The heritability of hypothalamus pituitary adrenal axis responses to psychosocial stress is context dependent.
Identifieur interne : 000728 ( PubMed/Corpus ); précédent : 000727; suivant : 000729The heritability of hypothalamus pituitary adrenal axis responses to psychosocial stress is context dependent.
Auteurs : Ilona S. Federenko ; Mitsue Nagamine ; Dirk H. Hellhammer ; Pathik D. Wadhwa ; Stefan WüstSource :
- The Journal of clinical endocrinology and metabolism [ 0021-972X ] ; 2004.
English descriptors
- KwdEn :
- Adolescent, Adrenocorticotropic Hormone (metabolism), Adult, Anxiety (etiology), Anxiety (psychology), Heart Rate, Humans, Hydrocortisone (metabolism), Hypothalamo-Hypophyseal System (physiopathology), Male, Mathematics, Mental Processes, Pituitary-Adrenal System (physiopathology), Saliva (metabolism), Smoking, Social Environment, Speech, Stress, Psychological (genetics), Stress, Psychological (physiopathology), Stress, Psychological (psychology).
- MESH :
- chemical , metabolism : Adrenocorticotropic Hormone, Hydrocortisone.
- etiology : Anxiety.
- genetics : Stress, Psychological.
- metabolism : Saliva.
- physiopathology : Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Stress, Psychological.
- psychology : Anxiety, Stress, Psychological.
- Adolescent, Adult, Heart Rate, Humans, Male, Mathematics, Mental Processes, Smoking, Social Environment, Speech.
Abstract
Individual differences in the response of the hypothalamus pituitary adrenal axis to stress are known to play an important role in health and disease risk. The origins, or determinants, of these individual differences are not well understood. To date, no study has examined the effects of context on the heritability of psychoendocrine stress responses. In the present study, 58 male twin pairs were exposed to a psychosocial stressor (Trier Social Stress Test) three times at weekly intervals, and their salivary and total cortisol, ACTH, and heart rate responses were assessed. Modest heritabilities were observed for all measures at the first stress exposure (all h2 < 0.33), but heritability estimates increased substantially with repetition of the stressor (T3: all h2 > 0.97). Concurrently, only the first but not the second and third Trier Social Stress Test exposure induced a significant increase in state anxiety (T1: P < 0.01, T2 and T3: n.s.), suggesting low heritabilities in a new, anxiety-evoking context and high heritabilities in a familiar, low-anxiety context. These findings challenge previous reports on a low heritability of markers of stimulated hypothalamus pituitary adrenal axis activity and are the first to document the relevance of context for psychoendocrine heritability estimates.
DOI: 10.1210/jc.2004-0981
PubMed: 15579784
Links to Exploration step
pubmed:15579784Le document en format XML
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Wadhwa</name></author><author><name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2004">2004</date><idno type="RBID">pubmed:15579784</idno><idno type="pmid">15579784</idno><idno type="doi">10.1210/jc.2004-0981</idno><idno type="wicri:Area/PubMed/Corpus">000728</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000728</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The heritability of hypothalamus pituitary adrenal axis responses to psychosocial stress is context dependent.</title><author><name sortKey="Federenko, Ilona S" sort="Federenko, Ilona S" uniqKey="Federenko I" first="Ilona S" last="Federenko">Ilona S. Federenko</name><affiliation><nlm:affiliation>Department of Clinical and Theoretical Psychobiology, University of Trier, Germany. ifederen@uci.edu</nlm:affiliation></affiliation></author><author><name sortKey="Nagamine, Mitsue" sort="Nagamine, Mitsue" uniqKey="Nagamine M" first="Mitsue" last="Nagamine">Mitsue Nagamine</name></author><author><name sortKey="Hellhammer, Dirk H" sort="Hellhammer, Dirk H" uniqKey="Hellhammer D" first="Dirk H" last="Hellhammer">Dirk H. Hellhammer</name></author><author><name sortKey="Wadhwa, Pathik D" sort="Wadhwa, Pathik D" uniqKey="Wadhwa P" first="Pathik D" last="Wadhwa">Pathik D. Wadhwa</name></author><author><name sortKey="Wust, Stefan" sort="Wust, Stefan" uniqKey="Wust S" first="Stefan" last="Wüst">Stefan Wüst</name></author></analytic><series><title level="j">The Journal of clinical endocrinology and metabolism</title><idno type="ISSN">0021-972X</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adrenocorticotropic Hormone (metabolism)</term><term>Adult</term><term>Anxiety (etiology)</term><term>Anxiety (psychology)</term><term>Heart Rate</term><term>Humans</term><term>Hydrocortisone (metabolism)</term><term>Hypothalamo-Hypophyseal System (physiopathology)</term><term>Male</term><term>Mathematics</term><term>Mental Processes</term><term>Pituitary-Adrenal System (physiopathology)</term><term>Saliva (metabolism)</term><term>Smoking</term><term>Social Environment</term><term>Speech</term><term>Stress, Psychological (genetics)</term><term>Stress, Psychological (physiopathology)</term><term>Stress, Psychological (psychology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adrenocorticotropic Hormone</term><term>Hydrocortisone</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Anxiety</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saliva</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Anxiety</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Heart Rate</term><term>Humans</term><term>Male</term><term>Mathematics</term><term>Mental Processes</term><term>Smoking</term><term>Social Environment</term><term>Speech</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Individual differences in the response of the hypothalamus pituitary adrenal axis to stress are known to play an important role in health and disease risk. The origins, or determinants, of these individual differences are not well understood. To date, no study has examined the effects of context on the heritability of psychoendocrine stress responses. In the present study, 58 male twin pairs were exposed to a psychosocial stressor (Trier Social Stress Test) three times at weekly intervals, and their salivary and total cortisol, ACTH, and heart rate responses were assessed. Modest heritabilities were observed for all measures at the first stress exposure (all h2 < 0.33), but heritability estimates increased substantially with repetition of the stressor (T3: all h2 > 0.97). Concurrently, only the first but not the second and third Trier Social Stress Test exposure induced a significant increase in state anxiety (T1: P < 0.01, T2 and T3: n.s.), suggesting low heritabilities in a new, anxiety-evoking context and high heritabilities in a familiar, low-anxiety context. These findings challenge previous reports on a low heritability of markers of stimulated hypothalamus pituitary adrenal axis activity and are the first to document the relevance of context for psychoendocrine heritability estimates.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15579784</PMID><DateCreated><Year>2004</Year><Month>12</Month><Day>06</Day></DateCreated><DateCompleted><Year>2005</Year><Month>02</Month><Day>03</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-972X</ISSN><JournalIssue CitedMedium="Print"><Volume>89</Volume><Issue>12</Issue><PubDate><Year>2004</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Journal of clinical endocrinology and metabolism</Title><ISOAbbreviation>J. Clin. Endocrinol. Metab.</ISOAbbreviation></Journal><ArticleTitle>The heritability of hypothalamus pituitary adrenal axis responses to psychosocial stress is context dependent.</ArticleTitle><Pagination><MedlinePgn>6244-50</MedlinePgn></Pagination><Abstract><AbstractText>Individual differences in the response of the hypothalamus pituitary adrenal axis to stress are known to play an important role in health and disease risk. The origins, or determinants, of these individual differences are not well understood. To date, no study has examined the effects of context on the heritability of psychoendocrine stress responses. In the present study, 58 male twin pairs were exposed to a psychosocial stressor (Trier Social Stress Test) three times at weekly intervals, and their salivary and total cortisol, ACTH, and heart rate responses were assessed. Modest heritabilities were observed for all measures at the first stress exposure (all h2 < 0.33), but heritability estimates increased substantially with repetition of the stressor (T3: all h2 > 0.97). Concurrently, only the first but not the second and third Trier Social Stress Test exposure induced a significant increase in state anxiety (T1: P < 0.01, T2 and T3: n.s.), suggesting low heritabilities in a new, anxiety-evoking context and high heritabilities in a familiar, low-anxiety context. These findings challenge previous reports on a low heritability of markers of stimulated hypothalamus pituitary adrenal axis activity and are the first to document the relevance of context for psychoendocrine heritability estimates.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Federenko</LastName><ForeName>Ilona S</ForeName><Initials>IS</Initials><AffiliationInfo><Affiliation>Department of Clinical and Theoretical Psychobiology, University of Trier, Germany. ifederen@uci.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagamine</LastName><ForeName>Mitsue</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Hellhammer</LastName><ForeName>Dirk H</ForeName><Initials>DH</Initials></Author><Author ValidYN="Y"><LastName>Wadhwa</LastName><ForeName>Pathik D</ForeName><Initials>PD</Initials></Author><Author 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