Title: Biological explanations of eating behaviour.
1- Biological explanations of eating behaviour.
2Keywords you will come across in this topic.
- Satiation
- Aphagia
- Leptin
- Hyperphagia
- Neuropeptide Y
- Lateral hypothalamus
- Ventromedial hypothalamus
- Paraventricular nucleus
- Amygdala
- Inferior frontal cortex
3 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!
4The 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 consumedthis is signalled in
the brain in different ways.
5The Hypothalamus.
The hypothalamus is responsible for all of these
bodily functions. A bit like the fat controller!!
6Hunger 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?
7Karl 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
Lets pause for thought!!! Q So if hunger is not
a reflex what is it??
8Karl 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.
9Lashleys 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.
10The breakdown of the hypothalamus
11So 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.
12Theres 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.
13So what is a peptidean example!
Leptide is secreted.
- 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.
Hypothalamus is Signalled.. calories are high
enough.
Body ceases to release fat cells
Hypothalamus detects this dropfeelings of
hunger.
14How 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 mindfulthese cases are rare.
15Over 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.
16Other 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.
17So are the the same or different?
- 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..its concentration
in blood falls after each meal and rises until
the next.
18Glucose is another signal
- As glucose levels decrease hunger levels increase
- Increase in glucose levels means satiation
reached.
19Satiation
- 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.
20Set 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.
21Overall 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.