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PSYC370 Ch 12.pdf

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PSYC 370
Janet L Menard

PSYC  370   Chapter  12   Hunger,  Eating,  and  Health     Statistics  of  American  food  consumption   -­‐ Average  3,800  calories  per  day  –  twice  the  necessary  intake   -­‐ 65%  of  people  are  overweight  or  obese  –  epidemic   -­‐ 300,000  people  die  each  year  from  disorders  related  to  excessive  eating     3%  of  Americans  suffer  from  anorexia  or  bulimia.       Most  people  believe  that  our  bodies  send  out  a  hunger  signal  when  we  reach  a  certain  set  point  of   low  energy.  This  is  not  the  case.   -­‐ Amnesic  patients  will  eat  food  that  is  offered,  even  right  after  finishing  a  meal     Digestion,  energy  storage,  and  energy  utilization     Digestion.     Digestion:  gastrointestinal  process  of  breaking  down  food  and  absorbing  its  constituents  into  the   body.     Food  has  not  been  consumed  until  it  has  been  digested.       1. Food  is  broken  down  and  mixed  with  saliva  during  chewing.     2. Saliva  lubricates  the  food  –  beginning  of  digestion.     3. Mouth  -­‐-­‐  esophagus  -­‐-­‐  stomach     4. HCl  breaks  food  down  into  particles.  Pepsin  breaks  proteins  down  into  amino  acids.       5. Stomach  –  (pyloric  sphincter)  –  duodenum  (where  most  absorption  takes  place).     6. Digestive  enzymes  in  the  duodenum  break  down  proteins  into  amino  acids,  starch  and   complex  sugars  into  simple  sugars.  These  enter  the  bloodstream  and  go  on  to  the  liver.     7. Fats  are  emulsified  (broken  into  droplets)  in  the  duodenum  by  bile.  These  go  on  to  the   lymphatic  system.     8. Remaining  water  and  electrolytes  are  absorbed  in  the  large  intestine.  The  remaining  waste   is  ejected  from  the  anus.       Many  of  the  digestive  enzymes  in  the  duodenum  come  from  the  gall  bladder  or  pancreas.     Bile  is  produced  by  the  liver  and  stored  in  the  pancreas.     (12  :  1)   PSYC  370   Energy  storage  in  the  body.     Energy  comes  to  the  body  as  lipids,  amino  acids,  and  glucose.     Lipids:  fats.     Amino  acids:  breakdown  products  of  proteins.     Glucose:  simple  sugar  broken  down  from  complex  carbohydrates.     The  body  is  always  using  energy  even  though  it  is  not  always  taking  it  in.  This  emphasizes  the   importance  of  energy  storage.     Energy  is  stored  in  the  body  as  fats,  glycogen,  and  proteins.  Most  of  the  energy  is  stored  in  fats.       Glycogen  is  readily  converted  to  glucose,  the  body’s  main  source  of  usable  energy.       Why  is  most  energy  in  the  body  stored  as  fat?   -­‐ One  gram  of  fat  can  store  twice  as  much  energy  as  one  gram  of  glycogen   -­‐ Fat  repels  water  (unlike  glycogen,  which  attracts  and  holds  onto  it)     Three  phases  of  energy  metabolism.     Energy  metabolism:  chemical  changes  by  which  energy  is  made  available  for  use.       1. Cephalic  phase:  preparatory  stage;  when  you  are  anticipating  food.  Ends  when  food  starts   to  be  absorbed  into  the  bloodstream.     2. Absorptive  phase:  energy  from  the  meal  entering  the  bloodstream  meets  body’s   immediate  energy  needs.       3. Fasting  phase:  all  unstored  energy  from  the  previous  meal  has  been  used,  to  the  body  goes   to  its  energy  stores  to  meet  its  immediate  needs.       Energy  metabolism  is  mediated  by  insulin  and  glucagon.     Insulin:  hormone  with  the  following  functions.   -­‐ Promotes  use  of  glucose  as  primary  energy  source   -­‐ Conversion  of  energy  in  the  blood  into  stored  forms     - Glucose  à  glycogen  and  fat   - Amino  acids  à  proteins   -­‐ Storage  of  ...   - Glycogen  à  liver  and  muscle   - Fat  à  adipose  tissue   - Proteins  à  muscle     (12  :  2)   PSYC  370   Pancreas  releases  insulin  during  the  cephalic  and  absorptive  phases.     Fasting  phase  is  characterized  by  high  glucagon  levels  and  low  insulin  levels.     What  happens  when  insulin  levels  are  low?   -­‐ Glucose  has  a  hard  time  entering  body  cells.  This  means  that  insulin  will  not  be  able  to   serve  as  the  primary  energy  source  for  the  body.   -­‐ Glucose  can  still  enter  the  brain  without  insulin   -­‐ Glycogen  and  protein  are  converted  to  glucose     Gluconeogenesis:  conversion  of  protein  to  glucose.     What  happens  when  glucagon  levels  are  high?   -­‐ Free  fatty  acids  are  released  from  adipose  tissue  and  used  as  the  body’s  primary  fuel   -­‐ Conversion  of  free  fatty  acids  to  ketones  (used  by  the  muscles  and  the  brain  –   conserves  glucose  levels  further)     Phase(s)   Hormones   Activities   Cephalic  phase       preparatory  phase  which   -­‐  Insulin  levels  high   Promotes   is  initiated  by  the  sight,     -­‐ Blood  glucose  as  source  of  energy   smell,  or  expectation  of   food.   -­‐  Glucagon  levels  low   -­‐ Conversion  of  excess  glucose  to  glycogen     and  fat   &   -­‐ Conversion  of  amino  acids  to  proteins   -­‐ Storage  of  glycogen  in  liver  and  muscle,  fat     in  adipose  tissue,  and  protein  in  muscle   Absorptive  phase   Nutrients  for  a  meal     meeting  the  body’s   Inhibits   immediate  energy   -­‐ Conversion  of  glycogen,  fat,  and  protein   requirements,  with  the   into  directly  usable  energy  (e.g.,  glucose,   excess  being  stored.   free  fatty  acids,  ketones)     Fasting  phase       Energy  being  withdrawn   -­‐ Glucagon  levels  high   Promotes   from  stores  to  meet     -­‐ Conversion  of  fats  to  free  fatty  acids  +  using   body’s  immediate  needs.   -­‐ Insulin  levels  low   free  fatty  acids  as  a  source  of  energy   -­‐ Conversion  of  glycogen  to  glucose,  free  fatty   acids  to  ketones,  and  protein  to  glucose     Inhibits   -­‐ Using  glucose  in  the  body  (but  not  in  the   brain)   -­‐ Conversion  of  glucose  to  glycogen  and  fat,   and  amino  acids  to  protein   -­‐ Storage  of  fat  in  adipose  tissue   (12  :  3)   PSYC  370   Theories  of  hunger  and  eating:  set  points  versus  positive  incentives     Set-­‐point  assumption.     Set-­‐point  assumption:  we  become  hungry  because  of  an  energy  deficit,  and  we  eat  as  a  means  to   restore  energy  levels  to  optimal  levels.     Components  of  set-­‐point  systems   -­‐ Set-­‐point  mechanism:  defines  the  set-­‐point.   - Detector  mechanism:  detects  deviation  from  the  set-­‐point.   - Effector  mechanism:  eliminates  deviations.     All  set-­‐point  systems  are  negative  feedback  systems.       Glucostatic  and  lipostatic  set-­‐point  theories  of  hunger  and  eating.     Glucostatic  theory:  extension  of  the  set-­‐point  theory  that  posits  that  we  feel  hunger  when  our   blood  glucose  levels  go  under  a  set  level.     Lipostatic  theory:  extension  of  the  set-­‐point  theory  that  posits  that  we  feel  hunger  when  our   blood  fat  levels  go  under  a  set  level.   -­‐ Adult  body  weight  does  not  tend  to  change  too  much     These  theories  complement  one  another  (they  are  not  mutually  exclusive).     -­‐ Glucostatic  theory  –  meal  initiation  and  termination  (short-­‐term  maintenance)   -­‐ Lipostatic  theory  –  long-­‐term  maintenance     Problems  with  set-­‐point  theories  of  hunger  and  eating.     -­‐ Do  not  account  for  current  obesity  epidemic     -­‐ Does  not  jive  with  evolutionary  theory:  humans  needed  to  eat  lots  of  food  when  it  was   available  to  fill  up  their  reserves.  They  would  die  if  they  stopped  eating  as  soon  as  their   immediate  energy  needs  were  met.     -­‐ If  these  set-­‐point  theories  actually  account  for  what  is  happening  in  the  body,  then  they   should  be  able  to  be  duplicated  in  the  lab.  Eating  was  stimulated  when  mice  experienced  a   large  drop  in  blood  glucose  (insulin  injection)  or  loss  of  body  fat  (starvation),  but  these   were  extreme  deviations  that  are  not  seen  day-­‐to-­‐day,  and  cannot  be  duplicated  in  the  lab.     -­‐ If  blood  fat  level  is  naturally  at  a  set-­‐point,  below  which  eating  begins  and  above  which   eating  stops,  then  having  a  high-­‐calorie  drink  or  appetizer  before  a  meal  would  trigger  you   not  to  have  the  meal  to  follow,  but  it  doesn’t.     -­‐ Do  not  account  for  learning,  social  factors,  cultural  factors,  and  taste.     (12  :  4)   PSYC  370   Positive-­‐incentive  perspective.     Positive-­‐incentive  perspective:  theory  that  humans  are  drawn  to  eat  because  of  the  anticipated   pleasure  it  will  bring.   -­‐ Hunger  is  brought  on  by  craving  the  experience  of  eating     -­‐ Evolution  has  shaped  us  to  crave  food   -­‐ Theory  applies  to  animals  as  well     Positive-­‐incentive  value:  the  anticipated  pleasure  of  a  behaviour.       Level  of  hunger  experienced  depends  on  the  positive-­‐incentive  value  of  the  experience.  Factors:   -­‐ Flavour  of  the  food   -­‐ Learned  effects  of  the  food   -­‐ Amount  of  time  since  last  consumption   -­‐ Quantity  and  type  of  food  in  your  gut   -­‐ If  other  people  are  present  and  eating   -­‐ Blood  glucose  levels       Factors  that  determine  what,  when,  and  how  much  we  eat     Factors  that  determine  what  we  eat.     Flavours  that  humans  crave   -­‐ Sweet   -­‐ Fatty   -­‐ Salty     These  are  associated  with  energy-­‐rich  foods.  Taste  aversion  for  bitter  foods,  which  can  be   indicative  of  toxins.       Animals  learn  the  following  paradigm:   -­‐ Prefer  foods  that  are  accompanied  by  an  influx  of  calories   -­‐ Avoid  foods  that  precede  illness   -­‐ Preference  for  foods  chosen  by  conspecifics     If  animals  develop  aversion  to  diets  that  lack  the  nutrients  they  need,  then  why  do  humans  choose   unhealthy  foods  and  diets  lacking  in  nutrition?   -­‐ Food  is  designed  to  suit  our  taste  preferences,  often  at  the  expense  of  nutrition     In  the  animal  model,  the  rats  would  develop  aversion  to  diets  that  were  completely  lacking  in  a   nutrient  and  would  prefer  a  diet  that  contained  the  nutrient.  This  is  easy  when  there  are  two   diets  to  choose  from.  We  get  some  of  the  nutrients  we  need  in  our  diet,  so  we  don’t  develop   illness  or  obvious  aversion,  but  we  also  lose  the  ability  to  detect  which  foods  are  or  aren’t   healthy.   (12  :  5)   PSYC  370   Factors  that  influence  when  we  eat.     Most  mammals  prefer  many  small  snacks  if  they  have  continuous  access  to  food.     Number  of  times  we  eat  is  influenced  by...   -­‐ Work  schedule   -­‐ Cultural  norms   -­‐ Family  routine   -­‐ Personal  preferences   -­‐ Wealth     Since  humans  tend  to  eat  large  meals  at  certain  times  of  day,  they  feel  most  hungry  at  these  times.   Malaise  (headache,  nausea,  inability  to  concentrate)  is  likely  if  a  meal  is  skipped.     Premeal  hunger.     Before  a  meal,  the  body  is  at  homeostasis.  After  a  meal,  there  are  new  substances  incorporated   into  the  body  which  cause  a  deviation  from  homeostasis.         Claim  that  the  body  anticipates  meals  (routine  mealtimes)  and  enters  the  cephalic  stage  in     preparation  –  defense  of  homeostasis.  Insulin  is  released,  blood  glucose  decreases.  This     manifests  as  feeling  hunger.       Hunger  =  expectation  of  food.     Rats  were  conditioned  to  expect  food  when  they  heard  a  buzzer.  Once  the  conditioning  phase  was   complete,  they  were  given  constant  access  to  food.  They  chose  to  eat  when  the  buzzer  sounded.     Factors  that  influence  how  much  we  eat.     Satiety:  motivational  state  that  causes  us  to  stop  eating  a  meal  when  there  is  food  remaining.   -­‐ Plays  a  major  role     Satiety  signals.     -­‐ Food  in  the  gut  and  glucose  in  the  blood  trigger  satiety  signals   -­‐ Depends  on  volume  of  food  and  nutritive  density     Nutritive  density:  calories  per  unit  volume  of  food.                 (12  :  6)   PSYC  370   Sham  eating.     Sham  eating:  tube  is  implanted  in  the  esophagus  of  a  rat.  When  the  rat  eats,  the  food  exits  the   body  immediately  (before  consumption  can  take  place).     Interesting  study  of  sham  eating  in  a  rat  model:     -­‐ Tube  was  implanted  in  the  rats     -­‐ Two  conditions:  familiar  diet  or  new  diet     -­‐ Rats  that  ate  from  the  familiar  diet  ate  the  same  quantities  that  they  had  in  the  past,  even   though  they  were  not  getting  any  nutrition  from  it.  Food  intake  increased  gradually  over   time.     -­‐ Rats  that  ate  from  the  new  diet  age  large  quantities  of  the  food  immediately.       -­‐ Findings  suggest  that  the  amount  we  eat  is  based  on  previous  experience  of  the   physiological  effects  of  the  food,  more  so  than  the  current  physiological  effects.           Other.     Appetizer  effect:  small  amounts  of  food  consumed  before  a  meal  increase  hunger.       -­‐ Evidence  against  the  set-­‐point  theory     Greater  serving  sizes  corresponds  to  more  eating.     We  eat  more  (up  to  60%  more)  when  we  are  with  others.     (12  :  7)   PSYC  370   Sensory-­‐specific  satiety.     Cafeteria  diet:  offering  a  wide  range  of  appealing  foods.   -­‐ Increases  consumption     Sensory-­‐specific  satiety:  consumption  of  one  food  increases  the  satiety  of  that  particular  food   but  not  necessarily  for  others.     -­‐ This  relates  to  the  cafeteria  diet  –  after  you  have  gotten  your  fill  of  one  dish,  you  will  not   want  any  more  of  it  (satiated)  but  you  may  continue  on  eating  other  foods       Interesting  study  on  this  vein:     -­‐ Participants  were  given  a  high-­‐calorie,  high-­‐carbohydrate  liquid  meal.  They  were  asked  to   rate  the  palatability  of  various  foods  afterward.     -­‐ Immediate  decrease  in  palatability  ratings  for  foods  with  similar  taste  as  the  drink.     -­‐ No  immediate  decrease  in  palatability  ratings  for  foods  with  different  flavours.     -­‐ After  30  minutes,  global  decrease  in  all  palatability  ratings.     Effects  of  sensory-­‐specific  satiety:   -­‐ Immediate  (decrease  in  positive  incentive  value  of  similar  foods  but  not  other  types  of   foods)   -­‐ Longer  term  (influences  choices  from  meal  to  meal)     Foods  that  do  not  seem  to  be  impacted  by  sensory-­‐specific  satiety  (i.e.,  they  can  be  eaten  almost   every  day  without  decline  in  palatability)   -­‐ Rice   -­‐ Potatoes   -­‐ Bread   -­‐ Sweets   -­‐ Green  salad     Adaptive  benefits   -­‐ Promotes  variety   -­‐ Promotes  eating  a  lot  (eat  your  fill  of  one  food  then  move  on  to  the  next  food)                   (12  :  8)   PSYC  370   Physiological  research  on  hunger  and  satiety     Role  of  blood  glucose  levels  on  hunger  and  satiety.     Blood  glucose  levels  are  fairly  constant  (do  not  change  more  than  2%)  throughout  the  day,  except   right  before  a  routine  mealtime  (deviates  by  8%).  Reasons  why  this  does  not  necessarily  support   the  glucostatic  theory:     -­‐ Drop  in  blood  glucose  level  corresponds  with  expected  meal  –  does  not  occur  when  eating  is   unexpected.     -­‐ Premeal  decrease  in  blood  glucose  occurs  because  of  the  intention  to  start  eating  (i.e.,   spontaneously  dropping  blood  glucose  levels  does  not  motivate  intention  to  start  eating).       -­‐ If  expected  meal  is  not  served,  blood  glucose  levels  return  to  normal.     -­‐ Insulin  injections  only  trigger  hunger  when  they  are  drastic  –  i.e.,  injections  large  enough  to   reduce  blood  glucose  levels  by  50%  (does  not  occur  in  real  life).     Myth  of  hypothalamic  hunger  and  satiety  centres.     1950s  beliefs  –  the  hypothalamus  as  the  control  centre  for  eating  behaviour.   -­‐ Ventromedial  hypothalamus  –  satiety   -­‐ Lateral  hypothalamus  –  feeding     Ventromedial  hypothalamus  –  satiety  centre.     Hyperphagia:  excessive  eating.     Lesions  to  the  ventromedial  hypothalamus  can  produce  hyperphagia  and  obesity  in  rats.       -­‐ Dynamic  phase:  immediately  after  surgery  the  rat  begins  to  eat  excessive  amounts  and   gain  significant  weight.   -­‐ Static  phase:  eating  eventually  tapers  off,  although  obesity  is  maintained.     Important:  excessive  body  weight  is  maintained  in  the  static  phase.       Lateral  hypothalamus  –  feeding  centre.     Aphagia:  complete  cessation  of  eating.     Adipsia:  complete  cessation  of  drinking.     LH  syndrome:  name  for  symptom  of  aphagia  and  adipsia  caused  by  lateral  hypothalamus  lesions.     (12  :  9)   PSYC  370   Lesions  to  the  lateral  hypothalamus  caused  aphagia  and  adipsia  in  rats.       -­‐ True  also  of  rats  that  had  been  made  hyperphagic  by  VMH  lesions.     -­‐ Recovery  if  kept  nourished  by  tube  feeding     Reinterpretation  of  the  effects  of  VMH  and  LH  lesions.     -­‐ Ventromedial  hypothalamus  –  regulation  of  energy  metabolism     - Rats  do  not  eat  and  then  become  obese,  they  become  obese  and  so  they  eat.   - Explains  the  finding  why  rats  with  this  condition  did  not  have  greater   motivation  to  eat     What  is  actually  happening  in  rats  with  ventromedial  hypothalamus  lesions:     -­‐ Increase  in  blood  insulin  causes  increase  in  lipogenesis  (production  of  body  fat)  and   decrease  in  lipolysis  (breakdown  of  body  fat  into  useable  forms).     -­‐ Need  to  eat  a  lot  to  make  sure  that  there  are  enough  calories  to  meet  immediate  needs    -­‐  if   calories  are  being  converted  quickly  into  fats  and  are  not  being  broken  down  into  useable   forms,  you  need  to  consume  a  lot  to  make  sure  that  there  is  enough  free  energy.     Lipogenesis:  production  of  body  fat.     Lipolysis:  breakdown  of  body  fat  into  useable  forms.       -­‐ Additionally,  structures  besides  the  ventromedial  hypothalamus  are  damaged     - Ventral  noradrenergic  bundle  
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