Neural and Hormonal Mechanisms in Eating Behaviour Flashcards
What is homeostasis?
Maintenance of body’s constant internal environment
What are the two homeostatic mechanisms within the body?
1) Increase food intake
2) Stop food intake
What is the process of the homeostatic mechanism designed to INCREASE food intake?
1) Glucose decreases as hunger increases
2) Activates the LH which results in feelings of hunger
3) Causes a rise in glucose
What is the process of the homeostatic mechanism designed to reduce food intake?
1) Glucose rise activates VMH causing feelings of satiation
2) Reduces further feeding
What is a limitation of this homeostatic explanation of eating behaviour?
- 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
Why does homeostatic explanations not being in keeping with evolutionary theories limit its explanation?
It is not in keeping with evolutionary perspective in which our biology has evolved
However, what is an argument in favour of the homeostatic explanation?
- Primary inflence for hunger is foods positive-incentive value
- Taste developed for foods that promote survival
- Behaviours simply evolved to aid our survival
How does the hypothalamus play a role in our feeding behaviours?
- Damage to LH can cause aphagia in rats (absence of eating)
- Stimulation of LH can elicit feeding behaviours
In regards to the hypothalamus, how can neurotransmitters affect the LH?
-NPY injections caused obesity in rats in just a few days, illustrating its role in stimulating the LH and causing eating behaviour
What is a criticism of research into the role of the hypothalamus?
The assumption it serves as an on/off switch for eating behaviour
What is a limitation of the assumption it serves as an on/off switch for eating behaviour?
- 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
The assumption it serves as an on/off switch for eating behaviour is false, showing what?
- Reductionist view as does not take alternative processes into account
- Limits expl as unable to provide an explanation for other processes happening within hypothalamus
What is a methodological flaw of research into role of the hypothalamus?
- Highly artificial NPY amounts, normal amount would not induce behaviour to same degree, affecting internal validity and generalisation, lacks mundane realism
Further criticism of research into Hypothalamus..
- 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
What is a positive application of the role of the hypothalamus?
- 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
Other neural explanations suggest that the A..
Amygdala and interior pre-frontal cortex influence eating behaviour
What is the role of the amygdala?
Selects food on the basis of past experience
What is the role of the pre frontal cortex
Receives messages regarding smell from olfactory bulb, which if damaged, can affect the taste of food
What did Rolls and Rolls find when they removed the amygdala of rats?
Consumption of familiar and unfamiliar foods indifferently, compared to those with theirs intact which avoided unfamiliar foods
An application of this research is that the wider-insight offered can help our understanding of feeding abnormalities in Kluver-Bucy patients..
- 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
What does Kluver-Bucy patients show?
Evidence to support neural control of cognitive factors in eating behaviour
Opposing research from Lutter shows that hunger may not be under purely neural control, but hormones instead…
- 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
Why might the approach of reducing ghrelin be problematic?!
- Removes ghrelins beneficial effect as part of the bodies response to stress
- Instead, we should address the root cause of comfort eating (the stress)
