The Mediation and Suppression Effect of Demoralization in Breast Cancer Patients After Primary Therapy: A Structural Equation Model.

BACKGROUND: Because of the increasing 5-year survival rate of breast cancer, adjustment to breast cancer survivorship is pertinent to the patient's life after diagnosis. Despite the psychological changes occurring during the transitional period (first 5 years after diagnosis) and after primary therapy having a known, critical effect on survivorship status, the data related to this topic are very limited. PURPOSE: This study was designed to examine the relationships among demoralization, stress, sleep disturbance, and psychological well-being in women with breast cancer after primary therapy. METHODS: Two hundred eight women with breast cancer (mean age = 51.96 ± 8.27) participated in a cross-sectional study in central Taiwan. Recruitment was conducted using convenience snowball sampling at a local teaching hospital. All of the participants had completed primary therapy and were in the 5-year postdiagnosis period. The average duration of cancer was 28 months. The participants completed the Stress of Breast Cancer after Primary Therapy Scale, Demoralization Scale, Pittsburgh Sleep Quality Inventory, and Ryff's Psychological Well-Being Scale-Short Form. Data were analyzed using a structural equation model to find plausible path relationships among stress, demoralization, sleep disturbances, and psychological well-being. RESULTS: Demoralization was shown to completely mediate the effect of stress on sleep disturbances. In addition, the predictive effect of sleep disturbances on psychological well-being was overwhelmingly explained by demoralization when competing with sleep disturbances. Furthermore, a positive path was found between stress and psychological well-being because of the suppression effect of demoralization. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: Demoralization was found to be a mediator that suppressed the relationships among stress, sleep disturbances, and psychological well-being in the adaptation process of patients with breast cancer after primary therapy. This article adds to the limited research on women with breast cancer after primary therapy who are in their initial 5 years of diagnosis. In addition, this study used structural equation model to find the plausible path relationships among the psychological factors involved in the well-being of women with breast cancer. Supporting patients with cancer and effectively reducing their perceived demoralization will be key to transforming stress into personal growth and a facilitator of long-term recovery.

Stearidonic and eicosapentaenoic acids inhibit interleukin-6 expression in ob/ob mouse adipose stem cells via Toll-like receptor-2-mediated pathways.

Increased adipose tissue positively correlates with circulating inflammatory cytokines such as IL-6. We previously reported that adipose stem cells from genetically obese ob/ob mice produce significantly higher levels of IL-6 compared with other cell types such as adipocytes and macrophages within adipose tissue. We also demonstrated that (n-3) PUFA have antiinflammatory effects on adipocyte IL-6 secretion. Based on these findings, we hypothesized that EPA [20:5 (n-3)] and stearidonic acid [SDA, 18:4 (n-3)] would decrease LPS (200 µg/L)-induced IL-6 secretion and IL-6 mRNA content in the adipose stem cells. SDA (100 µmol/L) and EPA (100 µmol/L) significantly reduced LPS-induced IL-6 secretion and decreased IL-6 mRNA expression. To determine the underlying intracellular mechanisms, we tested whether LPS-induced Toll-like-receptor (TLR) 4 and TLR2 expression were modulated by these fatty acids using Western-blot analysis. EPA and SDA suppressed LPS-induced TLR2 but not TLR4 protein expression in the adipose stem cells. Furthermore, SDA and EPA significantly lowered the activation and translocation of NF-κB, a TLR2 downstream signaling target, while protein expression of extracellular signal-regulated kinases-1/2 were unaffected. Collectively, our results suggest that EPA and SDA inhibit LPS-induced IL-6 secretion and IL-6 mRNA expression in the adipose stem cells by decreasing TRL2-mediated signaling pathways.