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Sensory-Specific Satiety and Nutrition
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
It is apparent that sensory-specific satiety, or sensory generalized satiety, has an impact upon both the hedonics and consumption of food. It has potential practical application in the management of obesity. Why does sensory-specific satiety exist in humans? Sensory-specific satiety is a logical evolutionary adaptation. If the type of food corresponds with nutrients, then sensory-specific satiety is a physiological way to prevent nutrient excess and switch consumption to other foods with other needed nutrients. While cafeteria-style food would act to reduce the effect of sensory-specific satiety and increase weight, flavoring all food eaten in a similar manner should act to decrease consumption. The problem with such monotonous diet is a matter of compliance. Possibly a diet based on satiety index or using other modalities to enhance sensory-specific satiety (Dougherty, Chapter 13) would be one mechanism of overcoming such monotony effect and still maximize this homeostatic and physiologic mechanism of sensory-specific satiety.
Obesity
Published in Geoffrey P. Webb, Nutrition, 2019
In a classical paper, Rolls et al. (1982) reviewed a series of experiments which showed that increasing food variety may encourage consumption. Volunteers were asked to rate their pleasantness after eating various foods. Previous consumption of a food reduced its pleasantness rating and the desire to consume more of it but had little effect on that of other foods – they termed this phenomenon “sensory specific satiety”. When people ate sausages, then their rating for sausages was reduced but the pleasantness rating for other foods e.g. fruit or cookies was largely unaffected by eating sausages. Subjects offered successive plates of sandwiches ate more if the sandwiches contained different fillings than if they were all the same. More surprisingly, subjects offered successive plates of pasta ate more if the pasta shape was varied than if the shape was the same. Variation in taste or appearance increased the amount eaten. If a diet is monotonous, we are less likely to overeat than if it is varied. This is not too surprising a conclusion – most of us can usually be persuaded to accept a little dessert even when satiated by earlier courses of the meal. Even laboratory rats eat much more when they are offered a variety of foods (cafeteria feeding).
Review of brain imaging in anorexia and bulimia nervosa
Published in Stephen Wonderlich, James E Mitchell, Martina de Zwaan, Howard Steiger, Annual Review of Eating Disorders Part 2 – 2006, 2018
Walter H Kaye, Angela Wagner, Guido Frank, Ursula F Bailer
Recent studies have shown that it is possible to study taste and smell in conjunction with fMRI which may inform studies in the ED population (De Araujo et al. 2003; Cerf-Ducastel and Murphy 2004). In brief, the insula cortex shows the primary response to taste recognition and the orbitofrontal cortex (OFC) shows secondary response to various taste stimuli. Stimuli such as pleasant taste activate the OFC. This activation declines when the same food is presented repeatedly which is called sensory-specific satiety. New studies now show that the dorsolateral prefrontal cortex is responsive to gustatory activation (Krin-gelbach et al. 2004). This area is a cognitive processing center and may suggest cognitive reflection of the taste experience, perhaps on a tertiary level. In a review of their own and studies of other investigators, this group proposes that the OFC activity may be separated into anterior-posterior and medial-lateral compartments with task-specific responsiveness (Kringelbach et al. 2004). With the notion that the OFC is involved in the evaluation of the reward value that a stimulus has, the medial part may then be active to reinforcing and the lateral part to aversive stimuli. This may also be the case for olfactory stimuli (Gottfried et al. 2002). The anterior part was hypothesized to be more involved in abstract stimuli such as monetary reward as opposed to more primitive experiences including taste or pain.
Prior exposure to nutritive and artificial sweeteners differentially alters the magnitude and persistence of sucrose-conditioned flavor preferences in BALB/c and C57BL/6 inbred mouse strains
Published in Nutritional Neuroscience, 2019
Sam LaMagna, Kerstin Olsson, Deena Warshaw, Gabriela Fazilov, Ben Iskhakov, Agata Buras, Richard J. Bodnar
Long-term exposure to sucrose has been shown to alter subsequent behavioral and physiological responses to sweeteners.26–30 Prior extended sucrose exposure reduced subsequent saccharin and maltose dextrin, but not sucrose consumption in adult rats.31 Outbred rodents given unlimited access to sucrose subsequently displayed decreased motivation for sucrose.27–29,32 Sucrose exposure respectively increased and decreased subsequent breakpoints of sucrose responding on a progressive ratio schedule of reinforcement in female and male rats.33 Further, exposure to a high-sugar, but not a high-fat diet produced a subsequent conditioned place preference in adult rats for the side associated with fat, but not sugar, indicating a deficit in sugar preference.34 Long-term exposure to either ‘junk food’ or ‘natural food’ cafeteria diets reduced subsequent sweet taste intake but did not impair a flavor-nutrient sugar-CFP in rats.35 In contrast, adult sensory-specific satiety was intact in rats made obese on a high-fat, high-sugar choice diet.36 Finally, exposure to artificial sweeteners such as saccharin also alter subsequent behavioral intake31,37 and weight38,39 as well as impairing glucose homeostasis40 in rats relating this to effects following lowcalorie sweetener use in humans.41,42
The effect of intestinal glucose load on neural regulation of food craving
Published in Nutritional Neuroscience, 2021
Marion A. Stopyra, Hans-Christoph Friederich, Sebastian Sailer, Sabina Pauen, Martin Bendszus, Wolfgang Herzog, Joe J. Simon
Our findings demonstrate that intragastral glucose administration without the cephalic phase of gastric secretion has no measurable effect on both neural food processing and overall subjective experience of food craving. This finding is intriguing given that blood glucose is considered to play a pivotal role in the regulation of food intake [33]. Low blood glucose levels are related to increased hunger and therefore motivate foraging behaviour [34], however our findings suggest that high levels of blood glucose do not reduce overall craving for appetizing foods. Interestingly, Page and colleagues [35] demonstrated that low blood glucose levels increase the neural reward response to food cues, whereas normal- or high blood glucose levels increase activity in regions related to inhibitory control. However, the exact relation between blood glucose and self-control has been a matter of debate in recent years. Studies investigating the influence of blood glucose levels on behavioural reports of craving observed conflicting results; with some studies reporting reduced control of craving under low blood glucose levels [36] and others reporting no influence of blood levels on craving [37]. Another factor that might have affected our results is sensory-specific satiety which could have occurred, given that our participants were only administered glucose. Sensory-specific satiety refers to the phenomenon that when a particular food is consumed to satiety, the pleasantness of that particular food item declines in comparison to foods that have not been previously consumed [38]. In fact, our participants exhibited increased subjective craving for savoury foods compared to sweet foods after the administration of glucose. This difference of subjective craving was only statistically significant during the viewing condition, further emphasising that distraction from food is equally effective for savoury and sweet flavoured foods. This finding further supports that sensory-specific satiety is not exclusively a sensory-based, top-down phenomenon but is also regulated from the bottom-up level. Indeed, sweet taste signalling mechanisms are present in the oral cavity as well as the gastrointestinal system [39] and our findings suggests that the gastrointenstinal sensing of glucose is sufficient to influence craving preference towards a particular food flavour. Thus, even though glucose administration had no effect on overall subjective hunger levels, it still had an influence over food preferences. Despite the long held assumption that the gut is primarily involved in the inhibition of food consumption, it is now evident that the nutrient sensing receptors in the gut are also involved in food preferences [40].