A"tudes  to  Food  and  Ea.ng  Behaviour  •  There  are  two  explana.ons  into  a1tudes  towards  food  and  ea.ng  behavior;  SLT  

and  cultural  influences.  •  Bandura’s  Social  Learning  Theory  emphasises  the  idea  that  people  observe  

modeled  behaviour  from  other  people.  Children  may  learn  a1tudes  and  behaviours  towards  ea.ng  from  their  parents  and  the  parents’  preferences  and  sa.sfac.on.  Through  this  vicarious  learning,  children  will  model  the  behaviour  themselves.  

•  Brown  et  al  found  a  consistent  correla.on  between  ea.ng  habits  of  parents  and  their  children  in  terms  of  snack  food  intake  and  body  dissa.sfac.on.  Moreover,  parents  also  mould  a  child’s  ea.ng  habits  as  they  dictate  what  kinds  of  food  enter  the  household.  

•  The  SLT  is  supported  by  Gast  et  al;  boys  and  girls  aged  10-­‐12  were  surveyed  and  they  found  a  +e  correla.on  between  peer  influence  and  disordered  thinking  of  food.  An  important  element  that  determined  this  correla.on  was  the  likeability  by  peers,  which  is  in  line  with  the  SLT  because  the  more  the  child  iden.fies  with  the  model  the  more  likely  the  model  will  shape  their  behaviour.    

•  Moreover,  Fisher  et  al  found  that  a  good  indicator  of  a  daughter’s  ea.ng  habits  came  from  looking  at  their  mother’s  restrained  die.ng  and  how  the  mother  perceived  the  risks  of  their  daughters  becoming  overweight.  This  would  suggest  that  daughters  learnt  behaviors  from  their  mothers  which  supports  this  explana.on.  

•  SLT  is  also  evident  in  the  impact  of  TV  and  magazines  as  McIntyre  found  that  the  media  significantly  impacted  what  people  ate  and  their  a1tudes  towards  certain  foods  e.g.  new  5:2  diet  fad.    

A"tudes  to  Food  and  Ea.ng  Behaviour  •  There  are  two  explana.ons  into  a1tudes  towards  food  and  ea.ng  behavior;  SLT  and  cultural  influences.  •  Bandura’s  Social  Learning  Theory  emphasises  the  idea  that  people  observe  modeled  behaviour  from  other  

people.  Children  may  learn  a1tudes  and  behaviours  towards  ea.ng  from  their  parents  and  the  parents’  preferences  and  sa.sfac.on.  Through  this  vicarious  learning,  children  will  model  the  behaviour  themselves.  

•  Brown  et  al  found  a  consistent  correla.on  between  ea.ng  habits  of  parents  and  their  children  in  terms  of  snack  food  intake  and  body  dissa.sfac.on.  Moreover,  parents  also  mould  a  child’s  ea.ng  habits  as  they  dictate  what  kinds  of  food  enter  the  household.  

•  The  SLT  is  supported  by  Gast  et  al;  boys  and  girls  aged  10-­‐12  were  surveyed  and  they  found  a  +e  correla.on  between  peer  influence  and  disordered  thinking  of  food.  An  important  element  that  determined  this  correla.on  was  the  likeability  by  peers,  which  is  in  line  with  the  SLT  because  the  more  the  child  iden.fies  with  the  model  the  more  likely  the  model  will  shape  their  behaviour.    

•  Moreover,  Fisher  et  al  found  that  a  good  indicator  of  a  daughter’s  ea.ng  habits  came  from  looking  at  their  mother’s  restrained  die.ng  and  how  the  mother  perceived  the  risks  of  their  daughters  becoming  overweight.  This  would  suggest  that  daughters  learnt  behaviors  from  their  mothers  which  supports  this  explana.on.  

•  SLT  is  also  evident  in  the  impact  of  TV  and  magazines  as  McIntyre  found  that  the  media  significantly  impacted  what  people  ate  and  their  a1tudes  towards  certain  foods  e.g.  new  5:2  diet  fad.    

•  Another  explana.on  into  a1tudes  towards  food  and  ea.ng  behaviour  is  cultural  influences.  •  Ethnicity  seems  to  play  a  role  in  determining  ea.ng  behaviour;  Khan  et  al  found  that  white  women  were  more  

likely  to  have  body  dissa.sfac.on  and  ea.ng  disorders  such  as  anorexia  nervosa  than  Asian  or  black  women.  This  suggests  that  ethnicity  will  impact  whether  a  woman  is  more  likely  to  develop  ea.ng  disorders,  which  may  be  because  Western  cultures  tend  to  promote  a  beauty  standard  achieved  through  thinness.    

•  Moreover,  Kennedy  et  al  supports  these  findings;  over  14,000  women  aged  18-­‐23  were  studied  and  they  found  that  the  longer  these  women  lived  in  Australia,  the  more  likely  they  were  to  portray  a1tudes  and  ea.ng  behaviours  similar  to  women  born  in  Australia.  This  is  known  as  the  accultura.on  effect.    

•  On  the  other  hand,  Mumford  et  al  found  completely  opposite  results;  they  found  that  the  incidence  rates  of  bulimia  were  higher  among  Asian  schoolgirls  than  their  white  counterparts.  This  suggests  that  ethnicity  may  not  necessarily  play  a  role  in  determining  ea.ng  behaviour.    

•  Similarly,  Striegel-­‐Moore  found  that  a  ‘drive  for  thinness’  was  more  evidence  in  black  girls  than  in  white  girls.  This  further  emphasises  the  idea  that  ethnicity  impacts  ea.ng  behaviour,  further  weakening  this  explana.on.  

A"tudes  to  Food  and  Ea.ng  Behaviour  •  Social  class  has  found  to  determine  a1tudes  towards  food.  In  Dornbusch  et  al’s  survey  of  7000  

American  adolescents,  they  found  that  the  upper-­‐class  women  were  more  like  to  strive  for  thinness  than  those  of  lower  social  classes.  This  suggests  that  social  class  may  influence  body  image.  To  emphasise  this,  Goode  et  al  found  that  such  individuals  were  also  more  likely  to  achieve  this  and  a  posi.ve  correla.on  between  income  and  healthy  ea.ng  was  established.    

•  This  is  supported  by  Xie  et  al  who  found  that  teenagers  from  higher-­‐income  background  were  found  to  eat  more  healthy  foods  than  those  from  lower-­‐income  families.  They  consume  less  saturated  fats,  more  protein  and  calcium  and  ate  closer  to  the  daily  guidelines.  This  suggests  that  income  impacts  ea.ng  behaviour  and  a1tudes  towards  certain  foods.  However,  a  weakness  in  this  research  is  that  we  cannot  infer  a  cause  and  effect  for  certain  that  higher  incomes  relates  to  healthier  ea.ng  habits.  There  may  be  confounding  unknown  variables  contribu.ng  to  this  correla.on,  such  as  the  stress  of  actually  being  poor  contribu.ng  to  poor  ea.ng  habits.  

•  On  the  other  hand,  Story  et  al  found  that  in  a  sample  of  American  students,  higher  social  class  was  related  to  greater  sa.sfac.on  with  weight  and  lower  rates  of  weight  control  behaviours.  This  completely  opposes  the  social  class  explana.on  of  cultural  influences,  weakening  the  explana.on.    

•  However,  research  into  cultural  influences  on  ea.ng  behaviour  and  a1tudes  is  arguably  culturally  biased,  as  a1tudes  towards  certain  foods  may  be  specific  to  that  culture  alone.  Thus,  what  may  be  valid  for  one  culture  may  not  necessarily  be  true  for  another;  for  example,  the  Western  ideals  of  being  skinny  may  not  apply  to  cultures  where  the  focus  is  to  avoid  starva.on.    

•  Most  studies  have  focused  purely  on  women  and  their  a1tudes  to  ea.ng  behaviour,  which  suggests  that  many  of  these  explana.ons  suffer  from  beta  bias  as  they  a[empt  to  be  generalised  to  men.  This  is  an  issue  because  men  have  different  body  types  and  different  metabolic  reac.ons  so  they  may  not  be  prone  to  cultural  influences  or  models  in  the  same  way  as  women  may  be.  Therefore,  these  explana.ons  lack  popula.on  validity  because  their  applica.on  is  limited  to  women  solely.  

•  Moreover,  there  are  issues  in  generalizability  as  some  studies  are  based  on  women  diagnosed  with  ea.ng  disorders,  some  are  based  on  people  with  subclinical  condi.ons  and  other  studies  are  based  on  people  who  may  be  experiencing  temporary  depressed  moods.  The  problem  here  is  that  we  cannot  generalise  findings  from  such  specific  circumstances  to  other  groups  or  even  the  wider  popula.on  itself.  Therefore,  the  findings  from  these  studies  may  lack  in  external  validity  because  the  studies  aren’t  measuring  how  ea.ng  behaviour  is  affected  in  a  way  that  can  be  generalised  beyond  that  niche  group  of  individuals.      

Failures  of  Die.ng  •  There  are  two  explana.ons  into  failures  of  die.ng;  the  restraint  theory  and  the  role  of  denial.    •  One  explana.on  for  the  failure  of  die.ng  is  the  Restraint  Theory;  this  theory  suggests  that  when  people  

consciously  a[empt  to  eat  less  and  restrain  their  intake,  they  actually  end  up  overea.ng.  This  is  o]en  because  the  dieter  has  periods  of  restraint  that  are  very  hard  to  maintain.    This  then  means  that  the  restraint  is  followed  by  periods  of  dis-­‐inhibi.on.  Dis-­‐inhibi.on  has  been  defined  as  ea.ng  more  as  a  result  of  loosening  restraints  in  response  to  emo.onal  distress,  intoxica.on  or  preloading.    

•  A  study  by  Wardles  and  Beales  highlighted  how  die.ng  contributed  to  overea.ng;  27  obese  women  were  put  either  into  a  diet  condi.on  that  focused  on  restrained  ea.ng  pa[erns,  an  ‘exercise’  condi.on  or  a  non-­‐treatment  condi.on  for  7  weeks.  Assessments  on  food  intake  and  appe.te  were  made  before  and  a]er  they  ate  a  snack  at  week  4  and  6  (under  stressful  condi.ons);  it  was  found  that  women  in  the  die.ng  condi.on  ate  more  than  those  in  the  other  condi.ons.  Thus,  this  suggests  that  overea.ng  is  caused  by  peoples’  a[empts  to  diet.      

•  Herman  and  Polivy’s  Boundary  Model  a[empts  to  explain  why  die.ng  leads  to  overra.ng;  it  suggests  that  ‘hunger’  ensures  we  don’t  eat  less  than  the  minimum  level,  whilst  ‘sa.ety’  ensures  we  don’t  eat  more  than  the  maximum  level.  Psychological  factors  are  believed  to  play  a  role  between  these  two  levels,  with  those  die.ng  believed  to  have  a  larger  range  between  sa.a.on  and  hunger.  This  could  be  because  it  takes  longer  for  dieters  to  feel  hungry.  Once  restrained  dieters  don’t  eat,  they  may  find  themselves  ea.ng  more  than  they  had  planned  because  it  takes  longer  for  sa.a.on  to  begin.    

•  However,  one  weakness  of  this  theory  is  that  it  cannot  explain  why  some  people  successfully  lose  weight  through  restrained  ea.ng  or  why  ea.ng  disorders  such  as  anorexia  exist.  Therefore,  this  suggests  that  other  factors  may  be  involved  and  so  the  theory  is  simplis.c  in  focusing  only  on  people  ea.ng  less  as  the  main  cause  for  failures  of  die.ng  when  the  nature  of  die.ng  is  in  fact  very  complex.  Thus,  this  weakens  the  restraint  theory  model.    

•  Moreover,  we  cannot  therefore  infer  cause  and  effect  between  research  findings  into  restrained  ea.ng  resul.ng  in  overea.ng  and  diets  failing  as  this  is  based  on  correla.onal  research.  There  may  be  other  extraneous  variables  like  nega.ve  cogni.ons  that  lead  to  overea.ng.      

Failures  of  Die.ng  •  This  is  cri.cised  by  another  explana.on  into  the  failure  of  die.ng  which  is  the  role  of  denial.  This  suggests  that  

a[emp.ng  to  suppress  thoughts  has  a  counterproduc.ve  effect,  as  it  will  make  the  thought  even  more  prominent  in  our  head.    Wegner  et  al’s  study  highlights  the  basis  for  this;  par.cipants  were  asked  to  not  think  about  a  white  bear  but  ring  a  bell  every  .me  they  did  whereas  a  control  group  were  asked  to  ac.vely  think  about  the  white  bear;  it  was  found  that  those  asked  not  to  think  about  it  rang  the  bell  more  frequently  than  those  in  the  control  group.  It’s  referred  to  as  being  the  ‘theory  of  ironic  process  of  mental  control’  as  denial  of  a  thought  leads  to  it  occurring  more  o]en.  Thus,  when  dieters  a[empt  to  not  eat  certain  foods  or  reduce  intake,  the  foods  then  become  more  temp.ng  and  prominent  in  their  minds,  leading  to  the  failure  of  diets.  

•  Soetens  lends  experimental  support  to  this  theory;  par.cipants  were  divided  into  two  groups:  restrained  and  unrestrained.  The  restrained  group  was  further  subdivided  into  those  who  were  either  high  or  low  in  disinhibi.on;  those  in  the  disinhibited  restrained  group  used  more  thought  suppression  than  the  other  groups  and  also  showed  a  rebound  effect  a]erwards.  This  shows  that  restrained  eaters  who  tend  to  overeat  try  to  suppress  thoughts  about  food  more  o]en,  strengthening  the  role  of  denial  explana.on.    

•  However,  an  issue  to  consider  is  whether  people  have  the  free  will  to  control  their  weight  loss  or  whether  it’s  biologically  determined.  For  example,  lipoprotein  lipase  (LPL)  is  an  enzyme  produced  by  fat  cells  to  help  store  calories  as  food;  a  person  who  produces  an  overload  of  LPL  will  regain  lost  weight  faster  than  others.  This  is  supported  by  Kern  et  al,  whereby  9  people  had  their  LPL  levels  measured  before  and  a]er  losing  90  pounds;  people  who  were  fa[er  at  the  start  were  found  to  have  higher  LPL  levels  post-­‐weight  loss,  sugges.ng  that  the  body  was  figh.ng  harder  in  those  people  to  retain  the  lost  weight.  The  weight  loss  would  have  ac.vated  the  produc.on  of  LPL,  which  may  explain  why  some  people  struggle  to  lose  weight.  This  weakens  both  explana.ons  into  failures  of  die.ng  as  it  argues  that  there  is  an  individualis.c  explana.on  that  exists  for  each  person.    

•  Moreover,  another  issue  is  that  research  into  die.ng  has  found  to  be  culturally  biased  as  some  cultural  groups  find  it  more  difficult  to  diet  successfully  due  to  the  natural  inclina.on  to  obesity  where  they  are;  for  example,  Asian  adults  are  more  prone  to  obesity  than  European  adults.  This  weakens  the  explana.ons  as  they  do  not  take  into  account  culture  and  therefore  cannot  be  extrapolated  across  cultures.    

•  Furthermore,  studies  into  die.ng  are  based  on  anecdotal  accounts  of  individuals.  These  are  not  100%  accurate,  cannot  be  replicated  nor  have  controls,  which  means  that  the  studies  suppor.ng  the  explana.ons  are  not  fully  valid  nor  reliable,  therefore  weakening  them.  This  can  be  fixed  by  using  scien.fic  means  of  acquiring  data.  

Neural  Mechanisms  into  Ea.ng  Behaviour  •  The  hypothalamus  is  a  gland  in  the  brain  responsible  for  homeostasis.  Homeostasis  has  two  mechanisms:  to  

detect  whether  the  body  has  enough  nutrients  and  to  correct  a  situa.on  to  restore  the  op.mum  environment.  Thus,  the  hypothalamus  is  believed  to  play  a  role  within  ea.ng  behaviour.  There  is  a  large  .me  lag  between  the  two  mechanisms  and  the  body  registering  their  effects,  so  the  body  has  evolved  two  separate  systems  to  overcome  this  .me  lag;  one  to  turn  ea.ng  behaviour  on  and  the  other,  off.  Glucose  levels  play  a  key  role  in  producing  the  feeling  of  hunger;  hunger  increases  when  glucose  levels  fall,  ac.va.ng  the  lateral  hypothalamus.  Once  food  is  consumed,  glucose  levels  rise,  ac.va.ng  the  ventromedial  hypothalamus,  which  causes  feelings  of  sa.a.on,  helping  stop  further  feeding.      

•  However,  one  weakness  for  the  homeosta.c  explana.on  is  that  hunger  mechanisms  should  theore.cally  be  adap.ve  to  an.cipate  and  prevent  deficits  in  energy  as  opposed  reac.ng  to  them.  The  idea  that  hunger  and  ea.ng  is  triggered  only  due  to  low  glucose  levels  doesn’t  fit  into  evolu.onary  perspec.ve  in  which  our  biology  has  evolved.  

•  On  the  other  hand,  researchers  found  that  damage  to  the  lateral  hypothalamus  in  rats  caused  aphagia,  the  absence  of  ea.ng,  suppor.ng  the  lateral  hypothalamus  explana.on  as  the  LH  couldn’t  be  ac.vated.    

•  In  contrast  however,  damage  to  the  LH  has  shown  to  cause  deficits  in  other  aspects  too  such  as  sex  as  opposed  to  just  hunger.  Recent  studies  have  also  found  that  neural  circuits  running  throughout  the  brain  play  a  role  in  ea.ng  behaviour  too.  This  suggests  that  LH  does  not  have  an  essen.al  role  in  controlling  the  ea.ng  centre.  Therefore,  the  view  that  the  LH  and  VMH  are  alone  responsible  is  simplis.c,  as  it  appears  there  are  more  complex  processes  occurring,  thus  weakening  the  theory.    

•  Yet,  Wickens  found  that  s.mula.on  to  the  lateral  hypothalamus  through  injec.on  of  neuropep.de  Y  (type  of  neurotransmi[er)  caused  them  to  begin  feeding.  This  suggests  that  there  is  an  ON  switch  and  that  NPY  found  in  the  hypothalamus  plays  a  role  both  in  s.mula.ng  lateral  hypothalamus  and  increasing  ea.ng  behaviour.    

•  Conversely,  Mariah  et  al  manipulated  mice  to  disable  them  from  producing  NPY  through  gene.c  modifica.on.  They  found  no  subsequent  decrease  in  their  ea.ng  behaviour.  This  suggests  that  hunger  s.mulated  by  NPY  injec.ons  may  have  been  an  experimental  artefact  in  that  NPY  flooding  causes  the  opposite  behaviour.  This  would  mean  that  the  research  into  NPY  lacks  external  validity  as  they  are  conducted  in  laboratory  se1ngs.  This  suggests  that  it  cannot  be  generalised  to  real  world  findings.  

•  Addi.onally,  another  cri.cism  is  the  use  of  animals  as  much  of  the  empirical  evidence  is  based  on  non-­‐human  animals.  It  can  therefore  be  suggested  that  the  findings  cannot  be  extrapolated  to  human  beings  because  our  gene.c  makeup  and  biology  are  significantly  different.    This  also  suggests  that  such  studies  may  lack  internal  validity,  as  observa.ons  made  in  animal  may  not  apply  to  human  ea.ng  behaviour,  thus  weakening  the  theory.  

Neural  Mechanisms  into  Ea.ng  Behaviour  •  On  the  other  hand,  researchers  have  found  that  damage  to  the  ventromedial  hypothalamus  resulted  in  rats  

overea.ng  due  the  lack  of  a  “stop  signal”  for  sa.a.on  onset,  leading  to  hyperphagia  which  is  excessive  hunger.  S.mula.on  of  the  VMH  was  also  found  to  inhibit  and  stop  feeding,  again  sugges.ng  this  neural  mechanism  controls  ea.ng  behaviour.      

•  Suppor.ng  this,  Hetherington  and  Ranson  made  lesions  on  an  area  of  the  ventromedial  nucleus  in  rats.  This  caused  them  to  over-­‐eat  and  become  drama.cally  obese.  It  was  found  that  this  lesion  destroyed  a  centre  that’s  vital  for  the  control  of  feeding  behaviour;  this  centre  was  thought  to  be  the  sa.ety  centre.    

•  However,  damage  to  nerve  fibres  passing  through  the  VH  possibly  damages  another  area  in  the  hypothalamus,  the  PVN.  Gold  suggests  that  damage  to  the  PVN  alone  causes  hyperphagia  and  found  that  lesions  to  the  VMH  alone  did  not  result  in  hyperphagia,  weakening  the  hypothesis  that  VMH  damage  leads  to  hypoerphagia.  

•  However,  the  issue  with  Gold’s  findings  are  that  no  subsequent  research  has  managed  to  replicate  the  findings.  This  suggests  that  the  claims  are  unreliable,  as  researchers  have  actually  found  the  contrary;  that  lesions  to  the  VMH  caused  over-­‐ea.ng  and  weight  gain.      

•  Other  neural  explana.ons  suggest  that  the  amygdala  and  the  inferior  prefrontal  cortex  affect  ea.ng  behaviour  through  cogni.ve  and  neural  factors.  The  amygdala  is  believed  to  influence  food  choice  though  previous  experience.  Rolls  and  Rolls’  findings  confirm  this  as  they  found  that  removing  the  amygdala  in  rats  would  cause  them  to  consume  both  familiar  and  unfamiliar  foods.  The  prefrontal  cortex  receives  messages  regarding  smell,  which,  if  damaged,  can  affect  the  taste  of  food.    

•  In  contrast,  research  has  found  that  hunger  and  ea.ng  pa[erns  may  not  be  under  the  control  of  neural  mechanisms;  LuLer  et  al  found  the  body  produced  extra  ghrelin  when  stressed,  which  has  been  associated  with  an  increase  in  appe.te.  The  view  that  neural  mechanisms  alone  affects  hunger  is  thus  simplis.c  because  there  may  be  combina.on  of  different  processes  involved  in  hunger  management.  Yet,  research  into  neutral  mechanisms  may  be  responsible  for  affec.ng  ea.ng  behaviour  in  real  life.  For  example,  drugs  with  Lep.n  may  be  developed  to  increase  weight  loss  or  drugs  that  inhibited  LH  may  help  people  reduce  feelings  of  cravings.  This  suggests  that  there  are  real  world  applica.ons  that  can  help  people  struggling  with  obesity.    

•  Moreover,  cogni.ve  factors  may  play  a  bigger  role  in  determining  sa.ety  and  when  a  person  is  full.  People  are  aware  of  when  they  have  eaten  and  they  could  therefore  conclude  that  they  are  full,  leading  to  sa.a.on.  This  explana.on  accounts  for  the  role  of  free  will  because  people  have  the  choice  to  eat  or  not.    

Evolu.onary  Explana.ons  of  Food  Preferences    •  Humans  evolved  from  hunter-­‐gatherers  and  their  diet  would  have  consisted  of  what  was  available  in  their  

environment  e.g.  plants  and  animals.  •  Preferences  for  fa[y  foods  would  have  been  adap.ve  because  it  provides  valuable  energy  resources,  which  

were  vital  in  an  environment  where  an  individual’s  next  meal  was  never  guaranteed.  Calories  were  less  available  within  the  EEA  and  thus  it  would  have  been  adap.ve  for  humans  to  develop  a  preference  for  highly  calorific  foods,  as  these  foods  would  provide  them  with  the  longest  period  of  energy.    

•  Moreover,  Gibson  and  Wardle  support  the  idea  the  importance  of  calorific  foods  in  an  ancestral  diet;  they  showed  that  children  aged  4-­‐5  preferred  fruit  and  vegetables  that  were  dense  in  calories,  such  as  bananas  and  potatoes,  as  opposed  to  foods  high  in  protein  or  sweetness.  This  suggests  that  a  fa[y  food  preference  had  evolved,  suppor.ng  the  fa[y  food  preference  explana.on.    

•  To  support  this,  Stanford  conducted  a  study  on  Tanzanian  chimpanzees;  when  coming  close  to  starva.on,  it  was  found  that  the  chimpanzees  would  kill  and  eat  the  most  fa[y  parts  of  a  colobus  monkey  such  as  the  brain  or  bone  marrow,  leaving  tender  nutri.ous  flesh.  This  emphasises  how  our  own  behaviour  may  have  been  shaped  in  the  EEA  and  thus  supports  the  fa[y  food  preference  explana.on.  

•  Furthermore,  humans  also  developed  a  preference  for  sweet  foods  as  it’s  associated  with  high-­‐energy  and  not  being  toxic  so  it  would  be  beneficial  for  survival.  In  contrast,  our  ability  to  detect  and  reject  bi[er  and  sour  tasted  also  makes  evolu.onary  sense  because  these  tastes  would  be  indica.ve  of  poison  or  toxins  that  plants  produce  to  repel  predators  such  as  humans.  Thus,  us  having  a  natural  dislike  to  bi[er  and  sour  taste  makes  sense  because  they  would  be  dangerous  if  consumed.  Humans  have  30  genes  that  code  for  bi[er  taste  receptors  so  humans  have  a  wider  scope  to  recognise  bi[er  and  possibly  toxic  foods.    

•  In  support  of  the  evolu.onary  advantage  to  bi[er/sour  food  development,  Desor  and  Steiner  found,  judging  by  facial  expressions,  that  neonates  were  more  sensi.ve  to  bi[er  tastes  and  preferred  sweet  foods,  which  was  an  innate  preference;  these  neonates  are  young  and  lack  environmental  experience  to  know  which  foods  are  safe  to  eat.  This  suggests  that  being  more  prone  to  bi[er/sour  tastes  would  have  had  an  evolu.onary  advantage.  A  strength  of  this  study  is  that  it  rules  out  extraneous  variables  such  as  social  learning  factors  because  the  neonates  are  too  young  to  have  learnt  preferences,  making  the  findings  more  valid.  On  the  other  hand,  interpre.ng  preference  using  facial  expressions  is  subjec.ve  and  can  easily  be  misinterpreted  and  unreliable.  Thus,  this  methodological  flaw  observed  may  weaken  the  study  because  expressions  observed  may  not  necessarily  imply  a  preference.  This  can  be  fixed  by  using  quan.ta.ve  means  of  obtaining  the  results.  

•  Moreover,  if  sweet  preference  was  determined  by  evolu.on,  it  would  be  found  across  cultures  and  would  be  universal.  However,  Stefansson  found  that  Copper  Inuit’s  were  disgusted  by  the  taste  of  sugar  when  they  first  tried  it.  This  undermines  the  evolu.onary  explana.on  behind  sweet  preferences  and  can  instead  be  explained  by  the  lack  of  exposure  to  sweet  foods  from  their  environment  instead.    

Evolu.onary  Explana.ons  of  Food  Preferences    •  Humans  have  the  ability  to  learn  taste  aversion  to  toxic  foods,  which  can  be  explana.on  through  

evolu.onary  explana.ons.  Taste  aversion  is  when  toxic  food  is  ingested  and  we  subsequently  develop  a  dislike  towards  it  a]er  consump.on  and  illness.  This  would  have  been  beneficial  for  survival  from  an  evolu.onary  perspec.ve  because  if  we  survived  the  ini.al  consump.on,  our  body  would  adapt  by  learning  to  avoid  the  foods  and  developing  a  natural  dislike  for  them.  The  opposite  can  also  occur,  with  a  preference  for  foods  that  enhance  health.  

•  One  study  that  supports  the  evolu.onary  explana.on  of  taste  aversion  is  by  Garcia  et  al.  They  found  that  when  a  rat  with  a  thiamine  (vitamin  B)  deficiency  consumed  food  with  a  dis.nc.ve  taste  followed  by  a  thiamine  injec.on,  the  rat  would  subsequently  develop  a  preference  for  this  dis.nc.ve-­‐tas.ng  food.  This  therefore  supports  the  taste  aversion  explana.on  as  thiamine  enhances  health  hence  why  rats  consumed  foods  that  contained  thiamine.    

•  Moreover,  Sandell  and  Breslin’s  study  supports  the  evolu.onary  explana.on  of  taste  aversion;  35  adults  were  screened  for  the  hTAS2R38  bi[er  taste  receptor  gene  and  par.cipants  were  asked  to  rate  the  bi[erness  of  various  vegetables.  Some  of  these  vegetables  contained  glucosinates,  a  mild  toxic  known  to  be  dangerous  in  high  dosages.  It  was  found  that  those  with  the  sensi.ve  version  of  hTAS2R38  rated  vegetables  containing  glucosinates  as  60%  more  bi[er  than  those  with  the  insensi.ve  version  of  the  gene.  This  suggests  an  adap.ve  ability  to  detect  and  avoid  toxic  foods,  which  would  explain  why  such  genes  are  more  widespread,  suppor.ng  the  evolu.onary  explana.on  of  taste  aversion.  

•  Furthermore,  real-­‐world  applica.ons  can  be  made  by  understanding  how  taste  aversion  and  preference  works;  cancer  pa.ents  have  reported  developing  an  aversion  to  food  they  consume  prior  to  chemotherapy,  which  has  resulted  in  the  ‘scapegoat  technique’  to  help  pa.ents  con.nue  enjoying  their  foods  post-­‐treatment.  This  involves  giving  cancer  pa.ents  a  novel  food  along  with  something  they’re  familiar  with  prior  to  treatment;  results  have  found  that  pa.ents  form  an  aversion  to  the  novel  food  and  not  to  the  familiar  food,  allowing  them  to  con.nue  ea.ng  familiar  foods.    

 

Psychological  Explana.ons  for  AN  •  There  are  two  psychological  explana.ons  into  anorexia  nervosa:  the  SLT  and  the  psychodynamic  

explana.on.    •  Within  Western  society,  people  learn  that  beauty  is  equated  to  thinness  and  this  ideal  of  a[rac.on  is  

thought  to  be  a  contributor  towards  AN.  The  media  is  then  used  to  ensure  that  body  ideals  are  maintained  in  adolescents  through  the  influence  of  TV,  magazines  and  fashion.  All  of  these  consistently  reinforce  this  cultural  ideal  within  the  popula.on  as  one  study  found  that  16%  of  all  15-­‐18  year  old  girls  in  the  UK  were  ‘currently  on  a  diet’.  This  could  be  because  girls  internalise  culturally  defined  standards  of  female  beauty,  leading  to  unhappiness  over  their  own  body  type  not  matching  this  ideal  and  an  obsession  with  die.ng  and  food,  thus  people  observe  and  imitate  the  model  ideal,  leading  to  AN.    

•  One  study  that  supports  the  impact  of  learning  from  the  media  has  on  body  type  was  conducted  by  Becker  et  al;  it  was  carried  out  in  Fiji  where  TV  was  introduced  in  1995;  ea.ng  disorders  were  absent  un.l  the  introduc.on  of  the  TV  and  influence  of  the  West  as  the  girls’  a1tudes  began  to  shi]  towards  a  desire  to  lose  weight.  It  was  found  that  a]er  5  years,  there  was  a  significant  increase  in  the  number  of  girls  suffering  from  anorexia  and  bulimia  nervosa.  This  highlights  how  the  media  may  contribute  to  the  onset  of  AN  indirectly,  thus  strengthening  the  explana.on.  However,  one  weakness  of  this  study  is  that  it  lacks  internal  validity  because  we  cannot  conclude  for  certain  that  the  shi]  in  a1tude  towards  body  image  directly  led  to  AN  as  there  may  be  other  factors  that  contributed  to  the  onset  of  AN;  this  is  emphasised  by  Jones  and  Buckingham  who  argue  that  not  everyone  is  influenced  by  the  media  in  the  same  and  that  it’s  usually  those  with  low  self-­‐esteem  who  are  more  likely  to  be  influenced.  Therefore  this  directly  highlights  the  fact  that  we  don’t  all  learn  to  be  thin  because  of  individual  differences,  which  would  explain  why  there  are  people  who  don’t  fit  into  the  Western  ideals.  

•  On  the  other  hand,  Gomesz’s  meta-­‐analysis  of  25  studies  found  a  consistent  support  for  the  idea  that  slender  beauty  ideals  led  to  body  dissa.sfac.on,  which  contributed  to  the  development  of  ea.ng  disorders,  primarily  under  19s.    

•  Moreover,  to  support  the  role  of  learning  AN,  Lai  et  al  found  that  the  rate  of  AN  began  to  increase  amongst  people  in  Hong  Kong  as  the  culture  become  more  modernised  and  therefore  westernised,  sugges.ng  that  learning  does  influence  AN.    

Psychological  Explana.ons  for  AN  •  However,  another  explana.on  that  directly  cri.cises  the  idea  of  learning  AN  is  the  psychodynamic  

theory  by  Bruch.  The  principles  of  the  psychodynamic  theory  is  that  adolescents  do  not  want  to  grow  up  and  separate  from  their  parents  so  they  become  fixated  at  the  oral  stage  where  they  are  completely  dependent  on  their  parents.  Those  with  AN  will  want  to  lose  weight  so  that  they  lose  secondary  sexual  characteris.cs  to  remain  childlike  and  asexual,  enabling  them  to  return  to  the  safety  of  their  families.  Bruch  argued  that  AN  is  ac.vated  in  early  childhood,  sugges.ng  that  it  is  caused  by  how  parents  respond  to  their  child’s  needs;  effec.ve  parents  recognise  their  needs  and  feed  them  when  they’re  hungry  whereas  ineffec.ve  parents  fail  to  respond  to  their  child’s  needs  by  feeding  the  child  when  they  are  not  hungry  or  vice  versa.  Children  with  ineffec.ve  parents  grow  up  confused  about  their  internal  needs,  becoming  more  reliant  on  them.  Therefore,  they  may  find  it  difficult  to  establish  autonomy  when  they  become  adolescent,  as  they  don’t  feel  control  over  their  own  bodies.  Thus,  to  overcome  their  sense  of  helplessness,  they  develop  abnormal  ea.ng  habits  and  take  excessive  control  over  their  body  shape  and  size.  As  a  result,  anorexia  nervosa  is  an  a[empt  to  control  ones  life  and  strive  for  autonomy.  Moreover,  Crisp  developed  the  idea  of  remaining  pre-­‐pubescent  through  starva.on,  leading  to  amenorrhoea,  underdeveloped  hips  and  breasts.    

•  Steiner  supports  Bruch’s  psychodynamic  explana.on  of  AN,  as  they  found  that  parents  of  AN  pa.ents  have  a  tendency  of  defining  their  child’s  physical  needs  than  allowing  the  child  to  be  autonomous  in  defining  their  own.  Thus,  this  suggests  that  AN  enables  teenagers  with  AN  to  strive  for  the  autonomy  they  have  been  deprived  of,  strengthening  the  theory.    

•  However,  Minuchin  disagrees  and  suggests  that  the  onset  of  AN  is  actually  related  to  family  problems  and  developed  the  family  system  approach.  Anorexia  diverts  a[en.on  from  family  problems  so  it’s  a  misguided  a[empt  at  keeping  the  family  together  as  they  will  start  to  worry  about  the  child  and  ignore  other  issues.    

•  Furthermore,  the  psychodynamic  approach  has  been  cri.cised  for  being  unscien.fic  because  it  is  based  on  small  case  studies,  for  example  Bruch’s  studies  are  based  on  qualita.ve  case  studies.  This  means  that  it  cannot  be  replicated  so  it  lacks  validity  and  cannot  be  tested  using  the  scien.fic  method.  

•  On  the  other  hand,  the  explana.on  into  AN  is  personality,  which  is  a  gene.c  characteris.c,  directly  cri.cizes  both  the  SLT  and  the  psychodynamic  theory.  Personality  traits  are  thought  to  play  an  important  causal  role  on  the  onset  and  maintenance  of  AN.  Those  with  a  perfec.onist  personality  are  more  likely  to  have  AN  as  Strober  et  al  retrospec.vely  studied  boys  and  girls  receiving  treatment  of  AN  and  found  high  levels  of  perfec.onism  amongst  them.    

•  To  emphasise  the  link  between  perfec.onism  and  AN,  Nilsson  et  al’s  longitudinal  study  found  that  those  with  a  short  period  of  AN  were  less  perfec.onist,  strengthening  the  personality  explana.on.    

•  Halmi  et  al  supports  this  explana.on.  They  inves.gated  the  rela.onship  between  AN  and  perfec.onism  in  322  women  in  the  US  and  Europe.  They  found  that  women  with  a  history  of  AN  scored  higher  on  the  Mul.dimensional  Perfec.onism  Scale  when  compared  to  a  control  group.  Moreover,  they  found  that  the  extent  of  perfec.onism  was  directly  related  to  the  severity  of  AN.    

•  As  part  of  this  study,  Halmi  et  al  also  included  rela.ves  of  those  with  AN  and  found  that  perfec.onism  as  a  personality  traits  appears  to  be  passed  on  from  rela.ves  and  thus  represents  a  gene.c  vulnerability  for  the  onset  of  AN.  Therefore,  this  suggests  that  biological  explana.ons  can  cause  the  onset  of  AN.  This  means  that  a  diathesis-­‐stress  model  may  be[er  explain  how  both  nature  and  nurture  play  a  role,  with  perfec.onism  being  gene.c  but  influenced  by  the  environment.  

•  However,  most  of  the  research  is  also  based  on  females  so  all  the  explana.ons  into  AN  may  suffer  from  beta  (gender)  bias;  the  same  psychological  factors  impac.ng  women  may  not  necessarily  explain  the  onset  of  AN  in  men  as  they  may  perceive  the  world  differently,  thus  weakening  the  psychological  explana.ons  into  AN.    

Psychological  Explana.ons  for  AN  

Biological  Explana.ons  for  AN  •  There  are  two  biological  explana.ons  into  the  onset  of  AN:  neurotransmi[ers,  the  reproduc.ve  

suppression  hypothesis  and  the  hypothalamus  dysfunc.on  theory.      •  Neurotransmi[ers  are  thought  to  cause  the  AN.  Neurotransmi[ers  involved  include  serotonin  &  

dopamine.    •  Kaye  et  al  found  that  drugs  such  as  SSRIs  that  alter  serotonin  levels  were  effec.ve  in  recovering  

AN  pa.ents  as  they  prevented  relapse.  SSRIs  alter  serotonin  levels  by  blocking  uptake  of  serotonin  from  the  synap.c  cle]s,  which  maintains  higher  serotonin  levels.  This  suggests  that  there  is  a  link  between  serotonin  levels  and  the  onset  of  AN,  suppor.ng  the  explana.on.    

•  Although  it  ahs  been  suggested  that  serotonin  is  involved  it’s  the  dopamine,  the  second  neurotransmi[er,  that  is  the  most  responsible  for  the  onset  of  AN  is  dopamine.  Kaye  et  al’s  PET  scan  compared  dopamine  ac.vity  in  the  brains  of  10  women  recovering  from  AN  and  12  healthy  controls.  They  found  that  in  the  AN  women,  there  was  an  over  ac.vity  in  dopamine  receptors  in  the  basal  ganglia  where  dopamine  plays  a  part  in  interpreta.on  of  harm  and  pleasure.  Increase  dopamine  ac.vity  in  the  basal  ganglia  seems  to  alter  the  way  people  interpret  rewards  so  those  with  AN  find  it  harder  to  associate  good  feelings  with  things  that  people  find  pleasurable  such  as  food.  However,  one  weakness  of  this  study  is  that  it  has  a  small  sample  size  that  only  uses  women;  therefore,  we  cannot  be  certain  that  the  imbalances  in  dopamine  would  be  the  same  in  men  with  AN  and  the  small  sample  size  means  that  we  cannot  generalise  the  findings  to  men,  let  alone  the  general  popula.on.  As  a  result,  it  lacks  external  validity    and  thus  weakens  the  explana.on  of  dopamine’s  effect  on  AN.    

•  Furthermore,  Castro-­‐Fornieles  et  al  found  that  AN  teenage  girls  had  higher  levels  of  homovanilic  acid  (waste  product  of  dopamine)  than  a  control  group  and  they  also  found  that  improvement  in  weight  levels  normalised  homovanilic  acid.  This  suggests  weight  gain  decreased  the  ac.vity  of  dopamine  levels  hence  the  decreased  homovanilic  acid,  strengthening  the  theory.    

Biological  Explana.ons  for  AN  •  Another  biological  explana.on  is  the  hypothalamus  dysfunc.on  theory,  which  suggests  that  people  have  a  set  

weight  for  their  bodies;  as  weight  increases  or  decreases,  the  body  adapts  to  make  adjustments  in  food  regula.on  to  return  the  individual  to  their  set  weight.  The  hypothalamus  is  believed  to  have  a  role  in  hunger  and  sa.a.on  as  the  lateral  hypothalamus  turns  ea.ng  behaviour  on  whilst  the  ventromedial  hypothalamus  turns  sa.a.on  on  to  decrease  feeding.  Thus,  Garfunkel  et  al  argued  that  a  disturbed  hypothalamus  causes  AN  through  the  LH  as  it  stops  sending  signals  to  eat  or  the  VMH  being  overac.ve  with  the  individual  receiving  signals  telling  them  they  are  full.    

•  Brobeck  supports  this  theory,  as  they  found  that  damaged  LH  in  rats  lead  to  aphagia  which  is  the  failure  to  eat  when  hungry.  This  provides  support  for  the  idea  that  damage  of  the  hypothalamus  could  lead  to  reduced  ea.ng,  suppor.ng  this  theory.    Moreover,  Stellar  et  al  found  that  s.mula.ng  VMH  inhibited  feeding,  which  again  support  the  idea  that  possible  over-­‐ac.va.on  of  the  VMH  could  lead  to  the  onset  of  AN.    

•  However,  biological  explana.ons  e.g.  hypothalamus  dysfunc.on  theory  can  be  cri.cised  as  biologically  determinis.c  as  they  ignore  the  free  will  and  ability  of  individuals  to  control  their  own  behaviour.  They  suggest  that  if  someone  has  par.cular  genes  or  biochemical  imbalances  they  will  inevitably  have  an  ea.ng  disorder,  which  ignores  the  individual’s  mo.va.on  to  resist  or  overcome  ea.ng  disorder,  thus  weakening  the  theory.  

•  Evolu.onary  explana.ons  involve  the  reproduc.ve  suppression  hypothesis.  The  reproduc.ve  suppression  hypothesis  assumes  that  weight  loss  was  a  strategy  for  suppressing  reproduc.ve  capability  when  food  was  in  limited  supply  as  pregnancy  would  have  been  risky  for  the  mother  and  survival  changes  for  the  infant  would  have  been  reduced.  Reproduc.on  is  costly  to  females  so  when  a  female  faces  condi.ons  that  are  unfavourable  to  reproduc.on  she  can  increase  her  life.me  reproduc.ve  success  by  delaying  reproduc.on  un.l  condi.ons  improve.  Because  a  minimum  amount  of  fat  is  needed  before  menstrua.on  begins  and  for  regular  ovula.on  to  be  maintained,  Frisch  et  al  argues  that  this  could  have  been  an  effec.ve  mechanism  for  controlling  sexual  matura.on  and  fer.lity  in  ancestral  females.  

•  However,  a  major  cri.cism  of  this  explana.on  is  that  AN  appears  more  maladap.ve  overall  than  adap.ve,  especially  during  harsh  condi.ons  in  the  EEA.  AN  causes  an  individual  to  be  weak,  frail  and  vulnerable  as  well  as  a  liability  to  the  group  and  it  seems  unlikely  any  benefit  could  be  achieved  from  such  a  weak  person.  Also,  the  basics  for  survival  also  become  difficult,  e.g.  hun.ng  for  food  which  is  necessary  for  all  animals.  This  further  undermines  the  evolu.onary  explana.on.    

•  Moreover,  a  further  cri.cism  is  that  AN  cannot  be  evolu.onary  because  it  cannot  be  passed  down  gene.cally  as  those  with  AN  would  die  out  of  malnutri.on.  AN  kills  which  therefore  contradicts  with  the  idea  that  it  helps  us  survive.