1/63
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
ventral medial hypothalamus (VMH)
helps you know when you’re full
lesions (destruction) cause overeating/elevated weight
stimulation causes starvation
lateral hypothalamus (LH)
helps you know when you’re hungry
lesions (destruction) cause starvation
stimulation causes overeating/elevated weight
brain activity and neurotransmitters
within brain cells (neurons), signals are carried electronically
between neurons, signals are transmitted by chemicals (NTs)
serotonin (5-HT)
dopamine
norepinephrine
serotonin/EDs
serotonin involved in regulation of appetite, mood, impulse control
decreases food intake/weight
serotonin hypothesis of EDs
AN caused by over-function of serotonin
BN caused by under-function of serotonin
studies:
studies DON’T support serotonin hypothesis for AN
evidence showed serotonin function is reduced in AN
studies DO support serotonin hypothesis for BN
higher binge frequency associated w/ lower cerebrospinal fluid serotonin levels
leptin
reduces food intake
genetic mutation makes mice unable to make leptin
overeat, low metabolism, weight gain, development of diabetes in adulthood (impacts of not being able to make leptin)
impacts in EDs
BN patients have lower levels of leptin compared to controls
consequence of weight suppression
AN patients have lower levels of leptin compared to controls
consequence of low weight
ghrelin
“hunger hormone”
results in increased food intake
functions in EDs compared to controls
AN → elevated
BN → elevated
BED → mixed
PD → elevated
cholecystokinin (CCK)
regulates gastric emptying and induces satiety
function in EDs compared to controls
AN → mixed
BN → lower
BED → normal
PD → normal
glucagon-like peptide 1 (GLP-1)
stimulates insulin secretion
function in EDs compared to controls
AN → mixed
BN → lower
BED → normal
PD → normal
peptide tyrosine tyrosine (PYY)
“satiety hormone”
function in EDs compared to controls
AN → mixed
BN → nixed
BED → mixed
PD → elevated
twin studies
MZ
DZ
results:
concordance (shared genes) for EDs is higher in MZ compared to DZ teens post-pubertally
one twin most likely to have ED after puberty if other twin has ED
twins are not at increased risk for EDs
steiger et al. (2011)
if certain alleles/genotypes are most common in ED participants than controls, then this allele/genotype may increase risk for ED
background
women w/ BN more likely to report histories of sexual/physical abuse
women w/ BN have higher cortisol levels, suggesting HPA-axis dysfunction
the C-allele (compared to G allele) of the Bcl 1 gene has been linked to higher cortisol response following a stressor via its influence on glucocorticoid receptors
hypothesis:
C allele of the Bcl 1 gene represents a diathesis (vulnerability) and abuse represents a stress that causes BN
there should be a significant interaction between history of abuse/Bcl 1 gene in predicting presence vs. absence of BN
IVs
either no history or only history
genotype (CC, GC, or GG)
GG
C allele carrier (CC or CG/GC)
DVs
presence vs. absence of BN
129 female patients w/ BN
98 “normal-eating” women
results
C allele
women w/ BN more likely to carry allele of Bcl 1 gene
abuse
women w/ BN report greater history of abuse compared to controls
odds ratio
individual affects of either a allele or abuse are eliminated in their interaction together
interaction between them is significant → they influence each other
conclusions
women w/ BN report greater history of abuse compared to normal eaters
women w/ BN more likely to carry C allele of Bcl 1 gene
both effects eliminated when evaluating interaction
combination of diathesis (c allele)/stress (abuse) that particularly predicts risk for BN
having both together increases risk for BN, not them individually
consequences of starvation
dry, brittle hair, skin, nails
fine hairs grow on body → lanugo; tries to keep you warm due to the lack of fat on the body
constipation
amenorrhea
osteoporosis/bone fractures
impaired immune system
muscle loss
major organ failures
cardiovascular complications
arrhythmia, heart failure
purging complications
electrolyte imbalance due to self-induced vomiting/diuretic/laxative mouse (can lead to heart failure)
electrolyte imbalance is the effect of multiple purging methods
erosion of dental enamel
hypersensitive gag reflex
ruptured esophagus/stomach
consequences of binge eating
elevated weight
correlated cardiovascular, metabolic consequences
compromised gastrointestinal function
enlarged gastric capacity
delayed gastric emptying
gastric emptying (rare but deadly)
inpatient treatment
this is when the patient is admitted to the hospital
reserved for the medically severe cases/those at-risk of suicide
most expensive
average cost of one month of this treatment → $30k
residential treatment
full-time treatment → go to a center where everyone’s getting treatment
resource intensive
average duration is about 83 days → average cost is $956/day, $79,348 (2006)
this is mostly limited to individuals w/ resources to cover the costs
insurance and disposable
outpatient treatment
this is when the patient sees a therapist/professional
costs substantially less compared to the other methods
$4k for a full course of CBT; $200/hr.
about $1,689 for full-course CBT w/ Medicare/Medicaid reimbursement level
have to consider the safety/health, efficacy
if someone’s at risk of death, this may not be the right treatment method for them
within-subjects designs
participant serves as their own control → changes in the same person over time
assess the baseline symptom level
begin treatment → reassess symptom level
discontinue after effective component of treatment → reassess symptom level
if the treatment is impacting the symptoms, then changes in the symptoms should be observed w/ changing presence and absence of the active treatment
limits:
limited generalizability → what works for one may not work for others
once patient is recovered, they never have the opportunity to test whether a different treatment would have been better/worse
not ethical to withhold treatment that you know works
between-subjects designs
comparing the outcomes between two groups → those who receive intervention vs. those that don’t receive intervention (or receive another one)
different people are the controls
IV → treatment condition or the group to which the patients belonged
DV → recovery, symptom reduction, something along those lines
randomized controlled trials (rct)
type of between-subjects design
active treatment group or control group (random assignment)
observes outcomes after treatment → did the number of people who recovered differ between the groups?
random assignment
increases the representativeness of those in a condition to the population that’s seeking treatment
reduces the likelihood that differences before the treatment (ex: differences in symptom severity) influence comparison of outcomes between the conditions
empirically supported interventions
evidence suggests that this is a good treatment
produce superior outcomes compared to control conditions
no treatment/waitlist or placebo or alternative treatment
also called evidence-based treatments
waitlist control
between-subjects design (w/ treatment group)
compare people who receive the intervention to the people placed on a waiting list for the treatment
whether the treatment is better than doing nothing
placebo control
between-subjects design (w/ treatment group)
compare people who receive intervention to people who receive fake treatment
mimics treatment pills (thinking you’re getting the treatment may actually help even if you’re not actually getting it)
alternative treatment control
between-subjects design (w/ treatment group)
compare people who receive the treatment to people given a different kind of intervention
two treatments studied compared to just one
comparing treatment modes
gowers et al. (2010)
three types:
specialized inpatient treatment
specialized outpatient treatment
general (routine) treatment through a service in England
acceptance/satisfaction
acceptance of randomization (treatment) greater for the outpatient care
both specialist treatments preferred over general outpatient treatment
outcome
no differences in outcome across treatment modalities
didn’t matter what you received in terms of the final improvements
improvement observed over time (good, but slow)
cost effectiveness
to achieve the same outcomes from cheapest to most expensive
specialist outpatient → general outpatient → inpatient
conclusions
specialist outpatient treatment determined to be the superior treatment modality
it’s acceptable to patients and results in higher satisfaction
produces outcomes that are just as good as the other options
costs the least amount of money
CBT for BN
Fairburn’s three stages
CBT Stage 1
CBT Stage 2
CBT Stage 3
Fairburn’s stage 1
identify the triggers and tackle them
establish control over eating w/ behavioral techniques
self-monitoring of food intake/symptoms w/ diary
prescription of a regular pattern of eating
ex: every 2/3 hours → 3 meals + 2/3 snacks
stimulus control (identify triggers to binge eating + avoid/employ incompatible behaviors)
psychoeducation on weight regulation, dieting, risks of purging
fairburn’s stage 2
explore the distorted thoughts and poke holes in them
reduce dieting/body image disturbance though a combination of behavioral/cognitive techniques, engaging in problem solving
Fairburn’s stage 3
maintenance of progress/reduction of risk for future relapse
ex: recognize and challenge dichotomous thinking to prevent lapses from becoming relapses
frequency of sessions transitions from initially being twice/week, once/week to twice/month, once/month, ending
disease-specific pathways model
focuses on specific factors that increase risk for EDs within individuals
their presence increases the risk of an ED but the absence does nothing
ex: weight/shape concerns
prevention would seek to reduce body dissatisfaction
success depends on the accurate identification of these risk factors
nonspecific vulnerability-stressor model
focus on nonspecific risk factors within individuals that contribute to EDs and other problems (ex: depression, anxiety disorders, SUDs)
ex: increased negative affect (sadness, anxiety) is a nonspecific risk factor for EDs (and depression, anxiety disorders, SUDs)
prevention would seek to reduce stress
these are the general risk factors that contribute to the etiology of many related problems
health promotion paradigm
focuses on protective factors that increase health when present and do nothing when absent (their absence does not make you sick)
focuses on the individual and the community
ex: people wouldn’t resort to unhealthy weight control behaviors if they had healthy approaches
prevention would promote healthy eating and exercise patters at the individual and community level (like workplace incentives for joining a gym)
empowerment-relational model
focuses on using the individual to change the community to help both the individual and society (based on feminist theory)
employs girls/young women as agents of change
ex: recruit girls to participate in letter-writing campaigns to ad agencies to focus on what women can do rather than appearance; empowers these girls and reduces sociocultural risk factors
universal prevention programs
includes everyone → works w/ the general population (like students in a school setting)
knowledge → improved significantly
attitudes → improved modestly in some
behaviors → largely unchanged
selective prevention programs
subsets of the population → focuses on the individual at increased risk for EDs
knowledge → improved significantly
attitudes → improved significantly
behaviors → improved significantly for in some but not all studies
more interactive programs more likely to reduce risks
indicated prevention programs
focuses on those w/ emerging problems → have already begun reporting some eating problems
knowledge → improved significantly
attitudes → improved significantly
behaviors → improved significantly
usually more effective than the universal programs
challenges for prevention
need for greater understanding of risk factors for EDs for disease-specific pathways model
narrow focus on sociocultural risk factors w/ assumptions that these have the greatest influence/easiest to change
constraints on duration/intensity of the programs
particularly true of universal programs where prevention takes time away from regular curriculum
selective/indicated preventions also face statistical/methodological challenges
selective biases may reduce difference from control conditions
individuals volunteering for prevention study may be motivated to improve regardless of efficacy of prevention
“regression to the mean” may contribute to improvements regardless of condition
planet health
a type of universal prevention program
uses the health promotion paradigm
employs longer duration/intensity than prior programs
school-based curriculum to prevent childhood elevated weight
results
elevated weight
both boys/girls showed reduced TV viewing/increased fruit/veggie consumption
prevalence of elevated weight decreased by half in intervention schools compared to control schools in girls, but not boys
in girls, reduced TV time predicted decreases in rates of elevated weight
EDs
at follow-up, 6.2% of girls in the control schools vs. 2.8% of girls in intervention schools reported use of purging to control weight
reduced time watching TV predicted reduced purging at 3-year follow-up
regression to the mean
when you test the same group at two time points; individuals w/ extreme scores (either very high or low) on the first test tend to produce scores closer to the average on the second test
scores on a test/measure reflect two things:
actual levels you’re testing/measuring
random error (ex: misreading an item)
actual levels may stay the same over time or change as an effect of intervention
random error is random and thus unlikely to affect scores the same way on the second test, allowing the score to move closer to the mean (though rank order may be relatively stable over time)
efficacy
demonstrated when intervention produces superior outcomes to the control conditions (no treatment/waitlist vs. placebo vs. alternative treatment) in RCT
this is done in a controlled setting
effectiveness
demonstrated when intervention produces improvement in naturalistic setting that mirrors how it will be employed in the real world
primary prevention
stopping an event before it occurs
hard to tackle this b/c it’s difficult to pinpoint when they may start
secondary prevention
stopping emerging problems from developing into more serious ones
outcome
how well the patients are doing at some point after they were initially encountered
where you end up at a given time
% recovered at 10-year follow-up
% ill at 10-year follow-up
course
path the patients have taken between when they were first encountered and when the outcomes assessed
how you get there
changes in illness status assessed repeatedly over follow-up
Becker et al. (2008)
background
cognitive dissonance (CD) based prevention programs
higher and lower risk groups compared to the active control group (media advocacy (MA))
IVs
treatment condition (CD vs. MA)
risk status (high vs. low)
DVs
internalization of thin ideal
body dissatisfaction
dietary restraint
bulimic pathology
results summary
hypotheses only partially supported
CD did produce improvements (for both high/low); some effects diminished over time
effects of MA, when observed, did not diminish as much as expected
across 3 DVs, CD worked well in both high/low participants whereas MA only worked in high-risk participants
this could show that MA is only good for high-risk populations
wilksch et al. (2017)
background
purely online intervention has key advantages (helps spread this a lot)
delivery does not require training of therapists/interventionists
no risk for loss of fidelity to program
no limit to number of participants
objectives
test online version of Student Bodies w/out moderator (therapist/trained interventionist) and against an active condition
develop and test an online version of Media Smart
test both in general population community w/ full range of eating pathology
results → acceptability
no differences in initiating/completing first nodule of MS-T vs. SB
among those who completed first module, significant more completed all 9 session in MS-T
only MS-T had weekly email reminders of the modules
primary results (EDE-Q global score):
no difference among those who initiated intervention/controls
follow-up measures → MS-T had lower EDE-Q scored than controls (good thing)
secondary results (weight concerns, depression, etc.):
MS-T pretty much better for everything over SB/controls
tertiary results (prevention/remission):
prevention → no significant differences
remission → MS-T significantly less likely to keep DE, but not significantly different from SB
discussion
ITT analyses produced no differences across conditions on primary outcome (not ideal)
didn’t eliminate people w/ higher symptoms b/c this mimics how interventions would be used in the real world
engagement was lower than in prior intervention studies
completely online test to fully scalable intervention
engagement even lower in SB than MS-T, suggesting value of automated email reminders
where differences were found, they favored MS-T
mortality
type of outcome domain
% dead
standardized mortality ratio (SMR) = actual mortality rate/expected mortality rate
AN associated w/ one of the highest risks of premature death of any premature death of any disorder
more recent evaluation of global burden of mental illness/SUDs suggests that Eds are 5th place for premature death (whiteford et al., 2013)
number could be due to the fact that non-Western areas also included
cause of death determined by what was on the death certificate
recovery
type of outcome domain
% w/ no symptoms (full remission)
% w/ symptoms below threshold for diagnosis (partial remission)
% still ill (non-recovery, current ED)
relapse
type of outcome domain
among those who achieved remission, % who returned to full-threshold diagnosis
crossover
type of outcome domain
% who migrate from one ED diagnosis to another one
prognostic factors
type of outcome domain
variables that predict any of the other outcome variables
mortality
recovery
relapse
crossover
crow et al. (2009)
background
several studies have supported increased risk of death in AN, including increased risk of death by suicide
fewer studies completed on BN, but small number of studies of not support increased mortality
no systematic studies on EDNOS
purpose: assess mortality in large sample of AN, BN, EDNOS w/ follow-up durations of 8 to 25 years
hypothesis
mortality rates would be high in AN
elevated mortality rates would be found in BN (due to longer duration of follow-up)
only modest elevation in mortality would be found for EDNOS
measures of mortality
crude mortality rate (CMR)
standardized mortality ratio (SMR)
results
hypothesis only partially supported
CMR for AN slightly lower than observed in previous studies; SMR not elevated significantly
CMR for BN higher than observed in previous studies; SMR significantly elevated for both all causes/suicide
CMR for EDNOS not lower for AN/BN; SMR significantly elevated for both all causes/suicide
crude mortality rate (cmr)
% of patients who died by follow-up
standardized mortality rate (smr)
ratio of observed deaths in patients to the expected number of deaths in the demographically matched sample
size of sample determines confidence interval around SMR, which determines where it differs significantly from 1
mortality in AN
franko et al. (2013)
9-year follow-up
11.6
22-year follow-up
4.37
what this tells us:
mortality goes down over the years (factoring aging death)
mortality in BN
franko et al. (2013)
9-year follow-up
1.3
22-year follow-up
2.33
what this tells us:
mortality slightly goes up
remission in AN
franko et al. (2013)
9-year follow-up
31.4%
22-year follow-up
62.8%
what this tells us:
still has recovery over 2 decades after treatment
tells patients that recovery is still possible even if they think they’re losing hope/there’s no reason to continue
positive linear relationship in recovery
remission in BN
franko et al. (2013)
9-year follow-up
68.2%
22-year follow-up
68.2%
what this tells us:
recovery pretty much stays the same; there’s not much difference
positive linear relation up until 20 years, in which it then becomes to level off
franko et al. (2018)
long-term recovery
methods:
participants
176 women originally recruited for a longitudinal study of AN/BN over 20 years previously completed interviews at follow-up
40 w/ baseline AN-R diagnosis
60 w/ baseline AN-BP diagnosis
76 w/ baseline BP diagnosis
interview: longitudinal interval follow-up evaluation EDs version
wave I: 1987-1996 → assessed every 6-12 months
wave II: 2011-2013 → assessed once and asked to recall over the past 12 months
psychiatric status rating (PSR) score for ED made weekly based on retrospective recall
5/6 = meets diagnostic criteria
3/4 = subthreshold criteria
1/2 = remission/minimal symptoms
results
for AN-R (vs. recovered) at wave II
intake diagnosis of AN-R vs. BN
intake diagnosis of MDD
for AN-BP (vs. recovered) at wave II
older age
lower BMI
higher % of weeks meeting diagnostic criteria for AN/BN
for BN (vs. recovered) at wave II
higher % of week meeting diagnostic criteria for BN
discussion
for those w/ AN-R, treatments to address both ED symptoms and depression may be important
for those w/ AN-BP/BN, features of the disorder predict the presence of the disorder at long-term follow-up
agras et al. (1974)
positive reinforcement can work when it comes to caloric intake
caloric intake can increase when being positively reinforced
this effect can still last even if you don’t actually give them the reinforcer, as long as they have done it before
diathesis
a genetic or biological vulnerability
ex: C allele of there Bcl 1 gene
Eisler et al. (2016)
MFT-AN vs. FT-AN
MFT-AN a more intensive version of FT
hypotheses
primary: MFT-AN will be more effective tan FT-AN in restoring healthy nutritional state
secondary: satisfaction will be higher in MFT-AN compared to FT-AN
methods
RCT comparing efficacy of MFT-AN and FT-AN
results
58% of FT vs. 76% of MFT in the good/intermediate category after follow-up (12 months)
other secondary outcomes:
mostly no differences (but there was a lot of missing data for secondary outcomes)
discussion
MFT-AN was superior to FT-AN
caveat: participants spent more time in MFT-AN than FT-AN
both treatments had high acceptability in terms of treatment acceptance (only one drop-out after randomization)
few hospitalizations during treatment (35) or entire study (7%)