CH 12: Hunger, Eating & Health Flashcards
Describe the process of DIGESTION.
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
Explain how energy is stored in the body.
- 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
List the 3 phases of energy metabolism.
- Cephalic Phase
- Absorptive Phase
- Fasting Phase
Describe the CEPHALIC PHASE.
- Cephalic Phase:
= Preparatory phase
- Begins w/ sight, smell or thought of food
- Ends when food starts to be absorbed into bloodstream
Describe the ABSORPTIVE PHASE.
- Absorptive Phase:
- When E absorbed into bloodstream from meal is meeting the body’s immediate E needs
Describe the FASTING PHASE.
- 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
Describe the SET-POINT ASSUMPTION.
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
Describe the GLUCOSTATIC Set-Point Theory.
What is it thought to account for?
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
Describe the LIPOSTATIC Set-Point Theory.
What evidence supports this?
What is it thought to account for?
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.
Outline 3 problems w/ set-point theories of hunger & eating.
- They’re inconsistent w/ basic eating-related evolutionary pressures
- Ancestors didn’t know when get next meal
- -> Eat large quantities of food when available - 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 - These theories are deficient bc they fail to recognize the major influences on hunger & eating ie) taste, learning, social influences
Describe the POSITIVE-INCENTIVE THEORY
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.
Describe 2 factors that determine WHAT we eat.
- 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) - 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
Describe 2 factors that determine WHEN we eat.
- 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
- PAVLOVIAN CONDITIONING OF HUNGER:
- Experiment where rats trained to eat each time buzzer & light were presented, even though recently completed a meal
List 6 factors that influence HOW MUCH we eat.
- Satiety signals
- Sham eating
- Appetizer effect & satiety
- Serving size & satiety
- Social influences & satiety
- Sensory-specific satiety
Define SATIETY.
Describe how Satiety Signals influence HOW MUCH we eat.
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
Define SHAM EATING.
Describe how Sham Eating influences HOW MUCH we eat.
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
Define APPETIZER EFFECT.
Describe how the Appetizer Effect & satiety influence HOW MUCH we eat.
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?
Describe how Serving Size & satiety influence HOW MUCH we eat.
- Amount consumed informed by serving size
- -> Larger servings = more we eat
Describe how Social influences & satiety influence HOW MUCH we eat.
- Feelings of satiety depend on eating alone vs. w/ others
- -> Consume more when eating w/ others
Define SENSORY-SPECIFIC SATIETY.
Describe how Sensory-Specific Satiety influence HOW MUCH we eat.
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
Explain the relationship b/w blood glucose levels & hunger & satiety (4).
- 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 - Eliminating the primal drop in blood glucose does NOT eliminate the meal
- If an expected meal is NOT served, blood glucose soon returns to its previous level
- The glucose levels in extracellular fluids that surround CNS neurons stay ~constant, even when blood glucose levels drop
***Critically evaluate the concept of hypothalamic hunger & satiety centres.
see pg 313-315
Describe the role of the gastrointestinal tract in satiety.
- 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)
Describe the discovery of hunger & satiety PEPTIDES.
- 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
Describe the role of SEROTONIN in satiety (3).
Study on rats showed serotonin-produced satiety had 3 major properties:
- Serotonin caused rats to resist powerful attraction of highly palatable cafeteria foods
- Serotonin reduced amount of food consumed during meal rather than reducing the # of meals
- Serotonin ass. w/ shift in food preferences away from fatty food
–> Suggests that serotonin may be useful in combating obesity in humans
Describe the symptoms & ethology of PRADER-WILLI SYNDROME.
What happens if left untreated?
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
Evaluate what the Set-Point Theory assumes about about variability of body weight (2).
Why are these assumptions wrong?
VARIABILITY OF BODY WEIGHT
- Set-point theory assumes adults can’t gain/lose large amounts of weight
- -> wrong bc can’t explain obesity - 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
Evaluate what the Set-Point Theory claims about obtaining optimal health (1).
Why is this assumption wrong?
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
Evaluate what the Set-Point Theory claims about the regulation of body weight.
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
Describe the SETTLING-POINT model of body-weight regulation.
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
Compare the Set-Point & Settling-Point models of body-weight regulation.
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
Describe, from an evolutionary perspective, why there’s a current epidemic of obesity.
- 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
Obesity = E ____ > E ____.
Obesity = E input > E output
Explain 4 reasons as to why some ppl become obese whereas others do not.
- DIFFERENCES IN CONSUMPTION:
ie) some ppl consume ^E bc:
- ^preference for taste of high-caloric foods
- cultures that promo excessive eating - 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 - DIFFERENCES IN GUT MICROBIOME COMPOSITION:
- Microbes influence brain & behaviour - GENETIC & EPIGENETIC FACTORS:
- Some loci (regions) on chromosomes linked to obesity
- Some genes influence likelihood of obesity via affecting gut micro biome
Explain 3 reasons why weight-loss programs are typically ineffective.
- Physical exercise accounts for only small proportion of total E expenditure
- Bodies are efficient machines
- Only burns small # calories during workout - Ppl feel free to consume extra drinks/foods containing more calories after workout
Describe LEPTIN - explain how its feedback signals regulate body fat.
Leptin:
= Peptide hormone (protein) synthesized in fat cells
- Acts as (-) feedback signal normally released by fat stores
- -> Decreases appetite & ^fat metabolism
Describe INSULIN - explain how its feedback signals regulate body fat (3).
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
Why are there 2 different feedback signals?
- 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
List 2 sorts of treatments for obesity.
- Serotonergic Agonists
2. Gastric Surgery
Describe SEROTONERGIC AGONISTS.
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
Describe GASTRIC SURGERY - what are the 2 types?
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
Define ANOREXIA NERVOSA - what are its symptoms?
- Disorder of underconsumption
- Health-threatening weight loss
- Perceive themselves as fat
Define BULIMIA NERVOSA - what are its symptoms?
- 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
Explain the DIFFERENCES b/w Anorexia & Bulimia (2).
- Starving produce diff health problems than does repeated binging & purging
- 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
Explain why those starving due to Anorexia don’t appear to be as hungry as they should be.
- 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
Explain how anorexia might result from conditioned aversions.
- 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
