Department of Physical Medicine & Rehabilitation, Rehabilitation Medicine Research Center, Mayo Clinic, Rochester, MN 55905, USA.
Neuroscience Program, Mayo Clinic School of Biomedical Sciences, Rochester, MN 55905, USA.
Biochim Biophys Acta Mol Basis Dis. 2020 Jul 1;1866(7):165779. doi: 10.1016/j.bbadis.2020.165779. Epub 2020 Mar 26.
Oligodendrocytes not only produce myelin to facilitate nerve impulse conduction, but are also essential metabolic partners of the axon. Oligodendrocyte loss and myelin destruction, as occurs in multiple sclerosis (MS), leaves axons vulnerable to degeneration and permanent neurological deficits ensue. Many studies now propose that lifestyle factors such as diet may impact demyelinating conditions, including MS. Most prior reviews have focused on the regulatory role of diet in the inflammatory events that drive MS pathogenesis, however the potential for dietary factors to modulate oligodendrocyte biology, myelin injury and myelin regeneration remain poorly understood. Here we review the current evidence from clinical and animal model studies regarding the impact of diet or dietary factors on myelin integrity and other pathogenic features of MS. Some limited evidence exists that certain foods may decrease risk or influence the progression of MS, such as increased intake of fish or polyunsaturated fatty acids, caloric restriction and fasting-mimicking diets. In addition, evidence suggests adolescent obesity or insufficient vitamin D levels increase the risk for developing MS. However, no clear or consistent evidence exists that dietary components exacerbate disease progression. Cumulatively, current evidence highlights the need for more extensive clinical trials to validate dietary effects on MS and to identify diets or supplements that may be beneficial as food-based strategies in the management of MS alone or in combination with conventional disease modifying therapies.
少突胶质细胞不仅产生髓鞘来促进神经冲动的传导,而且还是轴突的重要代谢伙伴。多发性硬化症(MS)中发生的少突胶质细胞损失和髓鞘破坏,使轴突容易发生退化,随后会出现永久性神经功能缺损。许多研究现在提出,生活方式因素(如饮食)可能会影响脱髓鞘疾病,包括多发性硬化症。大多数之前的综述都集中在饮食在驱动 MS 发病机制的炎症事件中的调节作用上,然而,饮食因素调节少突胶质细胞生物学、髓鞘损伤和髓鞘再生的潜力仍知之甚少。在这里,我们综述了关于饮食或饮食因素对多发性硬化症髓鞘完整性和其他发病特征影响的临床和动物模型研究的现有证据。有一些有限的证据表明,某些食物可能会降低多发性硬化症的风险或影响其进展,例如增加鱼类或多不饱和脂肪酸、热量限制和模拟禁食的饮食的摄入。此外,有证据表明青少年肥胖或维生素 D 水平不足会增加患多发性硬化症的风险。然而,没有明确或一致的证据表明饮食成分会加剧疾病进展。总之,现有证据强调需要进行更多的临床试验,以验证饮食对多发性硬化症的影响,并确定可能有益的饮食或补充剂,这些饮食或补充剂可以作为单独管理多发性硬化症或与传统疾病修正治疗联合管理的基于食物的策略。