Abstract

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.

Highlights

  • Scientific advances often come from uncovering a hitherto unseen aspect of things as a result, not so much of using some new instrument, but rather of looking at objects from a different angle (Jacob, 1977)A large population-based twin study in Finland reported that most women diagnosed with anorexia nervosa recovered clinically within 5 years and thereafter progressed toward full recovery (Keski-Rahkonen et al, 2007)

  • The hypothesis offered here is but one of several possible hypotheses that emerges from our framework and aims at establishing the link among eating behavior, the brain, and psychological epiphenomena. Another question comes to mind: if psychiatric symptoms in patients with mental disorders are different from the “psychiatric symptoms” of anorexic patients, what is the dimension(s) underlying these symptoms in anorexia nervosa?

  • The mental causation hypothesis, formalized as the OCDand ADHD-hypothesis, has not been supported possibly because mental disorders vary along continuous dimensions and cannot be divided into discrete categories

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Summary

INTRODUCTION

Scientific advances often come from uncovering a hitherto unseen aspect of things as a result, not so much of using some new instrument, but rather of looking at objects from a different angle (Jacob, 1977). An extensive literature on the evolutionary importance of foraging had accumulated at the time (Stephens and Krebs, 1986) This suggestion was novel because it departed from the mental causation hypothesis as recognized by Guisinger (2003), and today evidence has accumulated that an evolutionary perspective can inform our understanding of anorexia as suggested by Epling and Pierce. The neuroendocrine cells in the hypothalamic arcuate nucleus that are activated by starvation are involved in “shaping (the) behavioral choices” needed for foraging, and these behaviors outcompete most other behavioral choices (Chen et al, 2015; Dietrich et al, 2015; Burnett et al, 2016; Södersten et al, 2019b) The importance of this behavioral shift is obvious, as starving animals and humans must find food. It is the case that the mental/behavioral effects of starvation are reversible with appropriate re-feeding (Eckert et al, 2018)

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