What causes IBS (Irritable Bowel Syndrome) constipation?

Causes of IBS Constipation

IBS constipation is primarily caused by reduced colonic motility, fewer high amplitude propagating contractions, delayed transit, and visceral hyposensitivity, which collectively lead to impaired bowel function and constipation symptoms. 1

Pathophysiological Mechanisms of IBS-C

Altered Gut Motility and Transit

• Patients with IBS-C display:

  • Reduced colonic motility
  • Fewer high amplitude propagating contractions (HAPCs) of the colon
  • Delayed colonic transit time 1
  • Abnormal fasting and postprandial motility patterns even in patients with normal transit 1

• Serotonin (5-HT) metabolism plays a crucial role:

  • Low levels of serotonin are reported in IBS-C patients 1
  • This affects gut motility and secretion patterns

Visceral Sensitivity Abnormalities

• Approximately 20% of IBS patients are viscerally hyposensitive or insensitive to mechanical distension, more commonly in IBS-C than IBS-D 1
• The degree of insensitivity correlates with abdominal distension (physical increase in abdominal girth) 1
• This contrasts with IBS-D patients who typically experience visceral hypersensitivity 1

Brain-Gut Axis Dysregulation

• IBS-C involves dysregulation of the brain-gut axis 1
• Autonomic nervous system imbalance:
  • Reduction in parasympathetic activity
  • Increase in sympathetic nervous system activity 1
• Reduced vagal tone impacts gut motility, sensitivity, and gut permeability 1

Microbiome Alterations

• Changes in the gut microbiome can modify:
  • Gastrointestinal motility
  • Visceral sensation
  • Intestinal permeability
  • Stool consistency 1
• Both qualitative and quantitative differences have been observed in the gut microbiota of IBS patients compared to healthy individuals 2
• Antibiotic usage may be associated with either development or improvement of symptoms 1

Additional Contributing Factors

Immune Regulation and Inflammation

• Low-grade mucosal inflammation may arise from:
  • Compromised epithelial barrier
  • Dysbiosis
  • Altered stress levels 1
• Mast cell hyperplasia is present in some IBS patients, though more common in IBS-D than IBS-C 1

Genetic and Epigenetic Factors

• Familial clustering of IBS suggests genetic and shared environmental factors 1
• Various genetic single nucleotide polymorphisms have been associated with IBS subtypes 1
• Epigenetic changes, including alterations in DNA methylation, may play a role 1

Psychosocial Factors

• Psychological stress and other psychosocial factors can exacerbate GI symptoms via:
  • Alterations in gut motility
  • Changes in epithelial function
  • Modified perception of visceral stimuli 1
• Stress-reactivity and altered perception/modulation of visceral afferent signals contribute to symptom generation 1

Clinical Implications

The pathophysiology of IBS-C is multifactorial, with different mechanisms predominating in different patients. Understanding these mechanisms is crucial for developing effective treatment strategies that target the underlying causes rather than just managing symptoms.

A key clinical pitfall is assuming that all IBS-C patients have the same underlying pathophysiology. The evidence shows that multiple mechanisms can lead to similar symptoms, and treatment should be directed at the predominant mechanism when possible. For example, patients with primarily delayed transit may benefit from different interventions than those with primarily visceral sensitivity issues.

Another important consideration is that IBS subtypes can change over time, with approximately 25% of IBS patients changing their bowel habit predominance within a year 1, suggesting that the underlying pathophysiological mechanisms may also evolve.