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Central Adiposity and Increased Cortisol Reactivity to Stress: Potential Source of Increased Breast Cancer Risk among Women with a Family History of Breast Cancer

Bauchfett und erhoehte Cortisolreaktivitaet bei Stress: Potentielle Quelle fuer erhoehtes Brustkrebsrisiko bei Frauen mit familiaerer Haeufung von Brustkrebs

  • Objective: Only 20-25% of the variance for the two to four-fold increased risk of developing breast cancer among women with family histories of the disease can be explained by known gene mutations. Other factors must exist. Here, a familial breast cancer model is proposed in which overestimation of risk, general distress, and cancer-specific distress constitute the type of background stress sufficient to increase unrelated acute stress reactivity in women at familial risk for breast cancer. Furthermore, these stress reactions are thought to be associated with central adiposity, an independent well-established risk factor for breast cancer. Hence, stress through its hormonal correlates and possible associations with central adiposity may play a crucial role in the etiology of breast cancer in women at familial risk for the disease. Methods: Participants were 215 healthy working women with first-degree relatives diagnosed before (high familial risk) or after age 50 (low familial risk), or without breast cancer in first-degree relatives (no familial risk). Participants completed self-report measures of perceived lifetime breast cancer risk, intrusive thoughts and avoidance about breast cancer (Impact of Event Scale), negative affect (Profile of Mood States), and general distress (Brief Symptom Inventory). Anthropometric measurements were taken. Urine samples during work, home, and sleep were collected for assessment of cortisol responses in the naturalistic setting where work was conceptualized as the stressful time of the day. Results: A series of analyses indicated a gradient increase of cortisol levels in response to the work environment from no, low, to high familial risk of breast cancer. When adding breast cancer intrusions to the model with familial risk status predicting work cortisol levels, significant intrusion effects emerged rendering the familial risk group non-significant. However, due to a lack of association between intrusions and cortisol in the low and high familial risk group separately, as well as a significant difference between low and high familial risk on intrusions, but not on work cortisol levels, full mediation of familial risk group effects on work cortisol by intrusions could not be established. A separate analysis indicated increased levels of central but not general adiposity in women at high familial risk of breast cancer compared to the low and no risk groups. There were no significant associations between central adiposity and cortisol excretion. Conclusion: A hyperactive hypothalamus-pituitary-adrenal axis with a more pronounced excretion of its end product cortisol, as well as elevated levels of central but not overall adiposity in women at high familial risk for breast cancer may indicate an increased health risk which expands beyond that of increased breast cancer risk for these women.
  • Lediglich 20-25% der Varianz für das zwei- bis vierfach erhöhte Risiko an Brustkrebs zu erkranken wenn eine Familiengeschichte der Erkrankung vorliegt, kann durch derzeit bekannte Genmutationen erklärt werden. In dieser Arbeit wird ein Modell vorgeschlagen, in dem Überschätzung des eigenen Brustkrebsrisikos, genereller Distress und krebsspezifischer Distress zu einer Erhöhung von akuter Stressreaktivität führen. Dass Stressreaktionen mit Bauchfett assoziiert sind, ist wiederholt gezeigt worden. Bauchfett ist ein gut erforschter Risikofaktor für Brustkrebs. Teilnehmer dieser Studie waren 215 gesunde berufstätige Frauen mit hohem (HiFR), niedrigem (LoFR), und keinem (NoFR) familiären Brustkrebsrisiko. Neben der Erhebung von Frageboegen und Körpermassen wurden Urinproben zur Cortisolbestimmung während drei Zeitblöcken - Arbeitszeit, Freizeit, und Schlaf- gesammelt. Die Ergebnisse zeigten eine graduelle Steigerung der Arbeitszeitcortisolwerte über die drei Gruppen: von NoFR, über LoFR, zu HiFR. Brustkrebsintrusionen zeigten deutliche Effekte auf die Arbeitszeitcortisolwerte mit einer Reduzierung des Gruppeneffekts auf nicht-signifikantes Niveau. Eine gesonderte Analyse ergab erhöhte Bauchfettmasse, nicht jedoch generelles Übergewicht, in der Gruppe mit hohem familiären Risiko im Vergleich zu den beiden anderen Gruppen. Bauchfett korrelierte nicht mit den Cortisolreaktionen. Eine hyperaktive Hypothalamus-Hypophysen-Nebennierenrinden-Achse und erhöhte Bauchfettmasse stellen unter Umständen ein erhöhtes Gesundheitsrisiko für Frauen mit erhöhtem familiären Risiko für Brustkrebs dar.

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Metadaten
Author:Lucia Dettenborn
URN:urn:nbn:de:hbz:385-3277
Title Additional (English):Central Adiposity and Increased Cortisol Reactivity to Stress: Potential Source of Increased Breast Cancer Risk among Women with a Family History of Breast Cancer
Advisor:Dirk Hellhammer
Document Type:Doctoral Thesis
Language:English
Date of completion:2005/09/23
Publishing institution:Universität Trier
Granting institution:Universität Trier, Fachbereich 1
Date of final exam:2005/07/20
Release Date:2005/09/23
Tag:Bauchfett; Cortisol; Intrusionen
central adiposity; cortisol; familial risk; intrusions
GND Keyword:Anthropometrie; Brustkrebs; Stressreaktion
Institutes:Fachbereich 1 / Psychologie
Dewey Decimal Classification:1 Philosophie und Psychologie / 15 Psychologie / 150 Psychologie

$Rev: 13581 $