1.1 Appetite Control in Context
The worldwide increase in incidence of overweight and obesity represents one of the biggest public health challenges of recent times. Statistics on obesity are startling: the proportion of the population in the United States who meet World Health Organisation (WHO) criteria for obesity have risen from around 7% in 1985 to 30% in 2015. In 2014, more than one in four people were obese in countries as diverse as New Zealand, Mexico, Canada, Hungary and Chile. The WHO estimated that by 2014 39% of the world's population met the criteria for overweight, and 13% were obese, with more people overweight than malnourished for the first time in recorded history.
These statistics make understanding causes of weight gain an imperative. Weight gain is the consequence of storage of excess nutrients when there is an imbalance between energy intake and energy expenditure. Thus when intake of sources of energy in the diet, primarily fat and carbohydrate, exceeds short-term energy needs (the sum of basal metabolism, thermogenesis and energy needed for exercise and cognitive activity), the excess is stored. Most of the excess is converted to body fat, either directly by processing of ingested fat or through conversion of excess carbohydrate into fat by the liver. However, excess intake arises only when factors that encourage short-term intake are not regulated by the systems involved in promoting energy expenditure and, crucially in the context of this book, inhibiting further food intake. It is noteworthy that despite the worldwide increase in obesity, many consumers maintain a stable weight. This implies that even in the modern obesogenic environment it is possible to maintain an appropriate balance between energy input and output, but that individual differences in sensitivity to external cues promoting intake and homeostatic processes regulating appetite make some individuals prone to over-consumption. Since humans typically eat at prescribed times dictated by cultural convention, it has been argued that understanding the processes that lead to suppression of appetite after a meal are key to understanding how altering the food environment may help promote individual appetite regulation [1–5].
1.2 Satiation and Satiety: A Brief Overview
The modern interpretation of the terms “satiation” and “satiety” are most clearly encapsulated in the description of processes involved in appetite control commonly referred to as the “satiety cascade” [6]. In that descriptive model, satiation was defined as the processes that bring a meal to an end and satiety as the suppression of appetite post-ingestion. This specific interpretation of satiation and satiety is now widely accepted. The chapters in this book all examine aspects of two types of influence on satiation and satiety. The primary focus here is on how the sensory features of the foods and drinks we ingest influence the decisions that lead to meal termination (satiation) and also modify the processes that suppress appetite after ingestion (satiety). There are also chapters that highlight more cognitive elements that also modify both the interpretation of sensory cues and satiation and satiety more directly. Although models such as the satiety cascade fully recognised the importance of these cognitive and sensory influences, the majority of research on satiety remains focussed on physiological signals arising in the gut as a consequence of food ingestion. However, an understanding of these gut-derived signals is needed in order to put the main chapters in this volume into a broader context. The reader can find a more detailed description and discussion of these gut-based satiety signals in one of a number of more detailed reviews [3,7–10].
The view of satiety most commonly described when discussing the role of gut-based satiety signals sees the gut effectively as a sensor that sends signals about the nutrients it can detect to the brain [3,11,12]. This gut-to-brain signalling is clearly a major component of the physiological basis of satiety experienced post-ingestion. However, what the present volume clearly demonstrates is that these gut-derived physiological signals are only part of the story and that both cognitive and sensory cues at the point of ingestion can clearly modify the way the body experiences satiety from the same set of nutrients depending on the context in which those nutrients were ingested. Thus understanding gut-derived physiological signals is an important component of satiety, but they can only be interpreted in the context of all signals relating to ingestion, including those arising from both the sensory experience of food and beliefs about the likely effects of that food on appetite.
What then are the principle gut-derived signals? Arguably the most important signals are specific peptides released in the gut in response to specific nutrient signals and whose purpose is to regulate the passage of food though the gut to optimise digestion and nutrient absorption. One key aspect of that control process is to modify ingestion to ensure an appropriate supply of nutrients, and it is likely that the gut-based satiety signals have evolved at least partly for that reason. The first such signal to be identified was cholecystokinin, first shown to modify ingestion in rats in 1973 [13], but since then many more gut-based signals have been identified, most of which appear to have roles in suppressing appetite (and are described as satiety signals), including glucagon-like peptide 1 (GLP1), polypeptide YY (PYY), oxyntomodulin (OXM) and pancreatic polypeptide (PP). A further gut-derived signal, ghrelin, has the opposite effect, increasing the experience of appetite in humans and increasing food intake in humans [14–17] and other species [18,19]: see Hussain and Bloom and Guyenet and Schwartz [12,20] for recent reviews. Thus ghrelin stands apart as the only gut-derived hormonal “hunger signal”. The evidence supporting specific roles of these different gut signals in satiety typically involves a combination of studies in animals showing reduced food intake after administration of these compounds, evidence that such effects are consistent with a normal cessation of feeding rather than an indirect effect through malaise, and studies showing both reduced rated appetite and food intake in humans, again in the absence of any confounding malaise: this evidence has been reviewed at length by many authors [3,7,10,21], and a full review is beyond the scope of this introduction. What the current volume does do, however, is put these physiological satiety cues into the broader context of other signals associated with food ingestion, particularly those derived from the sensory characteristics of foods and drinks.
1.3 Sensory Influences on Satiation and Satiety: A Brief History
The chapters in this volume provide timely summaries of recent progress in understanding sensory and cognitive influences on satiation and satiety that build on ideas founded in classic studies in recent decades. Arguably the most influential concept during this time has been sensory specific satiety (SSS), and this concept is discussed from different perspectives in the chapters by Vickers (Chapter 2), De Graaf and Boesveldt (Chapter 3) and Piqueras Fiszman (Chapter 8). Sensory specific satiety is a concept founded in changes in liking for foods as a consequence of ingestion. The key observation is that liking for a food that is being consumed decreases, but liking for other foods which are not being consumed is maintained. The original observations came from studies in rats by the pioneering appetite researcher Jacques Le Magnen [22]: he observed that rats ate considerably more when provided with a variety of different-flavoured foods than when offered just a single food. The actual term SSS, however, came from seminal studies by Barbara and Edmund Rolls showing how rated liking for a consumed food decreased, but liking was unaltered for other non-consumed foods [23]. Although the change in liking occurs during ingestion and so may be better thought of as relating to satiation than satiety in our modern classification of a...