Su Shaoyong, Miller Andrew H, Snieder Harold, Bremner J Douglas, Ritchie James, Maisano Carisa, Jones Linda, Murrah Nancy V, Goldberg Jack, Vaccarino Viola
Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1256 Briarcliff Road NE, Suite-1 North, Atlanta, GA 30306, USA.
Psychosom Med. 2009 Feb;71(2):152-8. doi: 10.1097/PSY.0b013e31819082ef. Epub 2008 Dec 10.
To examine the extent to which a common genetic pathway is also involved in the relationship between depressive symptoms, in the absence of major depressive disorder (MDD), and inflammation. Recent data suggested that MDD and inflammation share common genes.
We recruited 188 male twins from the Vietnam Era Twin Registry who were free of symptomatic coronary artery disease and MDD, with mean +/- standard deviation (SD) age of 55 +/- 2.75 years, including 54 monozygotic and 40 dizygotic twin pairs. These pairs were assessed for two inflammatory markers, interleukin (IL)-6 and C-reactive protein (CRP). Current depressive symptoms were measured with the Beck Depression Inventory-II. Generalized estimating equations were used to examine the phenotypic association between depression and inflammatory markers. Biometrical genetic modeling was performed to estimate the genetic and environmental contributions to this association.
An association was observed between severity of current depressive symptoms and increased levels of inflammatory markers (p < .001 for IL-6 and p = .005 for CRP). After adjustment for other factors, the association was slightly attenuated but remained statistically significant for IL-6 (p = .002). The heritability of IL-6, CRP, and depressive symptoms were estimated as 0.37, 0.65, and 0.48, respectively. Genetic modeling found a significant genetic correlation between IL-6 and depressive symptoms (r(G) = 0.22, p = .046), indicating that about 66% of the covariance between them can be explained by shared genetic influences.
Current depressive symptoms are significantly correlated with inflammatory markers. This covariation is due, in large part, to genes that are common to depressive symptoms and inflammation.
探讨在无重度抑郁症（MDD）的情况下，常见遗传途径在抑郁症状与炎症之间的关系中所涉及的程度。近期数据表明，MDD与炎症存在共同的基因。
我们从越南战争时期双胞胎登记处招募了188名男性双胞胎，他们没有症状性冠状动脉疾病和MDD，平均年龄±标准差（SD）为55±2.75岁，包括54对同卵双胞胎和40对异卵双胞胎。对这些双胞胎进行了两种炎症标志物的评估，即白细胞介素（IL）-6和C反应蛋白（CRP）。使用贝克抑郁量表第二版测量当前的抑郁症状。采用广义估计方程来检验抑郁与炎症标志物之间的表型关联。进行生物统计学遗传建模以估计这种关联的遗传和环境贡献。
观察到当前抑郁症状的严重程度与炎症标志物水平升高之间存在关联（IL-6的p <.001，CRP的p =.005）。在对其他因素进行调整后，这种关联略有减弱，但对于IL-6仍具有统计学意义（p =.002）。IL-6、CRP和抑郁症状的遗传度分别估计为0.37、0.65和0.48。遗传建模发现IL-6与抑郁症状之间存在显著的遗传相关性（r(G) = 0.22，p =.046），表明它们之间约66%的协方差可由共同的遗传影响来解释。
当前的抑郁症状与炎症标志物显著相关。这种共变在很大程度上归因于抑郁症状和炎症所共有的基因。
