Hunger, eating and health Flashcards
digestion is how we convert food into
energy
energy supplied to the body in the form of
lipids, amino acids and glucose
energy use constant but
intake relatively infrequent
energy is stored as
- fat (adipose tissue - 85%)
- protein (muscles - 14.5%)
- glycogen (liver - 0.5%)
Glucose is
the brains energy sourcem needs to be readily available
-> stored as glycogen (in the liver) - easily converted back to glucose and released into circulation
pancreatic hormones
regulate the conversion process
glucagon
stimulates conersion from lycogen to glucose (ready energy)
insulin
stimulates conversion from glucose to glycogen (stored energy)
brain - does not need insulin, rest of the body does
fat is
preferred enrgy store
- provides 2x as much as energy as glycogen
- glycogen attracts water (heavy)
- fat either comes directly from food or is produced by the body from either glucose and other nutrients
3 phases of metabolism
1:cephalic
2: absoptive
3: fasting
Cephalic phase
preperatory phase, which is intiated by the sight, smell or expectation of food, ends with absorption into bloodstream
conditioned high release of insulin from pancreas (comparitvely little release of glucogen) in anticipation of glucose increase in the blood stream
insulin lowers level of bloodborne fuels by promoting:
1: use of glucose as primary energy sourse
2: conversion of bloodborn energy sources to storage of fuel
3: storage of glycogen in liver, muscle and fat
absorptive phase
nutrients from meal meeting the bodys immediate energy requirments, with the excess being stored
digestion promots release of gut hormone. some of these stimulate insulin release
more insulin is released by the pancreases
fasting phase
energy being withdrawn from stores to meet the bodys immediate needs (period between meals)
low level of insulin but high level of glucagon in the blood
because there are low insulin levels
1: glucose no longer main energy source (reserved for brain)
2: conversion of glycogen and protein to glucose promoted
pancreas starts secreting glucagon: high level of glucagon result in
1: release of free fatting acids from aipose tissue (converted to ketons - used by muscles during fasting phase)
2: conversion of glycogon back to glucose
theories of eating:
set point assumption (no longer seen as valid models)
- energy set point : based on homeostatic, negative feedback system
- homeostasis
hunger is driven by the need to have certain - glucostatic set point
- lipostatic set point
glucostaic and lipostatic set point theories
1: glucostatic theory:
- blood glucose (short term regulation)
responsible for intiating and terminating meals (diabieties disputes this theory)
2: lipostatic theory:
body fat (long term regulation)
While the glucostatic theory holds that hunger and satiety are due primarily to short-term shifts in blood glucose levels (or utilization rates), the lipostatic hypothesis states that the humoral signal which influences central structures must be related to long-term changes in the adipose tissue stores.
weaknesses of set point theories
- eating disorder, obseity epidemic..
- inconsistence with evolutionary pressures (banking food when available)
- major predictions of theories not conf
- chagnes in glucose needed to increase eating, not natural
- people with excess fat dont adjust meal size
- fail to recognise the pressures of taste, learning, social influences
positive incentive perspective
- developed to overcome shortcomings of set point
- about that inciticpated pleasure of eating and craving
animals eat in repsonse to: - preferred falvours
- past expereinces
- time since last meal
- others eating
factors that infleunce what we eat
- prfer sweet and salty
- aversion to bitter
- conditioned taste aversion and preferences
- craving for deficiencies :
- sodium, other vitamins
- dietry deficiencies?
: manufactoring of food to maximise profits - they maximise taste, and can just have poor nutritional value
factors that infleunce when we eat
when food is readily available:
- animals eat many small meals throughout the day, humans tend to focus on a few large meals per day
eating as a stresor:
- eating stresses the body because of the release of insulin
- malaise/ unpleasent feelings -> effects of the cephalic stage
Weingarten research
rat experiement (Ate each time conditioned stimulus was presented)
- hunger caused by expectations not energy deficiet
- we eat when we are used to eating
despite fact they had 6 meals aa day they still ate when stimulus came - they were conditioned to eat on the que
Satiety is
motivational state that causes us to stop eatin when there is food remaining)
Shame models
eat how much they are used to eating
appetizer effect
eating a small amount before meal increaes size of meal
the mroe variety of food
the more we eat today. problem in today soecity with abundance of food
sensory specific satiety
why we often missunderstand that full feeling.
when you feel full not neccsairly means you’r full but how interested you are in contuning to eat that food
@ive just had enough of that food, i want something else@
thats why we can eat desert after meal
when we have a lot of variety more likely to continue eating
Structures that play a role in satiety
early work the ventromedial hypothalamus was known as a satiety centre (increased eating)
The lateral hypothalamus was known as the hunfer centre (animals stopped eating and drinking when lesion here)
Hypothalamic nuclei now focus for research
problem with VMH as satiety centre
new reserch suggests they overeat becuase they become obese
many effects of VHM lesions are not attributed to VHM damage
humans expend most of their energy on
maintaining basal metabolis
which area of the hypothalamus seesm to be crtical for the ending of meals?
paraventicular nucleus
- the hypothalamus is a collction of nuclei. different parts have differnet functions
The PVN is the feeding centre - appreciate satiety peptides
when in fasting stage - leptin released nd send message to brain stopping arculate nucleous from send neuro peptide to PVN.
