Cues to overeat: psychological factors influencing overconsumption

Abstract

Human food intake is driven by necessity, but modern industrialized societies are characterized by food surfeit and an increasingly 'obesogenic' environment. This environment tends to discourage energy expenditure and to facilitate energy intake. The amount eaten in any given eating episode depends less on internal need state and more on environmental contextual factors such as the availability of highly-palatable energy-dense foods. In addition, the process of satiation can easily be disrupted by the introduction within a meal of different foods (variety effect), the presence of others (social context) and competing tasks (distraction). Properties of ingestants such as alcohol promote food intake and characteristics of individuals make them more or less susceptible to situational cues to overeat. In the present review the role of each of these environmental factors in promoting overconsumption is considered and the extent to which these factors might contribute to long-term weight regulation is discussed. Overconsumption: Energy intake: Weight regulation: Environmental factorsHuman food intake is motivated by need, but influenced by a myriad of complex factors including those that reside within the environment (availability, variety, portion size), those that characterize the food itself (energy density, macronutrient composition, sensory features) and the response of the individual to these factors. Most industrialized countries and many developing nations are now facing an exponential rise in overweight and obesity that must largely be a result of changes in the food environment. The relatively high levels of genetic predisposition to gain weight (Loos & Bouchard, 2003) in permissive environments suggest that the characteristics of the obesogenic environment and the response of the consumer to this environment must be understood if the obesity epidemic is to be tackled. In order to expose elements of the environment that may promote overeating, it is important to identify those controls of ingestion likely to be influenced by the food environment and then to examine how these features operate to derail homeostatic controls. Direct and indirect controls of meal sizeThe brain receives a constant stream of information to guide food intake based on stored energy as well as current energy and nutrient sources (Woods, 2005). Thus, the amount eaten within a meal will depend both on the metabolism of previous meals and the currently-available food. However, there is no simple relationship between energy deficit and energy intake. For example, consumers in Western cultures tend to eat their smallest meals after the longest period of energy depletion and their largest meal at the end of the day, in anticipation of this deficit (Weingarten, 1986). Meal size does not correspond well with the immediately preceding inter-meal interval (Le Magnen, 1969), suggesting that meal size is highly variable and subject to the influence of many different factors somewhat uncoupled from specific energy deficits (Wiepkema, 1971;Lowe & ...

Taste, olfactory and food texture reward processing in the brain and the control of appetite

“…Following Edmund Rolls' discovery of sensory-specific satiety revealed by the selective reduction in the responses of lateral hypothalamic neurons to a food eaten to satiety (3,5) , it has been shown that this is implemented in a region that projects to the hypothalamus, the orbitofrontal (secondary taste) cortex, for the taste, odour and sight of food (4,34) . This evidence shows that the reduced acceptance of food that occurs when food is eaten to satiety, the reduction in the pleasantness of its taste and flavour, and the effects of variety to increase food intake (6)(7)(8)(35)(36)(37)(38)(39)(40)(41)(42)(43) are produced in the OFC, but not at earlier stages of processing where the responses reflect factors such as the intensity of the taste, which is little affected by satiety (32,44) . In addition to providing an implementation of sensory-specific satiety (probably by habituation of the synaptic afferents to orbitofrontal neurons with a time course of the order of the length of a course of a meal), it is likely that visceral and other satiety-related signals reach the OFC (as indicated in Fig.…”

Evaluating the Power of Food Scale in obese subjects and a general sample of individuals: development and measurement properties

“…9,10 Eating behavior in humans is an extremely complex process modulated by internal homeostatic processes [11][12][13] and environmental and social influences. 14,15 As such, energy homeostasis aims to match energy intake with overall energy needs; however, total food intake is also influenced by external factors, such as food availability and palatability, which might lead to excess energy intake during any given meal. 16 This tendency to eat beyond immediate homeostatic needs has presumably evolved because the motivation to seek and consume calories contributed to survival when food sources were scarce and unpredictable.…”

Taste, olfactory and food texture reward processing in the brain and obesity

“…Following Edmund Rolls' discovery of sensory-specific satiety revealed by the selective reduction in the responses of lateral hypothalamic neurons to a food eaten to satiety, 24,25 it has been shown that this is implemented in a region that projects to the hypothalamus, the orbitofrontal (secondary taste) cortex, for the taste, odour and sight of food. 26,27 This evidence shows that the reduced acceptance of food that occurs when food is eaten to satiety, the reduction in the pleasantness of its taste and flavour, and the effects of variety to increase food intake, [28][29][30][31][32][33][34][35][36][37][38][39] are produced in the OFC, but not at earlier stages of processing in which the responses reflect factors such as the intensity of the taste, which is little affected by satiety. 22,40 In addition to providing an implementation of sensory-specific satiety (probably by habituation of the synaptic afferents to orbitofrontal neurons with a time course of the order of the length of a course of a meal), Figure 1 Schematic diagram showing some of the gustatory, olfactory, visual and somatosensory pathways to the OFC, and some of the outputs of the OFC, in primates.…”