Outline and evaluate the role of neutral and hormonal mechanisms in the
control of eating behaviour
The neutral and hormonal mechanisms in the control of eating behaviour is
preserved to indicate how the body consumes energy with evidence of hormonal
mechanisms. Homeostasis allows the body to maintain a constant state detecting
the body's balance. Within the dual centre model there are focuses of eating
behaviour, like the hypothalamus which is responsible for turning on and off eating.
The lateral hypothalamus has been identified as the hunger centre (turning on
eating) and the ventromedial hypothalamus as the satiety centre for “turning off
eating” By our blood sugars being low, signals are sent to the LH to trigger hunger.
The Ghrelin there is released from the stomach which stimulates the hypothalamus
to increase appetite and stimulate eating. When we eat it falls drastically, Leptin is
produced to reduce appetite after the fat has been satisfied. By not eating enough,
leptin drops which later triggers the body to hunger.
One strength of this role is that there is research support. For the dual centre model,
this comes from lesion studies in rats. For example, Hetherington and Randon 1942)
showed that the lesioning of the VMH as rats caused these animals to overeat and
eventually become severely obsese. This shows that creating surgical wounds in
various strategic brain areas confirms their roles in controlling eating behaviours. As
a result this strengthens the credibility of neural mechanisms, as the research
directly shows that the VMH is in control in satiety.
However, a weakness of this is that the explanation is oversimplified as it ignores
other biological factors. Eg, a hormone called cholecystokinin is produced in the
upper intestine. It activates the nerve that signals from the gastrointestinal tract of
the hypothalamus. This signal indicates satiety and contributes to the "stop eating
mechanism". It might even be that CCK is an even more powerful appetite
suppressant than leptin. Several other neurotransmitters such as serotonin and
dopamine also appear to be involved in eating behaviour. This suggests that eating
behaviour is more complex than this explanation perceives it to be.
Another weakness of this explanation is that it ignores the role of social and cultural
factors. For example, normal meal time is more less under neurochemical control
and is usually initiated by the social and cultural factors that are related to lifestyle.
Therefore, Woods (2004) suggests that the view that the LH feeding centre always
detects falls in blood glucose levels and stimulates hunger is outdated. Infact, this
only occurs in "emergency" conditions of severe energy deprivation. This suggests
that a pure biological approach to understanding eating behaviour tends to ignore
potentially important non-biological factors that may be more influential.
control of eating behaviour
The neutral and hormonal mechanisms in the control of eating behaviour is
preserved to indicate how the body consumes energy with evidence of hormonal
mechanisms. Homeostasis allows the body to maintain a constant state detecting
the body's balance. Within the dual centre model there are focuses of eating
behaviour, like the hypothalamus which is responsible for turning on and off eating.
The lateral hypothalamus has been identified as the hunger centre (turning on
eating) and the ventromedial hypothalamus as the satiety centre for “turning off
eating” By our blood sugars being low, signals are sent to the LH to trigger hunger.
The Ghrelin there is released from the stomach which stimulates the hypothalamus
to increase appetite and stimulate eating. When we eat it falls drastically, Leptin is
produced to reduce appetite after the fat has been satisfied. By not eating enough,
leptin drops which later triggers the body to hunger.
One strength of this role is that there is research support. For the dual centre model,
this comes from lesion studies in rats. For example, Hetherington and Randon 1942)
showed that the lesioning of the VMH as rats caused these animals to overeat and
eventually become severely obsese. This shows that creating surgical wounds in
various strategic brain areas confirms their roles in controlling eating behaviours. As
a result this strengthens the credibility of neural mechanisms, as the research
directly shows that the VMH is in control in satiety.
However, a weakness of this is that the explanation is oversimplified as it ignores
other biological factors. Eg, a hormone called cholecystokinin is produced in the
upper intestine. It activates the nerve that signals from the gastrointestinal tract of
the hypothalamus. This signal indicates satiety and contributes to the "stop eating
mechanism". It might even be that CCK is an even more powerful appetite
suppressant than leptin. Several other neurotransmitters such as serotonin and
dopamine also appear to be involved in eating behaviour. This suggests that eating
behaviour is more complex than this explanation perceives it to be.
Another weakness of this explanation is that it ignores the role of social and cultural
factors. For example, normal meal time is more less under neurochemical control
and is usually initiated by the social and cultural factors that are related to lifestyle.
Therefore, Woods (2004) suggests that the view that the LH feeding centre always
detects falls in blood glucose levels and stimulates hunger is outdated. Infact, this
only occurs in "emergency" conditions of severe energy deprivation. This suggests
that a pure biological approach to understanding eating behaviour tends to ignore
potentially important non-biological factors that may be more influential.
