1   704 150 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           
2  3579  34 IMPACT OF PATERNAL EDUCATION ON EPIGENETIC AGEING IN ADOLESCENCE AND MID-ADULTHOOD: A MULTI-COHORT STUDY IN THE USA AND MEXICO. BACKGROUND: BOTH PARENTAL AND NEIGHBOURHOOD SOCIO-ECONOMIC STATUS (SES) ARE LINKED TO POORER HEALTH INDEPENDENTLY OF PERSONAL SES MEASURES, BUT THE BIOLOGICAL MECHANISMS ARE UNCLEAR. OUR OBJECTIVE WAS TO EXAMINE THESE INFLUENCES VIA EPIGENETIC AGE ACCELERATION (EAA)-THE DISCREPANCY BETWEEN CHRONOLOGICAL AND EPIGENETIC AGES. METHODS: WE EXAMINED THREE USA-BASED [CORONARY ARTERY RISK DISEASE IN ADULTS (CARDIA) STUDY, FRAGILE FAMILIES AND CHILD WELLBEING STUDY (FFCWS) AND PROGRAMMING RESEARCH IN OBESITY, GROWTH, ENVIRONMENT AND SOCIAL STRESSORS (PROGRESS)] AND ONE MEXICO-BASED (PROJECT VIVA) COHORT. DNA METHYLATION WAS MEASURED USING ILLUMINA ARRAYS, PERSONAL/PARENTAL SES BY QUESTIONNAIRE AND NEIGHBOURHOOD DISADVANTAGE FROM GEOCODED ADDRESS. IN CARDIA, WE EXAMINED THE MOST STRONGLY ASSOCIATED PERSONAL, PARENTAL AND NEIGHBOURHOOD SES MEASURES WITH EAA (HANNUM'S METHOD) AT STUDY YEARS 15 AND 20 SEPARATELY AND COMBINED USING A GENERALIZED ESTIMATING EQUATION (GEE) AND COMPARED WITH OTHER EAA MEASURES (HORVATH'S EAA, PHENOAGE AND GRIMAGE CALCULATORS, AND DUNEDINPOAM). RESULTS: EAA WAS ASSOCIATED WITH PATERNAL EDUCATION IN CARDIA [GEES: BETASOME COLLEGE = -1.01 YEARS (-1.91, -0.11) AND BETA<HIGH SCHOOL = 1.05 (0.09, 2.01) VS COLLEGE GRADUATES] AND FFCWS [GEES: BETA<HIGH SCHOOL = 0.62 (0.00, 1.24)]. WE FOUND STRONGER ASSOCIATIONS FOR SOME PATERNAL EDUCATION CATEGORIES AMONG WHITE ADULTS (FOR GEE, BETASOME COLLEGE = -1.39 (-2.41, -0.38)], MEN (BETASOME COLLEGE = -1.76 (-3.16, -0.35)] AND WOMEN [BETA<HIGH SCHOOL = 1.77 (0.42, 3.11)]. CONCLUSIONS: THESE FINDINGS SUGGEST THAT EAA CAPTURES EPIGENETIC IMPACTS OF PATERNAL EDUCATION INDEPENDENTLY OF PERSONAL SES LATER IN LIFE. LONGITUDINAL STUDIES SHOULD EXPLORE THESE ASSOCIATIONS AT DIFFERENT LIFE STAGES AND LINK THEM TO HEALTH OUTCOMES. EAA COULD BE A USEFUL BIOMARKER OF SES-ASSOCIATED HEALTH AND PROVIDE IMPORTANT INSIGHT INTO THE PATHOGENESIS AND PREVENTION OF CHRONIC DISEASE.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        
3  4061  24 MATERNAL ADVERSITIES DURING PREGNANCY AND CORD BLOOD OXYTOCIN RECEPTOR (OXTR) DNA METHYLATION. THE AIM OF THIS STUDY WAS TO INVESTIGATE WHETHER MATERNAL ADVERSITIES AND CORTISOL LEVELS DURING PREGNANCY PREDICT CORD BLOOD DNA METHYLATION OF THE OXYTOCIN RECEPTOR (OXTR). WE COLLECTED CORD BLOOD OF 39 BABIES BORN TO MOTHERS PARTICIPATING IN A CROSS-SECTIONAL STUDY (N = 100) CONDUCTED IN BASEL, SWITZERLAND (2007-10). MOTHERS COMPLETED THE INVENTORY OF LIFE EVENTS (SECOND TRIMESTER: T2), THE EDINBURGH POSTNATAL DEPRESSION SCALE (EPDS, THIRD TRIMESTER: T3), THE TRIER INVENTORY OF CHRONIC STRESS (TICS-K, 1-3 WEEKS POSTPARTUM) AND PROVIDED SALIVA SAMPLES (T2, T3) FOR MATERNAL CORTISOL PROFILES, AS COMPUTED BY THE AREA UNDER THE CURVE WITH RESPECT TO GROUND (AUCG) OR INCREASE (AUCI) FOR THE CORTISOL AWAKENING RESPONSE (CAR) AND FOR DIURNAL CORTISOL PROFILES (DAY). OXTR DNA METHYLATION WAS QUANTIFIED USING SEQUENOM EPITYPER. THE NUMBER OF STRESSFUL LIFE EVENTS (P = 0.032), EPDS SCORE (P = 0.007) AND CORTISOL AUCGS AT T2 (CAR: P = 0.020; DAY: P = 0.024) WERE NEGATIVELY ASSOCIATED WITH OXTR DNA METHYLATION. OUR FINDINGS SUGGEST THAT DISTINCT PRENATAL ADVERSITIES PREDICT DECREASED DNA METHYLATION IN A GENE THAT IS RELEVANT FOR CHILDBIRTH, MATERNAL BEHAVIOR AND WELLBEING OF MOTHER AND OFFSPRING. IF A REDUCED OXTR METHYLATION INCREASES OXTR EXPRESSION, OUR FINDINGS COULD SUGGEST AN EPIGENETIC ADAPTATION TO AN ADVERSE EARLY ENVIRONMENT.	2016	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              
4  4067  32 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                    
5  2949  32 GENETIC AND EPIGENETIC CONSEQUENCE OF EARLY-LIFE SOCIAL STRESS ON DEPRESSION: ROLE OF SEROTONIN-ASSOCIATED GENES. EARLY-LIFE ADVERSITY CAUSED BY POOR SOCIAL BONDING AND DEPRIVED MATERNAL CARE IS KNOWN TO AFFECT MENTAL WELLBEING AND PHYSICAL HEALTH. IT IS A FORM OF CHRONIC SOCIAL STRESS THAT PERSISTS BECAUSE OF A NEGATIVE ENVIRONMENT, AND THE CONSEQUENCES ARE LONG-LASTING ON MENTAL HEALTH. THE PRESENCE OF SOCIAL STRESS DURING EARLY LIFE CAN HAVE AN EPIGENETIC EFFECT ON THE BODY, POSSIBLY RESULTING IN MANY COMPLEX MENTAL DISORDERS, INCLUDING DEPRESSION IN LATER LIFE. HERE, WE REVIEW THE EVIDENCE FOR EARLY-LIFE SOCIAL STRESS-INDUCED EPIGENETIC CHANGES THAT MODULATE JUVENILE AND ADULT SOCIAL BEHAVIOR (DEPRESSION AND ANXIETY). THIS REVIEW HAS A PARTICULAR EMPHASIS ON THE INTERACTION BETWEEN EARLY-LIFE SOCIAL STRESS AND GENETIC VARIATION OF SEROTONIN ASSOCIATE GENES INCLUDING THE SEROTONIN TRANSPORTER GENE (5-HTT; ALSO KNOWN AS SLC6A4), WHICH ARE KEY MOLECULES INVOLVED IN DEPRESSION.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  
6  4168  27 MEDITERRANEAN DIET AS A TOOL TO COMBAT INFLAMMATION AND CHRONIC DISEASES. AN OVERVIEW. SINCE ANCIENT TIMES, THE QUALITY OF NOURISHMENT IS A MILESTONE FOR THE MAINTENANCE OF HEALTH AND AS IT IS STATED 'PREVENTION IS BETTER THAN CURE', AMONGST THE SO-CALLED 'HEALTHY' DIETS MEDITERRANEAN DIET (MD) CLAIMS THE LION'S SHARE. IT STANDS IN GOOD STEAD BECAUSE OF A VARIETY OF VALUABLE MACRO- AND MICRONUTRIENTS. SO, ADHERENCE TO A MD IS ASSOCIATED WITH THE REDUCTION OF INFLAMMATION AND NON-COMMUNICABLE (NCD) OR CHRONIC DISEASES. NUMEROUS STUDIES TRY TO SCRUTINIZE THE ROLE OF MD COMPONENTS AS REGARDS REDUCING INFLAMMATION, LOWERING RATE, AND MORTALITY FOR DISORDERS AND ILLNESSES, AND PREVENTING NCD. MD REGIME OF THE INHABITANTS OF THE MEDITERRANEAN BASIN INCLUDES A VARIETY OF ETHNIC NUTRITIONAL HABITS AND REGULATES AN ARRAY OF EFFECTS AND EPIGENETIC CHANGES THAT AFFECT HUMAN WELLBEING. THE RESEARCH IS STILL ONGOING AND ENDEAVORS TO ELUCIDATE EVERY ASPECT OF THIS ISSUE. THIS REVIEW FOCUSES ON THE IMPACT OF MD ON INFLAMMATION HIGHLIGHTS POSITIVE RESULTS REGARDING NCD AND INDICATES THE NEED FOR MORE HIGH-QUALITY EXPERIMENTS AND TRIALS IN ORDER TO OVERCOME ANY DISCREPANCIES.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
7  6478  34 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
8  2646  28 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                        
9  1746  23 EARLY LIFE ADVERSITY, PUBERTAL TIMING, AND EPIGENETIC AGE ACCELERATION IN ADULTHOOD. BACKGROUND: GIVEN ASSOCIATIONS LINKING EARLY LIFE ADVERSITY, PUBERTAL TIMING, AND BIOLOGICAL AGING, WE EXAMINED THE DIRECT AND INDIRECT EFFECTS OF EARLY LIFE TRAUMA ON ADULT BIOLOGICAL AGING (VIA AGE OF MENARCHE). METHODS: PARTICIPANTS WERE PREMENOPAUSAL WOMEN (N = 183). PATH MODELS EVALUATED WHETHER EARLY LIFE TRAUMA PREDICTED EARLY PUBERTAL TIMING AND THEREBY, ADULT EPIGENETIC AGE ACCELERATION (INDEXED VIA FOUR EPIGENETIC CLOCKS: HORVATH DNAM AGE, HANNUM DNAM AGE, DNAM PHENOAGE, AND DNAM GRIMAGE). SECONDARY ANALYSES EXPLORED THE EFFECTS OF TYPE OF TRAUMA (ABUSE AND NEGLECT) AND ADULT CHRONIC STRESS STATUS (CAREGIVER OF CHILD WITH AUTISM AND NON-CAREGIVER). RESULTS: EARLY LIFE TRAUMA AND EARLIER AGE AT MENARCHE INDEPENDENTLY PREDICTED ACCELERATED AGING BASED ON ONE OF THE FOUR EPIGENETIC CLOCKS, DNAM GRIMAGE, THOUGH EARLY LIFE TRAUMA WAS NOT ASSOCIATED WITH AGE OF MENARCHE. CHILDHOOD ABUSE, BUT NOT NEGLECT, PREDICTED FASTER EPIGENETIC AGING; RESULTS DID NOT DIFFER BY CHRONIC STRESS STATUS. CONCLUSIONS: EARLY TRAUMA AND EARLY MENARCHE APPEAR TO EXERT INDEPENDENT EFFECTS ON DNAM GRIMAGE, WHICH HAS BEEN SHOWN TO BE THE STRONGEST EPIGENETIC PREDICTOR OF MORTALITY RISK. THIS STUDY IDENTIFIES A POTENTIAL CORRELATE OR DETERMINANT OF ACCELERATED EPIGENETIC AGING-MENARCHEAL AGE. FUTURE RESEARCH SHOULD ADDRESS THE LIMITATIONS OF THIS STUDY BY USING RACIALLY DIVERSE SAMPLES.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  
10  5316  35 PSYCHOLOGICAL STRESS IN EARLY LIFE AS A PREDISPOSING FACTOR FOR THE DEVELOPMENT OF CHRONIC PAIN: CLINICAL AND PRECLINICAL EVIDENCE AND NEUROBIOLOGICAL MECHANISMS. A WEALTH OF RESEARCH OVER THE PAST 2 DECADES HAS EXPANDED OUR UNDERSTANDING OF THE IMPACT OF EARLY-LIFE ADVERSITY ON PHYSIOLOGICAL FUNCTION AND, CONSEQUENTLY, HEALTH AND WELLBEING IN LATER LIFE. EARLY-LIFE ADVERSITY INCREASES THE RISK OF DEVELOPING A NUMBER OF DISORDERS, SUCH AS CHRONIC PAIN, FIBROMYALGIA, AND IRRITABLE BOWEL SYNDROME. ALTHOUGH MUCH OF THE RESEARCH HAS EXAMINED THE IMPACT OF PHYSICAL MALTREATMENT, AN INCREASING NUMBER OF STUDIES HAVE BEEN PUBLISHED OVER THE PAST FEW YEARS EXAMINING THE EFFECT OF CHILDHOOD PSYCHOLOGICAL STRESS AND TRAUMA ON THE DEVELOPMENT OF VARIOUS TYPES OF CHRONIC PAIN CONDITIONS. WE REVIEW THE CLINICAL AND PRECLINICAL DATA EXAMINING THE LINK AMONG EARLY-LIFE PSYCHOLOGICAL STRESS, ALTERED NOCICEPTIVE BEHAVIOR, AND CHRONIC PAIN IN LATER LIFE. EVIDENCE SUPPORTING A ROLE FOR CERTAIN KEY NEUROBIOLOGICAL SUBSTRATES, INCLUDING THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS; MONOAMINERGIC, OPIOIDERGIC, ENDOCANNABINOID AND IMMUNE SYSTEMS; AND EPIGENETIC MECHANISMS IN THE ASSOCIATION BETWEEN EARLY-LIFE PSYCHOLOGICAL STRESS AND CHRONIC PAIN, IS PROVIDED. GREATER UNDERSTANDING OF THE IMPACT OF EARLY-LIFE STRESS MAY INFORM THE DEVELOPMENT OF PERSONALIZED TREATMENTS FOR CHRONIC PAIN IN LATER LIFE AND STRATEGIES TO PREVENT ITS ONSET IN SUSCEPTIBLE INDIVIDUALS. (C) 2016 WILEY PERIODICALS, INC.	2017	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                              
11  6042  38 THE COLON REVISITED OR THE KEY TO WELLNESS, HEALTH AND DISEASE. THE HYPOTHESIS BEING ADVANCED IN THIS PAPER IS THAT THERE IS A NEW MEDICAL PARADIGM EMERGING FROM THE BIOMEDICAL RESEARCH CARRIED OUT IN THIS CENTURY, MAINLY DUE TO THE EXPLOSION OF THE SO CALLED "OMICS" AND ASSOCIATED TECHNIQUES. THE MAIN IDEA IS THAT THERE IS A COMMON PATHWAY FROM WELLBEING AND HEALTH TO CHRONIC DISEASE ("CHRONOPATHY") AND EVEN TO DEATH, WHICH COMPRISES FOLLOWING STEPS: 1) UNHEALTHY DIET, SEDENTARY LIFE STYLE AND PERMANENT EXPOSITION TO XENOBIOTICS AND ALL KINDS OF NOXIOUS STIMULI;-->2) INTESTINAL DYSBIOSIS;-->3) ALTERATION OF THE INTESTINAL MUCUS LAYER (ESPECIALLY THAT OF THE COLON);-->4) DISRUPTION OF THE ENDOTHELIAL TIGHT JUNCTIONS;-->5) METABOLIC ENDOTOXEMIA+BACTERIAL TRANSLOCATION;-->6) INFLAMMATION;-->7) EXACERBATION OF THE ENTERIC NERVOUS SYSTEM (ENS) AND CONSEQUENT MALADAPTATION AND MALFUNCTIONING OF THE COLON;-->8) EPIGENETIC MANIFESTATIONS;-->9) "CHRONOPATHY" AND PREMATURE DEATH. THEREFORE, IN ORDER TO MAINTAIN A GOOD HEALTH OR TO IMPROVE OR EVEN REVERSE CHRONIC DISEASES IN A PERSON, THE MAIN OUTCOME TO LOOK FOR IS A HOMEOSTATIC BALANCE OF THE INTESTINAL MICROBIOTA (EUBIOSIS), MOST OF WHICH IS LOCATED IN THE COLON. LYNN MARGULIS WAS ONE OF THE MAIN SCIENTISTS TO HIGHLIGHT THE IMPORTANCE OF THE ROLE PLAYED BY BACTERIA NOT ONLY IN THE ORIGIN OF ALL BIOLOGICAL SPECIES NOW PRESENT ON EARTH, BUT ALSO ON THEIR ROLE IN GLOBAL HOMEOSTASIS. BACTERIA DO NOT RELY ON OTHER LIVING BEINGS FOR THEIR EXISTENCE, WHILE THE LATTER DEPEND COMPLETELY ON THE FORMER. HUMANS ARE NO EXEMPTION, AND NEW EVIDENCE EMERGES EACH DAY ABOUT THE PIVOTAL ROLE OF INTESTINAL MICROBIOTA IN HUMAN HEALTH, DISEASE AND, IN GENERAL, IN ITS WELLBEING. THE FOLLOWING FACTS ABOUT INTESTINAL MICROBIOTA ARE NOWADAYS GENERALLY ACCEPTED: THERE ARE ABOUT 10 TIMES MORE BACTERIA IN THE GUT THAN HUMAN CELLS IN EVERY HUMAN BEING; THE MICROBIOMA IS ABOUT 100-150 TIMES BIGGER THAT THE HUMAN GENOME, AND THERE IS A CLEAR LINK BETWEEN INTESTINAL MICROBIOTA AND MANY OF THE MOST COMMON CHRONIC DISEASES, FROM OBESITY AND DIABETES TO DEPRESSION AND PARKINSON DISEASE AND DIFFERENT KINDS OF CANCER. THE MAIN IMPLICATION OF THIS THEORY IS THAT WE SHOULD BECOME A SORT OF MICROBIOTA FARMERS, THAT IS, WE OUGHT TO BE MORE CONSCIOUS OF OUR INTESTINAL MICROBIOTA, TAKE CARE OF IT AND MONITOR IT PERMANENTLY. THUS, AS PART OF OUR GOOD LIFE HABITS (HEALTHY EATING, PHYSICAL EXERCISE), WE SHOULD PROBABLY UNDERGO PERIODIC SEASONS OF FASTING AND COLON CLEANSING, AS IT WAS COMMON IN OLDER TIMES.	2017	
                                                                            
12  3630  46 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	
                                                                                                                                                                                                                
13  6483  42 TOXIC STRESS, EPIGENETICS AND CHILD DEVELOPMENT. OBJECTIVES: TO DESCRIBE THE CONCEPT OF TOXIC STRESS, PRESENT THE BASICS OF EPIGENETICS AND DISCUSS THEIR RELATIONSHIP WITH CHILD DEVELOPMENT. DATA SOURCE: NARRATIVE LITERATURE REVIEW THROUGH A SEARCH IN THE SCIELO, LILACS, MEDLINE DATABASES USING THE TERMS ADVERSE CHILDHOOD EXPERIENCE OR EARLY LIFE STRESS, EPIGENOMIC OR EPIGENETIC, CHILD DEVELOPMENT OR INFANT DEVELOPMENT. DATA SYNTHESIS: CONTINUING STRESS RESPONSE, KNOWN AS TOXIC STRESS, CAN OCCUR WHEN A CHILD EXPERIENCES INTENSE, FREQUENT, AND/OR PROLONGED ADVERSITY-SUCH AS PHYSICAL OR EMOTIONAL ABUSE, CHRONIC NEGLECT, FOR EXAMPLE-WITHOUT ADEQUATE ADULT SUPPORT. THIS TOXIC STRESS CAN HAVE HARMFUL EFFECTS ON LEARNING, BEHAVIOR, AND HEALTH THROUGHOUT LIFE. EPIGENETICS, AN EMERGING SCIENTIFIC RESEARCH AREA?, SHOWS HOW ENVIRONMENTAL INFLUENCES AFFECT GENE EXPRESSIONS AND EXPLAINS HOW EARLY EXPERIENCES CAN IMPACT THROUGHOUT LIFE. CONCLUSIONS: TOXIC STRESS CAUSES CHANGES IN THE HUMAN BODY RESPONSE SYSTEMS THAT CAN BE EXPLAINED IN PART BY EPIGENETIC CHANGES, WHICH CAN BE TEMPORARY OR LONG-LASTING. PEDIATRICIANS MUST BE AWARE OF THESE MECHANISMS AND THEIR CONSEQUENCES, SEEKING TO PREVENT THEM AND THUS PROMOTE THE HEALTH, WELL-BEING, AND QUALITY OF LIFE OF CHILDREN, CONTRIBUTING TO THEIR FULL DEVELOPMENT.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                             
14  5311  35 PSYCHOLOGICAL AND BIOLOGICAL RESILIENCE MODULATES THE EFFECTS OF STRESS ON EPIGENETIC AGING. OUR SOCIETY IS EXPERIENCING MORE STRESS THAN EVER BEFORE, LEADING TO BOTH NEGATIVE PSYCHIATRIC AND PHYSICAL OUTCOMES. CHRONIC STRESS IS LINKED TO NEGATIVE LONG-TERM HEALTH CONSEQUENCES, RAISING THE POSSIBILITY THAT STRESS IS RELATED TO ACCELERATED AGING. IN THIS STUDY, WE EXAMINE WHETHER RESILIENCE FACTORS AFFECT STRESS-ASSOCIATED BIOLOGICAL AGE ACCELERATION. RECENTLY DEVELOPED "EPIGENETIC CLOCKS" SUCH AS GRIMAGE HAVE SHOWN UTILITY IN PREDICTING BIOLOGICAL AGE AND MORTALITY. HERE, WE ASSESSED THE IMPACT OF CUMULATIVE STRESS, STRESS PHYSIOLOGY, AND RESILIENCE ON ACCELERATED AGING IN A COMMUNITY SAMPLE (N = 444). CUMULATIVE STRESS WAS ASSOCIATED WITH ACCELERATED GRIMAGE (P = 0.0388) AND STRESS-RELATED PHYSIOLOGIC MEASURES OF ADRENAL SENSITIVITY (CORTISOL/ACTH RATIO) AND INSULIN RESISTANCE (HOMA). AFTER CONTROLLING FOR DEMOGRAPHIC AND BEHAVIORAL FACTORS, HOMA CORRELATED WITH ACCELERATED GRIMAGE (P = 0.0186). REMARKABLY, PSYCHOLOGICAL RESILIENCE FACTORS OF EMOTION REGULATION AND SELF-CONTROL MODERATED THESE RELATIONSHIPS. EMOTION REGULATION MODERATED THE ASSOCIATION BETWEEN STRESS AND AGING (P = 8.82E-4) SUCH THAT WITH WORSE EMOTION REGULATION, THERE WAS GREATER STRESS-RELATED AGE ACCELERATION, WHILE STRONGER EMOTION REGULATION PREVENTED ANY SIGNIFICANT EFFECT OF STRESS ON GRIMAGE. SELF-CONTROL MODERATED THE RELATIONSHIP BETWEEN STRESS AND INSULIN RESISTANCE (P = 0.00732), WITH HIGH SELF-CONTROL BLUNTING THIS RELATIONSHIP. IN THE FINAL MODEL, IN THOSE WITH POOR EMOTION REGULATION, CUMULATIVE STRESS CONTINUED TO PREDICT ADDITIONAL GRIMAGE ACCELERATION EVEN WHILE ACCOUNTING FOR DEMOGRAPHIC, PHYSIOLOGIC, AND BEHAVIORAL COVARIATES. THESE RESULTS DEMONSTRATE THAT CUMULATIVE STRESS IS ASSOCIATED WITH EPIGENETIC AGING IN A HEALTHY POPULATION, AND THESE ASSOCIATIONS ARE MODIFIED BY BIOBEHAVIORAL RESILIENCE FACTORS.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
15  1221  43 CRITICAL CONNECTIONS AMONG EMBEDDING OF CHILDHOOD ADVERSITY AND ADULT CHRONIC GASTROINTESTINAL AND GENITOURINARY DISORDERS: A REVIEW OF THE LITERATURE. BACKGROUND: A GAP IN THE LITERATURE EXISTS DEMONSTRATING ASSOCIATIONS BETWEEN ADVERSE CHILD EXPERIENCES (ACES) AS POTENTIAL A PRIORI CONTRIBUTING FACTORS AND GASTROINTESTINAL (GI)/GENITOURINARY (GU) DISORDERS. PURPOSE: A NARRATIVE REVIEW OF THE LITERATURE WAS CONDUCTED TO EXPLORE CRITICAL CONNECTIONS BETWEEN ACES AND GI/GU DISORDERS WITH A WORKING HYPOTHESIS OF A DOSE-RESPONSIVE RELATIONSHIP EXISTING AMONG THEM. METHODS: A LITERATURE SEARCH WAS CONDUCTED USING MEDLINE, CUMULATIVE INDEX OF NURSING AND ALLIED HEALTH LITERATURE, PUBMED, AND WEB OF SCIENCE USING SEARCH TERMS ADVERSE CHILDHOOD EXPERIENCES, CHILDHOOD ADVERSITY, OBESITY, GASTROINTESTINAL DISORDERS, AND GENITOURINARY DISORDERS, AND SECONDARY SEARCHES OF OBESITY AND SPECIFIC GI/GU DISORDERS (EG, IRRITABLE BOWEL SYNDROME, PELVIC PAIN). DUPLICATES AND ARTICLES WITH INAPPROPRIATE FOCUS WERE DISCARDED AFTER REVIEW. RESULTS: A TOTAL OF 58 ARTICLES WERE INCLUDED. RESEARCH IDENTIFIED SHOWED THAT ACES DO PLAY A ROLE IN ADULT GI AND GU MORBIDITIES IN A DOSE-RESPONSE MANNER, AND SELECTED FACTORS SUCH AS SOCIOECONOMIC STATUS, RACE, GENDER IDENTITY, AND PHYSIOLOGIC STATE (EG, OBESITY) CONFER HIGHER RISK. RESEARCH ALSO SUGGESTED THAT GENETIC/EPIGENETIC MECHANISMS ARE AT PLAY IN DISEASE OCCURRENCE, AND THE IMPACT OF ACES MAY BE MITIGATED WITH POSITIVE LIFE EXPERIENCES. CONCLUSION: RESEARCH ON THE RELATIONSHIP BETWEEN ACES AND GI/GU DISORDERS IS HETEROGENEOUS, NOTABLY DUE TO WIDE VARIATIONS IN HOW TYPES OF ACES ARE DEFINED AND SCREENING METHODS USED. DESPITE THIS LIMITATION, ASSOCIATIONS ARE DEMONSTRATED. AWARENESS OF A POSSIBLE CORRELATION BETWEEN ACES AND RISK OF GI/GU DISORDERS HAS THE POTENTIAL TO IMPROVE PATIENT CARE, ESPECIALLY THROUGH TRAUMA-INFORMED STRATEGIES.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
16  5169  33 PRECONCEPTIONAL STRESS AND RACIAL DISPARITIES IN PRETERM BIRTH: AN OVERVIEW. OBJECTIVE: WE REVIEWED THE EVIDENCE FOR THREE THEORIES OF HOW PRECONCEPTIONAL PSYCHOSOCIAL STRESS COULD ACT AS A CONTRIBUTING DETERMINANT OF EXCESS PRETERM BIRTH RISK AMONG AFRICAN AMERICAN WOMEN: EARLY LIFE DEVELOPMENTAL PLASTICITY AND EPIGENETIC PROGRAMMING OF ADULT NEUROENDOCRINE SYSTEMS; BLUNTING, WEATHERING, OR DYSFUNCTION OF NEUROENDOCRINE AND IMMUNE FUNCTION IN RESPONSE TO CHRONIC STRESS ACTIVATION THROUGH THE LIFE COURSE; INDIVIDUALS' ADOPTION OF RISKY BEHAVIORS SUCH AS SMOKING AS A RESPONSE TO STRESSFUL STIMULI. METHODS: BASIC SCIENCE, CLINICAL, AND EPIDEMIOLOGIC STUDIES INDEXED IN MEDLINE AND WEB OF SCIENCE DATABASES ON PRECONCEPTIONAL PSYCHOSOCIAL STRESS, PRETERM BIRTH AND RACE WERE REVIEWED. RESULTS: MIXED EVIDENCE LEANS TOWARDS MODEST ASSOCIATIONS BETWEEN PRECONCEPTIONAL CHRONIC STRESS AND PRETERM BIRTH (FOR EXAMPLE COMMON ODDS RATIOS OF 1.2-1.4), PARTICULARLY IN AFRICAN AMERICAN WOMEN, BUT IT IS UNCLEAR WHETHER THIS ASSOCIATION IS CAUSAL OR EXPLAINS A SUBSTANTIAL PORTION OF THE BLACK-WHITE RACIAL DISPARITY IN PRETERM BIRTH. THE STRESS-PRETERM BIRTH ASSOCIATION MAY BE MEDIATED BY HYPOTHALAMIC-PITUITARY-ADRENAL AXIS DYSFUNCTION AND SUSCEPTIBILITY TO BACTERIAL VAGINOSIS, ALTHOUGH THESE MECHANISMS ARE INCOMPLETELY UNDERSTOOD. EVIDENCE FOR THE ROLE OF EPIGENETIC OR EARLY LIFE PROGRAMMING AS A DETERMINANT OF RACIAL DISPARITIES IN PRETERM BIRTH RISK IS MORE CIRCUMSTANTIAL. CONCLUSIONS: PRECONCEPTIONAL STRESS, DIRECTLY OR IN INTERACTION WITH HOST GENETIC SUSCEPTIBILITY OR INFECTION, REMAINS AN IMPORTANT HYPOTHESIZED RISK FACTOR FOR UNDERSTANDING AND REDUCING RACIAL DISPARITIES IN PRETERM BIRTH. FUTURE STUDIES THAT INTEGRATE ADEQUATELY SIZED EPIDEMIOLOGIC SAMPLES WITH MEASURES OF STRESS, INFECTION, AND GENE EXPRESSION, WILL ADVANCE OUR KNOWLEDGE AND ALLOW DEVELOPMENT OF TARGETED INTERVENTIONS.	2011	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               
17  1750  32 EARLY LIFE STRESS AND PEDIATRIC POSTTRAUMATIC STRESS DISORDER. TRAUMATIC STRESS EXPOSURE DURING CRITICAL PERIODS OF DEVELOPMENT MAY HAVE ESSENTIAL AND LONG-LASTING EFFECTS ON THE PHYSICAL AND MENTAL HEALTH OF INDIVIDUALS. TWO THIRDS OF YOUTH ARE EXPOSED TO POTENTIALLY TRAUMATIC EXPERIENCES BY THE AGE OF 17, AND APPROXIMATELY 5% OF ADOLESCENTS MEET LIFETIME CRITERIA FOR POSTTRAUMATIC STRESS DISORDER (PTSD). THE ROLE OF THE STRESS SYSTEM IS THE MAINTENANCE OF HOMEOSTASIS IN THE PRESENCE OF REAL/PERCEIVED AND ACUTE/CHRONIC STRESSORS. EARLY-LIFE STRESS (ELS) HAS AN IMPACT ON NEURONAL BRAIN NETWORKS INVOLVED IN STRESS REACTIONS, AND COULD EXERT A PROGRAMMING EFFECT ON GLUCOCORTICOID SIGNALING. STUDIES ON PEDIATRIC PTSD REVEAL DIVERSE NEUROENDOCRINE RESPONSES TO ADVERSE EVENTS AND RELATED LONG-TERM NEUROENDOCRINE AND EPIGENETIC ALTERATIONS. NEUROENDOCRINE, NEUROIMAGING, AND GENETIC STUDIES IN CHILDREN WITH PTSD AND ELS EXPERIENCES ARE CRUCIAL IN UNDERSTANDING RISK AND RESILIENCE FACTORS, AND ALSO THE NATURAL HISTORY OF PTSD.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       
18  5178  38 PREGNANCY AS A FUNDAMENTAL DETERMINANT OF CHILD HEALTH: A REVIEW. PURPOSE OF REVIEW: MATERNAL CONDITIONS AND EXPOSURES DURING PREGNANCY INCLUDING OVER- AND UNDERNUTRITION ARE ASSOCIATED WITH POOR CHILDBIRTH OUTCOMES, GROWTH, DEVELOPMENT AND CHRONIC CHILDHOOD DISEASES. WE EXAMINED CONTEMPORARY PREGNANCY-RELATED DETERMINANTS OF CHILD HEALTH. RECENT FINDINGS: WHILE MATERNAL UNDERNUTRITION REMAINS A MAJOR CONTRIBUTOR TO LOW BIRTH WEIGHT, MATERNAL OBESITY AFFECTS FOETAL GROWTH, BIRTH WEIGHT, SURVIVAL AND IS ASSOCIATED WITH CHILDHOOD OBESITY, ASTHMA AND AUTISTIC SPECTRUM DISORDERS. EMERGING EVIDENCE SUGGESTS THAT EPIGENETIC CHANGES, THE PRENATAL MICROBIOME AND MATERNAL IMMUNE ACTIVATION (MIA), A NEUROINFLAMMATORY PROCESS INDUCED BY DIET AND OTHER EXPOSURES CAUSE FOETAL PROGRAMMING RESULTING IN THESE CHRONIC CHILDHOOD DISEASES. MATERNAL DIET IS POTENTIALLY A MODIFIABLE RISK FACTOR FOR CONTROLLING LOW BIRTH WEIGHT, OBESITY AND CHRONIC DISEASE IN CHILDHOOD. FURTHER STUDIES ARE WARRANTED TO REFINE GUIDANCE ON DIETARY RESTRICTION AND PHYSICAL ACTIVITY DURING PREGNANCY AND DETERMINE HOW MIA AND PRENATAL MICROBIOTA CAN BE APPLIED TO CONTROL CHILDHOOD DISEASES ARISING FROM PROGRAMMING.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                           
19  6894  23 [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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
20  1779  40 EDITORIAL: MATERNAL INFLAMMATION DURING PREGNANCY: A MODIFIABLE PATHWAY TOWARD IMPROVING OFFSPRING SOCIOEMOTIONAL OUTCOMES IN CHILDHOOD AND ADOLESCENCE. CHILDHOOD PSYCHOPATHOLOGY IS A WELL-ESTABLISHED PREDICTOR OF POOR ADULT LIFE-COURSE OUTCOMES INCLUDING LOWER RATES OF EDUCATIONAL ATTAINMENT AND REDUCED FAMILY INCOME, WITH A TOTAL ECONOMIC LOSS OF $2.1 TRILLION IN THE UNITED STATES.(1) GIVEN THIS HIGH LEVEL OF INDIVIDUAL AND SOCIETAL BURDEN, MUCH EFFORT HAS BEEN DEVOTED TO IDENTIFYING THE MODIFIABLE RISK FACTORS THAT CONFER RISK FOR PSYCHIATRIC DISORDERS DURING EARLY CHILDHOOD. INDEED, NUMEROUS ASPECTS OF EARLY LIFE ADVERSITY, SUCH AS SOCIOECONOMIC DISADVANTAGE, STRESSFUL/TRAUMATIC LIFE EVENTS, AND DISRUPTED PARENT-CHILD RELATIONSHIPS, DEMONSTRATE STRONG ASSOCIATIONS WITH SOCIOEMOTIONAL PROBLEMS AND PSYCHIATRIC DISORDERS INTO ADOLESCENCE.(2) HOWEVER, THE UNDERLYING BIOLOGICAL MECHANISMS THAT ALSO CONTRIBUTE TO THIS RISK TRAJECTORY REMAIN LESS WELL UNDERSTOOD. ONE PROPOSED BIOLOGICAL MECHANISM THAT IS RAPIDLY GAINING MOMENTUM IN THE FIELD OF DEVELOPMENTAL PSYCHOPATHOLOGY CONCERNS EXCESSIVE IMMUNE SYSTEM ACTIVATION AND/OR PROINFLAMMATORY RESPONSES IN THE ORIGINS OF HEALTH AND DISEASE.(3) OF PARTICULAR INTEREST IS THE PRENATAL PERIOD, REPRESENTING A WINDOW OF VULNERABILITY IN WHICH PRENATAL EXPOSURES PREPARE OR PROGRAM THE FETUS FOR THE EXPECTED POSTNATAL ENVIRONMENT.(3-5) MORE SPECIFICALLY, FETAL PROGRAMMING POSITS THAT THE EFFECTS OF MATERNAL ADVERSITY DURING PREGNANCY ARE, AT LEAST IN PART, TRANSMITTED TO THE FETUS VIA MULTIPLE RELATED PATHWAYS INCLUDING CHRONIC MATERNAL INFLAMMATION AND/OR OVERACTIVATION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS, RESULTING IN ABERRANT MATERNAL-FETAL IMMUNE/GLUCOCORTICOID SYSTEMS AND DOWNSTREAM EPIGENETIC ALTERATIONS IN THE DEVELOPING FETUS. TOGETHER, THESE FACTORS WORK TO INCREASE THE SUSCEPTIBILITY OF OFFSPRING TO ADVERSITY IN THE POSTNATAL ENVIRONMENT AND, IN TURN, ENHANCE RISK FOR PSYCHIATRIC DISORDERS.(3-6) HOWEVER, MUCH OF THE EXISTING LITERATURE IS BASED ON PRECLINICAL ANIMAL MODELS WITH COMPARATIVELY FEWER CLINICAL STUDIES.(3) AS SUCH, THERE REMAINS A PAUCITY OF LARGE, PROSPECTIVELY DESIGNED CLINICAL STUDIES EXAMINING MATERNAL PROINFLAMMATORY CONDITIONS DURING PREGNANCY IN RELATION TO PSYCHOPATHOLOGY IN OFFSPRING. AS PART OF THE LANDMARK NATIONAL INSTITUTES OF HEALTH-FUNDED ECHO (ENVIRONMENTAL INFLUENCES ON CHILD HEALTH OUTCOMES) CONSORTIUM, THE STUDY BY FRAZIER ET AL.(7) REPRESENTS ONE OF THE LARGEST INVESTIGATIONS LINKING PERINATAL MATERNAL PROINFLAMMATORY CONDITIONS WITH CO-OCCURRING PSYCHIATRIC SYMPTOMS IN CHILDREN AND ADOLESCENTS.	2023