Hickie I B, Bansal A S, Kirk K M, Lloyd A R, Martin N G
School of Psychiatry, University of New South Wales, Sydney, Australia.
Twin Res. 2001 Apr;4(2):94-102. doi: 10.1375/1369052012209.
Risk factors to prolonged fatigue syndromes (PFS) are controversial. Pre-morbid and/or current psychiatric disturbance, and/or disturbed cell-mediated immunity (CMI), have been proposed as etiologic factors. Self-report measures of fatigue and psychologic distress and three in vitro measures of CMI were collected from 124 twin pairs. Crosstwin-crosstrait correlations were estimated for the complete monozygotic (MZ; 79 pairs) and dizygotic (DZ; 45 pairs) twin groups. Multivariate genetic and environmental models were fitted to explore the patterns of covariation between etiologic factors. For fatigue, the MZ correlation was more than double the DZ correlation (0.49 versus 0.16) indicating strong genetic control of familial aggregation. By contrast, for in vitro immune activation measures MZ and DZ correlations were similar (0.49-0.69 versus 0.42-0.53) indicating the etiologic role of shared environments. As small univariate associations were noted between prolonged fatigue and the in vitro immune measures (r = -0.07 to -0.12), multivariate models were fitted. Relevant etiologic factors included: a common genetic factor accounting for 48% of the variance in fatigue which also accounted for 4%, 6% and 8% reductions in immune activation; specific genetic factors for each of the in vitro immune measures; a shared environment factor influencing the three immune activation measures; and, most interestingly, unique environmental influences which increased fatigue but also increased markers of immune activation. PFS that are associated with in vitro measures of immune activation are most likely to be the consequence of current environmental rather than genetic factors. Such environmental factors could include physical agents such as infection and/or psychologic stress.
长期疲劳综合征（PFS）的风险因素存在争议。病前和/或当前的精神障碍，和/或细胞介导免疫（CMI）紊乱，已被提出作为病因。从124对双胞胎中收集了疲劳和心理困扰的自我报告测量值以及CMI的三项体外测量值。对完整的同卵双胞胎（MZ；79对）和异卵双胞胎（DZ；45对）组估计了跨双胞胎-跨性状相关性。拟合多变量遗传和环境模型以探索病因因素之间的协变模式。对于疲劳，MZ相关性是DZ相关性的两倍多（0.49对0.16），表明家族聚集存在强大的遗传控制。相比之下，对于体外免疫激活测量，MZ和DZ相关性相似（0.49 - 0.69对0.42 - 0.53），表明共享环境的病因作用。由于在长期疲劳和体外免疫测量之间发现了小的单变量关联（r = -0.07至-0.12），因此拟合了多变量模型。相关病因因素包括：一个共同的遗传因素，占疲劳方差的48%，也导致免疫激活分别降低4%、6%和8%；每项体外免疫测量的特定遗传因素；一个影响三项免疫激活测量的共享环境因素；最有趣的是，独特的环境影响增加了疲劳，但也增加了免疫激活标志物。与体外免疫激活测量相关的PFS最有可能是当前环境而非遗传因素的结果。此类环境因素可能包括感染和/或心理压力等物理因素。
