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Neurological (central nervous system disease, spinal cord injury, chronic idiopathic intestinal pseudo‐obstruction, idiopathic autonomic degeneration)
Decreased motility or gut transit
Opiates
Anticholinergics
GLP‐1 receptor agonists
L‐dopa
Tricyclic antidepressants
Calcium channel antagonists
Nitrates
Phosphodiesterase type 5 inhibitors (e.g. sildenafil)
Clonidine (an α‐2 agonist)
Sumatriptan (a 5‐HT‐1P agonist)a
Increased motility or gut transit
Metoclopramide
Domperidone
Erythromycin (a motilin agonist)b
Prucalopride
Beta blockers
Selective serotonin reuptake inhibitors
Cholinesterase inhibitors
Excess thyroxine

      a Relaxes the gastric fundus and slows gastric emptying but increases oesophageal motility.

      b Stimulates gastric emptying but slows small‐intestinal transit.

Photo depicts scintigraphic gastric emptying study.

      There is some evidence for altered responses to the presence of nutrients in the small intestine in the elderly compared to the young. In particular, intraduodenal nutrients stimulate greater cholecystokinin (CCK) release in the healthy elderly, even allowing for elevated fasting concentrations of CCK in this group,52 while intraduodenal glucose is more satiating than in the young. This enhanced small intestinal feedback could contribute to both delayed gastric emptying and impaired appetite. Furthermore, there is some evidence that the higher prevalence of Helicobacter infection and atrophic gastritis in the elderly compared to the young is associated with a decline in levels of the orexigenic peptide, ghrelin.53

      While small intestinal function is critical to good nutrition in the elderly, its motility does not appear to be substantially altered with healthy ageing but can be affected by a number of systemic illnesses.

      Changes in small‐intestinal motor function related to ageing

      The small intestine is more difficult to study than the oesophagus or stomach due to its length and relative inaccessibility. Like the stomach, the frequency of its contractions are linked to an underlying electrical rhythm – in this case, between 8 and 12 cycles per minute. The small intestine displays the same fasting cyclical activity as the stomach. However, small‐intestinal manometry, which is carried out in specialised laboratories, has relatively limited clinical application. Transport through the small intestine can be measured more readily by either a breath test (which detects an increase in hydrogen resulting from the breakdown of ingested non‐absorbable carbohydrate, such as lactulose, by colonic bacteria, and therefore reflects oro‐cecal transit) or by scintigraphy.

      Small‐intestinal MMC periodicity was not altered in healthy elderly volunteers age 81–91 when compared with the young, using ambulatory jejunal recording, although the propagation velocity of phase III was modestly slower. In the elderly, the amplitude and frequency of pressure waves were comparable to the young during phase III of the MMC and postprandially, but more propagated clustered contractions during fasting and postprandial recordings.54 The functional significance of the latter phenomenon is unclear, but similar patterns are seen in patients with irritable bowel syndrome. Nevertheless, small‐intestinal transit in the healthy elderly seems to be comparable to that in the young, in contrast with the delayed transit characteristic of the colon.13 This is consistent with the observation that small‐bowel bacterial overgrowth is uncommon in healthy older individuals.55

      Ageing is associated with an increased prevalence of conditions such as diabetes that potentially affect small‐intestinal motility as well as small intestinal diverticula. Such conditions may induce stasis of small‐intestinal contents and, together with the reduction in gastric acid secretion often seen on the elderly, predispose to bacterial overgrowth, a potential cause of malnutrition and diarrhoea.56 However, it should be noted that bacterial overgrowth is rare in the healthy elderly.57 Small bowel bacterial overgrowth may be diagnosed by culture of duodenal aspirates or by hydrogen breath tests (with glucose or xylose as a substrate), although reports as to their sensitivity and specificity

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