Satiety and Satiation

Satiety and satiation are two important principles in the study of food intake regulation. Satiety is defined as the state of eating cessation, and it delays the initiation of subsequent meals. Satiation, on the other hand, is the process of feeling full during the course of eating, a form of intra-meal satiety that affects meal size and is assessed by measuring energy content of the consumed meal (see figure below).

Food consumption triggers a multitude of neural and hormonal signals, originating from the periphery and interacting with the central nervous system, that regulate food intake according to energy requirements. In response to the macronutrient composition in one’s diet, the body releases hormones—gastrointestinal, pancreatic, and adipose derived—that ultimately signal the hypothalamus to contribute to the cessation of eating (i.e. satiation). This powerful feedback system is sensitive to the overall macronutrient composition of the diet and not specific to its sugars content per se.

Generally speaking, there is a positive association between glycemic response and satiety. In the short term, carbohydrates that tend to elicit a higher glycemic response are associated with lower food intake at the next meal. The initial release of glucose and insulin signals satiety centres in the central nervous system to suppress appetite and food intake.

Sugars and Appetite Control

Scientific evidence does not support the notion that sugars bypass the regulatory mechanisms that control food intake. The magnitude of effect of sugars may vary by the source, the food matrix, the dose, the inter-meal interval, and the time-point of measure. Sugars suppress food intake and, like other macronutrient sources, activate the normal hormonal cascade of signals that contribute to the suppression of food intake. Sugars, similar to other carbohydrates, do not bypass regulatory mechanisms of food intake [e.g. fructose, glucose, and sucrose all suppress ghrelin (a "hunger hormone" produced by ghrelin cells in the gastrointestinal tract) to a similar extent].

For more information, see Dr. Bellissimo's contribution to our 2015 resource <a data-cke-saved-href="/SUGAR/media/Sugar-Main/PDFs/CarbNews2015-6panel-ENG(s).pdf" href="/SUGAR/media/Sugar-Main/PDFs/CarbNews2015-6panel-ENG(s).pdf" onclick="_gaq.push (['_trackEvent', 'health_professionals', 'download', 'the_current_science']); target=" blank"="">Carbohydrate News - Sugars and Health: The Current Science


There is a popular belief that sugar consumption can lead to addiction similar to that of drug or alcohol dependency. In 2009, a scientific review conducted by Dr. David Benton from the University of Swansea, United Kingdom, examined the plausibility of sugar addiction in humans and its potential role in the development of obesity and binge eating disorders. Using an addiction model as a framework, a series of predictions were developed based on the hypothesis that an addiction to sucrose consumption can develop. Relevant scientific literature was examined in order to determine the validity of these predictions.

The findings of this review revealed that human studies do not support the widespread belief that sugar is addictive. It looked for the symptoms of addiction such as withdrawal, craving, and tolerance, and could find no evidence of an association with sugar consumption. The author also found no support from the human literature that addiction to food, or specifically sucrose, plays a role in obesity and eating disorders. Key findings from the review include:

  • The study of food preferences and cravings does not support a specific role for sucrose or sweet taste in increasing food cravings as an addiction model would predict;
  • A preference for a sweet taste or palatable foods should not be confused with addiction;
  • Fasting did not increase cravings for sweet items as would be expected in sugar addiction;
  • Although there is a genetically determined liking for sweetness, individuals differ in their response to sweetness and preference declines with age, opposite to that predicted by the addiction hypothesis;
  • Food cravings are commonly reported for a wide variety of foods, often reported as savoury/salty and sweet/fatty but most foods craved are high in fat rather than high in sugar;
  • Any palatable food results in the release of dopamine; in fact, any pleasant event, even a joke or a smile, will cause dopamine release;
  • Obese individuals did not find sweetness alone to be particularly attractive or prefer sucrose-containing foods relative to other palatable foods;
  • The notion that binge eating reflects an addiction to sweet foods is not supported by the evidence which indicates that a wide range of highly palatable foods are eaten during bingeing.

The author concludes that it is important to examine the underlying mechanisms of eating behaviour so that this knowledge can lead to appropriate interventions. If it is falsely believed that sucrose is addictive and leads to obesity, treatment may inappropriately concentrate on this ingredient while ignoring more beneficial responses.

For further information, see Dr. Benton's contribution to our 2015 resource Carbohydrate News - Sugars and Health: The Current Science.


Additional readings