The document discusses biological explanations for eating behavior, focusing on the role of neural mechanisms and homeostasis. It describes how the hypothalamus, specifically the lateral hypothalamus (hunger center) and ventromedial hypothalamus (satiety center), regulate eating through feedback loops involving glucose levels and hormones like ghrelin and CCK. Evidence from studies on rats and humans supports the dual-center theory, though some findings have limitations and physiological drives can be overridden by other factors.

1. Biological explanations to
eating behaviour
Role of neural mechanisms
Evolutionary explanations

2. Answer the following -
• Did you have breakfast this morning?
• Why did you stop eating the food?
• What are your favourite foods? Why?
• How do you feel after a large meal?

3. Role of neural mechanisms
in eating behaviour
• Eating behaviour = ingestive behaviour
• Homeostasis
– if we are hot – we sweat
– if we are dehydrated – thirsty
– If we need food – hunger
• Homeostasis is maintained via a negative feedback
loop: this assumes that all body variables have a set
point (or range)
• The digestive tract and the hypothalamus play a
significant role in homeostasis in eating behaviour.
The process by which the
body maintains a constant
internal environment

4. Homeostasis
• 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!

5. GLUCOSE
LEVELS
Decrease in glucose
levels
As glucose levels decrease hunger levels increase
Increase in glucose levels means satiation reached.
Activates this area – feel
hungry.
Individual
searches for
food and eats
Increase in glucose
levels
Activates this area –
feeling of satiation –
inhibits further feeding

6. Body weight
• Each individual has a set point and their
weight is regulated around that set point
• Body regulates hunger based possibly on
– Fat stores
– Glucose levels
– Cellular energy

8. Dual-Centre Theory of feeding
behaviour
• 2 areas of the hypothalamus involved in
eating behaviour
– Ventro Medial Hypothalamus (VMH) as a "satiety
centre" = full up!
– Lateral Hypothalamus (LH) as a "Hunger centre".
• NOTE: VMH and LH are also called VMN and
LN sometimes

9. Dual-Centre Theory of feeding behaviour

10. The lateral hypothalamus
• Contains the
feeding centre
• This initiates eating.
• It responds to
decreased blood
glucose and
increase in ghrelin a
hormone released
from the stomach
when it is empty.

11. Ventro medial
hypothalamus
• Contains the satiety
centre.
• This inhibits eating
behaviour when we are
full.
• Responds to
– an increase in blood
glucose,
– a decrease in ghrelin and
to release of CCK, a
hormone released when
food is detected in the
duodenum
– leptin a long term satiety
signal released by fat
cells.

12. The hypothalamus – research
evidence comes from…
• Case studies -patients with tumours in the
hypothalamus tend to become obese
• Methods used to research hypothalamus
– Lesioning in animals
– Investigation of feeding
patterns after brain damage
– Effects of neurotransmitters
introduced into parts of brain
– Impact of drugs on eating
– Use of fMRI (Functional
MRI scans)

13. Role of hypothalamus - evidence
• Aphagia (failure to eat when hungry) can be
caused by damage to the LH.
• Rats whose VMH had been lesioned developed
overeating and obesity
• Wickens (2000) Rats: Injected with NPY = became
obese!
• However, Gold (1973) found that lesions
restricted to the VMH alone did NOT result in
hyperphagia and only produced overeating when
they included other areas.

14. Hetherington and Ranson (1942)
The VMH Rat
Made lesions on an area of the VMH
(part of the hypothalamus) in rats.
Caused the rats to overeat and be
dramatically obese.
This lesion destroyed a centre that
is vital for the control of feeding
behaviour. Its destruction led to an
increase in feeding and body weight.
It was assumed that this was a
satiety centre – which is normally
activated when the animal is full at
the end of the meal.
Satiety – the feeling or
state of being fully
satisfied. Satiety centres
function is to stop feeding

15. The role of the hypothalamus -
evaluation
Is it really the ‘ON’ switch??
Damage to LH also affects thirst and sex drives.
Recent research suggests eating is more widely
spread
It is thought that the hypothalamus plays a role but
it is not solely responsible

16. Ao2 Role of ghrelin - evidence
• Cummings (2004) monitored PPs’ ghrelin levels every 5 minutes
• PPs had to assess their level of hunger every 30 mins.
• In 5 of the 6 participants there was a significant correlation between
ghrelin levels, emptiness of the stomach and hunger.
• The results support the theory of the role of ghrelin in eating
behaviour
• In addition ghrelin injections result in increased food intake in
animals
• Gastric bands used in treating obesity reduce ghrelin secretion.
• However: The study used a small sample limiting how far the
findings can be generalised.
• It is likely that the participant’s subjective judgements of hunger
were influenced by expectations of food based on meal times
(cultural factors rather than biological factors)

17. Role of neurotransmitters
Neurotransmitters
that increase food intake
• Neuropeptide Y–Rats injected with neuropeptide Y
continue eating large amounts of food even
when full
– It also seems to cause a preference for carbohydrates

18. Ao2 Supporting evidence:
Marie et al (2005)
role of neuropeptide Y
• Injections of NPY in mice cause hunger...
• However:
Genetically manipulated mice so that they did
not produce neuropeptide Y. Found no
subsequent decrease in their feeding
behaviour!!

19. Neurotransmitters and modulators
that decrease food intake
• (CCK) –released into bloodstream during meals
– Causes reduction in appetite.
– Suppresses weight gain

20. Evaluation of neural mechanisms and
eating behaviour
++Insight into brain chemicals – could be used to develop
medical interventions to help change what we eat
+Provides explanation of some differences in eating behaviour
+Studies such as those involving lesions to the LH and VMH in
rats have supported the role of the hypothalamus in
regulating eating behaviour
+Studies involving electrical stimulation of these centres have
confirmed their role in feeding and satiety.
+Such studies provide sound scientific evidence but there is
the issue of extrapolating finding from rats to humans.
+Research evidence
• Cumming et al, 2004 - ghrelin

21. Cont.
-Reductionism: focus exclusively on biological aspects of hunger and
satiety
-Biological determinism: focus exclusively on the role of nature and no
space left to choice and cultural and social influences
-there is substantial and convincing evidence that social, cultural and
psychological factors affect our eating behaviours as is evident from
psychological explanations of eating disorders
-Use of animals in research implies a lack of generalisability- we must
be cautious of findings
-Highly controlled lab experiments may lack ecological validity
-Physiological drives can be overriden (eg desire to lose weight; dislike
of certain foods; fear of losing control; social cues to continue
eating; food availability)

22. • Ethical issues with non-human animalsissues
• Is the biological approach reductionist?
• Free will vs determinism (can biological drives
be overridden?)
debates
• You contrast explanations to eating behaviour
• Biological,
• Learning (Behaviourist)
• Cognitive
• Social
approaches