Important episodic signals are those physiological events which are triggered as responses to the ingestion of food.  These form the inhibitory processes which first of all stop eating and then prevent its re-occurrence and so are termed satiety signals.  The types of signals involved in terminating a meal (satiation) and preventing further consumption (post meal satiety) can be represented by the satiety cascade.  The cascade demonstrates how satiation, the complex of processes which brings eating to a halt (cause meal termination), and satiety, those events which arise from food consumption which serve to suppress hunger (the urge to eat) and inhibit further eating, coordinate our eating behaviour controlling the size and frequency of eating episodes (Blundell et al. 1994).

Initially the brain is informed about the amount of food ingested and its nutrient content via sensory input. The gastrointestinal tract is equipped with specialised chemo- and mechano-receptors that monitor physiological activity and pass information to the brain mainly via the vagus nerve (Mei, 1985).  This afferent information constitutes one class of `satiety signals’ and forms part of the pre-absorptive control of appetite. It is usual to identify a postabsorptive phase that arises when nutrients have undergone digestion and have crossed the intestinal wall to enter the circulation. These products, which accurately reflect the food consumed, may be metabolised in the peripheral tissues or organs or may enter the brain directly via the circulation. In either case, these products constitute a further class of metabolic satiety signals. Additionally, products of digestion and agents responsible for their metabolism may reach the brain and bind to specific chemoreceptors, influence neurotransmitter synthesis or alter some aspect of neuronal metabolism. In each case the brain is informed about some aspects of the metabolic state resulting from food consumption.

It seems likely that chemicals released by gastric stimuli or by food processing in the gastro-intestinal tract are involved in the control of appetite (Read, 1990).  Many of these chemicals are peptide neurotransmitters, and many peripherally administered peptides cause changes in food consumption (Smith & Gibbs, 1995). Currently, a good deal of interest is being shown in these peripheral signals of appetite control, and some will be described below.

CCK is a hormone released in the proximal small intestine mediating meal termination (satiation) and possibly early phase satiety. CCK reduces meal size and also suppresses hunger before the meal; these effects do not depend on the nausea that sometimes accompanies an IV infusion (Greenough et al. 1998).   Food consumption (mainly protein and fat) stimulates the release of CCK (from duodenal mucosal cells) which in turn activates CCK-A type receptors in the pyloric region of the stomach. Fat in the form of Free Fatty Acids (FFA) of carbon chain lengths C12 and above produce pronounced CCK releases (Feltrin et al., 2004; Little et al., 2007). This signal is transmitted via afferent fibres of the vagus nerve to the nucleus tractus solitarius (NTS) in the brain stem. From here the signal is relayed to the hypothalamic region where integration with other signals occurs.

Animal data suggest that endogenous CCK release mediates the pre-absorptive satiating effect of intestinal fat infusions, and may in turn be critical in regulating the intake of fat (Greenberg et al. 1992).  As in rats, intestinal infusions of fat produce a reduction in food intake and promote satiety in humans (Welch et al. 1985). In humans the satiety effect of fat infused directly into the duodenum can be blocked by the CCKA receptor antagonist loxiglumid (Lieverse et al. 1994). High fat breakfasts have been shown to produce both greater feelings of satiety (signified by reduced levels of hunger, desire to eat and prospective consumption) and elevated endogenous plasma CCK levels. Collectively, these studies support the theory that CCK plasma levels are a potent fat (or fatty acid) -stimulated endogenous satiety factor, whose effects on food intake and feeding behaviour are mediated by CCKA receptors.

It has also been shown that synthetic CCK-A type agonists suppress food intake in humans. A drug, known by the number - ARL1718 – caused a significant reduction in meal size and had a longer duration of action than observed after infusions of CCK itself (Greeenhough et al, 2000). A number of other CCK analogues / CCK 1 receptor agonists treatments have been developed including most recently GW181771 (GlaxoSmithKline) and SR146131 (Sanofi-Aventis). Studies with such drugs, together with those on the peptide hormone itself, do suggest that CCK has the properties of a true satiation signal which contributes, under normal circumstances, to the termination of a meal. The action of CCK certainly acts in concert with other meal related events, such as gastric distention for example.

Glucagon-like peptide (GLP)-1 is an incretin hormone, released from the gut into the blood stream in response to intestinal nutrients. Endogenous GLP-1 levels increase following food intake, particular of carbohydrate (Lavin, et al. 1998; Ranganath et al. 1996). These studies suggest a role for GLP-1 in mediating the effects of carbohydrate (specifically glucose) on appetite.

In healthy men of normal weight, infusions of synthetic human GLP-1 (7-36) during the consumption of a fixed breakfast test meal, enhanced ratings of fullness and satiety when compared to the placebo infusion (Flint et al. 1998).  During a later ad libitum lunch, food intake is also significantly reduced by the earlier GLP-1 infusion. Intravenous GLP-1 also dose-dependently reduces spontaneous food intake and adjusts appetite in lean male volunteers. This marked reduction in food intake and enhancement in satiety is also observed in overweight/obese male patients with type 2-diabetes. In obese men, intravenous GLP-1 potently reduces food intake either during or post-infusion (Näslund et al. 1998) and, at lower sub-anorectic doses, slows gastric emptying. Reductions in intake and slowed gastric emptying are accompanied by decreased feelings of hunger, desire to eat and prospective consumption, and a prolonged period of post-meal satiety. These data demonstrate that exogenous GLP-1 reduces food intake and enhances in satiety in humans, both lean and obese.  However, it should be kept in mind that the doses of GLP-1 often administered, are usually higher than the normal values seen in blood after a meal. Consequently, although GLP-1 receptors could be a possible target for anti-obesity drugs, the physiological role of GLP-1 itself in the normal mediation of satiety is still not confirmed. None the less, GLP-1 through its action as an incretin which prompts the release of insulin, will certainly have some indirect role on the pattern of eating behaviour.

Peptide YY _3-36(PYY _3-36) is one of the two main endogenous forms of PYY. It is produced from the cleavage of PYY _1-36(the other major form of PYY) by dipeptidyl peptidase IV (DPP IV).  PYY is a 36 amino acid ‘hind gut’ peptide released from endocrine cells in the distal small intestine and large intestine. This hormone is similar in structure to the orexigenic neuropeptide NPY (70% amino acid sequence identity), and in the past, peptide YY (PYY) has been regarded, like NPY, as a potent stimulator of food intake. However, in a series of studies in rats, mice and in one human study (all included in one paper), (Batterham et al. 2002) have demonstrated that peripheral PYY _3-36administration reduces food intake and inhibits weight gain in rodents. These effects on intake and body weight are not observed in transgenic animals lacking NPY Y2 receptors (the NPY Y2 receptor knock-out), thereby implicating these receptors in mediating the anorectic effects of PYY.  PYY release in the distal intestine is triggered by a variety of nutrients, including fats (particularly free fatty acids), some forms of fibre and bile acid  (Ongaa et al., 2002; Feltrin et al., 2006; Weickert et al., 2006; Little et al., 2007).  In humans, endogenous PYY is released predominantly after rather than during a meal (Batterham et al., 2002; 2003) and causes a decrease in gastric emptying (the so-called ‘ileal brake’).  Thus, it is more associated with post-meal satiety. PYY (including PYY _3-36) can cross the blood brain barrier via a non-saturatable mechanism.  Moreover, some of the effects of peripheral PYY _3-36on food intake are should be either ‘independent of’ or ‘dependent on’ vagal afferents running from the periphery to the brain (Renshaw and Batterham 2005; Koda et al., 2005).  

With regard to the effect of PYY on human appetite, Batterham et al. (2002) demonstrated that in healthy humans a 90-minute PYY _3-36infusion reduced hunger and subsequent food intake two hours later.  In a further report, PYY infusions in both lean and obese subjects caused a 30% reduction in lunch intake post infusion and decreased the 24 h energy intake by 23% in lean and by 16% in the obese (Batterham et al, 2003). The natural plasma levels of PYY were lower in the obese than in the lean subjects, and were inversely correlated with the body mass index. The lower levels of PYY in the obese could mean a weaker satiety signaling through this hormone and therefore a greater possibility of over-consumption. The effects of PYY _3-36on human food intake have been described in three other studies to date.  However, as the authors noted these effects required doses greater than the normal physiological range of endogenous PYY and marked nausea was observed in one experiment (Degan et al. 2005; Sloth et al; 2007a,b).  Nonetheless, PYY _3-36(in the form of a PYY _3-36nasal spray from Nastech Pharmaceuticals, AC162352 a synthetic version of human PYY _3-36from Amylin Pharmaceuticals, and CJC-1681 from Conjuchem) and an Y2 agonist (TM30338 7TM Pharma) are currently in clinical development.

Much recent research has also focused on amylin, a pancreatic rather than a gastrointestinal hormone, which also has a potent effect on both food intake and body weight (Reda et al. 2002).  Peripheral administration of amylin reduces food intake in mice and rats, and meal size in rats. Chronic or peripheral administration of amylin over a period of 5 to 10 days produces significant reductions in cumulative food intake, body weight and body mass of rats (Rushing et al. 2001).   Amylin administration blocks the hyperphagic effects of (Morris & Nguyen, 2001). Thus, amylin appears to be a component part of the appetite regulation system. The effects of amylin on human food intake, food choice or appetite expression has yet to be fully assessed. However, pramlintide (a human amylin analogue), given to replace deficits in endogenous amylin in diabetics, has been shown to alter body weight in diabetic insulin treated obese (Hollander et al., 2003; 2004; Riddle et al., 2007) and non-diabetic obese (Aronne et al., 2007).  In lean health volunteers pramlintide induces reductions in meal intake and duration, and reduces pre meal appetite (Chapman et al., 2007).  Similar effects of pramlintide on intake and eating behaviour are reported in obese (with and with out type 2 diabetes) (Chapman et al., 2005; Smith et al., 2007).

In the overall control of the eating pattern, the sequential release and then de-activation of the peptides, described above, can account for the evolving biological profile of influence over the sense of hunger and the feeling of fullness.  (Blundell and Naslund, 1999).  The actions of these hormones therefore contribute to the termination of an eating episode  (thereby controlling meal size) and subsequently influence the strength and duration of the suppression of eating after a meal. Individual variability in the release and maintenance of the levels of hormones (or the sensitivity of receptors) may determine whether some individuals are prone to snacking between meals or to other forms of opportunistic eating. The overall strength or weakness of the action of these peptides will help to determine whether individuals are resistant or susceptible to weight gain.

One of the classical theories of appetite control has involved the notion of a so-called long-term regulation involving a signal which informs the brain about the state of adipose tissue stores. This idea has given rise to the notion of a lipostatic or ponderstatic mechanism (Weigle, 1994).  Indeed this is a specific example of a more general class of peripheral appetite (satiety) signals believed to circulate in the blood reflecting the state of depletion or repletion of energy reserves which directly modulate brain mechanisms. Such substances may include satietin, adipsin, tumour-necrosing factor (TNF or cachectin—so named because it is believed to be responsible for cancer induced anorexia), adiponectin and resistin together with other substances belonging to the family of neural active agents called cytokines.

In 1994 a landmark scientific event occurred with the discovery and identification of a mouse gene responsible for obesity. A mutation of this gene in the ob/ob mouse produces a phenotype characterized by the behavioural trait of hyperphagia and the morphological trait of obesity. The gene controls the expression of a protein (the ob-protein) by adipose tissue and this protein can be measured in the peripheral circulation. The identification and synthesis of the protein made it possible to evaluate the effects of experimental administration of the protein either peripherally or centrally (Campfield et al. 1995).  Because the ob-protein caused a reduction in food intake (as well as a possible increase in metabolic energy expenditure) it has been termed `leptin’. There is some evidence that leptin interacts with NPY, one of the brain’s most potent neurochemicals involved in appetite, and with the melanocortin system. Together these and other neuromodulators are involved in a peripheral-central circuit which links an adipose tissue signal with central appetite mechanisms and metabolic activity.

In this way the protein called leptin probably acts in a similar manner to insulin which has both central and peripheral actions; for some years it has been proposed that brain insulin represents a body weight signal with the capacity to control appetite.

At the present time, the precise relationship between the ob-protein and weight regulation has not been determined. However, it is known that in animals and humans which are obese the measured amount of ob-protein in the plasma is greater than in lean counterparts. Indeed there is always a very good correlation between the plasma levels of leptin and the degree of bodily fattiness (Maffei et al. 1995).  Therefore although the ob-protein is perfectly positioned to serve as a signal from adipose tissue to the brain, high levels of the protein obviously do not prevent obesity or weight gain. However, the ob-protein certainly reflects the amount of adipose tissue in the body. Since the specific receptors for the protein (namely ob-receptor) have been identified in the brain (together with the gene responsible for its expression) a defect in body weight regulation could reside at the level of the receptor itself rather than with the ob-protein. It is now known that a number of other molecules are linked in a chain to transmit the action of leptin in the brain. These molecules are also involved in the control of food intake, and in some cases a mutation in the gene controlling these molecules is known and is associated with the loss of appetite control and obesity. For example, the MC4-R mutation (melanocortin concentrating hormone receptor 4) leads to an excessive appetite and massive obesity in children, similar to leptin deficiency.

Leptin based obesity treatments for most obese individuals seem inappropriate given they appear leptin insensitive rather than leptin deficient.  Nonetheless, studies have shown for individuals with leptin deficiency leptin treatment produces dramatic weight loss, an affect associated with marked decreases in hunger (Farooqi et al., 1999; 2002; Williamson et al., 2005).  The administration of exogenous leptin to humans, with either an insufficiency in or a specific deficit of endogenous leptin appears to strengthen within meal satiation and post meal satiety (Williamson et al., 2005; McDuffie et al. 2004).  Under the right physiological conditions such as diet induced normalization of endogenous leptin levels, the effects of exogenous leptin on human appetite could be still exploited to treat obesity (Heini et al., 1998; Keim et al., 1998; Mars et al., 2006).  However, this has yet to be robustly demonstrated.

Ghrelin is found both in the gut and the brain, the gut being the major source of plasma ghrelin. The highest concentrations of ghrelin are found in the stomach, and then in the small intestine. Endogenous ghrelin levels appear responsive to nutritional status; for instance, human plasma ghrelin immunoreactivity increases during fasting and decreases after food intake. It is also found in hypothalamic nuclei critical to energy regulation (Cummings, 2006).  Unlike the other peripheral peptides described earlier, ghrelin stimulates rather than inhibits feeding behaviour. Both peripheral and central infusions of ghrelin have been shown to stimulate food intake in rats and mice (Wren et al. 2000).  Decreased endogenous ghrelin levels are observed in genetically obese rats and mice, and in dietary-induced obese rats exposed to a high fat diet (Ariyasu et al. 2002).  The peripheral effects of ghrelin may be vagally mediated but a direct effect of circulating ghrelin on the CNS cannot be ruled out given that receptors are found for it on the Accurate Nucleus outside the blood brain barrier and that it can cross the blood brain barrier also (Cummings. 2006).

It has been proposed that ghrelin – linked to the initiation of eating – acts as a compensatory hormone. This means that in obese people and in animals experimentally made fat, ghrelin levels would be reduced in an apparent attempt to restore a normal body weight status. Therefore ghrelin illustrates the characteristics of both an episodic and tonic signal in appetite control. From meal to meal the oscillations in the ghrelin profile act to initiate and to suppress hunger; over longer periods of time, some factor associated with fat mass applies a general modulation over the profile of ghrelin and therefore, in principle, over the experienced intensity of hunger. This means that when weight is lost, for example following a period of food restriction and weight loss, ghrelin levels would rise and therefore promote the feeling of hunger. This is likely to be one of the signals that makes the loss of body weight so difficult to maintain and so ghrelin blockade may prove a useful anti-obesity treatment.

Appetite sensitivity is related to the capacity to detect over- or under-consumption (positive or negative energy balance) and to exert a compensatory response. This can be achieved through the modulation of satiation signals and by compensating for a particular energy intake by adjusting the size of the next meal. There is some evidence to suggest that regular exercisers, or habitually physically active individuals, have a better capacity to regulate their food intake and energy balance because of an increased appetite sensitivity. Recently, (Long et al. 2002) demonstrated that habitual exercisers have an increased accuracy of short-term regulation of energy intake in comparison to non-exercisers. In this study, participants were given either a low or high energy preload for lunch, and were then asked to eat ad libitum from a test meal buffet. Energy intake did not significantly differ following the two preloads in the non-exercise group, indicating a weak compensation. However, the habitual exercisers demonstrated nearly full compensation (~90%) by reducing their energy intake following the high energy preload compared to the low energy preload. Insulin sensitivity has been proposed as one mechanism by which activity-induced improvements in appetite regulation occur. Exercise is known to increase insulin sensitivity (e.g. Andersson et al. 1991; Donnelly et al. 2000; Poehlman et al. 2000), and insulin sensitivity is known to be involved in satiety induced by particular foods (Holt et al. 1992) and in the compensatory response to high energy loads (Speechly and Bufferstein, 2000). A further mechanism by which exercise could affect appetite is through altering gut peptide action. For example, cholecystokinin (CCK) is implicated in the short-term regulation of appetite, and levels of CCK have been shown to rise after exercise (Bailey et al. 2001). The effects of exercise on other gut peptides, such as GLP-1, PYY and ghrelin, involved in the episodic regulation of appetite are to date, unknown. However, a recent study showed that PPY was not associated with changes in hunger or food intake (Martins et al, 2007).

Most studies examining the effects of exercise on body weight and food intake tend to report the mean data and overlook the inter-individual variability. It is unlikely that a fixed dose of exercise will be effective to the same extent in all individuals. The concept of individual variability is not necessarily new. Indeed, the classic genetic studies conducted by Claude Bouchard were instrumental in identifying the variability in response to over-feeding interventions in twins (Bouchard et al. 1990). Recent evidence shows that despite performing mandatory and supervised exercise, there is a large inter-individual variability in weight loss following 12 weeks of exercise (King et al, 2007). Figure 2 shows clearly the range in weight loss and that some individuals lose more than, while other lose less than the predicted weight loss of 3.7kg. Further analysis of the data revealed that individuals who lost less then the predicted weight were compensating via an increased drive to eat and food intake. Although acute studies show that exercise does not immediately drive up food intake, it has been demonstrated that compensation does begin to occur if daily physical activity persists. Over periods of up to 16 days partial compensation occurs so that increased eating accounts for approximately 30% of the increase in energy expended (Blundell et al. 2003).

Figure 2. Variability in weight loss response to 12 weeks supervised exercise (King et al. 2007). BW – body weight; FM – fat mass. It is possible that a compensatory increase in food intake could also be due inappropriate food choices and a feeling that food self-reward is justified, or from misjudgments about the energy cost of physical activity (calories expended) relative to the rate of eating-induced intake (calories consumed). Empirical evidence demonstrates that when physical activity is combined with high-fat, energy dense foods, the beneficial effects of activity on energy balance can be reversed (King & Blundell, 1995; Tremblay et al, 1994). An increase in physical activity does not automatically protect against inappropriate food choice.

Although the loose coupling between exercise-induced EE and EI has positive implications for weight control for increases in EE, unfortunately it has negative implications for decreases in EE. Recent findings have confirmed that there is no down regulation of appetite and EI remains at some stable preferred level when EE is reduced. Inactivity-induced reductions in EE occur in the natural, free-living environment due to a variety of reasons (e.g., injury, increase in energy-saving devices, increase car use). Two independent studies have demonstrated that EI is not down-regulated in response to activity-induced reductions in EE, hence a positive energy balance occurs (Murgatroyd et al, 1999; Stubbs et al, 2004). Therefore, a reduction in EE does not automatically reduce food intake. Considering eating tends to be a sedentary activity, inactivity could even increase food intake.

Advances in our understanding of the molecular and neural mechanisms behind food intake regulation and appetite control are revealing how the reward system can interact with homeostatic mechanisms.  For example, cannabinoid receptors and their endogenous ligands (e.g. anandamide) are implicated in the reward system.  Peripheral and central administration of anandamide increased appetite in rodents, and this seemed to be related to alterations in incentive value (desire) for palatable foods (Kirkham & Williams, 2001).  However, the cannabinoid system has been shown to interact with homeostatic processes in a number of ways (Stanley et al. 2005):  Leptin signalling becomes defective when hypothalamic endocannabinoid levels are high (Di Marzo et al. 2001); activation of CB1 receptors prevent the melanocortin system from altering food intake (Verty et al. 2004); furthermore, CB1 receptors can be found on adipocytes where they may directly increase lipogenesis (Cota et al. 2003).  Opioid neurotransmission also forms part of the biological substrate mediating reward processes of consumption.  For example, endogenous opioids are associated with the reinforcing effect of food (especially when palatable) (Welch et al. 1996; Yamamoto et al. 2000).  However, there is evidence to show that in a fasted state, the reinforcing effect of food can be reinstated in enkephalin and β-endorphin knock-out mice (Hayward et al. 2002).  Therefore, homeostatic processes may interact with hedonic signalling to override selective reward deficit.  Erlanson-Albertsson (2005) summarized how ingestion of palatable food can offset normal (homeostatic) appetite regulation (figure 3).  In the brain, research shows that energy deficit is registered in the hypothalamus leading to the release of hunger signals and the activation of their receptors.  Consumption of ‘standard’ food generates information on its energy content and taste in the brain stem.  This information is transmitted to the hypothalamus leading to the release or upregulation of various satiety peptides, causing consumption to cease.  However, a different scenario is apparent when the reward system is activated by highly palatable food.  With ingestion of palatable food, taste sensing is different than with standard food; information is transmitted to the reward circuit, leading to the release or upregulation of reward mediators like dopamine, endocannabinoids, and opiates.  The reward circuit has connections with appetite-controlling neurones in the hypothalamus that can increase the expression of hunger peptides such as NPY and orexins, while blunting the signalling of satiety peptides like insulin, leptin and cholecystokinin.  Therefore when food is highly palatable, the drive to eat is maintained, with continued eating now mediated by reward rather than biological need (see figure 3).

Figure 3. Hunger and satiety signalling during consumption of standard (left) and palatable (right) food (Erlanson-Albertsson, 2005). Left. Hunger and satiety signalling during intake of a standard meal. Hunger signals, such as ghrelin in the stomach and NPY, orexin, AgRP in the hypothalamus, are depressed after intake of standard food, while satiety signals like CCK, GLP-1, PYY, insulin and leptin are raised. Food intake is terminated as a result. Right. Hunger and satiety signalling after a period on a diet of palatable food. Hunger signals are either depressed, like ghrelin in the stomach and NPY in the hypothalamus, in response to a meal consisting of palatable food or raised, as for orexin and AgRP in the hypothalamus. Satiety signals like insulin and leptin are increased. Palatable food induces resistance to several satiety signals, documented for CCK, insulin and leptin, resulting in overeating. Food intake is driven by an increased activity in the reward system (dopamine, serotonin and opiates), triggered by the attractiveness of the taste.

Hence although homeostatic and hedonic systems can be given separate identities (Blundell & Finlayson 2004), they are also – to an extent – inseparable, with neural cross-talk permitting functional interactions which may influence the organization of feeding behaviour.  From this standpoint, the interaction of homeostatic and non-homeostatic pathways in the neuro-regulatory control of feeding may be more important than the two systems studied in isolation.  From behavioural and anatomical observations, Berthoud (2006) suggested that projections from the hypothalamus to the nucleus accumbens may modulate the motivation to feed via metabolic signals.  Furthermore, direct and indirect projections from the accumbens to the hypothalamus may explain the ability for mesolimbic processes – activated by relevant environmental cues and incentives – to essentially hijack the homeostatic regulatory circuits and drive up energy intake.  Further research is necessary to identify the pathways that mediate such interactions; however some progress has been made (see Berthoud 2004).

“Liking” and “wanting” are emerging constructs in a conceptual approach to food hedonics where separable processes of affect and motivation can be viewed as major influences on food intake.  Liking and wanting achieve importance in light of the recognition of the contrast between homeostatic and hedonic processes that control eating (Finlayson et al. 2007).

The liking and wanting constructs stem from research exploring the neural basis of palatability and addictive behaviour (see Berridge, 1996).  With principle focus on distinct dopamine and opioid pathways in the brain, the research suggests that processes of liking and wanting can be separately manipulated to produce patterns of behaviour that are either exclusively affective (rewarding) or motivational (driving) in conjunction with a food stimulus.  The proposal that food reward may comprise separable liking and wanting components has since attracted a great deal of attention and controversy among scientists concerned with human food intake and obesity.  Many people would assume that liking and wanting are identical phenomena, both of which signify a positive attraction to food.  The logical view is that liking and wanting co-vary in a natural two-way sequence.  In behavioural terms we assume that a change in liking will lead to proportional adjustments in wanting and, likewise, differences in wanting will predict changes in liking.  Therefore, some researchers suggest that a clear behavioural distinction might not be possible.  However, there are strong grounds for recognizing that liking and wanting can be clearly dissociated and have distinct identities.  This means that they have much greater resolving potential for understanding the role of hedonics on eating and therefore on overconsumption.  Thus, the issue of liking vs. wanting is concerned with the functional significance of these two distinguishable processes, operating within the hedonic domain, for overconsumption and weight regulation in humans.  Liking and wanting are thought to reflect ‘core’ processes that can operate without conscious awareness.  This means that they have implicit components.  However, their explicit counterparts express themselves subjectively in the form of hedonic feelings from the ingestion of a specific food (i.e. explicit liking) and the intent or desire to consume a specific food (i.e. explicit wanting).  Under normal circumstances, explicit liking (“I like this”) is closely associated with explicit wanting (“I want this”).  However, there is also evidence to suggest that wanting can be ‘irrational’; i.e. when implicit wanting for a food is greater than explicit wanting, and not proportional to experienced or expected liking (see Berridge 2004).

Liking and wanting appear to have separate and disproportionate roles in promoting overconsumption.  In terms of liking, some individuals at risk of weight gain may experience an exaggerated hedonic response to palatable foods, so that foods are enjoyed more and therefore eaten in greater amounts for longer periods of time (Blundell et al. 2005; Le Noury et al. 2002).  Conversely, susceptible individuals may have a diminished ability to experience pleasure from food and therefore consumption of palatable food is driven up to satisfy an optimum level of stimulation (see Davis and Fox, 2008).  Processes of wanting may also bring about vulnerability to weight gain through increased reactivity towards cues signalling the availability of food (e.g. Saelens & Epstein, 1996).  Moreover, a reduced ability to resist the motivation to eat when satiated may promote non-homeostatic overconsumption (e.g. Nasser et al. 2007).  A widely held notion is that wanting rather than liking may be the crucial process in maintaining an obese state.  For example, research on chronic drug abusers indicate that repeated drug taking behaviour and strong motivation to obtain a ‘fix’ can occur in the absence of any pleasant sensations during ingestion (Lamb et al 1991).  Moreover, food liking is often a rather stable characteristic within an individual and appears relatively uninfluenced by increasing weight status (Cox et al. 1999).  The implication is that liking may be important in establishing the motivational properties of food, but once these are retained it is the upregulation of wanting in an obesigenic environment – insensitivity to homoeostatic signals but over-reactivity to external cues – that promotes overconsumption by influencing what and possibly how much is eaten from moment to moment.