Price Rebecca C, Christou Nicolas V, Backman Steven B, Stone Laura, Schweinhardt Petra
Faculty of Medicine, McGill University, Strathcona Anatomy and Dentistry Building, Bldg Rm M/19, 3640 Rue University, Montreal, QC, H3A 0C7, Canada.
Alan Edwards Center for Research on Pain, McGill University, Strathcona Anatomy and Dentistry Building, Bldg Rm M/19, 3640 Rue University, Montreal, QC, H3A 0C7, Canada.
Psychopharmacology (Berl). 2016 Dec;233(23-24):3869-3879. doi: 10.1007/s00213-016-4417-4. Epub 2016 Sep 22.
Endogenous opioids inhibit nociceptive processing and promote the experience of pleasure. It has been proposed that pain and pleasure lie at opposite ends of an affective spectrum, but the relationship between pain and pleasure and the role of opioids in mediating this relationship has not been tested.
Here, we used obese individuals as a model of a dysfunctional opioid system to assess the role of the endogenous opioid peptide, beta-endorphin, on pain and pleasure sensitivity.
Obese (10M/10F) and age- and gender-matched non-obese (10M/10F) controls were included in the study. Pain sensitivity using threshold, tolerance, and subjective rating assessments and perceived sweet pleasantness using sucrose solutions were assessed in two testing sessions with placebo or the opioid antagonist, naltrexone (0.7 mg/kg body weight). Beta-endorphin levels were assessed in both sessions.
Despite having higher levels of baseline beta-endorphin and altered beta-endorphin-reactivity to naltrexone, obese individuals reported a similar increase in pain and decrease in pleasantness following naltrexone compared to non-obese individuals. Beta-endorphin levels did not correlate with pain or pleasantness in either group, but naltrexone-induced changes in pain and pleasantness were mildly correlated. Moreover, naltrexone-induced changes in pain were related to depression scores, while naltrexone-induced changes in sweet pleasantness were related to anxiety scores, indicating that pain and pleasantness are related, but influenced by different processes.
内源性阿片类物质抑制伤害性感受处理并促进愉悦体验。有人提出疼痛和愉悦处于情感光谱的两端,但疼痛与愉悦之间的关系以及阿片类物质在介导这种关系中的作用尚未得到验证。
在此,我们以肥胖个体作为功能失调的阿片系统模型,来评估内源性阿片肽β-内啡肽对疼痛和愉悦敏感性的作用。
本研究纳入了肥胖者(10名男性/10名女性)以及年龄和性别匹配的非肥胖对照者(10名男性/10名女性)。在两个测试环节中,使用阈值、耐受性和主观评分评估疼痛敏感性,并使用蔗糖溶液评估感知到的甜味愉悦度,测试时分别给予安慰剂或阿片拮抗剂纳曲酮(0.7毫克/千克体重)。在两个环节中均评估β-内啡肽水平。
尽管肥胖个体的基线β-内啡肽水平较高,且对纳曲酮的β-内啡肽反应性改变,但与非肥胖个体相比,肥胖个体在服用纳曲酮后报告的疼痛增加和愉悦度降低情况相似。两组中β-内啡肽水平均与疼痛或愉悦度无关,但纳曲酮引起的疼痛和愉悦度变化呈轻度相关。此外,纳曲酮引起的疼痛变化与抑郁评分相关,而纳曲酮引起的甜味愉悦度变化与焦虑评分相关,这表明疼痛和愉悦度相关,但受不同过程的影响。