Channing Division of Network Medicine, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, 181 Longwood Avenue, 3rd Floor, Boston, MA 02115, USA; Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA; Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 135 Dauer Drive, 2101 McGavran-Greenberg Hall, CB #7435, Chapel Hill, NC, 27599-7435, USA.
Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 135 Dauer Drive, 2101 McGavran-Greenberg Hall, CB #7435, Chapel Hill, NC, 27599-7435, USA; Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Breast. 2018 Jun;39:63-69. doi: 10.1016/j.breast.2018.03.013. Epub 2018 Mar 31.
Previous research has reported associations between social relationships and carcinogenesis. Inflammation is a potential mediator of these associations. To clarify these links for one tumor site, we examined associations between social relationships, circulating inflammation markers, and breast cancer incidence.
Among 132,262 participants from the prospective Women's Health Initiative, we used linear and logistic regression to evaluate associations between social relationship characteristics (social support, social strain, social network size) and inflammation markers of C-reactive protein (CRP) and white blood cell count (WBC). Cox regression was used to evaluate associations between inflammation markers and breast cancer incidence, as well as associations between social relationship characteristics and breast cancer incidence with and without adjustment for inflammation markers.
Larger social networks were associated with lower continuous CRP (beta = -0.22, 95% CI -0.36, -0.08) and WBC (beta = -0.23, 95% CI -0.31, -0.16). Greater social strain was associated with higher continuous CRP (beta = 0.24, 95% CI 0.14, 0.33) and WBC (beta = 0.09, 95% CI 0.04, 0.14). When WBC was dichotomized at 10,000 cells/uL, high WBC was associated with greater hazards of in situ breast cancer (HR = 1.65, 95% CI 1.17, 2.33) but not invasive breast cancer. Social relationship characteristics were not associated with incidence of invasive or in situ breast cancer.
Larger social networks were associated with lower inflammation and greater social strain was associated with higher inflammation. Higher inflammation might be associated with development of in situ breast cancer, but this appeared to be due to factors other than social relationships.
先前的研究报告了社会关系与致癌作用之间的关联。炎症是这些关联的潜在介质。为了澄清一个肿瘤部位的这些联系,我们检查了社会关系、循环炎症标志物与乳腺癌发病率之间的关系。
在来自前瞻性妇女健康倡议的 132262 名参与者中,我们使用线性和逻辑回归来评估社会关系特征(社会支持、社会压力、社交网络规模)与 C 反应蛋白(CRP)和白细胞计数(WBC)的炎症标志物之间的关联。使用 Cox 回归评估炎症标志物与乳腺癌发病率之间的关联,以及在不调整炎症标志物的情况下,社会关系特征与乳腺癌发病率之间的关联,以及调整炎症标志物后与乳腺癌发病率之间的关联。
更大的社交网络与连续 CRP(β=-0.22,95%CI-0.36,-0.08)和 WBC(β=-0.23,95%CI-0.31,-0.16)呈负相关。更大的社会压力与连续 CRP(β=0.24,95%CI0.14,0.33)和 WBC(β=0.09,95%CI0.04,0.14)呈正相关。当 WBC 以 10000 个细胞/μL 为界分为二项时,高 WBC 与原位乳腺癌的风险增加相关(HR=1.65,95%CI1.17,2.33),但与浸润性乳腺癌无关。社会关系特征与浸润性或原位乳腺癌的发病率无关。
更大的社交网络与更低的炎症相关,而更大的社会压力与更高的炎症相关。更高的炎症可能与原位乳腺癌的发展有关,但这似乎是由于社会关系以外的因素造成的。