The PK – Membrane Stabilizing – Protocol For Neurological Disorders
Patricia C. Kane, Ph.D., Mark O’Neal Speight, M.D.,
Katrin Bieber, M.D., Meinrad Milz, MD,
Shideh Pouria, MB BS BSc MRCP (UK) PhD CMT,
Damien Downing, M.D., Annette L. Cartaxo, MD, Edward Kane
Background: The lipid soluble nature of toxicity has led us to seize the complexity of neurological presentations by addressing them from a cell membrane perspective. Examination of red cell lipids and identification of nuclear DNA adducts as chemicals, pesticides, microbials and metals in subjects with Motor Neuron Disease, Autism, Multiple Sclerosis, Post Stroke, Epilepsy, Alzheimer’s and Parkinson’s Disease over the past eleven years in 9000 analyses has revealed a characteristic accumulation of very long chain fatty acids (VLCFAs), which comprise lipid rafts, or ceramides, revealing cell membrane derangement. Membrane phospholipid abnormalities with elevation of VLCFAs may be indicative of exposure to fat soluble neurotoxins resulting in suppressed peroxisomal beta oxidation of VLCFAs. Disturbances in methylation due to toxic exposure may destabilize the membrane phospholipid structure and alter DNA expression due to deficits in the enzymes Methylene Tetrahydrofolate Reductase (MTHFR) and Methionine Synthase.
Objective: The use of oral and IV lipids may facilitate stabilization of phospholipids in cellular membranes thereby addressing cell membrane integrity. The addition of intravenous phenylbutrate addresses neuroinflammation by increasing the beta oxidation of VLCFAs.
Procedure: To clear the bioaccumulation of toxins and stabilize membrane function we have embarked on a clinical treatment plan for the past five years to address the accumulation of aberrant lipids and ceramides with oral and IV phenylbutyrate, bolus intravenous phosphatidylcholine as Essentiale, methylation factors (folinic acid, riboflavin, methylcobalamin, tetrahydrobiopterin), and sulfation support (IV Glutathione).
Results: We have noted significant and sustained clinical neurological improvement within the first few weeks after initiation of oral and intravenous treatment in our patient population of 300 subjects.
Conclusion: The administration of Phosphatidylcholine, Leucovorin/Folinic acid, Glutathione and Phenylbutyrate may offer a new therapeutic strategy for neurological disorders involving neurotoxic exposure.