Outline and evaluate the role of neural and hormonal mechanisms in controlling eating.
Different components of the brain, such as the neurons, neurotransmitters and hormones,
influence eating behavior. The hypothalamus is referred to as the ‘hunger centre’ of the
brain and is involved in maintaining homeostasis. Acting like a ‘thermostat’ to initiate or stop
eating behavior. Different areas of the hypothalamus are responsible for different aspects of
hunger and satiation feelings. Glucose-sensing neurons in the hypothalamus detect
fluctuations in blood glucose concentrations, which act as the bodies main source of energy.
These levels can then be regulated by the hypothalamus influencing hormones such as
insulin and glucagon, secreted by the pancreas. The neural mechanism for controlling food
intake is located within the hypothalamus and works like an ‘on switch’ for feeling hungry,
this is the lateral hypothalamus (LH). On the other hand the ventromedial hypothalamus
(VMH) works like an ‘off switch’, inciting feeling of satiety and fullness. This works on a
feedback received from the stomach via hormone secretions. In Reeves & Plum’s case study,
a woman who’s weight more than doubled in a year, was found to have a tumor on her VMH
in a post-mortem exam. This caused the normal ‘stop eating’ function to fail.
The dual-centre model of eating details this. The LH is activated when glucose levels fall
below a certain level and this causes the individual to become hungry. A neurotransmitter
called neuropeptide U (NPY) is secreted and this increases hunger and reduced physical
activity. Once glucose levels rise above a set point, activity in the VMH is triggered and LH
activity is inhibited which make a person feel full and stop eating. Ghrelin is a hormone
released from the stomach which stimulates the hypothalamus to increase appetite and
stimulate eating. The concentration of ghrelin in our blood rises before we eat and falls after
a meal before progressively rising again which indicates to us that we are hungry. Leptin is a
fat hormone produced in fat cells and released into the blood to signify to the hypothalamus
to reduce appetite. Levels of leptin increase with fat levels, which are detected by VMH,
acting as a an appetite suppressant to contribute to satiety. Unlike ghrelin, leptin acts as a
long-term signal indicating the amount of fat stored in the tissue. For example, if someone is
not eating enough and losing body fat as a consequence, the amount of leptin produced
drops. The body interprets this as a lack of energy (calories) which in turn stimulates hunger
triggering us to eat.
Research has aided the treatment of obesity and anorexia. This is due to a better
understanding of the neural and hormonal mechanisms controlling eating behavior. Licinio
et al (2004) studies a rare genetic condition whereby individuals are unable to produce
leptin naturally. This condition is associated with severe obesity. There was a reduction of
food intake of 49% when given leptin-replacement therapy over 18 months. The successes
of this method to treatment allows huge financial savings for the NHS due to reduced
volume of patients with diet related illnesses such as coronary heart disease. Costs like these
are estimated at around £6bn annually in the UK. Life expectancy and quality of life of
individuals is also able to be increased, increasing welfare and productivity. Therefore there
are good practical applications to understanding neural and hormonal mechanisms in eating.
The control of eating behaviors is a straightforward account in the dual-centre model.
Research continues to reveal more neural and hormonal influences on eating behavior. Even
putting social and cultural factors to one side, the biological contributions are numerous.
Different components of the brain, such as the neurons, neurotransmitters and hormones,
influence eating behavior. The hypothalamus is referred to as the ‘hunger centre’ of the
brain and is involved in maintaining homeostasis. Acting like a ‘thermostat’ to initiate or stop
eating behavior. Different areas of the hypothalamus are responsible for different aspects of
hunger and satiation feelings. Glucose-sensing neurons in the hypothalamus detect
fluctuations in blood glucose concentrations, which act as the bodies main source of energy.
These levels can then be regulated by the hypothalamus influencing hormones such as
insulin and glucagon, secreted by the pancreas. The neural mechanism for controlling food
intake is located within the hypothalamus and works like an ‘on switch’ for feeling hungry,
this is the lateral hypothalamus (LH). On the other hand the ventromedial hypothalamus
(VMH) works like an ‘off switch’, inciting feeling of satiety and fullness. This works on a
feedback received from the stomach via hormone secretions. In Reeves & Plum’s case study,
a woman who’s weight more than doubled in a year, was found to have a tumor on her VMH
in a post-mortem exam. This caused the normal ‘stop eating’ function to fail.
The dual-centre model of eating details this. The LH is activated when glucose levels fall
below a certain level and this causes the individual to become hungry. A neurotransmitter
called neuropeptide U (NPY) is secreted and this increases hunger and reduced physical
activity. Once glucose levels rise above a set point, activity in the VMH is triggered and LH
activity is inhibited which make a person feel full and stop eating. Ghrelin is a hormone
released from the stomach which stimulates the hypothalamus to increase appetite and
stimulate eating. The concentration of ghrelin in our blood rises before we eat and falls after
a meal before progressively rising again which indicates to us that we are hungry. Leptin is a
fat hormone produced in fat cells and released into the blood to signify to the hypothalamus
to reduce appetite. Levels of leptin increase with fat levels, which are detected by VMH,
acting as a an appetite suppressant to contribute to satiety. Unlike ghrelin, leptin acts as a
long-term signal indicating the amount of fat stored in the tissue. For example, if someone is
not eating enough and losing body fat as a consequence, the amount of leptin produced
drops. The body interprets this as a lack of energy (calories) which in turn stimulates hunger
triggering us to eat.
Research has aided the treatment of obesity and anorexia. This is due to a better
understanding of the neural and hormonal mechanisms controlling eating behavior. Licinio
et al (2004) studies a rare genetic condition whereby individuals are unable to produce
leptin naturally. This condition is associated with severe obesity. There was a reduction of
food intake of 49% when given leptin-replacement therapy over 18 months. The successes
of this method to treatment allows huge financial savings for the NHS due to reduced
volume of patients with diet related illnesses such as coronary heart disease. Costs like these
are estimated at around £6bn annually in the UK. Life expectancy and quality of life of
individuals is also able to be increased, increasing welfare and productivity. Therefore there
are good practical applications to understanding neural and hormonal mechanisms in eating.
The control of eating behaviors is a straightforward account in the dual-centre model.
Research continues to reveal more neural and hormonal influences on eating behavior. Even
putting social and cultural factors to one side, the biological contributions are numerous.
