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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.
In letzter Zeit mehren sich psychoneuroimmunologische Forschungsbefunde, die darauf hindeuten, dass bestimmte chronische Schmerzsyndrome mit Dysregulationen der Hypothalamus-Hypophysen-Nebennierenrindenachse und des sympathoadrenalen Systems einhergehen können. Es wird davon ausgegangen, dass diese möglicherweise durch psychischen Stress bedingbaren Dysfunktionen zu einer potenzierten Sekretion von Entzündungsmediatoren und damit zur Sensibilisierung von peripheren Schmerzrezeptoren sowie zentralen nozizeptiven Neuronen führen. Aus den aktuell vorliegenden Studien lässt sich jedoch nicht ohne weiteres eine kausale Beeinflussung des Schmerzgeschehens durch Mediatorhormone des Stresssystems folgern. Vor diesem Hintergrund wurde untersucht, ob sich Zusammenhänge zwischen Cortisol (Hydrocortison) und Schmerzempfindlichkeit humanexperimentell realisieren und psychophysisch quantifizieren lassen. Durch Prüfung der Idoneität diverser Modelle peripher- und zentralnervöser Entzündungsschmerzprozesse konnte eine prinzipiell ursächliche Beeinflussung des Schmerzgeschehens durch Cortisol nachgewiesen und Befunde aus klinischen Studien validiert werden. Die Experimentalbefunde deuten auf eine spezifische Regulation algetischer Prozesse hin, die sich vielfach von bekannten antiinflammatorischen Corticosteroideffekten abhebt. Daraus ableitbare Anwendungen für die Schmerztherapie insbesondere präemptive Analgesie werden diskutiert.