Pain in Motion International Research Group, Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education & Physiotherapy, Vrije Universiteit Brussel , Brussels, Belgium.
Chronic Pain Rehabilitation, Department of Physical Medicine and Physiotherapy, University Hospital Brussels , Brussels, Belgium.
Expert Opin Ther Targets. 2020 Aug;24(8):793-803. doi: 10.1080/14728222.2020.1784142. Epub 2020 Jun 28.
Few treatment programs for chronic pain nowadays take a dietary pattern or adipose status into account.
An important role of neuroinflammation in chronic pain is now well established, at least in part due to increased central nervous system glial activation. Based on preclinical studies, it is postulated that the interaction between nutrition and central sensitization is mediated via bidirectional gut-brain interactions. This model of diet-induced neuroinflammation and consequent central sensitization generates a rationale for developing innovative treatments for patients with chronic pain. Methods: An umbrella approach to cover the authors' expert opinion within an evidence-based viewpoint.
A low-saturated fat and low-added sugar dietary pattern potentially decreases oxidative stress, preventing Toll-like receptor activation and subsequent glial activation. A low-saturated fat and low-added sugar diet might also prevent afferent vagal nerve fibers sensing the pro-inflammatory mediators that come along with a high-(saturated) fat or energy-dense dietary pattern, thereby preventing them to signal peripheral inflammatory status to the brain. In addition, the gut microbiota produces polyamines, which hold the capacity to excite N-methyl-D-aspartate receptors, an essential component of the central nervous system sensitization. Hence, a diet reducing polyamine production by the gut microbiota requires exploration as a therapeutic target for cancer-related and non-cancer chronic pain.
如今，很少有治疗慢性疼痛的方案将饮食模式或脂肪状况考虑在内。
神经炎症在慢性疼痛中的重要作用现已得到充分证实，这至少部分归因于中枢神经系统胶质细胞的激活增加。基于临床前研究，人们推测营养与中枢敏化之间的相互作用是通过双向肠-脑相互作用介导的。这种饮食诱导的神经炎症和随之而来的中枢敏化模型为开发慢性疼痛患者的创新治疗方法提供了依据。
采用伞状方法涵盖作者在循证观点内的专家意见。
低饱和脂肪和低糖饮食模式可能会降低氧化应激，从而阻止 Toll 样受体的激活和随后的胶质细胞激活。低饱和脂肪和低糖饮食也可能阻止感知伴随高（饱和）脂肪或高能量饮食模式而来的促炎介质的传入迷走神经纤维，从而防止它们向大脑发出外周炎症状态的信号。此外，肠道微生物群产生多胺，多胺具有兴奋 N-甲基-D-天冬氨酸受体的能力，而 N-甲基-D-天冬氨酸受体是中枢神经系统敏化的重要组成部分。因此，减少肠道微生物群多胺产生的饮食需要作为癌症相关和非癌症慢性疼痛的治疗靶点进行探索。
