Stress can cause stomach ulcers even in the absence of Helicobacter pylori

What is it about?

For most of the 20th century, based on clinical observations, it was assumed that ulcers of the stomach and some types of bowel inflammation were due to stress. Experimental evidence for this was embodied in a 1936 letter to Nature by Hans Selye. The astonishing 2005 Nobel prize winning discovery in the stomach of bacteria led to the belief that stomach ulcers are due entirely to these bacteria (Helicobacter pylori). The present review adduces evidence that stress indeed can cause stomach ulcers, even in the absence of these bacteria.

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Why is it important?

Hans Selye in a note to Nature in 1936 initiated the field of stress research by showing that rats exposed to nocuous stimuli responded by way of a ‘general adaptation syndrome’ (GAS). One of the main features of the GAS was the ‘formation of acute erosions ("ulcers") in the digestive tract, particularly in the stomach, small intestine and appendix’. This hypothesis was challenged by Marshall and Warren’s Nobel Prize (2005)-winning discovery of a causal association between bacteria, Helicobacter pylori, and peptic ulcers. However, clinical and experimental studies suggest that stress can still cause peptic ulceration in the absence of Helicobacter pylori. Predictably, the etiological pendulum of gastric and duodenal ulceration has swung from ‘all stress’ to ‘all bacteria’ followed by a sober realization that both factors can play a role, separately as well as together. This raises the question as to whether stress and Helicobacter pylori interact, and if so, how? Central dopamine mechanisms seem to be involved in the stress induction of peptic ulceration. In contrast, activation of the sympathetic nervous system and central and peripheral corticotrophin-releasing factor appears to mediate stress-induced inflammatory bowel disease.

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