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Biological explanations of eating behaviour. Keywords you will come across in this topic. Satiation Aphagia Leptin Hyperphagia Neuropeptide Y Lateral hypothalamus Ventromedial hypothalamus Paraventricular nucleus Amygdala Inferior frontal cortex.

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keywords you will come across in this topic
Keywords you will come across in this topic.
  • Satiation
  • Aphagia
  • Leptin
  • Hyperphagia
  • Neuropeptide Y
  • Lateral hypothalamus
  • Ventromedial hypothalamus
  • Paraventricular nucleus
  • Amygdala
  • Inferior frontal cortex
do you remember this phrase from gcse science homeostasis
Do you remember this phrase from GCSE science..Homeostasis
  • It involves mechanisms that can detect and correct.
  • Detect – check whether the body has enough nutrients (internal environment)
  • Correct – restore the body to its optimal state.
  • Body evolved 2 separate systems in order to cope with the time lag between restoring equilibrium and body registering their effect.
  • Turning eating on and turning eating off!
the role of neural mechanisms involved in controlled eating satiation
The role of neural mechanisms involved in controlled eating & satiation

You should understand………..

  • Hunger is activated by many cues.
  • All animals have a motivation to eat… these motivations increase as energy levels decrease.
  • An imbalance occurs when the energy expended exceeds the amount consumed…this is signalled in the brain in different ways.
the hypothalamus
The Hypothalamus.

The hypothalamus is responsible for all of these bodily functions.

A bit like the fat controller!!

hunger pangs
Hunger pangs?

Water + balloons =?

Stomach or neural mechanism?

What do balloons have to do with it?

What evidence is this based upon?

Who is Washburn & cannon?

karl lashley 1938
Karl Lashley (1938)
  • Mr Lashley was the first psychologists to suggest that stomach contractions were more of a strong incentive rather than indication of hunger.
  • Hunger is not just a reflex to a empty stomach

Let’s pause for thought!!!

Q: So if hunger is not a reflex what is it??

karl lashleys research
He used rats to support his growing belief that neural mechanisms are involved in decision making.

These were hungry rats!

He cut out different areas of the brain to see the effect on their ability to negotiate a maze successfully and reach the food placed at the exit as a reward.

Karl Lashleys research
lashleys findings
Lashleys findings.
  • He discovered how vital the role of the hypothalamus is in playing a part in the regulating of food intake.
  • In particular the lateral hypothalamus, this was identified as the main hunger centre.
  • The ventromedial hypothalamus as the main satiety centre.
  • After the lesions to the lateral hypothalamus, animals stopped eating spontaneously, and the reverse occurred after the lesions to the ventromedial hypothalamus.
so what does this tell us
So what does this tell us???
  • The hypothalamus is a very complex part of the brain.
  • It contains a number of different types of specialised nerve cell and controls different physiological functions.
  • There is a further section named the arcuate nucleus...this too plays a vital role.
there s more
It contains a several different nerve cells, one of which makes a neuropeptide (called neuropeptide Y or NPY).

Neuropeptides are small proteins that are encoded by genes- they serve as chemical messengers between neurons and the brain.

There’s more!!!!!!
so what is a peptide an example
The fat hormone leptide is an example of a peptide that is secreted from fat cells into the blood and signals the brain (via hypothalamus) that caloric storage is high.

When you do not eat sufficient amounts of food fat storage is used up to fuel the body and the fat cells cease to secrete and these levels fall in the blood.

The hypothalamus detects this drop and & interprets the drop in leptin as lack of calories and generate the feeling of hunger.

So what is a peptide…an example!

Leptide is

secreted.

Hypothalamus is

Signalled..

calories are

high enough.

Body ceases

to release

fat cells

Hypothalamus

detects this drop=feelings of hunger.

how do we know this
How do we know this???
  • Studies have shown individuals with leptin deficiency have ‘atypical’ eating behaviours.
  • They cannot control their eating and frequently become obese, injecting leptin can help them return to typical weight.

Be mindful…these cases are rare.

over to you ao2 or not ao2 that is the question
Over to you……….AO2 or not AO2, that is the question.
  • Zhang et al (1994)
  • Yang et al 2008
  • Kluver-Bucy syndrome
  • Homeostasis
  • Sakurai et al (1998)
  • Marie et al (2005)
  • Investigate these select pieces of research and apply them to the different mechanisms we have discussed so far.

How does each piece of research become an AO2 point.

What research does it support or refute.

other neuropeptides
Other Neuropeptides.
  • Agouti-gene-related peptide (AGRP) appears to signal hunger.
  • A rat that is food deprived has demonstrated levels of (NPY) and AGRP are...... increased in the brain.
  • If the rat is satiated and AGRP/NPY is injected into the rat what do you expect to happen?
  • He becomes ravenous.
so are the the same or different
So are the the same or different?

NPY

AGRP

Slow to increase during deprivation and slow to fall upon feeding.

A single injection of AGRP will cause a rat to overeat for several days

  • Increases levels rapidly food deprivation.
  • NPY injections induce feeding for a few minutes.
  • Gherlin is activated by NPY. A hormone that is secreted from a empty stomach..it’s concentration in blood falls after each meal and rises until the next.
glucose is another signal
Glucose is another signal
  • As glucose levels decrease hunger levels increase
  • Increase in glucose levels means satiation reached.
satiation
Satiation
  • Eating stops when satiation is reached. This occurs when the stomach muscles stretch and become distended by food.
  • Cholecystokinin (CCK) is secreted in the stomach during a meal and activates receptors.
  • These signals reach the hypothalamus and the ‘anorexigenic’ peptides are released.
set point hypothesis
Set point hypothesis
  • Everyone has a certain metabolic rate, a certain weight our bodies are set to, which determined by our hypothalamus, metabolism or rate at which we burn calories.
  • This point can change due to other factors (exercise). When we diet our leptin levels decrease and this causes hunger pangs to be triggered by the hypothalamus.
  • Thus the point maybe higher for obese people and lower for healthier people and thus is involved in many different aspects of eating behaviour.
overall evaluation
Overall evaluation.
  • Neural mechanisms still unclear
  • Influence of biological rhythms
  • Set point theory
  • Psychological hunger
  • Evidence for other biological theories.
  • Using these headings formulate at least two sentences for each heading to use as AO2 evaluation.