Genetics and familial factors
Family history tends to be positive in patients with Irritable Bowel Syndrome (IBS). This means there may be individuals suffering from the condition in the family.
However, environment also plays a role. Studies on twins living apart has shown that the environmental contribution plays a greater role than the genetic influence as the concordance between parent and child was greater than the concordance between dizygotic twins. The familial influence plays a role through parental reinforcement of illness or children modelling their parents.
Genes implicated in the pathogenesis of IBS are genes for :-
- serotonin transporter (HTT-5)
- α adrenergic receptor
- interleukin-10 (IL-10)
- tumor necrosis factor α(TNF-α).
5-HTT polymorphism had been emphasized greatly but recent studies show that the previous results might have been confounded by the association of these polymorphisms with anxiety or somatization. Somatization is genetically determined and might be the reason behind familial aggregation.
Genetic factors, if present, play a minor role and better understanding of IBS and psychological influences are required before definite conclusions are drawn.
Alterations in gastrointestinal motility
Previously IBS was termed by names like “spastic colon” and “irritable colon” suggesting a motility disorder. The motor disturbances present are usually varied and even change in the same person. Some patients have an associated delayed gastric emptying particularly those with constipation or dyspepsia.
Small intestinal motor disturbances reported are increased frequency and duration of cluster contractions, increased frequency of migrating motor complex (MMC) and greater retrograde or backwards duodenal and jejunal contractions. There may be an exaggerated motor response to meals and ileal distension.
These motility disturbances that decrease the intestinal transit time are more common in IBS presenting with diarrhoea. This is associated with pain and the retrograde movements are found to worsen symptoms of diarrhoea. Another feature is that colonic distension does not inhibit duodenal motility.
Colonic dysmotility has been held as the major pathogenic mechanism behind IBS. In patients presenting with diarrhoea there is a greater number of high amplitude propagating contractions (HAPC) and decreased colonic transit time and the reverse features are present in patients with constipation.
Allergic reactions or hypersensitivity
These motor events occur in normal subjects without the development of symptoms and thus IBS patients have a visceral hypersenstivity to these motions. IBS patients have greater sense of discomfort after experimental gut stimulation which accounts for the heightened responsiveness. Both the peripheral and central nervous systems are involved in this.
6-17% of patients give a history of gastroenteritis preceding onset of IBS. This is accompanied by increase in gut inflammatory cells (T-lymphocytes) that might be responsible for the peripheral sensitization.
Brain imaging and neurophysiological means has shown that certain areas of the brain in IBS patients involved in pain processing have an altered or exaggerated response to gut stimulation.
There are descending inhibitory pathways from the brain to the spinal cord which modulate the behavioural response to painful stimuli. Another phenomenon termed diffuse noxious inhibitory control inhibits the stimulation of spinal cord when a noxious stimuli is applied.
Further Reading
Exploring the gut-brain link: How diet and nutrient absorption impact digestive disorders