Reading on appetite regulation Flashcards
CCK and BN
1998 Geracioti and Liddle-In their 1988 study, Geracioti & Liddle explored the relationship between cholecystokinin (CCK) release and satiety in individuals with bulimia nervosa (BN). They found that people with bulimia nervosa exhibited blunted CCK release in response to a test meal, which contributed to delayed satiety.
Key Points of the Study:
Cholecystokinin (CCK) and Satiety:
CCK is a hormone released from the small intestine in response to eating, particularly when fats and proteins are consumed.
It promotes satiety by slowing gastric emptying and signaling the brain to stop eating. CCK is part of the feedback loop that helps regulate meal size and prevent overeating.
Blunted CCK Release in Bulimia Nervosa:
The study by Geracioti & Liddle showed that individuals with bulimia nervosa (BN) had a diminished or delayed CCK response to a meal.
This blunted release means that people with BN experience delayed satiety, meaning it takes longer for them to feel full after eating.
Impact on Eating Behavior:
Because satiety signals like CCK are delayed or weaker in people with BN, they may continue eating beyond normal limits, contributing to the binge-eating behavior often observed in bulimia nervosa.
The delayed release of CCK may also disrupt the normal regulation of hunger and fullness, making it difficult for individuals with BN to control portion sizes or stop eating when full.
Conclusion:
The findings from Geracioti & Liddle (1988) highlight that blunted CCK release plays a significant role in the dysregulation of satiety in individuals with bulimia nervosa, contributing to overeating and binge episodes. This suggests that physiological factors, in addition to psychological components, contribute to the disordered eating patterns seen in BN.
the satiety cascade
blundell and rodgers 1991
Blundell and Rogers’ “satiety cascade” is a model that explains how the body regulates hunger and fullness through a series of biological and psychological signals in response to food intake. This cascade involves three main phases:
Sensory and Cognitive: The sight, smell, and thought of food trigger initial feelings of hunger or desire to eat.
Gastrointestinal: During eating, the stomach and intestines send fullness signals to the brain through hormones (like ghrelin and leptin).
Post-Absorptive: After digestion, nutrients enter the bloodstream, influencing long-term satiety and energy needs
Hypothalamic control of eating- study on damage to the control of eating
Damage to either the arcuate nucleus or the lateral hypothalamic area results in withdrawal from normal eating behaviours and the loss of body weight (Hetherington and Ranson, 1940). The location and severity of damage is correlated with duration of suffering and chances of recovery from anorexia (Cuppples, 2002) highlighting neurons in this region are responsible for releasing neurotransmitters to make one eat.
food cycles
eating behaviour is cyclical- Throughout the day CART AND POMC inhibit the release of NPY and AgRP at mealtimes, NPY AND AGRP turn the tables on CART AND POMC and initiate one episodic eating cycle.
these cycles are set early in life, paretnal influence setting the strength and number of cycle (in the west its 3)
the evolutionary argument to overeating
We are biologically wired to overconsume and not underconsume.
it is necessary to have a system to allow for overconsumption so we can create fat stores to provide energy for leaner times
The brainstem and cortical control of eating
The brainstem function includes perception of taste.
Parts of the brainstem involved include the NTS, Somatosensory cortex and the frontol lobe.
Information is passed from taste receptors on the tongue and processed by the brainstem. And these send signals to different parts of the brain
For example some pathways go to the frontal lobe, which controls reward mechanisms associated with taste, i.e liking and wanting food.
It is important to have separate liking and wanting as the system must be able to override an animals food preferences sometimes- for example if the body really needs food, but the animal does not like the food, the animal may still eat it, simply because it has to
‘liking’ food
liking is controlled by the pathway between the nucleus of the solitary tract and the nucleus accumbens. EOP signals have been shown to increase food intake. When food is tasted, EOP signals stimulate the release of GABA, and communicate to the brain if we ‘like’ the food or not.
Hunger can also affect ‘likeness’ (Cabanac 1992) as signals are recieved from the hypothalamus about how hungry we are.
Allesthesia is the phenomenon of changing what foods we like and dislike. It can also change due to time of day. Allesthesia is an important component of food selection as it has the potential to moderate liking and therefore has implications for eating behaviour.
Humans having different taste preferences and pallets
some people are more sensitive to different tastes than others- known as taste sensitivity. (controlled in the brainstem)
‘super tasters’- these people are sought after in the food and perfume industry. To find people with more sensitive taste, a liquid solution containing PROP is used- those with highly sensitive taste can taste it very strongly- the ability to taste PROP is inherited from our parents, and people with PROP have the ability to differentiate tastes within the same food (Tepper, 1999)- an argument that food preferences are inherited and genetically factored.
‘wanting’ food
liking food is not enough to make use consume it, this is where wanting comes into play.
wanting is controlled by a single neurotransmitter pathway that extends from the brainstem to the forebrain. The signal it uses is dopamine (reward)
dopamine here is the key difference between liking and wanting- removing dopamine from the brain leaves an animal without motivation to consume a particular food but there are still signs of liking food if placed on the tongue.
reward sensitivity is controlled by concentrations of dopamine in the brain, people with higher concentrations of dopamine tend to be more responsive to food cues, especially if they like that foo d(Volkow et al., 2002)
Individuals with higher reward sensitivity, is also linked with impulsivity, and have been linked to have higher body mass indexes and food cravings (Franken & Muris, 2005)- another genetic factor to food preference. and is also linked with a stronger preference for ‘unhealthy’ sweet and salty foods (davis et a;., 2007)
