In the 1970s and 1980s there was a real enthusiasm for "psychosomatic" causes of irritable bowel syndrome. I recall by the early 1980s, however, neuroendocrine studies of the bowel suggested that natural was highly conservative -- the same neurotransmitters and receptors were used in the gut and the brain. I think it was pretty common even then to figure one day we'd find out that some gut motility disorders reflected a neurotransmitter defect that was probably also present in the brain; later an association between bowel dysfunction and autism underscored that hypothesis (though that's been usually misinterpreted as having something to do with gluten).
Now, 20 yeas later, we have some data.
...''You can run any test you want on people with I.B.S., and their GI tracts look essentially normal,' Dr. Mawe said. The default assumption has been that the syndrome is a psychosomatic disease. [jf: that was the assumption in 1980, the journalist is being dramatic here]But do they, as expected, have the same problem with SERT function in the brain?
But it turns out that irritable bowel syndrome, like depression, is at least in part a function of changes in the serotonin system. In this case, it is too much serotonin rather than too little.
In a healthy person, after serotonin is released into the gut and initiates an intestinal reflex, it is whisked out of the bowel by a molecule known as the serotonin transporter, or SERT, found in the cells that line the gut wall.
People with irritable bowel syndrome do not have enough SERT, so they wind up with too much serotonin floating around, causing diarrhea.
The excess serotonin then overwhelms the receptors in the gut, shutting them down and causing constipation.
When Dr. Gershon, whose work has been supported by Novartis, studied mice without SERT, he found that they developed a condition very much like I.B.S. in humans.
Several new serotonin-based drugs - intestinal antidepressants, in a way - have brought hope for those with chronic gut disorders.