taste, food intake and obesity

© 2001 The International Association for the Study of Obesity. obesity reviews 2, 213–218 213

Taste, food intake and obesity

incorporated throughout the article and summarized at theend.

Taste perception and obesity

Sweet, salty, and umami tastes are usually well accepted byhumans and contribute to the palatability of foods, that is,perception of these basic tastes in foods tends to promotetheir intake. Bitter and sour tastes are usually unacceptableto humans especially at high concentrations, and thereforecontribute to the reduced palatability of foods. Sensitivityto basic tastes does not seem to differ between lean and obese humans, however, increases in bitter and soursensitivity and decreases in sweet and salt sensitivity arereported in the morbidly obese after gastric bypass surgery(4,5). Mixtures of sugar, a source of sweetness, and fat areconsidered especially palatable by obese humans (6,7,8),however, Cox et al. (9) suggest that overall, lean and obesehumans do not differ in the selection of foods with perceived tastes and hedonic attributes.

The lack of reported differences in taste perceptions and food selections between lean and obese humans seemscounter-intuitive as good taste is usually the number onereason given for eating a food (10), and a decrease in goodtaste is a reason given for stopping food intake (11). It is possible that individual genetic and/or physiological

obesity reviews

Department of Psychiatry, Division of

Substance Abuse, Columbia University

College of Physicians and Surgeons; and,

New York Obesity Research Center, St.

Luke’s/Roosevelt Hospital Center, New York,

NY, USA

Received 15 February 2001; revised 11

April 2001; accepted 18 April 2001

Address reprint requests to: Jennifer Nasser,

New York State Psychiatric Institute, Unit 66,

1051 Riverside Drive, New York, NY 10032,

USA

E-mail: [email protected]

J. Nasser PhD

AbstractResearch in human eating behaviour prior to 1990 has shown that taste impactsthe palatability and selection of food for intake; sensory-specific satiety; satiation;and thermic effect of food. Research in the last decade has added information tothese areas; expanded the field to comparisons of the impact of ‘wanting’ vs.‘liking’ food on intake, and provided insight into the relationship of food intakeand brain functioning through new imaging techniques. This article will reviewliterature from the last decade on research in the area of taste and its impact onfood intake. Emphasis will be placed on differences seen between lean and obesehumans and how these may contribute to the development of human obesity. Suggestions for future research directions will also be discussed.

Keywords: Food intake, obesity, palatability, taste.

obesity reviews (2001) 2, 213–218

Introduction

Consumers tend to use the word taste to refer to all oralsensory sensations associated with food in the mouth,namely, taste, retronasal olfaction and chemosensation (1).In general, taste refers to four basic oral perceptions: sweet,salty, sour, and bitter, with some also including the taste ofstarch and umami (taste of monosodium glutamate) in thiscategory (2). Since most human taste and food-intakestudies are performed without the use of nose clips, theyreally measure flavor, which is a composite of taste per-ception and retronasal olfaction. In this article addressingtaste and obesity, no distinction will be made between tasteand flavor. Contributions of chemosensation to food intakewill not be addressed in this article.

Evidence in humans suggests that taste contributes to theselection of foods to be eaten and to palatability, definedby Yeomans (3) as ‘the hedonic evaluation of orosensoryfood cues under standardized conditions’. Taste also contributes to the development of sensory-specific satiety(SSS) (64,65), satiation (68,69), thermic effect of food(75,76,78,79), and the ‘reward value’ of food (81). Thisreview will examine literature from the last 10 years withparticular emphasis on the differences between lean andobese humans and how the differences may contribute toobesity. Suggestions for future research directions will be

differences within the lean and obese phenotypes confounddetection of differences in taste perceptions between thesegroups. For example, we know that lean individuals withobese parents are at greater risk of developing obesity thanthose with lean parents; however, the contribution of famil-ial obesity history to taste responses and food choice inhumans has only been reported in a few studies (12,13). Therelationship of the genetic ability to detect the bitter taste ofPROP(6-propylthiouracil) with the intensity of sweet andfat perception, relative preferences for sweet and fatty foodsand body mass index has recently been reviewed (14,15).Inclusion of PROP taster status as a grouping variable instudies examining the impact of taste on obesity may revealadditional differences between the lean and the obese.

Physiological impacts on taste

Among the obese, the distribution of body fat is associatedwith variations in physiology such as hyperinsulinaemia(16), hyperleptinaemia and leptin resistance (17,18). Theimpact of these physiological differences on responses totaste stimuli and food intake needs further study given thatboth insulin and leptin are involved in the hypothalamiccontrol of food intake (19). Obesity is associated with thehyperinsulinaemia that precedes Type 2 diabetes (20), andaltered taste responses have been reported in Type 2 dia-betics (21,22). Using lean humans, Rodin and co-workers(23) independently manipulated plasma insulin and glucoselevels, and reported that the acute hyperinsulinaemiaresulted in increased palatability of sweet solutions. How-ever, the impact of chronic hyperinsulinaemia on tasteresponses in the obese, as well as the time course for thedevelopment of altered taste responses in relation to thedevelopment of Type 2 diabetes in the obese have not beenreported.

Leptin, which can decrease food intake (19), suppressesoral responses to sweet stimuli when administered periph-erally to lean mice, but not to obese, diabetic, leptin recep-tor defective db/db mice (24). Taste cells in the lean miceexpress the leptin receptor, but no report has been made ofleptin receptors in human taste cells. There are conflictingreports of the relationship of leptin to perceptions of foodpleasantness (i.e. a contributing factor to the palatabilityresponse) in obese humans. Karhunen and co-workers(25,26) found that high leptin levels in obese women wereassociated with decreased responsiveness to food stimuli,reduced dietary energy and fat intakes. Raynaud and co-workers (27), however, report that fasting plasma levels ofleptin in humans, even when corrected for body mass index(BMI), are positively correlated with palatability ratings ofa 75-g carbohydrate-load breakfast. The positive correla-tion of plasma leptin with carbohydrate palatability sug-gests a potential role for leptin resistance in the reportedtaste preference for sugar/fat mixtures seen in obese women

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and weight cyclers (28). Further studies are needed to deter-mine the impact of leptin on taste sensitivity and its relationship to food intake in humans.

Evaluation of taste perception

An additional confounding factor in evaluating humantaste perceptions and its impact on food intake and obesitymay be the use of visual analogue scales (VAS) to compareratings of perceptions between individuals and groups.While VAS have been reported to have reproducibility(29,30) for rating appetite sensations, Bartoshuk (31) sug-gests that these instruments are prone to insensitivity andceiling effects associated with placement of verbal descrip-tors along the measurement line, and variation in usage ofthe verbal descriptors among individuals (for example, seeYeomans and Symes (32) for variations in the use of palata-bility). This could limit their usefulness in making inter-group comparisons and possibly obscure true differencesbetween individuals and groups of individuals as to theimpact of taste on food intake and obesity.

One approach for addressing this concern may be the use of the Labelled Magnitude Scale (LMS) (33). In a side-by-side comparison of VAS with LMS, Lucchina and co-workers (34) demonstrated increased sensitivity andelimination of a ceiling effect in the evaluation of sweet-ness intensity and PROP taste sensitivity. Recent advancesin instrumental electromyographic (EMG) recordings re-ported by Hu and co-workers (35,36) as well as work byRousmans and co-workers (37) utilizing variations in auto-nomic nervous system parameters to evaluate pleasantnessand palatability of various taste solutions suggest possiblemethods for calibrating individual VAS ratings of hedonicperceptions against continuous, objective instrumentaloutput. This type of calibration may allow for more sensi-tive interindividual and intergroup comparisons of tasteperceptions.

Taste and palatability

Smith (38) states that taste provides a feed-forward signalfor promoting food intake. The palatability response ofhumans to the taste of individual foods and whole mealsaccounts for a large with-in individual variation in foodintake but only a small variation between subjects (39).(For detailed reviews of the effects of taste and palatabil-ity on food intake see 3,40,41,42,43).

Palatability, a measure of the pleasantness of food, isrelated to the intake response towards a food, and is corre-lated with the energy density (kJ g -1) of a food. High energy-dense foods (>6.0kJg -1) are more palatable than low energydense foods (<4 kJ g -1) (40), and promote their own inges-tion, where low energy-dense foods promote satiety. Foodswith a high fat content or high percent of sugar/fat mixtures

tend to be high in energy density and are preferred by theobese (44–47). Mixtures of fat with salt are commonlyfound in high-fat, high energy-dense snacks and fast foods,which currently contribute 11% of total dietary fat in theAmerican diet (45,48). Salt contributes to the palatability ofhigh-fat foods by suppressing bitterness (49), which candevelop during cooking from the oxidation of fatty acidscontained in the fat (50). Since humans eat a constantvolume of food (51), the higher the energy density of thefood, the greater the caloric intake. This is one way in whichtaste may contribute to the development of obesity due toenergy intake in excess of energy expenditure over a pro-longed period of time. (For a review of efforts to dissociateenergy density from palatability see 52).

In addition to providing a feed-forward signal for foodintake, taste in animals can also determine the amounteaten. Numerous laboratory studies, reviewed by Sclafani(53), have reported the development of obesity in rats due to over-consumption of a palatable, cafeteria-style diet.Recent papers have also described the effect of taste to limitfood intake independent of postingestive satiety signals.Pass and Foley (54) and Stapley and co-workers (55) reportthat the taste of bitter secondary plant metabolites causes a dose-dependent reduction in plant intake in Australianbrush tail possums. In addition, orosensory detection of freefatty acids by rats (56–58), described as bitter by humans(50), is reported to reduce the amount of fat eaten by carbohydrate-preferring, but not fat-preferring, rats (59).

Such a fatty acid-sensitive, orosensory based inhibitorysystem for fat intake has not yet been described in humans,possibly due to the fact that fatty acids are removed fromprocessed fat sources(e.g. vegetable oils used in taste andfood intake studies) prior to being offered for sale (forhealth and safety reasons, as well as product stability concerns). However, correlation of decreased consumeracceptance of products, such as milk, home-ground wheatflour, and frozen fish, containing milligram quantities of freefatty acids has been reported (60–62). Preliminary work by Nasser and co-workers (63) suggests that detection ofmicrogram levels of free fatty acids in a high fat food ispositively correlated to PROP Taster status. Such a lowdetection level for fatty acids would provide a 1000-foldgradient over which to demonstrate dose-dependent intakereduction before consumer product rejection. Furtherstudies are needed to determine the contribution of orosen-sory, fatty acid-based signals to the control of dietary fatintake in humans.

Taste and sensory specific satiety

Brain imaging in non-human primates has shown that thereare sets of neurones in the caudolateral orbitofrontal cortexthat respond to tastes of food only when the animal ishungry (64). The response of these neurones decreases to

almost zero when the animal has eaten to satiety and is spe-cific for the food eaten. This observed event is referred to assensory-specific satiety (SSS), a decreased desire to consumemore of a food just eaten while still desiring more food. It isobserved in human eating behaviour and is directly relatedto the sensory properties of foods (65–67). SSS contributesto satiation, that is, the termination of a meal (68,69).

Of interest is whether there are differences in SSSbetween the lean and obese, or among various ethnicgroups where obesity is more prevalent. Evans and Foltin (70) report preliminary results suggesting that obesewomen have reduced SSS both to food eaten and food just tasted, compared to lean women. Schiffman and co-workers (71) report that overweight African-Americanwomen, compared to overweight European Americanwomen, show an elevated and sustained desire for sweettasting foods in a SSS, oral habituation test procedure.They suggest that since sweet tasting foods can have highenergy density when mixed with fat, this propensity forsweet taste may well contribute to development of obesityin this ethnic group.

Additional support for reduced SSS in the obese is foundin Epstein and co-workers (72). In this study obese womenwere found to have a significantly slower decline in saliva-tion due to repeated food cues. Reduced decline in saliva-tion is also consistent with a difference in reinforcing valueof food between the lean and obese. In rats, SSS has been associated with changes in dopamine efflux in thenucleus accumbens and prefrontal cortex of the brain, sitesassociated with the reward circuitry of the brain (73).Recently positron emission tomography (PET), a techniquethat measures changes in brain blood flow or neurotrans-mitter receptor binding by detecting positrons (positivelycharged particles emitted by injected radio-labelled sub-stances), has been used to image brain dopamine receptorsin obese and lean humans (74). Wang and co-workers (74)report that the obese have significantly fewer dopaminereceptors than the lean, and suggest two possibilities forthis phenomena, namely, down regulation of receptors dueto chronic high dopamine levels from overeating, OR, over-eating to produce increased dopamine release, which wouldcompensate for fewer receptors and under activation ofreward circuits. In either case, reduced sensitivity to SSSsignals in humans could be another way in which altered tasteresponses promote excessive energy intake and contributeto the development or maintenance of obesity in humans.

Taste, thermic effect of food and satiation

Thermic effect of food (TEF) refers to the increase in energyexpenditure associated with food intake. It is dependent on palatable, sensory stimulation (75) and is reduced inobese compared to lean humans (75–77). This reduction isrelated to impaired insulin sensitivity seen in obesity (77).

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TEF is associated with the satiating power of foods (78,79).Westerterp-Plantenga and co-workers (80) suggest that thisfunction of TEF is also reduced in the obese, which wouldagain promote over-consumption of energy and foster thedevelopment of obesity.

Taste, food liking, and food wanting

The perceived ‘liking’ of a food, which Berridge (81) suggests corresponds closely with palatability, is under thecontrol of brain opioid and serotonin pathways (81,82),while ‘wanting’ food (or appetite) (81), is modulated bydopamine pathways (81,83). The impact of ‘liking’ on foodintake in animals and humans has recently been reviewedby Sclafani (84) and Mela (85), and will not be coveredhere. It should be noted that the opioid and serotonin path-ways can modulate meso-limbic dopaminergic activity(83), suggesting a link between ‘liking’ and ‘wanting’ foodand a possible basis for ‘food craving’ (86). However,Rogers and Smit (87) suggest that craving is dependent onpsychological rather than neurophysiological processes.

The association of taste with ‘wanting’ food and foodreward (positive reinforcement) is related to the release ofdopamine in the meso-limbic circuitry of the brain (88).Dopamine release due to food stimuli (i.e. taste) is phasic,and contingent on stimulus novelty (89). Habituation tothe stimulus develops over time (83), leading to decreasedreinforcement as is seen in development of SSS during ameal (90). Dopamine release also has a role in associativelearning (91) whereby sensory stimulus reward is associ-ated with the metabolic consequences of energy intake.Saelens and Epstein (92) report that food is more reinforc-ing in the obese than the lean, and differences in function-ing of the dopaminergic pathway between the lean andobese are beginning to be revealed (74). Further work isneeded to determine the impact of differences in dopamin-ergic pathways on taste perceptions, reinforcing value offood and the development and maintenance of obesity.

Summary

Taste contributes to food palatability, which promotesintake, and to thermic effect of a meal and SSS, whichpromote termination of intake. Reduced sensitivity to thesesensory-based termination signals, coupled with possibleincreased incentive salience of food stimuli and decreasedactivation of food-reward circuits, may contribute to theover-consumption of energy that leads to obesity.

Suggestions for future research

This summary of suggestions for future research was generated from discussions with experienced taste andeating behaviour researchers (see acknowledgements) and



is offered for additional consideration and discussion:determination of the impact of leptin level on taste per-ceptions and food intake, identification of an orosensorybased fat intake inhibition system, answers to questionssuch as: how different does a food have to taste to get amore rapid SSS effect? and can we titrate taste perceptionsso as to maximize food reward value and minimize energyintake and identification of genetic differences that modu-late the potency of foods as unconditioned stimuli in thedevelopment of conditioned sensory preferences?

Acknowledgements

The author wishes to thank Drs Linda Bartoshuk (YaleUniversity), Adam Drewnowski (University of Washing-ton), Allan Geliebter (Columbia University), Harry Kissileff(Columbia University), David Mela (Unilever, the Nether-lands), Barbara Rolls (Pennsylvania State University) andAnthony Sclafani (City University of New York) for shar-ing their expertise and suggestions for future research.

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