Eating Disorders 1: Presentations, theories, causes, and maintaining factors

Define an eating disorder, and understand the diagnoses involved Detail how many cases of eating disorders exist in the population Distinguish and detail theories of causation and of maintenance Use this understanding of causation and maintenance to explain cases

internal balance mechanism in body

homeostasis

homeostasis function

keep eating evenly and diversely, ensure well nourished

what two concepts r being balanced by homeostasis in eating

hunger

satiety

problems w homeostasis

hunger and satiety influenced by interfering factors

influences on hunger - problems for homeostasis

genetics

learning

social learning

influence on satiety- problems for homeostasis

social pressures

food industry

toxic environment

eating disorders (Fairburn & Walsh, 2002)

a persistent disturbance of eating behaviour or behaviour intended to control weight, which significantly impairs physical health or psychosocial functioning

ed diagnoses- over time

change over time, suggesting not rly there yet

icd tends to follow dsm

what

bmi

weight in kg) / (height in m)²

healthy range bmi

19-25

bmi- how is it determined

• not biologically

• varies w factors like ethnicity

bmi and younger ppl

• not very meaningful for them

• use expected weight for height, adjusted for age

bmi underweight categories for u18s

< 85% underweight

< 70% dangerously underweight

overweight bmi

> 25 < 30

obese bmi

> 30

anorexia nervosa - diagnostic criteria, meet all of these features:

• persistent restriction of energy intake leading to significantly low body weight

• either: intense fear of gaining weight or becoming fat or persistent behaviour that interferes w weight gain (even tho signif low weight)

anorexia nervosa- diagnostic criteria, meet at least one of these features:

• disturbance in the way one’s body weight or shape is experienced

• undue influence of body shape and weight on self-evaluation

• persistent lack of recognition of the seriousness of the current low body weight

subtypes of anorexia nervosa

• restricting

• bing-eating/ purging

critical thought re anorexia definition

• ppl differ in set point for weight- limitation of using weight/bmi

• various suggestions for bmi marker over years- e.g.: atleast 15% below, under 17.5, adjust for ethnic groups- all have conceptual and practical problems

• athletes tend to count as overweight (more muscle)

• ballerina and gymnasts sanctioned to b underweight

• weight not a surefire indicator

weight and anorexia

• better at spotting extreme examples

• esp when seen b4 and after states

• or weight loss is way beyond bmi of 17.5

  • hwvr might be starvation for other reasons e.g. the Dutch Hunger Winter

The Dutch Hunger Winter

• 1944-1945

• famine

• german occupied netherlands

• esp in densely populated western provinces north of great rivers

bulimia nervosa- diagnostic criteria

• recurrent episodes of binge eating

• recurrent inappropriate compensatory behaviour in order to prevent weight gain

• binges and compensatory behaviours both occur, on avg, at least 1x week for 3mo

• self-eval unduly influenced by body shape/weight

• not occur exclusively during episodes of AN

binge eating definition

• eating, in a discrete period of time, more than most wld eat during similar period and under similar circumstances

• a sense of lack of control, overeating

inappropriate compensatory behaviour in BN

• self induced vomiting

• misuse of laxatives, diuretics, other meds

• fasting

• excessive exercise

issues w bulimia nervosa definition

• limitations of binge definition

-subjective (loss of control)

-objective (loss of control + excessive intake)

-what counts as excessive? over 2-3000?

• defining compensatory behaviours

-is vomiting always self-induced?
-exercise for health or to control weight?

• keep changing freq/often/amount of behaviours

binge eating disorder- diagnostic criteria

• recurrent episodes of binge eating

• marked distress re binge eating

• bingeing at least 1x per week for 3mo (mean)

• no purging or compensatory behaviours

• episodes associated w 3 or more of 6 behaviours

binge eating

•eating, in a discrete period of time more than most people would eat during a similar period and under similar circumstances

•a sense of lack of control over eating during the episode

what must episodes be associated w in BED

at least three of the following:

•eating much more rapidly than normal

•eating until feeling uncomfortably full

•eating large amounts of food when not feeling physically hungry

•eating alone because of feeling embarrassed by how much one is eating

•feeling disgusted with oneself, depressed or very guilty afterward

when was binge ED first proposed

1980s, took many years to be adopted

accessibility of treatment w BED

most towards AN and BN so may be more difficult to access

critical thghts of BED definition

• same as BN- issues defining binge

• recent formal diagnosis (only formalised in 2013 w DSM-5) → so still some debate re definitions (number of binges, over how long)

• need to understand motivation for bringing in this category

motivation for bringing in BED category

• genuine distress and need for treatment

• access to insurance funding for clinicians as way of treating a lot of overweight/obese patients

name for eating disorders which are atypical

other specified feeding and eating disorders (OSFED)

what was OSFED previously known as

EDNOS

OSFED definition

• present w many symptoms of other EDs but do not meet full criteria for diagnosis

• significant EDs

why were OSFED introduced

• clinical reasons in USA- need diagnosis for insurance to pay for treatment and services

• also to help progress research by better defining group

OSFEDs

• atypical anorexia nervosa

• atypical bulimia nervosa

• atypical binge eating disorder

• purging disorder

• night eating syndrome

atypical anorexia nervosa

despite significant weight loss, individual’s weight is within or above normal range

atypical bulimia nervosa

of low frequency and/or limited duration

atypical binge eating disorder

of low frequency and/or limited duration

ARFID

avoidant/restrictive food intake disorder

ARFID- who

primarily but not exclusively children and young ppl

ARFID- criteria

• disturbance in eating or feeding

-substantial weight loss/lack of weight gain

-nutritional deficiency

-dependence on supplements

• absence of typical ed beliefs abt food or fear of weight gain

• replacing and extending what was called selective or fussy eating

subtypes of ARFID

• sensory-based avoidance

• lack of interest

• food associated w fear-evoking stimuli

refusal of food intake based on smell, texture, colour, brand, presentation

sensory based avoidance ARFID

what is the lack of interest in in ARFID

in consuming food or tolerating it nearby

how have fear evoking stimuli developed in ARFID

thru a learned history

effective ARFID treatments

primarily behavioural, focusing on anxiety/exposure

Fairburn et al (2003): criticism of eating disorder diagnosis

diagnosis of specific eating disorders does not do what it should

evidence for Fairburn et al . (2003)’s criticism

diagnosis of specific EDs does not do what it shld:

• 40-50% of cases do not fit neatly into diagnoses

• atypical cases (OSFED) are single largest group

• many fail to stay in one diagnosis

• does not even indicate best treatment

as consequence to Fairburn et al. (2003)’s criticism, what is happening?

something of a shift away from rigid diagnoses- transdiagnostic model

Fairburn et al., (2003), Waller, 1993: eating disorders

transdiagnostic model

the underlying biological causes and consequences of EDs mean the following must be considered:

• co-occuring psych problems

• anxiety disorders (ocd, social)

• depressed mood (low serotonin)

• complex emotional and relational needs (personality disorders (anxiety and impulsivity based))

• alcohol and substance use (alc as higher risk)

high mortality rates of EDs due to range of problems, incl:

•cardiac complications

•muscular weakness (including cardiac failure)

•osteoporosis

•liver damage

•oesophageal tearing

•fainting

incidence definition

number of new cases in set window of time

prevalence definition

number of current cases (point …) or number of people who have had the problem over the past year (annual …) or case over lifetime (lifetime …)

types of prevalence

• point

• annual

• lifetime

why is it hard to calculate ed incidence

slow onset + secrecy + slow diagnosis

do we focus on prevalence or incidence of EDs and why

• hard to calc incidence

• can take a while to detect new cases

• so focus on prevalence

prevalence rates- Beat (2012)

est about 750,000 in UK

c.1% of population

prevalence rates- Beat (2012)

prevalence - issues

depends on assumptions made

most focus on young, female population (14-30yo)

lifetime prevalence of AN (van Eeden et al., 2021)

4% women

0.3% men

lifetime prevalence of BN (van Eeden et al., 2021)

3% women

1% men

lifetime prevalence of BED (Galmiche et al., 2019)

2.8% women

1% men

what does Galmiche et al., 2019 indicate

OSFED highest lifetime prevalence

highest lifetime prevalence

OSFED Galmiche et al., 2019

Silen & Rahkonen, 2022

in western cultures, binge eating lifetime prevalence up to 6.1% in women and 0.7% of men

medical records revises and case numbers of EDs- can they tell us number of cases?

• no, only say how many were spotted not how many there were

• beware reports re epidemics and rocketing numbers- cld be raised awareness

• gps miss cases even where v undeweight and esp if person is not young, white, and female

what is happening year

seems like epidemic of EDs

acc bc more awareness being raised (Currin et al., 2005)

not abt new cases

what is related to increasing identifcation and prevalence of EDs

westernisation

Curacao study

showing more cases among non-whites in recent years (Hoek, 2006)

Fiji study (Becker et al., 2011)

clear link w prevalence to introduction of western media

both TV and more social network based exposure e.g. home DVD

objective of Curacao study

AN once thght to only occur in affluent societies, cases now been documented globally so, to examine whether AN emerges in societies undergoing socioeconomic transition

what did authors study in Curacao study

incidence of AN on Caribbean island Curacao

method Curacao study

• contacted full range of community health service providers, incl dieticians, school counsellors, all 82 GPs

• studied inpatient records for 84,420 admission to Curacao General Hospital and two private hospitals in 1995-1998

• probable incident subjects were interviewed

results of Curacao study

incidence rates in 1995–1998 per 100,000 person-years for AN were 1.82 (95% confidence interval [CI]=0.74–2.89) for the total population

were 17.48 (95% CI=4.13–30.43) for the high-risk group of 15–24-year-old females.

no cases were found among the majority black population.

for mixed and white population, the incidence rate per 100,000 person-years for anorexia nervosa was 9.08 (95% CI=3.71–14.45)

Curacao study: incidence rates in 19__-____ per 100,000 person-years for AN were ____ for the total population

1995-1998

1.82

Curacao study: incidence rates in 1995-1998 per 100,000 person-years for AN were ____ for the high-risk group of __________

17.48

15-24 yo females

Curacao study: how many cases of AN found in majority Black population?

zero

Curacao study: incidence rates in 1995-1998 per 100,000 person-years for AN were ____ for the mixed and white population

9.08

Curacao study: conclusions

• overall incidence of AN much lower than in affluent societies of USA and Western Europe

• sociocultural factors appear to be associated w differential incidence rates of AN

• incidence of AN amongst majority black population is zero

• incidence among minority mixed and white ppl similar to that of USA and Netherlands

causation of EDs

• lots of sociocultural and neurobiological factors

neurobiological factors + clarity

• unclear

• hypotheses more common than acc evidence

• genetics

- some evidence e.g. twin studies

-dk where responsible genes r

-are genes responsible for ed.s directly or for other risk factors. e.g. perfectionism, serotonin mechanisms that predispose to impulsivity or compulsivity

• hypothalamic damage, preventing hunger?

-but AN patients report lots of hunger

issues underpinning identification of neurobiology in EDs

• exacerbated by issue of causality

• does dysfunctional biology result in ED or does ED result in dysfunctional biology

which starvation effects seem to go away when a person eats

• mood deficits

• cognitive deficits

• social isolation

• behavioural inactivation

→ important re treatment planning

important questions re ed maintenance

•If we cannot identify clear, universal pattern of predictors, can we identify what keeps the problem going once it has started?

•Eating disorders can and do last for years, so how to stop them as soon as possible?

•If we identify maintaining factors, can we interrupt them?

cognitive patterns common in EDs

• low self esteem

• negative self attribution

• perfectionism

what do cognitive patterns each have in EDs

self-maintaining cycle

self maintaining cycle, low self esteem

means do not look for positive things about ourselves. so remains that way

self maintaining cycle, high perfectionism

meaning we avoid things wrong, rather than we are good at anything, so have to keep striving

two main central belief systems/ cog patterns

• broken cognitive link

• overvaluation

broken cognitive link between…

eating and weight; driving restriction, then binging, then gaining weight, then restricting

what does broken cog link have

strong cognitive dissonance element

Waller and Mountford (2015)

• assumption even a small amount of eating will lead to disproportionate weight gain

• assumption that any weight gain will be uncontrollable and unstoppable

• therapeutic task is help rebuild broken cog link

assumptions re broken cog link by Waller and Mountford 2015

• even small amt of eating will lead to disproportionate weight gain

• any weight gain will be uncontrollable and unstoppable

what do Waller and Mountford 2015 say the therapeutic task is

help rebuild the link

overvaluation…

of appearance and weight as defining ourselves as being acceptable people

what are safety behaviours

behaviours that calm us temporarily when we are anxious but where the long term consequence is that we feel worse