No Brain, No Gain: The Role of Cognitive Processes in Irritable Bowel Syndrome

By Lackner, Jeffrey M. | Journal of Cognitive Psychotherapy, Summer 2005 | Go to article overview

No Brain, No Gain: The Role of Cognitive Processes in Irritable Bowel Syndrome


Lackner, Jeffrey M., Journal of Cognitive Psychotherapy


This article seeks to summarize research supporting the influence of psychological factors in general and cognitive factors in shaping the onset, expression, and outcome of irritable bowel syndrome (IBS). To this end, 6 lines of research are reviewed, with a focus on studies showing (a) the lack of correspondence between IBS symptoms and measured gut motility; (b) IBS patients as a group tend to label visceral sensations negatively and show a lower tolerance for visceral sensations; (c) neuroimaging studies showing abnormalities in central pain processing mechanisms in response to rectal stimuli among IBS vs. healthy controls; (d) high rates of psychiatric comorbidity among treatment seeking IBS patients, particularly of psychiatric disorders marked by cognitive dysfunction (e.g., depression, Generalized Anxiety Disorder); (e) the effects of cognitive factors on IBS and its outcome; and (f) frequency of comorbid functional somatic symptoms whose pathophysiology involves central processing abnormalities (e.g., fibromyalgia, headache). These data provide a strong conceptual foundation for formulating and treating IBS from a cognitive therapy orientation.

Keywords: irritable bowel syndrome; cognitive processes; pain; psychopathology

Irritable bowel syndrome (IBS) is a chronic gastrointestinal (GI) disorder with a worldwide prevalence of 10-20% (Camilleri & Choi, 1997). Its primary symptoms include abdominal pain/discomfort associated with altered bowel function (e.g., diarrhea, constipation, or both) that occurs in the absence of organic disease. Because the locus of the problem is in how the gut functions and not in abnormalities of its physical structure, IBS is considered a functional disorder. While IBS is only one of 25 functional GI disorders concentrated in one of five anatomic regions (esophagus, gastroduodenal, biliary, intestines, and anorectum; Drossman, 1994), it is the most prevalent, costly, and disabling type.

In the United States, approximately 20 to 40 million individuals-1 in 6 Americans-suffer from IBS (Lynn & Friedman, 1993). These figures make IBS not only one of the most prevalent chronic pain disorders (Crombie, Croft, Linton, LeResche, & Von Korff, 1999) but also one of the most prevalent chronic illnesses in general. The prevalence rate of IBS is at least as common as, if not more common than, that of hypertension and is much more common than the prevalence rates of asthma, diabetes, and congestive heart failure (Adams & Benson, 1991). Although the great majority (80% to 90%) of IBS patients do not seek medical attention, the 10% to 20% who consult physicians represent 28% of all visits to GI practices and 12% of all primary care visits. The financial costs on the U.S. health care system were estimated in 1995 to have been $8 billion annually (Talley, Gabriel, Harmsen, Zinsmeister, & Evans, 1995). Episodes can have serious debilitating effects on physical function. IBS has been identified as second only to the common cold as a cause of work absenteeism (Drossman et al, 1993). It has been reported that approximately 30% of IBS sufferers take sick leave because of the disorder, with half of these individuals being absent from work at least 2 weeks per year. IBS affects quality of life as much as, or more than, does congestive heart failure (Whitehead, Burnett, Cook, & Taub, 1996).

BIOPSYCHOSOCIAL MODEL

As a functional disorder, IBS lacks a pathophysiological marker and is therefore best understood from a biopsychosocial perspective (Drossman, 1997). The biopsychosocial model holds that individual biology (e.g., genetic predisposition, GI physiology), behavior, and higher order cognitive processes (e.g., coping, illness beliefs, abnormal central processing of gut stimuli) influence IBS through their interaction with each other, with early-life factors (e.g., trauma, modeling), and with the individual's social and physical environments (e.g., reinforcement contingencies). …

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