Stressors, mental and physical, are an everyday encounter necessary for growth and change but trauma inhibits these. Think of your muscles: stress is a strain, it can wear you out; extreme or inescapable stress is trauma; it is an injury, a wound causing long-term or permanent damage. You are changed after trauma. Most people will experience some kind of trauma at some point in their life. If the trauma is acute or chronic enough, or if the person is especially susceptible, post-traumatic stress disorder will develop which can greatly hinder a person’s quality-of-life or ruin it completely. The prognosis mostly depends on the patient’s education, their metabolism, their resources, and their environment.

Around 24 million Americans have PTSD. To this day, many popular health resources propagate the oft-thought household idea that PTSD only results from witnessing a “serious”, destructive or near-fatal accident, wars, terrorist attacks, deaths of loved ones, things like rape, or “other life-threatening events”. While those things all cause PTSD, the specificity of “serious” trauma and exclusion of a large fraction (~20%) of sufferers tell you the authors haven’t updated their lexicon in a while, as is common with American medical professionals and practitioners. The customization of what is “serious” by those writing the DSM can be read as evidence of authoritative snobbery. Despite regressive U.S. “liberals” further destroying credibility for genuine sufferers by trivializing “triggers” and “trauma” to nearly anything that irks them, there is much stirring and growing recognition for PTSD induced by bullying, failure, shame, illness, isolation, verbal abuse and emotional abuse among other things (Bisson et al., 2015).

Symptoms of PTSD include flashbacks, nightmares, disturbing thoughts, avoidance behavior, anxiety, anger, emotional hypersensitivity, psychogenic amnesia, dissociation, and major depression. PTSD sufferers have a dysfunctional hypothalamic-pituitary-adrenal axis, releasing epinephrine and norepinephrine inappropriately. Their body overreacts to relatively benign events as if they were being physically attacked (Simeon et al., 2006).

Patients with borderline personality disorder, an illness characterized by unstable sense of self and dissociation, reported experiencing higher amounts of abuse than patients with other personality disorders (Frias et al., 2016). The Department of Psychology at the University of Leuven in Belgium studied 90 sufferers of Chronic Fatigue Syndrome. 54% admitted to experiencing some type of early trauma, 46% of the abused specified emotional abuse (Kempke et al., 2014). Usually, the earlier the trauma and the higher the amount, the more severe symptoms and sickness develop (Murrough, 2011). People with low cortisol are more susceptible to PTSD, which is characterized by destabilized cortisol levels (Gill et al., 2008). Generally, low cortisol levels are associated with more abuse and less neglect at a young age while high cortisol is associated with less abuse and more neglect at a young age (Vegt et al., 2009; Flory et al., 2009). Abuse numbs the cortisol reaction to stress. In chronic fatigue syndrome, the cortisol response is blunted, and there is an inverse relationship of cortisol blunting and severity of symptoms; that is, with more cortisol blunting there is more chronic fatigue. Self-critical perfectionism was associated with the cortisol blunting in CFS. (Kempke et al., 2016). Treatment with cortisone is not usually successful for CFS and many patients react adversely to it. Vitamin B6, pyridoxine, is low in many CFS patients. CFS patients have made complete recoveries using B vitamins, most specifically B1 thiamine, B2 riboflavin, B3, B6, B12 cobalamin and B9 folate (Heap et al., 1999).

Trauma can cause dysautonomia, or postural orthostatic tachycardia syndrome (POTS). Dysautonomia involves hyperadrenergic response of the nervous system, where excess catecholamines like norepinephrine are easily released. There is constant overexcitability. POTS is comorbid with chronic fatigue and mast cell activation syndrome, which involves hyper responsive and destabilized immunological mast cells. Theanine, progesterone, cyproheptadine, and niacinamide (not niacin) stabilize mast cells (Finn and Walsh, 2013).

Serotonin 5-HT receptors are altered in PTSD, which then alters dopamine release. Dopamine is needed for satisfaction, motivation, and pleasure. Dysfunction of the dopaminergic system causes anhedonia, apathy, and addiction. Normally, doctors want to raise the serotonin in their patients, but serotonin 5-HT1B antagonists are now being suggested for PTSD treatment to lower serotonin. (Krystal, et al., 2009). Serotonin is elevated under stress, and continued stress distorts the 5-HT receptors (Chaouloff et al., 1999). Cyproheptadine, an antihistamine and antiserotonergic, has been effective in treating nightmares in PTSD.

There is decreased cerebrospinal fluid of the neurosteroid allopregnanolone in women with PTSD and depression and in people under social isolation. Increasing neurosteroids has been suggested as a PTSD treatment and SSRIs have been found to do this (Rasmusson et al., 2006; Pinna, 2013)

There is little success in the treatment of PTSD, dissociative disorders, psychosis, bipolar, schizophrenia, etc. Popular treatments are shoddy and the alternative and “holistic” health communities continually churn up flavors of the week to take desperate peoples’ money. As for the success of psychiatry, Dr. Abram Hoffer put it well when he said something like “doctors judge their treatment successful if they get the patient to shut up and spend their time drooling in front of the television all day, every day”.

Hypersensitivity of the norepinephrine system and overactivation of the norepinephrine receptors in the prefrontal cortex in PTSD and other mental illness are mediators of flashbacks and nightmares. This derangement of the system decreases the ability to experience and process the current environment thus increasing flashback intensity. Something is stuck and not reverting back to normal even though the trauma is long gone. Trauma increases the risk of developing personality disorders and psychotic illnesses like schizophrenia (Ingo Schäfer et al., 2011).

Dissociation is comorbid with many mental illnesses. Two common symptoms are derealization, a sense that the world is unreal, and depersonalization, a sense that the self is unreal. These physiological states can be chronic or episodic. Some sufferers get “stuck” in them for decades, seemingly forever, and anxiety about the condition increases the feelings of unreality. Dissociative disorders can be triggered by trauma, stress, drugs, or an unknown impetus. Severity of trauma predicts the dissociative symptoms within PTSD but the susceptibility to dissociation is also predicted by “pre-existing biological vulnerabilities” (Wolf et al., 2014).

There is high oxidative stress and inflammation in mental illness, including PTSD and anxiety (Hovatta, et al., 2010; Miller and Sahed, 2014).  Niacinamide, vitamin B3, prevents physical damage from stress and significantly reduces oxidative stress. It has been successfully used to treat schizophrenia, psychosis, and depression. Antidepressants may deplete B3. Niacinamide has a similar but safer action to benzodiazepines. Niacinamide improves metabolism, glucose oxidation, function of tissues, protects against radiation, prostaglandins, free radicals, brain and spinal cord injury, hypertension, and increases lifespan (Hoane et al., 2006; Goffus et al., 2010; Peat).

A girl I spoke with online told me her chronic depersonalization improved only with treatment of vascular symptoms related to her brain. She credited niacinamide as the most important remedy with cyproheptadine, aspirin, and progesterone as adjunctive. She highlighted niacinamide as a potent histone deacetylase inhibitor, which reprograms cell epigenetics so that they respond more healthily and adaptably to stimuli.

Contemporary research is finding connections to trauma and epigenetic changes. Environment, experience, conditioning, and internal physiology change gene expression by turning them on or off. Involved in these changes are DNA methylation, histone modifications, and chromatin remodeling. Epigenetics has been highlighted in inflammation, obesity, diabetes, and heart disease, but it is only now suspected to be “an important mechanism in the unknown etiology of many diseases” (Choi and Friso, 2010).

Stress, trauma, and the resulting methylation can cause cancer. P53, a tumor-suppressor gene, is turned off by excess methylation. The drugs novocaine, azacitidine, and decitabine are demethylating agents used to inhibit the growth of cancer. (Stefanska et al., 2012).

Ray Peat, PhD proposed the need for demethylating measures in disease. “A high metabolic rate and production of carbon dioxide would increase the adaptability of the organism by decreasing the limiting genetic imprints.” Prolonged carbon dioxide deficiency contributes to overmethylation and the inflammatory lactate metabolism. A similar process methylates histones, which increases with aging. Histones regulate genetic activity. […] With aging, DNA methylation is increased. I suggest that methylation stabilizes and protects cells when growth and regeneration aren’t possible (and that it’s likely to increase when CO2 isn’t available). Hibernation and sporulation appear to use methylation protectively. […] Parental stress, prenatal stress, early life stress, and even stress in adulthood contribute to ‘imprinting of the genes,’ partly through methylation of DNA and the histones. […] Several diseases and syndromes are now thought to involve abnormal methylation of genes. Prader-Willi sydrome, Angelman’s syndrome, and various “autistic spectrum disorders,” as well as post-traumatic stress disorder and several kinds of cancer seem to involve excess methylation. (“Protective CO2 and aging”)

Dr. Peat suggests paper bag breathing,  calcium, salt, baking soda, and going to higher altitudes to produce carbon dioxide. Restricting dietary methyl donors encourages demethylation. He lists hypothyroidism and excess estrogen as related detriments. Niacinamide modulates histone acetylation, reversing aging characteristics (Matuoka et al., 2001).

Common in mental illness is dysregulation of appetite and eating. Some people eat little or nothing and others overeat but I think undereating is far more detrimental. Many people overly obsessed with their health which includes many people with brain symptoms, read a lot about “detox” and “cleansing” but not enough about nutrition and anabolism. Malnutrition and under eating increase the risk of infection because it weakens every part of the immune system, including the destruction of the thymus gland. The eyes become dry, the hair dull and brittle, the skin dry and wrinkled, the muscles weak, the belly bloated, the bones aching, and the personality lethargic and apathetic. Fasting induces malaise, dampens cognition, and alters electrical brain activity (Mays, 1995).

Caloric restriction, ketosis, and fasting induce a catabolic state wherein the liver’s glycogen is depleted. The liver destroys your tissues for energy, including your brain. All organs suffer, stress hormones are high, and the body is unable to heal itself or protect from toxins. In the Minnesota Starvation Experiment, students eating 1600 calories per day for 6 months experienced lethargy, irritability, anxiety, dizziness, cold intolerance, soreness, hair loss, reduced cognition, edema, low libido, and ringing in the ears. Some withdrew from their classes. One became suicidal and one cut off three of his fingers, and both were psychiatrically hospitalized. Refeeding quickly relieved depression, lethargy, and dizziness but the other symptoms persisted for months. Caloric restriction does increase lifespan and protect mitochondria in yeasts and rats.

Patients with Kleine-Levin syndrome which is characterized by intermittent dissociation and cognitive impairment were shown to have persistent brain hypoperfusion (lack of oxygen) even during asymptomatic periods. The herbs Gingko Biloba and vinpocetine and infrared light increase brain oxygenation. Caloric restriction induces brain hypoperfusion which increases fear and “fear memory” (Riddle et al., 2013).

Depersonalization sufferers have significantly altered brain metabolism; it is lower in some areas and higher in others, compared to healthy individuals (Simeon et al., 2000).

The common treatments for PTSD and comorbid disorders are SSRIs and psychotherapy with a possible mood stabilizer or antipsychotic. This doesn’t work for everybody and SSRIs especially can be detrimental instead of therapeutic. There are safer and lesser known treatments that can be effective.

Traumatic brain injury and PTSD share similarities in their alterations of brain circuitry. Red light therapy improves cognition after brain injury and treats PTSD (Yennu et al., 2016; Naesar et al., 2011). Red light upregulates Cytochrome C, which is crucial for mitochondria and ATP synthesis. Thus it can be useful in diseases characterized by mitochondrial dysfunction, like chronic fatigue and dysautonomia. Dr. Andrzej Slominski said, “life on earth since inception has depended on a constant source of energy from the burning gases of our sun” (Tafur and Mills, 2008).

Breath meditation reduced PTSD symptoms in war veterans (Seppälä et al., 2014). Yoga stimulates the vagus nerve which oxygenates the brain and heart, heals heart lesions, improves cognition and energy and slows heart rate. Yoga dramatically improves PTSD and anxiety (Zope and Zope, 2013; Balaji et al., 2012).

Naltrexone and naloxone, opioid antagonists, reduce dissociation and improve hyperarousal symptoms in PTSD. These drugs blocks opioids like endorphins, the body’s painkillers. Alterations of the opioid system are seen in dissociation. In an open trial with 16 patients using 120 mg/day, there was an average of 30% reduction of depersonalization symptoms (Simeon et al., 2005). In 15 trauma patients using 2-6 mg/day, 11 reported immediate improvements in dissociation and 7 described lasting positive effects (Pape and Wöller, 2015). 25 to 100 mg reduced dissociative phenomena, emotional numbness, psychomotor retardation, and tension in borderline personality disorder (Bohus et al., 1999). Naltrexone treats alcoholism and reduces alcohol dependence in PTSD. High doses of naltrexone can affect liver function (Qazi et al., 2014; Allen et al., 2016).

Lamotrigine modulates the glutaminergic system which is implicated in dissociative symptoms, PTSD, depression, and suicide. Lamictal improves dissociative symptoms and treats PTSD, mania, and depression. It improves cognition and sociality in autism (Belsito et al., 2001). It is commonly used as an add-on to SSRIs in depersonalization treatment (Sierra et al., 2006).

Cyproheptadine treats nightmares associated with PTSD. In veterans with combat nightmares, dosages of 16-24 mg were successful (Brophy, 1991). Antihistamines, specifically H2 receptor antagonists like famotidine reduce symptoms in treatment-resistant schizophrenia (Meskanen et al., 2013).

Case studies show amphetamine salts as possibly effective for dissociation and PTSD (Scarella and Franzen, 2016; Daly, 2000).

Lysergic acid diethylamide (LSD) impairs fear recognition and enhances empathy and sociality. LSD promotes happiness, trust, closeness to others, and impaired the recognition of sad and fearful faces. LSD enhanced the participants’ desire to be with other people and increased their prosocial behavior” (Dolder et al., 2016). There were lower rates of mental problems in a sample of 21,967 psychedelic users (Krebs and Johansen, 2013). Private use of 10-20 microgram doses is popular in online groups.

I think the successful use of stimulants and psychedelics requires an already stabilized and robust metabolism which can be achieved through sufficient diet, nutrition, stimulation, and environment.

Eye movement desensitization and reprocessing (EMDR) is a form of psychotherapy wherein the brain’s adaptive processing mechanisms are used along side-to-side eye movements to process and desensitize the patient’s response to trauma among other things. It is more effective and works faster than cognitive therapy for PTSD, depression, and anxiety. (Shapiro, 2014; Chen et al., 2014).

Mercury toxicity causes brain damage which creates neuropsychiatric symptoms and exacerbates existing ones. Other heavy metals can do this but mercury is most prominent (Fagala and Wigg, 1992; Ross and Sholiton, 1983; Candura et al., 2000).  When organic mercury goes into the brain, it converts to inorganic mercury which stays forever.  Autopsies on human and monkey brains show bioaccumulation of mercury with age and a previously estimated half-life of 27.4 years was consistent with physical evidence (Rooney, 2014). The only safe way to chelate mercury out of the brain is with the Cutler Protocol, created by Andy Cutler, PhD PE. This costs almost nothing, and can be learned for free online. The organosulfur compounds alpha lipoic acid and DMSA or DMPS are used. Alpha lipoic acid is required to remove brain mercury while DMSA and DMPS are optional adjuncts. Success stories exist all over the internet for recovery from a variety of illnesses. Lipoic acid depletes thiamine, and vitamins C, E, zinc and magnesium are essential adjuncts. Since Cutler’s protocol is the only one predicated on objective pharmacokinetics of the chelators, all other protocols are dangerous and harmful.

When applicable knowledge based in reality is given to people instead of theoretical knowledge based in authority, amazing things become possible.

Further reading:


Works Cited

Allen, John P., Eric F. Crawford, and Harold Kudler. “Nature and Treatment of Comorbid Alcohol Problems and Post-Traumatic Stress Disorder Among American Military Personnel and Veterans.” Alcohol Research : Current Reviews. National Institute on Alcohol Abuse and Alcoholism, 2016. Web. 05 Dec. 2016.

Bisson, Jonathan, and Martin Andrew. “Psychological Treatment of Post-traumatic Stress Disorder (PTSD).” Cochrane Database of Systematic Reviews (2007). Print.

Bohus, Martin J., G. Bernhard Landwehrmeyer, Christian E. Stiglmayr, Matthias F. Limberger, Renate Böhme, and Christian G. Schmahl. “Naltrexone in the Treatment of Dissociative Symptoms in Patients With Borderline Personality Disorder.” The Journal of Clinical Psychiatry 60.9 (1999): 598-603. Print.

Carpenter, Linda L., Audrey R. Tyrka, Nicole S. Ross, Lamya Khoury, George M. Anderson, and Lawrence H. Price. “Effect of Childhood Emotional Abuse and Age on Cortisol Responsivity in Adulthood.” Biological Psychiatry 66.1 (2009): 69-75. Print.

Chaouloff, Francis, Olivier Berton, and Pierre Mormède. “Serotonin and Stress.” Neuropsychopharmacology 21 (1999). Print.

Chen, Ying-Ren, Kuo-Wei Hung, Jui-Chen Tsai, Hsin Chu, Min-Huey Chung, Su-Ru Chen, Yuan-Mei Liao, Keng-Liang Ou, Yue-Cune Chang, and Kuei-Ru Chou. “Efficacy of Eye-Movement Desensitization and Reprocessing for Patients with Posttraumatic-Stress Disorder: A Meta-Analysis of Randomized Controlled Trials.” PLoS ONE 9.8 (2014). Print.

Choi, S.-W., and S. Friso. “Epigenetics: A New Bridge between Nutrition and Health.” Advances in Nutrition: An International Review Journal 1.1 (2010): 8-16. Print.

“Cyproheptadine for Combat Nightmares in Post-traumatic Stress Disorder and Dream Anxiety Disorder.” Military Medicine. U.S. National Library of Medicine. Web. 05 Dec. 2016.

Daly, Oscar E. “The Use of Stimulants in the Treatment of Post Traumatic Stress Disorder: Case Report.” Human Psychopharmacology: Clinical and Experimental 15.4 (2000): 295-300. Print.

Davison, Karen M., and Bonnie J. Kaplan. “Food Intake and Blood Cholesterol Levels of Community-based Adults with Mood Disorders.” BMC Psychiatry 12.1 (2012). Print.

Dolder, Patrick C., Yasmin Schmid, Felix Müller, Stefan Borgwardt, and Matthias E. Liechti. “LSD Acutely Impairs Fear Recognition and Enhances Emotional Empathy and Sociality.” Neuropsychopharmacology 41.11 (2016): 2638-646. Print.

Fagala, Gwen E., and Cindy L. Wigg. “Psychiatric Manifestations of Mercury Poisoning.” Journal of the American Academy of Child & Adolescent Psychiatry 31.2 (1992): 306-11. Print.

Finn, D. F., and J. J. Walsh. “Twenty-first Century Mast Cell Stabilizers.” British Journal of Pharmacology 170.1 (2013): 23-37. Print.

Flory, Janine D., Rachel Yehuda, Robert Grossman, Antonia S. New, Vivian Mitropoulou, and Larry J. Siever. “Childhood Trauma and Basal Cortisol in People with Personality Disorders.” Comprehensive Psychiatry 50.1 (2009): 34-37. Print.

Frias, Alvaro, Carol Palma, Núria Farriols, Laura Gonzalez, and Anna Horta. “Anxious Adult Attachment May Mediate the Relationship between Childhood Emotional Abuse and Borderline Personality Disorder.” Personality and Mental Health 10.4 (2016): 274-84. Print.

Gasser, Peter, Dominique Holstein, Yvonne Michel, Rick Doblin, Berra Yazar-Klosinski, Torsten Passie, and Rudolf Brenneisen. “Safety and Efficacy of Lysergic Acid Diethylamide-Assisted Psychotherapy for Anxiety Associated With Life-threatening Diseases.” The Journal of Nervous and Mental Disease 202.7 (2014): 513-20. Print.

Gill, Jessica, Meena Vythilingam, and Gayle G. Page. “Low Cortisol, High DHEA, and High Levels of Stimulated TNF-α, and IL-6 in Women with PTSD.” Journal of Traumatic Stress 21.6 (2008): 530-39. Print.

Goffus, Andrea M., Gail D. Anderson, and Michael R. Hoane. “Sustained Delivery of Nicotinamide Limits Cortical Injury and Improves Functional Recovery Following Traumatic Brain Injury.” Oxidative Medicine and Cellular Longevity 3.2 (2010): 145-52. Print.

Harkness, Jon M., and Todd Tucker. “The Great Starvation Experiment: Ancel Keys and the Men Who Starved for Science.” The Journal of American History 96.1 (2009): 278. Print.

Hase, Michael, Ute Mirian Balmaceda, Adrian Hase, Maria Lehnung, Visal Tumani, Christian Huchzermeier, and Arne Hofmann. “Eye Movement Desensitization and Reprocessing (EMDR) Therapy in the Treatment of Depression: A Matched Pairs Study in an Inpatient Setting.” Brain and Behavior 5.6 (2015). Print.

Hoane, Michael R., Shelby A. Kaplan, and Amy L. Ellis. “The Effects of Nicotinamide on Apoptosis and Blood–brain Barrier Breakdown following Traumatic Brain Injury.” Brain Research 1125.1 (2006): 185-93. Print.

Hovatta, Iiris, Juuso Juhila, and Jonas Donner. “Oxidative Stress in Anxiety and Comorbid Disorders.” Neuroscience Research 68.4 (2010): 261-75. Print.

Institute of Medicine (US) Committee on Military Nutrition Research. “Impact of Underconsumption on Cognitive Performance.” Not Eating Enough: Overcoming Underconsumption of Military Operational Rations. U.S. National Library of Medicine, 01 Jan. 1995. Web. 05 Dec. 2016.

Iosifescu, Dan V. “The Relation between Mood, Cognition and Psychosocial Functioning in Psychiatric Disorders.” European Neuropsychopharmacology 22 (2012). Print.

Kas, A., S. Lavault, M.-O. Habert, and I. Arnulf. “Feeling Unreal: A Functional Imaging Study in Patients with Kleine-Levin Syndrome.” Brain 137.7 (2014): 2077-087. Print.

Kempke, Stefan, Patrick Luyten, Sarah De Coninck, Boudewijn Van Houdenhove, Linda C. Mayes, and Stephan Claes. “Effects of Early Childhood Trauma on Hypothalamic–pituitary–adrenal (HPA) Axis Function in Patients with Chronic Fatigue Syndrome.” Psychoneuroendocrinology 52 (2015): 14-21. Print.

Kempke, Stefan, Patrick Luyten, Linda C. Mayes, Boudewijn Van Houdenhove, and Stephan Claes. “Self-critical Perfectionism Predicts Lower Cortisol Response to Experimental Stress in Patients with Chronic Fatigue Syndrome.” Health Psychology 35.3 (2016): 298-307. Print.

Krystal, John H., and Alexander Neumeister. “Noradrenergic and Serotonergic Mechanisms in the Neurobiology of Posttraumatic Stress Disorder and Resilience.” Brain Research 1293 (2009): 13-23. Print.

“Lamotrigine Reviews & Ratings at” Lamotrigine Reviews & Ratings at Web. 05 Dec. 2016.

“Lamotrigine Therapy for Autistic Disorder: A Randomized, Double-blind, Placebo-controlled Trial.” Journal of Autism and Developmental Disorders. U.S. National Library of Medicine. Web. 05 Dec. 2016.

Matuoka, K., K. Y. Chen, and T. Takenawa. “Rapid Reversion of Aging Phenotypes by Nicotinamide through Possible Modulation of Histone Acetylation.” Cellular and Molecular Life Sciences 58.14 (2001): 2108-116. Print.

Meerson, F. Z. “Stress Damage to Nonischemic Divisions of the Heart in Experimental Infarction and Its Prevention.” Clinical Cardiology 6.4 (1983): 163-70. Print.

Meewisse, M.-L., J. B. Reitsma, G.-J. De Vries, B. P. R. Gersons, and M. Olff. “Cortisol and Post-traumatic Stress Disorder in Adults: Systematic Review and Meta-analysis.” The British Journal of Psychiatry 191.5 (2007): 387-92. Print.

Meskanen, Katarina, Heidi Ekelund, Jarmo Laitinen, Pertti J. Neuvonen, Jari Haukka, Pertti Panula, and Jesper Ekelund. “A Randomized Clinical Trial of Histamine 2 Receptor Antagonism in Treatment-Resistant Schizophrenia.” Journal of Clinical Psychopharmacology 33.4 (2013): 472-78. Print.

Miller, M. W., and N. Sadeh. “Traumatic Stress, Oxidative Stress and Post-traumatic Stress Disorder: Neurodegeneration and the Accelerated-aging Hypothesis.” Molecular Psychiatry 19.11 (2014): 1156-162. Print.

Murrough, James W. “The Effect of Early Trauma Exposure on Serotonin Type 1B Receptor Expression Revealed by Reduced Selective Radioligand Binding.” Archives of General Psychiatry 68.9 (2011): 892. Print.

Naeser, Margaret A., Anita Saltmarche, Maxine H. Krengel, Michael R. Hamblin, and Jeffrey A. Knight. “Improved Cognitive Function After Transcranial, Light-Emitting Diode Treatments in Chronic, Traumatic Brain Injury: Two Case Reports.” Photomedicine and Laser Surgery 29.5 (2011): 351-58. Print.

Pinna, Graziano. “Targeting Neurosteroidogenesis as Therapy for PTSD.” Frontiers in Pharmacology 4 (2014). Print.

“Psychedelics and Mental Health: A Population Study.” PloS One. U.S. National Library of Medicine. Web. 05 Dec. 2016.

Qazi, Hamid, Heshan Wijegunaratne, Ravi Savajiyani, and Maju Mathew Koola. “Naltrexone and Prazosin Combination for Posttraumatic Stress Disorder and Alcohol Use Disorder.” The Primary Care Companion For CNS Disorders (2014). Print.

Rasmusson, Ann M., Graziano Pinna, Prashni Paliwal, David Weisman, Christopher Gottschalk, Dennis Charney, John Krystal, and Alessandro Guidotti. “Decreased Cerebrospinal Fluid Allopregnanolone Levels in Women with Posttraumatic Stress Disorder.” Biological Psychiatry 60.7 (2006): 704-13. Print.

“Ray Peat, PhD Quotes on Therapeutic Effects of Niacinamide.” Ray Peat, PhD Quotes on Therapeutic Effects of Niacinamide – Functional Performance Systems (FPS). Web. 05 Dec. 2016.

Riddle, Megan C., Morgan C. Mckenna, Yone J. Yoon, Siobhan S. Pattwell, Patricia Mae G Santos, B. J. Casey, and Charles E. Glatt. “Caloric Restriction Enhances Fear Extinction Learning in Mice.” Neuropsychopharmacology 38.6 (2013): 930-37. Print.

Rooney, James P.k. “The Retention Time of Inorganic Mercury in the Brain — A Systematic Review of the Evidence.” Toxicology and Applied Pharmacology 274.3 (2014): 425-35. Print.

Ross, W. D., and M. C. Sholiton. “Specificity of Psychiatric Manifestations in Relation to Neurotoxic Chemicals.” Acta Psychiatrica Scandinavica 67 (1983): 100-04. Print.

Scarella, Timothy M., and Jamie R. Franzen. “Case Report: Improvement in Dissociative Symptoms with Mixed Amphetamine Salts.” Journal of Trauma & Dissociation (2016). Print.

Schfer, Ingo, Colin A. Ross, and John Read. “Childhood Trauma in Psychotic and Dissociative Disorders.” Psychosis, Trauma and Dissociation: 135-50. Print.

Shapiro, Francine. “The Role of Eye Movement Desensitization and Reprocessing (EMDR) Therapy in Medicine: Addressing the Psychological and Physical Symptoms Stemming from Adverse Life Experience.” The Permanente Journal (2014): 71-77. Print.

Sierra, Mauricio, Dawn Baker, Nicholas Medford, Emma Lawrence, Maxine Patel, Mary L. Phillips, and Anthony S. David. “Lamotrigine as an Add-on Treatment for Depersonalization Disorder.” Clinical Neuropharmacology 29.5 (2006): 253-58. Print.

Simeon, Daphne, Orna Guralnik, Erin A. Hazlett, Jacqueline Spiegel-Cohen, Eric Hollander, and Monte S. Buchsbaum. “Feeling Unreal: A PET Study of Depersonalization Disorder.” American Journal of Psychiatry 157.11 (2000): 1782-788. Print.

Simeon, Daphne, Margaret Knutelska, Rachel Yehuda, Frank Putnam, James Schmeidler, and Lisa M. Smith. “Hypothalamic-Pituitary-Adrenal Axis Function in Dissociative Disorders, Post-Traumatic Stress Disorder, and Healthy Volunteers.” Biological Psychiatry 61.8 (2007): 966-73. Print.

Simeon, Daphne, and Margaret Knutelska. “An Open Trial of Naltrexone in the Treatment of Depersonalization Disorder.” Journal of Clinical Psychopharmacology 25.3 (2005): 267-70. Print.

Stefanska, B., H. Karlic, F. Varga, K. Fabianowska-Majewska, and Ag Haslberger. “Epigenetic Mechanisms in Anti-cancer Actions of Bioactive Food Components – the Implications in Cancer Prevention.” British Journal of Pharmacology 167.2 (2012): 279-97. Print.

Tafur, Joseph, and Paul J. Mills. “Low-Intensity Light Therapy: Exploring the Role of Redox Mechanisms.” Photomedicine and Laser Surgery 26.4 (2008): 323-28. Print.

Vegt, Esther J.m. Van Der, Jan Van Der Ende, Clemens Kirschbaum, Frank C. Verhulst, and Henning Tiemeier. “Early Neglect and Abuse Predict Diurnal Cortisol Patterns in Adults.” Psychoneuroendocrinology 34.5 (2009): 660-69. Print.

Viljoen, Margaretha, Annie Swanepoel, and Priyesh Bipath. “Antidepressants May Lead to a Decrease in Niacin and NAD in Patients with Poor Dietary Intake.” Medical Hypotheses 84.3 (2015): 178-82. Print.

“Vitamin B Status in Patients with Chronic Fatigue Syndrome.” Journal of the Royal Society of Medicine. U.S. National Library of Medicine. Web. 05 Dec. 2016.

Wittenborn, J. Richard. “Niacin in the Long-Term Treatment of Schizophrenia.” Archives of General Psychiatry 28.3 (1973): 308. Print.

Wolf, Erika J., Ann M. Rasmusson, Karen S. Mitchell, Mark W. Logue, Clinton T. Baldwin, and Mark W. Miller. “A Genome-Wide Association Study Of Clinical Symptoms Of Dissociation In A Trauma-Exposed Sample.” Depression and Anxiety 31.4 (2014): 352-60. Print.

Yennu, Amarnath, Fenghua Tian, Alexa Smith-Osborne, Robert J. Gatchel, Fu Lye Woon, and Hanli Liu. “Prefrontal Responses to Stroop Tasks in Subjects with Post-traumatic Stress Disorder Assessed by Functional near Infrared Spectroscopy.” Scientific Reports 6 (2016): 30157. Print.

“[Low Dose Naltrexone in the Treatment of Dissociative Symptoms].” Der Nervenarzt. U.S. National Library of Medicine. Web. 05 Dec. 2016.

“[Occupational Poisoning with Psychiatric Manifestations].” Giornale Italiano Di Medicina Del Lavoro Ed Ergonomia. U.S. National Library of Medicine. Web. 05 Dec. 2016.

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