Hypothalamic-pituitary-adrenocortical activity and response to cognitive behavior therapy in unmedicated, hospitalized depressed patients
OBJECTIVE: Surprisingly little research supports the hypothesis that depressions characterized by objective measures of neurobiological dysregulation respond poorly to psychotherapy. Moreover, relevant studies testing this hypothesis have been compromised by low rates of neurobiological abnormality...
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creator | THASE, M. E DUBE, S BOWLER, K HOWLAND, R. H MYERS, J. E FRIEDMAN, E JARRETT, D. B |
description | OBJECTIVE: Surprisingly little research supports the hypothesis that
depressions characterized by objective measures of neurobiological
dysregulation respond poorly to psychotherapy. Moreover, relevant studies
testing this hypothesis have been compromised by low rates of
neurobiological abnormality in outpatient samples. The authors therefore
investigated response to cognitive behavior therapy in relation to
pretreatment measures of hypothalamic-pituitary- adrenocortical (HPA)
activity in hospitalized, yet unmedicated, patients. METHOD: The subjects
were 29 unmedicated, hospitalized patients with major depression (DSM-III-R
and Schedule for Affective Disorders and Schizophrenia/Research Diagnostic
Criteria), nonpsychotic/nonbipolar subtype. After a 7- to 14-day
evaluation, urinary free cortisol levels and dexamethasone suppression
tests (DSTs) were obtained. Patients were treated for an average of 3 weeks
with intensive individual cognitive behavior therapy. Response was assessed
in relation to clinical severity of illness and pretreatment HPA
parameters. RESULTS: Response to inpatient cognitive behavior therapy was
inversely associated with pretreatment urinary free cortisol
concentrations, although not strongly correlated with DST results. Overall,
12 (92%) of 13 cortisol suppressors on the DST who had normal urinary free
cortisol concentrations responded to treatment, compared with only seven
(44%) of the 16 patients characterized by nonsuppression of cortisol and/or
elevated urinary free cortisol excretion. The relation between response to
cognitive behavior therapy and HPA activity was not explained by clinical
measures of symptom severity. CONCLUSIONS: Results are consistent with the
hypothesis that patients with increased HPA function are less responsive to
psychotherapy and, hence, might require somatic interventions. It is
proposed that the negative impact of hypercortisolism on neurocognitive
function mediates this relationship. |
doi_str_mv | 10.1176/ajp.153.7.886 |
format | Article |
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depressions characterized by objective measures of neurobiological
dysregulation respond poorly to psychotherapy. Moreover, relevant studies
testing this hypothesis have been compromised by low rates of
neurobiological abnormality in outpatient samples. The authors therefore
investigated response to cognitive behavior therapy in relation to
pretreatment measures of hypothalamic-pituitary- adrenocortical (HPA)
activity in hospitalized, yet unmedicated, patients. METHOD: The subjects
were 29 unmedicated, hospitalized patients with major depression (DSM-III-R
and Schedule for Affective Disorders and Schizophrenia/Research Diagnostic
Criteria), nonpsychotic/nonbipolar subtype. After a 7- to 14-day
evaluation, urinary free cortisol levels and dexamethasone suppression
tests (DSTs) were obtained. Patients were treated for an average of 3 weeks
with intensive individual cognitive behavior therapy. Response was assessed
in relation to clinical severity of illness and pretreatment HPA
parameters. RESULTS: Response to inpatient cognitive behavior therapy was
inversely associated with pretreatment urinary free cortisol
concentrations, although not strongly correlated with DST results. Overall,
12 (92%) of 13 cortisol suppressors on the DST who had normal urinary free
cortisol concentrations responded to treatment, compared with only seven
(44%) of the 16 patients characterized by nonsuppression of cortisol and/or
elevated urinary free cortisol excretion. The relation between response to
cognitive behavior therapy and HPA activity was not explained by clinical
measures of symptom severity. CONCLUSIONS: Results are consistent with the
hypothesis that patients with increased HPA function are less responsive to
psychotherapy and, hence, might require somatic interventions. It is
proposed that the negative impact of hypercortisolism on neurocognitive
function mediates this relationship.</description><identifier>ISSN: 0002-953X</identifier><identifier>EISSN: 1535-7228</identifier><identifier>DOI: 10.1176/ajp.153.7.886</identifier><identifier>PMID: 8659610</identifier><identifier>CODEN: AJPSAO</identifier><language>eng</language><publisher>Washington, DC: American Psychiatric Publishing</publisher><subject>Adolescent ; Adult ; Behavior therapy. Cognitive therapy ; Biological and medical sciences ; Brain ; Circadian Rhythm ; Cognition & reasoning ; Cognitive Therapy ; Depressive Disorder - diagnosis ; Depressive Disorder - metabolism ; Depressive Disorder - therapy ; Dexamethasone ; Female ; Hospitalization ; Humans ; Hydrocortisone - blood ; Hydrocortisone - urine ; Male ; Medical sciences ; Middle Aged ; Neurology ; Psychiatric Status Rating Scales ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Severity of Illness Index ; Therapy ; Treatment Outcome ; Treatments</subject><ispartof>The American journal of psychiatry, 1996-07, Vol.153 (7), p.886-891</ispartof><rights>1997 INIST-CNRS</rights><rights>Copyright American Psychiatric Association Jul 1996</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a407t-c2c547abcddc217e80ebbfd804347202030a0113e030356f1cfb2a500ceb5c7d3</citedby><cites>FETCH-LOGICAL-a407t-c2c547abcddc217e80ebbfd804347202030a0113e030356f1cfb2a500ceb5c7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://psychiatryonline.org/doi/epdf/10.1176/ajp.153.7.886$$EPDF$$P50$$Gappi$$H</linktopdf><linktohtml>$$Uhttps://psychiatryonline.org/doi/full/10.1176/ajp.153.7.886$$EHTML$$P50$$Gappi$$H</linktohtml><link.rule.ids>314,780,784,2859,21629,27869,27924,27925,77791,77792</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2749387$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8659610$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THASE, M. E</creatorcontrib><creatorcontrib>DUBE, S</creatorcontrib><creatorcontrib>BOWLER, K</creatorcontrib><creatorcontrib>HOWLAND, R. H</creatorcontrib><creatorcontrib>MYERS, J. E</creatorcontrib><creatorcontrib>FRIEDMAN, E</creatorcontrib><creatorcontrib>JARRETT, D. B</creatorcontrib><title>Hypothalamic-pituitary-adrenocortical activity and response to cognitive behavior therapy in unmedicated, hospitalized depressed patients</title><title>The American journal of psychiatry</title><addtitle>Am J Psychiatry</addtitle><description>OBJECTIVE: Surprisingly little research supports the hypothesis that
depressions characterized by objective measures of neurobiological
dysregulation respond poorly to psychotherapy. Moreover, relevant studies
testing this hypothesis have been compromised by low rates of
neurobiological abnormality in outpatient samples. The authors therefore
investigated response to cognitive behavior therapy in relation to
pretreatment measures of hypothalamic-pituitary- adrenocortical (HPA)
activity in hospitalized, yet unmedicated, patients. METHOD: The subjects
were 29 unmedicated, hospitalized patients with major depression (DSM-III-R
and Schedule for Affective Disorders and Schizophrenia/Research Diagnostic
Criteria), nonpsychotic/nonbipolar subtype. After a 7- to 14-day
evaluation, urinary free cortisol levels and dexamethasone suppression
tests (DSTs) were obtained. Patients were treated for an average of 3 weeks
with intensive individual cognitive behavior therapy. Response was assessed
in relation to clinical severity of illness and pretreatment HPA
parameters. RESULTS: Response to inpatient cognitive behavior therapy was
inversely associated with pretreatment urinary free cortisol
concentrations, although not strongly correlated with DST results. Overall,
12 (92%) of 13 cortisol suppressors on the DST who had normal urinary free
cortisol concentrations responded to treatment, compared with only seven
(44%) of the 16 patients characterized by nonsuppression of cortisol and/or
elevated urinary free cortisol excretion. The relation between response to
cognitive behavior therapy and HPA activity was not explained by clinical
measures of symptom severity. CONCLUSIONS: Results are consistent with the
hypothesis that patients with increased HPA function are less responsive to
psychotherapy and, hence, might require somatic interventions. It is
proposed that the negative impact of hypercortisolism on neurocognitive
function mediates this relationship.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Behavior therapy. Cognitive therapy</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Circadian Rhythm</subject><subject>Cognition & reasoning</subject><subject>Cognitive Therapy</subject><subject>Depressive Disorder - diagnosis</subject><subject>Depressive Disorder - metabolism</subject><subject>Depressive Disorder - therapy</subject><subject>Dexamethasone</subject><subject>Female</subject><subject>Hospitalization</subject><subject>Humans</subject><subject>Hydrocortisone - blood</subject><subject>Hydrocortisone - urine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Psychiatric Status Rating Scales</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Severity of Illness Index</subject><subject>Therapy</subject><subject>Treatment Outcome</subject><subject>Treatments</subject><issn>0002-953X</issn><issn>1535-7228</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>K30</sourceid><recordid>eNp1kc2KFDEUhQtRxp7RpUshqLgQq81PpZJeyjA6woAbBXfFrSRlp6lOYpIaaN_At_YO3QwiusoJ58vJ5Z6mecbomjHVv4NdWjMp1mqtdf-gWaGWreJcP2xWlFLebqT49rg5L2WHVyoUP2vOdC83PaOr5tf1IcW6hRn23rTJ18VXyIcWbHYhmpirNzATMNXf-nogECzJrqQYiiM1EhO_B4-eI6Pbwq2PmdSty5AOxAeyhL2zGFCdfUu2sWA-zP6ns8S6hDEFVYLqXajlSfNogrm4p6fzovn64erL5XV78_njp8v3Ny10VNXWcCM7BaOx1nCmnKZuHCeraSc6xSmnggJlTDgUQvYTM9PIQVJq3CiNsuKieX3MTTn-WFypw94X4-YZgotLGZRmrBOaIfjiL3AXlxxwtoFz2slu020Qevk_iEmmRcclvYtqj5TJsZTspiFlv8c9D4wOdy0O2CI-EIMasEXkn59SlxE3eE-fakP_1cmHgvVMGYLx5R7jCifTCrE3RwxS8n8M9s8_fwPajbWe</recordid><startdate>19960701</startdate><enddate>19960701</enddate><creator>THASE, M. E</creator><creator>DUBE, S</creator><creator>BOWLER, K</creator><creator>HOWLAND, R. H</creator><creator>MYERS, J. E</creator><creator>FRIEDMAN, E</creator><creator>JARRETT, D. 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E ; DUBE, S ; BOWLER, K ; HOWLAND, R. H ; MYERS, J. E ; FRIEDMAN, E ; JARRETT, D. B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a407t-c2c547abcddc217e80ebbfd804347202030a0113e030356f1cfb2a500ceb5c7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Behavior therapy. Cognitive therapy</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Circadian Rhythm</topic><topic>Cognition & reasoning</topic><topic>Cognitive Therapy</topic><topic>Depressive Disorder - diagnosis</topic><topic>Depressive Disorder - metabolism</topic><topic>Depressive Disorder - therapy</topic><topic>Dexamethasone</topic><topic>Female</topic><topic>Hospitalization</topic><topic>Humans</topic><topic>Hydrocortisone - blood</topic><topic>Hydrocortisone - urine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Psychiatric Status Rating Scales</topic><topic>Psychiatry</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Severity of Illness Index</topic><topic>Therapy</topic><topic>Treatment Outcome</topic><topic>Treatments</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THASE, M. 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E</au><au>DUBE, S</au><au>BOWLER, K</au><au>HOWLAND, R. H</au><au>MYERS, J. E</au><au>FRIEDMAN, E</au><au>JARRETT, D. B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypothalamic-pituitary-adrenocortical activity and response to cognitive behavior therapy in unmedicated, hospitalized depressed patients</atitle><jtitle>The American journal of psychiatry</jtitle><addtitle>Am J Psychiatry</addtitle><date>1996-07-01</date><risdate>1996</risdate><volume>153</volume><issue>7</issue><spage>886</spage><epage>891</epage><pages>886-891</pages><issn>0002-953X</issn><eissn>1535-7228</eissn><coden>AJPSAO</coden><abstract>OBJECTIVE: Surprisingly little research supports the hypothesis that
depressions characterized by objective measures of neurobiological
dysregulation respond poorly to psychotherapy. Moreover, relevant studies
testing this hypothesis have been compromised by low rates of
neurobiological abnormality in outpatient samples. The authors therefore
investigated response to cognitive behavior therapy in relation to
pretreatment measures of hypothalamic-pituitary- adrenocortical (HPA)
activity in hospitalized, yet unmedicated, patients. METHOD: The subjects
were 29 unmedicated, hospitalized patients with major depression (DSM-III-R
and Schedule for Affective Disorders and Schizophrenia/Research Diagnostic
Criteria), nonpsychotic/nonbipolar subtype. After a 7- to 14-day
evaluation, urinary free cortisol levels and dexamethasone suppression
tests (DSTs) were obtained. Patients were treated for an average of 3 weeks
with intensive individual cognitive behavior therapy. Response was assessed
in relation to clinical severity of illness and pretreatment HPA
parameters. RESULTS: Response to inpatient cognitive behavior therapy was
inversely associated with pretreatment urinary free cortisol
concentrations, although not strongly correlated with DST results. Overall,
12 (92%) of 13 cortisol suppressors on the DST who had normal urinary free
cortisol concentrations responded to treatment, compared with only seven
(44%) of the 16 patients characterized by nonsuppression of cortisol and/or
elevated urinary free cortisol excretion. The relation between response to
cognitive behavior therapy and HPA activity was not explained by clinical
measures of symptom severity. CONCLUSIONS: Results are consistent with the
hypothesis that patients with increased HPA function are less responsive to
psychotherapy and, hence, might require somatic interventions. It is
proposed that the negative impact of hypercortisolism on neurocognitive
function mediates this relationship.</abstract><cop>Washington, DC</cop><pub>American Psychiatric Publishing</pub><pmid>8659610</pmid><doi>10.1176/ajp.153.7.886</doi><tpages>6</tpages></addata></record> |
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language | eng |
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source | MEDLINE; Psychiatry Legacy Collection Online Journals 1844-1996; Periodicals Index Online |
subjects | Adolescent Adult Behavior therapy. Cognitive therapy Biological and medical sciences Brain Circadian Rhythm Cognition & reasoning Cognitive Therapy Depressive Disorder - diagnosis Depressive Disorder - metabolism Depressive Disorder - therapy Dexamethasone Female Hospitalization Humans Hydrocortisone - blood Hydrocortisone - urine Male Medical sciences Middle Aged Neurology Psychiatric Status Rating Scales Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Severity of Illness Index Therapy Treatment Outcome Treatments |
title | Hypothalamic-pituitary-adrenocortical activity and response to cognitive behavior therapy in unmedicated, hospitalized depressed patients |
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