Corcos M, Guilbaud O, Paterniti S, Moussa M, Chambry J, Chaouat G, Consoli S M, Jeammet P
Department of Psychiatry Adolescent and Young Adult Psychiatry, 42 Boulevard Jourdan, 75014 Paris, France.
Psychoneuroendocrinology. 2003 Apr;28(3):229-49. doi: 10.1016/s0306-4530(02)00021-5.
A number of findings from clinical and animal studies indicate that pro-inflammatory cytokines may play roles in eating disorders. The measurement of pro-inflammatory cytokines (IL-1, IL-6, TNFalpha), which are known to decrease food intake, provides highly variable data from which firm conclusions cannot be drawn. In most of the longitudinal studies where pro-inflammatory cytokines have been shown to be impaired in anorexia or bulimia nervosa, a return to normal values was observed after renutrition. However these findings do not exclude the possibility that pro-inflammatory cytokines might be overproduced in specific brain areas and act locally without concomitantly increased serum or immune production. It was also pointed out that the production of the major type-1 cytokines (especially IL-2) was depressed in anorexia nervosa. It remains unclear whether this is due to undernutrition or to a specific underlying cause common to eating disorders. The impaired cytokine profile observed in eating disorders could be related to several factors including impaired nutrition, psychopathological and neuroendocrine factors. More particular attention should be devoted to the deregulation of the anti/pro-inflammatory balance. Deregulation of the cytokine network may be responsible for medical complications in eating disorder patients who are afflicted with chronic underweight.
临床和动物研究的一些发现表明,促炎细胞因子可能在饮食失调中起作用。已知会减少食物摄入量的促炎细胞因子(白细胞介素-1、白细胞介素-6、肿瘤坏死因子α)的测量提供了高度可变的数据,无法从中得出确凿的结论。在大多数纵向研究中,厌食症或神经性贪食症患者的促炎细胞因子已被证明受损,重新营养后观察到其值恢复正常。然而,这些发现并不排除促炎细胞因子可能在特定脑区过度产生并在局部起作用而血清或免疫产物不随之增加的可能性。还指出,神经性厌食症患者主要的1型细胞因子(尤其是白细胞介素-2)的产生受到抑制。目前尚不清楚这是由于营养不良还是饮食失调共同的特定潜在原因所致。饮食失调中观察到的细胞因子谱受损可能与多种因素有关,包括营养受损、精神病理和神经内分泌因素。应更加特别关注抗炎/促炎平衡的失调。细胞因子网络的失调可能是患有慢性体重过轻的饮食失调患者出现医学并发症的原因。