Feature articles

Sensory science: what do we know?

About the author

Pat Silcock, Product Development Research Centre, University of Otago, is a specialist food scientist with an expert understanding of how the many different components of foods interact and contribute to the final product. As Manager of the Product Development Research Centre, Pat provides professional consulting services for food companies on both technical and food safety issues. His specialties are food and flavour chemistry and new product development. His research interests include factors influencing flavour perception and flavour generation.

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The role of sweet perception in flavour, food intake and metabolism - an overview

Sweet perception is a taste sensation that plays important roles in sensory perception, food acceptability and metabolism. Sweet taste perception occurs when sweet tasting compounds interact with taste receptors that are housed in taste cells within papillae on the tongue. After the sweet tasting compound binds to the receptor a cascade of reactions sends a signal via the hypothalamus to the region of the brain where gustatory (taste) information processing occurs.

The function of taste

The main evolutionary function of taste sensations is to detect nutrients (e.g., sweet to detect sugar) or undesirable compounds (e.g., bitterness to detect toxins). Intense non-nutritive sweeteners (stevia, aspartame) taste sweet but they elicit different metabolic responses than nutritive sweeteners such as sucrose. For example, they elicit reduced hedonic brain responses and reduced satiety signalling (Van Opstal 2019), and produce unexpected glycemic effects in some subject groups (Pepino 2015). It is now thought that a number of pathways exist for sweet detection and this may help explain these differences.

How sweet?

The major sweet taste receptor consists of two proteins, T1R2 and T1R3, which exist bound together (T1R2/T1R3) and enable detection of all sweet tasting compounds. Though a minor receptor T1R3/T1R3 can also form which is able to bind only a limited number of sweet compounds, mostly mono- and disaccharides (eg glucose, fructose, sucrose, lactose). Though T1R2 and T1R3 enable detection of all sweet compounds, variation in sweetness intensity occurs due to binding strength of the sweet tasting compound to the receptor and where on the receptor it binds.

Evidence also exists to suggest monosaccharides may be detected independently of T1R3 pathway and potentially the T1R pathway (Damak et al., 2003; Yee, Sukumaran, Kotha, Gilbertson, & Margolskee, 2011). In addition, taste cells have also been found to express enzymes that can breakdown starch (a-glucosidase) and disaccharides (Sukumaran et al., 2016).

Senses in concert

Sweet taste perception experienced during eating does not occur in isolation, rather sensory perception of food is a complex phenomenon where sensations occur in concert. This means that when eating and drinking you do not experience a bit of sweet, a bit of sour, some bitter and each of the multitude of individual aroma compounds present in your cup of coffee – you experience coffee flavour with maybe two to five separate flavour attributes.

Sweet taste interacts with other taste sensations perceived by the brain (e.g. bitterness) and the extent of the interaction depends on the relative strength of the sensory perception e.g., if the sourness is very high, a low level of sweetness will have no effect. Sweetness has been shown to supress sour and salty perceptions depending on the intensities of these perceptions relative to sweet intensity (Thomas‐Danguin, Barba, Salles, & Guichard, 2017).

Flavour perception is a great example of senses interacting together where taste, including sweetness along with odour, play dominant roles. In flavour perception, odour (aroma) and taste interact with tactile, sound, vision and trigeminal cues (e.g., chili heat) to contribute to this complex perception (Spence, 2017). Within this context sweet perception has been demonstrated to interact with other tastes, odour, tactile, sound, vision and trigeminal cues (Wang et al., 2019).

Though for integration to occur, congruency or the similarity between the odour and taste sensations is important. For example, an increase in benzaldehyde (almond-like favour) intensity has been shown when paired with a sweet perception in North American participants (Dalton, Doolittle, Nagata, & Breslin, 2000) and reportedly with an umami (savoury) perception in Japanese participants.

This reflects the different uses of almonds in USA and Japan. However, regardless of personal experience and cultural background the way the taste and odour senses combine (multisensory integration) occurs the same way in the brain, however how each individual perceives these specific combinations of signals will depend on that individual’s experience (Spence, 2017).

Sweet taste liking

Understanding how people’s liking of sweetness varies is important to help understand the role of diet in obesity and metabolic disease. It is generally believed sweet liking is innate however, even in children sweet liking is not uniform and they can exhibit an optimum preference for sweetness (Mennella, Lukasewycz, Griffith, & Beauchamp, 2011; Ventura & Mennella, 2011).

Consistently characterising this variation in liking has been difficult as a lack of consistent methodology has resulted in populations being classified differently (Iatridi, Hayes, & Yeomans, 2019b). Recently, consumer responses to a series of sucrose solutions were collected and analysed using a mathematical technique called hierarchal clustering to identify three distinct consumer groups – sugar likers, sugar dislikers and an ‘inverted u’ group.

Sugar likers showed an increase in liking over a concentration range of 10 g/100 mL to 34 g/100 mL sucrose, sugar dislikers showed a decrease in liking as sugar concentration increased and the inverted u group showed an increase in liking up to a point (generally about 8.5 g/100 mL sucrose threshold concentration) followed by a decrease in liking (Iatridi, Hayes, & Yeomans, 2019a).

It is reasonable that these individual hedonic responses will result in different food choices. An additional output of this study was a simplified method that could be applied to larger populations to more reliably classify sugar liking. Reviews by Keast (2016) and Han, Bagenna, & Fu 2019) pointed to conflicting evidence for correlations of food intake with sweet liking or sweet perception, respectively.

The conflicting evidence associated with sweet liking and food intake may be in part related to the different methodologies used to determine sweet liking (Iatridi et al., 2019b).

Does taste perception predict dietary intake?

The relationship between sensory perception of food and dietary energy intake was investigated by Cox, Hendrie, Lease, Rebuli, & Barnes (2018). Using a food sensory database and dietary intake data from the 2011/12 Australian Health Survey, they investigated how the sensory properties of food contributed to food energy intake. They found sweetness only made a small contribution to an energy intake model at a population level, and particularly in discretionary foods sensory cues were not a good indication of composition. 

Does taste influence metabolic disease risk?

At a metabolic level sweet perception has a role in hormone secretion and brain activation for appetite control (Han et al., 2019). In addition, sweet taste receptors are not only restricted to the tongue but are present in the gut, pancreas, brain and adipose tissue, where they appear to be involved in metabolism regulation and in particular for the regulatory hormones insulin, ghrelin and leptin (Belloir, Neiers, & Briand, 2017). Our food energy intake is modulated by leptin and the endocannabinoid system (Hillard, Weinlander, & Stuhr, 2012; Vasselli, Scarpace, Harris, & Banks, 2013).

Decreases in appetite are achieved through slight increase in leptin levels whereas increases in appetite have been linked to increases in lipids that form part of the endocannabinoid system (Niki et al., 2015). Interestingly, both leptin and the endocannabinoid system can influence the perception of sweetness (Tarragon & Moreno, 2017). This does not happen with other taste sensations indicating a unique role for sweetness in managing food intake amongst the five tastes.

Over-eating of energy dense food, particularly those high in fat and/or sugar/refined carbohydrates can lead to diet induced leptin resistance, via an inflammatory route (Alemany, 2013; Esmaillzadeh et al., 2007; Tarragon & Moreno, 2017). This means the body does not recognise that it has elevated levels of leptin and results in the inability to regulate energy intake and an increased risk of weight gain (Vasselli et al., 2013).

The endocannabinoid system helps in maintaining energy balance, stress recovery and modulating immune and anti-inflammatory responses (Di Marzo, Ligresti, & Cristino, 2009; Hillard et al., 2012). The inflammation that leads to leptin resistance also stimulates the endocannabinoid system potentially leading to an increased appetite (Rossi, Punzo, Umano, Argenziano, & Miraglia Del Giudice, 2018) suggesting that overeating can create a perpetuating cycle of overeating and metabolic dysregulation.

Summary

Sugar and sweet perception are complex and differences appear to exist between the perception of between nutritive and non-nutritive sweeteners.

Sweet perception interacts with other perceptual modes to provide a complete sensory perception. These sensory interactions can vary between individuals and depend upon subjective experiences such as food culture.

Sweet perception and/or sweet liking appear to have roles in food intake and energy balance but methodological variation may have clouded this relationship. Sugar/sweet perception appears to have a direct role in leptin and endocannabinoid regulation, which has implications for obesity and metabolic disease.

References

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Cox, D. N., Hendrie, G. A., Lease, H. J., Rebuli, M. A., & Barnes, M. (2018). How does fatty mouthfeel, saltiness or sweetness of diets contribute to dietary energy intake? Appetite, 131, 36-43. doi:https://doi.org/10.1016/j.appet.2018.08.039

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