Patricia Kane protocol
The Patricia Kane protocol (PK protocol) is an experimental treatment for neurological disease involving intravenous infusion of phospholipids and methylation factors, along with dietary changes and supplements.
It is based on the theory that in diseases that Kane classes as those of neurotoxicity (e.g., multiple sclerosis, Parkinson's disease, chronic fatigue syndrome), toxins destabilize cell membranes, leading to dysfunctions in cell signaling and homeostasis and neurodegeneration.
Kane's treatments have never undergone double-blind, placebo-controlled testing in order to substantiate her claims. In a 2008 article in a CBS affiliate discussed Dr. Kane's work at the Haverford Wellness Center. Patients reported Kane told them their neurological diseases were "a build up of toxins". Another patient reported that Kane took thousands of dollars from her for treatments, and told her that she wasn't dying [of ALS]. The patient is now deceased.[1]
Theory[edit | edit source]
Kane seeks to correct deficiencies of omega 6 and arachidonic acid in cell membranes and correct the over-expression of very long chain fatty acids.
Protocol[edit | edit source]
The protocol is individualized but involves several key components: intravenous infusion of phosphatidylcholine and sodium phenylbutyrate, pushes of glutathione and folinic acid (leucovorin), methylcobalamin injections, and increased intake of essential fatty acids.
Patricia Kane recommends elimination of all processed foods, regular intake of pastured eggs, and a "cell membrane stabilizing drink" consisting of liquid phosphatidylcholine, evening primrose oil, whey protein, and a blend of safflower oil and flaxseed oil in a 4:1 ratio of Omega-6 to Omega 3, and a blend of seeds. She also recommends a low carbohydrate, high fat diet.
Medical applications[edit | edit source]
Kane believes her protocol can offer clinical benefit in a range of neurological disorders including ALS, Parkinson's disease, Multiple sclerosis, Alzheimer's, autism, pervasive developmental delay, seizure disorders, post stroke, traumatic brain injury, metabolic]] and genetic abnormalities.
Evidence[edit | edit source]
There have been no clinical trials of the PK protocol for the treatment of any disease.
Some of the individual components of the protocol have been studied.
Sodium phenylbutyrate[edit | edit source]
In mouse models of Parkinson's, sodium phenylbutyrate was found to protect the loss of dopaminergic neurons.[2][3][4]
See also[edit | edit source]
References[edit | edit source]
- ↑ "I-Team Follow-Up: False Hope - cbs3.com". web.archive.org. March 7, 2009. Retrieved May 9, 2024.
- ↑ Iannitti, Tommaso; Palmieri, Beniamino (September 2011). "Clinical and Experimental Applications of Sodium Phenylbutyrate". Drugs in R&D. 11 (3): 227–249. doi:10.2165/11591280-000000000-00000. ISSN 1174-5886. PMC 3586072. PMID 21902286.
- ↑ Freed, Curt R.; Lebin, Jacob; Luong, Nancy; Cummiskey, Jessica; Bercury, Kathryn; Zhou, Wenbo (April 29, 2011). "Phenylbutyrate Up-regulates the DJ-1 Protein and Protects Neurons in Cell Culture and in Animal Models of Parkinson Disease". Journal of Biological Chemistry. 286 (17): 14941–14951. doi:10.1074/jbc.M110.211029. ISSN 0021-9258. PMID 21372141.
- ↑ Pahan, Kalipada; Gendelman, Howard E.; Brahmachari, Saurav; Liu, Xiaojuan; Jana, Arundhati; Ghosh, Anamitra; Roy, Avik (June 18, 2012). "Sodium Phenylbutyrate Controls Neuroinflammatory and Antioxidant Activities and Protects Dopaminergic Neurons in Mouse Models of Parkinson's Disease". PLOS ONE. 7 (6): e38113. doi:10.1371/journal.pone.0038113. ISSN 1932-6203. PMC 3377667. PMID 22723850.
