Biological aspects of eating behaviours

• Homeostasis:

  • Blood glucose is important for turning hunger on and off- it is a biological indicator.
  • When blood glucose is high= satiety
  • When blood glucose is low= hungry
  • This is all detected by the hypothalamus
• Neural:

  • LH- Lateral Hypothalamus (skinny), makes you feel hungry (feeding centre)
  • VMH- Ventramedial Hypothalamus (fat) and PVN- Paraventricular nucleus (satiety centre).
• Neural Mechanisms- hypothalamus:

  • Anand & Brobeck lesioned rats' lateral hypothalamus (LH) which led to the loss in feeding (aphagia). This area of the brain was named the 'feeding centre'. As the LH no longer signalled the feeling of hunger.
• Neural Mechanisms- hypothalamus:

  1. However, not that straight forward as damage to the LH can actually influence many other behaviours such as thirst & sex, rather than hunger alone. Also, more recent research has suggested that hunger is controlled by neural circuits that run throughout the brain and are not limited to just significant & important role in the control of hunger, it would be over-simplifying it to call if the 'feeding centre' of the brain.
• Neural Mechanisms- Hypothalamus:

  2. Hetherington & Ranson lesioned rats hypothalamus' (VMH) and showed that they became obese. This was named the 'satiety centre'. Rats became obese due to the VMH not signalling satiation, therefore they continued to eat past their physical requirements (hyperphagia). The VMH= closely linked to PVN through nerve fibres and it is now thought that damage to the PVN alone can cause hyperphagia. The PVN is thought to detect the need for specific nutrients and therefore responsible for cravings.
• Evaluation of neural mechanisms- strength:

  • Hetherington & Ranson lesioning rats hypothalamus' provides support for the role of the VMH in controlling satiation, damage to the VMH in humans has also been linked to hyperphagia- has been demonstrated numerous times in studies of many different species.
• Evaluation of neural mechanisms- weakness:

  • Study relies on evidence from use of non-human animals, so validity questioned when it comes to applying the results to humans- motivations & drives of hunger & satiation in a rat are likely extremely different to that of a human, eg human in office job may have a specific hour of day to eat lunch- regardless of hunger level/ satiation. Humans have more complex social & cultural influences like eating meals together as family or group of friends. Again, this will impact what & how much we eat-factors you would not expect to affect a rat.
• Role of ghrelin:

  • Ghrelin is a hunger hormone that is released by stomach in proportion with stomach emptiness.
• When there is a lot of ghrelin in the blood, it activates the LH to tell us that we feel hungry.
• Support for the role of ghrelin:

  • Wren et al in 2001
  • Did a randomised double-blind study of 9 healthy volunteers, & gave either intravenous saline or ghrelin to PPs one week and the same again following week, but PPs did the opposite condition (ABBA- counterbalancing). After the infusion, they were offered a free choice buffet & the amount they took & ate was measured.
  • PPs who received ghrelin ate more than those who received saline- with a mean difference of 28%.
  • The sample size was small- this is a negative.
• Leptin:

  • Leptin is released from adipocytes into blood & travels to hypothalamus and acts as a satiety signal to stop us eating.
  • Leptin is a long-term signal linked to the fat reserves.
• Leptin has two major functions: 1. Activate the VMH 2. Increase sympathetic nervous system to use fat reserves as energy.
• Evaluation for the role of leptin:

  • Strength- Smith et al, injections of leptin made a strain of genetically obese mice eat less and become a normal weight (they were missing a gene that produces hormone leptin).
  • Questioned why not just inject leptin into obese people to 'help them lose weight'. May expect humans to have low levels, hence they eat too much, true for some cases like it was genetic for mice, but for the majority, leptin levels are hormonal or even high.
  • The problem being, similar to type 2 diabetes, brain has stopped responding to the hormone over time due to over-exposure of it.
• Dual Centre Model:

  • Eating causes: leptin increase, increase in blood glucose, ghrelin decrease
  • This activates ventromedial hypothalamus (VMH) which 'turns off' eating
  • This causes satiety (being full)
  • This causes us to stop eating
  • This causes leptin decrease, decrease in blood glucose, ghrelin increase
  • This activates the lateral hypothalamus (LH) which 'turns on' eating
  • This causes hunger
  • This then causes eating
• Evaluation of Dual Centre Model:

  • Strength- there's research support from the studies of VMH & LH
  • Strength- there's research support from Wren et al & Ghrelin
  • Strength- there's research support from Smith et al & Leptin
• Evaluation from Dual Centre Model- weakness:

  • It's reductionist- oversimplifies complex human behaviour & ignores the role of learning, evolution, social context etc. Many other things influence our eating habits- Easter, Birthdays etc.