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Biological psychology > hapter 12 - Hunger, Eating and Health > Flashcards

hapter 12 - Hunger, Eating and Health Flashcards

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1
Q

Primary purpose of hunger

A

to increase the probability of eating

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2
Q

Primary purpose of eating

A

to supply the body with the molecular building block - hence, energy it needs to survive and function

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3
Q

Digestion

A

gastrointestinal process of breaking down foods and absorbing its constituents into the body

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4
Q

gut microbiome

A

the bacteria and other organisms that live inside our gastrointestinal tract

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5
Q

Energy is delivered to the body in three forms

A
  1. Lipids (fats)
  2. Amino acids (breakdown product of proteins)
  3. Glucose (simple sugar)
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6
Q

Energy is stored in three formats

A
  1. Fats
  2. Glycogen
  3. Proteins
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7
Q

Energy metabolism

A

the chemical changes by which energy is made available for an organism’s use

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8
Q

What are the three phases of energy metabolism?

A
  1. Cephalic phase
  2. Absorptive phase
  3. Fasting phase
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9
Q

Cephalic phase

A
  • preparatory phase
  • it often begins with sight, smell or even thought of food
  • ends with when the food starts to be absorbed into the bloodstream
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10
Q

Absortive phase

A

period during which the energy absorbed into the bloodstream from the meal is meeting the body’s immedeate energy needs

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11
Q

Fasting phase

A

period during which all of the unstored energy from the previous meal have been used and the body is drawing energ from its reserves to meet its immediate energy requirements.

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12
Q

Flow of energy during the three phases of energy metabolism is controlled by two pancreatic hormones

A
  • unsulin
  • glucagon
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13
Q

Insulin does what three things?

A
  1. promotes use of glucose as primary source of energy by the body
  2. promotes the conversion of bloodborne fuels to forms that can be stored by glycogen and amino acid to proteins.
  3. promotes the storage of glycogen in liver and muscle, fat in adipose tissue and proteins in muscle.
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14
Q

Gluconeogenesis

A

conversion of protein to glucose.

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15
Q

What is the set-point assumption?

A

the assumption that hunger is typically triggered by a decline in the body’s energy resevered below their seit point.

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16
Q

All set-point systems have three components

A
  1. Set-point mechansims
  2. Detector mechanisms
  3. Effector mechanisms
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17
Q

Set-point mechanisms

A

defines the set-point

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18
Q

Detector mechanisms

A

detects deviations from the set-point

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19
Q

Effector mechanisms

A

acts to elimicate the deviations

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20
Q

What are negative feedback systems?

A

systems in which feedback from changes in one direction elicit compensatory effects in the opposite direction

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21
Q

Glucostatic theory

A

eating is regulated by a system designes to maintain a blood glucose set point

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22
Q

Lipostatic theory

A

theory that eating is controlled by deviations from hypothetical body set-point

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23
Q

What are three major weaknesses of the set-point theory

A
  1. Inconsistent with evolution (people ate large amount of foods at once)
  2. Many people are overweight
    3.Theory fails to take into account that eating has also a big influence on taste, learning and social influence
24
Q

Positive-incentive theory

A

the idea that behaviors are motivated by their anticipated pleasurable effects

25
Q

Positive-incentive value

A

the anticipated pleasure associated with a particular action such as taking a drug

26
Q

Premeal hunger - Factors that influence when we wat

A
  • string, unpleasant feeling of hunger
  • sensation of your body’a preparations for the expected homeostasis-disturbing meal
27
Q

Pavlovian conditioning for hunger

A

hunger is often caused by the expectation of food, not the energy deficit

28
Q

Satiety

A

motivational state that causes us to stop eating a meal when there is food remaining

29
Q

Nutritive density (satiety signals)

A

calories per volume

30
Q

Sham eating

A

the experimental protocol in which an animals shews and swallows food, after which the food immediately exists the body through a tube implanted in it’s esophagus

31
Q

Appetizer effect

A

the small aount of food consumed before a meal actually increases hunger raten than reduces it

32
Q

What is meant by sensory specific satiety?

A

the fact that the consumption of a particular food produces greater satiety for foods the same taste than for other foods.

33
Q

Suggestion that eating behavior is controlled by two different regions of the hypothalamus.

A
  1. Satiety by the ventromedial hypothalamus (VMH)
  2. Feeding by the lateral hypothalamus (LH)
34
Q

VMH satiety centre

A

large bilateral lesions to the VMH produce hyperphagia and extreme obesity (VMH syndrome)

35
Q

The VMH syndrom has two different phases …

A
  1. Dynamic phase: begins soons after subject regains consciousness after the operation - groosly exessive eating
  2. Static phase: the animal maintains the new bodyweight.
36
Q

LH feeding center

A
  • bilateral lesion to the LH produces aphagia
  • aphagia is accompanied by adipsia
37
Q

Aphagia (1) vs. Adipsia (2)

A
  1. complete cessation of eating
  2. complete cessation of drinking
38
Q

Reinterpretation of the effects of VMH and LH lesions - what were the two lines of evidence?

A
  1. role of the hypothalamzs is the regulation of energy metabolism, not the regulation of eating.
  2. Many effects of VMH lesions are not attriutable to VHM damage (but lesions of adjacent fibres)
39
Q

Satiety peptides

A

bind to receptors in the brain, have been reported to reduce food intake.

40
Q

Hunger peptides

A
  • peptides that increase appetite
  • are also discovered
41
Q

Serotonin-produced satiety was found to have three major properties

A
  1. cause rats to reists the powerful attractions of highly palatable cafeteria diets
  2. Reduces amount of food consumed during each meal
  3. Shift in food preference away from fatty foods.
42
Q

What is the prader-Willy syndrome?

A
  • acidents of chromosomal replication
  • experience insatiable hunger
  • little or no satiety
  • exceptionally slow metabolism
43
Q

Three different lines of evidence - set point assumption avout body weight and eating

A
  1. Variability of body weight
  2. Set points and health
  3. Regulation of body weight by changes in efficiency of energy utilization
44
Q

Diet-induced thermogenesis

A

the homeostasis - defending increases in body temperature that are associated with increases in body fat (body controls its fats levels)

45
Q

basal metabolic rate

A

rate at which energy is utilized to maintain bodily processes when resting.

46
Q

Settling point model

A

the point at which various factors influence the level of some regulated function (such as body weight) achieve and equilibrium.

47
Q

Leaky barrel model

A

understanding that body weights is regulated by a settling-point system

48
Q

Leptin (def.)

A

peptide hormone, which is actively released by fat

48
Q

Why do some poeple become obese while others not?

A
  • differences in consumption
  • differences in energy expenditure
  • differences in gut microbiome composition
  • genetic and epigenetic factors
49
Q

Ob/ob mice

A

mice that are homozygous for the mutant gene ob
- their body produces no leptin
- they become very obese

50
Q

Serotonergic Agonists

A
  • have shown to reduce food consumption in both human and nonhuman subjects
  • considerable potential in treatment of obesity.
51
Q

Gastric bypass

A

surgigal treatment for extreme obesity, involves short-circuiting the normal path of forrd through digestive tract.

52
Q

Asjustable gastric band procedure

A

surgically postioning a hallow silicone band around the stamach to reduce the flow of food through it.

53
Q

Anorexia nervosa

A

disorders of underconsumtpion
- eating so little that one experiences life-threatening weight loss

54
Q

Bulimia nervosa

A

periods of not eating and peridos of binging, followed by efforts to immediately eliminate the consumed calories.

Biological psychology (11 decks)

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