1 4067 126 MATERNAL AND PEDIATRIC HEALTH AND DISEASE: INTEGRATING BIOPSYCHOSOCIAL MODELS AND EPIGENETICS. THE CONCEPTS OF ALLOSTASIS (STABILITY THROUGH ADAPTATION) AND ACCUMULATED LIFE STRESS (MCEWEN'S ALLOSTATIC LOAD) AIM TO UNDERSTAND CHILDHOOD AND ADULT OUTCOMES. CHRONIC MALNUTRITION, CHANGES IN SOCIAL CONDITION, AND ADVERSE EARLY-LIFE EXPERIENCES MAY PROGRAM PHENOTYPES AND CONTRIBUTE TO LONG-LASTING DISEASE RISK. HOWEVER, INTEGRATION OF LIFE COURSE APPROACHES, SOCIAL AND ECONOMIC CONTEXTS, AND COMPARISON AMONG DIFFERENT BIOPSYCHOSOCIAL MODELS HAS NOT GENERALLY BEEN EXPLORED. THIS REVIEW CRITICALLY EXAMINES THE LITERATURE AND EVALUATES RECENT INSIGHTS INTO HOW ENVIRONMENTAL STRESS CAN ALTER LIFELONG HYPOTHALAMIC-PITUITARY-ADRENAL AXIS AND IMMUNE SYSTEM RESPONSIVENESS AND INDUCE METABOLIC AND NEURODEVELOPMENTAL MALADAPTATION. MODELS OF BIOPSYCHOSOCIAL STRESS OVERLAP BUT MAY CONSIDER DIFFERENT CONDITIONS. CONCEPTS INCLUDE ALLOSTASIS, WHICH INCORPORATES HORMONAL RESPONSES TO PREDICTABLE ENVIRONMENTAL CHANGES, AND GERONIMUS'S "WEATHERING," WHICH AIMS TO EXPLAIN HOW SOCIALLY STRUCTURED, REPEATED STRESS CAN ACCUMULATE AND INCREASE DISEASE VULNERABILITY. WEATHERING EMPHASIZES ROLES OF INTERNALIZED/INTERPERSONAL RACISM IN OUTCOMES DISPARITIES. FOR MEXICAN IMMIGRANTS AND MEXICAN AMERICANS, THE "ACCULTURATION" FRAMEWORK HAS PROVEN ESPECIALLY USEFUL TO EXPLORE DISPARITIES, INCLUDING PRETERM BIRTH AND NEUROPSYCHIATRIC RISKS IN CHILDHOOD. COMPLEXITIES OF STRESS ASSESSMENTS AND RECENT RESEARCH INTO EPIGENETIC MECHANISMS MEDIATING EFFECTS OF PHYSICAL, NUTRITIONAL, PSYCHOLOGICAL, AND SOCIAL STRESS ARE REVIEWED. 2016 2 29 32 A BIOPSYCHOSOCIAL OVERVIEW OF THE OPIOID CRISIS: CONSIDERING NUTRITION AND GASTROINTESTINAL HEALTH. THE OPIOID CRISIS HAS REACHED EPIDEMIC PROPORTIONS IN THE UNITED STATES WITH RISING OVERDOSE DEATH RATES. IDENTIFYING THE UNDERLYING FACTORS THAT CONTRIBUTE TO ADDICTION VULNERABILITY MAY LEAD TO MORE EFFECTIVE PREVENTION STRATEGIES. SUPPLY SIDE ENVIRONMENTAL FACTORS ARE A MAJOR CONTRIBUTING COMPONENT. PSYCHOSOCIAL FACTORS SUCH AS STRESS, TRAUMA, AND ADVERSE CHILDHOOD EXPERIENCES HAVE BEEN LINKED TO EMOTIONAL PAIN LEADING TO SELF-MEDICATION. GENETIC AND EPIGENETIC FACTORS ASSOCIATED WITH BRAIN REWARD PATHWAYS AND IMPULSIVITY ARE KNOWN PREDICTORS OF ADDICTION VULNERABILITY. THIS REVIEW ATTEMPTS TO PRESENT A BIOPSYCHOSOCIAL APPROACH THAT CONNECTS VARIOUS SOCIAL AND BIOLOGICAL THEORIES RELATED TO THE ADDICTION CRISIS. THE EMERGING ROLE OF NUTRITION THERAPY WITH AN EMPHASIS ON GASTROINTESTINAL HEALTH IN THE TREATMENT OF OPIOID USE DISORDER IS PRESENTED. THE BIOPSYCHOSOCIAL MODEL INTEGRATES CONCEPTS FROM SEVERAL DISCIPLINES, EMPHASIZING MULTICAUSALITY RATHER THAN A REDUCTIONIST APPROACH. POTENTIAL SOLUTIONS AT MULTIPLE LEVELS ARE PRESENTED, CONSIDERING INDIVIDUAL AS WELL AS POPULATION HEALTH. THIS SINGLE COHESIVE FRAMEWORK IS BASED ON THE INTERDEPENDENCY OF THE ENTIRE SYSTEM, IDENTIFYING RISK AND PROTECTIVE FACTORS THAT MAY INFLUENCE SUBSTANCE-SEEKING BEHAVIOR. NUTRITION SHOULD BE INCLUDED AS ONE FACET OF A MULTIDISCIPLINARY APPROACH TOWARD IMPROVED RECOVERY OUTCOMES. CROSS-DISCIPLINARY COLLABORATIVE EFFORTS, NEW IDEAS, AND FISCAL RESOURCES WILL BE CRITICAL TO ADDRESS THE EPIDEMIC. 2019 3 6478 33 TOPICAL REVIEW: THE EMERGING FIELD OF EPIGENETICS: INFORMING MODELS OF PEDIATRIC TRAUMA AND PHYSICAL HEALTH. OBJECTIVE: TRAUMA EXPERIENCED DURING CHILDHOOD AND ADOLESCENCE HAS BEEN LINKED TO A NUMBER OF CHRONIC MEDICAL CONCERNS. WE HIGHLIGHT MAJOR FINDINGS FROM THE PEDIATRIC TRAUMA LITERATURE TO PROVIDE A MODEL FOR UNDERSTANDING THIS ASSOCIATION. METHODS: STUDIES EXAMINING THE EFFECTS OF TRAUMA WERE SYSTEMATICALLY REVIEWED AND SYNTHESIZED INTO A MODEL PROPOSING A CENTRAL ROLE FOR EPIGENETICS IN THE WAYS THAT CHILDHOOD EXPERIENCES CAN AFFECT HEALTH. RESULTS: EARLY HYPOTHALAMIC PITUITARY ADRENAL (HPA) AXIS RESPONSE MAY IMPACT INITIAL TRAUMA EXPERIENCE, WITH DOWNSTREAM EFFECTS ON POSTTRAUMA ADJUSTMENT REFLECTED IN POSTTRAUMA NEUROBIOLOGY, PSYCHOLOGICAL HEALTH, AND PHYSICAL HEALTH. CONCLUSIONS: PROSPECTIVE RESEARCH WITH CHILDREN AND ADOLESCENTS EXPOSED TO TRAUMA IS NEEDED TO BETTER CHARACTERIZE THE GENETIC AND EPIGENETIC INFLUENCES ON THE COURSE OF HPA AND IMMUNE PROCESSES AS RELATED TO POSTTRAUMA PSYCHOLOGICAL AND PHYSICAL HEALTH OUTCOMES. 2016 4 6266 17 THE NEUROBIOLOGY OF SUICIDE. THE STRESS-DIATHESIS MODEL POSITS THAT SUICIDE IS THE RESULT OF AN INTERACTION BETWEEN STATE-DEPENDENT (ENVIRONMENTAL) STRESSORS AND A TRAIT-LIKE DIATHESIS OR SUSCEPTIBILITY TO SUICIDAL BEHAVIOUR, INDEPENDENT OF PSYCHIATRIC DISORDERS. FINDINGS FROM POST-MORTEM STUDIES OF THE BRAIN AND FROM GENOMIC AND IN-VIVO NEUROIMAGING STUDIES INDICATE A BIOLOGICAL BASIS FOR THIS DIATHESIS, INDICATING THE IMPORTANCE OF NEUROBIOLOGICAL SCREENING AND INTERVENTIONS, IN ADDITION TO COGNITIVE AND MOOD INTERVENTIONS, IN THE PREVENTION OF SUICIDE. EARLY-LIFE ADVERSITY AND EPIGENETIC MECHANISMS MIGHT EXPLAIN SOME OF THE LINK BETWEEN SUICIDE RISK AND BRAIN CIRCUITRY AND NEUROCHEMISTRY ABNORMALITIES. RESULTS FROM A RANGE OF STUDIES USING DIVERSE DESIGNS AND POST-MORTEM AND IN-VIVO TECHNIQUES SHOW IMPAIRMENTS OF THE SEROTONIN NEUROTRANSMITTER SYSTEM AND THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS STRESS-RESPONSE SYSTEM IN THE DIATHESIS FOR SUICIDAL BEHAVIOUR. THESE IMPAIRMENTS MANIFEST AS IMPAIRED COGNITIVE CONTROL OF MOOD, PESSIMISM, REACTIVE AGGRESSIVE TRAITS, IMPAIRED PROBLEM SOLVING, OVER-REACTIVITY TO NEGATIVE SOCIAL SIGNS, EXCESSIVE EMOTIONAL PAIN, AND SUICIDAL IDEATION, LEADING TO SUICIDAL BEHAVIOUR. BIOMARKERS RELATED TO THE DIATHESIS MIGHT HELP TO INFORM RISK-ASSESSMENT PROCEDURES AND TREATMENT CHOICE IN THE PREVENTION OF SUICIDE. 2014 5 2509 21 EPIGENETICS AND PAIN: NEW INSIGHTS TO AN OLD PROBLEM. PHYSICIANS AND NEUROSCIENTISTS HAVE LONG OBSERVED THAT FACTORS SUCH AS THOUGHTS, EMOTIONS, AND EXPECTATIONS CAN INFLUENCE THE PERCEPTION OF PAIN. PAIN CAN BE DESCRIBED AS AN UNPLEASANT SENSATION THAT CAUSES PHYSICAL DISCOMFORT AND EMOTIONAL DISTRESS. IT ALERTS AN INDIVIDUAL TO SEEK HELP AND IS THE MAIN COMPLAINT THAT BRINGS INDIVIDUALS TO PHYSICIANS. THOUGH IT IS ASSOCIATED WITH PROBABLE TISSUE DAMAGE, SUCH DAMAGE MAY BE SUBTLE, SOMETIMES INVOLVING THE RELEASE OF ALGESIC CHEMICALS, AND ALSO INFLUENCED BY ATTITUDES, BELIEFS, PERSONALITY, AND SOCIAL FACTORS. THE PERCEPTION OF PAIN MAY VARY DUE TO A MULTITUDE OF THESE FACTORS INFLUENCING THE ASCENDING SENSORY IMPULSE PROPAGATION TO THE PRIMARY SOMATOSENSORY CORTEX. THE GENETICS AND EPIGENETICS OF PAIN MODULATORS HAVE BEEN PREVIOUSLY STUDIED, BUT THERE IS A LACK OF APPLICATION IN THE EVERYDAY MANAGEMENT AND TREATMENT OF PAIN DUE TO THE PAUCITY OF VALID EVIDENCE-BASED DATA. WE USED THE PUBMED DATABASE AS OUR PRIMARY TOOL FOR RESEARCHING CURRENT LITERATURE ON THIS TOPIC. THE MESH TERMS USED INCLUDED: GENE MODIFICATION, EPIGENETICS, GENES, PAIN, ANALGESIA, "TYPES OF PAIN, AND THEORIES OF PAIN. THE RESULTS WERE FILTERED AS FOLLOWS: PUBLICATIONS WITHIN THE LAST 10 YEARS, GENERALIZED PAIN STUDIES REGARDING THE BIOPSYCHOSOCIAL ASPECT OF PAIN, PERTINENT GENES, AND EPIGENETIC MODULATION OF THOSE GENES; 52 PUBLICATIONS WERE SELECTED FOR REVIEW. BY ADDRESSING THE EXTERNAL FACTORIAL CAUSES AND THE APPROPRIATE APPLICATION OF EPIGENETIC PRINCIPLES WHICH AFFECT PAIN PERCEPTION, IT IS HOPED THAT THIS REVIEW WILL MOTIVATE FUTURE ADVANCEMENTS IN THE MANAGEMENT OF ACUTE AND/OR CHRONIC PAIN. 2022 6 367 28 AMPLIFIED PAIN SYNDROMES IN CHILDREN: TREATMENT AND NEW INSIGHTS INTO DISEASE PATHOGENESIS. PURPOSE OF REVIEW: ALTHOUGH MANY DIAGNOSTIC TERMS ARE USED FOR PEDIATRIC CHRONIC PAIN, EVIDENCE SUGGESTS A COMMON THREAD OF SIGNAL AMPLIFICATION, LEADING TO THE UNIFYING TERM 'AMPLIFIED PAIN SYNDROMES'. ONGOING RESEARCH PROVIDES NEW INSIGHTS INTO BIOPSYCHOSOCIAL CONTRIBUTORS AND TREATMENTS FOR PEDIATRIC AMPLIFIED PAIN SYNDROMES. RECENT FINDINGS: BASIC SCIENCE INDICATES A COMPLEX INTERPLAY OF GENETIC, EPIGENETIC, NEUROCHEMICAL, ENDOCRINE, AND INFLAMMATORY CONTRIBUTORS, ALONG WITH ENVIRONMENTAL AND PSYCHOLOGICAL FACTORS. ALTHOUGH MEDICATIONS AND INTERVENTIONS REMAIN COMMON APPROACHES TO CHILDREN WITH CHRONIC PAIN, THEIR EVIDENCE IS LIMITED. PRELIMINARY EVIDENCE EXISTS FOR MINDFULNESS-BASED THERAPIES, YOGA, AND OTHER COMPLEMENTARY/ALTERNATIVE MEDICINE APPROACHES. THE STRONGEST EVIDENCE IS FOR EXERCISE-BASED AND COGNITIVE-BEHAVIORAL TREATMENTS, IN PARTICULAR, WHEN COMBINED IN A MULTIDISCIPLINARY FORMAT. INTENSIVE APPROACHES (PAIN REHABILITATION) HAVE THE POTENTIAL TO EFFECTIVELY AND EFFICIENTLY TREAT THOSE MOST DISABLED BY AMPLIFIED PAIN SYNDROMES, AND LEAD TO SUSTAINED IMPROVEMENT IN PAIN, FUNCTIONING, AND MEDICAL UTILIZATION. SUMMARY: ALTHOUGH UNDERSTANDING OF THE MECHANISMS UNDERLYING PEDIATRIC AMPLIFIED PAIN SYNDROMES EVOLVES, STANDARD OF CARE IS MULTIDISCIPLINARY EMPHASIZING EXERCISE THERAPY, COGNITIVE-BEHAVIORAL TREATMENT, AND SELF-REGULATION. TREATMENT SHOULD TARGET FULL RETURN TO PHYSICAL FUNCTION, WHICH LEADS TO SUBSEQUENT IMPROVEMENT OR RESOLUTION OF PAIN. MULTIDISCIPLINARY CARE CAN BE COORDINATED BY A RHEUMATOLOGIST OR OTHER PHYSICIAN WITH APPROPRIATE REFERRALS, OR THROUGH A MULTIDISCIPLINARY TEAM. 2014 7 3400 21 HOW CAN PRECISION MEDICINE BE APPLIED TO TEMPOROMANDIBULAR DISORDERS AND ITS COMORBIDITIES? THE EIGHTH SCIENTIFIC MEETING OF THE TMJ ASSOCIATION, LTD. WAS HELD IN BETHESDA, MARYLAND, SEPTEMBER 11-13, 2016. AS IN THE PAST, THE MEETING WAS COSPONSORED BY COMPONENTS OF THE NATIONAL INSTITUTES OF HEALTH WITH SPEAKERS INVITED TO REVIEW THE STATE OF TEMPOROMANDIBULAR DISORDER SCIENCE AND PROPOSE RECOMMENDATIONS TO FURTHER PROGRESS. THE THEME OF PRECISION MEDICINE, WHICH AIMS TO TAILOR DISEASE TREATMENT AND PREVENTION TO MATCH THE CHARACTERISTICS OF AN INDIVIDUAL PATIENT (GENETIC, EPIGENETIC, ENVIRONMENTAL, LIFESTYLE) UNDERSCORED THE CURRENT CONSENSUS THAT TEMPOROMANDIBULAR DISORDERS ARE NO LONGER VIEWED AS LOCAL CONDITIONS OF JAW PAIN AND DYSFUNCTION. RATHER, THEY REPRESENT A COMPLEX FAMILY OF BIOPSYCHOSOCIAL DISORDERS THAT CAN PROGRESS TO CHRONIC PAIN, MOST OFTEN ACCOMPANIED BY ONE OR MORE OTHER CHRONIC PAIN CONDITIONS. TEMPOROMANDIBULAR DISORDERS AND THESE COMORBIDITIES, CALLED CHRONIC OVERLAPPING PAIN CONDITIONS, PREDOMINANTLY OR EXCLUSIVELY AFFECT WOMEN IN THEIR CHILDBEARING YEARS AND REFLECT CENTRAL NERVOUS SYSTEM SENSITIZATION. PRESENTERS AT THE MEETING INCLUDED LEADERS IN TEMPOROMANDIBULAR DISORDER AND PAIN RESEARCH, TEMPOROMANDIBULAR DISORDER PATIENTS AND ADVOCATES, AND EXPERTS IN OTHER FIELDS OR IN THE USE OF TECHNOLOGIES THAT COULD FACILITATE THE DEVELOPMENT OF PRECISION MEDICINE APPROACHES IN TEMPOROMANDIBULAR DISORDERS. 2017 8 6620 25 UNDERSTANDING DEVELOPMENT AND PREVENTION OF CHRONIC PHYSICAL AGGRESSION: TOWARDS EXPERIMENTAL EPIGENETIC STUDIES. THE AIM OF THIS PAPER WAS TO HIGHLIGHT HOW DEVELOPMENTAL PSYCHOPATHOLOGY, EPIGENETICS AND PREVENTION EXPERIMENTS ARE STARTING TO BLEND TOGETHER TO EXPLAIN THE DEVELOPMENTAL CAUSES OF CHRONIC PHYSICAL AGGRESSION (CPA) AND, MORE IMPORTANTLY, TO HELP PREVENT CPA AND ITS ASSOCIATED PHYSICAL, MENTAL AND SOCIAL PROBLEMS. AFTER DEFINING THE KEYWORDS (PREVENTION, CHRONIC AND PHYSICAL AGGRESSION), A SELECTED REVIEW OF PUBLISHED STUDIES IS USED TO ANSWER THE FOLLOWING FOUR QUESTIONS: WHEN SHOULD WE ATTEMPT TO PREVENT ONSET OF CPA? WHAT ARE THE RISK FACTORS FOR CPA? HAVE EARLY CHILDHOOD INTERVENTIONS BEEN SHOWN TO PREVENT CPA? CAN EARLY PREVENTIVE INTERVENTIONS BENEFIT FROM EPIGENETIC STUDIES? THE LAST SECTION OF THIS PAPER GIVES TWO EXAMPLES OF EXPERIMENTAL PREVENTION DESIGNS THAT INTEGRATE PRESENT KNOWLEDGE OF CPA DEVELOPMENT, RISK FACTORS, EARLY CHILDHOOD PREVENTIVE INTERVENTIONS AND EPIGENETIC PROGRAMMING OF BRAIN DEVELOPMENT DURING PREGNANCY AND EARLY CHILDHOOD. I CONCLUDE THAT RANDOMIZED CONTROL TRIALS OF PREVENTIVE INTERVENTIONS DURING PREGNANCY AND EARLY CHILDHOOD WITH A SPECIFIC FOCUS ON EPIGENETIC EFFECTS ARE THE RESEARCH DESIGN MOST LIKELY TO ADVANCE OUR UNDERSTANDING OF THE BIOPSYCHOSOCIAL MECHANISMS THAT LEAD TO CPA, AND THE ONLY RESEARCH DESIGN THAT CAN IDENTIFY EFFECTIVE INTERVENTIONS FOR PREVENTING THE DEVELOPMENT OF CPA. 2008 9 6894 20 [SOCIAL INEQUALITY AND MENTAL HEALTH]. SOCIAL INEQUALITY REFERS TO THE INEQUITABLE DISTRIBUTION OF SOCIAL PROSPERITY INCLUDING THE RESOURCE OF HEALTH. THE RELATIONSHIP BETWEEN SOCIAL INEQUALITY AND MENTAL HEALTH CAN BE ESTABLISHED BY MEANS OF INDICATORS OF SOCIAL INEQUALITY THROUGHOUT ALL AGE GROUPS IN GERMANY. THERE ARE SOCIAL GRADIENTS OF MENTAL HEALTH ON THE POPULATION LEVEL, I.E. THE LINEAR RELATIONSHIP BETWEEN SOCIAL CLASSES OR STATUS AND STATE OF HEALTH. FUNDAMENTAL DETERMINANTS OF HEALTH DISPARITY ARE CULTURAL, SOCIAL, POLITICAL, AND GEOGRAPHICAL CONDITIONS, WHICH INTERACT WITH THE GENETIC MAKE-UP AND EPIGENETIC PROCESSES. THESE DETERMINANTS ALSO INFLUENCE THE MANAGEMENT OF DEVELOPMENTAL TASKS DURING THE LIFE COURSE AND ARE OF UTMOST IMPORTANCE FOR THE DEVELOPMENT OF MENTAL DISORDERS. THE MALADAPTATION TO CHRONIC STRESS IS AT THE CORE OF HEALTH DISPARITY. INTERVENTIONS AT THE INDIVIDUAL BEHAVIORAL LEVEL SHOULD COMPRISE THE DEVELOPMENT OF STRESS MANAGEMENT AND COPING STRATEGIES. 2019 10 2850 30 FROM CHILD ABUSE TO DEVELOPING BORDERLINE PERSONALITY DISORDER INTO ADULTHOOD: EXPLORING THE NEUROMORPHOLOGICAL AND EPIGENETIC PATHWAY. BORDERLINE PERSONALITY DISORDER (BPD) IS ONE OF THE MOST COMMON PERSONALITY DISORDERS SEEN IN THE GENERAL POPULATION. AMONG MULTIPLE IDENTIFIED RISK FACTORS, ONE OF THE MOST INFLUENTIAL ELEMENTS IS EXPOSURE TO AN ADVERSE CHILDHOOD EXPERIENCE IN TERMS OF EMOTIONAL, PHYSICAL, OR SEXUAL ABUSE. A CASCADE OF NEUROMORPHOLOGICAL AND EPIGENETIC CHANGES OCCURS IN RESPONSE TO THESE CHILDHOOD STRESSORS, WHICH MAY HAVE A STRONG LINK TO THE DEVELOPMENT OF BPD. PUBMED AND GOOGLE SCHOLAR WERE SEARCHED FOR ARTICLES RELEVANT TO CHILD ABUSE AND THE DEVELOPMENT OF BPD. THE SEARCH WAS NOT RESTRICTED TO ANY TIME FRAME OR GEOGRAPHIC LOCATION. SIGNIFICANT EPIGENETIC AND NEUROMORPHOLOGICAL CHANGES ARE SEEN WITH CHILD ABUSE, CONTRIBUTING TO THE DEVELOPMENT OF BPD. CHRONIC STRESSORS LEAD TO HYPOTHALAMIC-PITUITARY AXIS (HPA) ACTIVATION, RELEASING CORTISOL THAT ACTS ON THE PREFRONTAL CORTEX, AMYGDALA, AND HIPPOCAMPUS, PRODUCING THE BEHAVIORAL PATTERNS SEEN IN BPD. OVERSTIMULATION OF GRAY MATTER LEADS TO PERMANENT NEUROMORPHOLOGICAL CHANGES, WHICH CAN BE VISUALIZED IN FUNCTIONAL MRI/BRAIN SCANS. HYPERMETHYLATION OF MESSENGER RIBONUCLEIC ACID IN VARIOUS SITES SUGGESTS THE IMPACT OF CHILD ABUSE ON THE GENETIC LEVEL. INTERESTINGLY, THE PREVALENCE OF BPD IS SEEN EQUALLY IN BOTH GENDERS BUT IS DIAGNOSED MORE FREQUENTLY IN FEMALES BECAUSE THEY TEND TO BE MORE LIKELY TO SEEK HELP. UNDERSTANDING THE IMPACT OF EARLY AGE LIFE STRESSORS INTO ADULTHOOD CALLS FOR SERIOUS FOCUS ON EARLY DIAGNOSIS AND INTERVENTION. THIS IMPLIES THE NEED FOR MORE STUDIES IN PATIENTS WITH BPD WITH OR WITHOUT ANY CHILDHOOD TRAUMATIC EXPERIENCE AND A BETTER UNDERSTANDING OF THE CHANGES THAT OCCUR BIOPSYCHOLOGICALLY AND GENETICALLY IN RESPONSE TO TRAUMA. 2020 11 4006 29 LOST AMONG THE TREES? THE AUTONOMIC NERVOUS SYSTEM AND PAEDIATRICS. THE AUTONOMIC NERVOUS SYSTEM (ANS) HAS BEEN STRIKINGLY NEGLECTED IN WESTERN MEDICINE. DESPITE ITS PROFOUND IMPORTANCE FOR REGULATION, ADJUSTMENT AND COORDINATION OF BODY SYSTEMS, IT LACKS PRIORITY IN TRAINING AND PRACTICE AND RECEIVES SCANT ATTENTION IN NUMEROUS MAJOR TEXTBOOKS. THE ANS IS INTEGRAL TO MANIFESTATIONS OF ILLNESS, UNDERLYING FAMILIAR PHYSICAL AND PSYCHOLOGICAL SYMPTOMS. WHEN ANS ACTIVITY IS ITSELF DYSFUNCTIONAL, USUAL INDICATORS OF ACUTE ILLNESS MAY PROVE DECEPTIVE. RECOGNISING THE RELEVANCE OF THE ANS CAN INVOLVE SEEING THE FAMILIAR THROUGH FRESH EYES, CHALLENGING ASSUMPTIONS IN CLINICAL ASSESSMENT AND IN APPROACHES TO PRACTICE. ITS IMPORTANCE EXTENDS FROM PHYSICAL AND PSYCHOLOGICAL WELL-BEING TO PARENTING AND SAFEGUARDING, PUBLIC SERVICES AND THE FUNCTIONING OF SOCIETY. EXPLORATION OF ITS ROLE IN CONDITIONS RANGING FROM NEUROLOGICAL, GASTROINTESTINAL AND CONNECTIVE TISSUE DISORDERS, DIABETES AND CHRONIC FATIGUE SYNDROME, TO AUTISM, BEHAVIOURAL AND MENTAL HEALTH DIFFICULTIES MAY OPEN THERAPEUTIC AVENUES. THE ANS OFFERS A MECHANISM FOR SO-CALLED FUNCTIONAL ILLNESSES AND ILLUSTRATES THE IMPORTANCE OF RECOGNISING THAT 'STRESS' TAKES MANY FORMS, PHYSICAL, PSYCHOLOGICAL AND ENVIRONMENTAL, DESIRABLE AND OTHERWISE. EVIDENCE OF INTRAUTERINE AND POST-NATAL PROGRAMMING OF ANS REACTIVITY SUGGESTS THAT NEONATAL CARE AND SAFEGUARDING PRACTICE MAY OFFER PREVENTIVE OPPORTUNITY, AS MAY GREATER UNDERSTANDING OF EPIGENETIC CHANGE OF ANS ACTIVITY THROUGH, FOR EXAMPLE, ACCIDENTAL OR PSYCHOLOGICAL TRAUMA OR INFECTION. THE AIM OF THIS ARTICLE IS TO ACCELERATE RECOGNITION OF THE IMPORTANCE OF THE ANS THROUGHOUT PAEDIATRICS, AND OF THE POTENTIAL PHYSICAL AND PSYCHOLOGICAL COST OF NEGLECTING IT. 2014 12 47 34 A CONCEPTUAL MODEL OF BIOPSYCHOSOCIAL MECHANISMS OF TRANSITION FROM ACUTE TO CHRONIC POSTSURGICAL PAIN IN CHILDREN AND ADOLESCENTS. ACUTE AND CHRONIC PAIN ARE HIGHLY PREVALENT AND IMPACTFUL CONSEQUENCES OF SURGERY ACROSS THE LIFESPAN, YET A COMPREHENSIVE CONCEPTUAL MODEL ENCOMPASSING BIOPSYCHOSOCIAL FACTORS UNDERLYING ACUTE TO CHRONIC PAIN TRANSITION IS LACKING, PARTICULARLY IN YOUTH. BUILDING ON PRIOR CHRONIC POSTSURGICAL PAIN MODELS, WE PROPOSE A NEW CONCEPTUAL MODEL OF BIOPSYCHOSOCIAL MECHANISMS OF TRANSITION FROM ACUTE TO CHRONIC POSTSURGICAL PAIN. THIS REVIEW AIMS TO SUMMARIZE EXISTING RESEARCH EXAMINING KEY FACTORS UNDERLYING ACUTE TO CHRONIC POSTSURGICAL PAIN TRANSITION IN ORDER TO GUIDE PREVENTION AND INTERVENTION EFFORTS AIMED AT ADDRESSING THIS HEALTH ISSUE IN CHILDREN. AS PAIN TRANSITIONS FROM ACUTE NOCICEPTIVE PAIN TO CHRONIC PAIN, CHANGES IN THE PERIPHERAL AND CENTRAL NERVOUS SYSTEM CONTRIBUTE TO THE CHRONIFICATION OF PAIN AFTER SURGERY. THESE CHANGES INCLUDE ALTERATIONS IN SENSORY PAIN PROCESSING AND PSYCHOSOCIAL PROCESSES (PSYCHOLOGICAL, BEHAVIORAL, AND SOCIAL COMPONENTS), WHICH PROMOTE THE DEVELOPMENT OF CHRONIC PAIN. PATIENT-RELATED PREMORBID FACTORS (EG, DEMOGRAPHIC FACTORS, GENETIC PROFILE, AND MEDICAL FACTORS SUCH AS PREMORBID PAIN) MAY FURTHER MODULATE THESE CHANGES. FACTORS RELATED TO ACUTE INJURY AND RECOVERY (EG, SURGICAL AND TREATMENT FACTORS), AS WELL AS BIOLOGICAL RESPONSE TO SURGERY (EG, EPIGENETIC, INFLAMMATORY, AND ENDOCRINE FACTORS), MAY ALSO INFLUENCE THIS PROCESS. OVERALL, LONGITUDINAL STUDIES EXAMINING TEMPORAL PATHWAYS OF BIOPSYCHOSOCIAL PROCESSES INCLUDING BOTH RISK AND RESILIENCY FACTORS WILL BE ESSENTIAL TO IDENTIFY THE MECHANISMS INVOLVED IN THE TRANSITION FROM ACUTE TO CHRONIC PAIN. RESEARCH IS ALSO NEEDED TO UNRAVEL CONNECTIONS BETWEEN THE ACUTE PAIN EXPERIENCE, OPIOID EXPOSURE, AND SENSORY PAIN PROCESSING DURING ACUTE TO CHRONIC PAIN TRANSITION. FURTHERMORE, FUTURE STUDIES SHOULD INCLUDE LARGER AND MORE DIVERSE SAMPLES TO MORE FULLY EXPLORE RISK FACTORS IN A BROADER RANGE OF PEDIATRIC SURGERIES. THE USE OF CONCEPTUAL MODELS TO GUIDE INTERVENTION APPROACHES TARGETING MECHANISMS OF TRANSITION FROM ACUTE TO CHRONIC PAIN WILL SIGNIFICANTLY ADVANCE THIS FIELD AND IMPROVE OUTCOMES FOR CHILDREN AND ADOLESCENTS UNDERGOING SURGERY. 2020 13 6917 15 [WHOSE BORDERLINE IS IT? HYPOTHESIZED ETIOLOGIES OF BORDERLINE PERSONALITY]. BORDERLINE PERSONALITY IS A WELL KNOWN CONCEPT IN PSYCHIATRIC LITERATURE, HOWEVER, NOT FULLY UNDERSTOOD AS TO ITS VERY NATURE. THIS ARTICLE PRESENTS A SHORT REVIEW OF HYPOTHESIZED ETIOLOGIES OF THE BORDERLINE PERSONALITY, STARTING WITH SO CALLED TRADITIONAL THEORIES, NAMELY, BORDERLINE PERSONALITY AS A CONSOLIDATED PERSONALITY ORGANIZATION, IN WHICH THE PATIENT PATHOLOGICALLY DEALS WITH HIS OR HER INNER AGGRESSION, OR WITH AN ENDURING DEVELOPMENTAL FAILURE. MORE MODERN HYPOTHESES FOCUS ON POSSIBLE CHILDHOOD SEXUAL ABUSE AS THE ORIGIN OF THE BORDERLINE, VIEWING THE ADULT PERSONALITY AS A CHRONIC, UNRESOLVED, POST-TRAUMATIC DISORDER. ADDITIONALLY, A NEURO-EPIGENETIC VIEW HYPOTHESIZED THAT A UNIQUE CONGENITAL NEUROLOGICAL STRUCTURE INTERACTS WITH CONSEQUENTIAL EVENTS IN EARLY CHILDHOOD TO CREATE THE BORDERLINE PERSONALITY. 2008 14 6329 32 THE ROLE OF CHILDHOOD TRAUMA IN BIPOLAR DISORDERS. THIS REVIEW WILL DISCUSS THE ROLE OF CHILDHOOD TRAUMA IN BIPOLAR DISORDERS. RELEVANT STUDIES WERE IDENTIFIED VIA MEDLINE (PUBMED) AND PSYCINFO DATABASES PUBLISHED UP TO AND INCLUDING JULY 2015. THIS REVIEW CONTRIBUTES TO A NEW UNDERSTANDING OF THE NEGATIVE CONSEQUENCES OF EARLY LIFE STRESS, AS WELL AS SETTING CHILDHOOD TRAUMA IN A BIOLOGICAL CONTEXT OF SUSCEPTIBILITY AND DISCUSSING NOVEL LONG-TERM PATHOPHYSIOLOGICAL CONSEQUENCES IN BIPOLAR DISORDERS. CHILDHOOD TRAUMATIC EVENTS ARE RISK FACTORS FOR DEVELOPING BIPOLAR DISORDERS, IN ADDITION TO A MORE SEVERE CLINICAL PRESENTATION OVER TIME (PRIMARILY AN EARLIER AGE AT ONSET AND AN INCREASED RISK OF SUICIDE ATTEMPT AND SUBSTANCE MISUSE). CHILDHOOD TRAUMA LEADS TO ALTERATIONS OF AFFECT REGULATION, IMPULSE CONTROL, AND COGNITIVE FUNCTIONING THAT MIGHT DECREASE THE ABILITY TO COPE WITH LATER STRESSORS. CHILDHOOD TRAUMA INTERACTS WITH SEVERAL GENES BELONGING TO SEVERAL DIFFERENT BIOLOGICAL PATHWAYS [HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS, SEROTONERGIC TRANSMISSION, NEUROPLASTICITY, IMMUNITY, CALCIUM SIGNALING, AND CIRCADIAN RHYTHMS] TO DECREASE THE AGE AT THE ONSET OF THE DISORDER OR INCREASE THE RISK OF SUICIDE. EPIGENETIC FACTORS MAY ALSO BE INVOLVED IN THE NEUROBIOLOGICAL CONSEQUENCES OF CHILDHOOD TRAUMA IN BIPOLAR DISORDER. BIOLOGICAL SEQUELAE SUCH AS CHRONIC INFLAMMATION, SLEEP DISTURBANCE, OR TELOMERE SHORTENING ARE POTENTIAL MEDIATORS OF THE NEGATIVE EFFECTS OF CHILDHOOD TRAUMA IN BIPOLAR DISORDERS, IN PARTICULAR WITH REGARD TO PHYSICAL HEALTH. THE MAIN CLINICAL IMPLICATION IS TO SYSTEMATICALLY ASSESS CHILDHOOD TRAUMA IN PATIENTS WITH BIPOLAR DISORDERS, OR AT LEAST IN THOSE WITH A SEVERE OR INSTABLE COURSE. THE CHALLENGE FOR THE NEXT YEARS WILL BE TO FILL THE GAP BETWEEN CLINICAL AND FUNDAMENTAL RESEARCH AND ROUTINE PRACTICE, SINCE RECOMMENDATIONS FOR MANAGING THIS SPECIFIC POPULATION ARE LACKING. IN PARTICULAR, LITTLE IS KNOWN ON WHICH PSYCHOTHERAPIES SHOULD BE PROVIDED OR WHICH TARGETS THERAPISTS SHOULD FOCUS ON, AS WELL AS HOW CHILDHOOD TRAUMA COULD EXPLAIN THE RESISTANCE TO MOOD STABILIZERS. 2016 15 6073 19 THE DRESDEN BURNOUT STUDY: PROTOCOL OF A PROSPECTIVE COHORT STUDY FOR THE BIO-PSYCHOLOGICAL INVESTIGATION OF BURNOUT. OBJECTIVES: THE DRESDEN BURNOUT STUDY (DBS) IS A 12-YEAR LONGITUDINAL COHORT STUDY THAT AIMS TO PROVIDE A DESCRIPTION OF THE BURNOUT SYNDROME ON THE BASIS OF TIME AND SYMPTOM CRITERIA WITH A SPECIAL FOCUS ON THE SEARCH FOR BIOMARKERS. BIOLOGICAL AND PSYCHOSOCIAL APPROACHES ARE APPLIED TO EXAMINE THE LONG-TERM COURSE AND CONSEQUENCES OF BURNOUT WITHIN A POPULATION-BASED GERMAN-SPEAKING SAMPLE AGED 18 TO 68 YEARS. METHODS: DEMOGRAPHICS AND PSYCHOSOCIAL DATA ARE GENERATED BY ONLINE ASSESSMENTS, INCLUDING DEMOGRAPHICS AND QUESTIONNAIRES ON BURNOUT, BURNOUT-RELATED CONSTRUCTS, WORK-ENVIRONMENT, AND HEALTH-RELATED FACTORS. THE LAB-BASED BIOMARKER ASSESSMENT INCLUDES ENDOCRINE, PHYSIOLOGICAL, IMMUNOLOGICAL, AND EPIGENETIC MARKERS OBTAINED FROM BLOOD AND HAIR SAMPLES. IN ADDITION, HEART RATE VARIABILITY IS ALSO MEASURED REPEATEDLY. WITHIN THE FIRST 2 YEARS, THE DBS COLLECTED PSYCHOSOCIAL DATA FROM OVER 7,600 PARTICIPANTS WITH BIOLOGICAL DATA OBTAINED FROM MORE THAN 800 INDIVIDUALS. DURING THE FOLLOWING 10 YEARS, DETAILED ASSESSMENTS OF BIOMARKERS AND PSYCHOSOCIAL FACTORS WILL BE COLLECTED IN ANNUAL STUDY WAVES. RESULTS: RESULTS WILL BE GENERATED DURING THE FOLLOWING DECADE. CONCLUSION: THE FINDINGS OF THE DBS ARE EXPECTED TO PAVE THE ROAD FOR AN IN-DEPTH BIOPSYCHOSOCIAL CHARACTERIZATION OF BURNOUT AND TO GIVE INSIGHT INTO THE LONG-TERM COURSE AND POTENTIAL MENTAL AND PHYSICAL HEALTH CONSEQUENCES OF THE BURNOUT SYNDROME. 2018 16 3630 43 INCLUSION OF SOCIAL AND STRUCTURAL DETERMINANTS OF HEALTH TO ADVANCE UNDERSTANDING OF THEIR INFLUENCE ON THE BIOLOGY OF CHRONIC DISEASE. SOCIAL DETERMINANTS OF HEALTH (SDOH) CONSIDER SOCIAL, POLITICAL, AND ECONOMIC FACTORS THAT CONTRIBUTE TO HEALTH DISPARITIES IN PATIENTS AND POPULATIONS. THE MOST COMMON HEALTH-RELATED SDOH EXPOSURES ARE FOOD AND HOUSING INSECURITY, FINANCIAL INSTABILITY, TRANSPORTATION NEEDS, LOW LEVELS OF EDUCATION, AND PSYCHOSOCIAL STRESS. THESE DOMAINS DESCRIBE RISKS THAT CAN IMPACT HEALTH OUTCOMES MORE THAN HEALTH CARE. EPIDEMIOLOGIC AND TRANSLATIONAL RESEARCH DEMONSTRATES THAT SDOH FACTORS REPRESENT EXPOSURES THAT PREDICT HARM AND IMPACT THE HEALTH OF INDIVIDUALS. INTERNATIONAL AND NATIONAL GUIDELINES URGE HEALTH PROFESSIONALS TO ADDRESS SDOH IN CLINICAL PRACTICE AND PUBLIC HEALTH. THE FURTHER IMPLEMENTATION OF THESE RECOMMENDATIONS INTO BASIC AND TRANSLATIONAL RESEARCH, HOWEVER, IS LAGGING. HEREIN, WE CONSIDER A PRECISION HEALTH FRAMEWORK TO DESCRIBE HOW SDOH CONTRIBUTES TO THE EXPOSOME AND EXACERBATES PHYSIOLOGIC PATHWAYS THAT LEAD TO CHRONIC DISEASE. SDOH FACTORS ARE ASSOCIATED WITH VARIOUS FORMS OF STRESSORS THAT IMPACT PHYSIOLOGICAL PROCESSES THROUGH EPIGENETIC, INFLAMMATORY, AND REDOX REGULATION. MANY SDOH EXPOSURES MAY ADD TO OR POTENTIATE THE PATHOLOGIC EFFECTS OF ADDITIONAL ENVIRONMENTAL EXPOSURES. THIS OVERVIEW AIMS TO INFORM BASIC LIFE SCIENCE AND TRANSLATIONAL RESEARCHERS ABOUT SDOH EXPOSURES THAT CAN CONFOUND ASSOCIATIONS BETWEEN CLASSIC BIOMEDICAL DETERMINANTS OF DISEASE AND HEALTH OUTCOMES. TO ADVANCE THE STUDY OF TOXICOLOGY THROUGH EITHER QUALITATIVE OR QUANTITATIVE ASSESSMENT OF EXPOSURES TO CHEMICAL AND BIOLOGICAL SUBSTANCES, A MORE COMPLETE ENVIRONMENTAL EVALUATION SHOULD INCLUDE SDOH EXPOSURES. WE DISCUSS COMMON APPROACHES TO MEASURE SDOH FACTORS AT INDIVIDUAL AND POPULATION LEVELS AND REVIEW THE ASSOCIATIONS BETWEEN SDOH RISK FACTORS AND PHYSIOLOGIC MECHANISMS THAT INFLUENCE CHRONIC DISEASE. WE PROVIDE CLINICAL AND POLICY-BASED MOTIVATION TO ENCOURAGE RESEARCHERS TO CONSIDER THE IMPACT OF SDOH EXPOSURES ON STUDY RESULTS AND DATA INTERPRETATION. WITH VALID MEASURES OF SDOH FACTORS INCORPORATED INTO STUDY DESIGN AND ANALYSES, FUTURE TOXICOLOGICAL RESEARCH MAY CONTRIBUTE TO AN EVIDENCE BASE THAT CAN BETTER INFORM PREVENTION AND TREATMENT OPTIONS, TO IMPROVE EQUITABLE CLINICAL CARE AND POPULATION HEALTH. (C) 2022 WILEY PERIODICALS LLC. 2022 17 4622 20 NEUROBIOLOGICAL DEVELOPMENT IN THE CONTEXT OF CHILDHOOD TRAUMA. NEUROBIOLOGICAL SYSTEMS MAY BE PARTICULARLY SUSCEPTIBLE TO DELETERIOUS IMPACT OF CHILDHOOD TRAUMA, AND THE IMPACT OF CHILDHOOD TRAUMA ON DEVELOPMENT AND SUBSEQUENT FUNCTIONAL OUTCOMES ACROSS THE LIFESPAN HAS BEEN WELL-DOCUMENTED. THE CURRENT REVIEW ADDRESSES THE NEUROBIOLOGICAL IMPACT OF EXPOSURE TO INTERPERSONAL TRAUMA IN CHILDHOOD IN THE CONTEXT OF EXECUTIVE FUNCTION, EMOTION REGULATION, AND DISSOCIATION/INTEROCEPTIVE AWARENESS. SUBSEQUENT RISK FOR PTSD AND DEPRESSION IS ALSO DISCUSSED. THE PATHWAY OF RISK FROM CHILDHOOD TRAUMA TO THESE COGNITIVE, EMOTIONAL, AND PSYCHIATRIC OUTCOMES IS ADDRESSED IN TERMS OF POTENTIAL STRUCTURAL AND FUNCTIONAL ALTERATIONS WITHIN THE HIPPOCAMPUS, PREFRONTAL CORTEX, AND AMYGDALA RESULTING FROM CHRONIC OR REPEATED ACTIVATION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL (HPA) AXIS AND ITS INTERACTION WITH AND INFLUENCE ON GENETIC AND EPIGENETIC PROCESSES DURING SENSITIVE PERIODS OF DEVELOPMENT. IMPLICATIONS FOR PRACTICE ARE DISCUSSED. 2017 18 6626 27 UNDERSTANDING RESILIENCE. RESILIENCE IS THE ABILITY TO ADAPT SUCCESSFULLY IN THE FACE OF STRESS AND ADVERSITY. STRESSFUL LIFE EVENTS, TRAUMA, AND CHRONIC ADVERSITY CAN HAVE A SUBSTANTIAL IMPACT ON BRAIN FUNCTION AND STRUCTURE, AND CAN RESULT IN THE DEVELOPMENT OF POSTTRAUMATIC STRESS DISORDER (PTSD), DEPRESSION AND OTHER PSYCHIATRIC DISORDERS. HOWEVER, MOST INDIVIDUALS DO NOT DEVELOP SUCH ILLNESSES AFTER EXPERIENCING STRESSFUL LIFE EVENTS, AND ARE THUS THOUGHT TO BE RESILIENT. RESILIENCE AS SUCCESSFUL ADAPTATION RELIES ON EFFECTIVE RESPONSES TO ENVIRONMENTAL CHALLENGES AND ULTIMATE RESISTANCE TO THE DELETERIOUS EFFECTS OF STRESS, THEREFORE A GREATER UNDERSTANDING OF THE FACTORS THAT PROMOTE SUCH EFFECTS IS OF GREAT RELEVANCE. THIS REVIEW FOCUSES ON RECENT FINDINGS REGARDING GENETIC, EPIGENETIC, DEVELOPMENTAL, PSYCHOSOCIAL, AND NEUROCHEMICAL FACTORS THAT ARE CONSIDERED ESSENTIAL CONTRIBUTORS TO THE DEVELOPMENT OF RESILIENCE. NEURAL CIRCUITS AND PATHWAYS INVOLVED IN MEDIATING RESILIENCE ARE ALSO DISCUSSED. THE GROWING UNDERSTANDING OF RESILIENCE FACTORS WILL HOPEFULLY LEAD TO THE DEVELOPMENT OF NEW PHARMACOLOGICAL AND PSYCHOLOGICAL INTERVENTIONS FOR ENHANCING RESILIENCE AND MITIGATING THE UNTOWARD CONSEQUENCES. 2013 19 2646 26 EPIGENOMIC LINKS BETWEEN SOCIAL DETERMINANTS OF HEALTH AND SYMPTOMS: A SCOPING REVIEW. SOCIAL DETERMINANTS OF HEALTH (SDOH) IMPACT HEALTH AND WELLNESS. THE LINK BETWEEN SDOH AND ADVERSE HEALTH OUTCOMES, INCLUDING SYMPTOM OCCURRENCE AND SEVERITY, MAY BE EXPLAINED BY AN INDIVIDUAL'S PHYSIOLOGIC RESPONSE TO ONE OR MORE SDOH. ONE POTENTIAL MECHANISM UNDERLYING THIS PHYSIOLOGIC RESPONSE LINKING SDOH AND SYMPTOMS IS THE DYNAMIC EPIGENOME. THE PURPOSE OF THIS SCOPING REVIEW OF THE LITERATURE WAS TO EXAMINE DIFFERENTIAL SUSCEPTIBILITY FOR SYMPTOMS BY IDENTIFYING AND SUMMARIZING RESEARCH LINKING SDOH AND SYMPTOMS THROUGH EPIGENOMIC MECHANISMS. PUBMED WAS SEARCHED TO IDENTIFY EMPIRICAL RESEARCH WHERE AT LEAST ONE SDOH WAS AN INDEPENDENT OR DEPENDENT VARIABLE, AT LEAST ONE SYMPTOM WAS INVESTIGATED, AND THE INVESTIGATION INCLUDED AN EPIGENOMIC MEASURE. OF THE 484 ARTICLES INITIALLY RETRIEVED, AFTER THOROUGH VETTING, 41 ARTICLES MET ELIGIBILITY. THE MOST STUDIED SYMPTOM WAS DEPRESSIVE SYMPTOMS FOLLOWED BY ANXIETY, COGNITIVE FUNCTION, SLEEP DYSFUNCTION, AND PAIN. THE MOST FREQUENTLY STUDIED SDOH WERE: 1) STRESS, PARTICULARLY EARLY LIFE STRESS AND ACCULTURATIVE STRESS; AND 2) TRAUMA, PREDOMINANTLY CHILDHOOD TRAUMA. DNA METHYLATION AND TELOMERE LENGTH WERE THE MOST STUDIED EPIGENOMIC MEASURES. FOUR GENES (SLC6A4, BDNF, NR3C1, OXTR) HAD EVIDENCE FROM MULTIPLE STUDIES AND ACROSS METHODOLOGICAL APPROACHES LINKING SDOH TO SYMPTOMS. THIS REVIEW SUPPORTS THE INCLUSION OF EPIGENOMIC APPROACHES TO BETTER UNDERSTAND THE LINK BETWEEN SDOH AND SYMPTOMS AND PROVIDES EVIDENCE THAT SDOH IMPACT TELOMERE LENGTH AND THE METHYLATION OF GENES INVOLVED IN NEUROTRANSMITTER SIGNALING, NEURONAL SURVIVAL, BEHAVIOR, INFLAMMATION AND STRESS RESPONSE. 2023 20 704 32 BUILDING RESILIENCE AGAINST THE SEQUELAE OF ADVERSE CHILDHOOD EXPERIENCES: RISE UP, CHANGE YOUR LIFE, AND REFORM HEALTH CARE. A REFORMED APPROACH TO HEALTH CARE TACKLES HEALTH AT ITS ROOTS. ADVERSE CHILDHOOD EXPERIENCES (ACES) IN THOSE EXPOSED TO THEM MAY CONTRIBUTE SIGNIFICANTLY TO THE ROOT CAUSES OF MANY DISEASES OF LIFESTYLE. ACES ARE TRAUMATIC EXPERIENCES, SUCH AS PHYSICAL AND EMOTIONAL ABUSE AND EXPOSURE TO RISKY FAMILY ENVIRONMENTS. IN 1998, A GROUND-BREAKING STUDY FOUND THAT NEARLY 70% OF AMERICANS EXPERIENCE AT LEAST 1 ACE IN THEIR LIFETIME, AND GRADED EXPOSURE IS ASSOCIATED WITH THE PRESENCE OF MENTAL HEALTH DISORDERS, HEART DISEASE, CANCER, AND OTHER CHRONIC DISEASES. OVER THE PAST 20 YEARS, EVIDENCE HAS DEMONSTRATED FURTHER DISEASE RISK, OUTCOMES, AND EPIGENETIC UNDERPINNINGS IN CHILDREN AND ADULTS WITH ACES. BUILDING RESILIENCE-THE CAPACITY TO ADAPT IN HEALTHY WAYS TO TRAUMATIC EXPERIENCES-THROUGH LIFESTYLE MODIFICATION OFFERS POTENTIAL TO COMBAT THE NEGATIVE HEALTH EFFECTS ASSOCIATED WITH ACES. EMERGING RESEARCH DEMONSTRATES RESILIENCE IS CULTIVATED THROUGH INDIVIDUAL SKILLS (EMOTIONAL INTELLIGENCE, COPING, AND FOSTERING HEALTHY LIFESTYLE CHOICES), AND NURTURING SUPPORTIVE RELATIONSHIPS. BEING MINDFUL OF THE IMPACT AND PREVALENCE OF ACES AND DIVERSITY OF INDIVIDUALS' EXPERIENCES IN SOCIETY WILL HELP BUILD RESILIENCE AND COMBAT THE ROOT CAUSE OF CHRONIC DISEASE. THIS REVIEW AIMS TO CULTIVATE THAT AWARENESS AND WILL DISCUSS 3 OBJECTIVES: TO DISCUSS THE EFFECTS AND HYPOTHESIZED PATHOPHYSIOLOGICAL UNDERPINNINGS OF TRAUMATIC EXPERIENCES IN CHILDHOOD ON HEALTH AND WELLBEING THROUGHOUT LIFE, TO PRESENT WAYS WE CAN PROMOTE RESILIENCE IN OUR DAILY LIVES AND PATIENT ENCOUNTERS, AND TO DEMONSTRATE HOW ADVOCACY FOR THE REDUCTION OF ACES AND PROMOTION OF RESILIENT, TRAUMA-INFORMED ENVIRONMENTS ARE FUNDAMENTAL TO HEALTH CARE REFORM. 2019