INTEGRATING NEUROFEEDBACK, NUTRITION & NUTRIGENOMICS
A Case Study of Severe Traumatic Brain Injury Recovery (TBI)
Judith Ann Miller. PhD., Dallas Shepard, UP
ABSTRACT
This case study is to introduce a successful model of care for TBIs. TBI stands for Traumatic Brain Injury, which is the leading cause of death and disability. There were about 61,000 TBI-related deaths in the United States in 2019. That’s about 166 TBI-related deaths every day (CDC, 2019). TBI results from head trauma (concussions and other concussive injuries, falls, bumps on the head, car accidents, etc.) and is a diagnosis in more than 288,000 hospitalizations and 2.2 million ED visits annually. A moderate or severe TBI may lead to long-term or life-long health problems that may affect all aspects of a person’s life. These health problems have been described as being similar to the effects of a chronic disease (MaserBe, 2918). A moderate or severe TBI not only impacts the life of an individual and their family, but it also has a large societal and economic toll. The lifetime economic cost of TBI, including direct and indirect medical costs, was estimated to be approximately $76.5 billion. Additionally, the cost of fatal TBIs and TBIs requiring hospitalization account for approximately 90% of total TBI medical costs (Finkelstein et al, 2006). Symptoms of TBI include difficulty taking in and processing information, explosiveness, insomnia, movement deficits, anxiety, headaches/migraines, depression, personality changes and/or a host of other symptoms. The brain is significantly altered immediately following a TBI because of metabolic, hemodynamic, structural, and electro-physiologic changes. This process affects cognition and behavior and can leave the brain vulnerable for worse injury in the setting of repeat insult (Barkhoudarian, et al. 2016). This case study introduces a 3-N Model (Nutrition, Neurofeedback & Nutrigenomics) scientifically designed to provide relief for TBI victims.
CASE STUDY
In 2018, a 52-year-old female suffered a severe brain and bodily injury as she was thrown from her vehicle that had rolled 5 times. Her daughter and dog were left with no injuries but mother was found dead at the site. Revived, she lapsed into a coma and was transported to emergency services to spend 30 days in intensive care and the next entire year in a nursing home. She suffered multiple neck, shoulder and back fractures, severe memory loss and was near dysfunctional. In 2021 as she reported for therapy, she continued to experience many TBI symptoms including memory loss, severe pain from her many fractures, anxiety, depression and PTSD.
ASSESSMENT
1. The Central Nervous System Function Assessment (CNS) – The initial CNS assessment revealed that her symptoms included: tremors, headache, loss of appetite, tiredness, rapid and irregular heartbeat, agitation and restlessness. Problems with blurred vision, hearing, sense of smell, and problems with light and sense of touch. Sudden and unexplained changes in mood, fearfulness, anxiety, and depression. Problems with confusion, concentration, attention, sequencing, prioritizing, feeling foggy, unable to recall reading. Fatigue, lack of stamina and insomnia. Restlessness, irritability and cold hands and feet. Forgetting what she was doing and what to do next as well as remembering words and past experiences. Essentially she has suffered extreme loss of memory. It was clear that Ms. E suffered from TBI, anxiety, depression, and Post Traumatic Stress Disorder (PTSD).
The Vulnerable CNS - The Central Nervous System (CNS) is especially vulnerable to oxidative stress due to several factors: 1) The limited regenerative capacity of neural cells, because adult neurons are post-mitotic cells that do not replicate Yang & Hurrep, 2007); 2) Intrinsic metabolic and structural characteristics of neurons make them more sensitive to oxidation compared to cells in other organs (Friedman, 2011); 3) Neuronal membranes are rich in polyunsaturated fatty acids, that make the brain more vulnerable to lipid oxidation (Mason, et al, 2002); 4) Several neurotransmitters, such as dopamine, norepinephrine, and serotonin easily undergo autoxidation (Gunther, et al (2016); 5) Brain microglia when activated inappropriately, can produce massive amounts of reactive oxygen and nitrogen species (Choi, et al, 2005; Wilkinson & Landreth, 2006); and 6) CNS antioxidant defenses are relatively modest in comparison with those of other tissues. In particular, the CNS contains rather low levels of both glutathione peroxidase and catalase (Friedman, 2011; Pruchen, et al, 1997).
2. Medication Assessment: the patient was taking 1800 mg of Gabapentin (600 mg 3Xdaily) for pain and Lisinopril 150 mg for blood pressure.
GABAPENTIN - Uses - Gabapentin is known as an anticonvulsant or antiepileptic drug and is used to treat partial seizures. It’s taken together with other seizure medications in adults and in children 3 years of age and older who have epilepsy.
Side Effects - Changes in mood or anxiety. Symptoms can include: Thoughts of suicide or dying, attempts to commit suicide, anxiety that’s new or gets worse, crankiness that’s new or gets worse, restlessness, panic attacks, trouble sleeping, anger, aggressive or violent behavior, extreme increase in activity and talking, unusual changes in behavior or mood, dizziness, tiredness or drowsiness, loss of coordination, fever, jerky movements, nausea and vomiting, trouble speaking, double vision, unusual eye movements, tremor, swelling of legs and feet, emotional changes, aggressiveness, trouble concentrating, restlessness, hyper behavior, severe tiredness or weakness, unexpected muscle pain
.
LISINOPRIL - Uses - Lisinopril is used to treat high blood pressure. Lowering high blood pressure helps prevent strokes, heart attacks, and kidney problems. It is also used to treat heart failure and to improve survival after a heart attack. Lisinopril belongs to a class of
drugs known as ACE inhibitors. It works by relaxing blood vessels so blood can flow more easily.
Side Effects - Dizziness, lightheadedness, tiredness, or headache may occur as your body adjusts to the medication. Dry cough may also occur.
Serious side effects: fainting, symptoms of a high potassium blood level (such as muscle weakness, slow/irregular heartbeat). Although Lisinopril may be used to prevent kidney problems or treat people who have kidney problems, it may also rarely cause serious kidney problems or make them worse. Lisinopril may rarely cause serious (possibly fatal) liver problems. A very serious allergic reaction to this drug is rare, but may include: rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.
MATERIALS AND EQUIPMENT
Over the past decade we have treated a significant number of pharmaceutical medication dependents on different medications. The materials, equipment and methodology employed have demonstrated efficacy and include the following:
1. Nutrition – Nutritional Psychiatry is a rapidly growing field that provides a significant body of research evidence that strongly suggest that dietary patterns are relevant to common mental illnesses. Studies indicate that there are known consistent mechanistic, observational and interventional data that diet quality may be a modifiable risk factor for mental illness. These studies are based on the understanding that specific biological pathways mediate the observed relationships between diet, nutrition and mental health that point to the immune system oxidative biology, brain plasticity and the microbiome-gut-brain axis as key targets for nutritional interventions. (Wolfgang, et al, 2017; Jacka, 2017). Recent studies indicate a strong correlation between a poor diet and the exacerbation of mood disorders, including anxiety and depression (Adan, et al. 2019).
Ross (2018) notes that integrative neuro-nutritional therapy is an emerging paradigm in the treatment of mental health disorders, which focuses on the relationship between nutrition, brain neurochemistry, brain function and behavior. She reports current evidence to support the recognition that dietary habits, nutrition, and metabolic mechanism that include inflammation, microbiota imbalances oxidative stress, and impaired mitochondrial function are important variables that affect brain function, mental health, and, ultimately mood and behavior.
2. Low Energy Neurofeedback Systems (LENS) – Low Energy Neurofeedback System utilizes a gentle, non-invasive electroencephalogram (EEG) neurofeedback that optimizes function in the areas of mood, cognition, energy levels and other functions the brain controls. The LENS system has led to dramatic improvements in chronic debilitating neurological conditions such as brain injury, extreme stress, emotional trauma, attention deficit disorder, fibromyalgia, and chemical dependence. Other disorders effectively treated with LENS include traumatic brain injury, migraine headaches, addictive behaviors, anxiety and depression, PTSD, autism, spectrum disorders, seizure disorders, ADHD, cerebral palsy, and even optimal brain performance (Hammond 2001, 2007, 2011 A&B, 2012 A&B, Larsen, 2006, 2008, 2012, Ochs, 1994 a & b, 2011).
3. Nutrigenomics – Nutrigenomics is the study of how nutrients and naturally occurring compounds affect gene expression. Nuclear factor erythroid 2–related factor 2 (Nrf2) is a regulator of cellular resistance to oxidative stress and enhances the body’s natural defenses to make antioxidants and achieve optimal cellular balance. Nuclear respiratory factor 1 (NRF1) works on the cellular level to increase cellular energy by boosting mitochondrial function, while nicotinamide adenine dinucleotide (NAD) helps to support energy, mental clarity, and mood. These nutrigenomic products have been developed as a drug-free therapy to integrate genetic expression and remove neurotoxic contaminations. These key activators work to prevent oxidative stress and mitochondrial dysfunction which are pre-cursers to Substance Use Disorder and are strongly correlated with anxiety and depression (Klalifeh, et al, 2016) and autism (Chauhan & Chauhan, 2006). Neurofeedback researchers have found that integrating these nutrigenomic factors to neurofeedback clients creates a synergistic-effect in that total amplitudes of the brain waves become unsuppressed at a much faster rate (Miller & Shepard, 2020).
Nfr2 For TBI Relief - Nrf2 plays a key role in neuronal resistance to oxidative stress and glutamate-induced excitotoxicity (Miller, et al, 2014). Science has shown that Nrf2 has neuroprotective effects against oxidative damage injury following cerebral ischemia/reperfusion in rats (Shih & Murphy 2005; Shih, et al, 2007). Nrf2 deficiency has shown to affect the psychological behavior and neurotransmitter systems in mice, such as reduced mobility in swimming tests, possibly by increasing dopaminergic and serotonergic neurotransmitters[128].
The pre-activation of Nrf2 by electrophilic agents protects cells, partially through enhanced H2O2 scavenging by the glutathione/glutathione peroxidase system, and the detoxification of reactive quinones by NAD(P) H:quinone oxidoreductase 1 (Murmatsu, 2013). Still, excessive extracellular dopamine itself can be an endogenous signal to activate Nrf2-dependent neuroprotective pathways (Duffy, 1998). Studies with primary cell cultures have also revealed that excessive dopamine release can act as an endogenous Nrf2-inducing signal (Shih & Murphy, 2007).
A recent clinical study showed increased activation of Nrf2 in peripheral blood mononuclear cells of patients with depression, which indicates a pro-oxidative state (Lukic, et al, 2014). In fact, the chronic fluoxetine treatment suggested that fluoxetine-induced neuroprotection may operate via an unexpected mechanism involving 5-HT (serotonin receptor) and a serotonin transporter blockade with Nrf2 signaling (Mendez-David, et al, 2005). Considering the regulation of antioxidant defenses through the Nrf2 pathway, this factor has emerged as a promising approach for neuroprotection, and it is possible that Nrf2 may also play an important role in the regulation of brain inflammation via interactions with NF-κB. Nrf2 clearly has vital functions in various physiological and pathological stresses, and it has been implicated as a causative factor in the pathophysiology of many psychiatric disorders, including anxiety disorder (Sandberg, et al, 2014). Alessandra et al (2018) suggest that focus on reinforcing the body’s existing oxidative defense mechanisms, such as Nrf2 and the Proteasome, in conjunction with existing therapies may increase the efficacy of treatments for anxiety disorders.
The Nutrigenomic Activators – The Nrf2, NRF1 and NAD products are designed to activate energy and health. Clinical studies have shown them to reduce cellular stress by an average of 40% in 30 days and have been shown to increase Superoxidate dismutase levels by 30%, glutathione by 300% and catalase by 54%. The trisynergizers are scientifically designed to support increased healing, focus, energy, mental clarity and mood.
The Role of Superoxidate dismutase – Dr. Younus, (2018) reported:“Superoxide dismutase (SODs) constitute a very important antioxidant defense against oxidative stress in the body. The enzyme acts as a good therapeutic agent against reactive oxygen species-mediated diseases.
The Role of Catalase (CAT) – Dr. Imlay (2003) reported: “Catalase is one of the most important antioxidant enzymes as protects us from dangerous reactive oxidizing moleculesLiving with oxygen is dangerous. We rely on oxygen to power our cells, but oxygen is a reactive molecule that can cause serious problems if not carefully controlled. One of the dangers of oxygen is that it is easily converted into other reactive compounds. Inside our cells, electrons are continually shuttled from site to site by carrier molecules, such as carriers derived from riboflavin and niacin. If oxygen runs into one of these carrier molecules, the electron may be accidentally transferred to it. This converts oxygen into dangerous compounds such as superoxide radicals and hydrogen peroxide, which can attack the delicate sulfur atoms and metal ions in proteins. To make things even worse, free iron ions in the cell occasionally convert hydrogen peroxide into hydroxyl radicals. These deadly molecules attack and mutate DNA. One theory is that this type of oxidative damage accumulates over the years of our life, causing us to age.”
The Role of Glutathione – Judith Miller (2019, P. 119) reported that “Glutathione is a tripeptide derived from glutamine, glycine, and cysteine amino acids. It is an antioxidant than can be synthesized in all cells of the body. Glutathione is involved in many biological processes such as free radical neutralization, detoxification, transport and storage of cysteine, maintenance of cellular redox, ascorbic acid and vitamin E regeneration, transport of mercury out of cells and brain, and serving as a coenzyme. It is believed to help maintain the integrity of the blood-brain barrier.
4. Photon Stimulator – Light Therapy – Low level laser therapy (LLLT) is the application of light (usually a low power laser) to pathology to promote tissue regeneration, reduce inflammation and relieve both acute and chronic pain.
5. Care for Fractures – Our patient was referred to a science-based chiropractic clinic for pain relief. The medications were not even masking the pain symptoms.
METHODS – AN INTEGRATIVE APPROACH
Stephanie Ross (2014) reported: In regard to the complexity of mental health disorders, such as depression, anxiety, and insomnia, which are common comorbid psychiatric conditions, it would appear that a holistic treatment model that incorporates a complementary and integrative therapy approach within the framework of conventional health care would most effectively support optimal healing. This study coordinated nutrition, neurofeedback and nutrigenomics therapies for a successful outcome. Each is described below:
LENS - Following the initial assessment and diagnosis, LENS was administered. The initial Mapping indicated severely suppressed amplitudes for all brain waves. Suppression is the flexibility in sites measured by the standard deviation between the average of the wave lengths mean total amplitude or the individual wave length broken down by dominant, delta, theta, alpha or beta frequencies. When a site has a standard deviation less than .35 % that site is considered suppressed or inflexible. Lifting of suppression has been a key indicator in the improvement in brain processing which leads to behavioral, emotional, and physical improvements. We have found that LENS therapy assists in withdrawal from antidepressants by lifting suppressed sites or increasing the efficiency of the brain to process. After LENS sessions subjects are more relaxed and less depressed. Their thinking is clearer and they begin to have more emotional resilience instead of being overwhelmed by their emotions. When the nervous system is stabilized, they become less over-reactive Miller a,b,c). Three subsequent LENS trainings were provided to treat the suppressed EEG sites, 7 site at a time. The initial map and follow up map showed significant improvement for the Mean Total Amplitude reports and Mean Dominant Frequency Amplitude reports (See map reports in Results Section).
Nutrition – A balanced amino acid nutritional plan was introduced and subject began a new dietary regime to change her former nutritionally deficient diet.
Nutrigenomics – The plant based nutrigenomic products were introduced on a daily basis. These products are designed to activate energy and balance health on a cellular and genetic level. Clinical studies have shown them to reduce cellular stress by an average of 40%, glutathione by 300% and catalase by 54%. The tri-synergizers (Nrf2, NRF1 & NAD) are specifically designed to support an increase in healing, focus, energy, mental clarity and mood.
Titration from Gabapentin and Lisinopril – The client’s Gabapentin and Lisinopril usage was tapered off slowly by utilizing a carefully planned titration strategy to help avoid withdrawal symptoms. The synergistic effect of coordinating LENS, nutrition and Nutrigenomics assists in balancing feelings that would normally arise during times of stress (Miller, 2019).
Photon Stimulator – The photon stimulator was applied to the subject’s pain points and provided considerable relief.
Care for Fractures - The chiropractic clinic determined the cause of the pain; provided a myriad of integrative procedures to attain relief. The chiropractic care continues. It is unfortunate that in the past medications were prescribed to make the pain go away, instead of the actual healing care required.
RESULTS
Nutrition – A balanced amino acid nutritional plan was introduced and subject began a new dietary regime to change her former nutritionally deficient diet made a huge difference in her ability to function, handle anxiety, and go back to work. Her former diet consisted of unhealthy, processed foods which augment the inflammatory process that leads to decreased motivation and depression. Healthy eating and hydration which includes portion control, meal frequency and a balanced diet with adequate water is essential for all areas of health.
Neurofeedback - The two LENS suppression maps presented below represent the initial map, while the second map report indicates the significant changes in the Mean Total Amplitude and the Mean Dominant Frequency amplitudes following only three LENS sessions. The suppressed sites (orange sites hyper-suppressed) have less flexibility and do not meet our preset requirements of a normal range between .35% to .7%. These sites are not working as efficiently as they could with processing inhibited. The blue sites fall within our range that we are looking for over the period of our
treatments. The purple sites are hypo-suppressed meaning they are above the .7% range. Ideally we want more blue sites meaning the brain is becoming more flexible and can process information more efficiently. The difference between Map 1 and Map 2 is quite dramatic correlating to the physical, emotional and behavioral changes as described.
While we do not present correlation coefficients of a multiple variate analysis to determine the value of each therapy represented in the methodology, we are suggesting that there was a synergistic effect of nutrition, neuro
feedback and nutrigenomics to create such a remarkable, measurable difference. This assumption is based on past experiences of providing LENS trainings with no adjunct therapies and realizing a much slower, lower improvement in our attempt to raise the total amplitudes o
f suppressed sites. But what was most impressive is that her memory has returned, anxiety and depression are controlled, and is experiencing pain relief. By coordinating alternative therapies with LENS, we expect future sessions will be significantly improved.
SUMMARY
A paradigm shift has been taking place in the field of healthcare with a growing trend toward an Integrative Health Care model. In the United States alone we are witnessing a widespread movement as individuals look for a more holistic, integrative approach to health care management, disease prevention and healthy living. Harmonized Brain Centers, a multicenter integrative neurotherapy practice located in Colorado and Tennessee (USA) is a pioneer in the integration of neurofeedback, nutrition and nutrigenomics in patient treatment protocols that continue to demonstrate enhanced positive outcomes, supported by measurable results when using evidence-based integrative health strategies. These science-based integrated therapies are essential for optimal wellness.
CONCLUSION
Our client has responded well to this integrated approach on her healing journey and we encourage other practitioners to adopt similar approaches to help TBI clients recover.
It seems mandatory for research reports to call for continued research. This report is no exception and calls for further application for two reasons: 1) to establish a science-based efficacy for this 3-N model of care for TBIs and 2) most important, every time this study is replicated it will provide relief for the TBI victim and lead to brain and body optimal functioning.
REFERENCES
Adan, R. A. H., E. M. van der Beek, J. K. Buitelaar, J/ F/ Cryan, J. Hebebrand, S. Higgs, H. Schellekens, & S. L. Dickson (2019). Nutritional psychiatry: Towards improving mental health by what you eat. European Neuropsychopharmacology 29: 1321-1332. DOI.org 10.1016/j.euroneuro.2019.10.011.
Alessandra das, et al., (2018). The role of oxidative stress in anxiety disorder: Cause or consequence? Free Radic Res. 52(7).737-750. Published online 4. doi: 10.1080/10715762.2018.1475733
Barkhoudarian, G., D. A. Hovda, & C. C. Giza (2016). The molecular pathophysiology of concussive brain inury: An update. DOI: 10.1016/j.pmr.2016.01.003
Centers for Disease Control and Prevention. (2019). National Center for Health Statistics: Mortality data on CDC WONDER. Available at: https://wonder.cdc.gov/mcd.html.
Chauhan, A., & V. Chauhan (2006). Oxidative stress in autism. Pathophysiology 13, 171-181. DOI:10.1016/j.pathophys.2006.05.007.
Choi SH, et al., (2005).Thrombin-induced oxidative stress contributes to the death of hippocampal neurons in vivo: Role of microglial NADPH oxidase. Journal of Neuroscience, 25(16): p. 4082–4090. [PMC free article] [PubMed] [Google Scholar]
Duffy S, So A, & T. H. Murphy (1998). Activation of endogenous antioxidant defenses in neuronal cells prevents free radical-mediated damage. Journal of Neurochemistry, 71(1): p. 69–77. [PubMed] [Google Scholar]
Esty, M. L. & C.M. Schiffett (2014). Conquering concussion: Healing TBI symptoms with neurofeedback and without drugs. Round Earth Pulishing. Sewickley, PA.
Finkelstein E, Corso P, Miller T and associates. The Incidence and Economic Burden of Injuries in the United States. New York (NY): Oxford University Press; 2006.
Gunther M, et al., (2016). Neuronal Vulnerability to Oxidative Stress Is Affected by Genetic Polymorphism and Related to Susceptibility to Inflammation in the Central Nervous System. Journal of Neurotrauma, 33(3): p. A5–A5. [Google Scholar]
Friedman J. (2011). Why Is the Nervous System Vulnerable to Oxidative Stress? Oxidative Stress and Free Radical Damage in Neurology, p. 19–27. [Google Scholar]
Hammond, D. C. (2001).Neurofeedback treatment of depression with the Roshi. Journal of Neurotherapy, 5(2), 45-56.
Hammond, D. C. (2007a). LENS neurofeedback treat anosmia resulting from a head injury. Journal of Neurotherapy, 11(11).
Hammond, D. C. (2007). LENS: the Low Energy Neurofeedback System. The Hawthorne Medical Press. Binghampton, NY.
Hammond, D. C. (2010). QEEG evaluation of the LENS treatment of TBI. Journal of Neurotherapy, 14:2, 170-177.
Hammond, D. C. (2011b. What is neurofeedback: An update. Journal of Neurotherapy, 15:305-336. http://dx.doi.org/10.1080/10874208.2011.623090.
Hammond, D. C. (2012a). Post traumatic anosmia Pp. 212-214. In S. Larsen (ED). The neurofeedback solution: How to treat autism, ADHD, anxiety, brain injury, stroke, PTSD, and more. Healing Arts Press. Rochester, VT.
Hammond, D. C. (2012b). A case of serious TBI Pp 214-219. In S. Larsen (ED). The neurofeedback solution: How to treat autism, ADHD, anxiety, brain injury, stroke, PTSD, and more. Healing Arts Press. Rochester, VT.
Harper, S. H. 2009), The special applicability of the low energy neurofeedback system form of neurofeedback to traumatic brain injury: the Theory, Biofeedback. 37(3), 104-107.
Imlay, J. A. (2003) Pathways of oxidative damage. Annual Review of Microbiology 57, 395-418.
Jacka, F. N. (2007). Nutritional psychiatry: Where to next? Biomedicine 17: 24-39. Htpp://dx.doi.org/10.1016/j.ebiom.2017.02.020.
Khalifec, S. et al, (2016). Complexity of compensatory effects of NRF1: Linking undeveloped anxiety-like behavior to prevented mitochondrial dysfunction and oxidative stress. Cell Mol Neurobiol, 36(4):553-563. DO110.1007/s10571-015-0236-0.Epub2015 Jul23.
Larsen, S. (2006). The Healing power of neurofeedback: The revolutionary LENS technique for restoring Optimal Brain Function. Healing Arts Press, Rochester, VT.
Larsen, S. (2009). The special applicability of the Low Energy neurofeedback system form of neurofeedback to traumatic brain injury: The theory. Biofeedback, 37(3), 104-107.
Larsen, S. (2012). The neurofeedback solution: How to treat autism, ADHD, anxiety, brain injury, stroke, PTSD and more. Healing Arts Press, Rochester, VT.
Larsen, S, K. Harrington, & S. Hicks (2006). The LENS (Low Energy Neurofeedback System: A clinical and outcomes study of one hundred patients at Stone Mountain Clinic Center, New York. Journal of Neurotherapy, 10(2-3), 69-78.
Lukic I, et al. (2014). Lymphocyte Levels of Redox-Sensitive Transcription Factors and Antioxidative Enzymes as Indicators of Pro-Oxidative State in Depressive patients, Neuropsychobiology, 70(1): p 1-9. [PubMed] [Google Scholar]
Muramatsu H, et al. (2013). Nrf2 deficiency leads to behavioral, neurochemical and transcriptional changes in mice. Genes to Cells, 18(10): p. 899–908. [PubMed] [Google Scholar]
MaselBE, DeWitt D. (2018). Traumatic brain injury: a disease process, not an event. J Neurotrauma. 2010:1529-1540.
Mason JW, et al., (2002). Marked lability in urinary cortisol levels in subgroups of combat veterans with posttraumatic stress disorder during an intensive exposure treatment program. Psychosom Med, 64(2): p. 238–46. [PubMed] [Google Scholar]
Mendez-David I, et al. (2015). Nrf2-signaling and BDNF: A new target for the antidepressant-like activity of chronic fluoxetine treatment in a mouse model of anxiety/depression. Neuroscience Letters, 597: p. 121–126. [PubMed] [Google Scholar]
Miller DM, et al., (2014). The Nrf2-Are Pathway as a Therapeutic Target in Traumatic Brain Injury: Genetic and Pharmacological Approaches for Neuroprotection. Journal of Neurotrauma. 31(12): p. A86–A86. [Google Scholar]
Miller, J. A. (2019a). Boots on the ground: Neurotherapy for veterans combatting: PTSD, TBIs, Trauma, Anxiety, Depression & Addiction. Amazon Press, Simla, CO.
Miller, J. A. (2019b). Herding cats: Coordinated alternative therapies for TBIs, PTSD, anxiety, depression and substance use disorder. Amazon Press, Simla, CO.
Miller, J. A., & D. Eccher (2019). The judge’s gavel: Winning the drug war by empowering recovery, Amazon Press, Simla, CO.
Miller, J. A. & D. Shepard (2020), The Power of Nrf2 + NRF1 + NAD: Combating SUD and Mental Health Disorders. Unpublished Report. www.harmonizedbraincenters.com.
Nelson, D. V. & M. L. Esty (2012). Neurotherapy of traumatic brain injury/post-traumatic stress symptoms in OEF/OIF veterans. Journal of Neuropsychiatry and Clinical Neurosciences, 24(2), 237-240.
Nelson, D. V., & M. L. Esty (2015). Neurotherapy of traumatic brain injury/post-traumatic stress symptoms in Vietnam veterans. Military Medicine, 180,e, 1111-1114.
Ochs, L. (1994a). EEG-Driven stimulation and heterogeneous head injured patients extended findings. A peer-reviewed abstract from the 1994 Berrol Head Injury Conference, Las Vegas NV. {web page, cited March 15, 2000} Available from: URL: http://www.flexyx.com contents/pubs/Extended.htm./
Ochs, L. (1994b). EEG-Driven stimulation and mild head injured patients: Preliminary findings. A peer-reviewed abstract from the 1994 Berrol Head Injury Conference, Salt Lake City, UT {web page, cited March 15, 2000 Available from: URL http//www.flexyx.com/ contents/pubs/Preliminary.htm.
Ochs, L. (2011). Working with traumatic brain injury using the low energy neurofeedback system (the LENS). Neuroconnections, Winter 2011, pp.23-26.
Peuchen S, et al., (1997). Interrelationships between astrocyte function, oxidative stress and antioxidant status within the central nervous system. Progress in Neurobiology,52(4): p. 261–281. [PubMed] [Google Scholar]
Ross, S. M. (2014). Psychophytomedicine: An overview of clinical efficacy and phytopharmacology of treatment of depression, anxiety and insomnia. Holistic Nurse Practitioners. 28(4) 275-280. DOI:10.1097/HNP.00000000000000040.
Sandberg M, et al. (2014). NRF2-regulation in brain health and disease: implication of cerebral inflammation. Neuropharmacology, 79: p. 298–306. [PMC free article] [PubMed] [Google Scholar]
Schoenberger, N. E., S. C. Shiflett, M/ L/ Esty, L. Ochs, & R. J. Matheis (2001). Rexyx neurotherapy system in the treatment of traumatic brain injury: An initial evaluation. Journal of Head Trauma Rehabilitation, 16(3), 260-274.
Shih AY, Li P, & T. H. Murphy (2005). A small-molecule-inducible Nrf2-mediated antioxidant response provides effective prophylaxis against cerebral ischemia in vivo. Journal of Neuroscience, 25(44): p. 10321–10335. [PMC free article] [PubMed] [Google Scholar]
Shah ZA, et al., (2007). Role of reactive oxygen species in modulation of Nrf2 following ischemic reperfusion injury. Neuroscience, 147(1): p. 53–59. [PMC free article] [PubMed] [Google Scholar]
Ross, S. M. (2018). Integrative neuronutritional therapy: Metabolic brain parameters in mental health. Holistic Nurse Practitioners 32(1) 51-55. DOI:10.1097HNP.0000000000000250.
White, C. (2008). Restoring optimal brain function helps many health problems: ADD, autism, depression, fibromyalgia, anxiety, PTSD, learning disorders, strokes, Parkinson’s disease, multiple schlerosis, Townsend Letter, The Examiner of Alternative Medicine, April 2008. http:/www.townsenletter,com/april2008/ltr_white0408.htm.
Wilkinson BL & G.. E. Landreth (2006). The microglial NADPH oxidase complex as a source of oxidative stress in Alzheimer’s disease. Journal of Neuroinflammation, 3. [PMC free article] [PubMed] [Google Scholar]
Wolfgang, M., G. Moseley, M. Berk, & F. Jacka (2016 Nutritional psychiatry: The present state of evidence. Proceedings of the Nutrition Society, Joint Winter Meeting between the Nutrition Society and the Royal Society of Medicine held at the Royal Society of Medicine. P. 1-10. DOI: 10.1017/S0029665117002026.
Yang Y & K. Herrup (2007). Cell division in the CNS: Protective response or lethal event in post-mitotic neurons? Biochimica Et Biophysica Acta-Molecular Basis of Disease, 1772(4): p. 457–466. [PMC free article] [PubMed] [Google Scholar]
Younus, H. (2018). Therapeutic potentials of superoxide dismutase, International journal of Health Science, 12(3): 88-93
About the Authors
Judith Ann Miller, Ph.D., is a Colorado neuro-therapy specialist focusing on sustainable recovery of TBIs, PTSD, trauma, anxiety, depression, and substance use dependency. She is a certified neurofeedback practitioner and employs natural nutritional regimes, and science-based psychotherapies to enhance optimal brain functioning. Her premise is that it is more important to treat the causes of neural conditions rather than the symptoms.
Contact: 719-541-4912 redfeather7@earthlink.net.
Dallas Shepard, is the founding Director of Harmonized Brain Centers that was established in 2013 and has since expanded to four multi-centers located in Colorado and Tennessee. Dallas’ inspiration was out of a need to help his brain injured son that occurred in 2003. We use an integrated approach to help our clients achieve their Best Brain Ever by using LENS (Low Energy Neurofeedback Systems), Physical Vascular Therapy, Nutirgenomics, Low Light Laser Therapy and Psychotherapy Education. Traumatic Brain Injury (TBI), PTSD, ADHD, Autism, Anxiety, Depression and more… NO PROBLEM. After personally completing over 15,000 sessions of LENS, Dallas is confident and passionate about helping his clients improve their lives no matter their underlying condition.
Contact: 719-661-6422 Dallas@HarmonizedBrainCenters.com