Okay.  Great.  The slow movement of the colon in slow transit constipation occurs for a real reason.  There’s actually objective findings.  Super.

BUT WHAT CAUSED IT?  Here is where all of the great leads die.  All the fun and learning to get to this point–a hard, cold, concrete wall.  The etiology is unknown.  Don’t know.

Is there one of those changes discussed in the last post that could be a primary cause?  Or do these changes happen because of a discrete problem we haven’t connected and put together yet?  Or, more likely in my mind, are the changes a result of a multi-hit process in some of us?  I have had a problem with this since childhood, worsening, however, through the years.  Did it start as a dairy intolerance leading to inflammation?  The inflammation and food intolerance leading to constipation?  Constipation leading to chronic distention on the bowel wall?  Then worse constipation.  With the slowed transit did the bacterial flora get disturbed and changed?  Or did I have poor bacterial flora which in some way or other led to inflammation, constipation, distention, and worsening constipation?  I don’t know.  The hypotheses are endless for now.

• Inflammation:  Usually in slow transit constipation, no overt inflammation is noted.  (Interstitial Cells of Cajal in health and disease.)  However, a study in mice indicated that inflammation from an induced intestinal infection could cause loss of the normal function of Interstitial Cells of Cajal and GI function.  At the end of 60 days, though, ICC function had returned to normal.  A reassuring thought if this could apply to humans.  (Abstract only:  Interstitial cells of cajal and inflammation-induced motor dysfunction in the mouse small intestine.)

• Obstruction:  Could significant obstruction/bowel distention lead to abnormal cellular changes?  Could a severely, chronically constipated gut be considered as a form of “obstruction?”  Usually, in slow transit constipation, no overt bowel dilatation is noted. (1)  But could the constant, chronic pressure and distention lead to these cellular changes we’ve been discussing without overt changes?   Physically applied obstruction in mice studies showed loss of the ICC and GI function.  ICCs did return after removal of obstruction with time, again reassuring if any of this would apply to humans.  (Full text:  Loss of interstitial cells of Cajal and development of electrical dysfunction in murine small bowel obstruction.)  In another study, partially obstructed bowel in mice also showed a change in the way neurons in the gut processed neurotransmitters, presumably in response to increased work load.  (Abstract:  Enteric neuronal plasticity and a reduced number of interstitial cells of Cajal in hypertrophic rat ileum.)

• Food sensitivities:  Would these be a source of chronic inflammation in the bowel which could bring about these insidious cellular changes?  Particularly if it was to something common like wheat, dairy or eggs?  I certainly don’t have an answer to this.  But studies do support food intolerances leading to severe, chronic constipation.  This next link is an excellent review article.  It starts out talking about cow’s milk and constipation, but near the end it starts talking about multiple food intolerances leading to constipation.  They go on to discuss inflammatory changes seen in chronic constipation patients, such as eosinophilia of the rectal mucosa.  (Full text, Review article: chronic constipation and food hypersensitivity –an intriguing relationship.)
• Genetics:  Are you kidding me?  Of course!  Everything’s in your genes, slow transit constipation is no exception!  Researchers found an abnormal chromosome 1 in enteric neurons and glial cells.  (Abstract: Chromosomal study of enteric glial cells and neurons by fluorescence in situ hybridization in slow transit constipation.)  

These are the ones I found research supporting.  Fiber has been a mixed bag.  Bacterial flora is just starting to get sorted out.  So for now, this is it.  We are learning the structural, cellular, and hormonal changes that occur in slow transit constipation.  But we don’t know what initially causes all of it.

“Unfortunately, to date data are lacking on the possible factors causing neurenteric abnormalities in constipated patients. The current hypothesized mechanisms (often originating from experimental animal models) imply abnormalities in glial trophic factors leading to neural degeneration, and enteric localization of infective agents (bacteria, virus, prions) causing more or less selective degeneration of specific neurenteric cell populations (particularly EGC), whereas genetic factors or neurodegenerative changes due to aging seem to play a lesser role.”   (Full text,   Cellular and molecular basis of chronic constipation: Taking the functional/idiopathic label out.)

Citations are mostly links within the post.  Let me know if the links don’t work, please:

(1) http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2008.01109.x/full

Next up when time allows, what I think about as I approach this problem personally and the Metametrix report on short chain fatty acids/butyrate stuff.

Terri

Related articles

• Why Does My GI Tract Defy Gravity: Changes in Severe, Chronic Constipation (thehomeschoolingdoctor.com)
• Slow Transit Constipation: A True Enteric Neuropathy (thehomeschoolingdoctor.com)
• Butyrate and Constipation (thehomeschoolingdoctor.com)