Sensory Influences on Nutrient Utilization

Sensory stimulation in the head and neck region exerts nutritional effects beyond its role in food selection via cephalic phase responses. These salivary, gastric, pancreatic exocrine and endocrine, thermogenic, cardiovascular, and renal responses to the thought, sight, sound, odor, feel, or taste of foods appear to prime the body to better absorb and utilize ingested nutrients.

Though the existence of such reflexes has been documented in humans, their physiological role remains uncertain. This is due, in part, to the fact that they are short-lived (i.e., lasting several minutes), tend to be small relative to the comparable postingestive response, and are difficult to elicit reliably under experimental conditions. Nevertheless, evidence that postingestive responses are often shorter in duration, lower in magnitude, or in some way altered in the absence of any cephalic phase component supports a view that they serve to optimize energy and nutrient utilization. Generally, the more components of the normal ingestive process recruited, the larger will be the cephalic phase response. Thus, progressing from thoughts of food to combining this with the sight and then the smell followed by the taste of the item and finally swallowing, the magnitude of the response increases.

In some, but not all, studies the mere sight of food elicits a cephalic phase release of saliva. The response is strongest for items that evoke the largest release of saliva when ingested. Olfactory stimulation is a sufficient condition as odors alone can trigger a release of saliva. Gustatory stimulation, particularly with acidic solutions, elicits the largest cephalic phase salivary response. Whole-mouth salivary flow rates can rise from basal levels of approximately 0.3 ml/min to well over 1 ml/min. The nature of the response may be modified by an individual’s state of hunger and the palatability of the stimulus.

To the extent that the cephalic phase salivary response influences the release of saliva during food ingestion, it may exert an impact on digestion via three mechanisms. First, the passage of a food through the gastrointestinal tract is facilitated by the addition of fluid and glycoproteins derived from saliva. Second, saliva contains digestive enzymes that can initiate the breakdown of starch and lipids. The importance of starch digestion in the oral cavity is typically minimal since amylase is rapidly inactivated in the acidic environment of the stomach. Lipid digestion can be more important under certain conditions, such as feeding of the preterm infant. In such cases, salivary lipase is the principal digestive enzyme for lipids. Finally, there is limited evidence that saliva entry into the stomach inhibits gastric emptying.

Thought, sight, smell, and taste are each singly capable of eliciting a release of gastric acid. Cognitive, visual, and olfactory stimulation can elicit a release that averages between one-fourth and two-thirds of that noted following mastication, but not swallowing, of food. Gustatory stimulation is the strongest cephalic phase trigger. Responses are also directly related to stimulus palatability. Stimulation with an unpleasant or tasteless stimulus can have no effect on gastric acid release, whereas provision of a preferred food will result in a marked release of acid. An exaggerated response has been reported in duodenal ulcer patients.

A nutritional impact of the cephalic phase gastric response can be presumed owing to the magnitude of the response and importance of gastric digestive functions. The release of gastric acid may serve to activate preenzymes (e.g., pepsinogen) that then promote the formation of numerous digestive enzymes. The acidic secretion, as well as gastrin, may also enhance pancreatic secretion.

The passage of gastric contents into the duodenum elicits a release of pancreatic secretions, but an independent effect of cephalic stimulation has also been documented. Responses are observed in individuals who are achlorhydric (i.e., absence of hydrochloric acid in gastric juice) or who have undergone procedures to block the passage of gut contents into the duodenum. Combined visual, olfactory, and trigeminal stimulation is a sufficient stimulus for a pancreatic exocrine response, but taste is more potent. More palatable taste stimuli also lead to larger responses. Sham feeding (ingestion of food coupled with diversion of the food out of the body via a gastric fistula) has been associated with elevations of trypsin, lipase, and chymotrypsin of 35-66%, 16-50%, and 25-60%, respectively. The total volume of the pancreatic secretion is enhanced, but there appears to be a particularly marked effect on release of digestive enzymes.

Thus, an especially enzyme-rich secretion is produced. A cephalic phase release of pancreatic polypeptide has also been described. Pancreatic polypeptide is believed to inhibit gastric and pancreatic exocrine secretion and to relax the gallbladder and may thereby influence digestion.

The cephalic phase contribution to pancreatic exocrine responses to food ingestion may serve to augment the release of not only digestive enzymes but satiety hormones as well. For example, cholecystokinin, which can be released through a cephalic phase mechanism, is reported to possess satiety properties. In fact, the cephalic phase cholecystokinin response is attenuated in obese humans and perhaps could contribute to a lack of satiety in obese individuals.

The most extensively studied cephalic phase response is that of insulin. The thought, appearance, and odor of food have led to elevations of plasma insulin, though only a subset of test subjects display such a response in any given study. The poor reliability of the response may be due to its fragility, variations in experimental conditions, or the populations tested. For example, both attenuated and exaggerated responses have been reported in obese relative to normal-weight individuals and palatable stimuli are reported to either enhance or have no effect on the magnitude of cephalic phase insulin release.

Despite the reported variability, the presence of cephalic phase insulin release may be critical for the regulation of blood glucose. Animal studies indicate that the intragastric administration of glucose that bypasses the oropharyngeal receptors and therefore does not elicit cephalic phase reflexes results in hyperglycemia and hyperinsulinemia. In addition, although the role of insulin in the control of hunger and satiety has not been directly established, the cephalic phase insulin response may contribute to these sensations and their modification.

A larger thermogenic response to food ingested orally as compared to intragastrically suggests a role for sensory stimulation in postprandial thermogenesis. Mixed findings have been reported on an influence of food palatability on postprandial energy expenditure. Some work demonstrates enhanced thermogenesis following ingestion of a preferred meal, whereas other data reveal no effect. The extent to which sensory factors influence overall energy balance through modulation of the thermogenic response to foods is unknown.

Sham feeding also reportedly reduces cardiac output and may do so by increasing splanchnic blood flow. This could be a direct effect of oral stimulation on the sympathetic nervous system or one mediated by a secondary hormonal action. Increased blood flow in the splanchnic region could promote nutrient absorption.

Fluid balance may be influenced by sensory stimulation as well. Stimulation of the oral cavity with salt leads to antidiuresis in humans. Studies in rats indicate that this may be attributable to a neural effect on vasopressin release from the hypothalamus. Direct evidence for the effect of the cephalic phase responses on nutrient digestion and utilization is still hypothetical. However, suggestive observations have been reported. First, in a number of independent studies of preterm infants, those infants provided with oral stimulation during nasogastric feeds displayed enhanced growth efficiency. That is, greater weight gain was achieved on a comparable level of energy intake. The stimulus in each case was a rubber pacifier.

Similar results have been noted in infants provided nonoral tactile/kinesthetic stimulation so that mediation by cephalic phase responses cannot be assumed. Second, patients receiving total parenteral nutrition and thus receiving no oral stimulation have been reported to require unexpectedly high levels of energy to maintain body weight. However, recent studies also raise questions about this observation. Third, excursions of plasma glucose are greater when insulin is administered to diabetic individuals 15-30 minutes after a meal (thereby eliminating a priming signal) compared to when it is administered concurrently with food. Furthermore, the inhibition of early insulin release in normal subjects also results in hyperglycemia. Thus, under conditions of normal health and food intake, cephalic phase responses may serve more as the trigger or primer for responses that occur as food passes along the gastrointestinal tract than as an effective digestive response itself.