1. Introduction
Taste is primarily a nutrient sensing system. The texture of the food and the rate at which it is eaten, have a profound effect on the time of orosensory exposure to foods and to satiation [1]. It has been established that slower eating leads to a longer exposure to taste [2,3,4,5]. Many studies suggest that the duration of the exposure to taste contributes significantly to the onset of satiation and the termination of a meal [6,7,8]. A longer duration of exposure to taste leads to earlier satiation [1]. A gut–brain signaling system has also been clearly demonstrated to influence taste responses to the consumption of food. The nucleus tractus solitarius (NTS) is the main entry point of the vagus nerve in the central nervous system, and thus, it receives afferent projections from most of the organs of the gastrointestinal (GI) tract [9]. In addition, the NTS also receives some cranial nerve afferents (i.e., facial and glossopharyngeal nerves) that convey extensive information on food texture, taste, smell, appearance, and palatability from the orosensory area, and conveys the ascending fibers ipsilaterally to the thalamus and insula, whereas some of them cross at the upper pons or midbrain level [10]. The gustatory system, therefore, has a predominately ipsilateral projection with some fibers crossing at the central level [10]. This system seems to respond rapidly to meal loads and to drive fast chemosensory-related reactions to the consumption of food [11]. On the other hand, chemosensory changes due to dietary habits are found to mainly rely on a wider network of areas including the hypothalamus and its sub-region responses, involved in the control of body energy homeostasis and its connections with NTS [11,12].
The comprehension of the reliability of testing taste—including both psychophysical and objective evaluations—appears of outmost relevance. Many clinical investigations have studied changes in the sense of taste in response to the meal load or to dietary habits as an effort to further cause changes along the pathways that support the extensive connections between taste and food intake. Within psychophysical evaluation techniques, there is a distinction between chemical (natural) (including the three-drop method [13,14], taste tablets and wafers [15,16], taste-strips [17,18,19], and the fatty acid threshold [20,21,22] or similar less-standardized methods [23,24,25]) and electrical testing tools (i.e., electrogustometry) [26,27]. The former techniques use basic taste solutions (sweet, sour, salty, bitter, and/or umami) to stimulate taste, and the latter techniques apply electrical currents to the surface of the tongue in order to elicit taste perceptions [20]. Both techniques suffer from the same shortcomings of psychophysical tests in general, which means that the patient must cooperate and must not be suffering from dementia. The main advantage of both tests is that they are quick and easy to perform [21] and have been used extensively in routine clinical practice and are currently accepted to be equally useful to measure gustatory function before and after any interventions [22]. Objective evaluation techniques—including gustatory event-related potentials [28,29], neuroimaging techniques (such as functional Magnetic Resonance Imaging [fMRI] and Positron Emission Tomography [PET]) [30,31,32], and the confocal microscopy [33,34]—are more difficult to perform [27] and require likewise patients’ cooperation.
2. Impact of Nutritional Intervention on Taste Perception —A Scoping Review
The main findings of the current scoping review are that nutritional context or dietary habits may induce different degrees of changes on taste tests. The main tastants investigated were fatty acids [
21,
22,
42,
52,
53], salt [
40,
49,
51], sugar [
43,
47,
50], zinc [
41], alcohol [
39], and glutamate [
45]. Basic tastants (salty, sour, sweet and bitter) evaluation was instead performed in the only two studies evaluating on healthy volunteers the impact of fasting [
46,
48] and of two different types of coffee [
44]. The taste tests investigated, with different techniques and tastants concentrations, the detection threshold [
21,
39,
42,
44,
46,
47,
49,
50,
51,
52,
53]; the recognition threshold [
40,
44,
48,
49]; the intensity rating [
22,
39,
40,
41,
43,
45,
47]; and the preference [
40,
43] (
Table 2 and
Table 3). Significant changes in these domains were found especially in those studies in which the nutritional intervention, dietary habits or preferences, and interventional approach on the meal load specifically encompassed the tastants included in the taste test [
20,
21,
39,
44,
51]. This was clearly evident for those studies in which a concordance between the dietary habits or interventional meal load changes and the taste test was present: That is, works investigating the impact of changes in fatty acids levels of diet on detection threshold and intensity rating [
21,
22,
42,
52], changes of sodium chloride amount of diet on recognition—but not detection [
51]—threshold [
40,
49], of sweet foods intake on intensity rating [
47], and detection threshold [
50]. Further, it appeared clear that a specific diet change may not interfere on a taste test devised for different purposes. In the experience of Wise and co-workers [
47], sugar restrictions over a 3-month period only induced changes on sweet intensity and pleasantness without impacting the same scales for sodium chloride. Dalenberg et al. [
43] demonstrated that the exposure to sweetened beverages did not affect the perception of basic tastants while a decrease insulin sensitivity in the healthy participants receiving sucralose combined with maltodextrin was correlated with reductions in midbrain, insular, and cingulate brain areas with BOLD-responses to sweet, but not sour, salty or savory taste as assessed with fMRI. Beyond theories postulating changes in the expression of heterodimeric taste receptor proteins [
54,
55], these findings may support that (i) there is a common mechanism that affects peripheral insulin release and the brain response to sweet taste; (ii) peripheral insulin affects the brain response to sweet taste or; (iii) the brain response to sweet taste affects insulin secretion [
43]. However, it has been hypothesized that the decrease in insulin sensitivity induces changes in dopamine neuron regions that are important for encoding oral and post-oral reinforcing signals from food [
56], which in turn can influence peripheral insulin sensitivity [
43,
57].
On the other hand, a specific meal load or beverage may considerably affect several tastant thresholds or ratings. This is the case of the study of Fjaeldstad and Fernandes [
44] in which the detection threshold for the sweet tastant was found to be higher in a group of subjects regularly consuming coffee while the threshold for the bitter tastant was significantly lower in a group of participants regularly consuming decaffeinated coffee. Similarly, Mattes and DiMeglio [
39] found that a rinse with nonalcoholic beer led to a higher sweetness intensity compared with other conditions, and to higher saltiness and sourness ratings when compared with carbonated water and beer. Moreover, the results obtained by Umabiki et al. [
50] show how a weight-loss program based on a specific diet and exercise can lead to an improvement in sweet taste, which may be in part accounted for by the decrease in leptin in obese females. Noel et al. [
45] came to the same conclusion in an earlier study in relation to the association between increased consumption of umami-rich foods and impaired umami perception in a free-living human population, showing that repeated exposure to umami taste diminishes perceived umami intensity. Curiously, also perceived salt taste tended to decrease across the study period. It is interesting to notice how, mainly in women, the salty taste threshold is found to be affected not only by the deprivation of its stimulus [
49] but also by the exposure to umami food [
45], as mentioned above, or to zinc intake [
40]. This last study suggests that zinc intake plays an important role in determining salty taste acuity and shows how gustatory tests for salty taste work well when salty parameters in the diet are modified or retrospectively studied. Similarly, Kusaba et al. [
49] proved that sodium restriction improved the recognition threshold for salty taste in CKD subjects who commonly present taste dysfunction and zinc deficiency. The literature suggests that this internally driven action on salt taste might be regulated by volume or osmosensors in various organs, or by the suppression of hormones associated with salt appetite, or an elevation in cerebrospinal fluid sodium concentrations that has been shown to reduce salt appetite [
58]. However, in the study by Bolhuis et al. [
51], salty taste tests did not show altered taste responses to sodium and potassium supplementation after a low sodium and low potassium diet. This was hypothesized as possibly due to many biases, including the enrollment of patients with different diseases (e.g., hypertension vs. CKD in Kusaba et al. and Bolhuis et al. study, respectively) and the subsequent administration of various drugs, previously recognized to possibly impact on salty taste threshold [
49,
59,
60,
61,
62,
63].
Collectively, these results are in line with previous literature that suggests that the appetitive tastes of different tastants may be attenuated, or preferences shifted to more intense stimuli with a diet high in the respective taste stimuli [
21,
64]. These phenomena have been attributed to a down-regulation in expression of specific subunits of sensing G-protein coupled receptors of different nutrients such as umami and fats, which in some cases, given their cross-sensitivity, may also account for a downward trend also for the sensitivity regarding other tastants (e.g., sweet taste) [
65,
66]. Equivalent associations—suggesting an adaptive relationship that is plastic with either high or low exposure to stimuli—have been reported for diets low in sugar, salt, and especially fat [
21,
47,
67]. Examples of these findings are provided by the interventional studies conducted by Stewart and Keast [
21] and Newman et al., 2016 [
52,
53], which collectively found that taste sensitivity to oleic acid was modulated by exposure to or deprivation of dietary fats. Fat perception decreased in lean subjects following the high-fat diet, while no change was found among overweight/obese subjects [
21]. At the same time, in both lean and overweight/obese subjects, significant increases in fat perception were observed following the low-fat diet [
21,
52], indicating that differences in taste sensitivity to fatty acids may be a result of gustatory adaptation to a high-fat diet and may contribute to excess fat intake because of an attenuated taste response to fatty acids among individuals who habitually consume a high-fat diet [
20,
52,
68]. Interestingly, thresholds for sucrose and NaCl did not change, indicating that the decreases in fat taste threshold were specific to the reduction in fat intake throughout the study period [
52]. Further studies implemented these notions and showed that (i) higher fat intakes at the previous eating occasion were significantly associated with decreased intensity ratings [
22], (ii) fat taste sensitivity is associated with the proportion of fat consumed with respect to the total energy intake rather than to the total amount of fat consumed [
42], and (iii) repeated or long-term—rather than a very short-term—exposure to the tastant could be necessary to elicit a change in detection thresholds [
52,
53]. Based on similarities in receptor-mediated fatty acid detection within taste receptor cells and enteroendocrine cells of GI tract [
67,
68], it is suspected that oral fatty acid detection and adaptations to fat exposure would mirror events that occur in the GI tract. Indeed, modulation of fatty acid taste receptor expression has recently been reported in rodents exposed to a high-fat diet [
69], elucidating that physical changes in taste receptor expression can be induced by a high-fat diet. Considering all these data, taste tests for fatty acids may help develop personalized diets for obese or overweight people and monitor their daily fat intake with the diet.
Controversial results were obtained about the hypothesis, supporting increased sensitivity to nutrition-related tastants while fasting. Zverev et al. [
48] demonstrated that recognition thresholds for sucrose and salt in healthy subjects were significantly lower during caloric deprivation than after caloric loading and that the reactivity of taste to bitter solutions was not affected by food deprivation and satiety. On the other hand, Pasquet et al. [
46] failed to demonstrate any statistical difference in taste recognition thresholds between hungry and satiated states. Although these studies were acknowledged to be biased by different factors (such as lack of gender balance and different taste tests methods); open discussions about the reasons for the modulation of taste sensitivity in hungry and satiated states might be summarized as follows: (i) systemic activation of the brain during food motivation or satiety might alter the sensitivity of the central structures involved in the perception of taste stimuli [
70]; (ii) the “tuning” efferent influences (mediated through the glossopharyngeal and lingual nerves) on gustatory receptors evoked by hunger or satiety might affect the sensitivity of the gustatory receptors [
71]; and (iii) alteration of the autonomic nervous system activity during fasting might contribute to a modulation of the perception of taste stimuli [
72,
73]. Such findings may be relevant considering the increasing interest around fasting-mimicking diets [
74].
This entry is adapted from the peer-reviewed paper 10.3390/foods10112747
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