Clinical Neuroscience Research Unit, Department of Psychiatry and Behavioral Neuroscience, Pritzker School of Medicine, University of Chicago, Chicago, Illinois.
Department of Psychology, University of Colorado Colorado Springs, Colorado Springs.
JAMA Psychiatry. 2014 Feb;71(2):158-65. doi: 10.1001/jamapsychiatry.2013.3297.
Neurochemical studies in human aggression point to a modulatory role for a variety of central neurotransmitters. Some of these neurotransmitters play an inhibitory role, while others play a facilitatory role modulating aggression. Preclinical studies suggest a facilitatory role for inflammatory markers in aggression. Despite this, to our knowledge, no studies of aggression and inflammatory markers have been reported in psychiatric patients or in individuals with recurrent, problematic, impulsive aggressive behavior.
To test the hypothesis that plasma inflammatory markers will correlate directly with aggression and will be elevated in individuals with recurrent, problematic, impulsive aggressive behavior. DESIGN, SETTING, AND PARTICIPANTS Case-control study in a clinical research program in impulsive aggressive behavior at an academic medical center. Participants were physically healthy individuals with intermittent explosive disorder (n = 69), nonaggressive individuals with Axis I and/or II disorders (n = 61), and nonaggressive individuals without history of an Axis I or II disorder (n = 67).
Plasma levels of C-reactive protein and interleukin 6 were examined in the context of measures of aggression and impulsivity and as a function of intermittent explosive disorder.
Both plasma C-reactive protein and interleukin 6 levels were significantly higher in participants with intermittent explosive disorder compared with psychiatric or normal controls. In addition, both inflammatory markers were directly correlated with a composite measure of aggression and, more specifically, with measures reflecting history of actual aggressive behavior in all participants.
These data suggest a direct relationship between plasma inflammatory processes and aggression in humans. This finding adds to the complex picture of the central neuromodulatory role of aggression in humans.
人类攻击性的神经化学研究表明,各种中枢神经递质起着调节作用。其中一些神经递质起着抑制作用,而另一些则起着促进攻击性的作用。临床前研究表明,炎症标志物在攻击性中起着促进作用。尽管如此,据我们所知,在精神科患者或反复发作、有问题、冲动性攻击行为的个体中,尚未有关于攻击性和炎症标志物的研究报告。
检验以下假设,即血浆炎症标志物将与攻击性直接相关,并且在反复发作、有问题、冲动性攻击行为的个体中升高。
设计、地点和参与者:在学术医疗中心冲动性攻击行为临床研究项目中进行的病例对照研究。参与者为间歇性爆发障碍患者(n=69)、有或无轴 I 或轴 II 障碍的非攻击性个体(n=61)和无轴 I 或轴 II 障碍史的非攻击性个体(n=67)。这些个体身体健康。
在攻击性和冲动性的测量背景下,检查了 C 反应蛋白和白细胞介素 6 的血浆水平,并根据间歇性爆发障碍进行了检查。
与精神病或正常对照组相比,间歇性爆发障碍患者的血浆 C 反应蛋白和白细胞介素 6 水平均显著升高。此外,这两种炎症标志物与攻击性的综合衡量指标直接相关,更具体地说,与所有参与者反映实际攻击行为史的衡量指标直接相关。
这些数据表明,人类血浆炎症过程与攻击性之间存在直接关系。这一发现增加了人类攻击性的中枢神经调质作用的复杂情况。