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PSYC 304 > CH 12: Hunger, Eating & Health > Flashcards

CH 12: Hunger, Eating & Health Flashcards

1
Q

Describe the process of DIGESTION.

A

DIGESTION:

  • GI process of breaking down food & absorbing its constituents into body
  • -> Break down food via gut micro biome = bacteria that live inside our GI tract
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2
Q

Explain how energy is stored in the body.

A
  • E delivered to body in 3 forms (lipids, AA’s, glucose)
  • E stored in body in 3 forms (fats, proteins, glycogen)
  • -> Most E stored as FAT (rather than glycogen) bc:
    1. 1g fat can store 2x E as 1g glycogen
    2. Glycogen, unlike fat, attracts & holds ^quantities of H2O
  • -> weighs more
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3
Q

List the 3 phases of energy metabolism.

A
  1. Cephalic Phase
  2. Absorptive Phase
  3. Fasting Phase
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4
Q

Describe the CEPHALIC PHASE.

A
  1. Cephalic Phase:
    = Preparatory phase
    - Begins w/ sight, smell or thought of food
    - Ends when food starts to be absorbed into bloodstream
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5
Q

Describe the ABSORPTIVE PHASE.

A
  1. Absorptive Phase:

- When E absorbed into bloodstream from meal is meeting the body’s immediate E needs

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6
Q

Describe the FASTING PHASE.

A
  1. Fasting Phase:
    - When all unstirred E from previous meal has been used & body is withdrawing E from its reserves to meet its immediate E requirements
    - Ends w/ beginning of next cephalic phase
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7
Q

Describe the SET-POINT ASSUMPTION.

A

Set-Point Assumption:

  • Meal continues until the E level (required for physiological functioning) returns to its set point & the person no longer feels hungry
  • (-) feedback sys
  • -> Acts to maintain homeostasis
  • aka assumes hunger & eating work in same way as a thermostat-regulated heating system in cool climate
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8
Q

Describe the GLUCOSTATIC Set-Point Theory.

What is it thought to account for?

A

Glucostatic Theory:

  • We become hungry when our blood glucose levels drop significantly below their set point
  • We become satiated (not hungry) when eating returns our blood glucose levels to their set point

–> Thought to account for meal initiation & termination

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9
Q

Describe the LIPOSTATIC Set-Point Theory.

What evidence supports this?

What is it thought to account for?

A

Lipostatic Theory:
- Every person has a set point for body fat, & deviations from this set point produce compensatory adjustments int he level of eating that return levels of body fat to their set point

  • Support: adults’ body weight stay relatively consistent

–> Thought to account for long-term regulation.

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10
Q

Outline 3 problems w/ set-point theories of hunger & eating.

A
  1. They’re inconsistent w/ basic eating-related evolutionary pressures
    - Ancestors didn’t know when get next meal
    - -> Eat large quantities of food when available
  2. Major predictions of these theories haven’t been confirmed
    - ie) efforts to reduce meal-size by having ppl unknowingly consume high-calorie drink before eating have been unsuccessful
  3. These theories are deficient bc they fail to recognize the major influences on hunger & eating ie) taste, learning, social influences
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11
Q

Describe the POSITIVE-INCENTIVE THEORY

A

Positive-Incentive Theory:
- we’re drawn to eat via anticipated pleasure of eating (rather than by internal E deficits)

  • The degree of hunger you feel at depends on interaction of all the factors that influence the positive incentive value of eating
  • -> ie) food flavour, amount of time since last ate, quantity of food in gut, social aspects, etc.
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12
Q

Describe 2 factors that determine WHAT we eat.

A
  1. LEARNED TASTE PREFERENCES & AVERSIONS:
    - Learn to prefer tastes followed by ^^calories
    - Learn to avoid tastes followed by illness
    - Influenced by conspecifics (i.e. cultural preferences)
  2. LEARNING TO EAT VITAMINS & MINERALS:
    - Vitamin deficiencies influence diet selection
    - Low Na+ –> imm. preference for sodium salt taste
    - Low vitamin/mineral –> learn to consume foods that are rich in the missing nutrient by experiencing their positive effects
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13
Q

Describe 2 factors that determine WHEN we eat.

A
  1. PREMEAL HUNGER:
    - Right before usual meal time, body defends its homeostasis by entering the CEPHALIC phase
    - -> Takes steps to soften impact of impeding homeostasis-disturbing influx
    - -> Releases insulin into blood
    - -> Reduces blood glucose
  • **Mealtime hunger is caused by expectation of food, NOT by an E deficit
  1. PAVLOVIAN CONDITIONING OF HUNGER:
    - Experiment where rats trained to eat each time buzzer & light were presented, even though recently completed a meal
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14
Q

List 6 factors that influence HOW MUCH we eat.

A
  1. Satiety signals
  2. Sham eating
  3. Appetizer effect & satiety
  4. Serving size & satiety
  5. Social influences & satiety
  6. Sensory-specific satiety
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15
Q

Define SATIETY.

Describe how Satiety Signals influence HOW MUCH we eat.

A

SATIETY:
= Motivational state that causes us to stop eating a meal when there’s food remaining
–> Triggered by food in gut & glucose entering blood

  • Satiety signals depend on V of NUTRITIVE DENSITY (=calories per unit V) of the food
  • -> Once a stable baseline of consumption established, nutritive density of diet changes
  • -> Learn to adjust food V to maintain stable caloric intake & body weight
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16
Q

Define SHAM EATING.

Describe how Sham Eating influences HOW MUCH we eat.

A

SHAM EATING:
= Experimental protocol where animal chews & swallows food, after which the food immediately exits the body through a tube implanted in its esophagus

  • Predict that sham eating meals would be ^^larger
  • -> But experiments w/ rats showed that meal size were the same
  • -> ***aka satiety is function of previous experience, not the current increases in body’s E resources
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17
Q

Define APPETIZER EFFECT.

Describe how the Appetizer Effect & satiety influence HOW MUCH we eat.

A

APPETIZER EFFECT:
= The increase in hunger produced by the consumption of small amounts of food

  • Occurs bc consumption of small amounts of food elicits cephalic-phase responds

–> Appetizer Effect decreases satiety?

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18
Q

Describe how Serving Size & satiety influence HOW MUCH we eat.

A
  • Amount consumed informed by serving size

- -> Larger servings = more we eat

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19
Q

Describe how Social influences & satiety influence HOW MUCH we eat.

A
  • Feelings of satiety depend on eating alone vs. w/ others

- -> Consume more when eating w/ others

20
Q

Define SENSORY-SPECIFIC SATIETY.

Describe how Sensory-Specific Satiety influence HOW MUCH we eat.

A

SENSORY-SPECIFIC SATIETY:
= Fact that the consumption of a particular food produced greater satiety for foods of the same taste than for other foods

  • Eat one food
  • -> Positive-incentive value of all foods decline slightly
  • -> Positive-incentive value of that particular food plummets
  • -> Become satiated on that food & stop eating it
  • -> Bit if another food’s offered to you, you’ll begin eating again
21
Q

Explain the relationship b/w blood glucose levels & hunger & satiety (4).

A
  1. The time course of glucose decline is NOT consistent w/ idea that it reflects a gradual decline in the body’s E
    - It occurs suddenly just before eating begins
  2. Eliminating the primal drop in blood glucose does NOT eliminate the meal
  3. If an expected meal is NOT served, blood glucose soon returns to its previous level
  4. The glucose levels in extracellular fluids that surround CNS neurons stay ~constant, even when blood glucose levels drop
22
Q

***Critically evaluate the concept of hypothalamic hunger & satiety centres.

A

see pg 313-315

23
Q

Describe the role of the gastrointestinal tract in satiety.

A
  • GI satiety signals reaches brain through the blood
  • Bloodbourne satiety signals not a nutrient, but some CHEMICALS released from stomach IRT caloric value & V of food
  • -> Shown via experiment w/ rat w/ transplanted stomach (aka no functional nerves)
24
Q

Describe the discovery of hunger & satiety PEPTIDES.

A
  • PEPTIDES = short AA chains that function as hormones & NTs = chemicals released from stomach to brain
  • Ingested food
  • -> Interact w/ receptors in GI tract
  • -> Release peptides into bloodstream
  • ie) CCK = gut/satiety peptide = provides brain w/ info about quantity & nature of food in GI tract
  • -> Info plays role in satiety
  • -> aka CCK reduces appetite

ie) Grelin = hunger peptide = synthesized in brain (in hypothalamus)

  • *Several gut peptides shown to bind to receptors in brain in HYPOTHALAMUS**
  • -> Renews hypothalamus’ role in hunger & eating
25
Q

Describe the role of SEROTONIN in satiety (3).

A

Study on rats showed serotonin-produced satiety had 3 major properties:

  1. Serotonin caused rats to resist powerful attraction of highly palatable cafeteria foods
  2. Serotonin reduced amount of food consumed during meal rather than reducing the # of meals
  3. Serotonin ass. w/ shift in food preferences away from fatty food

–> Suggests that serotonin may be useful in combating obesity in humans

26
Q

Describe the symptoms & ethology of PRADER-WILLI SYNDROME.

What happens if left untreated?

A

Prader-Willi Syndrome:

  • Patients experience insatiable hunger, little/no satiety, ^^^slow metabolism
  • -> acts as if they’re starving

> Other symptoms:

  • Weak muscles
  • Small hands & feet
  • Feeding difficulties in infancy
  • Tantrums
  • Skin Picking
  • Results from accident of chromosomal replication

> If left untreated, patients:

  • ^^obese
  • Die in early adulthood from diabetes, heart disease, or other obese-related disorders
27
Q

Evaluate what the Set-Point Theory assumes about about variability of body weight (2).

Why are these assumptions wrong?

A

VARIABILITY OF BODY WEIGHT

  1. Set-point theory assumes adults can’t gain/lose large amounts of weight
    - -> wrong bc can’t explain obesity
  2. Set-point theory claims body weight regulation best maintained when ppl eat only when motivated by hunger
    - -> wrong bc ppl avoid obese only by resisting urge to eat
28
Q

Evaluate what the Set-Point Theory claims about obtaining optimal health (1).

Why is this assumption wrong?

A

SET POINTS & OPTIMAL HEALTH

  • Set-point theory claims that each person’s set point is optimal for that person’s health
  • -> wrong bc dietary restriction can have beneficial effects even if it’s initiated later on in life
  • ie) Japanese island pop who ate 20% less calories than other pops but still had good health
29
Q

Evaluate what the Set-Point Theory claims about the regulation of body weight.

A

REGULATION OF BODY WEIGHT BY CHANGES IN THE EFFICIENCY OF ENERGY UTILIZATION

  • As a person’s level of body fat declines, they start to use E resources ^efficiently
  • ^body fat
  • -> ^body temp
  • -> require ^E to maintain
  • -> decreases in body fat have opposite effect
  • Humans have diff basal metabolic rates
30
Q

Describe the SETTLING-POINT model of body-weight regulation.

A

Settling Point:
= Level at which the various factors that influence body weight achieve an equilibrium
- As body fat levels ^, changes occur that limit further ^ until balance is achieved b/w all factors that encourage weight gain & all those that discourage it

  • Provides a ~homeostatic regulation w/o mechanism to return body weight to a set point
  • Claims body weight remains stable as long as there’s no long-term changes in factors that influence it
  • -> If factors do influence it, their impact is limited by (-) feedback
31
Q

Compare the Set-Point & Settling-Point models of body-weight regulation.

A

Settling-Point model:

  • (-) feedback limits further changes in same direction
  • It’s possible to perm. change your body weight by perm. changing any factors that influence E intake/output

Set-Point model:

  • (-) feedback triggers return to set point
  • It’s impossible to perm. change body weight bc always drawn back to your body weight set point

see pg 321 for details on leaky-barrel analogy

32
Q

Describe, from an evolutionary perspective, why there’s a current epidemic of obesity.

A
  • Throughout evolution, ppl would eat a lot whenever resources available
  • The fittest ppl = high-calorie foods, ate to capacity when food available, store as many excess calories as possible in form of body fat, & use calorie stores as efficiently as possible
  • -> If can’t do this, then unlikely to survive food shortage or harsh winter

> Change in cultural practices:

  • Ppl eat 3meals/day, regardless of hunger
  • Food is focus of social gatherings
  • Meals saved progressively ^palatability = salt, sweets, fat
  • Unhealthy feeding habits by parents passed onto offspring
  • Our current environment differs from our ‘natural’ environ
  • -> i.e. Live in environment w/ endless variety of foods of highest positive-incentive & caloric value that’s readily & continuously available
  • -> consequence = ^^levels of consumption
33
Q

Obesity = E ____ > E ____.

A

Obesity = E input > E output

34
Q

Explain 4 reasons as to why some ppl become obese whereas others do not.

A
  1. DIFFERENCES IN CONSUMPTION:
    ie) some ppl consume ^E bc:
    - ^preference for taste of high-caloric foods
    - cultures that promo excessive eating
  2. DIFFERENCES IN E EXPENDITURE:
    - ie) differences in exercise
    - ie) differences in basal metabolic rate
    - ie) differences in NEAT = non-exercise activity thermogenesis = generated by activities
  3. DIFFERENCES IN GUT MICROBIOME COMPOSITION:
    - Microbes influence brain & behaviour
  4. GENETIC & EPIGENETIC FACTORS:
    - Some loci (regions) on chromosomes linked to obesity
    - Some genes influence likelihood of obesity via affecting gut micro biome
35
Q

Explain 3 reasons why weight-loss programs are typically ineffective.

A
  1. Physical exercise accounts for only small proportion of total E expenditure
  2. Bodies are efficient machines
    - Only burns small # calories during workout
  3. Ppl feel free to consume extra drinks/foods containing more calories after workout
36
Q

Describe LEPTIN - explain how its feedback signals regulate body fat.

A

Leptin:
= Peptide hormone (protein) synthesized in fat cells

  • Acts as (-) feedback signal normally released by fat stores
  • -> Decreases appetite & ^fat metabolism
37
Q

Describe INSULIN - explain how its feedback signals regulate body fat (3).

A

Insulin:
= Pancreatic peptide hormone

  • Serves as (-) feedback signal in regulation of body fat:
    1. Brain levels of insulin are positively correlated w/ levels of body fat
    2. Receptors for insulin were found in the brain
    3. Infusions of insulin into the brains of lab animals found to reduce eating & body weight
38
Q

Why are there 2 different feedback signals?

A
  • Leptin levels ^closely correlated w/ SUBCUTANEOUS FAT = fat stored under skin
    vs.
  • Insulin levels ^closely correlated w/ VISCERAL FAT = fat stored around internal organs of body cavity
39
Q

List 2 sorts of treatments for obesity.

A
  1. Serotonergic Agonists

2. Gastric Surgery

40
Q

Describe SEROTONERGIC AGONISTS.

A

Serotonergic Agonists:

  • Reduces food consumption via mech different from that of leptin & insulin
  • -> Produces LONG-TERM satiety signals based on fat stores
  • -> Also ^short-term satiety signals ass. w/ consumption of a meal
41
Q

Describe GASTRIC SURGERY - what are the 2 types?

A

ie) Gastric Bypass = short-circuiting normal path of food through digestive tract so that its absorption is reduced

ie) Adjustable Gastric Band Procedure = placing hollow silicone band around stomach tor educe flow of food
- can adjust circumference of band via saline injections
- can be readily removed
- -> unlike gastric bypass

42
Q

Define ANOREXIA NERVOSA - what are its symptoms?

A
  • Disorder of underconsumption
  • Health-threatening weight loss
  • Perceive themselves as fat
43
Q

Define BULIMIA NERVOSA - what are its symptoms?

A
  • Disorder characterized by periods of not eating interrupted by binging, followed by efforts to immediately eliminate the consumed calories from body via voluntary purging or extreme exercise
  • Either obese or normal weight
44
Q

Explain the DIFFERENCES b/w Anorexia & Bulimia (2).

A
  1. Starving produce diff health problems than does repeated binging & purging
  2. Anorexia & Bulimia requires different treatment

> Anorexia:

  • reduced metabolism
  • slow heart rate
  • low bp
  • low body temp & anemia

> Bulimia:

  • irrigation & inflammation of esophagus
  • vitamin & mineral deficiencies
  • electrolyte imbalance
  • dehydration
  • acid reflux
45
Q

Explain why those starving due to Anorexia don’t appear to be as hungry as they should be.

A
  • Decline in eating due to declining POSITIVE-INCENTIVE value for eating
  • Declining in positive-incentive value for various TASTES of foods for anorexic vs. controls
46
Q

Explain how anorexia might result from conditioned aversions.

A
  • Meals produce adverse but tolerable effects in healthy individuals
  • -> May be ^^^aversive for individuals who have undergone food deprivation
  • -> But severe anorexics don’t have ^increase in positive-incentive value of eating, similar to the ^ experienced by normal starving individuals
  • -> bc MEALS consumed by anorexic prod variety of conditioned taste aversions that REDUCE motivation to eat
  • -> Anorexics / anyone severely undernourished shouldn’t be permitted to eat meals
  • -> Should be fed/infused w/ small amounts of food intermittently throughout the day

PSYC 304 (18 decks)

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