Zusammenfassung der Ressource
Neural mechanisms in Eating Behaviour
- Homeostasis
- A01
- 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