Biopsychosocial construct of irritable bowel syndrome and role of psychological factors

In the biomedical model of medicine, IBS is often considered at the “functional” end of the “functional-organic” spectrum where a disorder is characterized by absence of detectable structural abnormalities using traditional diagnostic techniques, such as endoscopy or imaging. In the past 2 decades, there has been a surge in the research in the area of motility, brain imaging, and neurotransmitters, which has helped define the “brain-gut axis.” As a result, pathophysiological understanding of IBS has increased, leading to organification of a “functional” disorder. In fact, IBS can be best conceptualized with a biopsychosocial construct where an influence of central nervous system at spinal and supraspinal levels results in sensory and motor dysfunction of the GI tract. The trigger can be peripheral (eg, GI infection, abdominal surgery) or central (eg, history of abuse) but psychosocial factors often play an important role in perpetuation and clinical manifestation of this disorder through centrally mediated pathways. The influence of these factors becomes increasingly significant with increasing severity of these disorders.

Psychosocial factors can play a vital role at any and all stages in the natural history of IBS, being responsible for predisposition, precipitation, and perpetuation of symptoms and illness behavior. In one series, up to three-fourths of patients with FGID seeking care at a tertiary care referral center meet diagnostic criteria for a psychiatric disorder, most commonly anxiety and depression, although in general the prevalence is much lower for patients seen in primary care or even general gastroenterology practice. A history of major stressful life events, such as sexual abuse, separation, and personal losses are common in IBS, particularly for patients with more severe symptoms who perpetuate the severity via maladaptive illness behavior (catastrophizing). Abuse, life stress, and poor or maladaptive coping can directly influence symptom severity, health-related quality of life (HRQOL), and response to treatment. Feelings of distress in response to the GI condition can have adverse effects on psychological state or health status independent of presence of a preexisting psychiatric diagnosis. Furthermore, a negative workup, incomplete understanding, and an unsatisfactory explanation from the physician lead to constant worry, fear, and anxiety and often perpetuates the symptom severity. Postinfectious (PI)-IBS provides an ideal example of psychological factors on IBS disease process. Psychosocial distress at the time of infection has been shown to be an independent predictor of later development of PI-IBS. Stress has been proposed to act by overarching effects on inflammation and the brain-gut axis in PI-IBS.

In addition, a subgroup of patients with IBS, particularly with more severe and refractory symptoms, report many non-GI symptoms, and some have hypothesized the existence of broader neurophysiological processes (eg, so called “somatization”) in up to 15% to 45% of patients with IBS. In effect, these patients have central dysregulation of pain regulatory pathways and often have comorbid problems such as fibromyalgia, chronic fatigue, or chronic generalized pain. This understanding has important implications on using centrally acting treatments, alone or in combination, to target this broader polysymptomatic process with FGIDs and even predicting response to these agents. These individuals may set lower thresholds for symptom reporting and often turn out to be “nonresponders” to a variety of different, especially peripherally based, pharmacologic interventions.