Neurolipid Keto Membrane Stabilizing Protocol© NRF 2012-2016
NeuroLipid Keto Diet & NeuroLipid Keto Metabolic Support, IV PK Keto Protocol

Patricia C Kane PhD, Edward Kane, Thomas Wnorowski, PhDAnnette L Cartaxo, MD,
Sheryl Leventhal, MD, Neal Speight MDKristine Gedroic, MDKatrin Bieber, MD,
Meinrad Milz, MDShideh Pouria, MDDamien Downing, MD, Carrie Robinson Loughran, RD, LD

Maintaining the appropriate balance and content of lipids in cellular membranes is critical for normal neural processes. Accumulating evidence suggests that even subtle perturbations in the lipid content of neurons and myelin can disrupt their function. The membrane and organelles within the cell are the primary focus of electrical discharge within the central nervous system and can be stabilized with phospholipid therapy and a Phospholipase A2 (PLA2) suppressive diet.


Dietary intervention includes a targeted, essential fatty acid and phospholipid nutrient dense diet with low carbohydrate and moderate protein. The brain is 60% lipid, containing phospholipids, which comprise the plasma and organelle membranes, along with cardiolipin, located exclusively in the inner lipid membrane of mitochondria. Stabilization of cardiolipin is a primary therapeutic target in seizure disorders which may be addressed using lipid therapy. Recent research has revealed that in the brain myelin acts as one enormous mitochondrion. Examination of red cell lipids at Johns Hopkins Peroxisomal Diseases Laboratory in subjects with Epilepsy, Autism, Alzheimer’s, inborn errors in metabolism, Post Stroke, PDD, Multiple Sclerosis and Parkinson’s Disease over the past 15 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 per disturbance in peroxisomal respiration, which has a vital role in cell membrane integrity and function.


Membrane phospholipid abnormalities with elevation of VLCFAs may be indicative of exposure to neurotoxins resulting in suppressed peroxisomal beta oxidation of VLCFAs. Identification of nuclear and mitochondrial DNA adducts (toxins) at Acumen, a research laboratory in Devon, England, has revealed a link between toxic exposure, and the development of cell membrane derangement / dysfunction.


In our current study we have captured visual images of distorted phospholipid membranes and have linked the impact of the DNA adducts (toxins) altering gene expression t o aberrations in lipid metabolism, cellular dysfunction and alteration of the structure of phospholipids in the cell membrane characteristic to the presenting diagnosis and symptoms.


Our treatment protocol includes an oral targeted lipid therapy (targeted phospholipid based dietary therapy) and in some cases an intravenous infusion of phenylbutyrate, phosphatidylcholine, leucovorin, and glutathione to clear bioaccumulation of toxins impacting gene expression and stabilize cellular architecture. We have documented significant clinical neurological improvement in our patients, including cessation of seizures, along with marked normalization of cellular function (via laboratory analysis) following six months of an oral and intravenous lipid regime. The administration of our neurometabolic lipid protocol may offer a new therapeutic strategy for neurological disorders.