Patients with anorexia nervosa often have difficulties recognizing and regulating emotions. This conclusion that is largely based on data from common tests such as Reading the Mind in the Eyes assessing emotion recognition, and questionnaires like Difficulties in Emotion Regulation Scale (DERS) assessing emotion regulation (see my post here). Although that study compared currently ill patients with healthy controls (thus raising the possibility that the resulting data was due to the effects of starvation or due to the chronic nature of the ED in the sample, ~7.5 year on average), there is some evidence that some of these difficulties persist post-recovery.
Individuals with autism (ASD, or autism spectrum disorders) also have difficulties with emotion recognition and regulation, leading some investigators to hypothesize that AN and ASD may share common etiology. Providing further support for this hypothesis are studies suggesting that AN might be overrepresented in ASD and vice versa. (That is to say, the prevalence of AN in ASD patients or vice versa is higher than the population mean.)
This doesn’t mean that all patients with one disorder have the other, or even a majority – just that the prevalence is significantly higher than you’d predict based on epidemiological data. In my view, this observation and this line of research is important for understanding the biological basis of these disorders. (Keep in mind, too, that whereas DSM demarcations are artificial, human traits are continuous – there is always a spectrum of behaviour.)
In this study, Oldershaw et al evaluate patients with AN on various cognitive tasks utilized in studying autism spectrum disorders and compare the results with published ASD data. First, though, Oldershaw outlines three main neurocognitive theories regarding autism spectrum disorders:
Neurocognitive Theories of Autism Spectrum Disorders
Empathising-Systemising Hypothesis – (Baron-Cohen, 2002)
– hypothesis explains strengths and weaknesses in ASD patients
– patients with ASD have difficulties with inferring what another person thinks (Theory of Mind), deficits in the RME task
– patients with ASD tend to excel “working with systems”, strengths in systemising
Executive Dysfunction Theory – (Hill, 2004)
– attempts to explain the “need for sameness”, repetitive and restrictive behaviours in ASD
– poor set-shifting abilities (difficulty adapting to new rules, for example)
Weak Central Coherence – (Frith, 1989)
– seeks to explain obsessional preoccupations, need for sameness, and “niche abilities”
– weak central coherence is essentially the inability to “see the forest for the trees” or “see the bigger picture”
– poor global integration of information and excellent ability to focus on detail
There have been some studies suggesting that patients with AN score similarly to patients with ASD on tasks measuring central coherence and executive function, again, suggesting that there might be an overlap in the biological basis of these disorders.
The participants were 50 adult with AN, recruited from an outpatient unit. Two were male, and all had a BMI of less than 18.5. The sample was not limited to AN-restricting subtype, and included 9 AN-binge/purge subtype and 19 EDNOS (AN-type). I am a bit surprised by the decision to include AN-BP and AN-EDNOS, to be honest. I would have liked to see comparisons made based on subtype. No information was given about the length of the disorder or the average BMI, unfortunately.
The tests and questionnaires that Oldershaw used to assess the cognitive profiles of individuals with AN were: reading the mind in the eyes task (RME), reading the mind in the voice task (RMV), reading the mind in films (RMF) (theory of mind); Wisconsin card sorting task (WCST) (executive function); group embedded figure test (GEFT) (central coherence).
SUMMARY OF THE MAIN RESULTS
Theory of mind:
- groups were matched for age, but AN IQ was lower than in the ASD group
- compared to ASD, AN scored better on RME, the same on RMV and worse on RMF tasks
- AN older than ASD patients, but well matched for IQ
- no differences were found on the Wisconsin Card Sorting Task
- again, AN were older than ASD patients, but well matched for IQ
- no differences were found for the GEFT task (no differences between groups in the mean time to locate a simple shape within a complex design)
So, it seems that for the most part – at least for the tasks evaluated in this study – AN and ASD patients share similarities in neurocognitive profiles. This probably comes as no surprise to clinicians and caregivers of AN patients. What is surprising to me is that this similarity is apparent even in such a mixed AN group (restricting, binge-purge and ednos subtypes). My guess would have been that this similarity would be more apparent in a more long-term AN-R group that has never had symptoms of bingeing and purging.
The main question that still remains unresolved is whether these traits, in the AN group, are stable (that is, they were there before the AN diagnosis and likely persist after), and if so – to what extent? And conversely, to what extent are these results due to starvation?
ASD is a relatively consistent, lifelong developmental disorder whilst AN is a mental illness which can ﬂuctuate in severity and be recovered from. Patients included here were acutely ill and underweight and as such the pattern of cognitive deﬁcits in AN may represent non-speciﬁc consequences of the starved state (e.g. non-speciﬁc brain dysfunction) rather than speciﬁc traits associated with a diagnosis of AN.
Therefore, the deﬁnition of AN at the cognitive level requires additional research to confirm whether proﬁles are trait-like and this has crucial implications in the search for genetic markers. Research including recovered AN participants and longitudinal methodologies is in its infancy, but thus far indicates that weak central coherence (Lopez et al., 2009), executive dysfunction (Tchanturia, Morris, Surguladze, & Treasure, 2002; Tchanturia, Morris et al., 2004) and poor emotion recognition (Harrison, Sullivan, Tchanturia, & Treasure, 2010; Oldershaw et al., 2010) may be trait features of AN, while eToM difﬁculties may be restricted to the ill state (Oldershaw et al., 2010).
Are there alternative explanations?
Of course, there are other explanations that could explain the results. As an example, Oldershaw et al point out that obsessive-compulsive traits are not only predictive for the development of an ED but also could explain the rigid cognitive thinking styles present in AN. Another example is perfectionism, which may underlie the attention to detail seen in AN.
Since both perfectionism and obsessive-compulsive personality traits are heritable, they are thought to account for some of the genetic predisposition to AN (Anderluh et al., 2003). Therefore, an overlap at a cognitive level does not necessarily imply common underlying psychological, neurobiological or genetic bases for AN and ASD…
Basically, we need more research. (As if you didn’t know that already.)
As always, I try to point out the limitations of the study (most of which are mentioned by the authors themselves), to make sure that the results are interpreted in their proper context.
- the ASD data wasn’t collected by one research group (but was taken from previously published data)
- participants may represent extreme/severe examples (as they were recruited from a specialized care centre, this may exaggerate certain traits)
- ASD sample had higher IQ than AN (and thus may be not very generalizable)
- no data on the presence of ASD in AN sample or AN in ASD sample
- gender bias (AN is 95% female, ASD, at least 80% male) may bias results (women tend to score better on empathy, men tend to be faster and more accurate on GEFT)
- only the detail focus aspect of central coherence was studied (global integration still needs to be evaluated)
In any case, we have to wait and see to what extent – if any – these results can be replicated and whether they are state-related (due to the disorder) or trait-related (persist before and/or after the disorder) factors.
As always, I’m interested in reading your thoughts on this topic. I’m especially interested in hearing from those who have been diagnosed with both – do you think there is a connection or it is just by chance? What implications does this have – if true – for treatment and recovery?