Colloca Luana, Pine Daniel S, Ernst Monique, Miller Franklin G, Grillon Christian
University of Maryland, Baltimore, Baltimore.
National Institute of Mental Health, Bethesda, Maryland.
Biol Psychiatry. 2016 May 15;79(10):794-802. doi: 10.1016/j.biopsych.2015.07.019. Epub 2015 Aug 4.
Social cues and interpersonal interactions strongly contribute to evoke placebo effects that are pervasive in medicine and depend upon the activation of endogenous modulatory systems. Here, we explore the possibility to boost placebo effects by targeting pharmacologically the vasopressin system, characterized by a sexually dimorphic response and involved in the regulation of human and nonhuman social behaviors.
We enrolled 109 healthy participants and studied the effects of intranasal administration of an arginine vasopressin 1A and 1B receptor agonist against 1) no treatment, 2) oxytocin, and 3) saline in a randomized, placebo-controlled, double-blind, parallel design trial using a well-established model of placebo analgesia while controlling for sex differences.
Vasopressin agonists boosted placebo effects in women but had no effect in men. The effects of vasopressin on expectancy-induced analgesia were significantly larger than those observed in the no-treatment (p < .004), oxytocin (p < .001), and saline (p < .015) groups. Moreover, women with lower dispositional anxiety and cortisol levels showed the largest vasopressin-induced modulation of placebo effects, suggesting a moderating interplay between pre-existing psychological factors and treatment cortisol changes.
This is the first study that demonstrates that arginine vasopressin boosts placebo effects and that the effect of vasopressin depends upon a significant sex by treatment interaction. These findings are novel and might open up new avenues for clinically relevant research due to the therapeutic potentials of vasopressin as well as the possibility to systematically control for influences of placebo responses in clinical trials.
社会线索和人际互动在很大程度上有助于引发安慰剂效应,这种效应在医学中普遍存在,并且依赖于内源性调节系统的激活。在此,我们探讨通过药理学靶向血管加压素系统来增强安慰剂效应的可能性,该系统具有性别差异反应,并参与人类和非人类社会行为的调节。
我们招募了109名健康参与者,并在一项随机、安慰剂对照、双盲、平行设计试验中,使用成熟的安慰剂镇痛模型,同时控制性别差异,研究鼻内给予精氨酸血管加压素1A和1B受体激动剂对1)不治疗、2)催产素和3)生理盐水的影响。
血管加压素激动剂增强了女性的安慰剂效应,但对男性没有影响。血管加压素对预期性镇痛的作用显著大于未治疗组(p <.004)、催产素组(p <.001)和生理盐水组(p <.015)。此外,特质焦虑和皮质醇水平较低的女性显示出血管加压素诱导的安慰剂效应调节最大,这表明先前存在的心理因素与治疗引起的皮质醇变化之间存在调节性相互作用。
这是第一项表明精氨酸血管加压素可增强安慰剂效应且血管加压素的作用取决于治疗与性别的显著交互作用的研究。这些发现是新颖的,并且由于血管加压素的治疗潜力以及在临床试验中系统控制安慰剂反应影响的可能性,可能为临床相关研究开辟新的途径。