Satiety
Abstract
Bulimia Nervosa and Dysregulated Satiety
Bulimia Nervosa (BN) is influenced by multiple factors, according to research. One of the most significant issues in BN is periods of uncontrolled consumption of large amounts of food. A key factor in this behavior is dysregulated satiety. This paper will define satiety, explore its biological underpinnings, and discuss causes and potential interventions for altered satiety in individuals with Bulimia Nervosa.
Keywords: Bulimia Nervosa, energy intake, satiety
Satiety Definition
Research indicates that satiety is altered in individuals with Bulimia Nervosa (Brooks et al., 2011). According to the Cambridge Dictionary, satiety is “the state of being completely satisfied, especially with food or pleasure, so that you could not have any more.” In people with BN, satiety signals are often impaired, meaning that they may not feel satisfied after a meal, regardless of its size. This lack of satisfaction can drive continued eating in search of comfort. Understanding the biological basis of satiety provides insight into this dysregulation.
Factors Affecting Satiety
Satiety is primarily regulated by hormonal signals interacting with the gastrointestinal tract. Under normal conditions, positive feedback from food intake is followed by negative feedback that inhibits further ingestion, maintaining homeostasis. In BN, this cycle becomes dysregulated (Smith et al., 2002). The body, normally a highly adaptive system, adjusts its cycles based on eating habits. However, repeated fasting and binge-eating episodes disrupt this signaling, impairing the ability to recognize fullness and hunger (Hannon-Engel, 2012).
A key hormone in this process is Cholecystokinin (CCK), which functions as a negative feedback signal. CCK responds to gastric distension by signaling the brain to terminate eating. Individuals with BN often have an enlarged gastric capacity, which blunts CCK signaling, prolongs eating episodes, and increases food intake (Devlin et al., 1997).
Other hormones influencing satiety include Glucagon-like Peptide-1 (GLP-1), found in the small intestine and colon, which responds to nutrient intake, and Peptide YY (PYY), which aids in nutrient absorption. Dysregulation of these hormones further contributes to impaired satiety in BN.
Satiety Recovery
Biologically, restoring normal satiety involves regulating gastrointestinal hormone responses. Macronutrient composition of the diet plays a key role. Protein has been shown to stimulate satiety hormones during digestion, reducing overall food intake.
Fats and carbohydrates also contribute to satiety. Fats can delay gastric emptying and activate the ileal brake, which signals fullness. Certain oils rich in pinolenic acid, such as pine nut oil, may further reduce intake, though the mechanism is not fully understood.
The glycemic index (GI) of foods also affects satiety. Low-GI foods reduce energy intake by enhancing satiety-related hormonal responses. Long-term consumption of low-GI foods has been associated with naturally reduced energy intake (Warren et al., 2003).
Conclusion
Satiety is regulated by multiple gastrointestinal hormones through a cycle of positive and negative feedback. In individuals with BN, repeated fasting and binge-eating disrupt these signals, often enlarging gastric capacity and impairing fullness perception.
Dietary strategies that include high-protein, minimally processed, and low-GI foods may help restore satiety regulation in people with BN. Careful dietary planning, combined with further research on the mechanisms of satiety, is essential for improving treatment outcomes and understanding the biological factors underlying dysregulated eating behaviors.
Resources
Brooks, S. J., O′Daly, O. G., Uher, R., Friederich, H., Giampietro, V., Brammer, M., . . . Campbell, I. C. (2011). Differential neural responses to food images in women with BULIMIA versus anorexia nervosa. PLoS ONE, 6(7). doi:10.1371/journal.pone.0022259
Devlin MJ, Walsh BT, Guss JL, Kissileff HR, Liddle RA, Petkova E. Postprandial cholecystokinin release and gastric emptying in patients with bulimia nervosa. Am J Clin Nutr. 1997 Jan; 65(1):114-20.
Hannon-Engel, S. (2012, January). Regulating satiety in bulimia nervosa: The role of cholecystokinin. Retrieved February 25, 2021, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4625980/
Satiety. (n.d.). Retrieved February 25, 2021, from https://dictionary.cambridge.org/us/dictionary/english/satiety
Smith GP, Gibbs J. Peripheral physiological determinant of eating and body weight. In: Fairburn CG, Wilson GT, editors. Eating disorders and obesity: A comprehensive handbook. New York: Guilford Press; 2002. pp. 11–15.
Warren JM, Henry CJK, Simmonites V. Low glycemic index breakfasts reduced food intake in preadolescent children. Pediatrics. 2003;112:414–9.