few abstracts to send them yesterday, and I'm pasting two of them below. Also, they found a wonderful link on the diet for cancer patients: http://www.meandmydiabetes.com/wp-content/uploads/2010/03/ketogenic_en-1-cancer.pdf .
Let this work.
Epilepsy Res. 2011 Aug 30.
Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer? Seyfried TN, Marsh J, Shelton LM, Huysentruyt LC, Mukherjee P.
Source Biology Department, Boston College, Chestnut Hill, MA 02467, United States.
Abstract Malignant brain cancer persists as a major disease of morbidity and mortality. The failure to recognize brain cancer as a disease of energy metabolism has contributed in large part to the failure in management. As long as brain tumor cells have access to glucose and glutamine, the disease will progress [by restricting glucose and protein (glutamine is an amino acid, a building block of protein), you stop feeding the cancer.]. The current standard of care provides brain tumors with access to glucose and glutamine. The high fat low carbohydrate ketogenic diet (KD) will target glucose availability and possibly that of glutamine when administered in carefully restricted amounts to reduce total caloric intake and circulating levels of glucose. The restricted KD (RKD) targets major signaling pathways associated with glucose and glutamine metabolism including the IGF-1/PI3K/Akt/Hif pathway. The RKD is anti-angiogenic, anti-invasive, anti-inflammatory, and pro-apoptotic when evaluated in mice with malignant brain cancer. The therapeutic efficacy of the restricted KD can be enhanced when combined with drugs that also target glucose and glutamine. Therapeutic efficacy of the RKD was also seen against malignant gliomas in human case reports. Hence, the RKD can be an effective non-toxic therapeutic option to the current standard of care for inhibiting the growth and invasive properties of malignant brain cancer. [woohoo!]
Nutr Metab (Lond). 2010 Sep 10;7:74.
The ketogenic diet reverses gene expression patterns and reduces reactive oxygen species levels when used as an adjuvant therapy for glioma. Stafford P, Abdelwahab MG, Kim do Y, Preul MC, Rho JM, Scheck AC.
Source Neuro-Oncology Research, Barrow Neurological Institute7 of St, Joseph's Hospital and Medical Center, Phoenix, AZ, 85013, USA. Adrienne.Scheck@chw.edu.
Abstract BACKGROUND: Malignant brain tumors affect people of all ages and are the second leading cause of cancer deaths in children. While current treatments are effective and improve survival, there remains a substantial need for more efficacious therapeutic modalities. The ketogenic diet (KD) - a high-fat, low-carbohydrate treatment for medically refractory epilepsy - has been suggested as an alternative strategy to inhibit tumor growth by altering intrinsic metabolism, especially by inducing glycopenia.
METHODS: Here, we examined the effects of an experimental KD on a mouse model of glioma, and compared patterns of gene expression in tumors vs. normal brain from animals fed either a KD or a standard diet.
RESULTS: Animals received intracranial injections of bioluminescent GL261-luc cells and tumor growth was followed in vivo. KD treatment significantly reduced the rate of tumor growth and prolonged survival. [woohoo!] Further, the KD reduced reactive oxygen species (ROS) production in tumor cells. Gene expression profiling demonstrated that the KD induces an overall reversion to expression patterns seen in non-tumor specimens. Notably, genes involved in modulating ROS levels and oxidative stress were altered, including those encoding cyclooxygenase 2, glutathione peroxidases 3 and 7, and periredoxin 4.
CONCLUSIONS: Our data demonstrate that the KD improves survivability in our mouse model of glioma, and suggests that the mechanisms accounting for this protective effect likely involve complex alterations in cellular metabolism beyond simply a reduction in glucose.