Chapter 5 Ulcers, Colitis, and the Runs
I. Digestive system (In mammals, 10 to 23% of energy is spent on digestion)
A. Mouth: Breaks food down mechanically; adds saliva, which contains enzymes (amylases) that break
down complex carbohydrates into simpler carbohydrates and sugars.
B. Stomach: breaks down food both chemically (with acids and enzymes ) and mechanically.
B. Intestines: “snake dance of peristalsis”
1. Small intestine: adds bicarbonate to neutralize acid from stomach. Also has enzymes to break
down proteins and fats.
2. Large intestine: absorbs water
C. Sphincters: circular muscles at beginning and end of each organ. They serve as locks to prevent food
from moving to next step too quickly.
D. Water poured in to keep food in solution.
E. Effects of stress on digestion: shut down all of the above
1. Peptic ulcer: hole in wall of stomach or organs bordering it
2. Gastric ulcer: hole in wall of stomach.
3. Esophageal ulcer: in esophagus
4. Duodenal ulcer: in upper part of small intestine (duodenum)
B. One subtype forms rapidly in humans exposed to extremely stressful crises.
C. Most (85-100%) form due to a very common bacterium (Helicobacter pylori)
1. Acid-resistant structure, wrapped in bicarbonate coat. Lives in stomach wall.
2. Ulcers are now treated with antibiotics.
D. Duodenal ulcers: more likely in anxious, depressed, or stressed people.
E. Acid rebound
1. Stomach is protected from its own hydrochloric acid by coating its many layers with mucus.
2. (Sapolsky says that bicarbonate is released after the meal has left the stomach. However, my Physiology book says that the bicarbonate is released into the duodenum, not the stomach.)
3. During stress: little acid because digestion is shut down. During prolonged stressor, stomach
decreases thickness and decreases mucus and bicarbonate secretion.
4. After stressor is over: acid hits underprotected stomach. After prolonged parasympathetic
shutdown, it actually over-responds. Ulcers form primarily after the stressor is over.
F. Dramatic decrease in blood flow
1. May cause small infarcts, due to lack of oxygen à necrotic tissue.
a. Oxygen radicals: result from oxidative metabolism. Reduced during stressor, as are
protective radical scavengers. After stressor, oxygen delivery resumes and there is therefore
more metabolic activity by the stomach, but now there are fewer scavengers.
G. Immune suppression: less protection against Helicobacters.
H. Insufficient amounts of prostaglandins, which increase blood flow but are inhibited by glucocorticoids
during stress. Aspirin inhibits prostaglandin secretion, and therefore can aggravate ulcers.
I. Stomach contractions: may damage stomach walls that are not adequately protected by mucus.
III. Bowels in an uproar
A. Much of what we eat cannot be digested. Under acute stress, it’s dead weight. Get rid of it!
B. Sympathetic N.S.: decreases activity in stomach and small intestine, but actually increases muscle
movement in the large intestine.
C. Diarrhea because not enough time to absorb water out of contents.
IV. Colitis and irritable bowels
A. Irritable bowel syndrome (IBS): abdominal pain, diarrhea (large intestine too responsive to stress) or
constipation (small intestine too responsive to stress), passage of mucus, bloating, abdominal
B. Colitis: inflammation of the colon (bowels). Stress: more likely to worsen preexisting colitis than to
cause it. May be a factor in only some patients.
V. Stress and appetite
A. CRF (corticotropin releasing factor)
1. From hypothalamus to anterior pituitary, which in turn secretes ACTH (adrenocorticotropic
hormone), which then stimulates adrenal cortex to secrete glucocorticoids.
2. Also a neurotransmitter in the brain: turns on sympathetic N.S., increases vigilance, and
B. Urocortin: structurally similar to CRF and binds to one type of CRF receptor. It’s better at
suppressing hunger and causes less anxiety.
C. Glucocorticoids: stimulate appetite. May be important for recovery from stress response.
D. Timing: CRF is released quickly and has fast effects. Glucocorticoids are slower to be released, slower
to have effects, and slower to be cleared from the body. CRF overrides glucocorticoids if they’re both present. Lots of short stressful events à overeating; one long stressor à loss of appetite.
E. Leptin: released by fat cells into circulation. In hypothalamus, produces satiety and increases
1. Glucocorticoids increase production of leptin, but also decrease the efficacy of its effect in the
brain. Final story not clear.