Oral processing, satiation and obesity: Overview and hypotheses

Abstract

Increasing the speed of eating or decreasing the amount of chewing of a test meal significantly decreases its satiation, increases concomitant caloric intake, and influences entero-endocrine secretion. Speed of eating is a strong risk factor for obesity and longitudinal studies suggest an etiological relationship. Individuals with obesity have an increase in bite size, less chewing per bite, decreased satiation, and greater food intake. Oral processing in terms of bite size and amount of chewing per gram of food is influenced by food texture and textural complexity. Soft foods increase bite size and decrease chewing per gram of food and meal duration compared to hard foods. An ultra-processed diet can lead to greater weight gain than a non-processed diet and a significant increase in eating rate. Many children with obesity are noted by their parents to have persistent hunger on a questionnaire and this is often extreme. Results of attempts to change eating behavior have been mixed in terms of producing long-term changes in eating behavior and body weight. It is hypothesized that there may be a unidirectional relationship between changes in oral processing, satiation and weight gain. However, the presence of persistent hunger can produce a vicious cycle that may exacerbate obesity and make treatment difficult. The increased energy density of foods as found particularly in ultra-processed foods also influences energy intake and obesity.