The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis
Identifieur interne : 001972 ( Istex/Corpus ); précédent : 001971; suivant : 001973The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis
Auteurs : Christine Heim ; D. Jeffrey Newport ; Dieter Wagner ; Molly M. Wilcox ; Andrew H. Miller ; Charles B. NemeroffSource :
- Depression and Anxiety [ 1091-4269 ] ; 2002.
English descriptors
Abstract
Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/da.10015
Links to Exploration step
ISTEX:A3465810B79883EF9CA8C349DEF3447226E20814Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title><author><name sortKey="Heim, Christine" sort="Heim, Christine" uniqKey="Heim C" first="Christine" last="Heim">Christine Heim</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Newport, D Jeffrey" sort="Newport, D Jeffrey" uniqKey="Newport D" first="D. Jeffrey" last="Newport">D. Jeffrey Newport</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Wagner, Dieter" sort="Wagner, Dieter" uniqKey="Wagner D" first="Dieter" last="Wagner">Dieter Wagner</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wilcox, Molly M" sort="Wilcox, Molly M" uniqKey="Wilcox M" first="Molly M." last="Wilcox">Molly M. Wilcox</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Miller, Andrew H" sort="Miller, Andrew H" uniqKey="Miller A" first="Andrew H." last="Miller">Andrew H. Miller</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Nemeroff, Charles B" sort="Nemeroff, Charles B" uniqKey="Nemeroff C" first="Charles B." last="Nemeroff">Charles B. Nemeroff</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A3465810B79883EF9CA8C349DEF3447226E20814</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1002/da.10015</idno><idno type="url">https://api.istex.fr/document/A3465810B79883EF9CA8C349DEF3447226E20814/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001972</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001972</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title><author><name sortKey="Heim, Christine" sort="Heim, Christine" uniqKey="Heim C" first="Christine" last="Heim">Christine Heim</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Newport, D Jeffrey" sort="Newport, D Jeffrey" uniqKey="Newport D" first="D. Jeffrey" last="Newport">D. Jeffrey Newport</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Wagner, Dieter" sort="Wagner, Dieter" uniqKey="Wagner D" first="Dieter" last="Wagner">Dieter Wagner</name><affiliation><mods:affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</mods:affiliation></affiliation></author><author><name sortKey="Wilcox, Molly M" sort="Wilcox, Molly M" uniqKey="Wilcox M" first="Molly M." last="Wilcox">Molly M. Wilcox</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Miller, Andrew H" sort="Miller, Andrew H" uniqKey="Miller A" first="Andrew H." last="Miller">Andrew H. Miller</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation></author><author><name sortKey="Nemeroff, Charles B" sort="Nemeroff, Charles B" uniqKey="Nemeroff C" first="Charles B." last="Nemeroff">Charles B. Nemeroff</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Depression and Anxiety</title><title level="j" type="abbrev">Depress. Anxiety</title><idno type="ISSN">1091-4269</idno><idno type="eISSN">1520-6394</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002">2002</date><biblScope unit="volume">15</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="117">117</biblScope><biblScope unit="page" to="125">125</biblScope></imprint><idno type="ISSN">1091-4269</idno></series><idno type="istex">A3465810B79883EF9CA8C349DEF3447226E20814</idno><idno type="DOI">10.1002/da.10015</idno><idno type="ArticleID">DA10015</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1091-4269</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>chronic stress</term><term>corticotropin‐releasing factor</term><term>depression</term><term>development</term><term>trauma</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Christine Heim Ph.D.</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</json:string></affiliations></json:item><json:item><name>D. Jeffrey Newport M.D.</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</json:string></affiliations></json:item><json:item><name>Dieter Wagner M.S.</name><affiliations><json:string>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</json:string></affiliations></json:item><json:item><name>Molly M. Wilcox B.A.</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</json:string></affiliations></json:item><json:item><name>Andrew H. Miller M.D.</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</json:string></affiliations></json:item><json:item><name>Charles B. Nemeroff M.D., Ph.D.</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</json:string><json:string>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>trauma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>chronic stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>development</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>depression</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corticotropin‐releasing factor</value></json:item></subject><articleId><json:string>DA10015</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>2008</abstractCharCount><pdfWordCount>5968</pdfWordCount><pdfCharCount>38905</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>285</abstractWordCount></qualityIndicators><title>The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title><refBibs><json:item><author><json:item><name>O Agid</name></json:item></author><host><volume>4</volume><pages><last>172</last><first>163</first></pages><author></author><title>Mol Psychiatry</title></host><title>Environment and vulnerability to major psychiatric illness: a case control study of early parental loss in major depression, bipolar disorder and schizophrenia</title></json:item><json:item><author><json:item><name>DG Baker Jr</name></json:item></author><host><volume>156</volume><pages><last>588</last><first>585</first></pages><author></author><title>Am J Psychiatry</title></host><title>Serial CSF corticotropin‐releasing hormone levels and adrenocortical activity in combat veterans with posttraumatic stress disorder</title></json:item><json:item><author><json:item><name>M Biondi</name></json:item></author><host><volume>68</volume><pages><last>150</last><first>114</first></pages><author></author><title>Psychother Psychosom</title></host><title>Psychological stress and neuroendocrine function in humans: the last two decades of research</title></json:item><json:item><author><json:item><name>DD Blake</name></json:item></author><host><volume>8</volume><pages><last>90</last><first>75</first></pages><author></author><title>J Traum Stress</title></host><title>The development of a clinician‐administered PTSD scale</title></json:item><json:item><author><json:item><name>JD Bremner</name></json:item></author><host><volume>150</volume><pages><last>239</last><first>234</first></pages><author></author><title>Am J Psychiatry</title></host><title>Childhood physical abuse and combat‐related posttraumatic stress disorder in Vietnam veterans</title></json:item><json:item><author><json:item><name>JD Bremner</name></json:item></author><host><volume>154</volume><pages><last>629</last><first>624</first></pages><author></author><title>Am J Psychiatry</title></host><title>Elevated CSF corticotropin‐releasing factor concentrations in PTSD</title></json:item><json:item><author><json:item><name>JD Bremner</name></json:item></author><host><volume>12</volume><pages><last>12</last><first>1</first></pages><author></author><title>Depress Anxiety</title></host><title>The Early Trauma Inventory: Development, reliability, validity</title></json:item><json:item><author><json:item><name>DR Britton</name></json:item></author><host><volume>31</volume><pages><last>367</last><first>363</first></pages><author></author><title>Life Sci</title></host><title>Intraventricular corticotropin‐releasing factor enhances behavioral effects of novelty</title></json:item><json:item><author><json:item><name>PB Chappell</name></json:item></author><host><volume>6</volume><pages><last>2914</last><first>2908</first></pages><author></author><title>J Neurosci</title></host><title>Alterations in corticotropin‐releasing factor‐like immunoreactivity in discrete rat brain regions after acute and chronic stress</title></json:item><json:item><author><json:item><name>M Cloitre</name></json:item></author><host><volume>9</volume><pages><last>482</last><first>473</first></pages><author></author><title>J Trauma Stress</title></host><title>Childhood abuse and subsequent sexual assault among female inpatients</title></json:item><json:item><author><json:item><name>JD Coplan</name></json:item></author><host><volume>93</volume><pages><last>1623</last><first>1619</first></pages><author></author><title>Proc Natl Acad Sci USA</title></host><title>Persistent elevations of cerebrospinal fluid concentrations of corticotropin‐releasing factor in adult nonhuman primates exposed to early‐life stressors: implications for the pathophysiology of mood and anxiety disorders</title></json:item><json:item><host><volume>4</volume><issue>2</issue><author></author><title>Diagnostic and statistical manual of mental disorders, 4th edition. 1994. Washington: American Psychiatric Association.</title></host></json:item><json:item><author><json:item><name>AJ Dunn</name></json:item></author><host><volume>15</volume><pages><last>100</last><first>71</first></pages><author></author><title>Brain Res Rev</title></host><title>Physiological and behavioral responses to corticotropin‐releasing factor administration: is CRF a mediator of anxiety or stress responses?</title></json:item><json:item><host><volume>4</volume><issue>2</issue><author></author><title>First MB, Spitzer RL, Gibbon M, Williams JB. 1997. Structured clinical interview for DSM‐IV. Washington: American Psychiatric Press.</title></host></json:item><json:item><author><json:item><name>U Gotthardt</name></json:item></author><host><volume>268</volume><pages><last>873</last><first>865</first></pages><author></author><title>Am J Physiol</title></host><title>Cortisol, ACTH, and cardiovascular response to a cognitive challenge paradigm in aging and depression</title></json:item><json:item><author><json:item><name>MA Green</name></json:item></author><host><volume>43</volume><pages><last>649</last><first>643</first></pages><author></author><title>J Clin Psychology</title></host><title>Five psychosocial variables related to the existence of posttraumatic stress disorder symptoms</title></json:item><json:item><author><json:item><name>M Hamilton</name></json:item></author><host><volume>12</volume><pages><first>56</first></pages><author></author><title>J Neurol Neurosurg Psychiatry</title></host><title>A rating scale for depression</title></json:item><json:item><author><json:item><name>C Heim</name></json:item></author><host><volume>46</volume><pages><last>1522</last><first>1509</first></pages><author></author><title>Biol Psychiatry</title></host><title>The impact of early adverse experiences on brain systems involved in anxiety and affective disorders</title></json:item><json:item><author><json:item><name>C Heim</name></json:item></author><host><volume>284</volume><pages><last>597</last><first>592</first></pages><author></author><title>JAMA</title></host><title>Increased pituitary‐adrenal and autonomic responses to stress in adult women after sexual and physical abuse in childhood</title></json:item><json:item><author><json:item><name>AD Kanner</name></json:item></author><host><volume>4</volume><pages><last>39</last><first>1</first></pages><author></author><title>J Behav Med</title></host><title>Comparison of two modes of stress measurement: daily hassles and uplifts versus major life events</title></json:item><json:item><author><json:item><name>KS Kendler</name></json:item></author><host><volume>49</volume><pages><last>116</last><first>109</first></pages><author></author><title>Arch Gen Psychiatry</title></host><title>Childhood parental loss and adult psychopathology in women: a twin perspective</title></json:item><json:item><author><json:item><name>KS Kendler</name></json:item></author><host><volume>150</volume><pages><last>1148</last><first>1139</first></pages><author></author><title>Am J Psychiatry</title></host><title>The prediction of major depression in women: toward an integrated model</title></json:item><json:item><author><json:item><name>RC Kessler</name></json:item></author><host><volume>23</volume><pages><last>690</last><first>679</first></pages><author></author><title>Psychol Med</title></host><title>Childhood adversities and adult depression: basic patterns of association in a US national survey</title></json:item><json:item><author><json:item><name>RC Kessler</name></json:item></author><host><volume>48</volume><pages><last>214</last><first>191</first></pages><author></author><title>Annu Rev Psychol</title></host><title>The effects of stressful life events on depression</title></json:item><json:item><author><json:item><name>C Kirschbaum</name></json:item></author><host><volume>75</volume><pages><last>1530</last><first>1526</first></pages><author></author><title>J Clin Endocrinol Metab</title></host><title>Heritability of cortisol responses to human corticotropin‐releasing hormone, ergometry, and psychological stress in humans</title></json:item><json:item><author><json:item><name>C Kirschbaum</name></json:item></author><host><volume>28</volume><pages><last>81</last><first>76</first></pages><author></author><title>Neuropsychoendocrinology</title></host><title>The Trier Social Stress Test: a tool for investigating psychobiological stress responses in a laboratory setting</title></json:item><json:item><author><json:item><name>CO Ladd</name></json:item></author><host><volume>137</volume><pages><last>1218</last><first>1212</first></pages><author></author><title>Endocrinology</title></host><title>Persistent changes in corticotropin‐releasing factor neuronal systems induced by maternal deprivation</title></json:item><json:item><author><json:item><name>I Liberzon</name></json:item></author><host><volume>22</volume><pages><last>453</last><first>443</first></pages><author></author><title>Psychoneuroendocrinology</title></host><title>Stress‐restress: effects on ACTH and fast feedback</title></json:item><json:item><author><json:item><name>I Liberzon</name></json:item></author><host><volume>21</volume><pages><last>50</last><first>40</first></pages><author></author><title>Neuropsychopharmacology</title></host><title>Neuroendocrine and psychophysiologic responses in PTSD: a symptom provocation study</title></json:item><json:item><author><json:item><name>JH Liem</name></json:item></author><host><volume>23</volume><pages><last>1157</last><first>1141</first></pages><author></author><title>Child Abuse Negl</title></host><title>Contextualizing the effect of childhood sexual abuse on adult self‐ and social functioning: an attachment theory perspective</title></json:item><json:item><author><json:item><name>SJ Lupien</name></json:item></author><host><volume>10</volume><pages><last>39</last><first>17</first></pages><author></author><title>Rev Neurosci</title></host><title>Increased cortisol levels and impaired cognition in human aging: implication for depression and dementia in later life</title></json:item><json:item><author><json:item><name>J McCauley</name></json:item></author><host><volume>277</volume><pages><last>1368</last><first>1362</first></pages><author></author><title>JAMA</title></host><title>Clinical characteristics of women with a history of childhood abuse</title></json:item><json:item><author><json:item><name>AC McFarlane</name></json:item></author><host><volume>174</volume><pages><last>14</last><first>4</first></pages><author></author><title>J Nerv Ment Dis</title></host><title>Posttraumatic morbidity of a disaster: a study of cases presenting for psychiatric treatment</title></json:item><json:item><author><json:item><name>CB Nemeroff</name></json:item></author><host><volume>226</volume><pages><last>1344</last><first>1342</first></pages><author></author><title>Science</title></host><title>Elevated concentrations of CSF corticotropin releasing factor like immunoreactivity in depressed patients</title></json:item><json:item><author><json:item><name>MJ Owens</name></json:item></author><host><volume>43</volume><pages><last>473</last><first>425</first></pages><author></author><title>Pharmacol Rev</title></host><title>Physiology and pharmacology of corticotropin‐releasing factor</title></json:item><json:item><author><json:item><name>PM Plotsky</name></json:item></author><host><volume>18</volume><pages><last>200</last><first>195</first></pages><author></author><title>Mol Brain Res</title></host><title>Early, postnatal experience alters hypothalamic corticotropin‐releasing factor (CRF) mRNA, median eminence CRF content and stress‐induced release in adult rats</title></json:item><json:item><author><json:item><name>PM Plotsky</name></json:item></author><host><author></author><title>J Neuroscience. In press</title></host><title>The effects of neonatal rearing environment on CRF mRNA and CRF receptor levels in adult rat brain</title></json:item><json:item><author><json:item><name>HS Resnick</name></json:item></author><host><volume>61</volume><pages><last>919</last><first>884</first></pages><author></author><title>J Consult Clin Psychol</title></host><title>Prevalence of civilian trauma and posttraumatic stress disorder in a representative national sample of women</title></json:item><json:item><author><json:item><name>IG Sarason</name></json:item></author><host><volume>46</volume><pages><last>946</last><first>932</first></pages><author></author><title>J Consult Clin Psychol</title></host><title>Assessing the impact of life changes: development of the Life Experiences Survey</title></json:item><json:item><author><json:item><name>K Schaaf</name></json:item></author><host><volume>22</volume><pages><last>1133</last><first>1119</first></pages><author></author><title>Child Abuse Negl</title></host><title>Relationship of childhood sexual, physical, and combined sexual and physical abuse to adult victimization and posttraumatic stress disorder</title></json:item><json:item><author><json:item><name>TE Seeman</name></json:item></author><host><volume>39</volume><pages><last>84</last><first>69</first></pages><author></author><title>J Psychosom Res</title></host><title>Self‐esteem and neuroendocrine response to challenge: MacArthur studies of successful aging</title></json:item><json:item><author><json:item><name>DJ Sirinathsinghji</name></json:item></author><host><volume>305</volume><pages><last>235</last><first>232</first></pages><author></author><title>Nature</title></host><title>Corticotropin‐releasing factor is a potent inhibitor of sexual receptivity in the female rat</title></json:item><json:item><author><json:item><name>RE Sutton</name></json:item></author><host><volume>297</volume><pages><last>333</last><first>331</first></pages><author></author><title>Nature</title></host><title>Corticotropin releasing factor produces behavioural activation in rats</title></json:item><json:item><author><json:item><name>HH van Dijken</name></json:item></author><host><volume>58</volume><pages><last>64</last><first>57</first></pages><author></author><title>Neuroendocrinology</title></host><title>Short inescapable stress produces long‐lasting changes in the brain‐pituitary‐adrenal axis of adult male rats</title></json:item><json:item><author><json:item><name>R Yehuda</name></json:item></author><host><volume>33</volume><pages><last>486</last><first>479</first></pages><author></author><title>Biol Psychiatry</title></host><title>Criteria for rationally evaluating animal models of posttraumatic stress disorder</title></json:item><json:item><author><json:item><name>LY Zaidi</name></json:item></author><host><volume>7</volume><pages><last>42</last><first>33</first></pages><author></author><title>J Trauma Stress</title></host><title>Childhood abuse experiences and combat related PTSD</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>15</volume><publisherId><json:string>DA</json:string></publisherId><pages><total>9</total><last>125</last><first>117</first></pages><issn><json:string>1091-4269</json:string></issn><issue>3</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1520-6394</json:string></eissn><title>Depression and Anxiety</title><doi><json:string>10.1002/(ISSN)1520-6394</json:string></doi></host><publicationDate>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1002/da.10015</json:string></doi><id>A3465810B79883EF9CA8C349DEF3447226E20814</id><score>0.59882677</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/A3465810B79883EF9CA8C349DEF3447226E20814/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/A3465810B79883EF9CA8C349DEF3447226E20814/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A3465810B79883EF9CA8C349DEF3447226E20814/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><availability><p>Copyright © 2002 Wiley‐Liss, Inc.</p></availability><date>2002</date></publicationStmt><notesStmt><note>General Clinical Research Centers Program - No. PHS M01‐RR00039;</note><note>Psychobiology of Corticotropin‐Releasing Factor NIH - No. MH‐42088;</note><note>Conte Center for the Neurobiology of Mental Disorders - No. MIMH 58922;</note><note>Deutsche Forschungsgemeinschaft - No. He 2561/2‐1;</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title><author xml:id="author-1"><persName><forename type="first">Christine</forename><surname>Heim</surname></persName><roleName type="degree">Ph.D.</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation></author><author xml:id="author-2"><persName><forename type="first">D. Jeffrey</forename><surname>Newport</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation></author><author xml:id="author-3"><persName><forename type="first">Dieter</forename><surname>Wagner</surname></persName><roleName type="degree">M.S.</roleName><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</affiliation></author><author xml:id="author-4"><persName><forename type="first">Molly M.</forename><surname>Wilcox</surname></persName><roleName type="degree">B.A.</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation></author><author xml:id="author-5"><persName><forename type="first">Andrew H.</forename><surname>Miller</surname></persName><roleName type="degree">M.D.</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation></author><author xml:id="author-6"><persName><forename type="first">Charles B.</forename><surname>Nemeroff</surname></persName><roleName type="degree">M.D., Ph.D.</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</affiliation></author></analytic><monogr><title level="j">Depression and Anxiety</title><title level="j" type="abbrev">Depress. Anxiety</title><idno type="pISSN">1091-4269</idno><idno type="eISSN">1520-6394</idno><idno type="DOI">10.1002/(ISSN)1520-6394</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2002"></date><biblScope unit="volume">15</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="117">117</biblScope><biblScope unit="page" to="125">125</biblScope></imprint></monogr><idno type="istex">A3465810B79883EF9CA8C349DEF3447226E20814</idno><idno type="DOI">10.1002/da.10015</idno><idno type="ArticleID">DA10015</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>trauma</term></item><item><term>chronic stress</term></item><item><term>development</term></item><item><term>depression</term></item><item><term>corticotropin‐releasing factor</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2001-05-14">Received</change><change when="2001-09-17">Registration</change><change when="2002">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/A3465810B79883EF9CA8C349DEF3447226E20814/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1520-6394</doi><issn type="print">1091-4269</issn><issn type="electronic">1520-6394</issn><idGroup><id type="product" value="DA"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="DEPRESSION AND ANXIETY">Depression and Anxiety</title><title type="short">Depress. Anxiety</title></titleGroup><selfCitationGroup><citation type="ancestor" xml:id="cit1"><journalTitle>Depression</journalTitle><accessionId ref="info:x-wiley/issn/10626417">1062-6417</accessionId><accessionId ref="info:x-wiley/issn/15227162">1522-7162</accessionId><pubYear year="1996">1996</pubYear><vol>4</vol><issue>2</issue></citation><citation type="ancestor" xml:id="cit2"><journalTitle>Anxiety</journalTitle><accessionId ref="info:x-wiley/issn/10709797">1070-9797</accessionId><accessionId ref="info:x-wiley/issn/15227154">1522-7154</accessionId><pubYear year="1996">1996</pubYear><vol>2</vol><issue>5</issue></citation></selfCitationGroup></publicationMeta><publicationMeta level="part" position="30"><doi origin="wiley" registered="yes">10.1002/da.v15:3</doi><numberingGroup><numbering type="journalVolume" number="15">15</numbering><numbering type="journalIssue">3</numbering></numberingGroup><coverDate startDate="2002">2002</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley" registered="yes">10.1002/da.10015</doi><idGroup><id type="unit" value="DA10015"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="publisher">Copyright © 2002 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2001-05-14"></event><event type="manuscriptAccepted" date="2001-09-17"></event><event type="firstOnline" date="2002-04-24"></event><event type="publishedOnlineFinalForm" date="2002-04-24"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-16"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-17"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst">117</numbering><numbering type="pageLast">125</numbering></numberingGroup><correspondenceTo>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:DA.DA10015.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="46"></count><count type="wordTotal" number="6805"></count></countGroup><titleGroup><title type="main" xml:lang="en">The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title><title type="short" xml:lang="en">Research Article: Experience and Stress Reactivity</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christine</givenNames><familyName>Heim</familyName><degrees>Ph.D.</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>D. Jeffrey</givenNames><familyName>Newport</familyName><degrees>M.D.</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Dieter</givenNames><familyName>Wagner</familyName><degrees>M.S.</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Molly M.</givenNames><familyName>Wilcox</familyName><degrees>B.A.</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Andrew H.</givenNames><familyName>Miller</familyName><degrees>M.D.</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Charles B.</givenNames><familyName>Nemeroff</familyName><degrees>M.D., Ph.D.</degrees></personName><contactDetails><email>cnemero@emory.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">trauma</keyword><keyword xml:id="kwd2">chronic stress</keyword><keyword xml:id="kwd3">development</keyword><keyword xml:id="kwd4">depression</keyword><keyword xml:id="kwd5">corticotropin‐releasing factor</keyword></keywordGroup><fundingInfo><fundingAgency>General Clinical Research Centers Program</fundingAgency><fundingNumber>PHS M01‐RR00039</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Psychobiology of Corticotropin‐Releasing Factor NIH</fundingAgency><fundingNumber>MH‐42088</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Conte Center for the Neurobiology of Mental Disorders</fundingAgency><fundingNumber>MIMH 58922</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Deutsche Forschungsgemeinschaft</fundingAgency><fundingNumber>He 2561/2‐1</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Research Article: Experience and Stress Reactivity</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis</title></titleInfo><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Heim</namePart><namePart type="termsOfAddress">Ph.D.</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D. Jeffrey</namePart><namePart type="family">Newport</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dieter</namePart><namePart type="family">Wagner</namePart><namePart type="termsOfAddress">M.S.</namePart><affiliation>Center for Psychobiological and Psychosomatic Research, University of Trier, Trier, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Molly M.</namePart><namePart type="family">Wilcox</namePart><namePart type="termsOfAddress">B.A.</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew H.</namePart><namePart type="family">Miller</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Charles B.</namePart><namePart type="family">Nemeroff</namePart><namePart type="termsOfAddress">M.D., Ph.D.</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia</affiliation><affiliation>Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, WMRB, Suite 4000, Atlanta, GA 30322</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002</dateIssued><dateCaptured encoding="w3cdtf">2001-05-14</dateCaptured><dateValid encoding="w3cdtf">2001-09-17</dateValid><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="references">46</extent><extent unit="words">6805</extent></physicalDescription><abstract lang="en">Sensitization of stress‐responsive neurobiological systems as a possible consequence of early adverse experience has been implicated in the pathophysiology of mood and anxiety disorders. In addition to early adversities, adulthood stressors are also known to precipitate the manifestation of these disorders. The present study sought to evaluate the relative role of early adverse experience vs. stress experiences in adulthood in the prediction of neuroendocrine stress reactivity in women. A total of 49 women (normal volunteers, depressed patients, and women with a history of early abuse) underwent a battery of interviews and completed dimensional rating scales on stress experiences and psychopathology, and were subsequently exposed to a standardized psychosocial laboratory stressor. Outcome measures were plasma adrenocorticotropin (ACTH) and cortisol responses to the stress test. Multiple linear regression analyses were performed to identify the impact of demographic variables, childhood abuse, adulthood trauma, major life events in the past year, and daily hassles in the past month, as well as psychopathology on hormonal stress responsiveness. Peak ACTH responses to psychosocial stress were predicted by a history of childhood abuse, the number of separate abuse events, the number of adulthood traumas, and the severity of depression. Similar predictors were identified for peak cortisol responses. Although abused women reported more severe negative life events in adulthood than controls, life events did not affect neuroendocrine reactivity. The regression model explained 35% of the variance of ACTH responses. The interaction of childhood abuse and adulthood trauma was the most powerful predictor of ACTH responsiveness. Our findings suggest that a history of childhood abuse per se is related to increased neuroendocrine stress reactivity, which is further enhanced when additional trauma is experienced in adulthood. Depression and Anxiety 15:117–125, 2002. © 2002 Wiley‐Liss, Inc.</abstract><note type="funding">General Clinical Research Centers Program - No. PHS M01‐RR00039; </note><note type="funding">Psychobiology of Corticotropin‐Releasing Factor NIH - No. MH‐42088; </note><note type="funding">Conte Center for the Neurobiology of Mental Disorders - No. MIMH 58922; </note><note type="funding">Deutsche Forschungsgemeinschaft - No. He 2561/2‐1; </note><subject lang="en"><genre>keywords</genre><topic>trauma</topic><topic>chronic stress</topic><topic>development</topic><topic>depression</topic><topic>corticotropin‐releasing factor</topic></subject><relatedItem type="host"><titleInfo><title>Depression and Anxiety</title></titleInfo><titleInfo type="abbreviated"><title>Depress. Anxiety</title></titleInfo><genre type="journal">journal</genre><subject><genre>article-category</genre><topic>Research Article</topic></subject><identifier type="ISSN">1091-4269</identifier><identifier type="eISSN">1520-6394</identifier><identifier type="DOI">10.1002/(ISSN)1520-6394</identifier><identifier type="PublisherID">DA</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>117</start><end>125</end><total>9</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>DepressionAnxiety</title></titleInfo><identifier type="ISSN">1062-6417</identifier><identifier type="ISSN">1522-7162</identifier><identifier type="ISSN">1070-9797</identifier><identifier type="ISSN">1522-7154</identifier><part><date point="end">1996</date><detail type="volume"><caption>last vol.</caption><number>4</number></detail><detail type="issue"><caption>last no.</caption><number>2</number></detail></part></relatedItem><identifier type="istex">A3465810B79883EF9CA8C349DEF3447226E20814</identifier><identifier type="DOI">10.1002/da.10015</identifier><identifier type="ArticleID">DA10015</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Rhénanie/explor/UnivTrevesV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001972 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001972 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Rhénanie
|area= UnivTrevesV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:A3465810B79883EF9CA8C349DEF3447226E20814
|texte= The role of early adverse experience and adulthood stress in the prediction of neuroendocrine stress reactivity in women: A multiple regression analysis
}}
| This area was generated with Dilib version V0.6.31. |  |