Neural mechanisms: Ventromedial hypothalamus


Neural mechanisms: Lateral hypothalamus

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  • Research to support Gold comes from Hetherington and Ranson. They conducted a study that reported that lesions to the VMH caused rats to become dramatically obese. This supports the idea that if the VMH (satiety centre) is destroyed it can lead to uncontrolled eating.


  • Research into the vemtromedial hypothalamus is inconclusive. Gold (1973) found that lesions restricted to the VMH did not result in hyperphagia and only produced overeating when they included other areas such as the paraventricular nucleus (PVN). Subsequent research has failed to replicate Golds findings with most studies showing that lesions in the VMH caused animals to eat more and gain more weight.
  • Within this explanation the role of cognition is ignored. The neurons with cell bodies in the LH or VMH could be affected by sensory input relayed from other areas, in particular the frontal cortex. This is supported by the fact that we all have food preferences, and so cognition also plays a part in eating and stopping eating; these behaviours are not just automatic stimulus–response drives. Thus, hunger, eating, and satiety are not just a result of biological processes, and the LH and VMH control system is far from a set of simple on–off switches.


Overall, hunger and eating may not be under purely neural control which suggests these biological explanations are reductionist accounts of eating behaviour because they fail to take in psychological factors.For instance Lutter et al found how the body produces extra quantities of the ghrelin hormone in response to the psychological state of stress. Ghrelin boosts appetite which leads to increase comfort eating as an eating behaviour. Therefore blocking ghrelin would help people with a tendency to comfort-eat when stressed and control their weight.


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