Eating and appetite

Question 1

What does Keesey and Powley’s (1986) set point theory of hunger state?

Answer 1

That hunger is a consequence of an energy deficit - each individual has an optimal level of energy resources (set point) which the body seeks to return to = homeostasis.

Question 2

What are the main criticisms of the set point theory of hunger?

Answer 2

1. Evolutionarily unlikely and potentially incompatible (inconsistent resources, winter)
2. Not supported by evidence (blood glucose reduction would have to be substantial, consuming calories before a meal doesn’t affect what you eat)
3. Ignores environmental factors - effects of learning, preference and social factors.

Question 3

What did Lowe (1993) find about drinking a high calorie drink before a meal?

Answer 3

That it’s the participant’s belief about the drink that affects what they eat.

Question 4

Who came up with an example of a positive-incentive theory?

Answer 4

Berridge, 2004.

Question 5

Outline the positive-incentive theory.

Answer 5

1. Anticipation (expected pleasure = +ve incentive)
2. Craving initiates eating (enables you to take advantage of good food when available)
3. Multiple factors affect eating

Question 6

According to positive-incentive theory, what factors influence how much we eat?

Answer 6

Flavour, knowledge of food i.e. learning, time since last meal, food in gut, blood glucose levels etc.

Question 7

What determines what we eat?

Answer 7

• Learned taste preferences and aversions, e.g. Sclafani (1990), Dwyer, Haselgrove and Jones (2011).
• Social acquisition (Galef, 1995)

Question 8

What did Sclafani (1990) and Dwyer, Haselgrove and Jones (2011) do?

Answer 8

Training:
- Flavour A + glucose/ Flavour B
Test
- A>B
Training 2
- A + lithium chloride (ill)/ B
Test 2
- A was avoided.

Therefore we acquire preferences.

Question 9

What did Fudim (1976) find about associating salt with flavours?

Answer 9

All animals Almond+Salt and Banana+sugar. No injection = prefer banana. Formalin (induces salt craving) = prefer almond.

Question 10

Given Fudim (1976)’s findings, why do people have such a poor diet?

Answer 10

Our diets are too complex to be fixed by this paradigm - e.g. Harris et al. (1993) thyamine depleted rats learned to eat complete diet but effect weakened when choice was between 10 diets.

Question 11

What determines when we eat?

Answer 11

Collier (1986):
- Most mammals eat many small meals.
Initiated mainly by environmental cues, which cause physiological ones.

Question 12

How does Woods (1991) explain pre-meal hunger?

Answer 12

• Eating a meal stresses the body - influx of fuel moves it away from homeostasis.
• Signals for a meal evoke a cephalic phase in which insulin is released into the blood causing a decrease in blood glucose.
• Thus, hunger is the body preparing for homeostatic disruption.

Question 13

How did Weingarten (1983) investigate conditional hunger in rats?

Answer 13

Buzzer+Light–>food.

Light = CS, rats ate more when subsequently presented.

Question 14

What parts of the hypothalamus are involved in eating?

Answer 14

• Ventromedial = satiety centre

- Lateral = feeding centre

Question 15

What is the role of the ventralmedial area of the hypothalamus in eating?

Answer 15

• Hetherington and Ranson (1940) lesioned = hyperphagia (overeating)
• VMH syndrome (dynamic and static phase, lazy and picky.

Question 16

What is the role of the lateral hypothalamus in eating?

Answer 16

• Anand and Brobeck (1951) lesioned = aphagia (cessation).
• LH syndrome (Teitelbaum and Epstein, 1962) - accompanied by adipasia, recovery possible with tube feeding, soft food then normal.

Question 17

What are criticisms of the evidence suggesting the hypothalamus’ involvement in eating?

Answer 17

1. VMH lesions damaged PVN, PVN produces hyperphagia.
2. Hypothalamus regulates metabolism, not eating - VMH lesions -> increased insulin, increases lipogenesis and decreases lipolysis, rats must eat more to meet demand.
3. LH lesions also produce motor disturbances and lack of responsiveness.

Question 18

What did Cannon and Washburn (1912) do?

Answer 18

• When swallowed a balloon attached to a string, found that contractions caused by empty stomach correlated with hunger.
• However patients without stomachs still get hungry.
• Thus, stomach is sufficient but not necessary for hunger.

Question 19

What did Koopmans (1981) do?

Answer 19

• Transplanted an extra stomach and length of intestine into rats (joined major arteries and veins)
• Food injected into and held in stomach decreased eating
• But no functioning nerves?
• Satiety signal must therefore have reached the brain through blood flow.

Question 20

What are peptides?

Answer 20

Short chains of amino acids that can function as a hormone or neurotransmitter.

Question 21

What does ingested food stimulate receptors in the gastrointestinal tract to release into the bloodstream?

Answer 21

Amino acids.

Question 22

What did Gibbs, Young and Smith (1973) find?

Answer 22

A satiety peptide:

• Injected cholecystokinin (CCK) into hungry rats’ guts, they ate less.
• May induce illness (supports flavour aversion).

Question 23

What does a spontaneous genetic mutation causing no leptin to be produced/received cause, and why?

Answer 23

• Obesity - eating more, converting calories into fat more efficiently.
• Supposed to be a negative feedback signal to reduce appetite and enable fat metabolism.

Question 24

What did Seeley and Woods (2003) do?

Answer 24

Injected ob/ob rats with leptin, reduced eating = weight loss.

Question 25

Who has had success treating human obesity with leptin therapy?

Answer 25

Farooqi et al. (1999):

• Girl with no feeling of fullness was constantly hungry.
• Lost 36 pounds (almost all fat) in a year after leptin therapy
• No obvious side effects.