Tag Archives: Autism

Can the causes of autism also cause depression or anxiety?

I have been following the reaction to the Spectrum 10K project by monitoring the #Spectrum10K and #StopSpectrum10K hashtags (Spectrum 10K is a project aiming to gather the DNA of 10,000 autistic individuals). I have often seen the claim that the depression and anxiety which many autistic individuals experience cannot be caused by autism. Therefore, if we want to reduce the level of depression and anxiety in autistic people there is no point studying the causes of autism. In this blog post I will analyse this claim.

It is commonly claimed that many autistic individuals have such high levels of depression and anxiety because our society does not accept them or accommodate them. Some people can be hostile to other people who are different and this rejection can have a negative impact upon those people who are different. Also, society is set up to accommodate some people whereas other people whom it is not set up for face many barriers in daily living. These claims seem correct. The question is whether the cause of autism could cause depression or anxiety in addition to the depression and anxiety caused by societal response. I will now outline two possible reasons for thinking the causes of autism can cause depression or anxiety.

In relation to non-autistic individuals, depression and anxiety can result from many factors. Some people get depressed or anxious because how their life is going. To say they get depressed or anxious due to their genes would be a mistake. However, other people get depressed or anxious even though there life appears to be going well. There is no detectable environmental trigger of the depression or anxiety. In these cases it is plausible to say that causes internal to the individual are causing the depression and anxiety. So this is an example of depression and anxiety occurring for reasons other than how their lives are going. Could the same sometimes happen in autistic individuals? Now, it could be claimed that if this is happening in autistic individuals then this is due to the causes of depression or anxiety and not the causes of autism. However, do we actually know this? Is it possible that some causes of autism play a causal role in the characteristics associated with autism and can separately also play a causal role in producing depression and anxiety? I do not think this can be ruled out. The sheer complexity of genetics is immense, with any particular gene potentially acting very differently depending upon which other genes are present and what environmental interactions occur. We have only a very limited understanding of this. So it is possible that the causes of autism actually do also result in depression or anxiety which arise irrespective of an individuals life situation. To be clear, I am not saying this is the case, rather, I am saying we do not know enough to rule out this being the case.

Another reason to question the claim that autism cannot cause depression and anxiety is the possibility that what we call depression and anxiety in autistic people is different to depression and anxiety in non-autistic people. When an autistic person reports that they are depressed, and when an non-autistic person reports that they are depressed we take them as to both be experiencing the same thing, namely depression. However, it is possible that actually the phenomenological experience (how it actually feels) of autistic individuals when they report depression is different to the phenomenological experience of non-autistic people when they report depression. This phenomenological experience could arise because what autistic individuals and non-autistic individuals report as depression actually stems from different causes. This would give reason to think that actually what is being reported as depression is actually different in both cases. All this could also be the case for anxiety. If what we call depression or anxiety in autistic people arises from the causes of autism then the causes of autism actually can cause depression or anxiety in autistic people. Now, is there any evidence for this claim? The problem is that phenomenology is very difficult to do and it is very rarely actually done today, so this is not the sort of thing which we have much evidence upon (although I have often felt that my experience of depression seems different to phenomenology I have read relating to non-autistic individuals). Additionally, it raises a whole bunch of metaphysical and conceptual issues about what make two things instances of the same thing (I have published a couple of papers which partly discuss this sort of issue in psychiatry, but ultimately philosophers have discussed these issues for literally multiple millennia in areas other than psychiatry). Seeing depression and anxiety as the same, or not the same, in autistic and non-autistic people seems to be compatible with the evidence and with credible metaphysical and conceptual approaches. Again, I am not suggesting it is the case that depression and anxiety are different in autistic and non-autistic individuals, rather, I am showing that it could be a possibility.

In this blog post I am doing philosophy, aiming to show alternative possibilities rather than showing a particular interpretation is true. I aim to show that we cannot simply dismiss or discount the claim that autism can cause depression or anxiety. As such, I think this is not grounds, in itself, to object to biological research on autism. Of course, I have not addressed many of the other potential problems with biological research on autism in general and Spectrum 10K in particular which may give good reason to reject Spectrum 10K (I have discussed some scientific problems with Spectrum 10K in another blog post).

The potential and pitfalls of Spectrum 10K

There has been a lot of hostility to the Spectrum 10K project on twitter. In this blog post I will reflect upon this, alongside mention some additional aspects of Spectrum 10K which I have not seen commented upon.

Some autistic people are against all biological investigation of autism. For example, they might think it is eugenicist, a waste of time or a far lower priority compared to changing society. So it makes sense that people with these views would reject Spectrum 10K. However, given the level of hostility to Spectrum 10K, it seems that lots more autistic individuals are against all biological research on autism than I realised or a lot of people think there are specific problems with Spectrum 10K which are not present in at least some other biological research on autism. It is the latter group I have in mind for this discussion.

One reason why I was surprised by the hostility is that Spectrum 10K seems less problematic than most biological research (which is not to say it is problem free, I will discuss problems below). Most biological research on autism aims to correlate biological factors with autism itself, i.e. with people who meet the diagnostic criteria. So far as I can see, Spectrum 10K is aiming to do something different. It aims to correlate biological factors present in autistic people with environmental factors. In this regard, Spectrum 10K is studying an area which is completely ignored by much biological research on autism. It is actually including the environment in scientific research. If you think, as I do, that issues of flourishing and disability ultimately involve both biology and the environment (and much besides them) then this is a good thing.

It opens a range of possible practical benefits compared to most biological research on autism. For example, imagine it was discovered that some biological factors are correlated with some sensory issues caused by particular environments. This could lead to two options. Firstly, change the environment. Secondly, develop a medication which specifically targets that biological factor, alleviating the sensory issue. Contrast Spectrum 10K’s approach with typical biological research on autism. It generally just finds endless biological complexity. But imagine if typical biological research on autism found a relatively strong biological factor present in most autistic people. What practical benefits could follow from this? It does not give us information about what part of the environment to change. It also means that any medication developed would probably affect lots of autistic individuals in a major way. That starts to look like a so called ‘cure for autism’ which so many autistic individuals are against. So it seems to me that Spectrum 10K has more likelihood of producing practical benefits and less likelihood of being eugenicist compared to most biological research on autism.

There are certainly significant potential issues with Spectrum 10K. Firstly, scientists have lots of sophisticated tools for investigating biological data. Are they going to use equally sophisticated tools for investigating the effect of the environment? They need make sure that they study a wide range of environmental factors and categorise those environmental factors in a nuanced way. They also need to understand how these environments affect autistic individuals through using sophisticated measurements of wellbeing and through understanding the phenomenological experience of autistic individuals. Secondly, Spectrum 10K will have much more statistical power compared to most biological studies given the sample size. This could be a significant positive but it also could cause more harm than good. A larger sample size can often drown out individual variation. It might only find commonalities at a broad level and miss smaller groupings of commonalties which only exist on a smaller scale within the sample size. Thirdly, there is the problem of epigenetics. Spectrum 10K will look at the relationship between biology and the environment, such as establishing that people with a specific gene have problems in a specific environment. However, another relationship is possible, namely that the environment might turn on the gene. So Spectrum 10K might mistake one causal relationship, biology plus environment resulting in lower wellbeing, for another, biology being present due to the environment and is unconnected to lower wellbeing. I do not know how Spectrum 10K will tackle these problems but certainly many studies are deficient in these matters.

Finally, some people think that, in contrast the claims of Spectrum 10K, that this data may end up in the hands of other organisations which will misuse it. This is a potential problem inherent in all biological research on autism. If anyone has any detail on what track record Cambridge has in relation to breaking promises or on data breaches, I would certainly be interested to read it.

Overall, if someone rejects all biological research on autism then it makes sense to reject Spectrum 10K. However, for all its potential problems, it seems to me a step in the right direction compared to most biological research on autism. It might, like most biological research, produce nothing of use. However, as much as I think we need to radically redress the balance of funding between biological investigation of autism compared to non-biological investigation, I do think this type of biological research has more potential than most biological research on autism.

Report on subtyping autism workshop

On the 19th of November 2019 a workshop on subtyping autism was held at LSBU. The hosting organisation was PARC (Participatory Autism Research Collective). With help from individuals from PARC and LSBU, myself, Chloe Farahar and Annette Foster organised this workshop. The workshop lasted two and a half hours. There were five talks, each lasting twenty minutes followed by ten minutes of questions. Some papers argued against subtyping, some argued for subtyping and some looked at specific subtypes (or, in my own case, looked at multiple specific subtypes when I outlined the history of subtyping). I was pleased to see that the workshop was well attended, counting 37 people present at one point on a quick head count.

One aim of the workshop was to obtain the views of autistic people on the question of subtyping. I feel this was a success since some of the speakers identified as autistic whilst there were also autistic individuals in the audience. Some autistic people thought that questions about how to best formulate the diagnosis of autism should be largely determined by autistic people whereas other autistic people felt the views of autistic people should be one of many relevant factors. Either way, I hope this workshop went some way to facilitated autistic people, as well as the non-autistic, in providing views upon this issue.

Quite a number of speakers seemed to share a common vision of what a good psychiatric diagnosis should do, even though they disagreed about whether subtypes would help achieve those goals. In my presentation and in other presentations it was argued that there is more to autistic people than just a broadly defined autism. Rather, it is important to understand the specific ways in which a specific autistic person manifests autism (alongside understanding aspects of them unrelated to their diagnosis). Also, I and others argued that understanding how autistic people can change over time is important. It is also important to understand that different environments can influence how autistic people think, feel and behave. So in this reguard there was a level of shared commonality when it came to questions over what a good diagnostic system should do. Some people (including myself) felt that subtypes would help with understanding these factors whereas other felt this information could be best understood without subtyping autism.

I outlined a history of subtyping. I divided my history into three different areas, the 1930s to the 1970s, the 1980s until recently (around 2010) and finally I discussed the present day. I focused upon Lauretta Bender and Leo Kanner in the first period, then I focused upon DSM-III and Lorna Wing in the second period and finally I focused upon DSM-5 in the final period. I outlined how the subtypes which were employed heavily reflected the values held by psychiatrists in each era. I suggested that DSM-5 is still largely working within the values present in the 1980s even though our values are currently in a process of shifting away from those 1980s values. I then suggested that adopting subtypes would help better reflect the values we are currently moving towards.

The full list of talks was as follows:

Autistic observable and unobservable experiences, and erroneous subtyping: Introducing the Internal and External Autistic Space (Chloe Farahar  & Annette Foster )

Exploring an autistic derived classification of autism (Mary Doherty)

Online discourse on autism does not need autism subtyping (Dafne Zuleima Morgado Ramirez)

An historical overview of subtyping (Sam Fellowes)

Demand Avoidance Phenomena: The circularity, integrity and validity of PDA: a commentary on the PDA Conference held by the National Autistic Society (2018) (Richard Woods)

Subtyping autism workshop

On the 19th of November (16.30 to 19.00 at London South Bank University (LSBU)) I am hosting (with collaborators) a workshop on subtyping autism. Below are some reasons why I am interested in this topic and more details on the event (note that these are reasons why I, rather than my collaborators or the presenters, am interested in the topic of subtyping).

My main academic interest is showing that psychiatric diagnoses are in principle scientifically legitimate. I argue that some (though not all) psychiatric diagnoses can be used in a similar way to how models are used in more respectable sciences. They cannot do everything a typical model can do in other sciences. Also, what they can do is usually done with less precision than occurs in other sciences. However, what level of similarity that they do have means that they have significant scientific worth (and this is true even though they typically cover a heterogeneous symptom picture and are causally heterogeneous).

Of course, psychiatric diagnoses can vary significantly in their scientific worth. Various ways of formulating them can impact this. The main diagnosis I am interested in is autism and one alternative way of formulating it is to add subtypes. This could alter its scientific worth as well as having many practical impacts outside of the scientific domain. This workshop will hopefully generate interesting discussion about these issues. Also, many speakers and attendees have a diagnosis of autism (or are in the process of being assessed) so lived experience might contribute some insight to both scientific and practical consequences of subtyping. Below is the initial abstract that was part of the call for papers and then the list of speakers.

This was the initial call for papers: Prior to and after the publication of the 2013 DSM there was much controversy over whether Asperger’s syndrome should be removed from the diagnostic manual. Members of the neurodiversity movement made contributions to this debate, drawing upon their lived experience of being autistic and their knowledge of the ways in which being diagnosed can be (or is not) beneficial. This conference aims to consider the question of autism and subtypes more broadly. What benefits or disadvantages are there for autistic people in adding substantive subtypes to autism? It is commonly stated that autistic people can present in many different ways. Might subtypes help add accuracy and nuance to clinical pictures? On the other hand, the boundaries between subtypes are typically vague and they can be placed in multiple places. This raises the danger that they are arbitrary impositions which do not reflect autistic experience. This conference draws upon the experience of autistic people to help resolve these issues. Possible areas for discussion include whether self-understanding for those diagnosed would be increased through being diagnosed with a more specific subtype or if this would unhelpfully impose unnatural constraints? Would the non-autistic be better able to understand different ways autism can manifest if there are significant subtypes, or would it help perpetuate unhelpful stereotypes based on an imposed limited number of ways autism would be proposed to manifest? Would the neurodiversity movement benefit from the subtypes bringing greater focus upon different ways autism can manifest or would this lead to unhelpful fracturing of the autistic community?

These are the papers that are being presented:

Autistic observable and unobservable experiences, and erroneous subtyping: Introducing the Internal and External Autistic Space (Chloe Farahar  & Annette Foster )

Exploring an autistic derived classification of autism (Mary Doherty)

Online discourse on autism does not need autism subtyping (Dafne Zuleima Morgado Ramirez)

An historical overview of subtyping (Sam Fellowes)

Demand Avoidance Phenomena: The circularity, integrity and validity of PDA: a commentary on the PDA Conference held by the National Autistic Society (2018) (Richard Woods)

Reviewing Re-Thinking Autism

Re-Thinking Autism contains, to my knowledge, the most sustained attack upon the diagnosis of autism found within a single book. The editors claim it is the first book in the field of critical autism studies. It contains 17 different papers which are grouped into three areas, namely ‘What is autism’, ‘Deconstructing autism’ and ‘Challenging Practice’. The editors see critical autism studies as focusing on two questions. Firstly, is the diagnosis of autism valid and secondly, is it useful. Most articles are very critical of the diagnosis of autism. Since I felt I benefited immensely from being diagnosed with autism I was probably always going to have reservations. However, in the spirit of engaging with the critical autism studies movement, I will suggest that the book did not address some important questions and issues which would significantly help any attempted challenge to autism.

In relation to validity, multiple articles criticised the scientific foundations of autism. Some give an useful overview of the very heterogeneous causal underpinnings of autism. Whilst this is a very relevant point when assessing autism I feel the consequences were insufficiently explored. There were relatively few details about why the causal heterogeneity makes autism deeply flawed and in need of replacement. Some articles contain statements that autism is not a biological entity or a scientific entity but these are usually asserted rather than argued for. I think these claims face some challenges. Firstly, virtually all psychiatric diagnoses are causally heterogeneous. Therefore, I feel that critical autism studies scholars need either explain why autism need replacing whilst other diagnoses do not or need explicitly endorse a whole rejection of DSM type psychiatric diagnoses (perhaps in favour of person centred approaches). A few articles do seem closer to the latter approach though there are few explicit statements. Additionally, there is little discussion about why causal heterogeneity is problematic and why it makes something not a biological or scientific entity. There was also little mention of other important factors when assessing a scientific theory (such as simplicity, tractability or coherence). These are admittedly deeply philosophical questions which are debated by philosopher of psychiatry (and I was pleased to see a few articles reference philosophers of psychiatry) but I feel these are the sorts of questions which critical autism studies needs engage in. Perhaps the arguments which critical autism studies employ are fully defensible but they currently need more development.

In relation to usefulness, some articles question whether it is helpful to give people a label and other articles question whether it helps in educational settings or support settings. Some of these authors making these arguments have a wide range of experience and expertise. Consequently, I felt they had a viewpoint that was at minimum worth hearing. That said, there was very little input from people diagnosed with autism (only one author was described as being autistic). Very few of the reasons why I find being diagnosed so useful were mentioned. Of course, being autistic does not make me automatically correct on this issue. Perhaps my positive feelings about how useful being diagnosed was are based upon flawed reasoning. Despite this, it would have been good if the book engaged in reasons why some autistic people find being diagnosed so useful even if only to then challenge those reasons.

I feel the biggest problem was a lack of alternatives being outlined. If autism is deeply flawed then what should replace it? Even some vague suggestions (i.e. split it up, add subtypes, merge it with other diagnoses) would have been helpful if I am to assess whether an alternative to autism would be preferable. Additionally, outlining alternatives would give an easier route to challenge autism. There would be no need to argue autism is deeply flawed, rather, there would instead be the easier task of arguing that autism can be useful but an alternative diagnosis is even more useful.

It is worth nothing that the articles are quite diverse and so the degree to which these criticisms are applicable to any given article will vary significantly. Additionally, I felt around a quarter of the articles were pretty good (these were usually the ones which critically analysed autism rather than wished to replace the diagnosis).

To conclude, I felt many articles avoided important questions which are relevant for assessing scientific concepts. I would like to see the critical autism movement engage more with philosophy of science and philosophy of psychiatry. Also, it would be more helpful if criticisms of autism were also accompanied by actual concrete suggestions for alternatives to autism. Despite this, I am glad I bought it and read it. If you want a single book which contains multiple different criticisms of autism then this is the book to go for. I suspect I cite multiple articles from this volume (admittedly, mainly to criticise).

Reviewing Peter Hobson’s The Cradle of Thought

Peter Hobson’s The Cradle of Thought is a philosophically and scientifically informed discussion of how thought develops in early life. Hobson’s main argument is that “interpersonal engagement contributes to the development of the mind – and [that] disordered interpersonal relations affect development of thinking” (p.143). He discusses many scientific studies which show how the level and nature of interpersonal relationships can impact the capacity for thought, suggesting deficient interpersonal relationships can lead to impoverished thinking.

Hobson highlights this through discussing individuals who are often not as capable of interpersonal interactions as most humans. He primarily discusses autism in detail, suggesting the usual thinking of autistic individuals (such as theory of mind differences) arise from lack of normal social and emotional interactions in early life. He heavily emphasizes that autism has a genetic component which results in biological differences (rejecting notions of poor mothering causing autism which some psychoanalysis used to believe) but argues the abnormal thinking itself is not primarily just due to biological difference. Rather, the biological differences result in difficultly interacting normally socially and emotionally, and this abnormal social and emotional experience results in abnormal thinking.

One might ask, why not just say the biological differences are responsible for both the abnormal interactions and for the abnormal thinking? Hobson uses a novel strategy to answer this question, primarily by looking at other types of individuals who also can face difficulties interacting normally. He considers individuals who are blind from birth and individuals who had very little social or emotional interaction in early life when raised in Romanian orphanges. These individuals often could not relate to other people in early life in the same way as most children. He then shows that these individuals sometimes develop some symptoms of autism, at substantially higher probabilities than would occur at random. Autistic individuals have biologically abnormal minds, blind individuals lack sight and Romanian orphans presumably have no major biological differences, yet all can exhibit some similar behaviour we associate with autism. Therefore, Hobson argues, some autistic behaviour is not directly the product of the biologically abnormal mind, but the biologically abnormal mind sets up abnormal interpersonal relationships and those interpersonal relationships result in symptoms associated with autism. Hobson also provides some evidence from how mothers with boarderline personality disorder interact with their children and how chimpanzees lack some parts of human socialising, suggesting both these cases can contribute to less than fully developed thinking.

Even though considered a developmental disorder, there is often a suggestion within scientific literature that the psychological development purely follow biological developments, rather than biological development resulting in psychological developments which then result in further psychological developments. I think a simple biological leading to psychological approach often present in modern science is far too simplistic, but I am unsure whether I think Hobson is correct or if I prefer a middle ground between Hobson and that modern science picture. Reguardless, the book is highly recommended for raising some important questions, presenting a solid evidence basis (often from very diverse sources which are not usually discussed in the context of autism) and for being highly accessible, being effectively popular philosophy and popular science.