Nutrients, Vol. 14, Pages 5100: The Power of Suggestion: Subjective Satiety Is Affected by Nutrient and Health-Focused Food Labelling with No Effect on Physiological Gut Hormone Release

1. IntroductionThe control of energy intake from food is complex and is governed by the interaction of both metabolic and emotional/cognitive regulatory systems. Peoples’ food preferences and enjoyment of food appear to be subject to suggestibility from visual and cognitive cues. For example, people prefer the taste of a branded beverage when consumed from a brand-named cup [1]. In addition, functional magnetic resonance imaging (fMRI) shows that there is increased activity in areas of the brain involved in emotional processing when the beverage is consumed after being shown a brand image compared to when consumed with no image being shown [1]. Furthermore, when a low calorie drink is ingested following the spoken verbal descriptor ‘treat’, there is increased activity in the hypothalamus and midbrain, as measured by fMRI, compared to when it is described as ‘healthy’ [2]. In addition, labelling and describing food items with taste-promoting descriptors increases selection of the food item and increases taste scores following consumption compared to when the same food is promoted as healthy [3]. Indeed foods felt to be unhealthy are perceived to be tastier [4].Endeavouring to reduce rates of overweight and obesity, public health policies commonly aim to educate the public regarding making healthy food choices [5,6]. Food marketers have capitalised on the public’s desire to eat ‘healthily’, health and nutrient claims which imply that food have particular beneficial health or nutritional properties are often used to boost sales. Indeed, surveys have shown that people are willing to pay more for healthy food [7]. Using health claims on food labelling has been shown to influence peoples’ perception of food without them actually eating it, for example, driving the belief that a particular food will make them feel more full [8,9]. Placing nutritional content on food labelling of unhealthy food using health star ratings or multiple traffic lights, for example, can restrain a person’s selection of portion size [10]. Perceived macronutrient content has also been demonstrated to influence subsequent energy intake, with participants consuming more at a test meal after eating a preload labelled as ‘low fat’ comparted to participants who consumed the same preload labelled as ‘high fat’ [11]. However, studies evaluating the effects of food labelling on appetite have produced variable results. A study by Chambers et al. (2013) found that the sensory qualities of a smoothie preload influenced appetite ratings and subsequent food intake, but labelled messages regarding the satiating properties of the product did not [12]. A study by Yeomans et al. (2001) demonstrated that soup preloads labelled as ‘high fat’ were rated as being more pleasant and creamy than those labelled as ‘low fat’, regardless of actual fat content. However, energy intake at a subsequent test meal was unaffected by the preload label. Instead, energy intake was influenced by the actual fat content, with a higher fat preload associated with lower subsequent energy intake [13]. Studies have also demonstrated that claims such as ‘low-fat’ and ‘low sugar’ can actually encourage people to eat more, perhaps by a reduction in the anticipated guilt associated with eating the ‘healthy’ option, or by increasing the amount of food felt necessary to satiate due to calorie underestimation [14,15,16].There is emerging evidence that the influence of product claims can extend beyond perception to actually influence the physiological indicators of satiety. Cassidy et al. (2012) conducted a study where participants consumed oral liquid and solid preloads which, following observation of a falsified demonstration, they were led to believe either formed liquids or solids in the stomach when in fact all preloads either remained liquid or quickly turned to liquid on consumption. They found that preloads which were either liquid, or perceived to be liquid once in the stomach, elicited greater postprandial hunger and lower fullness sensations, and attenuated insulin and glucacon-like peptide 1 release compared to those consumed as a solid, or perceived to turn to solid in the stomach [17]. Ghrelin is an orexigenic peptide synthesised in the stomach and is the only gastrointestinal hormone known to stimulate appetite. A study by Crum et al. (2011) demonstrated that when participants believed they were consuming an ‘indulgent’ product versus one labelled as ‘sensible’, there was a significantly deeper decline in the levels of ghrelin, despite the products being nutritionally identical [18]. However, in this study there were no reported differences in subjective hunger scores after consuming the differently labelled products, and the study did not assess any subjective measures of satiety. The role of food descriptions in promoting satiety and the mechanisms underlying this are unclear, but if these mechanisms could be further explored and the effect on satiety could be replicated, it could have implications for food labelling and marketing, as well as public health strategy. The aim of the current study was therefore to investigate whether the consumption of a 380 kcal yoghurt and granola breakfast item resulted in different subjective satiety scores or gastrointestinal hormone levels that mediate appetite, depending on whether the product was labelled as an ‘indulgent’ 500 kcal product (high in fat and sugar) or a ‘sensible’ 250 kcal one (low in fat and sugar). To achieve this, self-reported appetite and the circulating concentrations of the gastrointestinal hormone acylated ghrelin were measured. Peptide tyrosine-tyrosine (PYY) and glucagon-like peptide-1 (GLP-1) are anorectic gut hormones released into the circulation post-prandially in response to luminal nutrients, signalling satiety and promoting meal cessation. Circulating concentrations of these hormones were also measured. 4. DiscussionEvidence is mounting that a person’s ideas and expectations about the food they are eating can alter taste, preference and consumption. Previous research has also suggested that this may alter the physiological response to food by accelerating the fall in post-prandial ghrelin [18]. If these effects on perceived satiety and gut hormone physiology could be demonstrated across a broad range of foods, food labelling could potentially be manipulated to maximise perceived and physiological satiation.Whilst it is appreciated that this study was exploratory in nature and involved testing at multiple timepoints, some useful insights were gained. This study demonstrated a significant increase in self-reported fullness after consumption of the “indulgent” breakfast versus the “sensible” breakfast which is what might be expected if the actual calorie and macronutrient content of the two products differed. The increase in self-reported fullness in the current study is likely secondary to the participants’ perceptions of the products based on the food labels. It is clear that participants had formed perceptions of the breakfast products healthiness both prior to, and during, product consumption; prior to consumption participants rated the indulgent breakfast as being less healthy and they reported feeling less healthy whilst consuming it. However, it is also possible that these effects are secondary to response bias, with participants feeling that they ought to feel fuller after the higher calorie product and reporting fullness as such. It is recognised that the participant population had a high level of education. Education has been shown to influence perception of taste and satiety from food labelling [8] and has been associated with increased interest in and use of food labels [28,29]. It would be useful therefore to explore whether the effects observed in this study are replicable across different levels of education.Some limitations of the study design are acknowledged. Firstly, the time and nature of the last meal the preceding evening was not specified which may have affected baseline measures of hunger. Furthermore, it is not known whether the participants were regular consumers of breakfast, or if they were familiar with the particular kind of breakfast product. Familiarity with the breakfast product may be associated with pre-existing ideas of taste and health and this may have affected subjective measures of hunger. The authors also acknowledge that there may be carry-over effects in cross-over studies of this kind that mean the effect of the manipulation may be underestimated [30]. However, the order of the breakfast products was randomly allocated to ensure the presentation of test conditions was counterbalanced to neutralise possible learning effects.In a study by Crum et al. (2011) there was a rise in ghrelin in anticipation of an “indulgent” milkshake when compared to anticipation of an identical milkshake described as “sensible”. This was followed by a significantly greater rate of reduction in ghrelin following consumption [18]. In the current study, there was no difference in circulating levels of acylated ghrelin between the breakfasts at any time point. There is some evidence that ghrelin rises physiologically in anticipation of an expected meal, rather than solely being responsible for meal initiation [31]. The mechanisms driving this are not fully understood and it is possible that the expected size or macronutrient composition of the anticipated meal may modify this effect. It is therefore possible that different food products could elicit different responses, with health claims further altering the response. There were no significant differences in subjective hunger ratings between the two groups in this study or in the study by Crum et al. This supports the notion that the ghrelin rise seen in the study by Crum et al. could be due to meal anticipation rather than changes in the metabolic parameters which drive hunger.Although this study demonstrated a significant increase in self-reported fullness after consumption of the “indulgent” breakfast versus the “sensible” breakfast, there were no significant differences in the circulating levels of GLP-1 or PYY between the breakfasts at any time point. This suggests that the increased perceived satiety following ingestion of the supposed “indulgent’ breakfast is independent of anorectic gut hormone signalling, possibly occurring via manipulation of the hedonistic rather than homeostatic pathways involved in appetite regulation. Individuals who report placing high importance on taste have both increased consumption and self-reported satiety on consumption of a salad labelled as being “hearty” versus a salad labelled as being “healthy” [32]. This contrasts with individuals who place low importance on taste who eat less but report similar satiety scores when eating the “hearty” versus the “healthy” salad. This increased susceptibility to food labelling demonstrated by individuals who place high importance on taste supports the role of non-homeostatic regulatory pathways in mediating the effect of food labelling on satiety.Prior to consumption of the breakfast products, participants rated the indulgent option as being more appealing. During consumption, however, participants did not report any difference in the taste, smell, overall palatability or enjoyment between the two breakfast items. This finding is contrary to studies which show that food labelled and described as tasty has higher taste scores following consumption compared to the same food described as healthy [3]. It is possible that suggestion from labelling associated with a differential in taste has more of an effect on the non-homeostatic regulation of food preference than suggested differentials in health.Evidence suggests that labelling a food as healthy encourages restrained eaters to eat more [21]. In this study restrained eaters did not report any differences between the breakfasts with regard to appetite change from anticipatory to post-consumption. They did, however, report a significantly lower mean change in their strength of desire to eat in anticipation of the “indulgent” breakfast compared to the “sensible” breakfast. The sensible breakfast was perhaps a more appealing option for restrained eaters due to its apparent lower calorie, fat and sugar content.Whilst in the current study food labelling influenced the sensation of fullness, the physiological state of eating inhibition, it did not impact other appetite sensations including hunger. It is possible that the timing between consumption and completing the self-reported appetite measures was insufficient for the processing of satiety signals. It is also possible that the study was inadequately powered to detect the changes in appetite measures. As this was an exploratory study based on a similar experiment [18], a formal power calculation was not used. The effect sizes on self-reported fullness demonstrated in this study and in other studies cited here are small. It is possible that other studies have been conducted which have demonstrated no such effects and remain unpublished. The clinical relevance of the results are therefore uncertain.The increase in self-reported fullness following consumption of the “indulgent” breakfast compared with the “sensible” breakfast is likely secondary to the participants’ perceptions of the products based on the food labels. However, the effect sizes were small and future studies could include a positive control condition where the actual energy content of the product is manipulated in an oro-sensory matched manner to determine relative effect sizes. Evidence suggests that nutrient and health claims used for marketing purposes such as ‘lower in fat’ could actually encourage people to eat more [14]. This could be mediated by calorie underestimation and subsequent overconsumption. The current study manipulated participants’ perception of both calorie content and hedonic expectations. It would be beneficial to evaluate the effect of manipulation of perception of energy content alone on reported satiety measures as this may be more easily incorporated into current product calorie labelling strategies. Obesity rates are rising despite simultaneous increases in availability and sales of ‘healthy’ food products. Further study is needed to determine the effects of nutritional labelling on levels of food consumption and risk of weight gain.As discussed above, participants rated the indulgent option as being more appealing prior to consumption but reported no difference in overall palatability during consumption. Other studies have found that taste-focussed labelling has more of an effect on food choice than health-focussed labelling [3]. Further research is needed to identify particular labelling ‘triggers’ that promote preference for that particular food. This could be particularly relevant for public health initiatives in promoting healthy food choices. If suggested taste is indeed a superior influencer of food choice, research into the cognitive pathways governing this could be of further interest. Given the evidence suggesting that restrained eaters associate unhealthy food items with superior taste, this could be of particular importance for this sub-group.The current study found no difference in the magnitude of change of gut hormone levels between the two breakfasts across the time points of the study, suggesting that the alterations in fullness scores observed are likely not mediated by gut hormone physiology. These findings are in contrast to a previous similar study that reported a relative preprandial rise in ghrelin followed by a steeper post-prandial decline [18]. It is possible that this ghrelin rise could be due to meal anticipation and further study of the variance in pre-prandial ghrelin release with different expectations of meal size and macronutrient content would be of interest. In the current study there were no significant differences in ghrelin levels at any time point when stratified by levels of restrained eating behaviour. However, previous studies have shown that restrained eaters have significantly higher ghrelin levels than non-restrained eaters, both in the fasting state and when consuming a palatable milkshake [20,33]. It is possible that the sample sizes in this study were insufficient to detect significant differences within the restrained eaters and further study is warranted to examine the differences in gut hormone secretion in those with restrained eating patterns.

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