Ingestive behaviours Flashcards
Definition of eating.
-> The action of taking SOLID FOOD in the mouth in order to nourish oneself…carried out by the insertion of foodstuff in the mouth, followed by mastication, swallowing and digestion… eating is not specifically the ingestion of non-food substances such as CLAY, CHALK and STONES… they also exclude such potential foodstuffs as BLOOD and URINE.
Why do we need food?
What does regulation of eating involve?
- Fuel: energy supply
- Nutrition: essential chemicals
> Bio/psycho/social factors
What does hunger motivate?
- Food seeking behaviour, thoughts + emotions
What is the biological interpretation of eating?
-
Mechanical and chemical digestion after eating, and its sequential physical and chemical digestion by GIT.
> Absorption of nutrients that help refuel the body and quench our need for more food
What is the role of of the CNS in hunger perception?
- The hypothalamus - key controller of food intake
What is the set point theory? What is wrong with this?
- Old fashioned : Long term regulation of body weight results from a complex integration of hormonal, metabolic and neural signals
What are the appetite signals when you are:
1- Hungry
2- Fed
3- If we have more long term energy reservoirs present
1- Hungry: Gremlin from stomach
2- Fed: Glucose + Insulin (PYY+ CCK)
3- If we have more long term energy reservoirs present(adipose): LEPTIN and RETINOL BINDING PROTEIN 4 (Rbp4) in proportion to fat content which reduces insulin sensitivity
Taste perception can be modulated by what?
Give examples
- Endocrine and chemokine messengers – suggesting that the state of the body alters our enjoyment of the food we ingest.
> Angiotensin II decrease sensitivity to salty tastes, but increases sensitivity to sweet tastes
Leptin increases sensitivity to sweet food
Insulin increases sensitivity to salty food
TNF-alpha decreases sensitivity to some bitter tasting foods
** (Decreased sensitivity → greater consumption)**
What is Pica?
- A craving to ingest non-food stuffs is associate with a variety of micronutrient deficiencies (e.g. iron, zinc, phosphorous, vitamins B, C and D). The biological mechanisms behind this link to dietary deficiency is unclear.
Why do we feel thirsty?
- Increases in plasma osmolarity and [Ang II] trigger feelings of thirst via stimulating subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT)
-> Modulatedby GI afferents and baroreceptor inputs. - Median preoptic nucleus sends signals to the Insula (interoception) and cingulate cortex(motivation/emotional processing)
1- What is sodium appetite?
2- What does sodium appetite require activation of?
1- Elicited by sodium depletion > increased palatability and drive to ingest salty substances
2- Activation of the RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM via aldosterone activated HSD2 neurones in the nucleus tractus solitarii
HSD2 neurones are salt sensitive and activated by sodium depletion, Why are HSD2 neurones unique?
- Express MINERALCORITCOID RECPETORS (MR) which are nuclear receptors that can be activated by both aldosterone and corticosteroids
> Normal conditions, cortisol is present at X100 greater concentration than aldosterone and will therefore block aldosterone’s effect on the HSD2 neurons. However, these neurons also have another receptor called 11-beta-hydroxysteroid dehydrogenase-type 2 which can metabolise corticosteroids.
What 3 models can explain our eating behaviour?
Describe the developmental model which explains eating behaviours.
- Focus on development of food preferences emphasises the role of exposure + learning.
> More likely to eat foods you have had previously and avoid novel foods (neophobia). What you are exposed so is dependent on cultural/ economical factors
> Associative learning: Positive reinforcement (food as a reward) OR limiting/controlling exposure to certain foods can make them more attractive.
> Social learning: Exposure to foods can be influenced by those around us e.g friends, family, peers, role models
= Acquisition + maintenance of eating habits is learned.
What is the Barker hypothesis?
-
Intrauterine growth restriction or a low birth weight might predispose children to obesity and metabolic syndrome.
= The deprived fetus develops a phenotype to survive in a nutrient-poor environment (Thrifty phenotype hypothesis) - Mismatch between the intra- and extra-uterine environment the neonate may be maladapted