Abstract
When we consume any nutritive product (i.e., foods or drinks), those ingested nutrients provide signals that act to reduce our desire to eat and drink for some time after consumption. This is captured by the concept of satiety, the state of inhibition of appetite post-ingestion. Likewise, our desire to eat decreases during a meal, and the processes which lead to that reduction are referred to as satiation. Simplistic models have traditionally interpreted satiation and satiety simply as a function of ingested nutrients. However, there is now an abundance of evidence that both satiation and satiety are influenced by multiple factors, including beliefs and information about products prior to ingestion, the specific sensory characteristics of the product experienced during ingestion, and the volume, weight, macronutrient profile, and energy density of the consumed product and the social context in which food is ingested. Thus satiation and satiety are viewed as the product of a cascade of signals which interact to generate the overall satiety state. Expectations about how filling a product will be modifies portion size selection and influence subsequent satiety. Sensory cues such as oral processing time and flavor intensity modify satiation, while liking for the consumed product, but not unrelated products, decrease. Once ingested, gut-based signals, including the release of satiety hormones stimulated by nutrient sensing, interact with cognitive and sensory cues from ingestion to produce satiety. But how much individuals respond to these cues varies, with weak satiety responsiveness a risk for subsequent weight gain. Overall, satiation and satiety are highly complex phenomena, but our increased understanding of this complexity paves the way for the food products of the future.
References
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