Authors's reply.
Authors: Lukas Van Oudenhove, Jan Tack
Journal: Gut (2007)

We read with great interest the comment by Creed,1 and the letter by Castle and Libby in this issue concerning a recent article published by our group in Gut.2 We wish to thank the authors for their interest in our work and their remarks. In this study, we reported that treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram considerably improved irritable bowel syndrome (IBS) symptoms, including abdominal pain, compared with placebo in non‐depressed patients with IBS. Moreover, this effect on core IBS symptoms was found to be independent of effects on anxiety and depression as measured by self‐report questionnaires.

We agree with both Creed1 and Castle and Libby that psychological processes including hypervigilance towards bodily sensations and abnormal attributions of these sensations (thus, abnormal illness beliefs) may play a key role in the pathophysiology of functional somatic syndromes (FSS)—somatoform disorders in general and IBS in particular.1,3,4,5,6 This hypothesis is in line with the concept of visceral‐specific anxiety as a key process in IBS, as proposed by Labus et al.7 The hypothetic aetiological concept “somatisation”, which is descriptively defined as “the presence of somatic symptoms that cannot be (adequately) explained by organic findings”,5 may indeed be frequent and important in IBS, and a reduction in somatisation (or the psychological processes underlying it) could be hypothesised as an important mechanism of action by which SSRIs may influence FSS, as proposed by Creed.1 However, evidence is growing that psychological processes may underlie the multidimensional phenomenon.3,5

Analysis of the SCL‐90R somatisation scores from our study showed significant improvement after 3 and 6 weeks of citalopram treatment, compared with run‐in and placebo (table 1​1).). Somatisation scores at the beginning of the first treatment period did not differ from those at the beginning of the second treatment period, so in contrast with IBS symptom severity, no carry‐over effect of citalopram was observed for the somatisation scores. Furthermore, no significant correlation was found between changes in somatisation scores and changes in overall or specific symptom scores (all r 0.05). Hence, as the effect of citalopram on IBS symptoms is independent of general anxiety, depression or somatisation, we do not agree that our study can be seen as directly supporting the assumptions formulated by Castle and Libby in their letter.



Table 1 Somatisation levels during treatment with citalopram or placebo, assessed using the symptom‐checklist‐90‐revised (SCL‐90R)



These observations do not exclude a primarily central action of citalopram on IBS symptomatology. As most somatisation symptoms are painful symptoms, the hypothesis that SSRIs work primarily through a central analgesic effect could be supported by our data. On the other hand, it remains conceivable that SSRIs may affect more subtle psychological processes, including (especially attention to bodily symptoms) those that may underlie somatisation. We believe that those psychological processes (especially attention to bodily symptoms) may interact in a complex way with central proanalgesic and analgesic systems8 and that SSRIs may influence this complex interaction. Thus, the hypotheses that SSRIs work through a central analgesic effect or through reduction in somatisation or the psychological processes underlying it may be complementary rather than contradictory.

Although we agree with several points formulated by the same authors in their recent review article,6 including the role of stress and abnormal illness beliefs, we do not believe that IBS can simply be seen as “an affective disorder in its own right”. Clearly, an important reciprocal interaction exists between gastrointestinal sensorimotor and emotional regulation (at the level of the brain),9 which may explain the observed similarities between FSS/IBS and affective disorders (high comorbidity, role of stress/life events, treatment, etc). However, as affective disorders are currently still defined on the basis of symptom criteria,11 it seems contradictory to call a disorder lacking key affective symptomatology “an affective disorder in its own right”.11 This does not exclude a role for affective disorders in somatic symptom generation in (large) subsets of patients with FSS/IBS. In our view, the dualistic distinction between “functional” and “organic” somatic disease is problematic,4 as evidence for an influence of psychological (including affective) factors on both is growing.5,12,13 As psychopathology (including “subthreshold” psychological disturbances) does not always explain bodily symptoms in the absence of readily identifiable bodily pathology, we support the proposal of considering bodily symptoms/syndromes in their own right. Their aetiology is likely to be multifactorial with interacting psychological, social and biological factors in all cases (see fig 1 in reference 4), consistent with the biopsychosocial model as proposed by George Engel almost 30 years ago.3,13,14