Of all aspects of bowel function, constipation must be the one that has shown least progress and most confusion. It goes with the territory.
Although constipation can occur in many diseases and be a side effect of many drugs, the majority of cases have no obvious cause. These patients are diagnosed with ‘idiopathic constipation’ – in other words, the cause is unknown. Specialists always try to segregate such unexplained illness into subtypes in the hope that this will elucidate specific disease mechanisms and treatments. Accordingly chronic idiopathic constipation has been divided into slow transit constipation, IBS-constipation and disordered defaecation. Slow transit constipation is otherwise known as ‘colonic inertia’, but recent more detailed recording of colonic motility indicates that the colon may be anything but inert. It may include a reduction of high amplitude propagated contractions, an increase in tone and stationary contractions in the sigmoid colon, lack of rectal tone and even the presence of retrograde contractions through the distal colon.
The distinction between slow transit constipation and IBS constipation is often based on the presence or absence of pain. Despite that somewhat arbitrary distinction, there is no other difference in physiology. I am therefore tempted to think that idiopathic constipation is a spectrum that stretches from milder forms that may be associated with pain and occasionally alternate with diarrhoea to more severe slow transit constipation that may last for days if not weeks and is associated with general ill health. Also it is tempting to think that IBS constipation is more likely to be associated with an increase in rectal sensitivity and what is often termed frustrated defaecation or incomplete evacuation, while slow transit constipation is more commonly associated with an insensitive rectum, but I am not sure that such a clear distinction has ever been established.
Most people who show disorders of defaecation have what is termed ano-rectal dyssynergia or anismus, which implies failure of the anus to relax during attempts at defaecation and even paradoxical contraction of the sphincter mechanism. This is not necessarily a constant disorder. It may come and go depending on how a person feels and in particular whether they experience a sensation of wanting to defaecate. It may also be present on occasions in people who do not otherwise consider themselves constipated. We can all have difficulty passing motions at times. And people are more likely to block their own defaecation when this is being observed under test conditions.
Ano-rectal physiologists have observed a considerable overlap between ano-rectal dyssynergia and slow colonic transit, suggesting that both may be different components of the same state of idiopathic constipation and not different causes or conditions. Nevertheless long term difficulty in defaecation may result in structural changes such as rectocoele, rectal intussusception and partial rectal prolapse, which further exacerbate the problem.
When I was running the ano-rectal function laboratory at The Royal Hallamshire Hospital in the shiny city of Sheffield (Harwich for the continent. Sheffield for the incontinent!), we found that most of our patients with severe constipation had a combination of abnormalities. These included slow colonic transit, rectal insensitivity, recto-anal dyssynergia and a blunting of pelvic reflexes. They also tended to have slow small bowel transit and delayed gastric emptying and many had difficulty in emptying their bladder. This indicated to us that constipation might represent an inhibition of the brain stem mechanism controlling evacuation. Nevertheless, there was no clinical evidence of neurological disease. Furthermore, enquiry into the circumstances preceding the onset of constipation suggested that trauma or prolonged stress had laid a heavy hand on the switch controlling defaecation, a supposition supported by the reversal of constipation in some patients after a change in circumstances or during psychotherapy. The activation of the sympathetic nervous system by stress is known to inhibit propulsion through the gut, especially the colon, and increases activity in sphincter regions and in the sigmoid colon.
If idiopathic constipation is due to inhibition of the brain stem control of defaecation, then it questions the role of diet. I am reminded of Dr Gerald Crean’s quip in a conference on IBS, I organised in 1983 at Chateau Impney near Droitwich, that if constipation is related to fibre deficiency then headache is probably related to aspirin deficiency. Nevertheless a high fibre diet can help to stimulate a recalcitrant colon. It is therefore a pity that the wheels have come off ‘the bran wagon’ in recent years while enthusiasm for the low FODMAP diet has made people wary of foods containing poorly absorbed laxative sugars. Dietitians often assert that a low FODMAP diet may help relieve constipation, but I know of no trial that has specifically addressed constipation. Instead I would suggest an alternative approach – that is to encourage the team at Monash or Kings College, London, to trial a high FODMAP diet for constipation.
Similarly, it seems that laxatives can stimulate a stubborn colon? In the last few years, several new prokinetic agents have appeared for treatment of severe constipation. They include Linaclotide (Constella), Prucalopride (Resolor), Lubiprostone (Amitiza) and the inhibitor of bile acid absorption, Elobixibat. To my knowledge, none of them have been directly compared with the traditional laxatives such as bisacodyl, sennosides or osmotic purgatives such as lactulose or Movicol (macrogol). So I am not entirely sure whether any of them constitute a significant advance, especially as the notion that sennosides might damage the enteric nervous system now seems to be discounted. .
Despite my increasing age and a somewhat elongated colon, I consider myself lucky that I am only occasionally afflicted with constipation. This I put down to an active life style, that includes a daily swim in the river, avoidance of unnecessary stress, a morning pot of herb tea that contains hibiscus and grated fresh ginger, breakfast consisting of a big bowel of muesli with a variety of dried fruit, and a predominantly vegetarian diet that includes a plethora of high FODMAP foods, especially roasted beetroot, lentils, onions, chick peas and fruit. My daily rituals follow a holistic principle although I do acknowledge that what works for me may not necessarily work for everybody. We all need to discover our own way.
Love your openness and honesty 🙂 Everyone has to explore from their own perspective and decide how best to manage their own conditions. Great info.
Thank you for your comment. Always very encouraging.
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