Neural Mechanisms Involved in Controlling Eating Behaviour

  • There are many complex theories to explain our biological drive to eat and become satiated. There are two neural mechanisms that are part of the dual centre model of feeding regulation. The role of the lateral hypothalamus and neuropeptide Y (NPY) and the role of the ventromedial hypothalamus.
  • The Lateral Hypothalamus:
  • Investigation into the role of the hypothalamus in eating behaviour began in the 1950s when researchers discovered that damage to the lateral hypothalamus in rats caused a condition called aphagia. Researchers also found that stimulation of the LH elicits feeding behaviour. These opposing effects of injury and stimulation led researchers to conclude that they had discovered the ‘on switch’ for eating behaviour. A neurotransmitter found in the hypothalamus called neuropeptide Y (NPY) is particularly important in turning on eating. When injected in the hypothalamus it caused feeding to begin, even when satiated (Wickens 2000). Repeated injections of NPY into the hypothalamus produced obesity in just a few days (of rats) (Stanley et al 1986).
  • LH is activated by low blood glucose
  • Activation results in feelings of hunger
  • This triggers a search for and consumption of food (on switch)

The Ventromedial Hypothalamus:

Researchers also found that damage to the ventromedial hypothalamus (VMH) caused overeating, leading to a condition called hyperphagia. Similarly, stimulation of this area inhibited feeding. This led researchers to conclude that the VMH signals ‘stop eating’ and is therefore the ‘off switch’. This is likely to be a result of the many glucose receptors in this area.

  • VMH is activated by high blood glucose
  • Activation of VMH results in feeling od satiation
  • This triggers ‘stop eating’ (off switch)
  • Damage to the VMH also tends to damage the paraventricular nucleus
  • Damage to the PVN alone may cause cravings.


Research has found that NPY has an important role in eating behaviour, this could explain real world situations of why overweight people continue to eat too much. It could be because their brain produces NPY in excessive amounts, telling the individual that they are constantly hungry. However, recent research in Canada by Yang et al (2008) has shown that NPY is also produced by abdominal fat. The researchers suggest that this leads to a vicious cycle where NPY produced in the brain leads to more eating and the production of more fat cells which leads to an increased production of NPY and so on. Yang believes that by targeting overweight individuals with this problem with drugs that turn of NPY production, they can prevent obesity. Therefore the research into neural mechanisms has real world benefits of helping those with obesity.

There are limitations with the view that the LH served as an ‘on switch’ for eating. For example, damage to the LH caused deficits in other aspects of behaviour rather than just hunger. Also, more recent research has shown that eating behaviour is controlled by neural circuits that run throughout the brain, and not just by the hypothalamus. Furthermore, recent research on NPY has cast doubt on whether its normal function is to influence feeding behaviour, as illustrated by Marie et al (2005) in mice. They found no subsequent decrease in feeding behaviour, suggesting that the hunger stimulated by NPY injections may actually be an experimental artefact, in that the flood of NPY during experimental manipulations could cause behaviour not like that caused by normal amounts of the neurotransmitter. Therefore, it may be a result of the experiment.

There is support for the role of the ventromedial hypothalamus from early researchers for example who found that lesions or damage to the VMH resulted in hyperphagia and obesity in a number of different species, including humans, concluding the VMH as the ‘satiety centre’ in eating behaviour. However, Gold (1973) found that lesions restricted to the VMH alone did not result in hyperphagia and only produced overeating when they included other areas, such as the PVN. Alternatively, subsequent research has failed to replicated Gold’s findings, with most studies showing that, compared to lesions in other brain areas such as the PVN, animals with VMH lesions ate substantially more and gained substantially more weight.


Leptin (fat cell hormone) is shown to be involved in sending signals to the brain to control hunger when body fat levels are high. Ghrelin ( stomach hormone) has been shown to send hunger signals. It is secreted by the mucous membrane of an empty stomach and, it has been suggested, stimulates appetite by inhibiting the activity of vagus nerve fibres. Its selection stops when food is eaten (Berthoud and Morrison 2008). It is an important hormone in indicating whether or not we are hungry.

Leptin leads to a decrease in appetite and increase in energy expenditure. Leptin is an  adiposity signal to the brain as it is secreted in direct proportion to the amount of fat stored in fat cells. (Therefore, the leaner you are, the less cells, the fatter, the more there are.) An increase in fat cells means an increase in the secretion of Leptin.


There is research support for the role of Ghrelin  in controlling eating behaviour. Lutter et al (2008) identified Ghrelin as an important hormone in indicating whether we are hungry or not, as Ghrelin is released by an empty stomach where it travels to the brain, indicating that we are hungry. However, the researchers also suggest that the hormone is important in our mood. They starved mice for four days and as a result their Ghrelin increased due to their empty stomachs. Compared to the mice who were allowed to eat freely, the hungry mice showed more anxiety and signs of depression when carrying out tasks such as maze running. They found the same result when they increased Ghrelin levels by making he mice stressed. These finings suggest that food, hunger, stress and anxiety are all somehow associated.

There is growing evidence that neural pathways in the hypothalamus are particularly sensitive to the action of leptin. Mayer and Thompson (1967) found that traumas to, or tumours of the VMH (which is sensitive to leptin) can cause hyperphagia and also obesity. Furthermore, there is evidence for the importance of leptin as an adiposity signal to the brain. For example, mice were studied who did not produce leptin or had a genetic mutation that interfered with the function of its receptors. Characteristically, these animals consume excessive amounts of food and become extremely obese (Zhang et al 1994).

Evidence suggests that hunger and eating may not be under purely neural control. Lutter et al (2008) illustrated through the body’s release ghrelin that it may be linked to stress, as its part of the body’s natural defence. However, ghrelin also boosts appetite, leader to increased comfort-eating, suggesting that blocking the body’s response to it may help people with a tendency to comfort eat control their weight. Alternatively, this approach might be problematic as it would reduce ghrelin’s beneficial effects as part of the body’s response to stress.