Eating and appetite Flashcards

1
Q

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

A

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.

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2
Q

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

A
  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.
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3
Q

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

A

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

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4
Q

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

A

Berridge, 2004.

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5
Q

Outline the positive-incentive theory.

A
  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
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6
Q

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

A

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

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7
Q

What determines what we eat?

A
  • Learned taste preferences and aversions, e.g. Sclafani (1990), Dwyer, Haselgrove and Jones (2011).
  • Social acquisition (Galef, 1995)
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8
Q

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

A
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.

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9
Q

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

A

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

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10
Q

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

A

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.

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11
Q

What determines when we eat?

A

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

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12
Q

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

A
  • 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.
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13
Q

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

A

Buzzer+Light–>food.

Light = CS, rats ate more when subsequently presented.

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14
Q

What parts of the hypothalamus are involved in eating?

A
  • Ventromedial = satiety centre

- Lateral = feeding centre

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15
Q

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

A
  • Hetherington and Ranson (1940) lesioned = hyperphagia (overeating)
  • VMH syndrome (dynamic and static phase, lazy and picky.
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16
Q

What is the role of the lateral hypothalamus in eating?

A
  • 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.
17
Q

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

A
  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.
18
Q

What did Cannon and Washburn (1912) do?

A
  • 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.
19
Q

What did Koopmans (1981) do?

A
  • 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.
20
Q

What are peptides?

A

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

21
Q

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

A

Amino acids.

22
Q

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

A

A satiety peptide:

  • Injected cholecystokinin (CCK) into hungry rats’ guts, they ate less.
  • May induce illness (supports flavour aversion).
23
Q

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

A
  • Obesity - eating more, converting calories into fat more efficiently.
  • Supposed to be a negative feedback signal to reduce appetite and enable fat metabolism.
24
Q

What did Seeley and Woods (2003) do?

A

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

25
Q

Who has had success treating human obesity with leptin therapy?

A

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.