Involved in maintaining homeostasis – balancing bodily processes within certain limits
Homeostasis regulates the level of glucose in the blood
Glucose is the most basic form of sugar and the body’s main energy source
Glucose-sensing neurons in the hypothalamus can detect changes in glucose levels
The hypothalamus can then regulate glucose levels by releasing either insulin or anti-insulin hormones
Dual-centre model of eating:
This model suggests that two structures of the hypothalamus provide homeostatic control:
Lateral Hypothalamus (LH)
The ‘on switch’ for hunger
Ventro-medial hypothalamus (VMH)
The ‘off switch’ of eating behaviour
Lateral hypothalamus- LH: on switch
Contains cells that detect glucose levels
LH is activated when glucose levels fall below certain level
This causes individual to become hungry – increases motivation to eat
The neurotransmitter NPY is also linked to the LH. It is a powerful stimulant of hunger. Rats injected with NPY directly into hypothalamus eat excessively and become obese
Ventro-medial hypothalamus (VMH) - off switch
Eating food provides glucose, so blood glucose levels increase
These glucose levels are detected by cells in the VMH
The VMH is activated if glucose levels pass a set point.
This also stops the LH from working so you stop eating
The individual feels full and stops eating
Damage to the VMH is linked to overeating past the point of satiety (feeling full)
Research found that tumour on woman’s VMH led to her weight doubling in two year
Hormonal mechanisms - role of ghrelin:
Ghrelin is a hormone secreted by the stomach
It’s closely related to how empty our stomach is
More ghrelin is released the longer we go without food
When the hypothalamus detects ghrelin levels have passed a certain point, NPY is released which stimulates hunger and motivates you to eat
Hormonal - role of leptin:
Leptin is a hormone secreted by fat cells
It is an appetite suppressant (stops you feeling hungry)
Leptin levels in the blood increase along with fat levels
This increase is detected by the brain by the VMH
Once levels increase beyond a certain point, the individual stops eating and feels full
Research shows that a rare genetic conditions, in which individuals are unable to produce leptin naturally, is associated with severe obesity
Neural and hormonal mechanisms :
A03:
A strength of the dual-centre model is that there is research to support it from studies on rats
Research shows that by lesioning the VMH of rats, they became hyperphagic (they would overeat) and eventually became severely obese
When researchers have lesioned the LH of rats, the outcome was aphagia (not eating)
This supports the model because it suggests that the LH is the ‘on switch’ for eating and the VMH is the ‘off switch’
A03:
A limitation of dual-centre model explanations of eating behaviour is that it is oversimplified
Valassi et al. (2008) point out that research continues to reveal more neural and hormonal influences on eating behaviour
For example, a hormone called CCK produced in the intestine may be an even more powerful appetite suppressant than leptin
Therefore, the dual-centre model does not accurately reflect the true complexity of how eating behaviour is controlled
A03:
A limitation of neural and hormonal explanations in the control of eating behaviour is that they ignore social and cultural factors
The LH (on switch) only identifies drops in glucose levels in ‘emergency’ conditions when energy levels are severely low
Normal meal onset is much less controlled by neurochemical factors and is usually initiated by social and culture factors related to lifestyle (e.g. Meal times)
Therefore, a purely biological approach to understanding eating behaviour tends to ignore potentially important non-biological factors that may be more influential
A03:
A strength of research into neural and hormonalmechanisms in eating behaviour is that this increased understanding can lead to treatments for obesity and anorexia
For example, the fact that researchers know that leptin suppresses the appetite means if someone has low leptin levels they can provide treatment to regulate leptin levels
This means they can treat individuals who may have genetically determined leptin deficiencies and treat their obesity
This would help the wider economy as it would reduce health costs for the NHS regarding health problems linked to obesity