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Review

Behavioral Symptoms after Breast Cancer Treatment: A Biobehavioral Approach

by
Christopher Fagundes
1,2,3,*,
Angie LeRoy
4 and
Maryanne Karuga
5
1
Department of Psychology, Rice University, Houston, TX 77005, USA
2
Department of Symptoms Research, MD Anderson Cancer Center, Houston, TX 77030, USA
3
Department of Psychiatry, Baylor College of Medicine, Houston, TX 77030, USA
4
Department of Psychology, University of Houston, Houston, TX 77004, USA
5
Department of Science, Technology, Engineering, and Mathematics, Dillard University, New Orleans, LA 70122, USA
*
Author to whom correspondence should be addressed.
J. Pers. Med. 2015, 5(3), 280-295; https://doi.org/10.3390/jpm5030280
Submission received: 7 April 2015 / Revised: 17 July 2015 / Accepted: 23 July 2015 / Published: 3 August 2015
(This article belongs to the Special Issue Long-term Cancer Survivorship)
Versions Notes

Abstract

:
Being diagnosed and treated for breast cancer is emotionally and physically challenging. Breast cancer is the most commonly diagnosed cancer and the second leading cause of death for women in the United States. Accordingly, women with a breast cancer history are the largest group of female cancer survivors. Psychological stress substantially augments adverse autonomic, endocrine, and immune discharge, including enhanced production of proinflammatory cytokines. Importantly, inflammation is a key biological mechanism underlying the symptom cluster of pain, depression, fatigue, and sleep disturbances; there is also good evidence that inflammation contributes to breast cancer recurrence. Stress may exert direct effects on psychological and physiological risk processes. In this review, we take a biobehavioral approach to understanding predictors and mechanisms underlying somatic symptoms in breast cancer survivors.

1. Introduction

Being diagnosed and treated for breast cancer is emotionally and physically challenging. Breast cancer is the most commonly diagnosed cancer and the second leading cause of death for women in the United States [1]. There are more than 2.3 million breast cancer survivors in the United States, a number that is expected to dramatically increase; advances in adjuvant therapy combined with early tumor detection have dramatically improved disease-free survival for breast cancer survivors [1]. Accordingly, women with a breast cancer history are the largest group of female cancer survivors.
When primary treatment-related problems subside, many breast cancer survivors continue to report a heavy symptom burden that includes fatigue, depression, and disrupted sleep [2,3]. The survivorship period requires management of these ongoing physical symptoms and fears of recurrence. As the number of breast cancer survivors is projected to dramatically increase, more attention is being devoted to these issues [4].
In this paper, we provide a brief overview of the current state of the literature on post-treatment symptom burden in breast cancer survivors. Using Medline, CINAHL, and Psychinfo, (1960-week-present), we searched using recognizable terms in the breast cancer survivorship literature. The following words were used in combination with breast cancer survivors: symptoms, quality of life, fatigue, depression, pain, somatic, and sleep. This paper is not intended to be a systematic literature review and thus the themes presented below should not be viewed as comprehensive.

2. Symptom Overview

Behavioral symptoms such as fatigue, depression and sleep disturbance are among the most common and deleterious post-treatment problems in breast cancer survivors [5]. Just over a decade ago, an NIH State of the Science review concluded that post-treatment symptoms were undermanaged in cancer care and recommended an increased effort to develop evidence that would support the rationale for behavioral and pharmaceutical interventions to reduce symptom burden [6]. Since then, there has been substantial progress toward understanding the mechanisms and predictors that underlie post-treatment symptom burden.
Researchers have perhaps made the most progress in the area of cancer-related fatigue. The National Comprehensive Cancer Network (NCCN) defines cancer-related fatigue as an unusual, persistent, subjective sense of tiredness related to cancer or cancer treatment that interferes with usual functioning [7]. Once thought to be a byproduct of depressive symptoms, it is now a widely accepted condition with distinct features that differ from depression. Indeed, depressive symptoms and disturbed sleep are the strongest predictors of fatigue, however it has become clear that fatigue is not explained solely by depression or poor sleep [8]. Depression, sleep disturbance, and fatigue are disparate such that the cognitive and emotional characteristics of depression represent important distinguishing features [9]. Fatigue is the most common complaint among long-term cancer survivors [2,3], and interferes most with daily life [6,10]. Fatigue is a normal and expected response to chemotherapy and radiation [11], however, fatigue persists many years beyond cancer treatment in a substantial number of cancer survivors [12,13]. Indeed, a large-scale, longitudinal study of 763 breast cancer survivors found that 34% of the women were fatigued 5–10 years after diagnosis, compared to 35% 1–5 years after diagnosis; 21% of the women were fatigued at both assessments, suggesting cancer-related fatigue is both severe and persistent [2].
In addition to fatigue, depression is also a significant problem for breast cancer survivors. Cancer patients are four times more likely to have major depression [14]. The inherent difficulty in differentiating depressive symptoms from normal adjustment after breast cancer makes diagnosis difficult. Depression is characterized by feelings of sadness, hopelessness, helplessness, anhedonia, as well as insomnia and fatigue [15]. Depressive symptoms are high among breast cancer patients [16]. After completion of cancer treatment, depression is still a major concern. Adults with a history of cancer had a greater risk for depression than those who did not have a cancer history [17]. Indeed, breast cancer survivors are more likely to have mental health contacts and use mental health services than those without a cancer history [18].
Poor sleep is also a substantial problem for breast cancer survivors [19,20]. Sleep is measured by polysomnography, actigraphy, and self-report questionnaires such as the Pittsburgh Sleep Quality Index [21]. In general, these assessment tools characterize sleep quality as sleep duration, sleep latency, number of arousals, as well as subjective aspects such as feeling restful [21]. Disrupted sleep impacts between 30% and 50% of cancer patients, and persists after primary treatment in a number of breast cancer survivors [19,20]. As in other populations, sleep disturbances are associated with anxiety and depressive symptoms [19,20].
Behavioral symptoms such as fatigue, depression, and sleep disturbance are associated with substantial impairment in quality of life and also contribute to disease related outcomes. Although independently assessed, these symptoms often cluster [22]. In addition to assessing symptom severity, the construct of symptom interference is frequently utilized by the survivorship community. Symptom interference is essentially the degree to which symptoms interfere with the major aspects of a patient’s daily life [23]. The combined effects of all symptoms (often referred to as symptom burden) relative to a patient’s ability to function as he or she did before the onset of the disease or therapy is a useful metric to understand how much post-treatment symptoms impair a breast cancer survivor’s quality of life [6].

3. Biological Mechanisms

3.1. Inflammation, Sickness Behaviors, and Symptom Burden

Based on similarities between post-treatment cancer-related symptoms and cytokine-induced sickness behavior in animal models, researchers have devoted considerable work to the notion that post-treatment symptoms in cancer survivors may have an inflammatory basis [24]. Animal studies on neural-immune signaling have demonstrated that proinflammatory cytokines signal the central nervous system to trigger a constellation of behavioral changes that include fatigue, sleep disturbance, and depressive-like symptoms. Indeed, sickness behavior responses are observed in animals after the administration of infectious or inflammatory agents or certain proinflammatory cytokines [25]. Physically ill humans and animals exhibit sickness behaviors when exposed to infections. These behaviors are adaptive in that they help sick people restructure their perceptions and actions in order to conserve energy and resources. As described below, several cancer-related symptoms may be a partial side effect of persistent low-grade inflammation, representing a maladaptive version of inflammatory induced sickness behaviors [26].
Inflammation has been found to be a key mechanism underlying the symptom cluster of fatigue, depression, and sleep disturbance [26]. Fatigued breast cancer survivors had higher levels of proinflammatory activity including interleukin-1 receptor antagonist (IL-1ra), soluble tumor necrosis factor receptor Type II (sTNF-RII), and neopterin (a marker of macrophage activation), than breast cancer survivors who were not fatigued [10]. In another study, fatigued survivors had higher levels of soluble markers of proinflammatory cytokines IL-1ra and soluble interleukin-6 receptor (sIL-6r) than non-fatigued survivors [27]. Similarly, ex vivo production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) by lipopolysaccharide (LPS) stimulated monocytes was higher among fatigued compared to non-fatigued breast cancer survivors [28]. Finally, fatigued breast cancer survivors had greater increased LPS-stimulated IL-1β (beta) and IL-6 production from baseline to 30 min after the Trier Social Stress Task (a standardized laboratory stressor) than non-fatigued survivors [29].
Inflammation not only induces symptoms of sickness and fatigue, but also major depressive disorder [30,31,32,33,34,35]. Indeed, both syndromal depression as well as higher levels of depressive symptoms has been linked to heightened inflammation [30,31,32,33,34,35]. Even mild depressive symptoms have been linked to elevated proinflammatory cytokine production [31,32,36]. Depression can also promote inflammation creating a problematic feedback loop [37]. Psychological stressors can provoke transient increases in proinflammatory cytokines [30,31,32,33,34,35,38,39,40,41,42,43,44,45,46,47]. Evidence from animal and human studies suggests that stress and depression can permanently alter the responsiveness of the immune system; stressors can prime the inflammatory response promoting larger cytokine increases in response to subsequent stressors and/or minor infectious challenges [34,41,48,49,50,51]. Thus, it is not surprising that chronic stressors have been linked to sustained overproduction of a key proinflammatory cytokine, IL-6 [46].
Recent work has highlighted that inflammation is also associated with sleep disturbances. Indeed, inflammation is common among individuals with sleep disorders, as well as among those with objectively assessed sleep disturbance [52,53,54,55,56,57]. Between 40% and 50% of breast cancer survivors report sleep problems that appear to be partially attributable to elevations in inflammation [22]. Although inflammation is common among individuals with sleep disorders that are objectively measured, the relationship between self-reported sleep problems and inflammation is tenuous [22].

3.2. Stress and Inflammation: A Pathway to Symptom Burden

As reviewed elsewhere, there are multiple different factors that likely contribute to inflammatory induced symptoms in breast cancer survivors [58]. A primary tenant of the biobehavioral model that guides our research is that stress modulates autonomic and neuroendocrine discharge, which in turn, ultimately dysregulates inflammatory activity. We propose that high levels of stress directly promote symptom burden through autonomic, neuroendocrine, and immune dysregulation.
Both physical and psychological stressors can directly provoke increases in proinflammatory cytokines [30,31,32,33,34,35,38,42,43,44,45,46,47]. Furthermore, stress and depression also contribute to greater risk for infection, prolonged infectious episodes, and delayed wound healing [59,60,61,62,63], all processes that indirectly fuel sustained proinflammatory cytokine production. Compounding these risks, poor sleep, one very commonplace consequence of stress and depression, enhances inflammation [54,55,56].
There is evidence that greater stress or distress is associated with greater immune dysregulation in both cancer [64,65,66,67,68,69,70], and non-cancer populations [31,71,72,73,74,75,76]. Elevations in inflammatory markers can also be induced experimentally, using a standardized experimental performance task, such as the Trier Social Stress Test (TSST) [77,78,79]. This allows for the observation of individual differences in acute stress reactivity under controlled experimental conditions. Breast cancer survivors who are more fatigued show a greater inflammatory stress response than those who are not fatigued. Indeed, in a sample of 10 fatigued breast cancer survivors and 15 non-fatigued breast cancer survivors, those who were fatigued showed greater cytokine production when exposed to an experimental stressor compared to those who were not fatigued [80]. In a non-cancer sample, a laboratory stressor led to higher IL-6 responses in those with more depressive symptoms, compared with those experiencing less depressive symptoms [77].
Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, and particularly the stress hormone cortisol, has been implicated in the etiology of depression, and to a lesser extent fatigue and sleep in a large body of animal and human research. A healthy cortisol pattern includes a peak early in the morning and then decreases throughout the day [10]. In one study, fatigued breast cancer survivors had lower levels of morning serum cortisol than non-fatigued controls [10]. In another study, fatigued breast cancer survivors had flatter cortisol slopes across the day than non-fatigued survivors, as well as a rapid decline in cortisol levels in the evening [81]. Although cortisol generally inhibits inflammation, the persistence of high cortisol levels can lead immune cells to decrease their response to cortisol. Once a cell has become insensitive to glucocorticoids like cortisol, proinflammatory cytokines are produced in an unregulated environment. In turn, this environment enhances inflammation [82].
The autonomic stress response enhances sympathetic activity, which drives the “fight or flight response.” It also typically dampens parasympathetic activity. Because the autonomic nervous system can directly innervate immune organs, this autonomic profile of higher sympathetic and lower parasympathetic activity can raise inflammation [2,3,29,83,84,85]. Mechanistically, norepinephrine-dependent adrenergic stimulation activates nuclear factor kappa B (NF-κB), and NF-κB activates gene expression and production of proinflammatory cytokines associated with cancer-related fatigue [86]. Furthermore, lower parasympathetic activity results in higher levels of inflammation via the cholinergic anti-inflammatory pathway that facilitates acetylcholine release [87]. When acetylcholine interacts with the macrophage’s alpha-7 nicotinic receptor, it inhibits proinflammatory cytokine production [87]. Fatigued breast cancer survivors had higher sympathetic activity (as indexed by the catecholamine, norepinephrine) and lower parasympathetic activity (as indexed by high frequency heart rate variability or HF-HRV) compared with those who were not fatigued. This study was replicated by another laboratory [3]. This profile of autonomic activity (especially low parasympathetic activity) has been linked to depression and sleep disturbance as well [88,89,90,91,92,93,94,95,96].

4. Psychosocial Moderators

Stress is thought to play an important role in symptom burden by dysregulating the autonomic, neuroendocrine, and immune systems [97]. Research on stress and symptom burden has typically conceptualized stress as an acute trigger for the onset of disease and associated symptoms [97]. Recently, behavioral scientists have taken a life-course perspective for the study of stress and disease [98]. This perspective highlights that cumulative exposure to various types of adversity has a profound impact on symptom burden by dysregulating the autonomic, neuroendocrine, and immune systems [98]. Accordingly, stressful life experiences such as abuse, being low socioeconomic status (SES), or being a victim of discrimination and prejudice may all impact cancer-related symptoms.
Trauma victims are particularly vulnerable to emotional distress and somatic symptoms after breast cancer treatment. Adult trauma survivors suffered more cancer-related distress than those who did not report traumatic experiences after treatment for breast cancer [99]. Further, breast cancer survivors who were abused or neglected as children reported more psychological distress, poorer functional well-being, and more cancer related fatigue compared with who did not report childhood abuse [100]. Child adversity was also associated with elevated markers of inflammation in breast cancer survivors [101]. It is possible that profound stressors such as these prime the inflammatory stress response making women particularly vulnerable to post-treatment symptoms after cancer treatment.
People of lower socioeconomic position are confronted with a number of important social and environmental conditions that contribute to chronic stress and depression, which leads to considerable cumulative stress exposure over the life course [102,103,104]. Socioeconomic disparities in cancer-related symptom burden exist such that those with lower socioeconomic status are disproportionally burdened by post-treatment cancer-related fatigue, depression, and sleep problems [2,5,10,13,27,85,105,106]. These findings echo the well-established inverse, monotonic relationship between socioeconomic status and other health outcomes [102].
Ethnic minority breast cancer survivors report significantly worse symptom burden than others [107]. These disparities are thought to arise from a combination of economic, social, and cultural factors. Among breast cancer survivors, African American and Hispanic survivors report significantly poorer physical functioning compared to Caucasian and Asian American survivors [108]. Among breast cancer survivors, African American and Hispanic survivors report significantly lower physical functioning compared to Caucasian and Asian American survivors [108]. The US Latino population is growing rapidly, and Mexican-Americans form the largest Latino subgroup. On average, Latinos have very low socioeconomic status [109]. It is possible that the effects of Latino ethnicity and low socioeconomic status are interactive. Specifically, the effects of low socioeconomic status may be heightened in Latinos due to exposure to stressors specific to being a minority.
Social support can serve as a protective factor for reducing cancer-related symptoms [110]. Although social support can be defined in many ways, it generally is the perception or experience that you are loved and cared for by others, esteemed and valued, and part of a social network [111]. Higher levels of social support predicted improvements in subjective well-being over time among breast cancer survivors [112]. Breast cancer patients who reported greater life stress also experienced less mood disturbances if they had more people in their support network [113]. The beneficial effects of social support seem to exist cross-culturally. In Taiwan, social support buffered breast cancer survivors’ depressive symptoms [114]. In other work, social support predicted the degree to which breast cancer survivors reported positive personal growth as a result of their cancer [112].

5. Exercise to Improve Symptom Burden

Exercise may be one of the most important health behaviors for cancer survivors to maintain. Physical activity level is related to symptom burden [115]. In one study, survivors who met the general physical activity recommendation had less symptom burden than those who did not [116]. As evidenced in multiple intervention studies, exercise may even be powerful enough to change cancer survivors’ post-treatment symptoms [117]. This seems to be true even among ethnic minorities. For example, an exercise intervention improved physical fitness, reduced perceived stress, and decreased cortisol levels among Hispanics [118]. Although intense exercise regiments are not always possible for breast cancer survivors, moderate exercise regiments, such as yoga, may be particularly helpful. Indeed, yoga improved mood, alleviated fatigue, and lowered inflammation in breast cancer survivors [119].

6. Pharmaceutical Treatments to Improve QOL

Several barriers have hindered the development of clinical trials in symptom management. First, the subjective nature of fatigue symptoms has limited innovative research into the mechanisms underlying these symptoms and the development of novel ways of treating or preventing them. However, patient-reported outcome research has recently been promoted by the U.S. Food and Drug Administration (FDA) for more accurate therapeutic agent evaluation, and symptom reduction has been recognized as a primary clinical benefit for drug approval [120,121]. In addition, until recently, there has been a lack of understanding of the biological mechanisms that underlie subjective symptoms.
Perhaps the most obvious drug to treat these post-treatment symptoms in breast cancer survivors is selective serotonin reuptake inhibitors (SSRIs). Indeed, newer antidepressants are widely used in women with breast cancer for treatment of depression and are prescribed for tamoxifen related hot flashes and various other indications. Although SSRIs are useful in the treatment of depression in this population, they do not appear to impact fatigue or pain [122].
The control or prevention of cancer-related cytokine dysregulation presents a novel opportunity for symptom reduction. However, many of the agents that might be effective in the control of inflammation are generic, and sometimes even over the counter. Nonsteroidal anti-inflammatory drugs (NSAIDs) are one such drug. NSAIDs inhibit proinflammatory cytokines by inhibiting the enzyme cyclooxygenase (Cox), which is responsible for inflammatory production. Different NSAIDs inhibit the activity of either cyclooxygenase-1 (COX-1) or cyclooxygenase-2 (COX-2), or both to different degrees, and thereby, the synthesis of prostaglandins and thromboxanes. NSAIDs are weak acids that are well absorbed from the stomach and intestinal mucosa where they are then metabolized in the liver.
Studies have investigated whether the use of anti-inflammatory agents improve the antidepressant response for treatment resistant depression where inflammation is the likely culprit. A recent meta-analysis of 10 trials (4258 participants) revealed that anti-inflammatory treatment reduces depressive symptoms compared with placebo [123]. Across 10 trials, NSAIDS reduced depressive symptoms without adverse effects. Importantly, the antidepressant effect was shown to be independent of pain relief. There have been no studies investigating the direct effect of NSAIDS on cancer-related symptoms; this is an interesting avenue for future research [123].

7. Conclusions

Being diagnosed and treated for breast cancer is emotionally and physically challenging. Even when treatment-related problems subside, many breast cancer survivors report symptoms of depression, fatigue, and sleep disturbance [5]. The physical and psychological effects of the aftermath of a cancer diagnosis and its treatment are notable. Psychological stress substantially augments adverse autonomic, endocrine, and immune discharge, including enhanced production of proinflammatory cytokines [124]. Importantly, inflammation is a key biological mechanism underlying the symptom cluster of depression, fatigue, and sleep disturbances; there is also good evidence that inflammation contributes to breast cancer recurrence [6,125]. Stress may exert direct effects on psychological and physiological risk processes [98,126]. As the population of breast cancer survivors grows, a biobehavioral approach to research and treatment will be needed.

Author Contributions

Christopher Fagundes was the main contributor of the paper’s conceptualization. Angie LeRoy contributed to the section on psychosocial moderators. Maryanne Karuga contributed to the introduction and conclusion, as well as formatting.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. DeSantis, C.; Ma, J.; Bryan, L.; Jemal, A. Breast cancer statistics, 2013. CA Cancer J. Clin. 2014, 64, 52–62. [Google Scholar] [CrossRef] [PubMed]
  2. Bower, J.E.; Ganz, P.A.; Desmond, K.A.; Bernaards, C.; Rowland, J.H.; Meyerowitz, B.E.; Belin, T.R. Fatigue in long-term breast carcinoma survivors: A longitudinal investigation. Cancer 2006, 106, 751–758. [Google Scholar] [CrossRef] [PubMed]
  3. Fagundes, C.P.; Lindgren, M.E.; Kiecolt-Glaser, J.K. Psychoneuroimmunology and Cancer: Incidence, Progression, and Quality of Life. In Psychological Aspects of Cancer; Springer: New York, NY, USA, 2013; pp. 1–11. [Google Scholar]
  4. Khatcheressian, J.L.; Hurley, P.; Bantug, E.; Esserman, L.J.; Grunfeld, E.; Halberg, F.; Hantel, A.; Henry, N.L.; Muss, H.B.; Smith, T.J.; et al. Breast cancer follow-up and management after primary treatment: American Society of Clinical Oncology clinical practice guideline update. J. Clin. Oncol. 2013, 31, 961–965. [Google Scholar] [CrossRef] [PubMed]
  5. Bower, J.E. Behavioral symptoms in patients with breast cancer and survivors. J. Clin. Oncol. 2008, 26, 768–777. [Google Scholar] [CrossRef] [PubMed]
  6. Cleeland, C.S.; Bennett, G.J.; Dantzer, R.; Dougherty, P.M.; Dunn, A.J.; Meyers, C.A.; Miller, A.H.; Payne, R.; Reuben, J.M.; Wang, X.S.; et al. Are the symptoms of cancer and cancer treatment due to a shared biologic mechanism? A cytokine-immunologic model of cancer symptoms. Cancer 2003, 97, 2919–2925. [Google Scholar] [CrossRef] [PubMed]
  7. National Comprehensive Cancer Network: NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines): Cancer-Related Fatigue; National Comprehensive Cancer Network (NCCN): Fort Washington, PA, USA, 2011.
  8. Bower, J.E. Prevalence and causes of fatigue after cancer treatment: The next generation of research. J. Clin. Oncol. 2005, 23, 8280–8282. [Google Scholar] [CrossRef] [PubMed]
  9. Brown, L.F.; Kroenke, K. Cancer-related fatigue and its associations with depression and anxiety: A systematic review. Psychosomatics 2009, 50, 440–447. [Google Scholar] [CrossRef]
  10. Bower, J.E.; Ganz, P.A.; Aziz, N.; Fahey, J.L. Fatigue and proinflammatory cytokine activity in breast cancer survivors. Psychosomatic Med. 2002, 64, 604–611. [Google Scholar] [CrossRef]
  11. Smets, E.; Garssen, B.; Schuster-Uitterhoeve, A.; de Haes, J. Fatigue in cancer patients. Br. J. Cancer 1993, 68, 220–224. [Google Scholar] [CrossRef] [PubMed]
  12. Prue, G.; Rankin, J.; Allen, J.; Gracey, J.; Cramp, F. Cancer-related fatigue: A critical appraisal. Eur. J. Cancer 2006, 42, 846–863. [Google Scholar] [CrossRef] [PubMed]
  13. Bower, J.E.; Ganz, P.A.; Desmond, K.A.; Bernards, C.; Rowland, J.H.; Meyerowitz, B.E.; Belin, T.R. Fatigue in breast cancer survivors: Occurrence, correlates, and impact on quality of life. J. Clin. Oncol. 2000, 18, 743–753. [Google Scholar] [PubMed]
  14. Kessler, R.; Berglund, P.; Demler, O.; Jin, R.; Koretz, D.; Merikangas, K.R.; Rush, A.J.; Walters, E.E.; Wang, P.S. The epidemiology of major depressive disorder: Results from the National Comorbidity Survey replication. JAMA 2003, 289, 3095–3105. [Google Scholar] [CrossRef] [PubMed]
  15. Stanton, A.L.; Bower, J.E. Psychological Adjustment in Breast Cancer Survivors. In Improving Outcomes for Breast Cancer Survivors; Springer: New York, NY, USA, 2015; pp. 231–242. [Google Scholar]
  16. Stommel, M.; Kurtz, M.E.; Kurtz, J.C.; Given, C.W.; Given, B.A. A longitudinal analysis of the course of depressive symptomatology in geriatric patients with cancer of the breast, colon, lung, or prostate. Health Psychol. 2004, 23, 564–573. [Google Scholar] [CrossRef] [PubMed]
  17. Reyes-Gibby, C.C.; Aday, L.A.; Anderson, K.O.; Mendoza, T.R.; Cleeland, C.S. Pain, depression, and fatigue in community-dwelling adults with and without a history of cancer. J. Pain Symptom Manag. 2006, 32, 118–128. [Google Scholar] [CrossRef] [PubMed]
  18. Hewitt, M.; Rowland, J.H. Mental health service use among adult cancer survivors: Analyses of the National Health Interview survey. J. Clin. Oncol. 2002, 20, 4581–4590. [Google Scholar] [CrossRef] [PubMed]
  19. Morin, C.M.; Ware, J.C. Sleep and psychopathology. Appl. Prev. Psychol. 1996, 5, 211–224. [Google Scholar] [CrossRef]
  20. Savard, J.; Simard, S.; Ivers, H.; Morin, C.M. Randomized study on the efficacy of cognitive-behavioral therapy for insomnia secondary to breast cancer, part II: Immunologic effects. J. Clin. Oncol. 2005, 23, 6097–6106. [Google Scholar] [CrossRef] [PubMed]
  21. Mollayeva, T.; Thurairajah, P.; Burton, K.; Mollayeva, S.; Shapiro, C.M.; Colantonio, A. The Pittsburgh sleep quality index as a screening tool for sleep dysfunction in clinical and non-clinical samples: A systematic review and meta-analysis. Sleep Med. Rev. 2015. [Google Scholar] [CrossRef] [PubMed]
  22. Bower, J.E.; Ganz, P.A.; Irwin, M.R.; Kwan, L.; Breen, E.C.; Cole, S.W. Inflammation and behavioral symptoms after breast cancer treatment: Do fatigue, depression, and sleep disturbance share a common underlying mechanism? J. Clin. Oncol. 2011, 29, 3517–3522. [Google Scholar] [CrossRef] [PubMed]
  23. Wang, X.S.; Zhao, F.; Fisch, M.J.; O'Mara, A.M.; Cella, D.; Mendoza, T.R.; Cleeland, C.S. Prevalence and characteristics of moderate to severe fatigue: A multicenter study in cancer patients and survivors. Cancer 2014, 120, 425–432. [Google Scholar] [CrossRef] [PubMed]
  24. Dantzer, R.; Heijnen, C.J.; Kavelaars, A.; Laye, S.; Capuron, L. The neuroimmune basis of fatigue. Trends Neurosci. 2014, 37, 39–46. [Google Scholar] [CrossRef] [PubMed]
  25. Dantzer, R.; Meagher, M.W.; Cleeland, C.S. Translational approaches to treatment-induced symptoms in cancer patients. Nat. Rev. Clin. Oncol. 2012, 9, 414–426. [Google Scholar] [CrossRef] [PubMed]
  26. Diamond, L.M.; Hicks, A.M.; Otter-Henderson, K.D. Every time you go away: Changes in affect, behavior, and physiology associated with travel-related separations from romantic partners. J. Personal. Soc. Psychol. 2008, 95, 385–403. [Google Scholar] [CrossRef] [PubMed]
  27. Bower, J.E.; Ganz, P.A.; Aiziz, N.; Fahey, J.L.; Cole, S.W. T-cell homeostasis in breast cancer survivors with persistent fatigue. J. Natl. Cancer Inst. 2003, 95, 1165–1168. [Google Scholar] [CrossRef] [PubMed]
  28. Collado-Hidalgo, A.; Bower, J.E.; Ganz, P.A.; Cole, S.W. Irwin MR: Inflammatory biomarkers for persistent fatigue in breast cancer survivors. Clin. Cancer Res. 2006, 12, 2759–2766. [Google Scholar] [CrossRef] [PubMed]
  29. Cohen, S.; Wills, T.A. Stress, social support, and the buffering hypothesis. Psychol. Bull. 1985, 98, 310–357. [Google Scholar] [CrossRef] [PubMed]
  30. Dentino, A.N.; Pieper, C.F.; Rao, M.K.; Currie, M.S.; Harris, T.; Blazer, D.G.; Cohen, H.J. Association of interleukin-6 and other biologic variables with depression in older people living in the community. J. Am. Geriatr. Soc. 1999, 47, 6–11. [Google Scholar] [CrossRef] [PubMed]
  31. Lutgendorf, S.K.; Garand, L.; Buckwalter, K.C.; Reimer, T.T.; Hong, S.Y.; Lubaroff, D.M. Life stress, mood disturbance, and elevated interleukin-6 in healthy older women. J. Gerontol.: Ser. A Biol. Sci. Med. Sci. 1999, 54, M434–M439. [Google Scholar] [CrossRef]
  32. Maes, M.; Song, C.; Lin, A.; de Jongh, R.; van Gastel, A.; Kenis, G.; Bosmans, E.; de Meester, I.; Benoy, I.; Neels, H. The effects of psychological stress on humans: Increased production of pro-inflammatory cytokines and a Th1-like response in stress-induced anxiety. Cytokine 1998, 10, 313–318. [Google Scholar] [CrossRef] [PubMed]
  33. Maes, M.; Lin, A.; Delmeire, L.; van Gastel, A.; Kenis, G.; de Jongh, R.; Bosmans, E. Elevated serum interleukin-6 (IL-6) and IL-6 receptor concentrations in posttraumatic stress disorder following accidental man-made traumatic events. Biol. Psychiatr. 1999, 45, 833–839. [Google Scholar] [CrossRef]
  34. Glaser, R.; Robles, T.; Sheridan, J.; Malarkey, W.B.; Kiecolt-Glaser, J.K. Mild depressive symptoms are associated with amplified and prolonged inflammatory responses following influenza vaccination in older adults. Arch. Gen. Psychiatr. 2003, 60, 1009–1014. [Google Scholar] [CrossRef] [PubMed]
  35. Suarez, E.C.; Lewis, J.G.; Krishnan, R.R.; Young, K.H. Enhanced expression of cytokines and chemokines by blood monocytes to in vitro lipopolysaccharide stimulation are associated with hostility and severity of depressive symptoms in healthy women. Psychoneuroendocrinology 2004, 29, 1119–1128. [Google Scholar] [CrossRef] [PubMed]
  36. Irwin, M. Psychoneuroimmunology of depression: Clinical implications. Brain Behav. Immun. 2002, 16, 1–16. [Google Scholar] [CrossRef] [PubMed]
  37. Miller, G.E.; Chen, E.; Parker, K.J. Psychological stress in childhood and susceptibility to the chronic diseases of aging: Moving toward a model of behavioral and biological mechanisms. Psychol. Bull. 2011, 137, 959–997. [Google Scholar] [CrossRef] [PubMed]
  38. Lutgendorf, S.K.; Logan, H.; Costanzo, E.; Lubaroff, D. Effects of acute stress, relaxation, and a neurogenic inflammatory stimulus on interleukin-6 in humans. Brain Behav. Immun. 2004, 18, 55–64. [Google Scholar] [CrossRef]
  39. Steptoe, A.; Hamer, M.; Chida, Y. The effects of acute psychological stress on circulating inflammatory factors in humans: A review and meta-analysis. Brain Behav. Immun. 2007, 21, 901–912. [Google Scholar] [CrossRef] [PubMed]
  40. Brydon, L.; Wright, C.E.; OʼDonnell, K.; Zachary, I.; Wardle, J.; Steptoe, A. Stress-induced cytokine responses and central adiposity in young women. Int. J. Obes. 2008, 32, 443–450. [Google Scholar] [CrossRef] [PubMed]
  41. Smith, T.W.; Uchino, B.N.; Florsheim, P.; Berg, C.A.; Butner, J.; Hawkins, M.; Henry, N.J.; Beveridge, R.M.; Pearce, G.; Hopkins, P.N.; et al. Affiliation and control during marital disagreement, history of divorce, and asymptomatic coronary artery calcification in older couples. Psychosomatic Med. 2011, 73, 350–357. [Google Scholar] [CrossRef] [PubMed]
  42. DeRijk, R.; Michelson, D.; Karp, B.; Petrides, J.; Galliven, E.; Deuster, P.; Paciotti, G.; Gold, P.W.; Sternberg, E.M. Exercise and circadian rhythm-induced variations in plasma cortisol differentially regulate interleukin-1b (IL-1b), IL-6, and tumor necrosis factor-a (TNF-a) production in humans: High sensitivity of TNF-a and resistance of IL-6. J. Clin. Endocrinol. Metab. 1997, 82, 2182–2192. [Google Scholar] [PubMed]
  43. Zhou, D.; Kusnecov, A.W.; Shurin, M.R.; DePaoli, M.; Rabin, B.S. Exposure to physical and psychological stressors elevates plasma interleukin 6: Relationship to the activation of hypothalamic-pituitary-adrenal axis. Endocrinology 1993, 133, 2523–2530. [Google Scholar] [PubMed]
  44. Brydon, L.; Edwards, S.; Mohamed-Ali, V.; Steptoe, A. Socioeconomic status and stress-induced increases in interleukin-6. Brain Behav. Immun. 2004, 18, 281–290. [Google Scholar] [CrossRef] [PubMed]
  45. Segerstrom, S.C.; Miller, G.E. Psychological stress and the human immune system: A meta-analytic study of 30 years of inquiry. Psychol. Bull. 2004, 130, 1–37. [Google Scholar] [CrossRef] [PubMed]
  46. Kiecolt-Glaser, J.K.; Preacher, K.J.; MacCallum, R.C.; Atkinson, C.; Malarkey, W.B.; Glaser, R. Chronic stress and age-related increases in the proinflammatory cytokine IL-6. Proc. Natl. Acad. Sci. USA 2003, 100, 9090–9095. [Google Scholar] [CrossRef] [PubMed]
  47. Pitsavos, C.; Panagiotakos, D.B.; Papageorgiou, C.; Tsetsekou, E.; Soldatos, C.; Stefanadis, C. Anxiety in relation to inflammation and coagulation markers, among healthy adults: The ATTICA study. Atherosclerosis 2006, 185, 320–326. [Google Scholar] [CrossRef] [PubMed]
  48. Johnson, J.D.; OʼConnor, K.A.; Deak, T.; Stark, M.; Watkins, L.R.; Maier, S.F. Prior stressor exposure sensitizes LPS-induced cytokine production. Brain Behav. Immun. 2002, 16, 461–476. [Google Scholar] [CrossRef] [PubMed]
  49. Johnson, J.D.; OʼConnor, K.A.; Deak, T.; Stark, M.; Watkins, L.R.; Maier, S.F. Prior stressor exposure primes the HPA axis. Psychoneuroendocrinology 2002, 27, 353–365. [Google Scholar] [CrossRef]
  50. Dantzer, R.; Wollman, E.; Vitkovic, L.; Yirmiya, R. Cytokines and depression: Fortuitous or causative association? Mol. Psychiatr. 1999, 4, 328–332. [Google Scholar] [CrossRef]
  51. Maes, M.; Ombelet, W.; de Jongh, R.; Kenis, G.; Bosmans, E. The inflammatory response following delivery is amplified in women who previously suffered from major depression, suggesting that major depression is accompanied by a sensitization of the inflammatory response system. J. Affect. Disord. 2001, 63, 85–92. [Google Scholar] [CrossRef]
  52. Vgontzas, A.N.; Chrousos, G.P. Sleep, the hypothalamic-pituitary-adrenal axis, and cytokines: Multiple interactions and disturbances in sleep disorders. Endocrinol. Metab. Clin. N. Am. 2002, 31, 15–36. [Google Scholar] [CrossRef]
  53. Vgontzas, A.N.; Papanicolaou, D.A.; Bixler, E.O.; Kales, A.; Tyson, K.; Chrousos, G.P. Elevation of plasma cytokines in disorders of excessive daytime sleepiness: Role of sleep disturbance and obesity. J. Clin. Endocrinol. Metab. 1997, 82, 1313–1316. [Google Scholar] [CrossRef] [PubMed]
  54. Vgontzas, A.N.; Papanicolaou, D.A.; Bixler, E.O.; Lotsikas, A.; Zachman, K.; Kales, A.; Prolo, P.; Wong, M.L.; Licinio, J.; Gold, P.W.; et al. Circadian interleukin-6 secretion and quantity and depth of sleep. J. Clin. Endocrinol. Metab. 1999, 84, 2603–2607. [Google Scholar] [CrossRef] [PubMed]
  55. Vgontzas, A.N.; Zoumakis, M.; Bixler, E.O.; Lin, H.M.; Prolo, P.; Vela-Bueno, A.; Kales, A.; Chrousos, G.P. Impaired nighttime sleep in healthy old versus young adults is associated with elevated plasma interleukin-6 and cortisol levels: Physiologic and therapeutic implications. J. Clin. Endocrinol. Metab. 2003, 88, 2087–2095. [Google Scholar] [CrossRef] [PubMed]
  56. Irwin, M.R.; Wang, M.G.; Campomayor, C.O.; Collado-Hidalgo, A.; Cole, S. Sleep deprivation and activation of morning levels of cellular and genomic markers of inflammation. Arch. Intern. Med. 2006, 166, 1756–1762. [Google Scholar] [CrossRef] [PubMed]
  57. Gustafson, P. Work-related travel, gender and family obligations. Work Employ. Soc. 2006, 20, 513–530. [Google Scholar] [CrossRef]
  58. Bower, J.E. Cancer-related fatigue: Links with inflammation in cancer patients and survivors. Brain Behav. Immun. 2007, 21, 863–871. [Google Scholar] [CrossRef] [PubMed]
  59. Kiecolt-Glaser, J.K.; Dura, J.R.; Speicher, C.E.; Trask, O.J.; Glaser, R. Spousal caregivers of dementia victims: Longitudinal changes in immunity and health. Psychosomatic Med. 1991, 53, 345–362. [Google Scholar] [CrossRef]
  60. Kiecolt-Glaser, J.K.; Glaser, R.; Gravenstein, S.; Malarkey, W.B.; Sheridan, J. Chronic stress alters the immune response to influenza virus vaccine in older adults. Proc. Natl. Acad. Sci. USA 1996, 93, 3043–3047. [Google Scholar] [CrossRef] [PubMed]
  61. Vedhara, K.; Cox, N.K.M.; Wilcock, G.K.; Perks, P.; Hunt, M.; Anderson, S.; Lightman, S.L.; Shanks, N.M. Chronic stress in elderly carers of dementia patients and antibody response to influenza vaccination. Lancet 1999, 353, 627–631. [Google Scholar] [CrossRef]
  62. Kiecolt-Glaser, J.K.; Marucha, P.T.; Malarkey, W.B.; Mercado, A.M.; Glaser, R. Slowing of wound healing by psychological stress. Lancet 1995, 346, 1194–1196. [Google Scholar] [CrossRef]
  63. Glaser, R.; Sheridan, J.F.; Malarkey, W.B.; MacCallum, R.C.; Kiecolt-Glaser, J.K. Chronic stress modulates the immune response to a pneumococcal pneumonia vaccine. Psychosomatic Med. 2000, 62, 804–807. [Google Scholar] [CrossRef]
  64. Andersen, B.L.; Farrar, W.B.; Golden-Kreutz, D.; Kutz, L.A.; MacCallum, R.; Courtney, M.E.; Glaser, R. Stress and immune responses after surgical treatment for regional breast cancer. J. Natl. Cancer Inst. 1998, 90, 30–36. [Google Scholar] [PubMed]
  65. Andersen, B.L. Psychological Interventions for Cancer Patients. In Evidence-Based Cancer Care and Prevention: Behavioral Interventions; Given, C.W., Given, B., Champion, V.L., Kozachik, S., deVoss, D.N., Eds.; Springer Publishing Company, Inc.: New York, NY, USA, 2003. [Google Scholar]
  66. Vitaliano, P.P.; Scanlan, J.M.; Ochs, H.D.; Syriala, K.; Siegler, I.C.; Snyder, E.A. Psychosocial stress moderates the relationship of cancer history with natural killer cell activity. Ann. Behav. Med. 1998, 20, 199–208. [Google Scholar] [CrossRef] [PubMed]
  67. Sachs, G.; Rasoul-Rockenschaub, S.; Aschauer, H.; Spiess, K.; Gober, I.; Staffen, A.; Zielinski, C. Lytic effector cell activity and major depressive disorder in patients with breast cancer: A prospective study. J. Neuroimmunol. 1995, 59, 83–89. [Google Scholar] [PubMed]
  68. Musselman, D.L.; Miller, A.H.; Porter, M.R.; Manatunga, A.; Gao, F.; Penna, S.; Pearce, B.D.; Landry, J.; Glover, S.; et al. Higher than normal plasma interleukin-6 concentrations in cancer patients with depression: Preliminary findings. Am. J. Psychiatr. 2001, 158, 1252–1257. [Google Scholar] [CrossRef] [PubMed]
  69. Antoni, M.H.; Lutgendorf, S.K.; Cole, S.W.; Dhabhar, F.S.; Sephton, S.E.; McDonald, P.G.; Stefanek, M.; Sood, A.K. The influence of bio-behavioural factors on tumour biology: Pathways and mechanisms. Nat. Rev. Cancer 2006, 6, 240–248. [Google Scholar] [PubMed]
  70. Costanzo, E.S.; Lutgendorf, S.K.; Sood, A.K.; Anderson, B.; Sorosky, J.; Lubaroff, D.M. Psychosocial factors and interleukin-6 among women with advanced ovarian cancer. Cancer 2005, 104, 305–313. [Google Scholar] [CrossRef] [PubMed]
  71. Kiecolt-Glaser, J.K. Norman Cousins Memorial Lecture 1998. Stress, personal relationships, and immune function: Health implications. Brain Behav. Immun. 1999, 13, 61–72. [Google Scholar] [CrossRef] [PubMed]
  72. Delahanty, D.L.; Dougall, A.L.; Schmitz, J.B.; Hawken, L.; Trakowski, J.H.; Jenkins, F.J.; Baum, A. Time course of natural killer cell activity and lymphocyte proliferation in response to two acute stressors in healthy men. Health Psychol. 1996, 15, 48–55. [Google Scholar] [CrossRef] [PubMed]
  73. Delahanty, D.L.; Dougall, A.L.; Baum, A. Neuroendocrine and Immune Alterations Following Natural Disasters and Traumatic Stress. In Psychoneuroimmunology; Ader, R., Felten, D.L., Cohen, N., Eds.; Academic Press: San Diego, CA, USA, 2001; Volume 2, pp. 335–348. [Google Scholar]
  74. Ironson, G.; Wynings, C.; Schneiderman, N.; Baum, A.; Rodriguez, M.; Greenwood, D.; Benight, C.; Antoni, M.; LaPerriere, A.; Huang, H.S.; et al. Posttraumatic stress symptoms, intrusive thoughts, loss and immune function after Hurricane Andrew. Psychosomatic Med. 1997, 59, 128–141. [Google Scholar] [CrossRef]
  75. Kop, W.J.; Gottdiener, J.S.; Tangen, C.M.; Fried, L.P.; McBurnie, M.A.; Walston, J.; Newman, A.; Hirsch, C.; Tracy, R.P. Inflammation and coagulation factors in persons >65 years of age with symptoms of depression but without evidence of myocardial ischemia. Am. J. Cardiol. 2002, 89, 419–424. [Google Scholar] [CrossRef]
  76. Miller, G.E.; Cohen, S. Psychological interventions and the immune system: A meta-analytic review and critique. Health Psychol. 2001, 20, 47–63. [Google Scholar] [CrossRef] [PubMed]
  77. Fagundes, C.P.; Glaser, R.; Hwang, B.S.; Malarkey, W.B.; Kiecolt-Glaser, J.K. Depressive symptoms enhance stress-induced inflammatory responses. Brain Behav. Immun. 2012, 31, 172–176. [Google Scholar] [CrossRef] [PubMed]
  78. Pace, T.W.W.; Mletzko, T.C.; Alagbe, O.; Musselman, D.L.; Nemeroff, C.B.; Miller, A.H.; Heim, C.M. Increased stress-induced inflammatory responses in male patients with major depression and increased early life stress. Am. J. Psychiatr. 2006, 163, 1630–1632. [Google Scholar] [CrossRef] [PubMed]
  79. Carpenter, L.L.; Gawuga, C.E.; Tyrka, A.R.; Lee, J.K.; Anderson, G.M.; Price, L.H. Association between plasma IL-6 response to acute stress and early-life adversity in healthy adults. Neuropsychopharmacology 2010, 35, 2617–2623. [Google Scholar] [CrossRef] [PubMed]
  80. Bower, J.E.; Ganz, P.A.; Aziz, N.; Olmstead, R.; Irwin, M.R.; Cole, S.W. Inflammatory responses to psychological stress in fatigued breast cancer survivors: Relationship to glucocorticoids. Brain Behav. Immun. 2007, 21, 251–258. [Google Scholar] [CrossRef] [PubMed]
  81. Bower, J.E.; Ganz, P.A.; Aziz, N. Altered cortisol response to psychologic stress in breast cancer survivors with persistent fatigue. Psychosomatic Med. 2005, 67, 277–280. [Google Scholar] [CrossRef] [PubMed]
  82. Barnes, P.J.; Adcock, I.M. Glucocorticoid resistance in inflammatory diseases. Lancet 2009, 373, 1905–1917. [Google Scholar] [CrossRef]
  83. Thayer, J.; Sternberg, E. Beyond heart rate variability: Vagal regulation of allostatic systems. Ann. N. Y. Acad. Sci. 2006, 1088, 361–372. [Google Scholar] [CrossRef] [PubMed]
  84. Fagundes, C.P.; Glaser, R.; Alfano, C.M.; Bennett, J.M.; Povoski, S.P.; Lipari, A.M.; Agnese, D.M.; Yee, L.D.; Carson, W.E.; Farrar, W.B.; et al. Fatigue and herpesvirus Latency in women newly diagnosed with breast cancer. Brain Behav. Immun. 2011, 26, 394–400. [Google Scholar] [CrossRef] [PubMed]
  85. Fagundes, C.P.; Murray, D.M.; Hwang, B.S.; Gouin, J.P.; Thayer, J.F.; Sollers, J.J.; Shapiro, C.L.; Malarkey, W.B.; Kiecolt-Glaser, J.K. Sympathetic and parasympathetic activity in cancer-related fatigue: More evidence for a physiological substrate in cancer survivors. Psychoneuroendocrinology 2011, 36, 1137–1147. [Google Scholar] [CrossRef] [PubMed]
  86. Bierhaus, A.; Wolf, J.; Andrassy, M.; Rohleder, N.; Humpert, P.M.; Petrov, D.; Fersti, R.; von Eynatten, M.; Wendt, T.; Rudofsky, G.; et al. A mechanism converting psychosocial stress into mononuclear cell activation. Proc. Natl. Acad. Sci. USA 2003, 100, 1920–1925. [Google Scholar] [CrossRef] [PubMed]
  87. Tracey, K.J. Reflex control of immunity. Nat. Rev. Immunol. 2009, 9, 418–428. [Google Scholar] [CrossRef] [PubMed]
  88. Fraley, R.C.; Shaver, P.R. Airport separations: A naturalistic study of adult attachment dynamics in separating couples. J. Personal. Soc. Psychol. 1998, 75, 1198–1212. [Google Scholar] [CrossRef]
  89. Vormbrock, J.K. Attachment theory as applied to wartime and job-related marital separation. Psychol. Bull. 1993, 114, 122–144. [Google Scholar] [CrossRef]
  90. Roby, H. Understanding the development of business travel policies: Reducing business travel, motivations and barriers. Transp. Res. Part. A: Policy Pract. 2014, 69, 20–35. [Google Scholar] [CrossRef]
  91. Lemke, M.R.; Brecht, H.M.; Koester, J.; Kraus, P.H.; Reichmann, H. Anhedonia, depression, and motor functioning in Parkinson’s disease during treatment with pramipexole. J. Neuropsychiatr. Clin. Neurosci. 2005, 17, 214–220. [Google Scholar] [CrossRef]
  92. Macht, M.; Schwarz, R.; Ellgring, H. Patterns of psychological problems in Parkinsonʼs disease. Acta Neurol. Scand. 2005, 111, 95–101. [Google Scholar] [CrossRef] [PubMed]
  93. Karlsen, K.; Larsen, J.P.; Tandberg, E.; Jørgensen, K. Fatigue in patients with Parkinsonʼs disease. Mov. Disord. 1999, 14, 237–241. [Google Scholar] [CrossRef]
  94. Breen, S.J.; Baravelli, C.M.; Schofield, P.E.; Jefford, M.; Yates, P.M.; Aranda, S.K. Is symptom burden a predictor of anxiety and depression in patients with cancer about to commence chemotherapy? Med. J. Aust. 2009, 190, S99. [Google Scholar] [PubMed]
  95. Glassman, A.H.; Covey, L.S.; Stetner, F.; Rivelli, S. Smoking cessation and the course of major depression: A follow-up study. Lancet 2001, 357, 1929–1932. [Google Scholar] [CrossRef]
  96. Cook, W.L.; Kenny, D.A. The Actor-Partner Interdependence Model: A model of bidirectional effects in developmental studies. Int. J. Behav. Dev. 2005, 29, 101–109. [Google Scholar] [CrossRef]
  97. Epping-Jordan, J.E.; Compas, B.E.; Osowiecki, D.M.; Oppedisano, G.; Gerhardt, C.; Primo, K.; Krag, D.N. Psychological adjustment in breast cancer: Processes of emotional distress. Health Psychol. 1999, 18, 315–326. [Google Scholar] [CrossRef] [PubMed]
  98. Bower, J.E.; Crosswell, A.D.; Slavich, G.M. Childhood adversity and cumulative life stress risk factors for cancer-related fatigue. Clin. Psychol. Sci. 2014, 2, 108–115. [Google Scholar] [CrossRef] [PubMed]
  99. Green, B.L.; Krupnick, J.L.; Rowland, J.H.; Epstein, S.A.; Stockton, P.; Spertus, I.; Stern, N. Trauma history as a predictor of psychologic symptoms in women with breast cancer. J. Clin. Oncol. 2000, 18, 1084–1093. [Google Scholar] [PubMed]
  100. Fagundes, C.P.; Lindgren, M.E.; Shapiro, C.L.; Kiecolt-Glaser, J.K. Child maltreatment and breast cancer survivors: Social support makes a difference for quality of life, fatigue and cancer stress. Eur. J. Cancer 2012, 48, 728–736. [Google Scholar] [CrossRef] [PubMed]
  101. Crosswell, A.D.; Bower, J.E.; Ganz, P.A. Childhood Adversity and Inflammation in Breast Cancer Survivors. Psychosom. Med. 2014, 76, 208–214. [Google Scholar] [CrossRef] [PubMed]
  102. Baum, A.; Garofalo, J.; Yali, A. Socioeconomic status and chronic stress: Does stress account for SES effects on health? Ann. N. Y. Acad. Sci. 1999, 896, 131–144. [Google Scholar] [CrossRef] [PubMed]
  103. Adler, N.; Boyce, T.; Chesney, M.; Cohen, S.; Folkman, S.; Kahn, R.L.; Syme, S.L. Socioeconomic status and health. Am. Psychol. 1994, 49, 15–24. [Google Scholar] [CrossRef] [PubMed]
  104. Adler, N.E.; Epel, E.S.; Castellazzo, G.; Ickovics, J.R. Relationship of subjective and objective social status with psychological and physiological functioning: Preliminary data in healthy white women. Health Psychol. 2000, 19, 586–592. [Google Scholar] [CrossRef] [PubMed]
  105. Bower, J.E.; Lamkin, D.M. Inflammation and cancer-related fatigue: Mechanisms, contributing factors, and treatment implications. Brain Behav. Immun. 2013, 30, S48–S57. [Google Scholar] [CrossRef] [PubMed]
  106. Donovan, K.A.; Small, B.J.; Andrykowski, M.A.; Munster, P. Jacobsen PB: Utility of a cognitive-behavioral model to predict fatigue following breast cancer treatment. Health Psychol. 2007, 26, 464–472. [Google Scholar] [CrossRef] [PubMed]
  107. Luckett, T.; Goldstein, D.; Butow, P.N.; Gebski, V.; Hons, M.; Aldridge, L.J.; McGrane, J.; Weng, N.; King, M.T. Psychological morbidity and quality of life of ethnic minority patients with cancer: A systematic review and meta-analysis. Lancet Oncol. 2011, 12, 1240–1248. [Google Scholar] [CrossRef]
  108. Paxton, R.J.; Phillips, K.L.; Jones, L.A.; Chang, S.; Taylor, W.C.; Courneya, K.S.; Pierce, J.P. Associations among physical activity, body mass index, and health-related quality of life by race/ethnicity in a diverse sample of breast cancer survivors. Cancer 2012, 118, 4024–4031. [Google Scholar] [CrossRef] [PubMed]
  109. Ward, E.; Jemal, A.; Cokkinides, V.; Singh, G.K.; Cardinez, C.; Ghafoor, A.; Thun, M. Cancer disparities by race/ethnicity and socioeconomic status. CA: Cancer J. Clin. 2004, 54, 78–93. [Google Scholar] [CrossRef]
  110. Simpson, J.S.; Carlson, L.E.; Beck, C.A.; Patten, S. Effects of a brief intervention on social support and psychiatric morbidity in breast cancer patients. Psychooncology 2002, 11, 282–294. [Google Scholar] [CrossRef] [PubMed]
  111. Wills, T.A. Comments on Heller, Thompson, Trueba, Hogg, and Vlachos-Weber, “peer support telephone dyads for elderly women”. Am. J. Commun. Psychol. 1991, 19, 75–83. [Google Scholar] [CrossRef]
  112. McDonough, M.H.; Sabiston, C.M.; Wrosch, C. Predicting changes in posttraumatic growth and subjective well-being among breast cancer survivors: The role of social support and stress. Psychooncology 2014, 23, 114–120. [Google Scholar] [CrossRef] [PubMed]
  113. Koopman, C.; Hermanson, K.; Diamond, S.; Angell, K.; Spiegel, D. Social support, life stress, pain and emotional adjustment to advanced breast cancer. Psychooncology 1998, 7, 101–111. [Google Scholar] [CrossRef]
  114. Huang, C.Y.; Hsu, M.C. Social support as a moderator between depressive symptoms and quality of life outcomes of breast cancer survivors. Eur. J. Oncol. Nurs. 2013, 17, 767–774. [Google Scholar] [CrossRef] [PubMed]
  115. Beesley, V.L.; Eakin, E.G.; Janda, M.; Battistutta, D. Gynecological cancer survivorsʼ health behaviors and their associations with quality of life. Cancer Causes Control 2008, 19, 775–782. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  116. Blanchard, C.M.; Stein, K.D.; Baker, F.; Dent, M.F.; Denniston, M.M.; Courneya, K.S.; Nehl, E. Association between current lifestyle behaviors and health-related quality of life in breast, colorectal and prostate cancer survivors. Psychol. Health 2004, 19, 1–13. [Google Scholar] [CrossRef]
  117. Duijts, S.F.; Faber, M.M.; Oldenburg, H.S.; van Beurden, M.; Aaronson, N.K. Effectiveness of behavioral techniques and physical exercise on psychosocial functioning and health-related quality of life in breast cancer patients and survivors—A meta-analysis. Psychooncology 2011, 20, 115–126. [Google Scholar] [CrossRef] [PubMed]
  118. Hughes, D.C.; Leung, P.; Naus, M.J. Using single-system analyses to assess the effectiveness of an exercise intervention on quality of life for Hispanic breast cancer survivors: A pilot study. Soc. Work Health Care 2008, 47, 73–91. [Google Scholar] [CrossRef] [PubMed]
  119. Kiecolt-Glaser, J.K.; Bennett, J.M.; Andridge, R.; Peng, J.; Shapiro, C.L.; Malarkey, W.B.; Emergy, C.F.; Layman, R.; Mrozek, E.E.; Glaser, R. Yoga’s impact on inflammation, mood, and fatigue in breast cancer survivors: A randomized controlled trial. J. Clin. Oncol. 2014. [Google Scholar] [CrossRef]
  120. Patrick, D.L.; Burke, L.B.; Powers, J.H.; Scott, J.A.; Rock, E.P.; Dawishna, S.; O'Neill, R.; Kennedy, D.L. Patient-reported outcomes to support medical product labeling claims: FDA perspective. Value Health 2007, 10, S125–S137. [Google Scholar] [CrossRef] [PubMed]
  121. Basch, E.; Torda, P.; Adams, K. Standards for patient-reported outcome-based performance measures. JAMA 2013, 310, 139–140. [Google Scholar] [CrossRef] [PubMed]
  122. Fann, J.R.; Thomas-Rich, A.M.; Katon, W.J.; Cowley, D.; Pepping, M.; McGregor, B.A.; Gralow, J. Major depression after breast cancer: A review of epidemiology and treatment. Gen. Hosp. Psychiatr. 2008, 30, 112–126. [Google Scholar] [CrossRef] [PubMed]
  123. Köhler, O.; Benros, M.E.; Nordentoft, M.; Farkouh, M.E.; Iyengar, R.L.; Mors, O.; Krogh, J. Effect of anti-inflammatory treatment on depression, depressive symptoms, and adverse effects: A systematic review and meta-analysis of randomized clinical trials. JAMA Psychiatr. 2014, 71, 1381–1391. [Google Scholar] [CrossRef] [PubMed]
  124. Dantzer, R.; Capuron, L.; Irwin, M.R.; Miller, A.H.; Ollat, H.; Perry, V.H.; Rousey, S.; Yirmiya, R. Identification and treatment of symptoms associated with inflammation in medically ill patients. Psychoneuroendocrinology 2008, 33, 18–29. [Google Scholar] [CrossRef] [PubMed]
  125. Cole, S.W. Chronic inflammation and breast cancer recurrence. J. Clin. Oncol. 2009, 27, 3418–3419. [Google Scholar] [CrossRef] [PubMed]
  126. Eversley, R.; Estrin, D.; Dibble, S.; Wardlaw, L.; Pedrosa, M.; Favila-Penney, W. Post-treatment symptoms among ethnic minority breast cancer survivors. Oncol. Nurs. Forum 2005, 32, 250–256. [Google Scholar] [CrossRef] [PubMed]

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Fagundes, C.; LeRoy, A.; Karuga, M. Behavioral Symptoms after Breast Cancer Treatment: A Biobehavioral Approach. J. Pers. Med. 2015, 5, 280-295. https://doi.org/10.3390/jpm5030280

AMA Style

Fagundes C, LeRoy A, Karuga M. Behavioral Symptoms after Breast Cancer Treatment: A Biobehavioral Approach. Journal of Personalized Medicine. 2015; 5(3):280-295. https://doi.org/10.3390/jpm5030280

Chicago/Turabian Style

Fagundes, Christopher, Angie LeRoy, and Maryanne Karuga. 2015. "Behavioral Symptoms after Breast Cancer Treatment: A Biobehavioral Approach" Journal of Personalized Medicine 5, no. 3: 280-295. https://doi.org/10.3390/jpm5030280

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