Chapter 5: Ulcers, Colitis, and the Runs

Under resting conditions, digestion represents an intricate orchestration of muscular activity, enzyme production, selective blood distribution, and fluid management coordinated by the parasympathetic nervous system. During acute stress, the sympathetic nervous system appropriately redirects these resources away from digestion toward immediate survival needs, a mechanism that evolved to benefit organisms like zebras escaping predators but becomes pathological when humans chronically activate this response to psychological threats. Sapolsky explains that peptic ulcers develop through multiple stress-mediated pathways including excessive acid production, acid rebound phenomena following stress cessation, compromised gastric blood flow reducing mucosal protection, diminished oxygen radical defenses, impaired prostaglandin-dependent healing mechanisms, bacterial proliferation under suppressed immunity, and disrupted gastric motility patterns. Critically, stress ulcers frequently emerge during recovery periods rather than active stress, when protective mechanisms remain suppressed. The chapter explores stress-induced diarrhea as a consequence of accelerated large intestinal contractions that prevent adequate water reabsorption, an evolutionary adaptation for reducing body weight during escape but problematic in modern social contexts. Irritable bowel syndrome and colitis represent stress-related conditions where intestinal dysynchronization produces alternating constipation and diarrhea alongside heightened visceral sensitivity to mild stressors. Sapolsky further analyzes appetite dysregulation, demonstrating that corticotropin-releasing factor suppresses early feeding while glucocorticoids stimulate consumption during recovery phases, with individual variability in hormone secretion patterns explaining divergent weight responses to chronic stress. The fundamental conflict emerges between digestion's requirement for long-term metabolic planning and the stress response's prioritization of immediate survival, producing gastrointestinal disease when this emergency system becomes chronically activated.