Satiety is a state or condition of fullness gratified beyond the point of satisfaction.
Satiation is the state of being sated.
Satiation refers to then cumulative effect of inhibitory sensory, cognitive, digestive, and hormonal signals that bring an eating occasion to an end.
Satiation helps control meal size, and snacking between meals.
Satiation is a psycho-biological process that suppresses hunger after eating and prevents further eating;
It is the opposite of hunger.
It is a state which induces meal termination.
It occurs when food is present in the GI tract after a meal satiety signals overrule hunger signals and intake ceases, after which satiety slowly fades as hunger increases.
Appetite is the desire to eat.
Appetite includes the biological urge to eat as well as the interplay between senses, habits, past experiences, future expectations and available food.
As both satiation and satiety are processes that inhibit eating.
Enhancing satiety could reduce overeating.
Satiety involves interaction of both physiological signals and psychological, environmental and social influences.
Satiety responsiveness varies between people.
People with low satiety responsiveness show a faster return of hunger after a meal.
The satiety center is located in ventromedial nucleus of the hypothalamus.
Satiety is signaled through the vagus nerve as well as circulating hormones.
During intake of a meal, the stomach stretches to accommodate the increased volume.
This gastric accommodation activates stretch receptors in the proximal stomach.
These receptors then signal through afferent vagus nerve fibers to the hypothalamus, increasing satiety.
As food moves into the duodenum, duodenal cells release multiple substances that affect digestion and satiety.
Peptides influence appetite:
Ghrelin released from the stomach, is also known as the hunger hormone because it stimulates food intake.
Satiety hormones cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1) and peptide YY (PYY) released from the small and large intestine inhibit food intake.
The Satiety Index: types of food eaten, its nutrients and physical form can influence satiety.
The highest Satiety Index (SI) measured is for boiled potatoes and it is seven times higher than the SI for a croissant.
SI scores correlated positively with the weight of foods, protein, fiber and water content.
Fat content is negatively associated with SI scores.
The increased satiating effect of potato has also been shown when compared to rice and pasta in a mixed meal.
The protein content of food is a strong determinant of satiation and short-term satiety, what happens afterwards is also important.
Carbohydrates may elicit more helpful post meal sensations than protein.
A high carbohydrate has a higher ratings for satisfaction, food joy and overall wellness and fullness than a high protein diet.
In addition, a high protein diet induces a higher desire for sweet foods after the meal and this may have implications for subsequent food and energy intake.
Dietary fiber in food promotes satiety and reduced food intake and may explain the association between fiber intake and lower body weight.
Fiber is thought to enhance satiety by adding bulk and viscosity to gut contents and altering gut hormones.
A good amount and variety of different dietary fibers in carbohydrate-containing plant foods can contribute to an optimal gut microbiome.
These microbes can produce metabolites that affect satiety.
Microbiota dysbiosis, or an imbalance in gut microbes, can stimulate food intake and contribute to weight gain and development of obesity.
Food structure influences how easily nutrients are absorbed and digested, with subsequent influence on gut hormone responses.
Whole nuts’ fiber content reduces the digestibility and slows the absorption of the fats they contain and this is likely enhances satiety.
High levels of food processing can make nutrients more accessible and reduce satiety.
Chewing food more also enhances satiety and reduces food intake.
A systematic review and meta-analysis on the influence of food texture on satiety found that there is a hierarchy of ability to reduce hunger, suggesting:
solids -> higher viscous (thick) food -> liquid -> low viscous (thin) food.
Solid foods trigger the early stages of the satiety, through visual and oral cues, and the later processes in the satiety cascade are not as affected by food form.
Liquids are consumed quickly, and spend less time in the mouth, have shorter oro-sensory exposure time,
Foods eaten slowly spend more time in the mouth and give a higher satiety response.
Sugar-sweetened beverages compared to milk show lower subjective fullness and satiety but no difference in subsequent energy intake.
Gastric distention activates satiety circuitry in the brain via the vagal nerves.
Faster gastric emptying rate is associated with less satiety and higher energy intake.
Air bubbles in beverages promotes fullness and lower hunger than non-aerated beverages, thought to be due to carbonated beverages having greater gastric volume.
The sense of taste is an important contributor to the satiating effect of foods.
Taste is a nutrient sensor of the brain.
Tasting food contributes to satisfaction of appetite, while triggering activation of taste and reward areas of the brain, suggesting sensory stimulation has an important role in satiation.
Food delivered to the stomach without oral sensory stimulation activates the brain, in different brain areas.
The drive to eat incorporates more than meeting nutritional needs.
Appetite is not just about hunger and satiety but includes other more subjective evaluations such as food pleasure and how it makes us feel.
The combination of taste and aroma may induce greater satiation and short-term satiety than either taste or aroma alone, suggesting that flavor quality and intensity play a role in subsequent food intake.
Sweet foods stimulate food intake but they also produce satiation as a result of their volume, nutrient and energy content.
Sweet taste detection and signalling in the mouth also operate in the gut.
High intensity sweeteners do not evoke the release of satiety hormones in the same way sugars do, as they do not activate the brain’s reward pathways as sugar does.
Non-nutritive sweeteners may uncouple the relationship between sweet taste and neuroendocrine signaling.
Sensory-specific satiety describes pleasantness declines as you eat more of one food compared to that of other foods: this describes how even though you’ve eaten dinner, you still have room for dessert or cheese plate.
High energy density foods tend to be palatable and less satiating, while low energy density foods, that tend to have the most water and least fat, tend to be less palatable and more satiating.
Preload specific foods or drinks given prior to offering other foods: whole foods such as fruits and vegetables, soups and salads eaten before a meal can reduce energy intake of the meal probably due to their volume, solid/semi-solid form and water content.
Intuitive eating is the practice of eating whatever is desired and stopping when satiated.
Intuitive eating matches the body’s that is well calibrated in infancy and early childhood but can become blunted or distorted over time.
The Western food and diet culture disrupts food intake regulation, as has the prevalence of hyper-palatable, energy-dense highly-processed foods.
People are poorly adapted to the abundance of energy-dense foods, and highly palatable foods that by-pass our drive to eat to fulfil nutritional needs.
The drive to eat may be even stronger for people with low-satiety responsiveness.
People with a low satiety phenotype experience higher hunger levels, greater liking and wanting of high fat foods, greater tendency to snack and higher energy intake.
Glucagon-like peptide-1 (GLP-1) is an incretin released by the duodenum that inhibits relaxation of the stomach.
This inhibition causes increased stretch of the stomach, increasing activation of proximal gastric stretch receptors. It also slows overall gut motility, increasing the duration of satiety.
This effect is used to increase weight loss and treat obesity through GLP-1 agonists.
Cholecystokinin (CCK) is gut peptide produced by the duodenum in response to fat and protiens.
CCK has the effect of slowing gut motility and increasing satiety as well as activating release of pancreatic digestive enzymes and bile from the gallbladder.