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Dual Centre Model of Feeding (AO1)


--> Eating behaviour is controlled by 2 main nuclei (cluster of cells) in the Hypothalamus.

Signals of food intake (rise in blood glucose), then VMH satiety centre activated, next feeding stops. Next signals of declining nutrient levels (decrease in blood glucose), then lateral hypothalamus activated, this causes feelings of hunger. Then the cycle starts again.

Dual = structure in hypothalamus

Hunger centre = Lateral Hypothalamus (LH)


i.e. feeding centre




Fullness centre = Ventromedial Hypothalamus (VMH)


i.e. satiety centre = being full

Dual Centre Model of Feeding (AO2)


Evidence


--> Hetherington and Ranson

Demonstrated that the VMH is a satiety centre, responsible for stopping hunger drives and eating behaviour.


Lesions (damage) to the VMH caused rats to overeat and become dramatically obese.


The lesion prevented the signals from the satiety centre being sent so the rats didn't feel 'full' therefore continued eating.

Dual Centre Model of Feeding (AO2)


Evidence


--> Anand and Brobeck

Found lesions to the LH led to a loss of feeding behaviour rats, also known as aphagia.



They suggested that this area was a feeding or hunger centre whose normal function was to stimulate hunger drives and feeding in hungry rats.


Dual Centre Model of Feeding (AO2)


Evidence


--> Etc

Later studies confirmed these findings. Electrical stimulation of the VMH inhibited feeding, while stimulation of the LH produced feeding, so confirming their normal function.

Using animals as research participants.

Human eating behaviour more complex: social influence, health awareness, emotional eating etc.


They are able to quash impulses whereas animals are not.

Rule of Hormones --> Dual Centre model evaluation

Dual centre model is to reductionist & simplistic to explain eating behaviour, even as a biological explanation --> also ignores social factors.




Neural mechanisms do not act in isolation, part of a complex biological system including hormones.

Ghrelin -->released from stomach

--> secretion happens when stomach is empty

Effect on LH = Stimulates

Effect on VMH = Blocks receptors


When secreted makes person hungry.


Release stops when full.

Cummings et al --> supports ghrelin and that focus on brain mechanisms in eating is too reductionist.

Found ghrelin levels fell immediately after eating lunch and reached its peak when ppts requested evening meals.


In 5/6 ppts ghrelin levels closely correlated with degree of hunger reported by the ppts.

Leptin --> sends signals from fat cells into bloodstream when full.

Effect on LH = Blocks --> preventing brain activity


Effect on VMH = stimulates


Suppresses hunger

Carlson --> supports leptin and that focus on brain mechanisms in eating is too reductionist.

Found when he injected leptin into the Ob mice they stopped eating as much and their weight eventually dropped.


Ob mice = genetically obese mice

Biological approach to eating behaviour is very reductionist...

Eating complex should not be reduced to role of individual's brain structure or/and hormones


Simplistic --> ignores:


Environment e.g. external eaters, conditioning, lifestyle.


Emotional triggers


Cognitive triggers (things about food that triggers neural mechanisms)