Autism (Associations (ASD and Anorexia:
Diagnosed when a person becomes…
ASD and Anorexia:
- Diagnosed when a person becomes significantly underweight due to restricted eating, reflecting an intense fear of putting on weight and a distorted body image (APA, 2013)
- Onset typically in adolescence/early adulthood, affects over 10 females to 1 male, and high rates of mortality
- Around 25% of women with AN meet criteria for ASD (Anckarsat et al., 2012)
- Rastam et al. (2003) 3 features that overlap between ASD and AN: impaired theory of mind (ability to recognise that people have independent mental states), impaired central coherence (ability to see the ‘bigger picture’) and impaired set shifting (ability to shift from one course of action to another fluently and with little difficulty), and conditions such as Alexithymia (inability to identify and describe states of emotion)
- Given treatment resistance in AN and high mortality rate, the categorical presence of ASDs in eating disorders may explain treatment resistance (Wallier et al., 2009) --> relate to females being less likely diagnosed
ASD and CPs:
- A pattern of behaviour ‘characterised by a failure to conform to society’s rules and expectations’ (Rutter and Rutter, 1993)
- Children with disruptive behaviour known to have problems with social understanding --> many studies focusing on how children with CPs misinterpret others' intent
- More recent: Donno et al. (2010) 26 children persistently disruptive at school more severe difficulties with reciprocal social interaction, more severe pragmatic language difficulties and greater difficulties with ToM than controls
35% of these qualified for an ASD diagnosis compared to 0% controls
- This was independent of IQ --> pragmatic difficulties are not just a function of intelligence
- Difficult to tell if influence if due to gender because less girls than boys engage in antisocial behaviour in elementary school
What happens when consider new model, and not high on both social impairment and inflexibility and sensory abnormality?
- low social problems but high inflexibility/sensory abnormality = anorexia
- high social problems but not low inflexibility/sensory abnormality = CPs
Huke et al. (2013) difficult to test whether ASD traits are artefacts of starvation
- 1) argument that ASD traits are purely a factor of starvation effects on cognition:
e.g. Keys et al. (1950) Minnesota starvation expt. Semi-starvation = obsessionality, inflexibility in previously healthy p’s
-Oldershaw et al. (2010) can be a recovery of theory of mind/emotional theory of mind with nutritional improvement, especially in recognition and experience of one’s own emotions(but not set-shifting)
- 2) argument that ASD traits apparent before:
-AN and ASDs coexist within families (Gillberg, 1983) --> sig. more individuals in AN group have 1st degree relatives with 2 or more of the 4 DSM-IV social impairment symptoms of autism (31% vs 12% controls)
-ASD sig. more likely to be apparent in retrospective AN sample compared with a control group after 10 years - Berkman et al. (2007)
-in an 18-year follow-up study of those fitting the ASD criteria, the comorbidity of AN was associated with a greater likelihood of a poor outcome than for those without (Wentz et al., 2009)
-Set-shifting difficulties appear to persist after recovery (Tchanturia et al. 2004) = it may represent as an endophenotype, to eating disorders.
Suggests social and communication elements of ASD that carry risk for CPs
- All children presenting with conduct problems, especially those of early onset, should be screened for ASD, and for ASD traits
- In particular social and communication difficulties should be considered and if present these should be incorporated in the formulation of CPs
Myth is that social and non-social (sensory and inflexible processing) impairment make up ASD in equal amounts/are highly correlated.
- Social = understanding rules of social behaviour, difficulty understand gestures and facial expressions
- Inflexibility and sensory processing - difficulty processing everyday sensory experiences (e.g. noise, light is overwhelming) and repetitive interests behaviours and activities
- Different developmental trajectories for different parts of the triad --> rigid/repetitive behaviours emerge later than social & communicative difficulties, are less good markers of autism in infancy, improve less with age, and respond less well to some intervention programs (Aldred et al. 2004)
- some measures e.g. social responsiveness scale are heavily weighted towards the social domain do not show fractionation of the triad at behavioural level = unclear what different findings can be attributed to differences in measures
Last half a century looked at cause and cures as a whole, based on a triad of behavioural impairments (social interaction, impaired communication and restricted and repetitive interests and activities)
- BUT, Ronald et al. (2006) modest to low correlations between ASD like behavioural traits in these 3 areas, and even social and communication impairments only modestly related
- Considerable no. children showed isolated difficulties in only one area of the triad e.g. 59% who showed social impairments showed only impairments in this aspect of the triad
Genes for autism or independent traits?
- Ronald et al. (2006) comparison of 3,000 MZ and DZ twin pairs at age 7 and 8 suggests that each aspect of the triad is highly heritable, across both the range of individual differences and at the extreme. BUT model-fitting analyses of cross-twin, cross-trait correlations suggest that more than half the genes that contribute to variation in, say, social (dis)ability are independent from those that contribute to variation in communicative skills or rigid/repetitive tendencies
= most of the genetic effects at middle school are specific, acting on just one part of the triad
- Kuhl et al. (2005) lack of preferential attention to speech in autism associated with specific abnormalities in EEG studies
- Gervais et al. (2004) lack of activation of superior temporal sulcus voice-selective regions in response to vocal sounds has been reported
Issues of construct validity:
- e.g. RIBA construct may comprise diverse behaviours that do not all share the same aetiology. Factor analyses have shown 2 factor model of repetitive interests behaviours and activities --> insistence on sameness and repetitive sensory motor actions (Richler et al. 2007)
Males and females
- Mandy et al. (2011) found no IQ sex differences
-By parent report and direct observation, females had less repetitive stereotyped behaviour (RSB), with male-equivalent levels of social and communication impairment.
-Teachers reported males with ASD as having greater externalising and social problems than females.
-The female phenotype we describe was stable across our sample’s age range.
-Their milder RSBs and less severe difficulties at school may lead to under-recognition of ASD in females.
Prevalence rates suggest more cases of ASD in boys than girls but does this actually represent incidence? e.g. less likely to be diagnose/more able to camouflage symptoms
- More women in non-referred than clinical samples = why aren’t as many women going into clinics for treatment?? Stigma attached?
- Constantino and Todd (2003) - 788 pairs of twins, used ‘social responsiveness scale’ (parent-ratings) levels of severity of autistic traits at or above the previously published mean for patients with pervasive developmental disorder were found in 1.4% of boys and 0.3% of girls.
The genes influencing autistic traits appear to be the same for boys and girls --> Lower prevalence (and severity) of autistic traits in girls may be the result of increased sensitivity to early environmental influences that operate to promote social competency
Why less diagnosed?
- Hiller et al. (2014) females have a higher social motivation than males = don't exhibit classic social impairments to extent males do?
- Culture-based gender role expectations may drive girls to adopt more interpersonal processes to modify their behaviours (e.g. censoring of behaviours, mimicry of salient gender-normative behaviours, adopting social scripts) --> also a role of the media in aiding these presentations -Kreiser and white (2014)
- Lai (2015) have a greater ability to camouflage autistic difficulties
- e.g. Mandy & Tchanturia (2015) --> can be conscious or automatic: masking (deciding to suppress stimming behaviours in public as they can attract negative attention) and compensation (copying popular peers in how they dress, use gesture, how they talk, etc.)
- Green et al. (2014) Meta analysis: females on average have less repetitive and restricted behaviours and interests than males (normal social communication difficulties) --> but these tests might be male biased because the items were formed with perception of longstanding male predominance
- Might be because when women have specific interests = tend to be more stereotypical e.g. fashion, and more normative/less unusual (Hiller, 2014)
- Beeger (2013) age of diagnosis is later in females than males --> what if the need for diagnosis differs? e.g. emerges later than males, in adolescents
- Identification issues: may reflect gender-based interpretation bias from sources of referral (e.g. family, school) or diagnostician e.g. interpreting social difficulties as "just being shy" (stereotyped as female-typical) - Goldman (2013)
- Greater diagnostic overshadowing/substitution in females by co-occurring/secondary conditions e.g. anxiety/depression, or misdiagnoses (Trubanova et al. 2013)
- Mandy et al. (2012) males more likely to also develop externalising disorders e.g. CP, whilst women more likely to develop internalising disorders e.g. eating disorders
- ‘Autism’ = label that describes a collection of phenomena, namely impairments in social interaction and communication, along with repetitive interests, behaviours and activities (American Psychiatric Association, 2000).
- Highly co-morbid with anxiety and depression but seen as a secondary symptoms i.e. result of lack of understanding of social interactions
- Based on behaviour: but, can have many different causes of the same behaviour, different manifestations of the same cause (not allowing for age, ability, good/bad days, education, temperament, family environment = hard to assess behaviourally), and means treatment of the symptoms rather than the cause of ASD
- Heterogeneity leads to it being referred to as an autistic spectrum in the literature --> varies in presentation, course and outcome (developmental differences, in the quality and intensity of their core autism symptoms, their adaptive and cognitive levels and responses to therapy)- Dover et al. (2007)
- Know there are biological causes, it is a biologically based condition:
Strong genetic component- concordance in MZ twins= around 90%, highest of any psychological disorder, rare genetic mutations account for 10-20% of cases and there are 400-1000 risk genes **(Daly et al. 2012). **
Site of impact in the brain
BUT can't diagnose biologically as no markers- not surprising given behavioural heterogeneity
Old view, DSM-IV:
New view, DSM-V:
- A rare, unitary neurodevelopmental disorder that mainly affects males, usually associated with intellectual disability, and categorically distinct from normal development and from other disorders.
- This description contains a number of myths that the new view, DSM-V, attempts to account for
- A relatively common, non-unitary neurodevelopmental disorder with a gender- specific presentation, usually associated with normal-range IQ, and representing the extreme of a trait distributions that extend throughout the general population.
ASD is rare
- Taylor et al. (2013):
between 2004-2010 in UK, prevalence rates for each year were steady at approximately 3.8/1000 boys and 0.8/1000 girls. Annual incidence rates each year were also steady at about 1.2/1000 boys and 0.2/1000 girls.
- Hansen et al. (2015):
assessed all children born alive from January 1, 1980, through December 31, 1991, in Denmark (n = 677 915). The children were followed up from birth until ASD diagnosis, death, emigration, or the end of follow-up on December 31, 2011, whichever occurred first. Found 60% of the increase in reported ASD prevalence could be explained by the change in diagnostic criteria and the inclusion of outpatient contacts = reporting practices are important in prevalence rates
- Verhoeven (2010) original estimate 40 years ago 4 per 10,000 changed into today’s epidemiologic studies of autism reporting a prevalence of 5-10 cases of classic autism per 10,000 to even 60–65 per 10,000 cases when including the entire spectrum.
- Prevalence does not mean incidence: change in part due to broadening of diagnostic spectrum or due to increased awareness of the condition = people being diagnosed who wouldn't have been 20-30 years ago (can't rule out a true rise over time)
Assumption that people with ASD have impaired intellectual ability, but many cases of people with high functioning autism
- Centers for Disease Control (2014) reported percentage of children with ASD, with and without intellectual disability: only 30% with intellectual disability, 70% normal intellectual functioning
- Autism was widely conceptualised as a discrete category, qualitatively different from other disordered as well as typical states (Jensen et al. 2006). But consensus is emerging that autism is actually a dimensional disorder, reflecting developmental difficulties at the extreme end of a continuum
- evidence for the dimensional approach provided by studies showing that autistic traits are found in large general population samples (not just in relatives of autistic people), and that they are continuously distributed, with no natural boundary between normality and psychopathology, as would have been evidenced by a bi-modal distribution (Posserud et al. 2006).