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17.6 Scintigraphic gastric emptying study. Part of the radiolabelled meal is evident in the stomach, while some has emptied into the small intestine (bottom left). Proximal and distal gastric regions of interest are outlined.

      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

Small intestine

      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 vary widely. A subsequent negative test following a course of antibiotics increases the diagnostic certainty. Treatment is with antibiotics such as metronidazole, tetracycline, or quinolones, or the non‐absorbed antibiotic rifaximin⁵⁸, given for one to four weeks, and may need to be repeated on a cyclical basis in the event of recurrence. However, there is a paucity of controlled data to guide practice in this area.

      Postprandial hypotension

      Blood pressure can decrease markedly after meals in the elderly, and this represents an important but often under‐recognised clinical problem predisposing to syncope and falls.⁵⁹ Older people with type 2 diabetes are at particular risk, probably because of the associated autonomic neuropathy. Postprandial hypotension can, in the broadest sense, be regarded as a gastrointestinal disorder since the postprandial decline in blood pressure is related to the regulation of splanchnic blood flow and the release of gastrointestinal peptide hormones and can be attenuated by administration of the somatostatin analogue, octreotide. Amongst the macronutrients, both carbohydrate and fat contribute to the fall in blood pressure. After oral or small‐intestinal administration of glucose, the magnitude of the fall in blood pressure is related to the rate at which glucose enters the small intestine. Dietary and pharmacologic approaches which slow gastric emptying (e.g. GLP‐1 receptor agonists such as lixisenatide⁶⁰) and small‐intestinal carbohydrate absorption (e.g. acarbose) may prove to be effective in the treatment of postprandial hypotension, while distending the stomach (e.g. by drinking a glass of water) can attenuate the postprandial fall in blood pressure. There is limited evidence for the use of caffeine, a combination of denopamine (a beta 1 agonist) with midodrine (an alpha 1 agonist), and withdrawal of diuretic therapy for the prevention of postprandial hypotension.⁵⁹

Systemic disorders associated with disturbance of gastrointestinal motility

      Although the effects of healthy ageing per se on gastrointestinal motility are modest, the prevalence of comorbidities that may impact gut function increases markedly with advancing age; Parkinson’s disease and diabetes are typical examples. Progressive systemic sclerosis is less common but has profound effects on gastrointestinal motility. Furthermore, numerous medications can affect gastrointestinal motility; some of these are listed in Table 17.3.

      Parkinson’s disease

      Gastrointestinal dysfunction represents a common manifestation of Parkinson’s disease⁶¹ and may both precede and predominate over the somatic motor symptoms.⁶² Involvement of the dorsal motor nucleus of the vagus may influence parasympathetic innervation, while abnormalities of the enteric nervous system (ENS) itself (such as Lewy bodies and loss of dopaminergic neurons) are also evident. Nevertheless, the pathophysiology of gastrointestinal complications of Parkinson’s disease has been insufficiently studied, and the relative contribution of loss of dopaminergic neurons in the ENS compared to defects of other aspects of neuronal function is unclear.

      Dysphagia affects a majority of patients (50–90%), impairs quality of life, and tends to become more severe with the progression of the disease, although it does not always parallel the main neurological features.⁶³ Disturbance of the oropharyngeal phase of swallowing with impaired mechanosensitivity at the base of the tongue,⁶⁴ and impaired oesophageal transit associated with non‐peristaltic or tertiary pressure waves, are prominent. Heartburn is a common symptom and could be related to impaired acid clearance. The effects of L‐dopa and anticholinergic therapy on swallowing disorders are inconsistent; both drugs may be associated with either improvement or deterioration in dysphagia. Limited data indicate benefit from apomorphine, which is administered by subcutaneous infusion.

      Gastric emptying is delayed in at least 70% of Parkinson’s patients attending neurological clinics, even in the absence of L‐dopa therapy, which is likely to slow gastric emptying further.⁶⁵ Delayed gastric emptying may contribute to the high prevalence of symptoms such as nausea and bloating and result in impaired nutrition and absorption of oral medications. In particular, L‐dopa may be metabolised to dopamine if retained in the stomach and unavailable for systemic absorption. In patients suffering from the ‘on‐off’ phenomenon of motor fluctuations, gastric emptying may normalise in the ‘on’ phase; conversely, variations in the rate of emptying may result in erratic L‐dopa absorption and thereby contribute to the on‐off phenomenon. Direct infusion of L‐dopa into the duodenum has been advocated as a solution to this problem, and it has also been suggested that the ratio of dopa decarboxylase

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