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1
Epigenetics and human health: Linking hereditary, environmental, and nutritional aspects. Weinheim: Wiley-VCH, 2010.
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Wang, Fushun, Jason H. Huang, Fang Pan, and Yi-Yuan Tang, eds. Early Life Stress-Induced Epigenetic Changes Involved in Mental Disorders. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-153-6.
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Fitzgerald, Hiram E., and Leon I. Puttler, eds. Alcohol Use Disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676001.001.0001.
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Chapters in this volume reflect, to one degree or another, eight critical aspects of contemporary research attempting to understand the etiologic processes that heighten risk or resilience factors for substance use disorders: (1) a focus on systemic frameworks for understanding developmental process, (2) the heterogeneity of developmental pathways, (3) the role of genes and epigenetic–experience transactions, (4) risk cumulative/cascade models of the effects of exposure to adverse childhood experiences, (5) negotiating developmental transitional periods, (6) neurobiological embodiment of adverse childhood experiences, (7) links between alcohol use disorder and tobacco addictive behaviors, and (8) longitudinal studies and data analysis within and between studies.
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Mastroeni, Diego F. An Epigenetics Perspective on Diseases of the Central Nervous System. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0011.
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In the next two decades epigenetics could revolutionize understanding and treatment of diseases of the central nervous system. New research already demonstrates that manipulation of epigenetic mechanisms in vivo and in vitro can ameliorate a host of pathogenic processes associated with neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD), amyotrophic lateral sclerosis (ALS), Huntington’s (HD), and multiple sclerosis (MS), among others. These advances have come relatively rapidly for a field that is still in its infancy compared to the much longer history of epigenetics in developmental biology. Epigenetic modifications are all-encompassing, from nucleotides to amino acids. They are capable of altering transcriptional to biochemical activity in a consistent manner across thousands of genes and hundreds of biologic pathways, yet they can do so differentially even in individuals or cells with identical gene codes. As such, epigenetic modifications are likely to touch on virtually all the mechanisms described in this book.
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Lucchesi, John C. Epigenetics, Nuclear Organization & Gene Function. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.001.0001.
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Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence. Epigenetic changes, consisting principally of DNA methylation, histone modifications and non-coding RNAs, maintain and modulate the initial impact of regulatory factors that recognize and associate with particular genomic sequences. This book’s primary goal is to establish a framework that can be used to understand the basis of epigenetic regulation and to appreciate both its derivation from genetics and its interdependence with genetic mechanisms. A further aim is to highlight the role played by the three-dimensional organization of the genetic material itself (the complex of DNA, histones and non-histone proteins referred to as chromatin) and its distribution within a functionally compartmentalized nucleus. Dysfunctions at any level of genetic regulation have the potential to result in an increased susceptibility to disease or actually give rise to overt pathologies. As illustrated in this book, research is continuously uncovering the role of epigenetics in a variety of human disorders, providing new avenues for therapeutic interventions and advances in regenerative medicine.
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Gorman, Jack M. Life Events Shape Us. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850128.003.0003.
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Psychiatry downplayed the importance of life events in causing mental illness from the 1960s on, favoring a view that all disorders except one are the result of abnormal genes affecting chemical processes in the brain. Studying the exception, posttraumatic stress disorder (PTSD), when it was defined in 1980 helped lead to renewed recognition that early life adversity is central to all psychiatric conditions. At the same time, neuroscientists showed that early life experiences are capable of changing life-long behavior and brain function in laboratory animals. One mechanism by which this occurs is through the epigenetic regulation of gene expression. Epigenetics is the way that the expression levels of genes are controlled without changing the underlying genetic code. Epigenetics is an attractive way of understanding how individual life experiences are translated in the brain into each person’s unique set of emotions, behaviors, abilities, and risks for psychiatric abnormalities.
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Peedicayil, Jacob, Dennis R. Grayson, and Dag Yasui. Neuropsychiatric Disorders and Epigenetics. Elsevier Science & Technology Books, 2016.
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Neuropsychiatric Disorders and Epigenetics. Elsevier, 2017. http://dx.doi.org/10.1016/c2013-0-15470-0.
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Peedicayil, Jacob, Dennis R. Grayson, and Dimitri Avramopoulos. Epigenetics in Psychiatry. Elsevier Science & Technology Books, 2014.
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Ponomarev, Igor. Alcohol Use Disorder. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190676001.003.0005.
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Alcohol use disorder (AUD) is characterized by clinically significant impairments in health and social function. Epigenetic mechanisms of gene regulation may provide an attractive explanation for how early life exposures to alcohol contribute to the development of AUD and exert lifelong effects on the brain. This chapter provides a critical discussion of the role of epigenetic mechanisms in AUD etiology and the potential of epigenetic research to improve diagnosis, evaluate risks for alcohol-induced pathologies, and promote development of novel therapies for the prevention and treatment of AUD. Challenges of the current epigenetic approaches and future directions are also discussed.
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Epigenetics of Stress and Stress Disorders. Elsevier, 2022. http://dx.doi.org/10.1016/c2019-0-03695-3.
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Miu, Andrei C., Judith R. Homberg, and Klaus-Peter Lesch, eds. Genes, brain, and emotions. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198793014.001.0001.
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With the advent of methods from behavioral genetics, molecular biology, and cognitive neuroscience, affective science has recently started to approach genetic influences on emotion, and the underlying intermediate neural mechanisms through which genes and experience shape emotion. The aim of this volume is to offer a comprehensive account of current research in the genetics of emotion, written by leading researchers, with extensive sections focused on methods, intermediate phenotypes, and clinical and translational work. Major methodological approaches are reviewed in the first section, including the two traditional “workhorses” in the field, twin studies and gene–environment interaction studies, and the more recently developed epigenetic modification assays, genome-wide association studies, and optogenetic methods. Parts 2 and 3 focus on a variety of psychological (e.g. fear conditioning, emotional action control, emotion regulation, emotional memory, decision-making) and biological (e.g. neural activity assessed using functional neuroimaging, electroencephalography, and psychophysiological methods; telomere length) mechanisms, respectively, that may be viewed as intermediate phenotypes in the pathways between genes and emotional experience. Part 4 concentrates on the genetics of emotional dysregulation in neuropsychiatric disorders (e.g. post-traumatic stress disorder, eating disorders, obsessive–compulsive disorder, Tourette’s syndrome), including factors contributing to the risk and persistence of these disorders (e.g. child maltreatment, personality, emotional resilience, impulsivity). In addition, two chapters in Part 4 review genetic influences on the response to psychotherapy (i.e. therapygenetics) and pharmacological interventions (i.e. pharmacogenetics) in anxiety and affective disorders.
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Zhou, Feng C., and Stephen Mason, eds. Genetics and Epigenetics of Fetal Alcohol Spectrum Disorders. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-573-2.
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McEwen, Bruce S., and Natalie L. Rasgon. The Brain and Body on Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0002.
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Neuroscientists have treated the brain in isolation from the rest of the body, while endocrinology and general medicine have viewed the body largely without regard to the influence of systemic physiology and pathophysiology on higher brain centers outside of the hypothalamus and pituitary gland. But now there is greater recognition of brain–body interactions affecting the limbic and cognitive systems of brain and altering systemic physiology; these are conceptualized as allostasis and allostatic load and overload. These concepts look at both the interactions of brain and body to stressors and health-promoting and health-damaging behaviors, and they help integrate behavior and mood with systemic functions. These interactions involve genetic predispositions and epigenetic alterations mediated by circulating steroid and metabolic hormones. Comorbidity and multi-morbidity of disorders will be illustrated by the relationship of systemic and brain insulin resistance to the psychopathology of depression and to the increased risk for dementia.
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Meaney, Michael J., and Rachel Yehuda. Epigenetic Mechanisms and the Risk for PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0017.
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This chapter discusses the epigenetic mechanisms involved in individual variation in and persistence of post-traumatic stress disorder (PTSD). Such mechanisms make it possible to trace vulnerability for PTSD to effects that predate development of PTSD. While some may be genetic in origin, others may involve parental stress occurring pre-conception, in utero changes in the maternal environment contributing to developmental programming, and childhood adversity, resulting in modifications of genes’ contribution to PTSD risk. The chapter discusses epigenetic alterations implicated in hypothalamic–pituitary–adrenal (HPA) function in PTSD that mark increased risk. Unlike the transient alterations in neural, endocrine, or immunological signals that follow exposure to trauma, certain epigenetic markers can be chemically stable over extended periods and can serve as a basis for understanding the persistence of PTSD symptoms. The chapter concludes with a discussion of how epigenetic modification may offer insights into future treatments for PTSD.
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Schulz, S. Charles, and Robert O. Friedel. Established and Novel Pharmacological Approaches to the Treatment of Personality Disorders. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0016.
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In the past few decades, the widely held belief of personality disorder patients being unresponsive to medication has been challenged. This chapter first reviews the current knowledge on medication for patients with personality disorders and then considers a number of novel pharmacological approaches that may yield additional beneficial results in the treatment of these disorders. It utilizes the neuroscience-based nomenclature for psychotropic agents, in which the presumptive modes and mechanisms of action of each drug form the basis of the nomenclature. A special emphasis of the chapter is laid on the role of clozapine in the treatment of personality disorders as well as new findings in the areas of pharmacogenetics and epigenetics.
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Wallace, Rodrick. Computational Psychiatry: A Systems Biology Approach to the Epigenetics of Mental Disorders. Springer, 2018.
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McKinlay Gardner, R. J., and David J. Amor. Uniparental Disomy and Disorders of Imprinting. Edited by R. J. McKinlay Gardner and David J. Amor. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199329007.003.0018.
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Uniparental disomy (UPD) is a fascinating pathogenetic mechanism, albeit that it is applicable to a small but important number of conditions. This chapter discusses the basis of UPD and the different mechanisms by which it may arise. It reviews the concept of epigenetics in this setting. This chapter considers UPD as it may have been observed in all the chromosomes, in some of which it appears to be without any effect, and others in which a UPD effect is well known, including the classic UPD conditions, of which Prader-Willi and Angelman syndromes are the archetypes. The differing reproductive risks in these different syndromes are noted.
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Nemeroff, Charles B., and Charles Marmar, eds. Post-Traumatic Stress Disorder. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.001.0001.
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Post-Traumatic Stress Disorder (PTSD) reviews current knowledge and controversies of PTSD. The history, nosology, epidemiology, pathophysiology, risk factors, diagnosis, and treatment of post-traumatic stress disorder are described in detail. Also covered are the evidence-based treatments for PTSD, including all psychopharmacological agents (such as antidepressants and antipsychotics) as well as individual psychotherapies. The book delves into a vast array of cases involving at-risk groups such as minorities and offers a closer look at the coverage of PTSD across the world. The authors present state-of-the-art findings in genetics, epigenetics, neurotransmitter function, and brain imaging to provide the most current and thorough review of this burgeoning field.
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Guffanti, Guia, Milissa L. Kaufman, Lauren A. M. Lebois, and Kerry J. Ressler. Genetic Approaches to Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0026.
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Post-traumatic stress disorder (PTSD) is a debilitating psychiatric disorder with an estimated genetic component accounting for 30%–40% of the variance contributing to risk for the disease. This chapter starts with a review of the biological hypotheses and related genetic mechanisms currently proposed to be associated with PTSD and trauma-related disorders. It will follow with a description of the state-of-the-art on the methodologies and their application to map genetic loci and identify biomarkers associated with PTSD. Finally, we will review the latest results from genome-wide association studies of genetic variants as well as those derived from the emerging fields of epigenetics and gene expression.
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Brüne, Martin. Textbook of Evolutionary Psychiatry and Psychosomatic Medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med:psych/9780198717942.001.0001.
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Psychiatry and psychosomatic medicine are concerned with medical conditions affecting the brain, mind, and behaviour in manifold ways. Traditional approaches have focused on a restricted array of potential causes of psychiatric and psychosomatic conditions, including adverse experiences such as trauma, neglect, or abuse, genetic vulnerability, and epigenetic regulation of gene expression. While essential for the understanding of mental disorders, these approaches have disregarded pertinent questions such as why the human mind is vulnerable to dysfunction at all. This Textbook of Evolutionary Psychiatry and Psychosomatic Medicine seeks to find answers to these questions by emphasizing an evolutionary perspective on psychiatric and psychosomatic conditions. It explains how the human brain/mind has been shaped by natural and sexual selection; why adaptations to environmental conditions in our evolutionary past may nowadays work in suboptimal ways; and how human cognition, emotions, and behaviour can be scientifically framed to improve our understanding of how people try to attain important biosocial goals pertaining to one’s status in society, mating, eliciting and providing care, and maintaining rewarding relationships. The evolutionary topics relevant to the understanding of psychiatric and psychosomatic conditions include the concepts of genetic plasticity, life-history theory, stress regulation, and immunological aspects. In addition, it is argued that an evolutionary framework is necessary to understand how psychotherapy and psychopharmacology work to improve the lives of patients with psychiatric and psychosomatic disorders.
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Post, Robert M. The Neurochemistry and Epigenetics of PTSD. Edited by Frederick J. Stoddard, David M. Benedek, Mohammed R. Milad, and Robert J. Ursano. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457136.003.0014.
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This chapter reviews the neurochemistry and epigenetics of posttraumatic stress disorder (PTSD). Traditional views of the neurochemistry of PTSD focus on alterations in classical central nervous system neurotransmitters serotonin and norepinephrine and pathological reactivity in the hypothalamic-pituitary-adrenal axis, and these are only briefly noted here. Instead, the chapter emphasizes a series of new conceptualizations and neurochemical data that have recently been elucidated. One is the recognition of the symptoms and neurobiology of PTSD as a moving target, being very different in different stages of illness evolution. Differences are apparent in the neurochemistry involved in early life stressor-related vulnerabilities to PTSD, the acute stress reaction, compensation and resolution phases, or ongoing chronicity with sleep disturbance, nightmares, flashbacks, hyperarousal, and dulling and depression. The neurochemical abnormalities vary as a function of this temporal unfolding and the common acquisition and progression of comorbid syndromes of alcohol and substance abuse.
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Maltzman, Sara. A Multidisciplinary, Biopsychosocial Approach to Treatment. Edited by Sara Maltzman. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199739134.013.43.
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This concluding chapter of theOxford Handbook of Treatment Processes and Outcomes in Psychologydescribes the importance of breaking down research and practice silos in favor of a multidisciplinary and biopsychosocial approach regarding human physical and mental health. The chapter summarizes why we can have more confidence in treatments and interventions that “fit” within the context of converging lines of evidence across these multilevel systems. What multidisciplinary research tells us is that treatmentdoesmatter, as evidenced by multiple lines of research in animal models, particularly in fear-based and anxiety disorders. This research affirms that psychological/behavioral treatments are active and not reducible to nonspecific placebo effects. However, data indicate that placebo may prove valuable as a deliberately applied adjunct to psychological/behavioral and pharmacological treatments. Individual differences in self-regulation and temperament; genetic and epigenetic factors that influence resilience or maladaptive responses to adverse conditions; the buffering effects of social support; and how these factors may influence treatment process and outcomes are reviewed. Research evaluating pharmacological adjuncts to psychological/behavioral treatment underscores the complexity of delivering optimal treatment. Newer methodologies, such as neuroimaging, will assist in explicating the above complex interrelationships. This chapter also calls attention to research evaluating treatment outcomes, including dose response relationships and the importance of evaluating the therapist’s unique contribution to outcomes.
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Burdick, Katherine E., Luz H. Ospina, Stephen J. Haggarty, and Roy H. Perlis. The Neurobiology and Treatment of Bipolar Disorder. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0020.
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Bipolar disorder (BPD) is a severe mood disorder that often has psychotic features. Its most severe forms are more common and significantly more likely to cause disability than originally thought. Studies of high-risk children have found them to be at increased risk for a variety of symptoms and neurobiological abnormalities. In contrast to schizophrenia, there is no formal prodromal syndrome that has been identified, and cognitive abnormalities do not precede the onset of the disorder. Abnormal sleep and circadian rhythms are prominent and have led to intriguing biological models. Neurobiological experiments have primarily focused on candidate pathways and include circadian abnormalities, epigenetic processes including histone modification, WNT/GSK3 signaling, other modulators of neuroplasticity, and mitochondrial dysfunction. Recent data suggest that BPD is a highly polygenic disease and that integration of prior modeling and data with the wide variety of new genetic risk loci will be productive in the future.
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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0038.
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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.
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Holroyd, Christopher R., Nicholas C. Harvey, Mark H. Edwards, and Cyrus Cooper. Environment. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0038_update_001.
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Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.
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Perkins, Elizabeth C., Shaun P. Brothers, and Charles B. Nemeroff. Animal Models for Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0024.
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Animal models of post-traumatic stress disorder (PTSD) provide a wellspring of biological information about this complex condition by providing the opportunity to manipulate trauma exposure and measure biological outcomes in a systematic manner that is not possible in clinical studies. Symptoms of PTSD may be induced in animals by physical (immobilization, foot shock, underwater stress) and psychological stressors (exposure to predator, social defeat, early life trauma) or a combination of both. In addition, genetic, epigenetic and transgenic models have been created by breeding animals with a behavioral propensity for maladaptive stress response or by directly manipulating genes that have been implicated in PTSD. The effect of stressors in animals is measured by a variety of means, including observation of behavior, measurement of structural alterations in the brain and of physiological markers such as HPA axis activity and altered gene expression of central nervous system neurotransmitter system components including receptors. By comparing changes observed in stress exposed animals to humans with PTSD and by comparing animal response to treatments that are effective in humans, we can determine the validity of PTSD animal models. The identification of a reliable physiological marker of maladaptive stress response in animals as well as standard use of behavioral cutoff criteria are critical to the development of a valid animal model of PTSD.
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Westfall, Nils C., and Charles B. Nemeroff. Child Abuse and Neglect as Risk Factors for Post-Traumatic Stress Disorder. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0025.
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Child abuse and neglect confer substantially increased risks of developing post-traumatic stress disorder (PTSD) for the victims and possibly even their offspring. Furthermore, they are associated with more severe and treatment-resistant PTSD and common comorbid conditions, such as major depressive disorder. This chapter begins by discussing the epidemiology of child abuse, neglect, and maltreatment-associated PTSD to provide a sense of the nature and scope of these major public health problems, then describes the major ways in which child abuse and neglect may contribute to increased liability to PTSD: maltreatment, victim, and environmental factors; neurobiological changes, including neuroendocrine, neurotransmitter system, structural and functional neuroimaging, inflammatory, and epigenetic changes; interactions with risk gene alleles; and cognitive, psychological, and behavioral changes. A discussion of the implications of this knowledge for future research and the development of new treatments for child maltreatment–associated PTSD follows.
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Kapczinski, Flávio, Michael Berk, and Pedro Vieira da Silva Magalhães, eds. Neuroprogression in Psychiatry. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198787143.001.0001.
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Psychiatric disorders are characterized by an overlapping set of pathophysiological pathways that include monoamines but also neurotrophins, apoptotic and mitochondrial pathways, epigenetics, and dysregulation of immunity and redox balance, counterbalanced by cellular resilience and defence pathways and the effects of treatment. These conspire in a subset of individuals to cause changes in brain function and, over time, the activity of these pathways in chronic psychiatric disorders can lead to cognitive sequelae and changes in brain structure. This can lead to differences between early and late stages of illness. These biological underpinnings could explain why late-stage patients are more prone to treatment refractoriness, progressive brain changes, and consequent cognitive and functioning impairment. This process is understood under the construct of neuroprogression, which refers to the pathological rewiring of the brain underlying the clinical and cognitive changes that underpin the staged progression of the illness, caused by activities of the aforementioned biological pathways. It is important to note that the brain can adapt to the challenges of the environment and respond to medications to ameliorate this process. Understanding the process of neuroprogression provides a window into the core biology of the disorder and opens the door to therapeutic approaches addressing these pathways. This book is an account of the state of the art in the field of neuroprogression in different psychiatric disorders.
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Barañano, Kristin W. Angelman Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0055.
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Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by maternal deficiency of the epigenetically imprinted gene UBE3A. It is characterized by severe developmental delay, an ataxic gait disorder, an apparent happy demeanor with frequent smiling or laughing, and severe expressive language impairments. Understanding the neurobiology of AS has focused on understanding how UBE3A is regulated by neuronal activity, as well as the targets of its ubiquitin E3 ligase activity. This has led to a model of the role of UBE3A in the regulation of experience-dependent sculpting of synaptic circuits. At this time, treatment is largely supportive, but efforts directed toward reversing the epigenetic silencing machinery may lead to improved synaptic function in AS patients.
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Survivor café: The legacy of trauma (and the) labyrinth of memory. Counterpoint, 2017.
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Johnston, Michael V. Coffin-Lowry Syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0057.
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Coffin-Lowry syndrome (CLS) is a relatively rare (1:50,000-100,000 incidence) sex-linked neurodevelopmental disorder that includes severe intellectual disability, dysmorphic features including facial and digital abnormalities, growth retardation, and skeletal changes. Most cases are sporadic with only 20% to 30% of cases having an additional family member. CLS is caused by variable loss of function mutations in the RPS6KA3 gene that maps to Xp22.2 and codes for the hRSK2 S6 kinase that phosphorylates the transcription factor CREB (cAMP response element binding protein) as well as other nuclear transcription factors. Phosphorylated CREB (pCREB) plays a major role in memory formation in fruit flies and mammals by activating specific genes through epigenetic histone acetylation.
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Post, Robert M. Depression as a Recurrent, Progressive Illness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0003.
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Clinical Highlights and summary of Chapter• Episodes of depression and bipolar illness progress in two ways:faster recurrences as a function of number of prior episodes, andgreater autonomy (decreased need for precipitation by stressors(Episode Sensitization)• Recurrent stressors result in increased reactivity to subsequent stressors(Stress sensitization) and bouts of stimulant abuse increase in severity with repetition(Stimulant-induced behavioral sensitization)• Each type of sensitization cross-sensitizes to the others and drives illness progression• Each type of sensitization involves specific memory-like epigenetic processes as well as nonspecific cellular toxicities• Childhood onset depression and bipolar illness have a more adverse course than adult onset illness and are increasing in incidence via a cohort (year of birth) effect• As opposed to genetic vulnerability, each type of sensitization can be prevented with appropriate clinical intervention and prevention, which should lessen illness severity and progression• Seeing depression and bipolar disorder as progressive illnesses changes the therapeutic emphasis away from acute treatment and instead to long term prophylaxis• Preventing recurrent depressions will likely protect the brain, the body, and the personWord count with Named refs = 6,417>Depression and bipolar disorder are illnesses which tend to progress with each new recurrence. Stressors, mood episodes, and bouts of substance abuse each sensitize (show increased reactivity) upon their repetition and cross-sensitization to the others. These sensitization processes appear to have a memory-like and epigenetic basis, in some instances conveying lifelong increased vulnerability to illness recurrence and progression. Greater numbers of episodes are associated with faster recurrences, lesser need for stress precipitation, cognitive dysfunction, pathological changes in brain, treatment refractoriness, and loss of many years of life expectancy, predominantly from cardiovascular disease. Such a perspective emphasizes the need for greater awareness of higher incidence of psychiatric and medical comorbidities in the United States compared to many European countries, and the need for earlier intervention and more sustained long term prophylaxis to prevent illness progression and its adverse consequences on brain and body.
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Charney, Dennis S., Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum, eds. Charney & Nestler's Neurobiology of Mental Illness. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.001.0001.
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In the years following publication of the DSM-5, the field of psychiatry has seen vigorous debate between the DSM’s more traditional, diagnosis-oriented approach and the NIMH’s more biological, dimension-based RDoC approach. Charney & Nestler’s Neurobiology of Mental Illness is an authoritative foundation for translating information from the laboratory to clinical treatment, and this edition extends beyond its reference function to acknowledge and examine the controversies and thoughts on the future of psychiatric diagnosis. In this wider context, this book provides information from numerous levels of analysis including molecular biology and genetics, cellular physiology, neuroanatomy, neuropharmacology, epidemiology, and behavior. Section I, which reviews the methods used to examine the biological basis of mental illness in animal and cell models and in humans, has been expanded to reflect important technical advances in complex genetics, epigenetics, stem cell biology, optogenetics, neural circuit functioning, cognitive neuroscience, and brain imaging. These established and emerging methodologies offer groundbreaking advances in our ability to study the brain and breakthroughs in our therapeutic toolkit. Sections II through VII cover the neurobiology and genetics of major psychiatric disorders: psychoses, mood disorders, anxiety disorders, substance use disorders, dementias, and disorders of childhood onset. Also covered within these sections is a summary of current therapeutic approaches for these illnesses as well as the ways in which research advances are now guiding the search for new treatments. The last section, Section VIII, focuses on diagnostic schemes for mental illness. This includes an overview of the unique challenges that remain in diagnosing these disorders given our still limited knowledge of disease etiology and pathophysiology. The section then provides reviews of DSM-5 and RDoC. Also included are chapters on future efforts toward precision and computational psychiatry, which promise to someday align diagnosis with underlying biological abnormalities.
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Incayawar, Mario, and Sioui Maldonado Bouchard, eds. Overlapping Pain and Psychiatric Syndromes. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190248253.001.0001.
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When a health practitioner is at the bedside of a patient suffering from chronic pain and a psychiatric comorbid condition, he is facing a true clinical conundrum. The comorbidity is frequent yet poorly understood, the diagnosis is difficult and the treatment that follows is less than appropriate. Pain conditions and psychiatric disorders have customarily been understood and treated as different and separate clinical entities, to the detriment of patients’ wellbeing. Fathoming the overlapping pain and psychiatric disorders is in the interest of everyone involved in healthcare, including doctors, nurses, pain specialists, psychiatrists, social workers, psychologists, hospital administrators, and health policymakers. There is a wide overlap of chronic pain conditions and psychiatric disorders. Pain and psychiatric comorbidity is frequent in the population, yet it is poorly understood. The societal burden of mental illness and pain is enormous; it could approach one trillion dollars annually in the USA. Compounding to the economic burden, are the liability related to stigma, shame, bias, discrimination, health disparities, inequities in care, and health injustice. Recent scientific and technological developments in digital medicine, artificial intelligence, pharmacogenetics, genetics, epigenetics, and neuroscience promise beneficial quality changes to medical care and education. The pain medicine and psychiatry of the future will consider patients as human beings embedded in their physical and social environments. This book provides a glimpse in that direction.
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Glover, Vivette. Maternal Stress During Pregnancy and Infant and Child Outcome. Edited by Amy Wenzel. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199778072.013.006.
Full textAbstract:
Many independent prospective studies show maternal stress, anxiety, or depression during pregnancy poses an increased risk for her child to have a wide range of adverse outcomes including emotional problems, ADHD or conduct disorder, or impaired cognitive development. Several studies have shown that these adverse outcomes are independent of possible confounding factors, such as postpartum anxiety and depression. Most children are not affected, and those who are can be affected in different ways, probably due to different genetic vulnerabilities and the quality of postpartum care. An evolutionary explanation for the observed changes is proposed. Underlying mechanisms are just starting to be understood: altered function of the placenta, allowing more of the stress hormone cortisol to pass through to the fetus, may well be important, as may epigenetic changes. The implications are that improved emotional care of pregnant women should improve outcomes for their children to a clinically significant degree.
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Krochmal, Robert. Nutritional Support and Addiction. Edited by Shahla J. Modir and George E. Muñoz. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190275334.003.0017.
Full textAbstract:
Nutrition occupies a central position in the treatment of SUDs. Given the paradox that food can have apparently opposing effects in either causing addiction or in influencing its remedy, it is important to clarify this difference. Evidence is mounting that diseases such as obesity, heart disease, diabetes, and mental health disorders including addiction have a common root cause related to the increase in sugar and processed food consumption rather than fat consumption as has been commonly held. In addition to new integrative approach models encompassing a holistic perspective, new developments in genetics and epigenetics as well as the human microbiome and gut-brain health provide further evidence of the mechanisms by which a healthy approach to nutrition can change outcomes. Building upon the neurobiological theory of addiction and reward deficiency, these breakthroughs lead to new hope for a successful approach to recovery.
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Beauchaine, Theodore P., and Maureen Zalewski. Physiological and Developmental Mechanisms of Emotional Lability in Coercive Relationships. Edited by Thomas J. Dishion and James Snyder. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199324552.013.5.
Full textAbstract:
Thestaticapproach to characterizing psychopathology classifies disorders syndromally, with little attention to development or social risk mediators. This approach, founded on biological reductionism, characterizes particular syndromes as arising from genetic and/or neural dysfunctions. In contrast, thehigh-riskapproach emphasizes exposure to adversity, with little consideration of neurobiology. Since neurobiological vulnerability × environmental risk interactions often account for more variance in developmental outcomes than do main effects, studying either in isolation can be misleading. This chapter presents an ontogenic process perspective in which neurobiological vulnerabilities interact with coercive family processes to shape and maintain emotional lability and emotion dysregulation—hallmarks of psychopathology. It emphasizes bidirectional transactions across levels of analysis (e.g., behavior ↔ autonomic function), mechanisms through which physiological systems adapt to coercion (neural plasticity, epigenesis), generalization of coercive behaviors across contexts (family, peer groups), and distinct functions of neurobiological systems in transmitting coercive behavior.
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Stoddard, Frederick J., and Robert L. Sheridan. Wound Healing and Depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0009.
Full textAbstract:
Depression and wound healing are bidirectional processes for adults and children consistent with the conception of depression as systemic. This systemic interaction is similar to the “bidirectional impact of mood disorder on risk for development, progression, treatment, and outcomes of medical illness” generally. And, evidence is growing that the bidirectional impact of mood disorder may be true for injuries and for trauma surgery. Animal models have provided some support that treatment of depression may improve wound healing. An established biological model for a mechanism delaying wound healing is increased cortisol secretion secondary to depression and/or stress, and impaired immune response, in addition or together with the other factors such as genetic or epigenetic risk for depression. Cellular models relate both to wound healing and to depression include cytokines, the inflammatory response (Miller et al, 2008), and cellular aging (Telgenhoff and Shroot, 2005) reflected in shorter leukocyte telomere length (LTL) (Verhoeven et al, 2016). Another model of stress impacting wound healing investigated genetic correlates—immediate early gene expression or IEG from the medial prefrontal cortex, and locomotion, in isolation-reared juvenile rats. Levine et al (2008) compared isolation reared to group reared samples, and found that, immediate gene expression in the medial prefrontal cortex (mPFC) was reduced, and behavioral hyperactivity increased, in juvenile rats with 20% burn injuries. Wound healing in the isolation reared rats was significantly impaired. They concluded that these results provide candidates for behavioral biomarkers of isolation rearing during physical injury, i.e. reduced immediate mPFC gene expression and hyperactivity. They suggested that a biomarker such as IEGs might aid in demarcating patients with resilient and adaptive responses to physical illness from those with maladaptive responses
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Masino, PHD, Susan A., ed. Ketogenic Diet and Metabolic Therapies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.001.0001.
Full textAbstract:
Ketogenic diets have been used to treat epilepsy for nearly a century. Alongside enduring clinical success with a ketogenic diet, metabolism’s critical role in health and in diseases in the central nervous system and throughout the body is increasingly appreciated. Furthermore, metabolism-based strategies have been proven equal or even superior to pharmacological treatments in specific cases and for specific diseases. Rather than causing unwanted off-target pharmacological side effects, addressing metabolic dysfunction can improve overall health simultaneously. Enduring interest in the ketogenic diet’s proven efficacy in stopping seizures and emerging efficacy in other disorders has fueled renewed efforts to determine key mechanisms and diverse applications of metabolic therapies. In parallel, multiple strategies are being developed to mobilize similar metabolic benefits without reliance on such a strict diet. Research interest in metabolic therapies has spread into laboratories and clinics of every discipline, and could yield entirely new classes of drugs and treatment regimens. This work is the first comprehensive scientific resource on the ketogenic diet, covering the latest research into the mechanisms, established and emerging applications, metabolic alternatives, and implications for health and disease. Experts in clinical and basic research share their research into mechanisms spanning from ion channels to epigenetics, their insights based on decades of experience with the ketogenic diet in epilepsy, and their evidence for emerging applications ranging from autism to Alzheimer’s disease to brain cancer.