1  5728 105 SLEEP QUALITY AND METHYLATION STATUS OF SELECTED TUMOR SUPPRESSOR GENES AMONG NURSES AND MIDWIVES. CHRONIC SLEEP RESTRICTION MAY AFFECT METABOLISM, HORMONE SECRETION PATTERNS AND INFLAMMATORY RESPONSES. LIMITED REPORTS SUGGEST ALSO EPIGENETIC EFFECTS, SUCH AS CHANGES IN DNA METHYLATION PROFILES. THE STUDY AIMS TO ASSESS THE POTENTIAL ASSOCIATION BETWEEN POOR SLEEP QUALITY OR SLEEP DURATION AND THE LEVELS OF 5-METHYLCYTOSINE IN THE PROMOTER REGIONS OF SELECTED TUMOR SUPPRESSOR GENES. A CROSS-SECTIONAL STUDY WAS CONDUCTED ON 710 NURSES AND MIDWIVES AGED 40-60 YEARS. DATA FROM INTERVIEWS REGARDING SLEEP HABITS AND POTENTIAL CONFOUNDERS WERE USED. THE METHYLATION STATUS OF TUMOR SUPPRESSOR GENES WAS DETERMINED VIA QMSP REACTIONS USING DNA SAMPLES DERIVED FROM LEUCOCYTES. NO SIGNIFICANT FINDINGS WERE OBSERVED IN THE TOTAL STUDY POPULATION OR IN THE TWO SUBGROUPS OF WOMEN STRATIFIED BY THE CURRENT SYSTEM OF WORK. A BORDERLINE SIGNIFICANCE ASSOCIATION WAS OBSERVED BETWEEN A SHORTER DURATION OF SLEEP AND AN INCREASED METHYLATION LEVEL IN CDKN2A AMONG DAY WORKING NURSES AND MIDWIVES. FURTHER STUDIES ARE WARRANTED TO EXPLORE THIS UNDER-INVESTIGATED TOPIC.	2018	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
2  1151  31 CONNECTIONS AMONG BIOLOGIC EMBEDDING OF CHILDHOOD ADVERSITY, ADULT CHRONIC ILLNESS, AND WOUND CARE: A REVIEW OF THE LITERATURE. ADVERSE CHILDHOOD EXPERIENCES (ACES) BIOLOGICALLY EMBED BY ALTERING BRAIN DEVELOPMENT AND INFLUENCING EPIGENETIC MECHANISMS. THESE EXPERIENCES MAY GENERATE HEALTH RISK FACTORS. PURPOSE: A LITERATURE REVIEW WAS CONDUCTED TO COMPARE ACE-GENERATED HEALTH RISK FACTORS WITH RISK FACTORS FOR WOUND DEVELOPMENT AND ABERRANT HEALING, AS WELL AS TO IDENTIFY A GAP IN LITERATURE REGARDING CRITICAL CONNECTIONS BETWEEN ACES, CHRONIC ILLNESS, AND WOUND DEVELOPMENT/HEALING, WITH ASSOCIATED PRACTICE IMPLICATIONS. METHODOLOGY: A LITERATURE SEARCH OF ENGLISH-LANGUAGE ARTICLES WAS CONDUCTED USING THE CUMULATIVE INDEX OF NURSING AND ALLIED HEALTH LITERATURE, MEDLINE, AND PUBMED USING THE SEARCH TERMS ADVERSE CHILDHOOD EXPERIENCES, ADULTS, WOUNDS, CHRONIC DISEASE OR ILLNESS, AND EPIGENETICS. THE SEARCHES YIELDED 561 PUBLICATIONS REGARDING ACES, CHRONIC ILLNESS OR DISEASE, AND ADULT; 182 FOR ACES; AND 547 FOR EPIGENETICS AND WOUNDS. ABSTRACTS WERE REVIEWED TO REMOVE DUPLICATES AND STUDIES WITH PARTICIPANTS WHO WERE <18 YEARS OLD. PUBLICATIONS WERE REVIEWED FOR SALIENCE; THOSE DISCUSSING THE BIOLOGIC PLAUSIBILITY OF ACES CONTRIBUTING TO ADULT ILLNESSES AND ASSOCIATED WOUND DEVELOPMENT AND HEALING WERE REVIEWED FOR INCLUSION. RESULTS: SIXTY-EIGHT (68) PUBLICATIONS WERE FOUND APPROPRIATE FOR REVIEW AND INCLUDED POPULATION-BASED STUDIES; LITERATURE REVIEWS; EPIDEMIOLOGIC DATA; META-ANALYSES; AND SYSTEMATIC, CROSS-SECTIONAL, OBSERVATIONAL, AND PROSPECTIVE STUDIES AS SINGULAR OR MIXED METHODS DESIGNS. A SUBSTANTIAL OVERLAP WAS FOUND IN TERMS OF RISK FACTORS GENERATED BY ACE EXPOSURE AND RISK FACTORS FOR WOUND DEVELOPMENT/HEALING, AS WAS A GAP IN THE LITERATURE REGARDING THIS RELATIONSHIP. EPIGENETIC MECHANISMS AND ALTERED BRAIN DEVELOPMENT ARE IMPLICATED IN PROCESSES THROUGH WHICH CHILDHOOD ADVERSITY ERODES HUMAN HEALTH. CONCLUSION: ADULT HEALTH RISKS AS A RESULT OF EXPOSURE TO ACES AND CRITICAL CONNECTIONS WITH RISKS FOR WOUND DEVELOPMENT AND DISRUPTED WOUND HEALING VIA EPIGENETIC INFLUENCES ARE RECOGNIZED IN THE LITERATURE. PRACTICE IMPLICATIONS INCLUDE CONSIDERING SCREENING FOR THE RISK FACTOR OF ACES EXPOSURE IN ADULT PATIENTS TO IDENTIFY THIS ADDITIONAL RISK FACTOR AND PRACTICING PATIENT-CENTERED, TRAUMA-INFORMED CARE. FURTHER RESEARCH INTO THE INTEGRATIVE ROLES OF THESE FACTORS IS WARRANTED.	2019	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                
3  5727  95 SLEEP QUALITY AND METHYLATION STATUS OF CORE CIRCADIAN RHYTHM GENES AMONG NURSES AND MIDWIVES. ABSTARCT POOR SLEEP QUALITY OR SLEEP RESTRICTION IS ASSOCIATED WITH SLEEPINESS AND CONCENTRATION PROBLEMS. MOREOVER, CHRONIC SLEEP RESTRICTION MAY AFFECT METABOLISM, HORMONE SECRETION PATTERNS AND INFLAMMATORY RESPONSES. LIMITED RECENT REPORTS SUGGEST A POTENTIAL LINK BETWEEN SLEEP DEPRIVATION AND EPIGENETIC EFFECTS SUCH AS CHANGES IN DNA METHYLATION PROFILES. THE AIM OF THE PRESENT STUDY WAS TO ASSESS THE POTENTIAL ASSOCIATION BETWEEN POOR SLEEP QUALITY OR SLEEP DURATION AND THE LEVELS OF 5-METHYLCYTOSINE IN THE PROMOTER REGIONS OF PER1, PER2, PER3, BMAL1, CLOCK, CRY1 CRY2 AND NPAS2 GENES, TAKING INTO ACCOUNT ROTATING NIGHT WORK AND CHRONOTYPE AS POTENTIAL CONFOUNDERS OR MODIFIERS. A CROSS-SECTIONAL STUDY WAS CONDUCTED ON 710 NURSES AND MIDWIVES (347 WORKING ON ROTATING NIGHTS AND 363 WORKING ONLY DURING THE DAY) AGED 40-60 YEARS. DATA FROM IN-PERSON INTERVIEWS ABOUT SLEEP QUALITY, CHRONOTYPE AND POTENTIAL CONFOUNDERS WERE USED. SLEEP QUALITY AND CHRONOTYPE WERE ASSESSED USING PITTSBURGH SLEEP QUALITY QUESTIONNAIRE (PSQI) AND MORNINGNESS-EVENINGNESS QUESTIONNAIRE (MEQ), RESPECTIVELY. MORNING BLOOD SAMPLES WERE COLLECTED. THE METHYLATION STATUS OF THE CIRCADIAN RHYTHM GENES WAS DETERMINED VIA QUANTITATIVE METHYLATION-SPECIFIC REAL-TIME PCR ASSAYS (QMSP) REACTIONS USING DNA SAMPLES DERIVED FROM LEUCOCYTES. THE PROPORTIONAL ODDS REGRESSION MODEL WAS FITTED TO QUANTIFY THE RELATIONSHIP BETWEEN METHYLATION INDEX (MI) AS THE DEPENDENT VARIABLE AND SLEEP QUALITY OR SLEEP DURATION AS THE EXPLANATORY VARIABLE. ANALYSES WERE CARRIED OUT FOR THE TOTAL POPULATION AS WELL AS FOR SUBGROUPS OF WOMEN STRATIFIED BY THE CURRENT SYSTEM OF WORK (ROTATING NIGHT SHIFT/DAY WORK) AND CHRONOTYPE (MORNING TYPE/INTERMEDIATE TYPE/EVENING TYPE). A POTENTIAL MODIFYING EFFECT OF THE SYSTEM OF WORK OR THE CHRONOTYPE WAS EXAMINED USING THE LIKELIHOOD RATIO TEST. NO SIGNIFICANT FINDINGS WERE OBSERVED IN THE TOTAL STUDY POPULATION. SUBGROUP ANALYSES REVEALED TWO STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN A SHORTER SLEEP DURATION AND 1) METHYLATION LEVEL IN PER2 AMONG DAY WORKERS, ESPECIALLY THOSE WITH THE MORNING CHRONOTYPE (OR = 2.31, 95%CI:1.24-4.33), AND 2) METHYLATION LEVEL IN CRY2 AMONG SUBJECTS WITH THE INTERMEDIATE CHRONOTYPE, PARTICULARLY AMONG DAY WORKERS (OR = 0.52, 95%CI:0.28-0.96). THE STUDY RESULTS DEMONSTRATED A POSITIVE ASSOCIATION BETWEEN AVERAGE SLEEP DURATION OF LESS THAN 6 HOURS AND THE METHYLATION LEVEL OF PER2 AMONG MORNING CHRONOTYPE SUBJECTS, AND AN INVERSE ASSOCIATION FOR CRY2 AMONG INTERMEDIATE CHRONOTYPE SUBJECTS, BUT ONLY AMONG DAY WORKERS. BOTH THE SYSTEM OF WORK AND THE CHRONOTYPE TURNED OUT TO BE IMPORTANT CONFOUNDERS AND MODIFIERS IN A NUMBER OF ANALYSES, MAKING IT NECESSARY TO CONSIDER THEM AS POTENTIAL COVARIATES IN FUTURE RESEARCH ON SLEEP DEFICIENCY OUTCOMES. FURTHER STUDIES ARE WARRANTED TO EXPLORE THIS UNDER-INVESTIGATED TOPIC.	2017	

4  1050  25 CLINICAL FEATURES ASSOCIATED TO REFRACTORY OBSESSIVE-COMPULSIVE DISORDER. SOME PATIENTS WITH OBSESSIVE-COMPULSIVE DISORDER (OCD) EXHIBIT AN UNSATISFACTORY REDUCTION IN SYMPTOM SEVERITY DESPITE BEING TREATED WITH ALL THE AVAILABLE THERAPEUTIC ALTERNATIVES. THE CLINICAL VARIABLES ASSOCIATED WITH TREATMENT-REFRACTORINESS IN OCD ARE INCONSISTENTLY DESCRIBED IN THE LITERATURE. METHODS: TO INVESTIGATE FACTORS ASSOCIATED WITH TREATMENT-REFRACTORINESS OF PATIENTS WITH OCD, WE CONDUCTED A CASE-CONTROL STUDY, COMPARING 23 PATIENTS WITH TREATMENT-REFRACTORY OCD TO 26 PATIENTS WITH TREATMENT-RESPONDING OCD. RESULTS: THE FACTORS ASSOCIATED WITH REFRACTORINESS OF OCD WERE HIGHER SEVERITY OF SYMPTOMS SINCE THE ONSET OF OCD (P<0.001), CHRONIC COURSE (P=0.003), LACK OF A PARTNER (P=0.037), UNEMPLOYMENT (P=0.025), LOW ECONOMIC STATUS (P=0.015), PRESENCE OF OBSESSIVE-COMPULSIVE SYMPTOMS OF SEXUAL/RELIGIOUS CONTENT (P=0.043), AND HIGHER SCORES ON FAMILY ACCOMMODATION (P<0.001). ONLY THE THREE LATTER VARIABLES REMAINED SIGNIFICANTLY ASSOCIATED WITH TREATMENT-REFRACTORINESS AFTER REGRESSION ANALYSES. LIMITATIONS: SMALL SAMPLE SIZE, THE BIASES AND DRAWBACKS INHERENT TO A CASE-CONTROL STUDY, AND THE INCLUSION CRITERIA USED TO DEFINE THE STUDY GROUPS MAY HAVE LIMITED THE GENERALISATION OF THE RESULTS. CONCLUSION: A MAJOR STRENGTH OF THIS STUDY IS THE SYSTEMATIC AND STRUCTURED EVALUATION OF A VAST ARRAY OF VARIABLES RELATED TO THE CLINICAL EXPRESSION OF OCD, INCLUDING EPIGENETIC FACTORS AND RATINGS DERIVED FROM INSTRUMENTS EVALUATING FAMILY ACCOMMODATION. THE PRESENCE OF SEXUAL/RELIGIOUS SYMPTOMS, LOW ECONOMIC STATUS AND HIGH MODIFICATION ON FAMILY FUNCTION DUE TO OCD WERE INDEPENDENTLY ASSOCIATED WITH TREATMENT-REFRACTORINESS. FUTURE LONGITUDINAL STUDIES ARE WARRANTED TO VERIFY IF THESE VARIABLES REPRESENT PREDICTIVE FACTORS OF TREATMENT NON-RESPONSE.	2006	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   
5  6096  33 THE EFFECTS OF STRESS AND MEDITATION ON THE IMMUNE SYSTEM, HUMAN MICROBIOTA, AND EPIGENETICS. CONTEXT * GLOBALLY, MORE THAN 25% OF INDIVIDUALS ARE AFFECTED BY ANXIETY AND DEPRESSION DISORDERS. MEDITATION IS GAINING POPULARITY IN CLINICAL SETTINGS AND ITS TREATMENT EFFICACY IS BEING STUDIED FOR A WIDE ARRAY OF PSYCHOLOGICAL AND PHYSIOLOGICAL AILMENTS. AN EXPLORATION OF STRESS PHYSIOLOGY IS AN ESSENTIAL PRECURSOR TO DELINEATION OF THE MECHANISMS UNDERLYING THE BENEFICIAL EFFECTS OF MEDITATION PRACTICES. OBJECTIVE * THE REVIEW OUTLINES A MODEL OF INTERCONNECTED PHYSIOLOGICAL PROCESSES THAT MIGHT SUPPORT THE CONTINUED INCLUSION AND EXPANSION OF MEDITATION IN THE TREATMENT OF DIVERSE MEDICAL CONDITIONS AND TO INVESTIGATE THE ROLE THAT GUT MICROBIOTA MAY PLAY IN REALIZING WELL-BEING THROUGH MEDITATION. DESIGN * THE AUTHORS CONDUCTED A SCIENTIFIC LITERATURE DATABASE SEARCH WITH THE GOAL OF REVIEWING THE LINK BETWEEN STRESS MANAGEMENT TECHNIQUES AND HUMAN MICROBIOTA. THEIR GOAL WAS ALSO TO IDENTIFY THE EXTENT OF UNDERLYING EPIGENETIC REACTIONS IN THESE PROCESSES. THE REVIEW WAS COMPLETED IN APPROXIMATELY 2 Y. DATABASES SEARCHED INCLUDED MEDLINE VIA PUBMED AND OVID, PSYCINFO VIA OVID, SPINET, PROQUEST CENTRAL, SAGE RESEARCH METHODS ONLINE, CINAHL PLUS WITH FULL TEXT, SCIENCE DIRECT, SPRINGER LINK, AND WILEY ONLINE LIBRARY. KEYWORDS SEARCHED INCLUDED, BUT WERE NOT LIMITED TO, STRESS, MEDITATION, MINDFULNESS, IMMUNE SYSTEM, HPA AXIS, SYMPATHETIC NERVOUS SYSTEM, PARASYMPATHETIC NERVOUS SYSTEM, MICROBIOTA, MICROBIOME, GUT-BARRIER FUNCTION, LEAKY GUT, VAGUS NERVE, PSYCHONEUROIMMUNOLOGY, EPIGENETIC, AND NF-KAPPAB. SETTING * THE STUDY TOOK PLACE AT NEW YORK UNIVERSITY (NEW YORK, NY, USA), THE UNIVERSITY OF CALIFORNIA, SAN DIEGO (LA JOLLA, CA, USA), AND THE CHOPRA FOUNDATION (CARLSBAD, CA, USA). RESULTS * PSYCHOLOGICAL STRESS TYPICALLY TRIGGERS A FIGHT-OR-FLIGHT RESPONSE, PROMPTING CORTICOTROPIN-RELEASING HORMONE AND CATECHOLAMINE PRODUCTION IN VARIOUS PARTS OF THE BODY, WHICH ULTIMATELY DISTURBS THE MICROBIOTA. IN THE ABSENCE OF STRESS, A HEALTHY MICROBIOTA PRODUCES SHORT-CHAIN FATTY ACIDS THAT EXERT ANTI-INFLAMMATORY AND ANTITUMOR EFFECTS. DURING STRESS, AN ALTERED GUT MICROBIAL POPULATION AFFECTS THE REGULATION OF NEUROTRANSMITTERS MEDIATED BY THE MICROBIOME AND GUT BARRIER FUNCTION. MEDITATION HELPS REGULATE THE STRESS RESPONSE, THEREBY SUPPRESSING CHRONIC INFLAMMATION STATES AND MAINTAINING A HEALTHY GUT-BARRIER FUNCTION. CONCLUSIONS * THE CURRENT RESEARCH TEAM RECOMMENDS THE INTEGRATION OF MEDITATION INTO CONVENTIONAL HEALTH CARE AND WELLNESS MODELS. CONCURRENTLY, STUDIES TO EXPLORE THE EFFECTS OF MEDITATION ON HUMAN MICROBIOTA ARE WARRANTED.	2017	
                                                                                                                                                                                                                                                                                                              
6  1058  26 CLINICAL MEASURES OF ALLOSTATIC LOAD IN CHILDREN AND ADOLESCENTS WITH FOOD ALLERGY, DEPRESSION, OR ANXIETY. PURPOSE: SUSTAINED HIGH STRESS EXPOSURE RESULTS IN CHRONIC ACTIVATION OF THE STRESS RESPONSE SYSTEM, DYSREGULATED STRESS RESPONSES, HIGH ALLOSTATIC LOAD, AND POOR LATER-LIFE HEALTH. CHILDREN AND ADOLESCENTS WITH CHRONIC HEALTH CONDITIONS FACE STRESSORS RELATED TO THEIR CONDITION IN ADDITION TO THOSE TYPICAL OF CHILDHOOD AND ADOLESCENCE, PLACING THEM AT RISK OF HIGH ALLOSTATIC LOAD. THE PURPOSE OF THIS SECONDARY ANALYSIS WAS TO EXAMINE WHETHER YOUTH WITH CHRONIC HEALTH CONDITIONS DIFFER FROM CONTROLS ON CLINICAL MEASURES OF ALLOSTATIC LOAD. DESIGN AND METHODS: A SECONDARY ANALYSIS OF TWO DATASETS, THE ELECTRONIC HEALTH RECORD OF A TERTIARY CHILDREN'S HOSPITAL AND DATA FROM THE SURVEY OF THE HEALTH OF WISCONSIN, COMPARED YOUTH WITH CHRONIC HEALTH CONDITIONS TO CONTROLS ON CLINICAL MEASURES OF ALLOSTATIC LOAD. ADDITIONAL ANALYSES EXPLORED WHETHER PARENTAL STRESS AND MENTAL HEALTH INFLUENCED THESE RELATIONSHIPS. RESULTS: ANALYSES IDENTIFIED DIFFERENCES IN BMI, BLOOD PRESSURE, AND WAIST CIRCUMFERENCE BETWEEN YOUTH WITH FOOD ALLERGY, ANXIETY, OR DEPRESSION, AND CONTROLS. THESE RELATIONSHIPS DIFFERED FOR MALES AND FEMALES AND FOR THOSE WITH COMORBID MENTAL AND PHYSICAL CONDITIONS, AND WERE INFLUENCED BY PARENT STRESS AND MENTAL HEALTH. CONCLUSIONS: RESULTS SUPPORT FUTURE STUDIES EXPLORING WHETHER HIGH STRESS IN YOUTH WITH CHRONIC HEALTH CONDITIONS LEADS TO INCREASED ALLOSTATIC LOAD. INCORPORATING BIOMARKERS AS WELL AS GENETIC AND EPIGENETIC FACTORS WILL PROVIDE CRITICAL INSIGHTS. PRACTICE IMPLICATIONS: YOUTH WITH MENTAL AND PHYSICAL CHCS MAY BE AT INCREASED RISK OF HIGH ALLOSTATIC LOAD, REFLECTED IN CLINICAL MEASURES OF METABOLISM, AND SHOULD HAVE REGULAR ASSESSMENTS OF THEIR METABOLIC HEALTH.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                      
7    92  20 A PILOT STUDY INVESTIGATING THE ROLE OF GENDER IN THE INTERGENERATIONAL RELATIONSHIPS BETWEEN GENE EXPRESSION, CHRONIC PAIN, AND ADVERSE CHILDHOOD EXPERIENCES IN A CLINICAL SAMPLE OF YOUTH WITH CHRONIC PAIN. CHRONIC PAIN IS A HIGHLY PREVALENT AND COSTLY ISSUE THAT OFTEN EMERGES DURING CHILDHOOD OR ADOLESCENCE AND PERSISTS INTO ADULTHOOD. ADVERSE CHILDHOOD EXPERIENCES (ACES) INCREASE RISK FOR SEVERAL ADVERSE HEALTH CONDITIONS, INCLUDING CHRONIC PAIN. RECENT EVIDENCE SUGGESTS THAT PARENTAL TRAUMA (ACES, POST-TRAUMATIC STRESS DISORDER (PTSD) SYMPTOMS) CONFERS RISK OF POOR HEALTH OUTCOMES IN THEIR CHILDREN. INTERGENERATIONAL RELATIONSHIPS BETWEEN PARENTAL TRAUMA AND CHILD CHRONIC PAIN MAY BE MEDIATED BY EPIGENETIC MECHANISMS. A CLINICAL SAMPLE OF YOUTH WITH CHRONIC PAIN AND THEIR PARENTS COMPLETED PSYCHOMETRICALLY SOUND QUESTIONNAIRES ASSESSING ACES, PTSD SYMPTOMS, AND CHRONIC PAIN, AND PROVIDED A SALIVA SAMPLE. THESE WERE USED TO INVESTIGATE THE INTERGENERATIONAL RELATIONSHIPS BETWEEN FOUR EPIGENETIC BIOMARKERS (COMT, DRD2, GR, AND SERT), TRAUMA, AND CHRONIC PAIN. THE RESULTS INDICATED THAT THE SIGNIFICANT BIOMARKERS WERE DEPENDENT UPON THE GENDER OF THE CHILD, WHEREIN PARENTAL ACES SIGNIFICANTLY CORRELATED WITH CHANGES IN DRD2 EXPRESSION IN FEMALE CHILDREN AND ALTERED COMT EXPRESSION IN THE PARENTS OF MALE CHILDREN. ADDITIONALLY, THE NATURE OF THE ACE (MALTREATMENT VS. HOUSEHOLD DYSFUNCTION) WAS ASSOCIATED WITH THE SPECIFIC EPIGENETIC CHANGES. THERE MAY BE DIFFERENT PATHWAYS THROUGH WHICH PARENTAL ACES CONFER RISK FOR POOR OUTCOMES FOR MALES AND FEMALES, HIGHLIGHTING THE IMPORTANCE OF CHILD GENDER IN FUTURE INVESTIGATIONS.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     
8  6112  34 THE EPIGENETIC CLOCK AS A PREDICTOR OF DISEASE AND MORTALITY RISK: A SYSTEMATIC REVIEW AND META-ANALYSIS. BACKGROUND: AGEING IS ONE OF THE PRINCIPAL RISK FACTORS FOR MANY CHRONIC DISEASES. HOWEVER, THERE IS CONSIDERABLE BETWEEN-PERSON VARIATION IN THE RATE OF AGEING AND INDIVIDUAL DIFFERENCES IN THEIR SUSCEPTIBILITY TO DISEASE AND DEATH. EPIGENETIC MECHANISMS MAY PLAY A ROLE IN HUMAN AGEING, AND DNA METHYLATION AGE BIOMARKERS MAY BE GOOD PREDICTORS OF AGE-RELATED DISEASES AND MORTALITY RISK. THE AIMS OF THIS SYSTEMATIC REVIEW WERE TO IDENTIFY AND SYNTHESISE THE EVIDENCE FOR AN ASSOCIATION BETWEEN PERIPHERALLY MEASURED DNA METHYLATION AGE AND LONGEVITY, AGE-RELATED DISEASE, AND MORTALITY RISK. METHODS: A SYSTEMATIC SEARCH WAS CONDUCTED IN LINE WITH THE PREFERRED REPORTING ITEMS FOR SYSTEMATIC REVIEWS AND META-ANALYSES (PRISMA) GUIDELINES. USING RELEVANT SEARCH TERMS, MEDLINE, EMBASE, COCHRANE CENTRAL REGISTER OF CONTROLLED TRIALS, AND PSYCHINFO DATABASES WERE SEARCHED TO IDENTIFY ARTICLES MEETING THE INCLUSION CRITERIA. STUDIES WERE ASSESSED FOR BIAS USING JOANNA BRIGGS INSTITUTE CRITICAL APPRAISAL CHECKLISTS. DATA WAS EXTRACTED FROM STUDIES MEASURING AGE ACCELERATION AS A PREDICTOR OF AGE-RELATED DISEASES, MORTALITY OR LONGEVITY, AND THE FINDINGS FOR SIMILAR OUTCOMES COMPARED. USING REVIEW MANAGER 5.3 SOFTWARE, TWO META-ANALYSES (ONE PER EPIGENETIC CLOCK) WERE CONDUCTED ON STUDIES MEASURING ALL-CAUSE MORTALITY. RESULTS: TWENTY-THREE RELEVANT ARTICLES WERE IDENTIFIED, INCLUDING A TOTAL OF 41,607 PARTICIPANTS. FOUR STUDIES FOCUSED ON AGEING AND LONGEVITY, 11 ON AGE-RELATED DISEASE (CANCER, CARDIOVASCULAR DISEASE, AND DEMENTIA), AND 11 ON MORTALITY. THERE WAS SOME, ALTHOUGH INCONSISTENT, EVIDENCE FOR AN ASSOCIATION BETWEEN INCREASED DNA METHYLATION AGE AND RISK OF DISEASE. META-ANALYSES INDICATED THAT EACH 5-YEAR INCREASE IN DNA METHYLATION AGE WAS ASSOCIATED AN 8 TO 15% INCREASED RISK OF MORTALITY. CONCLUSION: DUE TO THE SMALL NUMBER OF STUDIES AND HETEROGENEITY IN STUDY DESIGN AND OUTCOMES, THE ASSOCIATION BETWEEN DNA METHYLATION AGE AND AGE-RELATED DISEASE AND LONGEVITY IS INCONCLUSIVE. INCREASED EPIGENETIC AGE WAS ASSOCIATED WITH MORTALITY RISK, BUT POSITIVE PUBLICATION BIAS NEEDS TO BE CONSIDERED. FURTHER RESEARCH IS NEEDED TO DETERMINE THE EXTENT TO WHICH DNA METHYLATION AGE CAN BE USED AS A CLINICAL BIOMARKER.	2019	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                  
9  4066  30 MATERNAL AND PATERNAL PERICONCEPTIONAL NUTRITION AS AN INDICATOR OF OFFSPRING METABOLIC SYNDROME RISK IN LATER LIFE THROUGH EPIGENETIC IMPRINTING: A SYSTEMATIC REVIEW. AIMS: THIS REVIEW EXAMINED WHETHER MATERNAL AND PATERNAL PERICONCEPTIONAL NUTRITION EFFECTS AN OFFSPRING'S LIKELIHOOD OF DEVELOPING CHRONIC METABOLIC RELATED CONDITIONS DUE TO EPIGENETIC IMPRINTING. METHODS: A LITERATURE SEARCH WAS CONDUCTED IN MULTIPLE SCIENCE DATABASES AND LIMITED TO STUDIES PUBLISHED AFTER 2012, IN ENGLISH LANGUAGE AND PEER REVIEWED. THE DATA FROM SELECTED ARTICLES WERE EXTRACTED AND A QUALITATIVE APPROACH WAS EMPLOYED DUE TO HETEROGENEITY OF RESULTS. RESULTS: NEWBORNS FROM OBESE FATHERS SHOWED ALTERED METHYLATION OVERALL AND SIGNIFICANT HYPOMETHYLATION AT THE INSULIN-LIKE GROWTH FACTOR 2 (IGF2) GENE. HIGH MATERNAL PRE-PREGNANCY BODY MASS INDEX (BMI) WAS ASSOCIATED WITH ALTERED OFFSPRING DNA METHYLATION LEVELS AND GESTATIONAL DIABETES MELLITUS INDUCED SIGNIFICANTLY INCREASED METHYLATION LEVELS IN OFFSPRING. GESTATIONAL WEIGHT GAIN WAS NOT ASSOCIATED WITH DIFFERENTIALLY METHYLATED CORD BLOOD. BIRTH WEIGHT WAS HIGHER IN OFFSPRING EXPOSED TO FAMINE IN EARLY GESTATION. OFFSPRING BORN POST MATERNAL BARIATRIC SURGERY SHOWED A LOWER PERCENTAGE OF BODY FAT AND IMPROVED FASTING INSULIN LEVELS COMPARED TO SIBLINGS BORN PRE-MATERNAL BARIATRIC SURGERY. CONCLUSIONS: THE AVAILABLE EVIDENCE SUGGESTS THAT POOR MATERNAL AND PATERNAL PERICONCEPTIONAL NUTRITION CAN INCREASE THE RISK OF METABOLIC SYNDROME IN OFFSPRING, THROUGH EPIGENETIC IMPRINTING. POTENTIAL PARENTS SHOULD BE ADVISED THAT MAINTAINING A HEALTHY DIET AND BMI IS LIKELY TO REDUCE THE RISK OF METABOLIC SYNDROME IN OFFSPRING.	2017	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     
10  5085  31 PILOT STUDY OF ABSOLUTE TELOMERE LENGTHS IN PRETERM INFANTS. BACKGROUND: ANNUALLY, APPROXIMATELY 15 MILLION BABIES ARE BORN PRETERM (<37 WEEKS GESTATIONAL AGE) GLOBALLY. IN THE NEONATAL INTENSIVE CARE UNIT (NICU) ENVIRONMENT, INFANTS ARE EXPOSED TO REPEATED STRESSFUL OR PAINFUL PROCEDURES AS PART OF ROUTINE LIFESAVING CARE. THESE PROCEDURES HAVE BEEN ASSOCIATED WITH EPIGENETIC ALTERATIONS THAT MAY LEAD TO AN INCREASED RISK OF NEURODEVELOPMENTAL DISORDERS. TELOMERE LENGTH HAS BEEN NEGATIVELY ASSOCIATED WITH ADVERSE LIFE EXPERIENCES IN STUDIES OF ADULTS. OBJECTIVES: THIS PILOT STUDY AIMED TO DESCRIBE TELOMERE LENGTH IN A SAMPLE OF PRETERM INFANTS AT NICU DISCHARGE AND EXAMINE ANY ASSOCIATIONS WITH PAIN, FEEDING METHOD, AND NEURODEVELOPMENT. METHODS: THIS DESCRIPTIVE PILOT STUDY SAMPLE INCLUDES BASELINE ABSOLUTE TELOMERE LENGTH (ATL) OF 36 PRETERM INFANTS IMMEDIATELY PRIOR TO DISCHARGE. QUANTITATIVE POLYMERASE CHAIN REACTION WAS USED TO DETERMINE ATL. INFANT DEMOGRAPHICS, PAIN/STRESS, TYPE OF FEEDING, ANTIBIOTIC USE, NEURODEVELOPMENT, AND BUCCAL SWAB DATA WERE COLLECTED. DESCRIPTIVE DATA ANALYSIS WAS USED TO DESCRIBE THE TELOMERE LENGTH USING GRAPHS. RESULTS: AMONG OUR PRETERM INFANT SAMPLES, THE MEAN ATL WAS FAR GREATER THAN THE AVERAGE ADULT TELOMERE LENGTH. ALTHOUGH NO SIGNIFICANT ASSOCIATIONS WERE FOUND BETWEEN ATL AND PAIN, FEEDING METHOD, AND NEURODEVELOPMENT, A TREND BETWEEN SEX WAS NOTED WHERE MALE TELOMERE LENGTHS WERE SHORTER THAN FEMALES AS THEY AGED. DISCUSSION: THIS IS ONE OF FEW STUDIES TO EVALUATE PRETERM INFANT TELOMERE LENGTH. ALTHOUGH OTHER RESEARCHERS HAVE USED RELATIVE TELOMERE LENGTH, WE USED THE MORE ACCURATE ATL. WE FOUND NONSIGNIFICANT SHORTER TELOMERE LENGTHS AMONG MALES. ADDITIONAL LARGE-SCALE, LONGITUDINAL STUDIES ARE NEEDED TO BETTER IDENTIFY THE PREDICTORS OF TELOMERE LENGTH AT THE TIME OF DISCHARGE FROM NICU.	2021	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
11  2646  24 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                          
12  3797  15 INTERNATIONAL BREAST CANCER AND NUTRITION: A MODEL FOR RESEARCH, TRAINING AND POLICY IN DIET, EPIGENETICS, AND CHRONIC DISEASE PREVENTION. THIS ARTICLE SUMMARIZES PRESENTATIONS FROM THE INTERNATIONAL BREAST CANCER AND NUTRITION WORKSHOP HELD DURING THE ASN SCIENTIFIC SESSIONS AND ANNUAL MEETING AT EXPERIMENTAL BIOLOGY 2014 IN SAN DIEGO, CA, ON 28 APRIL 2014. AN INTERNATIONAL COLLABORATION WAS DESCRIBED AMONG TEAMS FROM LOW-, MIDDLE-, AND HIGH-INCOME COUNTRIES ADDRESSING ENVIRONMENTAL FACTORS, ESPECIALLY DIET, AND EPIGENETIC INTERACTIONS THAT AFFECT THE RISK OF CHRONIC DISEASE. SPEAKERS ADDRESSED OPPORTUNITIES AND CHALLENGES INVOLVED IN THIS TYPE OF INTERNATIONAL COLLABORATION, ASSESSING DIET AND NUTRITIONAL STATUS ACROSS A WIDE RANGE OF CULTURES, AND RESEARCH TOOLS AND DISCOVERIES FROM THIS GROUP.	2014	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
13  2734  33 EXPLORING THE RELATIONSHIP BETWEEN DNA METHYLATION AGE MEASURES AND PSYCHONEUROLOGICAL SYMPTOMS IN WOMEN WITH EARLY-STAGE BREAST CANCER. PURPOSE: THE EPIGENETIC CLOCK HAS BEEN ACKNOWLEDGED AS AN INDICATOR FOR MOLECULAR AGING, BUT FEW STUDIES HAVE EXAMINED POSSIBLE ASSOCIATIONS OF DNA METHYLATION (DNAM) AGE OR AGE ACCELERATION (AA) WITH SYMPTOM BURDEN IN INDIVIDUALS WHO ARE TREATED FOR CANCER. THIS STUDY EXPLORED THE ASSOCIATION OF DNAM AGE OR AA WITH PSYCHONEUROLOGICAL (PN) SYMPTOMS, INCLUDING COGNITIVE IMPAIRMENT, FATIGUE, SLEEP DISTURBANCES, PAIN, AND DEPRESSIVE SYMPTOMS, IN BREAST CANCER SURVIVORS OVER A 2-YEAR PERIOD. METHODS: WE MEASURED PN SYMPTOMS USING RELIABLE INSTRUMENTS AND DNAM LEVELS BY INFINIUM HUMANMETHYLATION450K BEADCHIP (N = 72). DNAM AGE WAS CALCULATED BY THE HORVATH, GRIM, AND HANNUM-BASED INTRINSIC AND EXTRINSIC AGE ESTIMATIONS. AA WAS DEFINED BY THE RESIDUAL REGRESSING ESTIMATED EPIGENETIC AGE ON CHRONOLOGICAL AGE. MIXED REGRESSION MODELS WERE FITTED FOR AA AND CHANGES IN AA TO STUDY THE ASSOCIATION OVER TIME. SEPARATE LINEAR REGRESSION MODELS AND A MIXED-EFFECTS MODEL WERE FITTED FOR AA AT EACH TIME POINT. RESULTS: HORVATH-AA, GRIM-AA, AND EXTRINSIC EPIGENETIC AA WERE SIGNIFICANTLY CHANGED OVER TIME, WHILE INTRINSIC EPIGENETIC AA DID NOT EXHIBIT ANY TEMPORAL CHANGES. INCREASED AA WAS ASSOCIATED WITH GREATER ANXIETY AND FATIGUE, AS WELL AS WORSE COGNITIVE MEMORY, ADJUSTING FOR RACE, BMI, INCOME, CHEMOTHERAPY, RADIATION THERAPY, AND CHRONOLOGICAL AGE. INCREASED DNAM AGE WAS ASSOCIATED WITH GREATER ANXIETY OVER 2 YEARS. CONCLUSION: OUR FINDINGS SUGGEST DNAM AGE AND AA MAY BE ASSOCIATED WITH PN SYMPTOMS OVER THE COURSE OF CANCER TREATMENT AND SURVIVORSHIP. SOME PN SYMPTOMS MAY BE AMENABLE TO PREVENTIVE INTERVENTIONS TARGETED TO EPIGENETIC CLOCKS THAT INFLUENCE AGING-ASSOCIATED PROCESSES.	2022	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       
14  1221  28 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               
15  1776  33 ECONOMIC HARDSHIP AND BIOLOGICAL WEATHERING: THE EPIGENETICS OF AGING IN A U.S. SAMPLE OF BLACK WOMEN. BACKGROUND: PAST RESEARCH HAS LINKED LOW SOCIO-ECONOMIC STATUS (SES) TO INFLAMMATION, METABOLIC DYSREGULATION, AND VARIOUS CHRONIC AND AGE-RELATED DISEASES SUCH AS TYPE 2 DIABETES, CORONARY HEART DISEASE, STROKE, AND DEMENTIA. THESE STUDIES SUGGEST THAT THE CHALLENGES AND ADVERSITIES ASSOCIATED WITH LOW SES MAY RESULT IN PREMATURE AGING AND INCREASED RISK OF MORBIDITY AND MORTALITY. OBJECTIVE: BUILDING UPON THIS RESEARCH, THE PRESENT STUDY INVESTIGATES VARIOUS AVENUES WHEREBY LOW INCOME MIGHT ACCELERATE BIOLOGICAL AGING. METHODS: STRUCTURAL EQUATION MODELING AND LONGITUDINAL DATA FROM A SAMPLE OF 100 BLACK, MIDDLE-AGED WOMEN RESIDING IN THE UNITED STATES WAS USED TO INVESTIGATE THE EFFECT OF INCOME ON A RECENTLY DEVELOPED EPIGENETIC MEASURE OF BIOLOGICAL AGING. THIS MEASURE CAN BE USED AS A "BIOLOGICAL CLOCK" TO ASSESS, AT ANY POINT DURING ADULTHOOD, THE EXTENT TO WHICH AN INDIVIDUAL IS EXPERIENCING ACCELERATED OR DECELERATED BIOLOGICAL AGING. RESULTS: LOW INCOME DISPLAYED A ROBUST ASSOCIATION WITH ACCELERATED AGING THAT WAS UNAFFECTED AFTER CONTROLLING FOR OTHER SES-RELATED FACTORS SUCH AS EDUCATION, MARITAL STATUS, AND CHILDHOOD ADVERSITY. FURTHER, OUR ANALYSES INDICATED THAT THE ASSOCIATION BETWEEN INCOME AND BIOLOGICAL AGING WAS NOT EXPLAINED BY HEALTH-RELATED BEHAVIORS SUCH AS DIET, EXERCISE, SMOKING, ALCOHOL CONSUMPTION, OR HAVING HEALTH INSURANCE. RATHER, IN LARGE MEASURE, IT WAS FINANCIAL PRESSURE (DIFFICULTY PAYING BILLS, BUYING NECESSITIES, OR MEETING DAILY EXPENSES) THAT ACCOUNTED FOR THE ASSOCIATION BETWEEN LOW INCOME AND ACCELERATED AGING. CONCLUSIONS: THESE FINDINGS SUPPORT THE VIEW THAT CHRONIC FINANCIAL PRESSURES ASSOCIATED WITH LOW INCOME EXERT A WEATHERING EFFECT THAT RESULTS IN PREMATURE AGING.	2016	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                               
16  2605  17 EPIGENETICS-A POTENTIAL MEDIATOR BETWEEN AIR POLLUTION AND PRETERM BIRTH. PRETERM BIRTH IS A MAJOR CAUSE OF INFANT MORBIDITY AND MORTALITY AND A POTENTIAL RISK FACTOR FOR ADULT CHRONIC DISEASE. WITH OVER 15 MILLION INFANTS BORN PRETERM WORLDWIDE EACH YEAR, PRETERM BIRTH POSES A GLOBAL HEALTH CONCERN. THERE IS A POSSIBLE ASSOCIATION BETWEEN AIR POLLUTION AND PRETERM BIRTH, THOUGH STUDIES HAVE BEEN INCONSISTENT, LIKELY DUE TO VARIATION IN STUDY DESIGN. HOW AIR POLLUTION INDUCES HEALTH EFFECTS IS UNCERTAIN; HOWEVER, STUDIES HAVE REPEATEDLY DEMONSTRATED THE EFFECTS OF AIR POLLUTION ON EPIGENETIC MODIFICATIONS. MORE RECENT EVIDENCE SUGGESTS THAT EPIGENETICS MAY, IN TURN, BE LINKED TO PRETERM BIRTH. DISCOVERY OF ENVIRONMENTALLY MODIFIABLE EPIGENETIC PROCESSES CONNECTED TO PRETERM BIRTH MAY HELP TO IDENTIFY WOMEN AT RISK OF PRETERM BIRTH, AND ULTIMATELY LEAD TO DEVELOPMENT OF NEW PRETERM BIRTH PREVENTION MEASURES.	2016	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            
17  1971  20 EPIGENETIC ALTERATIONS ASSOCIATED WITH CHILDHOOD TRAUMA AND ADULT MENTAL HEALTH OUTCOMES: A SYSTEMATIC REVIEW. OBJECTIVES: MULTIPLE, CHRONIC AND REPEATED TRAUMA EXPOSURE IN CHILDHOOD IS ASSOCIATED WITH ADVERSE MENTAL HEALTH OUTCOMES IN ADULTHOOD. IN THIS PAPER WE SYNTHESISE THE LITERATURE ON EPIGENETIC MODIFICATIONS IN CHILDHOOD TRAUMA (CT) AND THE MEDIATING EFFECTS OF DIFFERENTIAL EPIGENETIC MECHANISMS ON THE ASSOCIATION BETWEEN CT AND THE LATER ONSET OF PSYCHIATRIC DISORDERS.METHODS: WE REVIEWED THE LITERATURE UP TO MARCH 2018 IN FOUR DATABASES: PUBMED, WEB OF SCIENCE, EBSCOHOST AND SCOPUS. NON-HUMAN STUDIES WERE EXCLUDED. ALL STUDIES INVESTIGATING CT EXPOSURE BOTH IN HEALTHY ADULTS (18 YEARS AND OLDER) AND ADULTS WITH PSYCHIATRIC DISORDERS WERE INCLUDED.RESULTS: THIRTY-SIX PUBLICATIONS WERE INCLUDED. FOR MOOD DISORDERS, METHYLATION OF THE GLUCOCORTICOID RECEPTOR NR3C1 GENE, SPECIFICALLY AT THE NGFI-A BINDING SITE IN EXON 1F, AND CORRELATION WITH CT WAS A ROBUST FINDING. SEVERAL STUDIES DOCUMENTED DIFFERENTIAL METHYLATION OF SLC6A4, BDNF, OXTR AND FKBP5 IN ASSOCIATION WITH CT. COMMON PATHWAYS IDENTIFIED INCLUDE NEURONAL FUNCTIONING AND MAINTENANCE, IMMUNE AND INFLAMMATORY PROCESSES, CHROMATIN AND HISTONE MODIFICATION, AND TRANSCRIPTION FACTOR BINDING.CONCLUSIONS: A VARIETY OF EPIGENETIC MEDIATORS THAT LIE ON A COMMON PATHWAY BETWEEN CT AND PSYCHIATRIC DISORDERS HAVE BEEN IDENTIFIED, ALTHOUGH LONGITUDINAL STUDIES AND CONSISTENCY IN METHODOLOGICAL APPROACH ARE NEEDED TO DISENTANGLE CAUSE AND EFFECT ASSOCIATIONS.	2020	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   
18  5395  27 REDUCED EPIGENETIC AGE IN OLDER ADULTS WITH HIGH SENSE OF PURPOSE IN LIFE. PSYCHOSOCIAL RISK FACTORS HAVE BEEN LINKED WITH ACCELERATED EPIGENETIC AGING, BUT LITTLE IS KNOWN ABOUT WHETHER PSYCHOSOCIAL RESILIENCE FACTORS (EG, SENSE OF PURPOSE IN LIFE) MIGHT REDUCE EPIGENETIC AGE ACCELERATION. IN THIS STUDY, WE TESTED IF OLDER ADULTS WHO EXPERIENCE HIGH LEVELS OF PURPOSE MIGHT SHOW REDUCED EPIGENETIC AGE ACCELERATION. WE EVALUATED THE RELATIONSHIP BETWEEN PURPOSE AND EPIGENETIC AGE ACCELERATION AS MEASURED BY 13 DNA METHYLATION (DNAM) "EPIGENETIC CLOCKS" ASSESSED IN 1 572 OLDER ADULTS FROM THE HEALTH AND RETIREMENT STUDY (MEAN AGE 70 YEARS). WE QUANTIFIED THE TOTAL ASSOCIATION BETWEEN PURPOSE AND DNAM AGE ACCELERATION AS WELL AS THE EXTENT TO WHICH THAT TOTAL ASSOCIATION MIGHT BE ATTRIBUTABLE TO DEMOGRAPHIC FACTORS, CHRONIC DISEASE, OTHER PSYCHOSOCIAL VARIABLES (EG, POSITIVE AFFECT), AND HEALTH-RELATED BEHAVIORS (HEAVY DRINKING, SMOKING, PHYSICAL ACTIVITY, AND BODY MASS INDEX [BMI]). PURPOSE IN LIFE WAS ASSOCIATED WITH REDUCED EPIGENETIC AGE ACCELERATION ACROSS 4 "SECOND-GENERATION" DNAM CLOCKS OPTIMIZED FOR PREDICTING HEALTH AND LONGEVITY (FALSE DISCOVERY RATE [FDR] Q < 0.0001: PHENOAGE, GRIMAGE, ZHANG EPIGENETIC MORTALITY INDEX; FDR Q < 0.05: DUNEDINPOAM). THESE ASSOCIATIONS WERE INDEPENDENT OF DEMOGRAPHIC AND PSYCHOSOCIAL FACTORS, BUT SUBSTANTIALLY ATTENUATED AFTER ADJUSTING FOR HEALTH-RELATED BEHAVIORS (DRINKING, SMOKING, PHYSICAL ACTIVITY, AND BMI). PURPOSE SHOWED NO SIGNIFICANT ASSOCIATION WITH 9 "FIRST-GENERATION" DNAM EPIGENETIC CLOCKS TRAINED ON CHRONOLOGICAL AGE. OLDER ADULTS WITH GREATER PURPOSE IN LIFE SHOW "YOUNGER" DNAM EPIGENETIC AGE ACCELERATION. THESE RESULTS MAY BE DUE IN PART TO ASSOCIATED DIFFERENCES IN HEALTH-RELATED BEHAVIORS. RESULTS SUGGEST NEW OPPORTUNITIES TO REDUCE BIOLOGICAL AGE ACCELERATION BY ENHANCING PURPOSE AND ITS BEHAVIORAL SEQUELAE IN LATE ADULTHOOD.	2023	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                         
19  3630  27 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	
                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                   
20  6478  20 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