Involves mechanisms which keep
our bodies balanced
In equilibrium
When glucose levels drop hunger
increases + we look for food
Once G levels rise we
feel satisfied + stop
eating
There is a time lag between stimuli + mechanism
but body can account for that
A02
Limitations
Theory can be viewed as incompatible w/
evol. of hunger mechanisms
In order for it to be adaptive it must both anticipate +
prevent hunger (energy deficits)
Doesn't make sense for eating + hunger to be triggered
once energy levels are below their desired amount
Lateral hypothalamus
A01
When G levels in blood get low LH is triggered causing
hunger + makes someone go in search of food
NPY = neurotransmitter found in LH important for eating
A02
Problems w/ LH
A few probs. have been identified w/
idea LH acts as 'on switch' for eating
Damage causes deficits in other aspects of behaviour (thirst
+ sex) rather than just hunger
Sakurai et al
Found eating behaviour is
controlled by neural circuits all
over brain
Meaning while LH probably still plays important role it
isn't 'eating centre' as initially believed
Problems w/ NPY
Recent research has cast doubt on whether
neuropeptide Y's normal function is to
influence feeding
Marie et al
Genetically manipulated mice so that they didn't make NPY
Found no subsequent decrease in feeding behaviour
Suggest hunger stimulated by injections of NPY may be an experimental artefact
IDA - Real-world application
Yang et al
Found NPY is produced by abdominal fat + suggest this leads to vicious cycle where
NPY produced in brain leads to more eating + production of more fat cells, leading to
more NPY + fat cells + so on
By targeting those at risk they believe it should be
poss. to treat them w/ drugs that turn off NPY + this
prevent obesity
Ventromedial hypothalamus
A01
Part of H responsible for saying when
someone's satisfied after food due to lots of G
receptors
Damage to this area causes overeating
(hyperphagia) due to fact person no longer
'knows' when their full
A02
Research for VMH
Early research found damage to VMH led to
hyperphagia + obesity in a no. of species,
including humans
Led to VMH being named 'satiety centre'
However...
Gold
Found lesions restricted to VMH alone didn't result in hyperphagia + only
produced overeating when other areas (paraventriculeur nucleus) is also
damaged
Subsequent research has failed to replicate Gold's findings
Cognitive factors
A01
Amygdala + inferior pre-frontal cortex are
responsible for cognitive aspects of hunger
Amygdala means we choose food
based on our experience of that food
If you remove amygdala = rats eat novel +
familiar foods (when they would usually avoid
novel food)
Rolls + Rolls
Messages to IPFC come from part of brain responsible for smell
(olfactory bulb) meaning if IPFC is damaged there is a decrease in
eating
A02
Research support
Zald + Pardo
Provide psychological evidence to support
claim amygdala participates in emotional
processing of olfactory stimuli
Exposed healthy adult ppts to aversive olfactory stimuli
while measuring blood flow to amygdala via PET scan
Were significant blood flow increases to A when ppts where
exposed to unpleasant smells
Kluver-Bucy syndrome
Damage to amygdala + IPFC could explain
feeding abnormalities observed in K-B syndrome
Patients typically show increased appetite, indiscriminate
eating + even attempt to eat non-food items
Research suggests food cues no longer accurately
represent their real reward value to indivi.
IDA - Evol. approach
Evol. theorists suggest primary stimuli for hunger + eating is
foods positive-incentive value
People eat because they develop a relish for particular
tastes that are associated w/ foods that promote our survival