Eating behaviour- neural mechanisms

Question 1

what is the dual centre model

Answer 1

the hypothalamus has two structures
the lateral hypothalamus: (lean hamster- eat!) feeding centre
the ventromedial hypothalamus: (very loudly humous-don’t eat!) satiety centre

Question 2

sequence of events involved in feeding and the hypothalamus

Answer 2

1- food intake signals e.g rise in blood glucose
2- VHM activated
3- feeling full- feeding stops
4- decline in nutrient levels signals e.g decrease in blood glucose
5- LH activated
6- feeling hungry- feeding starts

Question 3

evidence for dual centre model: Hetherington and Ranson (1942)

Answer 3

demonstrated VMH- is satiety centre- responisble for hunger drives in eating behaviour.
Lesions (damage) to the VMH caused rats to overeat and become dramatically obese
conc: VMH under normal circumstances- is a satiety centre activated when the animal is full or satietated after eating.
lesions prevented these signals from being sent- no feeling of full so rats continued eating

Question 4

evidence for dual centre model: Anand and Brobeck (1951)

Answer 4

found a lesion to the LH led to a loss of feeding behaviour in rats also known as aphagia.
they suggested this area was a feeding or hunger centre whose normal function was to stimulate hunger drives and feeding in hungry rats.

Question 5

later findings from research into hypothalamus

Answer 5

confirmed findinds from Hetherington and Ranson and Anand and Brobeck
electrical stimulation of the VMH inhibited feeding, while stimulation of the VH produced feeding so confirmed their normal functions

Question 6

comment on use of animals as research participants

Answer 6

issues of generalisability
brain physiology similar to human BUT
we have ability to override neural impulses
human eating behaviour more complex: social influences, health awareness, emotional eating etc
issues of validity:
lesions and electrical stimulation may have affected other important areas of the brain as well
many replications= high reliability

Question 7

IDA- nature-nurture debate in relation to the dual centre model of feeding

Answer 7

highly nature based but also reductionist

complex eating behaviour reduced to two parts of the hypothalamus = criticism

Question 8

evaluation of dual centre model

Answer 8

brain not an island :
sends and receives signals from the body
key messenegers= hormones
travel in blood stream, diffuse into brain act on synapses ‘feedback’ from body
endocrine system
conclusion:
dual centre model too reductionist and simplistic to explain eating behaviour (not only because it ignores social/psychological reasons but also within biological terms- not only hypothalamus- hormones included

Question 9

Ghrelin

Answer 9

stimulates receptors in arcuate nucleus in both LH and VMH
inhibits activity of VMH
released from stomach when empty- stops when full
makes you hungry

Question 10

Leptin

Answer 10

stimulates receptors in arcuate nucleus in both LH and VMH
inhibits activity of LH
released from fat cells in adipose tissue
suppresses hunger
acts as an indicator f body weight to hypothalamic mechanisms controlling long term food intake

Question 11

AO2 dual model

Answer 11

neural mechanisms cannot control eating on their own, they require endocrine systems- focus on brain is simplistic e.g gherlin send signals to LH and stimulates the action of the LH which induces hunger because released from stomach when it’s empty and switches on receptors which allow signals to pass to LH creating hunger drives whist VMH is inhibited due to release of ghrelin
Cummings- found that gherkin levels fell immediately after eating lunch - as digestion kicked in the increase of gherkin occurred in 5/6 ppts G levels closely correlated with the degree of hunger.
reductionist! reduces eating behaviour the the action of the brain- it’s neural mechanisms

Question 12

adipose

Answer 12

fat storage cells of body

after digestion insulin enables fat in bloodstream to be stored in adipose cells

Question 13

OB mice

Answer 13

genetically obese mice. they lack the gene that controls the production of the satiety signal leptin from adipose tissue. with no leptin, they over eat and become obese

Question 14

cummings et al(2004) research evidence for ghrenlin

Answer 14

investigated changes in the blood gherkin levels over time between meals.
6 ppts ate lunch then monitored g levels every 5 mins until the evening meal
assessment of hunger every 30 mins
G levels fell immdiately after lunch- lowest 70 mins after
slowly began to rise peaking their evening meals.
5/6 g levels closely correlated with the degree of hunger reported by the pats.

Question 15

how does cummings support the role of gherkin in eating behaviour

Answer 15

ghrelin directly reflects stomach emptiness and are closely related to subjective feelings of hunger- therefore has a key role in appetite signalling in humans

Question 16

lutter et al (2008) research evidence for ghrelin

Answer 16

starved mice for 4 days
found that gherkin increased, mice showed anxiety and depression when maze running
ghrelin also increased when mice were stressed, shows that food, hunger, stress and anxiety seem to be associated (but use of animals may lead to unwarranted extrapolation and ethical issues)
study could be used to support the link between stress and increased food intake- comfort eating

Question 17

carlson 2007) research evidence for leptin

Answer 17

studied mice with a genetic mutation (genetically obese) OB mice
missing the gene that produces leptin- ombre didn’t produce leptons their hypothalamus does not receive a signal to stop eating and so they eat continuously and become obese
when he injected leptin the ob mice stopped eating and their body weight returned to normal
leptin was therefore thought as a potential treatment for human obesity- expected that overweight human would have low levels of leptin however NO
rare individuals who are over weight because of leptin deficiency - but majority have normal or even higher level of leptin—prob here is that brain mechanisms controlling feeding behaviour are insensitive to the effects ofleptin or that other neural mechanism override the leptin signals