Neural and Hormonal Mechanisms in Eating Behaviour Flashcards

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1
Q

What is homeostasis?

A

Maintenance of body’s constant internal environment

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2
Q

What are the two homeostatic mechanisms within the body?

A

1) Increase food intake

2) Stop food intake

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3
Q

What is the process of the homeostatic mechanism designed to INCREASE food intake?

A

1) Glucose decreases as hunger increases
2) Activates the LH which results in feelings of hunger
3) Causes a rise in glucose

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4
Q

What is the process of the homeostatic mechanism designed to reduce food intake?

A

1) Glucose rise activates VMH causing feelings of satiation

2) Reduces further feeding

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5
Q

What is a limitation of this homeostatic explanation of eating behaviour?

A
  • Should be able to anticipate and prevent energy deficits rather than just react if truly adaptive
  • Inconsistent with harsh environment in which the mechanisms would have been developed
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6
Q

Why does homeostatic explanations not being in keeping with evolutionary theories limit its explanation?

A

It is not in keeping with evolutionary perspective in which our biology has evolved

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7
Q

However, what is an argument in favour of the homeostatic explanation?

A
  • Primary inflence for hunger is foods positive-incentive value
  • Taste developed for foods that promote survival
  • Behaviours simply evolved to aid our survival
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8
Q

How does the hypothalamus play a role in our feeding behaviours?

A
  • Damage to LH can cause aphagia in rats (absence of eating)

- Stimulation of LH can elicit feeding behaviours

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9
Q

In regards to the hypothalamus, how can neurotransmitters affect the LH?

A

-NPY injections caused obesity in rats in just a few days, illustrating its role in stimulating the LH and causing eating behaviour

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10
Q

What is a criticism of research into the role of the hypothalamus?

A

The assumption it serves as an on/off switch for eating behaviour

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11
Q

What is a limitation of the assumption it serves as an on/off switch for eating behaviour?

A
  • Damage can also cause deficits in thirst and sex drive, not just hunger
  • Neural circuits running through brain also play an eating role
  • LH does play a role, but is not eating centre
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12
Q

The assumption it serves as an on/off switch for eating behaviour is false, showing what?

A
  • Reductionist view as does not take alternative processes into account
  • Limits expl as unable to provide an explanation for other processes happening within hypothalamus
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13
Q

What is a methodological flaw of research into role of the hypothalamus?

A
  • Highly artificial NPY amounts, normal amount would not induce behaviour to same degree, affecting internal validity and generalisation, lacks mundane realism
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14
Q

Further criticism of research into Hypothalamus..

A
  • NPY may not influence eating behaviour as much as thought
  • Mice genetically manipulated so no NPY did not show feeding decrease
  • Behaviour resulted from NPY injections may just be experimental side effects
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15
Q

What is a positive application of the role of the hypothalamus?

A
  • NPY produced by abdominal fat, leading to vicious cycle of more eating and the production of fat cells, leading to more NPY production
  • Knowledge can help us in understanding and treatment of obesity: target those at risk
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16
Q

Other neural explanations suggest that the A..

A

Amygdala and interior pre-frontal cortex influence eating behaviour

17
Q

What is the role of the amygdala?

A

Selects food on the basis of past experience

18
Q

What is the role of the pre frontal cortex

A

Receives messages regarding smell from olfactory bulb, which if damaged, can affect the taste of food

19
Q

What did Rolls and Rolls find when they removed the amygdala of rats?

A

Consumption of familiar and unfamiliar foods indifferently, compared to those with theirs intact which avoided unfamiliar foods

20
Q

An application of this research is that the wider-insight offered can help our understanding of feeding abnormalities in Kluver-Bucy patients..

A
  • Bilateral lesions of medial temporal lobe results in symptoms such as hyperphagia (overeating)
  • Extreme indiscriminate eating, attributed to damage to the amygdala, as cues such as smell and taste no longer represent a reward value
21
Q

What does Kluver-Bucy patients show?

A

Evidence to support neural control of cognitive factors in eating behaviour

22
Q

Opposing research from Lutter shows that hunger may not be under purely neural control, but hormones instead…

A
  • Ghrelin hormone in response to stress which increases the appetite
  • This knowledge can allow us to address comfort eating by blocking the production of ghrelin, which may aid in controlling weight
23
Q

Why might the approach of reducing ghrelin be problematic?!

A
  • Removes ghrelins beneficial effect as part of the bodies response to stress
  • Instead, we should address the root cause of comfort eating (the stress)