Elsevier

Appetite

Volume 57, Issue 1, August 2011, Pages 286-294
Appetite

Research review
“You Say it's Liking, I Say it's Wanting …”. On the difficulty of disentangling food reward in man

https://doi.org/10.1016/j.appet.2011.05.310Get rights and content

Abstract

According to the influential theory of Berridge, 1996, Berridge, 2009, food reward comprises two components: food ‘liking’ and ‘wanting’, with ‘liking’ referring to the pleasure derived from eating a given food and ‘wanting’ referring to appetitive motivation. Animal research shows that these two components have separate neural correlates. In examining reward driven eating in man, researchers have thus begun to develop interest in indicators of ‘liking’ and ‘wanting’. But validating ‘liking’ and ‘wanting’ requires the dissociation of these components when theory dictates they should diverge. One such circumstance is neural sensitization as this leads to exaggerated ‘wanting’ without increased ‘liking’. However, there are no data suggesting that such sensitization is the likely result of (over)eating. Without sensitization, one cannot determine whether task performance is indicative of true food ‘liking’ or ‘wanting’. It is concluded that it is important to assess appetite and palatability in the study of reward driven eating, but determining whether these measurements reflect either food ‘wanting’ or food ‘liking’ is not.

Highlights

► Food reward comprises ‘liking’ and ‘wanting’ food. ► ‘Liking’ and ‘wanting’ are thought to be important in determining reward driven eating. ► Validation of measures of ‘liking’ and ‘wanting’ in man is logically impossible. ► It is needless to speculate on the separate contribution of ‘liking’ and ‘wanting’ to food reward.

Introduction

One may argue that in environments where highly palatable foods are abundant and readily available, hunger and satiety do not play an important role in determining eating behavior (i.e., food intake and selection). Many scholars agree that in these settings appetite reflects hedonic motives rather than homeostatic needs (see e.g., Appelhans, 2009, Berridge, 2004, Eertmans et al., 2001, Finlayson et al., 2007b, Lowe and Levine, 2005, Papies et al., 2008, Stroebe et al., 2008, Yeomans et al., 2007). That does not mean that one denies that homeostatic drives influence affective processing of food and food cues (see e.g., Siep et al., 2009, Young, 1959), but in the absence of true physiological needs this influence may be limited. Apart from being a biological necessity, eating can be a source of joy, and particularly high energy dense palatable foods are potent rewards. Cuisine is often the central feature of a culture and people derive great pleasure from it as exemplified by the fact that some individuals will spend a lot of money on a carefully prepared meal at a top restaurant (de Castro et al., 2000, Rozin, 1996).

It is possible to define eating behavior in terms of need-free hedonic motivation: people eat the foods they like and avoid having to eat foods they do not like (Cabanac, 1992, Eertmans et al., 2001, Lowe and Butryn, 2007, Young, 1959). This hedonic eating behavior can be characterized as reward driven eating (Appelhans, 2009). What makes studies of food reward or reward driven eating especially relevant is that “hedonic hunger” (Lowe and Butryn, 2007, Lowe and Levine, 2005) can override homeostatic signals and hence promotes weight gain. Palatability is an important predictor of food intake, hedonic responses to foods are closely linked to food choice, food palatability induces overconsumption particularly when sated, and the mere exposure to a preferred food stimulates appetite (see e.g., Jansen et al., 2008, Mustonen et al., 2007, Yeomans et al., 2007). Clearly this “power of food” (Lowe & Butryn, 2007) undermines weight regulation and contributes to an excessive appetite. In line with this view the current rapid global rise in the prevalence of obesity has prompted much needed research investigating the role of food reward in eating.

Berridge, 1996, Berridge, 2007a argues that when examining the role of food reward in eating behavior one should make the distinction between food ‘liking’ and food ‘wanting’, with ‘liking’ roughly referring to palatability (i.e. the pleasure derived from eating a given food) and ‘wanting’ to an incentive motivation or disposition to eat. The division between food ‘liking’ and ‘wanting’ relies on animal research showing that different neural substrates underlie the expression of affective food (dis)likes and the disposition to eat (i.e. wanting). Food ‘wants’, incentive salience, or food cravings are induced by exposure to food and food-related cues, and heavily depend on mesocorticolimbic dopamine activity (i.e., dopamine neurotransmission; Berridge, 2007b). Food ‘liking’, the affective state triggered by tasting palatable foods, is associated with opioid activation in specific limbic forebrain structures, or “hedonic hotspots” (Berridge, 2009, Berridge and Kringelbach, 2008, Peciña et al., 2006). In animal research, such food ‘liking’ hotspots have been found within the medial shell of the nucleus accumbens (Peciña & Berridge, 2005) and the posterior ventral pallidum (Smith & Berridge, 2005). Mu-opioid receptor stimulation within these specific neural structures by micro-injections of the opioid agonist DAMGO typically increases sweet taste ‘liking’, whereas lesions to these areas – especially the ventral pallidum – may lead to a complete loss of appetite (Berridge, 2007a, Berridge, 2009). Interestingly, other neurotransmitter systems within these limbic structures (e.g., endocannabinoid system and GABA-ergic neurotransmission) may also affect food ‘liking’ and this suggests a complex interplay of neurotransmitter systems in determining hedonic responses to food (Berridge, 2007a, Cooper, 2004). Importantly, food ‘wanting’ can be disconnected from food ‘liking’. For example, treating rats with 6-OHDA leaves them dopamine depleted. These rats are aphagic but still display normal affective reactivity to sucrose (liked) and quinine (disliked) (Berridge & Robinson, 1998). Conversely, a surplus of dopamine in the rodent brain either as the result of a genetic mutation or due to the administration of amphetamine inducing dopamine release causes elevated sweet food ‘wanting’, but not ‘liking’ for sweet food rewards (Peciña et al., 2003, Tindell et al., 2005).

In sum, food reward comprises both ‘liking’ and ‘wanting’, and these two aspects of food reward each have their own, though interrelated, neural correlates. Importantly, this implies that food ‘liking’ and ‘wanting’ can be split under certain circumstances and contribute separately and differently to reward driven eating (Berridge, 2009). Finlayson et al. (2007b, p. 989) state that “if core processes of liking and wanting can independently modulate food reward …, it is important to understand how they can be approached and rendered suitable for the study of ingestive behaviour in humans”. In animals, food ‘liking’ and ‘wanting’ can be studied separately by imposing specific brain lesions. The difficulty in identifying and dissecting these food reward components in human eating behavior lies in the obvious fact that one cannot rely on lesion studies and this raises the question whether it is possible at all to dissociate ‘liking’ and ‘wanting’ in man. In the present article, the contention is that, given current theory and data, it is impossible to validate measures of true food ‘liking’ and ‘wanting’ in man implying that one cannot distinguish between pure ‘wanting’ and ‘liking’ when examining human reward driven eating, and that hence the parsing of food reward into ‘liking’ and ‘wanting’ is unnecessary.

Section snippets

Dissociating food ‘liking’ and ‘wanting’ in man

Inasmuch as reward driven eating in man is determined by dissociable ‘liking’ and ‘wanting’, investigating the separate contributions of ‘liking’ and ‘wanting’ to the experience of food reward requires that one is able to objectively measure these food reward components. To this end, various food ‘liking’ and ‘wanting’ tasks and tests have been developed or adapted, but it has proven to be very difficult to measure true ‘wanting’ separate from true ‘liking’. A selection of studies typifying

Individual differences in dissociated ‘liking’ and ‘wanting’

Food ‘liking’ and ‘wanting’ do not likely diverge with normal reward driven eating, but it may in the case of abnormal eating behavior. In fact, a disconnect between ‘liking’ and ‘wanting’ might be at the heart of aberrant dietary habits, such as binge eating in case of different eating disorders or regular caloric overconsumption associated with weight gain (Berridge, 2009, Yeomans et al., 2007). It has been suggested that the relative overconsumption of high energy dense palatable foods

Neural sensitization, food addiction, and obesity

With repeated drug use certain structures within the brain become more tolerant to the effects of the drug, but other parts or networks become sensitized, especially the reward related structures such as the nucleus accumbens and the ventral tegmental area. One can assess such neural sensitization with behavioral studies. The structures that tend to sensitize with drug use are partly involved in the regulation of overall behavioral activity or psychomotor arousal. Behavioral activity increases

Disentangling food ‘liking’ and ‘wanting’: “… Let's call the whole thing off”

According to Berridge, 1996, Berridge, 2009, there is cumulating evidence that separate neural structures and neurotransmitter systems are involved in the respective processing of incentive salience and food hedonics. One may doubt whether such a conclusion is warranted given the data, but that is a discussion outside the scope of the present article. The primary aim of this paper was to critically evaluate the recent attempts to measure the contributions of assumed separable food ‘wanting’ and

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    The author would like to thank Anne Roefs and Chantal Nederkoorn for discussions and for providing detailed comments on an earlier draft. The author would further like to thank the Jansen lab for helpful and much appreciated ‘Gedankenflapperflackern’.

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