section). In contrast, it seems that age has little, if any, effect on small intestinal or colonic motor function, and orocaecal and whole‐gut transit time are not affected in the healthy elderly. Healthy older people do have slower Phase III migration velocities and more frequent ‘propagated contractions’ in the small intestine, but no differences in duration of postprandial motility or amplitude or frequency of either fasting or postprandial pressure waves.24
Declining senses
Taste and smell contribute to a pleasurable eating experience. Although there are conflicting studies, the sense of taste likely deteriorates with age, which may influence food choice. There is also strong evidence that the sense of smell declines with age, particularly after age 50. This is thought to be due to a reduction in mucus secretion, thinning of the epithelium, and a decline in the regeneration of olfactory receptor cells.30 In one study, over 60% of subjects age 65–80 and over 80% age 80 or more exhibited major reductions in their sense of smell, compared with fewer than 10% of those under 50. As these changes may influence the type of food eaten, several studies have shown a strong correlation between impaired sense of smell and reduced interest in and intake of food. Consistent with this effect of ageing on the types of food eaten is the observation that ageing is associated with a less varied, more monotonous diet.31
Sensory‐specific satiety is the normal decline in the pleasantness of the taste of a particular food after it has been consumed. Sensory‐specific satiety leads to a decrease in the consumption of a previously eaten food and a tendency to shift consumption to other food choices during a meal. This acts to promote the intake of a more varied, nutritionally balanced diet. Older adults have a reduced capacity to develop sensory‐specific satiety, perhaps because of reduced senses of smell and taste. Reduced sensory‐specific satiety may in turn favour the consumption of a less varied diet and the development of micronutrient deficiencies.32
Hormones and neurotransmitters: a selective review
Hormones that influence food intake include leptin, ghrelin, and the orexins. Additionally, the central feeding system is dependent on the stimulatory effect of neurotransmitters, including the opioids, noradrenaline, neuropeptide Y (NPY), and galanin. A recent systematic review and meta‐analysis suggest that there are increased concentrations of inhibitory hormones including insulin, leptin, CCK, and PYY circulating in older adults.33
The short‐term peripheral satiety system is largely driven by gastrointestinal mechanisms. In the longer term, factors such as leptin and cytokines become more important. Gastrointestinal sensory and motor functions are essential in the regulation of satiation. Sensory signals induced by the distension by food contribute to initial sensations of fullness during a meal. These sensations are mediated via vagal mechanisms from mechanoreceptors situated within the stomach wall. In young adult humans, gastric distension using a barostat reduces food intake by up to 30%. Distension of the distal stomach (antrum) is related to increased sensations of fullness and is likely to be more important than distension of the proximal stomach (fundus). After eating, the stomach relaxes by a process of receptive relaxation, resulting in decreased intragastric pressure and increased gastric volume. This relaxation is particularly marked in the proximal stomach and results in a proximal fundic reservoir where food is retained. Not long before it is emptied into the small intestine, food is propelled distally from the fundus into the antrum. The extent of antral filling and distension relates more closely to feelings of fullness and satiety than does proximal gastric distension.30 Studies in animals and humans have demonstrated a relationship between postprandial satiety and the rate of gastric emptying. Slowing of gastric emptying may reduce appetite and food intake by increasing and prolonging antral distension and by prolonging the effect of small intestinal satiety signals. People with gastroparesis often exhibit symptoms of early satiety, loss of appetite, nausea, and vomiting, and studies in both animals and humans have shown that there is a relationship between postprandial satiation and the rate of gastric emptying.
Once food has entered the small intestine, chemoreceptors relay signals to the hypothalamus, resulting in the cessation of food intake. These signals are mediated by the release of gastrointestinal peptide hormones including CCK, peptide YY (PYY), and glucagon‐like peptide‐1 (GLP‐1). A number of gastrointestinal and pancreatic hormones, including CCK, GLP‐1 and amylin, have feedback effects on the stomach to slow gastric emptying, an effect associated with increased fullness and reduced food intake, by increasing and prolonging gastric distension and prolonging the effect of small intestinal satiety signals. Nutrient absorption and feedback signals from peripheral fat cells via leptin and, possibly, TNF‐α contribute to satiation.
Figure 13.1 illustrates the interplay of these mechanisms involved in appetite regulation. While evidence may be limited, Figure 13.2 summarizes which hormones are thought to be stimulatory and inhibitory.
Central neurotransmitters and hormones
Monoamines
The central aminergic system affects feeding, with noradrenaline having stimulating, serotonin having inhibiting, and dopamine having region‐specific stimulatory or inhibitory effects. Ageing may be associated with increased satiating effects of serotonin without apparent effects on dopamine or noradrenaline.
Figure 13.1 Overview of the mechanisms involved in appetite regulation.
Figure 13.2 The stimulatory and inhibitory effects of hormones.
Opioids
Endogenous opioids play a role in mediating the short‐term sensory reward response to food. Exogenous administration of opioid agonists increases food intake in animals, and opioid antagonists decrease food intake in animals and adult humans.34 There is evidence that ageing is associated with a reduced opioid feeding drive (reviewed by Horwitz et al.35). Elderly patients with idiopathic, senile anorexia have lower plasma and CSF β‐endorphin concentrations than normal‐weight, age‐matched controls.36 Intraperitoneal (i.p.) morphine injection increases food intake in young but not old mice, whereas i.p. naloxone decreases food intake in young but not older rats. Healthy older men are less sensitive to the inhibitory effects of subcutaneous naloxone on fluid intake than young men,37 and in one small study of feeding in humans, the suppression of food intake by naloxone was non‐significantly greater in the older than young adults: 16 vs. 8%.34 Overall, these results suggest that the stimulatory effect of endogenous opioids does decline somewhat with advancing age and may contribute to the anorexia of ageing. Further work is required to clarify these changes.
Neuropeptide Y
NPY is synthesized in the peripheral nervous system and brain and strongly stimulates food intake. There is preliminary evidence from animal studies that ageing may be associated with reduced NPY activity, perhaps more in males than females. Old rats have lower levels of arcuate nucleus prepro‐NPY mRNA than young rats, and hypothalamic NPY levels decrease with ageing in male but not female rats. Studies in humans, however, suggest, if anything, increased NPY activity with increasing age. CSF NPY levels increase with healthy ageing in women, and plasma and CSF levels are increased in elderly people with idiopathic anorexia. In rats, the feeding response to hypothalamic NPY injections diminishes with ageing, whereas the stimulation of feeding