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What percentage of people were obese in England and Wales in 2021
26%
What figure is there to show there’s a growing rate of dieters
42.2% of adolescents trying to lose weight in 2015, compared to 28.6% in 2005
Solmi et al. (2015): Changes in the Prevalence and Correlates of Weight-Control Behaviours and Weight Perception in Adolescents in the UK, 1986-2015 RESULTS
Increase in weight-control behaviour over time
Higher in girls BUT a steeper increase in boys
What is over-estimation of weight associated with
Higher depression scores
Fardouly et al: Appearance Comparisons
In person comparisons the most common context
Upward comparisons most common across contexts
Upward comparisons on social media were associated with the greatest negative outcomes
What are two key clinical features of ED’s
Persistent disturbance of eating, or eating-related behaviour
Impaired physical health and psychological wellbeing
Pica ED
Eating non-nutritive or nonfood substances
Rumination disorder
Repeated regurgitation of food
Anorexia Nervosa (AN): Characteristics and Subtypes
Characteristics
Restriction of energy intake relative to requirements, leading to significantly low body weight
Intense fear of gaining weight
Disturbance in the way one’s body weight or shape is experienced
Subtypes
Restricting
Binge-eating/purging
What is AN mortality rate compared to peers
AN has 5 times higher mortality rate than peers
Bulimia Nervosa (BN): Characteristics and Subtypes
Characteristics
Recurrent episodes of binge eating
Recurrent, inappropriate compensatory behaviours to prevent weight gain
Self-evaluation unduly influenced by body shape and weight
Not experiencing AN
Subtypes
Purging
Non-purging
How often should binge eating and compensatory behaviours occur on average to be clinically significant
1 per week for 3 weeks
If someone reaches the criteria threshold for both a AN and BN diagnosis, what will they be diagnosed and treated for?
AN due to higher mortality rates
What distinguishes Binge Eating Disoder (BED) from AN and BN
No compensatory behaviour
What is the frequency criteria for a BED diagnosis
At least once a week for three months
What are some common comorbidities of ED’s
Depression
OCD
Substance Use Disorders
Personality Disorders
ASD
Diagnositc crossovers (transitions) between AN, BN, and BED
Quite common in ED’s
Transition between two AN subtypes (AN-R and AN-BP) are common
AN and BED appear quite distinct (low transition)
Criticism that the diagnostic system is not doing a good job at categorizing these disorders
An argument behind moving to a trans-diagnositc approach
Using DSM-IV diagnostic criteria, what percentage of treatment seeking adolescents and adults are diagnosed with ‘EDNOS’ or Eating Disorder Not Otherwise Specified
60%
Who might be diagnosed with EDNOS?
Individuals who display quite severe symptoms but don’t quite meet the criteria for a diagnosis but still has a severe impact on their life
People may display symptoms across different diagnosis
What diagnosis supports a trans-diagnostic criteria?
EDNOS
Transdiagnostic CBT-Model
Developed to account for the high degree of movement between the different diagnosis
Useful model for individuals who fall under the EDNOS diagnosis
All of these might not apply to individual with ED, but useful for personalised understanding and treatment approach
Prevalence of ED’s: BED, BN, AN, ENDOS
Binge Eating Disorder: 2%
Bulimia Nervosa: 1%
Anorexia Nervosa: 0.9% women, 0.3% men
Other specified/unspecified ED’s: most common
Prevalence of AN over time
AN stable for the past decades, incidence among those under 15 years old has increased
Prevalence of BN over time
BN increased in the 1970s-1990s, now declining
In Bassett and Ewart (2023) study looking at media depictions of ED’s, what was the most commonly depicted demographic (sexuality, ethnicity, gender, age)
Heterosexual, White, Women, Under 30 years of age
Average age of onset: AN, BN, BED
AN
Age 16 to 20
BN
Age 21 to 24
BED
Age 30 to 50
Gender and ED disorders
Gender ratio previously thought to be 10:1, now estimated 3:1
Higher prevalence in gay and bisexual men than straight men
Biological Factors in EDs
Genetics
Hormones
Neurological factors
Biological Factors in EDs: Genetics through family
ED’s seem to run in families
Strober (2000) found ED’s at least 3x more common among relatives of individuals with AN or BN than among relatives of individuals without AN or BN
AN over 10 x more common in relatives of AN sufferers
BUT looking at families doesn’t allow us to separate potential genetic and environmental factors
AN Diagnosis in MZ vs. DZ Twins (Genetic Factor)
MZ twins show 58% concordance comapred to DZ twins (5%)
Conclusion
Some genetic contribution
If there is a genetic mechanism underlying the familial patterns, it is more consistent with increased susceptibility as opposed to an all-or-nothing mechanism
How is the genetic influence mediated
Three underlying mechanisms:
Via the determination of body weight/shape/size
Via the determination of brain chemistry
Via the determination of personality traits (including neurocognitive and socio-emotional profile)
Not necessarily mutually exclusive
What brain structures are involved with ED’s
Hypothalamus
Ventromedial and lateral hypothalamus are involved in satiety and appetite
Frontal Cortex
Temporal cortex is involved in body image perception
Orbitofrontal cortex is involved in monitoring the stimuli pleasantness (smell and taste)
Linked to development of AN and sometimes BN
Hypothalamus: Animal studies
Animal studies have found that lesions to the ventromedial hypothalamus increase hunger and the inability to regulate intake WHEREAS stimulating stops eating
Animal studies had found the opposite effects in the lateral hypothalamus (lesions stop eating and visa versa)
HOWEVER, there’s not a lot of clear evidence of abnormalities in the hypothalamus of individuals with ED’s, but still rationale to say it was a role in weight recognition
Maybe it is the network of this brain area to others (such as the amygdala) which is important
Neurotransmitters that have a role in ED’s
Serotonin and Dopamine
Neurotransmitters role in ED’s: Serotonin
Most popular neurotransmitter in AN research given its involvement in mood, obsessions, appetite regulation and impulse control
Patients with AN have low levels of serotonin metabolites (5-HIAA)
Following recovery, patients with previous AN or BN have higher levels of 5-HIAA than controls
Might experience over activity
Neurotransmitters role in ED’s: Dopamine
Recent interest given its role in reward systems
Foods high in sugar and fat usually what individuals engage with when binge eating
Also being less sensitive to food reward might ‘help’ individuals with restricting food intake
What is Set Point Theory
States there is a biological control method in humans that actively regulates weight towards a predetermined set weight for each individual
Body tries to keep us at this set weight, hormones may be used to regulate this
What are the Hormones involved in appetite and weight regulation: Set Point Theory
Leptin
Satiety hormone
Reduces food intake
Profoundly disturbed in AN
Grehlin
Hunger hormone
Increases food intake
Puberty and the Role of Sex Hormones
Puberty key risk period of ED onset
Before puberty, genetic influences account for ~0% of the variability in disordered eating, where as genetic factors account for over 50% during and after puberty
What is the hormone thought to “activate” genetic risk for disordered eating in girls during puberty
Ovarian hormones
Oestradiol is potent regulator of gene transcription in CNS, thought to activate genetic risk in girls during puberty
Fordouly et al. (2023): Social media mirco-interventions to improve young women’s body image and mood
A Facebook ‘micro-intervention’ to improve body image
Randomly assigned one of:
Body positive Facebook group
Appearance neutral Facebook group
Facebook as usual
Results
Body positive and neutral groups experienced decreased body dissatisfaction
Body positive group experienced decreased appearance comparisons
Small to medium effects