38-month long progression-free and symptom-free survival of a patient with recurrent glioblastoma multiforme: A case report of the Paleolithic Ketogenic Diet (PKD) used as a stand-alone treatment after failed standard oncotherapy
Studies in animal models have suggested that the ketogenic diet may be effective in the treatment of cancer. However, human cohort studies on the ketogenic diet have, thus far, failed to show benefits in cancer survival or in any other hard clinical endpoints of the disease. This paper presents a case report of a patient with glioblastoma multiforme. The patient had initially been treated with standard oncotherapy including surgery, radiotherapy and chemotherapy. Despite standard treatment, the patient experienced a recurrence of the glioblastoma seven months later. Subsequently, the patient refused radiotherapy and chemotherapy and opted to use the paleolithic ketogenic diet (PKD) as a stand-alone therapy. Following the adoption of the PKD, progression of the disease has been completely halted. At the time of writing, the patient has remained in remission for 38 months, is without side-effects and experiences an excellent quality of life without the use of any drugs.
In the classic ketogenic diet, the source of the foods is not stipulated; whereas in the PKD the source of the fats and proteins is of the utmost importance. In practical terms this means that the PKD excludes all dairy products, cereal grains, plant oils, nightshades, legumes and dietary supplements; i.e. all foods that were not routinely available before the advent of agriculture 10,000 years ago.
The classic ketogenic diet (and its variants), typically contain unrestricted amounts of dairy products, nuts and plant oils, which are normally excluded in the PKD. In our opinion, this difference accounts for the additional benefits conferred by the PKD as compared to the classic ketogenic diet. We believe that excluding the non-PKD food components results in the normalization of intestinal permeability, which is a critical factor in the mechanism of action of the PKD in cancer (Tóth et al., 2017).