What is the problem? There definitely is a problem, even if knowing what we know of the problem won’t help you move your bowels any more frequently yet. And of all these “problems,” we don’t know which is the primary problem, if any of them! I guess what I’m saying is, it’s good to know, but I’m sorry it won’t help you. Advances in science occur in spurts, and then it takes time to shape these advances into hypotheses and then theories. Even then, we may arrive at an incomplete understanding–as we may have in leading you to believe “fat is bad for you.”
I will describe in a later post how I use this and other information to try to gain any edge I can on my bowel function.
Please let me know if any of these links don’t work, please. It is fascinating information, and if it may help you with your disease process, I’d like to make sure you can read it!
- Less Interstitial Cells of Cajal (ICC). Normal movement of the GI tract requires interstitial cells of Cajal. These cells act as pacemakers and signallers between autonomic nerves and smooth muscle, causing the colon’s neurons to fire and bring about peristalsis, and alterations in their number and function are thought to bring about drastic functional changes. Decreased ICC numbers and abnormal integrity are considered a hallmark in the gut disorders of diabetic gastropathy and slow transit constipation. (1, 2, 4)
- Increased number of mast cells. Mast cells are immune cells which are often found in connective tissue, particularly in sites where there is close interaction with the “outside world”—the external environment—like in the GI tract. They are often associated with allergic responses, including food allergies. In the GI tract, mast cells are preferentially located next to nerve terminals in the region known as the lamina propria and play an important role in the regulation of gastrointestinal visceral sensitivity, vascular permeability, and motor function. Interestingly, they have also have been found to be elevated in many cases of irritable bowel syndrome. (1,3)
- Abnormal neurotransmitters and response to these neurotransmitters , including but not limited to– serotonin, vasoactive intestinal peptide, and substance P. (1, 3, 4, 9)
- Too many progesterone receptors. Progesterone slows the GI tract down. It does this, in part, by decreasing the effect of acetylcholine (the neurotransmitter that, in the bowel, leads to increased peristalsis) and serotonin. This may explain why constipation may worsen during pregnancy and at certain times in female cycles. Check. (1, 5)
- Reduced Substance P Fibers. Substance P brings about an increased GI motility effect. (1)
- Less neurons immunoreactive for ChAT. Basically saying there are less neurons sensitive to acetylcholine, which is necessary for peristalsis. (6)
- More neurons immunoreactive for NOS. Basically saying that there are more neurons sensitive to nitric oxide (NO), a substance that allows the distal gut to relax as peristalsis occurs. Having more NO sensitive neurons will make the gut more likely to be “relaxed” rather than peristalsing. (6)
- Less neuron density (50% less), decreased neuron numbers, reduced number of ganglia, reduced number of cells per ganglion, and reduced enteric glial cells. (6, 9)
- Reduction in high amplitude propagating contractions and a disruption of the coordinated peristaltic activity. Basically saying that there are less of the sweeping contractions that bring about defecation and that the whole system just is not coordinated at all like in normal person. (6)
- Weaker contraction to acetylcholine in the colon. (7)
- Relaxation to adrenalin stronger than a normal colon. (7)
- Possible antibodies to GnRH with decreased GnRH and its receptor in enteric neurons. GnRH is gonadotropin releasing hormone. (8)
- Excitatory nerve fibers present in the circular muscle are deficient in tachykinins and encephalin. (9)
- Expression of c-kit mRNA and c-kit protein was also found to be significantly decreased, which may lead to reduced interstitial cells of Cajal. (9)
In summary, your gut (and mine) doesn’t move, and we aren’t sure exactly why. However, there are MANY identifiable differences in a gut with slow transit constipation and a normal gut. The unique nervous system of the gut is disordered, in both the neurons, hormone production, hormone processing, and the supporting cells for the neurons.
More posts to follow along this topic: What could cause this problem? What I personally do about it. The role of butyrate and short chain fatty acids (SCFA) on the gut/my Metametrix result for SCFA.
(1) This requires a log-in. So you may not be able to pull this little review article up: http://www.medscape.org/viewarticle/770638_3
(9) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710411/#!po=11.3636 (I really liked this article for pulling things together and giving me leads to follow.)