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

2. Role of neural mechanisms in eating behaviour
Eating behaviour = ingestive behaviour
Homeostasis
if we are hot – we sweat
if we are dehydrated – thirsts
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 eating behaviour.
The process by which the body maintains a constant internal environment

3. 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 (lipostatic hypothesis)
Glucose levels (glucostatic hypothesis)
Cellular energy – adenosine trisophate (ATP) is a product of the breakdown of macronutrients (fats, carbohydrates and proteins) and considered important for the regulation and maintenance of homeostasis

4. The hypothalamus
Patient 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
Magnetic Resonance Imaging)

5. Dual-Centre Theory of feeding behaviour
2 areas of the hypothalamus involved in eating behaviour
Ventro Medial Hypothalamus (VMH) as a "satiety center"
Lateral Hypothalamus (LH) as a "Hunger center".
NOTE: VMH and LH are also called VMN and LN (N stands for NUCLEUS!!!)

6. Dual-Centre Theory of feeding behaviour
Hunger -> eating starts
Increase in blood glucose, decrease in ghrelin release
VMH satiety centre activated
Satiety – feeding stops...
...Feelings of declining nutrient levels
LH feeding centre activated

7. The lateral nucleus of the 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.

8. Ventro medial nucleus (VMN)of the 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 CCK, a hormone released when food is detected in the duodenum
leptin a long term satiety signal released by fat cells.

9. 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
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 such as the parvoventricular nucleus!
However, subsequent research has failed to replicate Gold’s findings...

10. Role of ghrelin - evidence
Cummings et al (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
AO3: The study used a small sample limiting how far the findings can be generalised and 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)
Ghrelin injections result in increased food intake in animals
Gastric bands used in treating obesity reduce ghrelin secretion.

11. Role of neurotransmitters
3 main neurotransmitters are found to influence appetite:
Catecholamines (dopamine, norepinephrine, and epinephrine): sympathomimetic "fight-or-flight" hormones that are released by the adrenal glands in response to stress
Serotonin: found extensively in the gastrointestinal tract, it activates the muscles used for feeding. Is also associated to aggression and “happiness”
Peptides: short polymers formed from the linking, in a defined order, of α-amino acids

12. Neurotransmitters that increase food intake
Norepinephrine (NE) – injections of NE in hypothalamus
can stimulate feeding if injected into the paraventricular nucleus
Can reduce feeding if injected into the perfornical area
Neuropeptide Y (33 amino acid peptide)– high concentrations in the paraventricular hypothalamus and perfornical hypothalamus.
Rats injected with neuropeptide Y continue eating large amounts of food even when full
It also seems to cause a preference for carbohydrates
Galanin (29 amino acid peptide)- particularly found in the paraventricular hypothalamus.
Injections of galanin into rats cause an increase of food intake and a preference for fats rather than carbohydrates

13. Marie et al (2005) role of neuropeptide Y
Genetically manipulated mice so that they did not produce neuropeptide Y
Found no subsequent decrease in their feeding behaviour!!
However, injections of NPY cause hunger...
...May be due to an experimental artefact, because of the unexpected intake of NPY in experimental conditions (through injection)

14. Neurotransmitters and modulators that decrease food intake
Cholecystokinin (CCK) – endogenous 33 amino acid peptide that is released into bloodstream during meals
Causes reduction in appetite and satiation
Suppresses weight gain
Bombesin – peptide found to reduce food intake in rats
Corticotropin-Releasing Hormone (CRH) – 41 amino acid peptide produced in the paraventricular hypothalamus and other regions of brain that reduces food intake
Serotonin (5HT) – neurotransmitter which decreases food intake.

15. KEY WORDS – matching exercise
Homeostasis
Negative feedback loop
Set point
Lipostatic hypothesis
Glucostatic hypothesis
adenosine trisophate (ATP)
Lateral Nucleus
Ventro Medial Nucleus
Ghrelin
CCK
Leptin
Neuropeptide Y (NPY)

16. Impact of drugs on eating behaviour
Nicotine – decreases food intake.
Smokers generally weigh 3 kg less than non-smokers (US Department of Health and Human Services, 1990)
Ogden (1994) some dieters use smoking as a weight-loss strategy and those who stop smoking increase their calorie intake, especially from sweet foods
Amphetamines - have a dramatic suppressant impact on both subjective hunger and food intake
Marijuana – increases hunger and food intake

17. Impact of drugs on eating behaviour
Alcohol – influences food intake in contradictory ways
Some studies indicate it can have a weak inhibitory effect
Others show it can stimulate hunger
Anti-psychotic drugs – both lithium and chloropromazine cause considerable weight gain
Tricyclic anti-depressants – cause cravings for sweet food and weight gain
Selective Serotonin Reuptake Inhibitors (SRRIs) – used for patients with depression, might promote weight loss...

18. Impact of drugs on eating behaviour
Analgesics – used for pain relief
Naloxone can trigger deceased food intake
Morphine has also a weak depressant effect on appetite
Appetite-suppressant drugs
have a consistent depressant effect on hunger and reduce food intake
Have been removed from the market because linked to heart problems

19. Does it increase or decrease hunger?
Morphine
Anti-psychotic drugs
Tricyclic anti-depressants
Selective Serotonin Reuptake Inhibitors (SRRIs)
Naloxone
Alcohol
Appetite-suppressant drugs
DECREASE
INCREASE
INCREASE
DECREASE
DECREASE
BOTH!
DECREASE

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

21. Evaluation of neural mechanisms and eating behaviour
+Reflection on people’s experience of hunger\satiety
+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, ghrelin

22. 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 lack of generalisability -Highly controlled lab experiments may lack ecological validity -Physiological drives can be overriden (eg desire to loose weight; dislike of certain foods; fear of losing control; social cues to continue eating; food availability)

23. Outline and evaluate the role of neural mechanisms involved in controlled eating and satiation(25 marks)
AO1:
Intro: homeostasis; negative feedback loop; set point
Lipostatic and glucostatic hypotheses
describe dual centre model (diagram will be also credited);
Role of LH and VMH;
neurotransmitters and hormones involved in eating regulation (ghrelin; CKK; leptin; norepinephrine; Neuropeptide Y...)
AO2:
research evidence for effects of hormones + contrasting evidence (eg Cummings et al, 2004 ghrelin AND Marie et, 2005 NEY al OR Gold, 1973 VMH lesioning) (4)
Impact of drugs (eg alcohol, anti-depressants...) on appetite confirms biological basis of eating behaviour
I: ethics with non-himan PPs; reductionism
D: free will vs determinism; nature vs nurture
A: biological vs social, behaviourist, psychodynamic
AO3
Lack of ecological validity
Lack of generalisability
Sampling issues (eg Cummings et al, 2004)