Neural mechanisms in Eating Behaviour

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Neural mechanisms in Eating Behaviour
1 Homeostasis
1.1 A01
1.1.1 Involves mechanisms which keep our bodies balanced In equilibrium
1.1.2 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
1.2 A02
1.2.1 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
2 Lateral hypothalamus
2.1 A01
2.1.1 When G levels in blood get low LH is triggered causing hunger + makes someone go in search of food
2.1.2 NPY = neurotransmitter found in LH important for eating
2.2 A02
2.2.1 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
2.2.2 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
2.2.3 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
3 Ventromedial hypothalamus
3.1 A01
3.1.1 Part of H responsible for saying when someone's satisfied after food due to lots of G receptors
3.1.2 Damage to this area causes overeating (hyperphagia) due to fact person no longer 'knows' when their full
3.2 A02
3.2.1 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
4 Cognitive factors
4.1 A01
4.1.1 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
4.1.2 Messages to IPFC come from part of brain responsible for smell (olfactory bulb) meaning if IPFC is damaged there is a decrease in eating
4.2 A02
4.2.1 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
4.2.2 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.
4.2.3 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

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