Södersten Per, Brodin Ulf, Zandian Modjtaba, Bergh Cecilia E K
Karolinska Institutet, Mandometer Clinics, Huddinge, Sweden.
Front Psychol. 2019 Sep 16;10:2110. doi: 10.3389/fpsyg.2019.02110. eCollection 2019.
Mental causation takes explanatory priority over evolutionary biology in most accounts of eating disorders. The evolutionary threat of starvation has produced a brain that assists us in the search for food and mental change emerges as a consequence. The major mental causation hypothesis: anxiety causes eating disorders, has been extensively tested and falsified. The subsidiary hypothesis: anxiety and eating disorders are caused by the same genotype, generates inconsistent results because the phenotypes are not traits, but vary along dimensions. Challenging the mental causation hypothesis in Feighner et al. (1972) noted that anorexic patients are physically hyperactive, hoarding for food, and they are rewarded for maintaining a low body weight. In 1996, Feighner's hypothesis was formalized, relating the patients' behavioral phenotype to the brain mechanisms of reward and attention (Bergh and Södersten, 1996), and in 2002, the hypothesis was clinically verified by training patients how to eat normally, thus improving outcomes (Bergh et al., 2002). Seventeen years later we provide evidence supporting Feighner's hypothesis by demonstrating that in 2012, 20 out of 37 patients who were referred by a psychiatrist, had a psychiatric diagnosis that differed from the diagnosis indicated by the SCID-I. Out of the 174 patients who were admitted in 2012, most through self-referral, there was significant disagreement between the outcomes of the SCID-I interview and the patient's subjective experience of a psychiatric problem in 110 of the cases. In addition, 358 anorexic patients treated to remission scored high on the Comprehensive Psychopathological Rating Scale, but an item response analysis indicated one (unknown) underlying dimension, rather than the three dimensions the scale can dissociate in patients with psychiatric disorders. These results indicate that psychiatric diagnoses, which are reliable and valid in patients with psychiatric disorders, are less well suited for patients with anorexia. The results are in accord with the hypothesis of the present Research Topic, that eating disorders are not always caused by disturbed psychological processes, and support the alternative, clinically relevant hypothesis that the behavioral phenotype of the patients should be addressed directly.
在大多数饮食失调的描述中，心理因果关系在解释上优先于进化生物学。饥饿的进化威胁产生了一个帮助我们寻找食物的大脑，心理变化随之出现。主要的心理因果关系假说：焦虑导致饮食失调，已经经过广泛测试并被证伪。辅助假说：焦虑和饮食失调由相同的基因型引起，产生了不一致的结果，因为表型不是特征，而是沿维度变化。费伊纳等人（1972年）对心理因果关系假说提出质疑，指出厌食症患者身体活动过度，囤积食物，并且因维持低体重而得到奖励。1996年，费伊纳的假说被形式化，将患者的行为表型与奖励和注意力的大脑机制联系起来（伯格和瑟德斯特恩，1996年），2002年，通过训练患者正常饮食从而改善结果，该假说得到了临床验证（伯格等人，2002年）。十七年后，我们通过证明在2012年，37名由精神科医生转诊的患者中有20名的精神科诊断与SCID-I所示诊断不同，为费伊纳的假说提供了证据支持。在2012年入院的174名患者中，大多数是通过自我转诊，在110例病例中，SCID-I访谈结果与患者对精神问题的主观体验之间存在显著差异。此外，但项目反应分析表明存在一个（未知的）潜在维度，而不是该量表在精神疾病患者中可以区分的三个维度。这些结果表明，在精神疾病患者中可靠且有效的精神科诊断，不太适合厌食症患者。这些结果与本研究主题的假说一致，即饮食失调并不总是由心理过程紊乱引起的，并支持另一种与临床相关的假说，即应直接处理患者的行为表型。
