Summary 1 Introduction 2 Physiological mechanisms of satiation and satiety 2.1  Physiological mechanisms of satiation 2.1.1  Gastric mechanisms of satiation 2.1.2  Intestinal mechanisms of satiation 2.2  Physiological mechanisms of satiety 2.2.1  Gut hormones – episodic signals of satiety 2.2.2  Tonic satiety signals 2.3  The integration of satiety signals in the brain 2.3.1  Anorexigenic pathways in the hypothalamus 2.3.2  Orexigenic pathways in the hypothalamus 2.3.3  Other areas of the brain involved in satiation and satiety 2.3.4  Reward pathways 3 Measuring satiation and satiety 3.1  Measuring satiation 3.2  Measuring satiety 3.2.1  Free living vs. laboratory studies 3.2.2  Preload studies 3.2.3  Self‐reported measures of satiety 3.2.4  Measuring food intake 3.2.5  Quantifying satiety 3.3  Confounders in satiety research 3.3.1  Physiological confounders 3.3.2  Behavioural confounders 4 The effects of foods and drinks on satiety 4.1  Protein and satiety 4.2  Carbohydrates and satiety 4.3  Fibre and satiety 4.4  Intense sweeteners and satiety 4.5  Fat and satiety 4.6  Liquids and satiety 4.7  Alcohol and satiety 4.8  Energy density and satiety 5 The effect of external factors on satiation and satiety 5.1  Palatability 5.2  Variety 5.3  Portion size 5.4  Sleep 5.5  Physical activity 5.6  Television viewing and other distractions 5.7  Social situations 6 Satiation, satiety and weight control 6.1  Obesity genes and satiety 6.2  Physiological differences in satiation and satiety responses in obese people 6.3  Behavioural differences in the response to satiation and satiety in obesity 7 Conclusions Summary: In the context of the rising prevalence of obesity around the world, it is vital to understand how energy balance and bodyweight are controlled. The ability to balance energy intake and expenditure is critical to survival, and sophisticated physiological mechanisms have developed in order to do this, including the control of appetite. Satiation and satiety are part of the body's appetite control system and are involved in limiting energy intake. Satiation is the process that causes one to stop eating; satiety is the feeling of fullness that persists after eating, suppressing further consumption, and both are important in determining total energy intake. Satiation and satiety are controlled by a cascade of factors that begin when a food or drink is consumed and continues as it enters the gastrointestinal tract and is digested and absorbed. Signals about the ingestion of energy feed into specific areas of the brain that are involved in the regulation of energy intake, in response to the sensory and cognitive perceptions of the food or drink consumed, and distension of the stomach. These signals are integrated by the brain, and satiation is stimulated. When nutrients reach the intestine and are absorbed, a number of hormonal signals that are again integrated in the brain to induce satiety are released. In addition to these episodic signals, satiety is also affected by fluctuations in hormones, such as leptin and insulin, which indicate the level of fat storage in the body. Satiation and satiety can be measured directly via food intake or indirectly via ratings of subjective sensations of appetite. The most common study design when measuring satiation or satiety over a short period is using a test preload in which the variables of interest are carefully controlled. This is followed by subjects rating aspects of their appetite sensations, such as fullness or hunger, at intervals and then, after a predetermined time interval, a test meal at which energy intake is measured. Longer‐term studies may provide foods or drinks of known composition to be consumed ad libitum and use measures of energy intake and/or appetite ratings as indicators of satiety. The measurement of satiation and satiety is complicated by the fact that many factors besides these internal signals may influence appetite and energy intake, for example, physical factors such as bodyweight, age or gender, or behavioural factors such as diet or the influence of other people present. For this reason, the majority of studies on satiation and satiety take place in a laboratory, where confounders can be controlled as much as possible, and are, therefore, of short duration. It is possible for any food or drink to affect appetite, and so it is important to determine whether, for a given amount of energy, particular variables have the potential to enhance or reduce satiation or satiety. A great deal of research has been conducted to investigate the effect of different foods, drinks, food components and nutrients on satiety. Overall, the characteristic of a food or drink that appears to have the most impact on satiety is its energy density. That is the amount of energy it contains per unit weight (kJ/g, kcal/g). When energy density is controlled, the macronutrient composition of foods does not appear to have a major impact on satiety. In practice, high‐fat foods tend to have a higher energy density than high‐protein or high‐carbohydrate foods, and foods with the highest water content tend to have the lowest energy density. Some studies have shown that energy from protein is more satiating than energy from carbohydrate or fat. In addition, certain types of fibre have been shown to enhance satiation and satiety. It has been suggested that energy from liquids is less satiating then energy from solids. However, evidence for this is inconsistent, and it may be the mode of consumption (i.e. whether the liquid is perceived to be a food or drink) that influences its effect on satiety. Alcohol appears to stimulate energy intake in the short‐term, and consuming energy from alcohol does not appear to lead to a subsequent compensatory reduction in energy intake. The consumption of food and drink to provide energy is a voluntary behaviour, and, despite the existence of sophisticated physiological mechanisms to match intake to requirements, humans often eat when sated and sometimes refrain from eating when hungry. Thus, there are numerous influences on eating behaviour beyond satiation and satiety. These include: the portion size, appeal, palatability and variety of foods and drinks available; the physiological impact on the body of physical activity and sleep; and other external influences such as television viewing and the effect of social situations. Because satiation and satiety are key to controlling energy intake, inter‐individual differences in the strength of these signals and responsiveness to their effects could affect risk of obesity. Such differences have been observed at a genetic, physiological and behavioural level and may be important to consider in strategies to prevent or treat obesity. Overall, it is clear that, although the processes of satiation and satiety have the potential to control energy intake, many individuals override the signals generated. Hence, in such people, satiation and satiety alone are not sufficient to prevent weight gain in the current obesogenic environment. Knowledge about foods, ingredients and dietary patterns that can enhance satiation and satiety is potentially useful for controlling bodyweight. However, this must be coupled with an understanding of the myriad of other factors that influence eating behaviour, in order to help people to control their energy intake.

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