Drivers of eating behaviour during chronic overconsumption: Role of food hedonics (liking & wanting) and peptide biomarkers on satiation and satiety.

This project will investigate the drivers of eating behaviour that occur during a prolonged period of overconsumption (excess intake of calories). Overconsumption is important as a major cause of weight (re)gain and obesity. The type of society which exists in many developed countries is said to represent an 'obesigenic' environment. This type of environment facilitates a high consumption of food (as well as encouraging sedentariness) and generates rapid weight gain that leads to obesity. The obesigenic environment 'offers' the possibility for people to overeat. People are able to eat too much of some foods because of excessive activation of hedonic (pleasure related) processes, or because of a defect in homeostatic processes. Firstly this means that people will eat more because of elevated sensations of pleasure during eating or heightened motivation to obtain a looked-for food. These (hedonic) processes are termed 'liking' & 'wanting'. Secondly, people will eat more because their physiological systems fail to shut off eating quickly (leading to large meals) or because food fails to suppress their hunger after eating. These last two processes are called 'satiation' and 'satiety'. The pleasure of eating can be divided into two components /'liking' & 'wanting'. Although these terms often occur together, they are quite different. Sometimes we do not have a strong wanting for foods that we like a lot; at other times we have a strong wanting for foods that are not especially liked (e.g. potatoes/food staples). Importantly, we have developed procedures that measure both the liking & wanting of foods. It is not known if overconsumption results from an increase in liking for certain foods, or from an increase in wanting for those foods. We will identify the types of foods selected during a prolonged period of overeating and whether this is driven to a greater degree by increased liking or wanting. At the same time it is important to be able to measure the actual changes in processes that control meal size (satiation) and which lead to the reduction of hunger after eating (satiety). We will identify which aspect of eating plays the major role in allowing overeating /a large meal size, or weak suppression of hunger. This will inform us how to use specific foods to control these two aspects of eating. It is important to be able to relate changes in sensations and behavior to underlying physiological processes. This means measuring chemicals in the blood that are known to be involved in appetite control. Some of these chemicals are thought to be involved mainly in hunger (ghrelin) or in satiety (GLP1, CCK) or in both hunger/satiety, liking & wanting (leptin). We will therefore assess the particular ways in which these signals influence overconsumption. Generating overconsumption in the long term leads to a gain in weight which may never be lost again and could impair health. We have therefore developed a 'safe' model of overconsumption that has arisen from a BBSRC project just finished. When overweight and obese people volunteer for a 12 week programme of supervised daily exercise (of fixed energy expenditure) some individuals lose weight and others do not. However, independent of weight loss all volunteers show decreases in heart rate, blood pressure, and an increase in fitness (key to becoming healthy). The reason behind this variability in response is that the poor responders who do not lose weight have increased their food intake to negate the energy lost. This increase can be interpreted as overconsumption and amounts to ~290 kcal/day. In absence of exercise this would lead to a dramatic weight increase of more than 6kg over a year. Therefore we can use this 'safe' form of overconsumption to examine changes in underlying behavioral drivers /liking & wanting, satiation and satiety/ and their association with signalling peptides. This provides a relevant long term method for investigating the drivers of food behaviour.

This project will examine how hedonic and homeostatic processes contribute to food intake behaviour during chronic (12wk) overconsumption, and will demonstrate the relationship of the behavioural change to biomarkers of appetite control. We will identify ways in which sensory and nutritional attributes of foods can be developed as novel foods to prevent overconsumption. We will examine key components of food hedonics (liking & wanting). Our approach quantifies these processes and includes measures of explicit liking (experienced pleasure during eating), and implicit wanting (motivation towards a target food). The adjustment of food intake caused by liking & wanting is necessarily expressed through changes in satiation (meal size) and/or satiety (post-meal suppression of desire to eat) and through food selection. We will measure liking & wanting, in conjunction with food selection, during satiation and satiety in order to understand the behavioural drivers associated with (chronic) overconsumption. Changes in hedonic and homeostatic variables reflect the operation of biomarkers for appetite. We will measure changes in episodic (CCK/GLP1/ghrelin) and tonic (leptin/ghrelin) signalling peptides periodically. An intensive probe day (wk13) will examine the postprandial profile of peptides in relation to changes in motivation and behaviour. It is unethical to induce chronic overconsumption as the weight gained may never be lost. We will use a safe form of overconsumption induced in approximately 40% of people in response to a daily schedule of fixed exercise (see BBS/B/05079). These people show compensatory increases in EI which offsets the energy deficit. This model of chronic overconsumption will be used in conjunction with nutritional challenges (wk0,6,12) to examine satiation and satiety. Measures of liking, wanting, hunger and peptide biomarkers will be superimposed and evaluated in relation to measured energy metabolism.