Department of Psychiatry and Behavioral Health, Stony Brook University, Stony Brook, New York, USA.
Department of Pediatrics and Microbiology/Immunology, University of Arkansas for Medical Sciences, Arkansas Children's Research Institute, Little Rock, AR, USA.
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Dec 20;95:109705. doi: 10.1016/j.pnpbp.2019.109705. Epub 2019 Jul 19.
One of the main challenges in suicide prevention is the limited understanding of the biological mechanisms underlying suicide. Recent findings suggest impairments in pain processing in acutely suicidal patients. However, little is known about the biological factors that may drive these discrete physiological abnormalities. In this study, we examined plasma peptides involved in analgesic and inflammatory responses and physical pain threshold in acutely suicidal patients.
Thirty-seven depressed patients of both sexes hospitalized for severe suicidal ideation or a recent suicide attempt were characterized clinically including history of suicidal ideation and behavior. Psychological and physical pain, and pressure pain threshold was also measured. Plasma levels of β-endorphin, neurotensin, agouti-related protein (AgRP), C-reactive protein (CRP), adrenocorticotropic hormone (ACTH), and brain-derived neurotrophic factor (BDNF) were run in Milliplex multiplex assays.
The number of lifetime suicide attempts was positively correlated with β-endorphin (r = 0.702; p = 0.007), and neurotensin (r = 0.728, p = 0.007) plasma levels. Higher pain threshold was measured in the suicide attempt group as compared to the suicidal ideation group. Pain threshold was strongly and negatively associated with CRP plasma levels (r = -0.548; p < 0.001). In patients reporting chronic pain, lower AgRP levels and lower pain threshold were observed (t = 4.472; p = 0.001).
Our results suggest that abnormalities in the opioid and neurotensin systems may underlie the increase in pain threshold found in suicide attempters, and possibly risk for suicidal behavior. Targeting pain circuits and systems may provide therapeutic mechanisms for suicide prevention.
预防自杀的主要挑战之一是对自杀背后的生物学机制的了解有限。最近的研究结果表明，急性自杀患者的疼痛处理受损。然而，对于可能导致这些离散生理异常的生物学因素知之甚少。在这项研究中，我们检查了参与镇痛和炎症反应以及躯体疼痛阈值的急性自杀患者的血浆肽。
对 37 名男女住院的重度自杀意念或近期自杀未遂的抑郁患者进行临床特征分析，包括自杀意念和行为史。还测量了心理和躯体疼痛以及压力疼痛阈值。通过 Milliplex 多重分析运行β-内啡肽、神经降压素、刺鼠相关蛋白（AgRP）、C 反应蛋白（CRP）、促肾上腺皮质激素（ACTH）和脑源性神经营养因子（BDNF）的血浆水平。
一生中自杀尝试的次数与β-内啡肽（r=0.702，p=0.007）和神经降压素（r=0.728，p=0.007）的血浆水平呈正相关。与自杀意念组相比，自杀未遂组的疼痛阈值更高。疼痛阈值与 CRP 血浆水平呈强烈负相关（r=-0.548，p<0.001）。在报告慢性疼痛的患者中，AgRP 水平较低，疼痛阈值较低（t=4.472，p=0.001）。
我们的结果表明，阿片肽和神经降压素系统的异常可能是自杀未遂者疼痛阈值升高的基础，并且可能是自杀行为的风险因素。针对疼痛回路和系统可能为预防自杀提供治疗机制。
