PSYCHONEUROIMMUNOLOGY

Resumen Recientemente, el interés por el estudio de la relación entre el sueño y el sistema inmunológico, ha incrementado. El Síndrome de Apnea Obstructiva del Sueño (SAOS), es un trastorno caracterizado por episodios repetidos de cese de la respiración que ocurren durante el sueño. Recientes estudios han defendido la necesidad de estudiar la relación entre SAOS y sistema inmune. El objetivo de este estudio fue analizar las posibles diferencias existentes entre sujetos con SAOS y sujetos sanos en cuanto a su sistema inmunológico. La muestra del estudio estuvo compuesta por 13 sujetos con SAOS seleccionados de un centro médico y 16 sujetos sanos. Un índice de apnea/hipopnea (IAH) ≥ a 10 confirmó el diagnostico de SAOS. Para establecer el diagnóstico de SAOS se utilizó una poligrafía cardiorrespiratoria de todas las horas de sueño a cada paciente. Los resultados indican que existen diferencias estadísticamente significativas en leucocitos (p< 0,01), y linfocitos (p< 0,01), entre los pacientes con apnea y el grupo control. No se encontraron diferencias significativas en monolitos.

It has been hypothesized that the immune system plays a pathogenetic role in psychiatric disorders, in particular in major depression and schizophrenia. This hypothesis is supported by a number of reports on altered circulating levels and in vitro production of cytokines in these disorders. However, the respective evidence is not consistent. This may be in part due to an incomplete control for numerous confounding in¯uences in earlier studies. We investigated the plasma levels of cytokines and soluble cytokine receptors in psychiatric patients (N = 361) upon hospital admission and compared the results to those obtained in healthy controls (N = 64). By multiple regression analysis we found that circulating levels of interleukin-1 receptor antagonist (IL-1Ra), soluble IL-2 receptor (sIL-2R), tumor necrosis factor-a (TNF-a), soluble TNF receptors (sTNF-R p55, sTNF-R p75) and IL-6 were signi®cantly aected by age, the body mass index (BMI), gender, smoking habits, ongoing or recent infectious diseases, or prior medication. Cytokine or cytokine receptor levels were signi®cantly increased in patients treated with clozapine (sIL-2R, sTNF-R p75), lithium (TNF-a, sTNF-R p75, IL-6) or benzodiazepines (TNF-a, sTNF-R p75). Taking all these confounding factors into account, we found no evidence for disease-related alterations in the levels of IL-1Ra, sIL-2R, sTNF-R p75 and IL-6, whereas levels of TNF-a and sTNF-R p55 in major depression and sTNF-R p55 in schizophrenia were slightly decreased compared to healthy controls. We conclude that, if confounding factors are carefully taken into account, plasma levels of the above mentioned cytokines and cytokine receptors yield little, if any, evidence for immunopathology in schizophrenia or major depression. #

Signs of an inflammatory process, in particular increased pro-inflammatory cytokines and increased levels of prostaglandine E 2 (PGE 2 ), have repeatedly been described in major depression (MD). As cyclooxygenase-2 (COX-2) inhibitors inhibit the PGE 2 production and the production of pro-inflammatory cytokines, we performed a therapeutic trial with the COX-2 inhibitor celecoxib. In a prospective, double-blind, add-on study, 40 patients suffering from an acute depressive episode were randomly assigned to either reboxetine and celecoxib or to reboxetine plus placebo. After a wash-out period, 20 patients received 4-10 mg reboxetine plus placebo and 20 received reboxetine plus 400 mg celecoxib for 6 weeks. The treatment effect was calculated by analysis of variance. There were no significant differences between groups in age, sex, duration or severity of disease or psychopathology, or reboxetine dose or plasma levels. Over 6 weeks, both groups of patients showed significant improvement in scores of the Hamilton Depression Scale. However, the celecoxib group showed significantly greater improvement compared to the reboxetine-alone group. Additional treatment with celecoxib has significant positive effects on the therapeutic action of reboxetine with regard to depressive symptomatology. Moreover, the fact that treatment with an anti-inflammatory drug showed beneficial effects on MD indicates that inflammation is related to the pathomechanism of the disorder, although the exact mechanisms remain to become elucidated.

It is by now widely recognized that acute and chronic stress have an impact on the immune system. Acute stress may have a stimulating effect on the immune system, while in the case of chronic stress-and in particular in depression-the immune system may be down-regulated. However, there is considerable individual variability in the immune response to stress. This seems to a large extent to be determined by the subject's way of dealing with stress. The perception and evaluation of a stressor and the specific ways of stress coping may in different ways be related to various aspects of the stress response: sympathetic nervous system (SNS) activation and activation of the hypothalamic-pituitary-adrenal (HPA) axis, both systems affecting the immune system. Prolonged exposure to stressors or to severe life stresses may outweigh the person's coping resources leading to feelings of depression. The affective changes with the accompanying changes in the HPA axis are one of the hypothesized mechanisms underlying the immune changes in depression. It should be noted that the relationship between depression and immunity is affected by several other factors, such as gender and age and other personal resources. Increasing the subject's abilities to cope with stress and to reduce the negative affect by psychological interventions may on the other hand have a beneficial effect on the immune system.

Research suggests that the immune system may be adversely affected by chronic stress. There is some evidence that relaxation-based practices may effect an increase in immune functioning, but recent findings suggest that acute stress may lead to similar increases. Given this, we used a counterbalanced within-subjects design to directly compare the effects of a stressful mental arithmetic task and a relaxation-based task on secretory immunoglobulin A (S-IgA). Thirty participants were seen in small groups of two or three where they were administered both a mental arithmetic (stress) task and a relaxing hypnosis task. Four-minute timed saliva samples were obtained immediately following the two experimental tasks and following two baseline periods. Results demonstrated that, compared with baseline, S-IgA concentration and secretion rate were significantly higher following both the relaxation-based task and stress task. Additionally, our data showed that the increases were short-lived, decreasing significantly within 8 min following the completion of each task. Our results indicate that both stress-reducing and stress-inducing tasks can increase S-IgA levels, and these results are discussed with reference to the potential differential mechanisms and clinical significance of such changes. Copyright © 2008 John Wiley & Sons, Ltd.

The use of placebo may have accompanied healing and medical practices since their origins (Plato; Charmides, 155-156). Recent experimental data indicate that we would be well advised to further consider placebo eVects in future therapeutic strategies, with a better knowledge of their potency, psychological basis and underlying neurobiological mechanisms. Current research in the areas of pain, depression and Parkinson's disease has uncovered some of the potential neurobiological mechanisms of placebo eVects. These data indicate that conscious expectation and unconscious behavioral conditioning processes appear to be the major neurobiological mechanisms capable of releasing endogenous neurotransmitters and/or neurohormones that mimic the expected or conditioned pharmacological eVects. To date, research on placebo responses aVecting immune-related diseases is scarce, but there are consistent indications that skin and mucosal inXammatory diseases, in particular, are strongly modulated by placebo treatments. However, the brain's capability to modulate peripheral immune reactivity has been impressively demonstrated by paradigms of behavioral conditioning in animal experiments and human studies. Thus, placebo eVects can beneWt end organ functioning and the overall health of the individual through positive expectations and behavioral conditioning processes.

This study tested the hypothesis that human behavioral responses to psycho-social stress are sexually dimorphic and conform to the 'flight-or-fight' response for males and 'tend-and-befriend' for females. One hundred and twenty young adults (60 male, 60 female), mostly college students, served as study participants. Participants were randomly assigned to either a stress condition (Trier Social Stress Test, a standardized laboratory procedure used to induce psychosocial stress) or a control condition. Stress induction was confirmed with self-report questionnaires about perceived stress and anxiety. Participants then underwent three social decision making tasks to assess their competitive and cooperative tendencies: an Ultimatum Game, a Prisoner's Dilemma, and a Prosocial Risk Taking task. We found evidence for interactive effects of stress and sex in all three tests, and all interactions were in the same direction. Relative to controls, stressed males made lower monetary offers to their partners and tended to be less willing to behave prosocially in a hypothetical risky situation, whereas stressed females offered higher monetary amounts in the Ultimatum Game and behaved more cooperatively in the Prisoner's Dilemma. These results suggest that stress renders males more selfish and competitive, while stressed females become more other-oriented, more generous, and more cooperative. These effects are consistent with the 'flight or fight' pattern for males and the 'tend and befriend' pattern for females, respectively. The role of risk taking and empathy as possible psychological mediators of the effects of acute psychosocial stress on social decision making in men and women needs to be further investigated, along with sex differences in physiological responsiveness to stress.

The biopsychosocial model describes interactions between psychosocial and biological factors in the etiology and progression of disease. How an individual interprets and responds to the environment determines responses to stress, influences health behaviors, contributes to the neuroendocrine and immune response, and may ultimately affect health outcomes. Health psychology interventions are designed to modulate the stress response and improve health behaviors by teaching individuals more adaptive methods of interpreting life challenges and more effective coping responses. These interactions are discussed in the context of aging.

Delayed type hypersensitivity (DTH) reactions are antigen-specific, cell-mediated immune responses which, depending on the antigen involved, mediate beneficial (resistance to viruses, bacteria, fungi, and certain tumors) or harmful (allergic dermatitis, autoimmunity) aspects of immune function. We have shown that acute stress administered immediately before antigenic challenge results in a significant enhancement of a skin DTH response in rats. A stress-induced trafficking or redeployment of leukocytes to the skin may be one of the factors mediating this immunoenhancement. Here we investigate the effects of varying the duration, intensity, and chronicity of stress on the DTH response and on changes in blood leukocyte distribution and glucocorticoid levels. Acute stress administered for 2 h prior to antigenic challenge, significantly enhanced the DTH response. Increasing the duration of stress from 2 h to 5 h produced the same magnitude enhancement in cutaneous DTH. Moreover, increasing the intensity of acute stress produced a significantly larger enhancement of the DTH response which was accompanied by increasing magnitudes of leukocyte redeployment. In contrast, chronic stress suppressed the DTH response when it was administered for 3 weeks before sensitization and either discontinued upon sensitization, or continued an additional week until challenge, or extended for one week after challenge. The stress-induced redeployment of peripheral blood lymphocytes was attenuated with increasing exposure to chronic stress and correlated with attenuated glucocorticoid responsivity. These results suggest that stress-induced alterations in lymphocyte redeployment may play an important role in mediating the bi-directional effects of acute versus chronic stress on cell-mediated immunity in vivo. ᭧ 1997 Academic Press

it has been shown that major depression may be accompanied by an increased production of interleukin-1 /3 ( IL-1 p ), an acute phase (AP) response and simultaneous signs of activation and suppression of cell-mediated immunity. The mterleukin-1 -receptor antagonist (IL-1 -rA) is released in vivo during an AP response and serum levels are increased in many Immune disorders. The release of IL-I-rA may limit the pro-inflammatory effects of IL-l. This study has been carried out to examine serum IL-I-Ra in 68 depressed subjects (21 minor, 25 simple major and 22 melancholic subjects) vs. 22 normal controls. Depressed subjects showed significantly higher serum IL-1-rA concentrations than healthy controls. 29% of all depressed subjects had serum IL-1 -rA levels higher than the mean value + 2 standard deviations of normal controls; 44% depressed subjects had IL-I-rA values greater than 0.215 ng/ml with a specificity of 90%. In depressed subjects, there was a significant and positive relationship between serum IL-1 -rA and severity of illness. In depression, there were no significant relationships between serum IL-I-rA concentrations and indicants of hypothalamic-pituitary-adrenal (HPA)-axis activity, such as 24-h urinary cortisol and postdexamethasone cortisol values. Women had significantly higher serum IL-I -t-A levels than men. The findings support the thesis that depression is accompanied by an immune-inflammatory response.

Memes that are destructive to the cohesion of a complex social system should be defined as pathogenic memes. As a result, it is my belief that a cognitive prophylaxis model is necessary, and feasible, when it comes to preventing a pathogenic meme outbreak.

L-Theanine is an amino acid contained in green tea leaves which is known to block the binding of L-glutamic acid to glutamate receptors in the brain. Because the characteristics of L-Theanine suggest that it may influence psychological and physiological states under stress, the present study examined these possible effects in a laboratory setting using a mental arithmetic task as an acute stressor. Twelve participants underwent four separate trials: one in which they took L-Theanine at the start of an experimental procedure, one in which they took L-Theanine midway, and two control trials in which they either took a placebo or nothing. The experimental sessions were performed by double-blind, and the order of them was counterbalanced. The results showed that L-Theanine intake resulted in a reduction in the heart rate (HR) and salivary immunoglobulin A (s-IgA) responses to an acute stress task relative to the placebo control condition. Moreover, analyses of heart rate variability indicated that the reductions in HR and s-IgA were likely attributable to an attenuation of sympathetic nervous activation. Thus, it was suggested that the oral intake of L-Theanine could cause anti-stress effects via the inhibition of cortical neuron excitation. #

Abstract: During evolution, DNA viruses have captured a broad array of cellular genes involved in immune recognition and growth control that are nonessential for viral replication. The encoded virokines and viroceptors may act as mimetics or antagonists of their cellular homologues, altering signal transduction and cell communication towards survival of virus-infected cells. Human herpesvirus type 8 (HHV8) is the most recently identified human oncogenic herpesvirus. It is associated with Kaposi's sarcoma and lymphoproliferative diseases, such as pleural effusion lymphomas and multicentric Castleman's disease. HHV8 has captured a unique number of cellular regulatory genes, which redirect gene expression and cell growth, prevent apoptosis and immune recognition, and interfere with tumor suppressor gene function. HHV8 encodes a unique virokine, viral interleukin-6, which is particularly relevant for the pathogenesis of HHV8-associated tumors, since it participates in transformation and mediates autocrine and paracrine mitogenic and proinflammatory effects. Viral IL-6 differs fundamentally from human IL-6 in receptor engagement for signal transduction and thus constitutes a singular model to understand the facets of human and viral cytokine biology. We provide an overview of the role of virokines in cancer, with a particular focus on the differences of human and viral IL-6 in the pathophysiology of HHV8-associated tumors.

Fibromyalgia is presented as an example of how an illness is learned along with its PNI correlates. In this work I argue that fibromyalgia, as well as most illnesses are learned patterns that have an initial preservation function. In the case of fibromyalgia, the patient may learn a functional hypervigilance in order to cope with a potential threat during sleep (possible physical threats during the day and/or sexual abuse while asleep). Initially, it was adaptive learning to sleep lightly (with the consequence of delta sleep deprivation, pro inflammatory products etc.), but as the contextual conditions change (i.e. no longer a need to be hypervigilant), the behavior becomes dysfunctional, and eventually its PNI damage reaches a critical mass where the symptoms, rather than the cause, emerge as an "illness".

Studies of interactions between the nervous and immune systems that eVect immunological and behavioral changes are relevant to our understanding biological issues pertinent to evolution, ethology, ecology, and aging, in addition to our understanding the immune and nervous systems per se. Psychoneuroimmunology also relates to homeland security, science education, and the practice of conventional as well as complementary and alternative medicine. This paper will highlight just some of these global implications of psychoneuroimmunology.  2005 Elsevier Inc. All rights reserved.

This article reviews evidence that shows a bidirectional relationship between the brain and the immune system. As a result of this relationship, mental factors such as stress and depression have been shown to affect immune system functioning, with both immunosuppression and immune activation being reported. Stress and depression also have been associated with worse outcomes in immune-related disorders including cancer and infectious diseases suggesting that stress/depression effects on the immune system are clinically relevant to disease expression. Conversely, several lines of evidence suggest that immune system activation such as during infectious diseases, cancer, and autoimmune disorders is associated with the development of behavioral symptoms similar to those seen in the context of chronic stress or major depression. These findings implicate a role for the immune system in the cause of behavioral disorders in a wide range of medical illnesses. Finally, a paradigm is proposed i...

The belief that adverse life stressors and the emotional states that can lead to major negative impacts on an individual's body functions and hence health has been held since antiquity. Adverse health outcomes such as coronary heart disease, gastrointestinal distress, and cancer have been linked to unresolved lifestyle stresses that can be expressed as a negative impact on human survival and ultimately a decrease of the human life span. Psychological modulation of immune function is now a well-established phenomenon, with much of the relevant literature published within the last 50 years. Psychoneuroimmunology and psychoneuroendocrinology embrace the scientific evidence of research of the mind with that of endocrinology, neurology and immunology, whereby the brain and body communicate with each other in a multidirectional flow of information that consists of hormones, neurotransmitters/neuropeptides, and cytokines. Advances in mind-body medicine research together with healthy nutrition and lifestyle choices can have a significant impact on health maintenance and disease prevention and hence the prolongation of the human life span.

Neuroscience was an integral part of psychosomatic medicine at its inception in the early 20th century. Since the mid-20th century, however, psychosomatic research has largely ignored the brain. The field of neuroscience has burgeoned in recent years largely because a variety of powerful new methods have become available. Many of these methods allow for the noninvasive study of the living human brain and thus are potentially available for integration into psychosomatic medicine research at this time. In this first paper we examine various methods available for human neuroscientific investigation and discuss their relative strengths and weaknesses. We next review some basic functional neuroanatomy involving structures that are increasingly being identified as relevant for psychosomatic processes. We then discuss, and provide examples of, how the brain influences end organs through "information transfer systems," including the autonomic, neuroendocrine, and immune systems. The evidence currently available suggests that neuroscience holds great promise for advancing the goal of understanding the mechanisms by which psychosocial variables influence physical disease outcomes. An increased focus on such mechanistic research in psychosomatic medicine is needed to further its acceptance into the field of medicine. Key words: neuroscience, brain imaging, information transfer systems, autonomic nervous system, neuroendocrinology, psychoneuroimmunology.

It is said that human mind is the most complex machine on earth. Psychologists have always been trying to know why we behave the way we do or the way our mind functions. It is a complex area of research where explanations have always fallen short. Humans differ in their mental capabilities. There are various tests available to analyze various mental abilities of a human mind which have a direct effect on their behaviour. Some such measures are IQ test, EQ test, personality tests, achievement test, aptitude test, etc. One such relatively new measure is AQ, which stands for adversity quotient. AQ is the predictor of success of a person in face of adversity, how he behaves in a tough situation, how he controls the situation, is he able to find the correct origin of the problem, whether he takes his due ownership in that situation, does he try to limit the effects of adversity and how optimistic he is that the adversity will eventually end. The science of AQ was developed by Dr. Paul G....

Author: Lameese Eldesouky

The Five Factor Model, one of the most commonly used models for assessing personality, consists of five main universal traits: extraversion, neuroticism, agreeableness, conscientiousness, and openness to experience (McCrae & John, 1992). Recently, its application to fields investigating the role of personality on physical and mental health has been extensive, with most traits producing consistent results across studies. The fifth of the model’s main traits, however, openness to experience, has produced inconsistent results. In this review, we attempt to understand why these findings have been mixed by analyzing various facets of this trait in depth. We evaluate the six facets of openness to experience: actions, ideas, values, aesthetics, fantasy, and feelings individually to better understand the implications of openness to experience on physical and mental health.

Connecting the dots between discoveries in neuroscience (neuroplasticity), psychoneuroimmunology(the brain-immune loop) and user experience (gadget rub-off) indicate the nature of our time spent with gadgets is a vector in human health - mentally, socially and physically. The positive design of our interactions with devices therefore can have a positive impact on economy, civilization and society. Likewise, the absence of design that encourages positive interaction may encourage undesirable behaviors. Much like the architecture of physical spaces and buildings, the consequences of the architecture of the 21stcentury conversation between man and machine may last generations. AI and the Internet of Things are primary vectors for positive and negative impacts of technology.  We describe a growing body of co-discoveries occurring across a variety of disciplines that support the argument for human sciences in technology design.    The paper brings the rigors of science to bear on the humanities and makes the case for its relevance at this juncture in time to the design of technology involved in conversation and behaviors between humans and machines .

Identity can be considered as the ideological signifier of our age, it also carries an ever increasing weight as a political emblem, even as this mostly concerns identification, for which we easily trade our true consciousness and core self.
Identity is an essential attribute of being. At a personal level, identity is not only what we think we are or the labels we are given. It includes our unconscious and is more than our personality, which is the expression of our identity in relation to others. It goes deeper than our subjective selfhood, the notion of me or self which provides the sense of sameness and continuity, but this stability is an illusion. We are not the same all the time, the continuity of a single ‘self’ is a chimera.
One of the central themes of this book is that our personal identity is not an indivisible, immutable, totally consistent given, but rather a dynamic matrix, often a repertoire of identities. This is not a pathological condition, but something many of us have, often resulting in inner conflicts, which eventually may cause depression or disease. To help understand these identity conflicts, in oneself and in others, this extensive and updated study present a new way to look at the formation and development of identity and notably substitute identities because of trauma dissociation and how these manifest and change.
Issues like the digital identities we all have in cyberspace, group mind, psychological immunity, trauma immunity, digestive identity social identity, the Western identity crisis, identity politics,  radicalization, and identification mechanisms are covered in this book, as are PTSD and auto-immune diseases. We show how there is resonance between cell-, organ- and personal-identity at the epigenetic level.
This book is full of new and daring insights and visualizations on how our psyche operates and how we function as humans and how group identity, mass hypnosis and social identity emerge. The impact of Corona on mass-formation, identity, autonomy, agency,  immunity etc. is discussed.
update nov 2022

Τι είναι η ΙΨΔ Η Ιδεοψυχαναγκαστική διαταραχή είναι μια διαταραχή που ανήκει στις αγχώδεις διαταραχές. Το άτομο που πάσχει από ΙΨΔ παγιδεύεται από μια σειρά επαναληπτικών σκέψεων που ονομάζονται ιδεοληψίες και επαναλαμβανόμενων συμπεριφορών που ονομάζονται ψυχαναγκασμοί και του προκαλούν μεγάλη δυσφορία. Η ΙΨΔ εμφανίζεται σε μέτρια έως σοβαρή μορφή. Όταν η μορφή που εμφανίζεται είναι σοβαρή και παραμείνει χωρίς θεραπεία μπορεί να αποδυναμώσει την δυνατότητα του ατόμου να λειτουργήσει ικανοποιητικά στην εργασία του, στο σχολείο κ.λπ Πόσο συχνή είναι η ΙΨΔ

Historical analysis and new concepts enable understanding of Riemann's Hypothesis (RH), his zeta function, mathematics, the principles enabling them, and ontological proofs. They enable new, post-modern metamathematics. New terms and definitions support comprehensive proof of new number theory, set theory, and proof theory. They enable deep understanding of the full scope of the historic context and causes of RH. The "Results" section provides basics and the technical context of work on RH and related problems. The "History" section summarizes the background of useful work and attempted solutions. Section 2 enables understanding of the work, enabling metalogic, and the domain of discourse. Section 3 provides comprehensively definitive, deeply explanatory proof of RH, and an integral critique of prior metatheory. It includes proofs of closely related problems, explanations, and how primal numbers may be rapidly, economically located. The new metatheorems of ontology, mathematics, numbers, sets, and proof also support new conjectures and possibilities. Disproof of the P/NP problem is included. Section 4 provides summary comments and predictions, for inspiration and verification.

This is a partially-completed, preliminary draft of an article that I wrote in the summer of 2009, with occasional additions thereafter. Additions to the article are based primarily upon subsequent literature review. 

In 2014, when I emailed an earlier draft of this article to Professor Guiles Guillemin--who was and continues to be the Head of the Neuroinflammation Group at Macquarie University, the Co-Director of the Motor Neuron Disease Research Center at Macquarie University, the Co-Director of the Neurodegenerative Diseases Research Centre at Macquarie University, and the Editor-in-Chief of The International Journal of Tryptophan Research--he sent me an enthusiastic reply, offering to co-author a revised and finalized version of the article for publication in The International Journal of Tryptophan Research. I had no background whatsoever in life sciences or medicine, and had immersed myself in the medical literature review for about eight months before writing the draft. Having such a highly-regarded co-author would have been an enormous benefit.

At that point in time, the draft provided an overview of the role of the kynurenine pathway as a cause of pathogenesis in Lyme neuroborreliosis and quite a few other chronic infections. The article explained how chronic activation of a hyperinflammatory immune response results in excitotoxicity, oxidative stress, impairment of antioxidant defenses, and devastating deactivation of the immune response against both intracellular and extracellular infections, such as Lyme neuroborreliosis, if those infections are the cause of the chronic, hyperinflammatory immune response that results in overactivation of the kynurenine pathway.  Because aggressive antibiotic treatment of advance Borrelia burgdorferi infection results in exacerbation of the inflammatory immune response, the article provides a well-researched hypothesis that in cases of prolonged infection with B. burgdorferi, such as my own 30 year history of infection with both B. burgdorferi and Babesia microti, aggressive antimicrobial treatment can damage such patients far more in a less than a year than the underlying, untreated  infections had damaged such a patient over the prior 30 years. Such was the case with me, when I was treated with two intravenous antibiotics simultaneously, along with oral antimicrobials, for both Lyme neuroborreliosis and infection with Babesia microti.

The article also provided a thoroughly-researched hypothesis concerning the mechanisms of action of ketamine as an antidepressant. And it provided my hypothesis that ketamine taken with buprenorphine would synergistically reduce depression. I had developed tolerance to such a high dose of ketamine that 300 mg intramuscular ketamine daily could not control my depression. Nor could buprenorphine any longer control my depression. But when I found a psychiatrist who was willing to prescribe both drugs together, my hypothesis turned out to be correct (sample size: one). Moreover, buprenorphine prevented me from developing any additional tolerance to ketamine. I was able to take 300 mg IM ketamine daily (10 injections @ 30 mg each daily) and 8 mg buprenorphine twice daily for six years--from August 2011 to early 2017--which reduced my depression from the severe-to-extreme range to the lower moderate range.

I was unable to accept Professor Guillemin's offer of co-authorship in 2014 because during the two years before I mailed him the draft, I had been diagnosed with additional medical disorders that have high fatality rates and were supposedly incurable. I had managed to cure those medical conditions after another round of intensive medical literature review, but I felt it was more important to continue my research and to find an even better treatment for depression.

Specifically, I had developed complex regional pain syndrome from the left elbow, along the left forearm, and into the left hand after falling out of bed in 2012 and landing on my left elbow on a hard wood floor. Immediately, I began experiencing peripheral neuropathy from the left elbow, down the left forearm, and throughout the left hand. Over a period of seven months, the tingling and numbness became an intense  burning sensation. And at that point, I suddenly began experiencing identical symptoms simultaneously in my right arm. At the eight month point, I discovered a case report of cure of CRPS using the exact model of near-infrared laser I already owned: a 7.5 watt, 980 nanometer Avicenna laser that emitted a divergent beam with a spot size of 1 square centimeter at 0 mm distance. After traveling three centimeters, the beam became 56% wider, and therefore 56% less powerful. I treated my left arm from the elbow to the end of the left hand with an output of 7.5 watts, holding the lens very close to the skin while moving the hand piece back and forth for 15 minutes, three days in-a-row. After the third daily treatment in 2012, I was completely cured , and have never experienced any recurrence of CRPS.

Because I had already developed tolerance to a very high dose of ketamine before discovering that buprenorphine prevented additional tolerance, I had to take 300 mg intramuscular ketamine daily combined with buprenorphine. After about 16 months, I developed excruciating ketamine-induced interstitial cystitis. A major hospital in Seattle was able to do nothing to alleviate my symptoms. It appeared that I would either have to stop taking ketamine, which would result in a relapse of extreme depression that I could not survive, or that I would destroy my bladder over the next month, leading to the same outcome  as well as a destroyed bladder. So I began treating the ureters and the bladder with my 7.5 watt laser. I had to treat each ureter for 30 minutes daily with that laser, from the top of the ureters down to the bladder. But within three days, the interstitial cystitis was under control. A week after I began treating myself with the laser, I went back to the hospital for a scope of my ureters and bladder. The doctors were astounded that they could find no damage. Among other things, the laser activates mesenchymal stem cells, which travel from the bone marrow to locations throughout the body that are damaged, and repair the damage. Over the next five years, I upgraded to more powerful lasers and a more effective wavelength. First, I upgraded to a 10 watt, 980 nm Diowave laser that emitted a divergent beam with a spot size of 3 square centimeters at 0 mm distance. I was able to treat myself less often than I had with the outdated 7.5 watt, 980 nm Avicenna laser. Then I upgraded to a hand piece that emits a collimated beam, which I used with the 10 watt laser. Immediately, I was able to treat myself 12 times less often to achieve the same result that I had achieved using a divergent beam. I was then able to significantly reduce the treatment time when I upgraded to a 15 watt, 810 nm Diowave laser that emits a collimated beam. And finally, when I upgraded to a 30 watt, 810 nm Aspen laser that emits a collimated beam, I was able to treat each ureter down to the bladder for five minute each month (10 minutes of treatment per month) to achieve the same results I had achieved with four hours of treatment weekly using the 7.5 watt, 980 nm Avicenna laser. I continued taking 300 mg ketamine and 8 mg buprenorphine BID that entire time. A with a wavelength of 810 nanometers penetrates into any part of the human body, including the brain, about three times more effectively than a 980 nm beam with the same power density.

In 2015, I a pilot study demonstrating that lasers at least 30 times less powerful than my 30 watt laser (effectively at least 30 times less powerful, because they emitted divergent beams) cured about 90% of patients with severe, suicidal depression caused by traumatic brain injury within two months after starting treatment, when treated twice per week for 20 minutes for those two months. But lasers with the power output in those pilot trials had no effect on my depression. I have never seen depression as extreme as mine described in any medical literature. Here is a one minute and eight second video of me that was taken in April 2011, almost four months before I found a psychiatrist who was willing to prescribe 300 mg IM ketamine and 8 mg buprenorphine BID. When this video was taken, I was taking only buprenorphine. https://www.dropbox.com/s/qsbza9huy2zb8w4/2011%2005-22%20Video%20of%20Anthony%20severely%20depressed%20%287%20on%20scale%20of%200%20to%2010%29.mp4?dl=0

In 2017, I continued to increase the treatment time when treating the temporal regions and frontal lobes using my 30 watt, 810 nm Aspen laser that emits a collimated beam. I treated for 10 minutes, and took a one minute break, and treated for another ten minutes. Finally, when I reached 50 minutes of treatment per day, I began experiencing dramatic antidepressant effects, enabling me to reduce my dose of ketamine from 300 mg daily to nothing at all in a period of six weeks. And I have been able to reduce the dose of buprenorphine by half.

I added information about near-infrared laser to this draft article, but not nearly to the extent that I would like to do so. I plan on turning this into two separate articles: one about ketamine and buprenorphine, and the other about high-power, near-infrared laser therapy.

One of the major philosophical aspirations in contemporary consciousness research is to find a framework of explanation that could successfully address the problem of mind-body relations. Descartes is often regarded as the father of dualism in modern philosophy of mind. Phenomenology and embodiment may dissolve the problem of dualism in the waters of the experiential features of the life-world and the subject.
Recent findings in psychoneuroimmunology have shown that somato-psychic mechanisms exist through which bodily stimuli
are translated into neuropsychological events resulting in alterations in certain behavioral patterns. These may as well include changes in the qualitative features of the lived body (Leib) resulting in an overall change in the subjective experience. The application of modern embodiment theories
in life sciences has the potential to create a novel, fruitful and heuristic approach, which may help us unveil features of the
“mind-body phenomenon” that have been hidden so far. In this paper, I will try to briefly outline a possible analytical framework
on the grounds of classic – Husserlian and Merleau-Pontian – phenomenology and biomedical sciences.

El estrés crónico y la Terapia Cognitiva Centrada en Mindfulness: Una nueva dimensión en psiconeuroinmunología En el presente artículo se hace una revisión del concepto de estrés crónico desde una perspectiva psiconeuroinmunólogica. Se examina un extenso número de estudios multidisciplinarios que demuestran las interacciones entre el cerebro y los sistemas nervioso, endocrino e inmune en el desarrollo de enfermedades. Se presenta una nueva visión acerca del estrés y se hacen las distinciones correspondientes en relación con la respuesta fisiológica, emocional, comportamental y estilo de vida del individuo. Se examina el impacto negativo del estrés crónico con un énfasis especial en la enfermedad del cáncer, y finalmente se hace referencia al programa de la Terapia Cognitiva Centrada en Mindfulness (TCCM) como una forma de intervención biopsicosocial promisoria para contrarrestar los efectos nocivos del estrés crónico. estrés crónico / calidad de vida / cáncer / mindfulness / psiconeuroinmunología

Background. As part of a new standard of quality cancer care, the Institute of Medicine has recommended inclusion of therapies that address psychosocial needs of cancer patients. A range of psychosocial therapies for managing acute and chronic stress have been developed for patients with cancer, based on the scientific framework of psychoneuroimmunology (PNI). The current review aimed to identify studies of new and emerging PNI-based psychosocial therapies in patients with cancer that have used neuroendocrine-immune biomarkers as outcomes. Specifically, this review aimed to evaluate studies based on the cancer populations involved, types of psychosocial therapies, and PNI measures employed. Methods. Methodology was guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The PubMed, EMBASE, PsychINFO, CINAHL, and Google Scholar online databases were searched using combinations of keywords obtained from previous reviews of psychosocial interventions. Studies from 2001 to 2012 were included if they (a) were published in English, (b) used experimental or quasi-experimental designs, (c) evaluated psychosocial therapies, (d) involved cancer patients, and (e) reported results on at least one neuroendocrine or immune outcome measure. The search strategy identified 403 records and 2 stages of screening were used to eliminate irrelevant studies. Results. A total of 24 cancer-specific studies of psychosocial therapies that used PNI-based outcome measures were included in this review. Most studies included early-stage breast cancer patients, and 2 major types of therapies emerged, cognitive-behavioral therapies and complementary medical therapies. Durations of interventions ranged widely, from 1.3 hours over a single week to 27 hours over 18 weeks. Considerable diversity in PNI outcomes made statistical comparisons problematic. Studies of cognitive-behavioral therapies were found to have reported the most success in impacting PNI-based measures, which were typically functional measures of the immune system, for example, cytokines. Conclusions. Several issues related to research methodology are discussed. Most important, studies examining dose-response associations and resource allocation are needed to guide future research. A standardized panel of psychosocial instruments and biomarkers for PNIbased studies would enhance comparability of findings across studies when evaluating this body of research and assist with integrating psychosocial therapies into the standard of cancer care.

Interest in the interplay between mind and body is deep-rooted. Written accounts in Western society are found as far back as the second century, when the physician Galen remarked that cancer seemed to occur more frequently in melancholic (depressed) than sanguine (happy, spirited) women [1]. In traditional Eastern medicine, mind and body have been considered entwined for centuries, and this attitude continues to today (see for an overview). Relative to these examples, it is only recently that scientific inquiry has taken an interest in the mind-body connection. The past three decades have witnessed an explosion of discoveries in this area, and we have seen psychological factors related to physical ailments from asthma to heart disease . The present review focuses on just one aspect of mindbody interaction, but one with far-reaching effects. We review evidence for the relationship between psychological stress and immune function. Using a conceptual model, we review psychological, behavioral, and physiological responses to stressful events before entering into a more in-depth discussion of the potential role of subjective experiences of stress.

During the second half of the last century, biopsychosocial research in psychosomatic medicine largely ignored the brain. Neuroscience has started to make a comeback in psychosomatic medicine research and promises to advance the field in important ways. In this paper we briefly review select brain imaging research findings in psychosomatic medicine in four key areas: cardiovascular regulation, visceral pain in the context of functional gastrointestinal disorders, acute and chronic somatic pain and placebo. In each area, there is a growing literature that is beginning to define a network of brain areas that participate in the functions in question. Evidence to date suggests that cortical and subcortical areas that are involved in emotion and emotion regulation play an important role in each domain. Neuroscientific research is therefore validating findings from previous psychosomatic research and has the potential to extend knowledge by delineating the biological mechanisms that link mind and body more completely and with greater specificity. We conclude with a discussion of the implications of this work for how research in psychosomatic medicine is conducted, the ways in which neuroscientific advances can lead to new clinical applications in psychosomatic contexts, the implications of this work for the field of medicine more generally, and the priorities for research in the next 5 to 10 years.

Case report of my own recovery from episodes of unremitting, severe-to-extreme depression per HDRS, lasting from late 2003 to late 2006 (at which point I requested a different psychiatrist to prescribe specific medications, resulting in remission within one week), and then another such episode, involving near-catatonia, which was caused by extremely aggressive antimicrobial therapy for a 30 year old cerebral infection with Borrelia burgdorferi and coinfection with Babesia microti. Because no medical professional was able to keep me alive, I immersed myself in medical literature, discovered that at least in my case, buprenorphine prevents tolerance to ketamine. I improved to a chronic state of mild-to-moderate depression after a psychiatrist recognized that the risk of suicide in my condition was 100%, that every known treatment had been attempted, and that I had provided a strong hypothesis as to the causes and pathological mechanisms involved in my illness, as well as a reasonable hypothesis that ketamine and buprenorphine should act synergistically to reduce depression (neither drug alone was sufficient in my case). I was able to enjoy a tolerable quality of life for over six years taking 300 mg intramuscular ketamine daily (10 injections daily) along with 8 mg buprenorphine twice daily -- with no change in dosage. I was then able to reduce my dose of ketamine from 300 mg daily to zero in a period of six weeks, with no difficulty, when I began treating the frontal lobes and temporal region bilaterally each evening with a 30 watt, 810 nanometer near-infrared laser, equipped with a hand piece that emits a collimated beam with a spot size of 2.5 sq. cm. A typical hand piece on an 810 nm laser emits a beam that becomes 70% more divergent, and therefore 70% less powerful than it is at the lens after passing through merely 3 cm. of air. I use three powerful 12 inch fans located about eight inches from the forehead and from each temple to prevent any thermal discomfort (shaving my head every night). I treat from the back-side of one temple, across the forehead, to the back-side of the other temple, moving the hand piece back and forth, for 10 minutes six times in a row (with a one minute pause between treatments). Thus, I deliver 90,000 Joules of energy to the treatment area each evening. Until I worked up to that power output, I did not experience benefits, although the pilot studies that have been published reveal about an 80% remission rate using lasers at least 24 times less powerful than mine twice per week (20 minutes of treatment per week) for a period of two months. I have been off ketamine completely for about two years, and now take half the dose of buprenorphine that I used to take. And my depression is under much better control than it had been. The paper provides more limited information about near-infrared laser therapy, but enough information, along with citations, to serve as an introduction to this treatment modality. I have no financial interests in any form of medical treatment. I am providing this information publicly merely to benefit others who appear to be beyond all possible hope. Please note that this article is being made available in early draft form; for instance, although much of the text is my own, I copied and pasted abstracts of studies and used those abstracts as place markers (with appropriate citations) in sections that will be rewritten in with far less detail.  I am providing the article in this preliminary format because I believe others who are suffering could benefit from the information I have provided, and I do not wish to prolong anyone's suffering by withholding the information until a finalized version is written.

Background: "Fright" is an English-speaking Caribbean idiom for an illness, or ethnomedical syndrome, of persistent distress. A parallel ethnopsychiatric idiom exists in the French Antilles as sésisma. Fright is distinct from susto among Hispanics, though both develop in the wake of traumatic events. West Indian ethnophysiology (ethnoanatomy) theorizes that an overload of stressful emotions (fear, panic, anguish or worry) causes a cold humoral state in which blood coagulates causing prolonged distress and increased risks of other humorally cold illnesses. Methods: Qualitative data on local explanatory models and treatment of fright were collected using participantobservation, informal key informant interviews and a village health survey. Ethnobotanical and epidemiological data come from freelist (or "free-list") tasks, analyzed for salience, with nearly all adults (N = 112) of an eastern village in Dominica, and a village survey on medicinal plant recognition and use (N = 106).

This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues. Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. In most cases authors are permitted to post their version of the article (e.g. in Word or Tex form) to their personal website or institutional repository. Authors requiring further information regarding Elsevier's archiving and manuscript policies are encouraged to visit: http://www.elsevier.com/copyright a b s t r a c t The immune system's efficacy in detecting and destroying cancer cells varies considerably throughout the stages of cancer development and its role may be critical particularly during the surgical period. Although surgery causes tumor cells to shed into the blood, immune cells have the capacity to destroy these tumor cells. However, surgery also suppresses cytotoxic capacity. It is particularly during this surgical period that psychological factors can have a significant dampening or strengthening impact on surgery-related immunomodulation response, thus exerting an effect on survival. This review describes the immune changes during the peri-surgical period and the influences psychological factors have on immune function, including the immune effects caused by psychological interventions in cancer patients. We recommend that future studies exploring the role of psychological factors on immune function and survival focus more on their influence during the peri-surgical period.

Psychoneuroimmunology (PNI) is a discipline that has evolved in the last 40 years to study the relationship between immunity, the endocrine system, and the central and peripheral nervous systems. In this manner, neurotransmitters, hormones, and neuropeptides have been found to regulate immune cells, and these in turn are capable of communicating with nervous tissue through the secretion of a wide variety of cytokines. Of critical importance is the effect of products of the CNS and nerves on the maintenance of the delicate balance between cell-mediated (Th1) and humoral (Th2) immune responses. A good example of how this concept operates in vivo becomes evident when analyzing the effects of stressors. Chronic stress affects significantly the function of the immune system as well as modifies the evolution of a variety of skin diseases, as psychosocial interventions have proved to be effective in their therapy.