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Biological Psychology 2 > Motivation: Eating, Hunger & Eating Disorders > Flashcards

Motivation: Eating, Hunger & Eating Disorders Flashcards

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1
Q

Define motivation.

A

It is what initiates, directs and maintains our behaviours.

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2
Q

Name the 5 main motivation theories.

A 
Instinct theories. 
Maslow's hierachy of needs. 
Arousal theory.
Drive-reduction theory.
Incentive theory.
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3
Q

What is instinct theory?

A

Behaviours are motivated by instinct that is innate and which are activated by environmental stimuli. Instinct drives all human behaviours.

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4
Q

What did McDougall say instincts are?

A

Identified 18 different instincts (e.g. hunger, sex).
Instincts are unlearned, innate, automatic.
Trigger behaviours that aid in survival.
Many reflexes in humans show instinctive behaviour.

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5
Q

What is the main weakness of instinct theory?

A

Can’t explain all behaviours.

Hard to test.

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6
Q

What is Maslow’s hierarchy of need?

A

Basic survival needs to be satisfied before we are motivated to satisfy higher-level needs (e.g. self-esteem, self-actualisation).
Hierarchy.

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7
Q

What are the weaknesses of Maslow’s hierarchy of need?

A

Only the first 2 needs are hierarchical.
Humans are motivated by a complex array of needs.
Hard to test.
Culturally-specific.

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8
Q

What is optimal arousal theory?

A

Behaviour is motivated by the need to achieve optimum levels of arousal.
Behaviour is in response to a need to raise or lower arousal levels.
Individual differences in optimal arousal.

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9
Q

Explain the Yerkes-Dodson Law (arousal theory).

A

Arousal levels influence our performance. Complex tasks more affected.

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10
Q

What are the two primary arousal systems?

A

Autonomic nervous system - arouses body.

Cortical arousal system - arouses brain.

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11
Q

How is the ascending reticular activating system related to arousal?

A

Regulates wakefulness + sleep-wake transitions.
Connects reticular formation in brainstem to cortex via thalamus. Coma if these are damaged.
Selectively increases/decreases arousal + attention in cortex by modulating neurotransmitter systems.

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12
Q

What is drive reduction theory?

A

Motivation originates from biological needs to maintain the body in a state of equilibrium.
Physiological need creates an aroused tension state that motivates an organism to satisfy the need.
Homeostasis is the aim.

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13
Q

What are the three phases of digestion?

A
  1. Cephalic/reflex phase - initiated by sight, smell, thought or taste of food. Modulated by appetite. Preparatory processes.
  2. Gastric/absorptive phase - triggered by food in stomach. Distension of stomach + rise of pH. Activates muscle contractions.
  3. Intestinal phase - speeds/slows rate at which stomach empties.
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14
Q

What are the three main constituents of food that serve as fuel molecules?

A

carbohydrates, fats + proteins.

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15
Q

Which cells use the three main constituents that are absorbed into the bloodstream?

A

Glucose - carbohydrates.
Lipids - fats.
Amino acids - protein.

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16
Q

What are the 3 forms that energy is stored in the body?

A

Fat.
Glycogen - made + stored by liver and muscle.
Protein - broken down and used for energy when other stores are depleted.

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17
Q

Define homeostasis.

A

The maintenance of a steady internal state.

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18
Q

What are the two hypothesis for what creates the drive in drive-reduction theory?

A

Glucostatic and lipostatic hypothesis.

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19
Q

What is the glucostatic hypothesis?

A

Low blood glucose levels cause increased appetite and trigger eating. Glucose levels are highly regulated.
During/after eating - insulin levels increase. Insulin allows cells to make use of glucose and promotes storage of excess glucose as glycogen.

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20
Q

Explain where insulin is produced and what its role is in the body (evidence for this?).

A

Pancreas.
Enters brain and can reduce appetite. Controls appetite.
Evidence: mice with disrupted brain insulin receptors = higher food intake + obesity.

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21
Q

Explain how diabetes occurs.

A

Insulin levels too low.
Blood glucose too high (cells can’t make use of it).
Increased appetite + food intake. But glucose is excreted rather than used. Fat stores used up instead - weight loss.

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22
Q

What are the three other main appetite hormones (not insulin)?

A

Ghrelin, PYY, Leptin.

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23
Q

What is ghrelin?

A

Peptide hormone made by stomach.
Levels in blood increase between meals and fall once food is consumed.
Appetite stimulant.

24
Q

What is PYY?

A

Produced by the lower gastrointestinal tract.
After 1-2 hours after eating, PYY levels peak. PYY concentrations are proportional to meal energy content.
Signals satiety + suppresses appetite.

25
Q

What is leptin?

A

Suppresses appetite.
Produced by fat, stomach and other organs.
Levels are + correlated with amount of body fat mass.
Secretion levels not driven by meal patterns - levels follow a daily rhythm peaking between midnight + early morning.

26
Q

What has genetic leptin deficiency in mice shown us?

A

Increased food intake, reduced energy usage - morbid obesity.
Corrected by leptin injections.

27
Q

What is the lipostatic hypothesis?

A

Levels of body fat influence regulation of food consumption to maintain a stable body weight.

28
Q

What are the 2 important appetite hormones in the lipostiatic hypothesis and why?

A

Leptin - suppresses appetite.

Ghrelin - appetite stimulant. Influenced by body fat levels (e.g. low in obese subjects).

29
Q

Explain how leptin plays a role in obesity and how this can be improved.

A

5% of obese individuals have congenital leptin deficiency.

Supplement with leptin - increase energy usage + decrease appetite.

30
Q

What is a weakness of using leptin supplements as a treatment for obesity?

A 
Obesity = decreased sensitivity to leptin rather than lack of.
Leptin resistance (also seen in pregnancy and hibernation!). 
Obesity is associated with damage to hypothalamus neutrons - decreased sensitivity to leptin. Physical exercise can help repair these cells!
31
Q

What is the role of the hypothalamus in appetite?

A

Regulatory functions - like a thermostat.
Regulation of ANS (including metabolic processes).
Contains receptors for many peptide hormones.
Important integration and control centre for feeding and metabolism.
Sensitive to leptin, ghrelin, insulin and other hormones.
Outputs to nucleus accumbent, OFC and amygdala - important for control of human eating behaviour.

32
Q

What happens when there is lesions in the lateral hypothalamus? What about the ventromedial hypothalamus?

A

Lateral - diminished appetite! Hunger centre?
Electrical stimulation of lateral = rats feed even when already fed-
Ventromedial - animals overeat and become obese. Satiety centre?
Shows how hypothalamus is critical in regulating appetite + feeding behaviours.
Dual centre model for feeding.

33
Q

What did later evidence suggest the lateral hypothalamus may be instead of the hunger centre?

A

Motivation centre.
Lesions also caused a wide range of severe motor disturbances. General lack of responsiveness to sensory input not just food,
Stimulation is not very localised! When stimulating the hypothalamus, actually activating dopamingeric system as well.

34
Q

What is set point theory?

A

When we fall below ideal weight - body increases hunger + decreases energy expenditure. When above set point - opposite.

35
Q

Set point theory is likely to relate to body composition rather than weight (lipostatic theory). Describe the evidence for this.

A

Most adults maintain a relatively stable body weight even with a substantial variation in energy intake + expenditure.

36
Q

What is the main weakness of set point theory?

A

Oversimplified model.
More factors can influence body weight and composition.
Set-point can move up depending on societal factors (overabundance, availability of food…). Can lower set-point through diets…
There is an interaction between biological + environmental factors - settling point.

37
Q

What is a settling point?

A

0 dynamic equilibrium. Interaction between biological and environmental factors - biological factors settle into an equilibrium with the environment.

38
Q

What is positive incentive theory?

A

Behaviour is motivated by internal and external incentives.
Motivated to eat by the anticipated pleasure of eating (positive incentive value) not energy deficits.
Social context, smell + sight of food, etc play a role.

39
Q

Give some examples of how external incentives can affect how much we eat.

A

Size of bowl/utensils, environment (lighting, temperature), effort, social influences (60% increase in eating when with others!), cultural norms, classical conditioning.

40
Q

Give some evidence on how classical conditioning can affect how much we eat.

A

Rats study.
Hungry rats - buzzer. Even when well-fed, eating could be triggered by an external stimulus previously associated with food.
Consistent with positive incentive but not drive reduction theory!

41
Q

How does food variety affect eating (evidence for this)?

A

More variety = more eaten.
Consistent with positive incentive but not drive reduction theory!
Evidence: rats had a 49% weight increase when they had a variety of food to choose from.

42
Q

What is sensory-specific satiety?

A

After eating a food to satiety there is a decrease in pleasantness consumption for that food.
As you eat one food, the positive-incentive value for all food declines slightly, but for that food it declines strongly.

43
Q

What pathway is key to the sensory-specific satiety theory and why?

A

Mesolimbic dopamine pathway - key reward circuit. Projects from VTA to nucleus accumbent, hippo + amygdala.
MDP projects to frontal cortex, OFC.
Feeding triggers dopamine release in uncles accumbent. Dopamine antagonists affect an animal’s ability to maintain feeding behaviours.

44
Q

Is food addictive?

A

Drug abuse = rise in accumbent dopamine. This becomes blunted with the development of addiction. Decrease in striatal D2 receptors with development.
Rats given high-sugar high-fat diets show behaviours and dopamine responses that resemble addiction. Obese people = reduced striatal D2 receptors - pathological eating a compensation for decreased dopamine???
Many people argue against this theory.

45
Q

Where to taste and olfactory pathways converge?

A

Amygdala and OFC. To represent flavour.

46
Q

What has cell recording in the OFC shown us?

A

That populations of neurons respond to particular tastes.

Responses of taste neutrons to a food fed to satiety in a monkey decrease to zero - sensory-specific satiety!

47
Q

What does the sight of chocolate activate?

A

Striatum + OFC. Larger effects in cravers.

48
Q

What is anorexia nervosa?

A

Persistent restriction of energy intake - low body weight. Intense fear of gaining weight. Disturbance in experience of own body weight.

49
Q

What is bulimia?

A

Recurrent episodes of binge eating. Lack of control operating.
Compensatory behaviour to prevent weight gain - vomiting, laxatives.
Self-evaluation affected by body shape/weight.

50
Q

What is binge eating disorder?

A

Eating more rapidly than normal, eating when not hungry, feeling disgusted with one-self afterwards.

51
Q

What are the two main biological explanations for anorexia? Explain them.

A

Hypothalamus dysfunction theory - disturbed hypothalamic functions = lack of weight thermostat. Grey matter atrophy in anorexia. BMI correlates with grey matter in hypothalamus.
Biochemical imbalance theory - dopamine system may be hypersensitive in anorexia. Amphetamine leads to anxiety in anorexia as opposed to euphoria in healthy controls. Explains why food-related dopamine = anxiety and not pleasure in anorexia.

52
Q

What is a weakness of the two anorexia theories?

A

Unable to establish cause and effect. Cause or effect of malnutrition?
Other factors important; early life experiences, sociocultural influences (e.g. social media).

53
Q

What is the biological explanation of bulimia nervosa?

A

Brain activity to food not reduced when full - striatum and amygdala.
Failure to devalue food reward when full up?

54
Q

What is Prader-Willi syndrome and how is it caused?

A

Genetic disorder.
Insatiable hunger, weak muscles, slow metabolism.
Chromosome 15 is missing. Disrupts development of hypothalamus + some neurotransmitters involved in eating.
Most people become extremely obese and die in adulthood when untreated.

55
Q

How is positive incentive theory better than drive reduction theory?

A

Can explain more findings - conditioned feeding behaviours to environmental cues, sensory specific satiety.

Biological Psychology 2 (11 decks)

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