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Neural mechanisms in Eating Behaviour
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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
- Once G levels rise we feel satisfied + stop eating
- Involves mechanisms which keep our bodies balanced
- 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
- Theory can be viewed as incompatible w/ evol. of hunger mechanisms
- Limitations
- A01
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
- Found eating behaviour is controlled by neural circuits all over brain
- A few probs. have been identified w/ idea LH acts as 'on switch' for eating
- 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
- Found no subsequent decrease in feeding behaviour
- Genetically manipulated mice so that they didn't make NPY
- Marie et al
- Recent research has cast doubt on whether neuropeptide Y's normal function is to influence feeding
- 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
- 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
- Yang et al
- Problems w/ LH
- A01
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
- Found lesions restricted to VMH alone didn't result in hyperphagia + only produced overeating when other areas (paraventriculeur nucleus) is also damaged
- Gold
- Early research found damage to VMH led to hyperphagia + obesity in a no. of species, including humans
- Research for VMH
- A01
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
- If you remove amygdala = rats eat novel + familiar foods (when they would usually avoid novel food)
- Amygdala means we choose food based on our experience of that food
- Messages to IPFC come from part of brain responsible for smell (olfactory bulb) meaning if IPFC is damaged there is a decrease in eating
- Amygdala + inferior pre-frontal cortex are responsible for cognitive aspects of hunger
- 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
- Exposed healthy adult ppts to aversive olfactory stimuli while measuring blood flow to amygdala via PET scan
- Provide psychological evidence to support claim amygdala participates in emotional processing of olfactory stimuli
- Zald + Pardo
- 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.
- Damage to amygdala + IPFC could explain feeding abnormalities observed in K-B syndrome
- 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
- Evol. theorists suggest primary stimuli for hunger + eating is foods positive-incentive value
- Research support
- A01
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- A mind map outlining the A01 and A02 points for an essay
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- bebe97
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