Updated: Jan 30
As luck and coincidence would have it, I began to have people find me who like me ( I have had 3) had suffered a TBI (traumatic brain injury) but failed to recover quickly ( less than 90 days), and experience pro-longed and incomplete healing. I am up to 10 clients now (including me) who have had TBI's that didn't fully heal initially, some from many years ago, some more recent (less than 5 years). Although this sample size certainly isn't statistically significant, the types of genetic mutations I see in common across this group are striking - and the rarity of these mutations in a normal population (thank you gnom AD Browser!) is uncanny.
This blog entry is a rough draft, and as the days go on I will tidy it up, add more information, and details, and more fully source with references and findings. However, i am leaping a bit here, as i am hopeful others who have struggled to heal from TBI's will take me up on my offer - to let me look at your genetic data for free - and see if the common patterns hold - so I can potentially increase my sample size. You don't need to become a client to be in my sample, just a data point. My intent is to get enough of a sample size (~30), where I can publish a paper, and have a couple of M.D.'s co-author with me who have expressed interest. So, if you have a TBI, and haven't healed and have your genetic data - please reach out. If you don't have your genetic data , I am open to discussing how we can get you a robust set - I will direct you how without charging you consulting fees.
COMMON PATTERN #1 - UPREGULATED iNOS (NOS2)
This is the most striking pattern I see in these clients. They all have one or both mutations on iNOS (NOS2) that have research demonstrating they upregulate the iNOS enzyme, producing excessive Nitric Oxide. One of these mutations has research that shows it upregulates iNOS over 4.5X! Why is excess nitric oxide so important, and what are the symptoms. I would like to outline 5 key things that happens when iNOS gets over expressed:
Free radicals and oxidative stress (super oxide, peroxynitrite, hydroxyl radicals) - fatigue, inflammation.
BH4 / Tetrahydrobiopterin gets oxidized and depleted - effects neurotransmitters (mood)
Low blood pressure (dizzyness), POTS like symptoms, poor circulation (cold hands and feet)
NAD / NADPH gets depleted (fatigue)
Platelet Activation - poor oxygen perfusion and delivery (fatigue, cognitive challenges)
First, we thank Martin Pall, who explored this years ago - related to Chronic Fatigue Syndrome. Excess nitric oxide combines with super oxide (free radical) and forms the more damaging free radical peroxynitrite - which can also go on and form the damaging free radical hydroxyl radical. Ouch! Lots of oxidative stress here. Further, Martin Pall, has published a ton of research that many cardiac events are preluded by "NOS Uncoupling" where the excess nitric oxide consumes all the available BH4 (Tetrahydrobiopterin) and then when BH4 runs out, it creates a massive cascade of free radicals and oxidative stress. This is a precursor to many cardiac events [1,2,4,18]. The second thing that excess nitric oxide does is it creates low blood pressure with symptoms like POTS, cold hand and feet, dizziness, etc. Excess nitric oxide also results in poor circulation and blood all over the body, including the brain, resulting in low oxygen delivery (cold hands and feet anybody!). Third, an upregulated iNOS enzyme uses NAD / NADPH as a cofactor in its reaction and consumes a ton of this - and NAD / NADPH is the most common co factor for enzymatic reactions in the body - when this gets depleted - people are TIRED! Its one reason why many athletes are now paying for expensive NAD IV treatments - its one of the basic common denominators in creating energy potential in the body. Fourth, excess nitric oxide oxidizes BH4 which is a cofactor in turning Tyrosine into Dopamine (low mood anyone!). And BH4 is also a cofactor for creating Serotonin from Tryptophan and 5HTP (anxiety anyone ?). Lastly, and perhaps most importantly, excess nitric oxide from iNOS causes platelet activation, which in turn leads to low oxygen perfusion and delivery - as the activated platelets clump up and grab on to red cells - which deliver oxygen. The impacts of these two mutations on iNOS are serious - and common across all 10 TBI clients. When this enzyme was stabilized through basic diet changes and basic supplementation - positive changes were seen.
Further, many have been concluding recently, based on Pall's initial work, and from further exploration into Covid 19 - that it is in fact eNOS (NOS3) that is needed most for endothelial health, and it is iNOS (NOS2) that can compete and disrupt eNOS and lead to NOS uncoupling, and then endothelial dysfunction and cardiac related issues .
COMMON PATTERN #2 - COMPROMISED PRODUCTION OF GLYCINE FROM SHMT1, SHMT2, AND / OR GCAT ENZYMES
All ten of these clients had significant compromise in one or more of the enzymes that create glycine from serine (SHMT1 - in the exosome and SHMT2 - inside the mitochondria) or from L-Threonine (GCAT). The cofactors for each of these reactions is B6 (p5p form), which is commonly depleted in many people for a variety of reasons. In another article to be explored more fully i will discuss how supplementing with glycine can draw glutamate down a pathway and away from the brain to reduce neuro excitatory / inflammation. It is for this reason, why i believe so many respond so well to glycine supplementation - in addition to being one of the three building blocks to glutathione (Glutamate, Cysteine, and Glycine). HOWEVER - CAUTION HERE FOLKS - NAC SUPPLEMENTATION - THE OTHER BUILDING BLOCK TO GLUTATHIONE ASIDE FROM GLUTAMINE - WILL COMBINE WITH EXCESS IRON AND CREATE HYDROXYL RADICALS (FATIGE ANYONE FROM NAC!).
COMMON PATTERN #3 - EXCESS GLUTAMATE
In the majority but not all 10 of these cases, there are compromises in the glutamate system that lead to a build up of glutamate. If there is a B6 or Magnesium deficiency, it becomes even more problematic - as glutamate isn't converted to GABA (calming neurotransmitter) efficiently. Like a train station, there are literally a half dozen escape routes for glutamate - but if they are compromised, glutamate can build up, and create all sorts of issues from poor sleep, to anxiety, to sensory overload, etc. Oxaloacetate is one of the pathways out of this train station intersection - and is marketed as a PMS supplement! What/why!? Because glutamate builds up during a woman's monthly cycle - there is a physiological reason for these issues! So, women, if this was an issue for you - glutamate is worthy of exploration.
COMMON PATTERN #4 - COMPROMISED NMDA RECEPTORS (GRIN ENZYMES)
This was first identified by Martin Pall years ago, and he correctly connect the NMDA receptors (GRIN genes) to the TRP receptors as well . These are also linked to EMF sensitivity and the CACNA1C gene. Although observationally, I have seen EMF sensitivity with no CANCNA1C mutations but with iNOS upregulations. When the NMDA receptors have significant mutations - it compounds glutamate sensitivity issues, along with EMF sensitivity issues. Almost all 10 cases had very significant NMDA mutations.
COMMON PATTERN #5 - COMPROMISED ANTIOXIDANT SYSTEMS - ESPECIALLY GLUTATHIONE. CATALASE AND SUPER OXIDE DISMUTASE ALSO NOTED.
Most folks are well versed in the basic anti oxidant systems (Glutathione, Catalase and Super Oxide Dismutase) [x]. The GST genes - glutathione S- transferese enzymes support detoxification of metals, chemicals, molds. The GPX genes - glutathione peroxidase enzymes - support the detoxification of hydrogen peroxide from reactions with ammonia, fatty acids, etc. The GPX enzyme play a critical role in platelet activation - because without proper disposal of the lipid by products - inflammatory compounds like Leukotrine B4 become excessive. In the absence of glutathione, the body will use carnosine to detox some of 12-HETE / 12-PETE by products in the ALOX 12 pathway. GPX4 is the only gpx enzyme expressed inside the mitochondria, just like SOD2. Mutations in GPX4 and SOD2 are impactful in creating oxidative stress inside the mitochondria - which can lead to downregulation of the krebs cycle (fatigue anybody!) as a response to manage the oxidative stress. Ron Davis has his own theory here on the - Aconotate Shunt. GPX1 is the most ubiquitously expressed GPX enzyme - and it has correlations with all cause mortality - its important! GPX1 mutations were very common in this group of 10 cases [x]. It is compromises in the GPX system that are most common in this group. iNOS / NOS2 is expressed primarily in the GI tract, as is GPX2. When there are mutations of upregulated iNOS and GPX2 - its double trouble for gut issues. Lots of super oxide, lots of hydrogen peroxide, which probably over whelms GPX2.
Its also important to note the GSR enzyme, it recycles oxidized glutathione back to reduced glutathione. If this gene is severely mutated, one must be very careful with exogenous glutathione supplementation or upregulation the GST or GPX enzymes. The first step is getting the GSR enzyme functioning!
Also of note in the anti oxidant system regulation are Keap1, NRF2, and HMOX1. Significant mutations were seen in these cluster of genes in this population - and they are also seen in CFS cases.
COMMON PATTERN #6:
COMPROMISE IN PLATELET ACTIVATION PATHWAYS - THERE ARE A DOZEN!
So this is a bit of catch all for platelet activation, but in fairness iNOS creates platelet activation too, so its in here, but described above. I will briefly note the 8 pathways I see related to this issue, acknowledging there may be more of course that we dont know about yet. Most of these separate pathways are connected in some way , as Martin Pall noted in his research years ago, its my best attempt to separate things into parts of a whole:
8a) Upregulated iNOS / NOS2 - See above
8b) Compromised CCR1, CCR3, CCR5 Enzymes (Rantes)
8c) TNF Alpha Pathway which includes - NFK Beta, HFE, IL-10, IL-6
8d) PLA2 pathway
8e) ALOX 5 Pathway
8f) ALOX 12 Pathway
8g) COX / PTGIS Pathway
8h) ACE 2 / Angiotensin 2 / HMOX1 pathway 
8i) Keap1 / NrF2 / HMOX 1 / BLRVA pathway
8j) Prostacyclin pathway
8k) Thromboxanne A2 pathway
8l) Protectins and Resolvins Pathway
8m) NOX1, NOX3, NOX4, NOX5, Il-6, SIRT1 pathway [4,10]
8N) GPX1-7, GSR, NRF2, Keap1 pathway
There is alot to the above regarding platelet activation as you can see - and i will devote an entire blog article to this specific topic to do it justice. Suffice to say, all 10 TBI clients had major compromises in multiple pathways, and every client that tested for elevated levels of two compounds that indicate activated platelets - all were elevated. In this blog article on Platelet Activation i will also describe a variety of tests you can explore to decipher if this is an issue from very inexpensive ones that make you suspicious its at play, to the full deal with over a dozen specific markers.
I haven't mentioned specific locations or SNP's related to the above genes - its intentional. Yes, in some cases some very specific SNP's are critical, but also the overall evaluation of the gene across many many locations - sometimes 100+. I encourage you to seek the counsel of somebody trained on how to evaluate specific SNP's as well as the aggregate level of mutations for a particular gene relative to a normal population to assess its level of compromise.
I also haven't mentioned specific solutions for each of the above, most have several options - and again encourage you to seek the counsel and guidance of somebody who knows based on research and has experience doing so.
Most of the 10 cases did have gut related issues as a consequence, not cause of their issues, and that also needed to be addressed, but secondarily. Fut2 mutations make things worse - as they compromise the ability to synthesize B vitamins - need for neurotransmitters and energy production (krebs cycle).
More to come, with references, research, and data....please check back in.....and please contact me if you have suffered a TBI and want to explore the genetics........I really do need more case examples. Most of these individuals experienced quick improvement related to course correcting some of the above issues. For some it was more of a gradual improvement over 3 to 6 months. Many were stuck for over a decade.
Minor update. I have had two people contact me that have had ECT injury. One was the primary source of their TBI - and provided their genetic data - their data revealed that many of the above major patterns were present genetically. The other has become a client, and we are awaiting to complete the genetic testing. My 10 case examples listed above were all from more traditional head impact TBI's (e.g. car wreck, fall, bike wreck, head to head combat, etc).
 Nitric oxide synthase partial uncoupling as a key switching mechanism for the NO/ONOO- cycle
 The NO/ONOO-Cycle as the Central Cause of Heart Failure; Martin L. PallInt J Mol Sci. 2013 Nov; 14(11): 22274–22330. Published online 2013 Nov 13. doi: 10.3390/ijms141122274; PMCID: PMC3856065; PMID: 24232452
 Approaches to Curing Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, Fibromyalgia, Multiple Chemical Sensitivity, Gulf War Syndrome and Possibly Many Others by Martin L. Pall, PhD. From the Townsend Letter; February / March 2010
 NOX5-induced uncoupling of endothelial NO synthase is a causal mechanism and theragnostic target of an age-related hypertension endotype. Mahmoud H. Elbatreek , Sepideh Sadegh, Elisa Anastasi, Emre Guney, Cristian Nogales, Tim Kacprowski, Ahmed A. Hassan, Andreas Teubner, Po-Hsun Huang, Chien-Yi Hsu, Paul M. H. Schiffers, Ger M. Janssen, Pamela W. M. Kleikers, Harald H. H. W. Schmidt. Published: November 10, 2020. https://doi.org/10.1371/journal.pbio.3000885
 NMDA Sensitization and Stimulation by Peroxynitrite, Nitric Oxide, and Organic Solvents as the Mechanism For Multiple Chemical Sensitivity. Martin L Pall, School of Molecular Bio Sciences, Washington State Univeristy. The FASEB Journal Volum 16, Issues 11, September 2002.
 The NO/ONOO– Cycle as the Etiological Mechanism of Tinnitus Martin L. Pall and Sabrina A. Bedient School of Molecular Biosciences, Washington State University, Pullman, Washington, USA
 High-dose Therapy with Ascorbate, Niacin, Folate and B12: Pauling was Right but for the Wrong Reason Martin L. Pall, PhD1 1 Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University and Research Director, The Tenth Paradigm Research Group. 638 NE 41st Ave. Portland, OR 97232-3312 USA
 Angiotensin II Decreases Endothelial Nitric Oxide Synthase Phosphorylation via AT1R Nox/ROS/PP2A Pathway Jing Ding1,2† , Min Yu1,2† , Juncai Jiang1,2 , Yanbei Luo1,2 , Qian Zhang1,2 , Shengnan Wang3 , Fei Yang4 , Alei Wang1,2 , Lingxiao Wang1,2 , Mei Zhuang5 , Shan Wu6 , Qifang Zhang7 , Yong Xia8 * and Deqin Lu1,2. This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology Received: 03 June 2020 Accepted: 08 September 2020 Published: 30 September 2020
 Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States Copy Right@ Ally A, Nauli SM This work is licensed under Creative Commons Attribution 4.0 License AJBSR.MS.ID.002087. American Journal of Biomedical Science & Research www.biomedgrid.com ISSN: 2642-1747 Research Article Tran N1, Garcia T1, Aniqa M1, Ali S1, Ally A1* and Nauli SM2* Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States. Am J Biomed Sci & Res. 2022 - 15(2). AJBSR.MS.ID.002087. DOI: 10.34297/AJBSR.2022.15.002087 Received: December 13, 2021 Published: January 04, 2022
 NOX5-induced uncoupling of endothelial NO synthase is a causal mechanism and theragnostic target of an age-related hypertension endotype Mahmoud H. ElbatreekID, Sepideh Sadegh , Elisa Anastasi , Emre Guney, Cristian Nogales, Tim Kacprowski, Ahmed A. Hassan , Andreas Teubner , PoHsun Huang, Chien-Yi Hsu, Paul M. H. Schiffers, Ger M. Janssen, Pamela W. M. Kleikers , Anil Wipat , Jan Baumbach, Jo G. R. De Mey, Harald H. H. W. Schmidt; email@example.com (MHE); firstname.lastname@example.org (HHHWS).
Martin Pall References
 A fantastic summary of Martin Pall's Work: https://www.medicalinsider.com/cardiac3.html
 Martin Pall's Article on BH4 and Sauna Therapy: "A study of sauna therapy in myalgic encephalomyelitis/chronic fatigue syndrome patients shows sauna action via raised tetrahydrobiopterin and confirms three predictions of the NO/ONOO cycle." https://www.thefreelibrary.com/A+study+of+sauna+therapy+in+myalgic+encephalomyelitis%2Fchronic+fatigue...-a0348313986
 Elevated Nitric Oxide/Peroxynitrite Theory of Multiple Chemical Sensitivity: Central Role of N-Methyl-d-Aspartate Receptors in the Sensitivity Mechanism. October 2003. Environmental Health Perspectives 111(12):1461-4. DOI:10.1289/ehp.5935. Source PubMed. Authors: Martin L Pall Washington State University
 The Vanilloid Receptor as a Putative Target of Diverse Chemicals in Multiple Chemical Sensitivity. Martin L. Pall &Julius H. Anderson. Pages 363-375 | Published online: 07 Aug 2010 https://doi.org/10.3200/AEOH.59.7.363-375
 "Maybe it's not just in your head". February 10, 2010, by Mary Aegerter. Washington State Magazine. Imagine trying to lead your life while avoiding diesel exhaust, perfume, cleaning fluids, the myriad chemicals that give off gas from new cars, carpets, or treated woods and fabrics–and a whole lot of other things.
 How Can We Cure NO/ONOO− Cycle Diseases? A Review . Approaches to Curing Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, Fibromyalgia, Multiple Chemical Sensitivity, Gulf War Syndrome and Possibly Many Others by Martin L. Pall, PhD. From the Townsend Letter
 Explaining Unexplained Illnesses: Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others
by Martin Pall. Publisher:Taylor & FrancisPublication date:04/23/2007 Series:Haworth Research Series on Malaise, Fatigue, and Debilitation .
 The NO/ONOO-Cycle as the Central Cause of Heart Failure. Martin L. Pall.
 Multiple Chemical Sensitivity: Toxicological Questions and Mechanisms Martin L. Pall. General and Applied Toxicology, Online 2009 John Wiley & Sons, Ltd. This article is 2009 John Wiley & Sons, Ltd. DOI: 10.1002/9780470744307.gat091 General and Applied Toxicology was renamed as General, Applied and Systems Toxicology in 2011 2011 John Wiley & Sons, Ltd  Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression. Journal of Chemical Neuroanatomy. Volume 75, Part B, September 2016, Pages 43-51. Martin L.Pall. https://doi.org/10.1016/j.jchemneu.2015.08.001
Glycine, Glutamate, NAC Related References
 Published: 23 December 2014. The Sleep-Promoting and Hypothermic Effects of Glycine are Mediated by NMDA Receptors in the Suprachiasmatic Nucleus. Nobuhiro Kawai, Noriaki Sakai, et al. Neuropsychopharmacology volume 40, pages1405–1416 (2015)
 Modulation of NMDA receptors by glycine — introduction to some basic aspects and recent developments. C. G. Parsons, W. Danysz, M. Hesselink, S. Hartmann, B. Lorenz, C. Wollenburg & G. Quack Amino Acids volume 14, pages207–216 (1998).
 Effects of sarcosine and N, N-dimethylglycine on NMDA receptor-mediated excitatory field potentials. Mei-Yi Lee, Yi-Ruu Lin, Yi-Shu Tu, Yufeng Jane Tseng, Ming-Huan Chan & Hwei-Hsien Chen Journal of Biomedical Science volume 24, Article number: 18 (2017).
 The NMDA receptor activation by d-serine and glycine is controlled by an astrocytic Phgdh-dependent serine shuttle. Samah Neame, Hazem Safory, Inna Radzishevsky, +8, and Herman Wolosker email@example.comAuthors Info & Affiliations. Edited by Solomon H. Snyder, Johns Hopkins University School of Medicine, Baltimore, MD, and approved August 29, 2019 (received for review June 1, 2019). September 23, 2019. 116 (41) 20736-20742. https://doi.org/10.1073/pnas.1909458116.
 Requirement for Glycine in Activation of NMDA-Receptors Expressed in Xenopus Oocytes. NANCY W. KLECKNER AND RAYMOND DINGLEDINEAuthors Info & Affiliations. SCIENCE. 12 Aug 1988. Vol 241, Issue 4867. pp. 835-837. DOI: 10.1126/science.2841759
 Interactions between the glycine and glutamate binding sites of the NMDA receptor
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 Clinical Psychopharmacology and Neuroscience 2006; 4(1): 3-10
The NMDA Receptor Hypofunction Hypothesis for Schizophrenia and Glycine Modulatory Sites on the NMDA Receptors as Potential Therapeutic Drugs. Kenji Hashimoto From the Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan
 Glycine Causes Increased Excitability and Neurotoxicity by Activation of NMDA Receptors in the Hippocampus David W. Newell,1 Alain Barth, Tom N. Ricciardi, and Alfred T. Malouf Department of Neurological Surgery, School of Medicine, University of Washington, Seattle, Washington 98195. EXPERIMENTAL NEUROLOGY 145, 235–244 (1997) ARTICLE NO. EN976463. t Department of Neurological Surgery, Harborview Medical Center, 325 9th Avenue, Seattle, WA 98104.
 Role of glycine decarboxylase in regulating NMDA receptor function Rudolph, Uwe. University of Illinois Urbana-Champaign, Champaign, IL, United States.
 Glycine triggers a non-ionotropic activity of GluN2A-containing NMDA receptors to confer neuroprotection. Published: 03 October 2016. Rong Hu, Juan Chen, Brendan Lujan, Ruixue Lei, Mi Zhang, Zefen Wang, Mingxia Liao, Zhiqiang Li, Yu Wan, Fang Liu, Hua Feng & Qi Wan
Scientific Reports volume 6, Article number: 34459 (2016) "Glycine protects against glutamate neurotoxicity-induced neuronal injury in cortical neurons through non-ionotropic activation of GluN2ARs."
Carnosine Alox 12, ALOX 15, ALOX 5, HETE, PETE Research
Dietary Carnosine Prevents Early Atherosclerotic Lesion Formation in Apolipoprotein E–Null Mice Oleg A. Barski, Zhengzhi Xie, Shahid P. Baba, Srinivas D. Sithu, Abhinav Agarwal, Jian Cai, Aruni Bhatnagar and Sanjay Srivastava
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Carnosine suppresses neuronal cell death and inflammation induced by 6-hydroxydopamine in an in vitro model of Parkinson's disease. Plos One, Maho Kubota, Nahoko Kobayashi, Toshifumi Sugizaki, Mikako Shimoda, Masahiro Kawahara*, Ken-ichiro TanakaID* Laboratory of Bio-Analytical Chemistry, Research Institute of Pharmaceutical Sciences, Faculty of Pharmacy, Musashino University, Tokyo, Japan
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The Author(s) 2022. Published by Oxford University Press on behalf of the American Society for Nutrition. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. Adv Nutr 2022;13:1914–1929; doi: https://doi.org/10.1093/advances/nmac059.