neural mechanisms 2012

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Biological explanations of eating behaviour Specification: The role of neural mechanisms involved in controlling eating and satiation

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Page 1: Neural mechanisms 2012

Biological

explanations

of eating

behaviourSpecification:

The role of neural

mechanisms involved in

controlling eating and

satiation

Page 2: Neural mechanisms 2012

How do we know when it is time

to eat?

• Hunger is activated by both

environmental and biological

factors.

This topic looks at biological

mechanisms involved in

eating.

•What makes us feel hungry?

•What tells us to stop eating

when we are full?

Page 3: Neural mechanisms 2012

Neural mechanisms in eating

and satiation

Homeostasis

Humans, along with all

mammals are

homeostatic animals, (we are designed to run our

bodies in a constant state

of balance)

Involves mechanisms that detect both the

state of the internal environment (e.g. Level

of nutrients) and correct the situation to

restore that environment to its optimal state

Our eating behaviour is a prime example of

this internal balance in that it is clear from

research that we have a “Feeding” centre

in the brain activated when we are hungry

and a “Satiety” centre activated when we

are full.

The body has evolved two separate systems

(both involving the hypothalamus)

Turning eating ON

- Lateral hypothalamus

Turning eating OFF

- Ventromedial

hypothalamus

The Dual Feeding System!

Page 4: Neural mechanisms 2012

The control of eating and satiation

Among humans, glucose levels play the most

important part in producing feelings of hunger

**Hunger increases as glucose levels decrease**

**Satiation (fullness) increases as glucose levels

increase**

Decreasing glucose and

the Lateral Hypothalamus1. A decline in glucose levels

in the blood activates the

Lateral Hypothalamus.

2. Feelings of hunger

3. Individual searches for and

then consumes food

- Glucose levels rise again

Rising glucose and the

Ventromedial Hypothalamus1. A rise in glucose levels in the

blood activate the VMH

2. Feeling of satiation (fullness)

This inhibits further feeding

Page 5: Neural mechanisms 2012

LH + NPY seem to control eating behaviour

In the 1950’s...

• Researchers found that damage to

the LH in rats caused aphagia(a failure to eat when hungry)

• Stimulation of the LH caused the

animal to want to feed

Neuropeptide Y (NPY) was also

found to be important in turning

eating on.

- When injected into the

hypothalamus of rats, NPY caused

them to start feeding, even when they

were full!

It was

concluded

therefore that

the LH was the

„ON‟ switch for

eating

behaviour

Repeated injections of

NPY caused obesity in a

matter of days

(Stanley 1986)

Page 6: Neural mechanisms 2012

What does this suggest about the

neural mechanisms of the LH in

controlling eating behaviour?

* It suggests that the LH is the main feeding centre

in rats and that the LH triggers feeding in response

to signals from the body.

* It also suggests that NPY is also important in

triggering the feeding response.

* The LH and NPY therefore turn feeding ON! (not

off)

Page 7: Neural mechanisms 2012

AO1 – Neural mechanisms

involved in the control of eating....

LH NPYHigh levels of

Ghrelin

Cause Hunger

All switch eating ON

Page 8: Neural mechanisms 2012

AO2: An evaluation of the role of the LH

in eating behaviour

Damage to the LH causes deficits in other aspects of

behaviour (e.g. Thirst and sex). Therefore LH does not only

control hunger.

More recent research has shown that eating behaviour is

controlled by neural circuits that run through the brain, not

just the hypothalamus

This shows that although LH undoubtedly plays an important

role in the control of eating behaviour, it may not, as

previously thought, be the brain’s sole feeding centre

Sakurai et al, 1998

Page 9: Neural mechanisms 2012

AO2: An evaluation of the role of

Neuropeptide Y in eating behaviour

Recent research on NPY has cast doubt on whether its

normal function is to influence feeding behaviour

Marie et al (2005) genetically manipulated mice so that they

did not make NPY. They found no subsequent decrease in

their feeding behaviour

This suggests that the hunger stimulated by the injections of

NPY may actually be a result of the experimental artefact, in

that the flood of NPY given to the rats during the

experimental manipulations could cause behaviour not like

that caused by normal amounts of the neurotransmitter

This shows that the relationship between NPY and feeding

behaviour remains unclear. Which means that we do not

know everything “as yet” about brain mechanisms which

control feeding behaviour.

Page 10: Neural mechanisms 2012

Hormone - Ghrelin

• Ghrelin is a hormone that is released from

an empty stomach

• The amount of ghrelin released is directly

proportional to the emptiness of the

stomach

i.e. As the time from the last meal increases

and we feel hungrier, so ghrelin secretion

is increased

Ghrelin is the hunger signal

Page 11: Neural mechanisms 2012

Research into the role of

GhrelinCummings et al (2004)

A – To investigate changes in blood ghrelinlevels over time between meals

P – 6 male participants were allowed to eat lunch, ghrelin levels were monitored via blood samples taken every 5 minutes until the participant requested their evening meal. Participants assessed their degree of hunger every 30 minutes

F – Cummings found that ghrelin levels fell immediately after eating lunch and then slowly began to rise, peaking as participants requested their evening meal. In 5/6 participants ghrelin levels were closely correlated to their self-report feelings of hunger

C – The researchers concluded therefore that ghrelin directly reflects stomach emptiness and are closely related to subjective feelings of hunger.

Ghrelin therefore has a key role in appetite

signalling in humans

A03? IDEAs?

Page 12: Neural mechanisms 2012

EvaluationGhrelin

Further research conducted by Cummings (2006) has found

that injections of ghrelin increases food intake in both animals

and humans

This provides biological evidence of the link between the

hormone ghrelin and the beginning of eating, satiety and

overeating.

Cummings

(2004)

Sample

Bias?

Cummings

(2004)

Correlation?

Cummings

(2006)

Ethical

Issues

Cummings

(2004)

Ps were

isolated

from time &

social cues

Page 13: Neural mechanisms 2012

Debates: DeterministicApproaches: Biological

Ignores other explanations (e.g.

evolutionary explanation)

Also, don‟t forget..AO3.. How

- ExtrapolationIssues:

Reductionist

Ethical issues

Page 14: Neural mechanisms 2012

Question exercise

Outline the role of neural

mechanisms involved in

controlling eating behaviour

(8 marks)

Page 15: Neural mechanisms 2012

Mind map

Make sure you construct a

mind map to organise the

AO1; AO2; AO3 and IDEAs

for the role of neural

mechanisms involved in

eating behaviours

Page 16: Neural mechanisms 2012

The Ventromedial Hypothalamus• Researchers discovered that

damage to the VMH caused rats to overeat leading to a condition called hyperphagia.

• Stimulation of the VMH inhibits feeding

A02 - However...

Damage to the nerves passing

through the VMH causes damage

to another part of the

hypothalamus, the paraventricular

nucleus (PVN) – it is thought that

damage to the PVN alone causes

hyperphagia

It was

concluded

therefore that

the VMH was

the „OFF‟

switch for

eating

behaviour

A02

The PVN also

detects the specific

foods our body

needs (may be

responsible for

cravings)

Page 17: Neural mechanisms 2012

EvaluationVentromedial Hypothalamus

Extensive research has supported the finding that

lesions/damage to the VMH results in hyperphagia and

obesity

Shows that the VMH plays an important part in signalling to

an individual when it’s necessary for them to cease eating

Hetherington & Ranson conducted research and reported

that lesions to the VMH caused rats to become dramatically

obese

Supporting the idea that if the VMH (satiety centre) is

destroyed it can lead to uncontrolled eating

Page 18: Neural mechanisms 2012

EvaluationVentromedial Hypothalamus

Gold (1973) found lesions/damage to the VMH alone did not

result in hyperphagia and only produced over eating when

other areas (such as the PVN) was also damaged

Suggesting that the VMH doesn’t appear to control

hunger/satiety alone

However...

Further research has failed to replicate

Gold’s findings, demonstrating that

animals with VMH lesions ate

substantially more and gained more

weight compared to those with lesions

in other brain areas

The

reliability of

Gold’s

research

can be

questioned

Page 19: Neural mechanisms 2012

The role of Leptin

• Leptin is a fat hormone

• It is secreted into the blood stream to

signal to the brain (via the hypothalamus)

that calorie storage is high.

• Basically telling the brain that the body has

sufficient fat stored

The body releases more leptin as more fat is

stored – how should the body respond to this?

STOP EATING!

Page 20: Neural mechanisms 2012

Therefore..Low levels of Leptin

also cause us to feel hungry

* When people don’t eat enough food, fat is used

up, the fat cells cease to secrete leptin.

* Leptin levels in the blood fall – the

hypothalamus detects the drop in leptin levels

and generates a feeling of hunger to increase

eating.

In summary.........

Page 21: Neural mechanisms 2012

Support for the role of leptin in eating behaviour comes from

conducting experiments using ‘ob’ mice (a stain of mice that

are genetically obese).

Studies have demonstrated that these mice are missing the

gene that produces leptin. They therefore eat continually. (remember, low levels of leptin are thought to cause hunger)

Furthermore, injections of leptin into the ob mice stop them

eating so much and their weight eventually returns to normal

This shows that there appears to be a strong link in the

relationship between low levels of leptin and over-eating

AO2: An evaluation of the role of

Leptin in eating behaviour

Page 22: Neural mechanisms 2012

However, some

humans who are

overweight have a

leptin deficiency but

most actually have

increased levels of

leptin!

AO2: An evaluation of the role of

Leptin in eating behaviour

Page 23: Neural mechanisms 2012

Debates: DeterministicApproaches: Biological

Ignores other explanations (e.g.

evolutionary explanation)

Also, don‟t forget..AO3.. How

- ExtrapolationIssues:

Reductionist

Ethical issues

Page 24: Neural mechanisms 2012

General EvaluationThe role of neural mechanisms are still unclear,

exactly how ghrelin and leptin reach their targets in the brain is not fully clear, both are large peptides what do not cross the blood brain barrier easily

Influence of biological rhythms, research has shown that rats become more active and start to eat soon after darkness descends. This and similar rhythms are controlled by another area of the hypothalamus (the SCN)

IDEA - Alternative approach – what other factors influence your hunger levels everyday?

Page 25: Neural mechanisms 2012

Diagram of the Dual Centre Model of Feeding

Feelings of hunger -feeding starts

Food intake, rise in

glucose levels and a

decrease in ghrelin

VMH satiety centre

satisfied

Satiety, feeling of fullness (feeding stops)

Signals of decline in nutrients

(decrease of glucose,

increase of ghrelin

LH feeding centre is activated