Breastfeeding and autism continued

"We found that the percentage of mothers who started breastfeeding was similar between the two groups, but mothers of children with ASD [autism spectrum disorder] breastfed for a shorter amount of time compared to mothers of children without ASD."

So said the findings reported by Gnakub Soke and colleagues [1] continuing a research theme that I've had some professional interest in down the years (see here) on whether breastfeeding (use, duration, etc) *might* have some important *links* to risk of offspring autism and/or related conditions (see here). The same caveats mention in some of my other musings on this topic come into effect when talking (briefly) about the Soke findings (i.e. no-one is saying that a lack of breastfeeding 'causes' autism). That being said, there might still however be some important science to do on how breastfeeding and/or the constituents of breast milk might have some important biological effects for the developing child (minus any psychobabble explanations).

The Study to Explore Early Development or SEED was the starting point for the Soke study (continuing an autism research theme), and specifically investigation into the: "associations between ASD and breastfeeding initiation (yes/no) and duration (months categorized in tertiles)." The findings suggested that (a) breastfeeding rates (initiation rates) were high in mums of children with ASD compared to not-autism controls (85% vs. 90%), and (b) "mothers of children with ASD were less likely to report duration of breastfeeding in the high (≥12 months) versus low tertile (<6 months)... or the middle (6-<12 months) versus low tertile."

I don't want to dwell too much on the whys-and-wherefores of the Soke findings but there are some important questions that need answering. Not least the question of why breastfeeding seems to end quicker for those mums of children who were subsequently diagnosed as having an ASD. Were these infants more difficult to feed (something which Kanner might have picked up on in his seminal paper describing autism)? What role does the presentation of the 'broader autism phenotype' (BAP) in mothers mentioned by Soke et al play in such findings? That last point in particular, draws on the need for lots more research into the experience of pregnancy and motherhood with the BAP (see here) and/or autism in mind (see here).

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[1] Soke GN. et al. Association Between Breastfeeding Initiation and Duration and Autism Spectrum Disorder in Preschool Children Enrolled in the Study to Explore Early Development. Autism Res. 2019 Mar 9.

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Putting Money on autoimmunity and autism

Go to Jail, go directly to jail... @ Wikipedia  

I owe a debt of gratitude to Natasa who brought me to the very short and very pay-walled communication by McDougle & Carlezon* discussing neuroinflammation and autism. Whilst the open-accessing of research is seemingly discussed in bulk these days, we are not quite there yet in making science free and accessible to all hence I can't refer you to the full-text paper at this time unfortunately.

No mind, the McDougle communication is brief but discusses some interesting themes, some of which have appeared before on this blog including:

• Kanner's original descriptions of autism describing so much more than just behaviour (see this post)
• The issue of autoimmunity and autism tracking back to the topic of today's post, the paper by John Money and colleagues** from 1971.
• And how mention of the paper that should not be mentioned (in my best Harry Potter voice) reflects the fact "that at least some subtypes [of autism] represent whole-body disorders, offering exciting new possibilities for therapy".

I'm not 100% sure if it is the same person or not but the psychologists out there might recognise the name John Money in relation to the very sad case of the late David Reimer. A quick scan through the scientific literature based on the name Money and other authors listed on the the 1971 paper leads me to believe it is the same person who undertook work on gender identity and who championed the chemical castration of certain types of offenders. I offer no opinion on these ideas by the way.

I've previously done a review of some older research before on this blog and in particular the wonderfully descriptive article by Mary Goodwin and colleagues (see this post) on the very earliest days of the gut-brain axis in cases of autism. Readers should consider this post of a similar ilk and indeed published in the same year and by the same journal.

Money and colleagues present a family study with a few interesting points noted:

• The particular family was one seen at The Johns Hopkins Hospital in Baltimore, USA.
• It presents on a case of autism presenting in a boy called Tommy also diagnosed with Addison's disease and moniliasis - fungal infection related to Candida to you and me.
• Tommy had several brothers (x3), 2 of whom also showed various signs and symptoms of autoimmune diseases including those found with Tommy. 
• The early presentation of Tommy has some interesting features. He was overdue, presented with jaundice, had poor weight gain, issues with bone age and quite a few issues related to his diagnosis of Addison's disease. Tonsilitis with convulsions and coma with seizures "attributed to hypogylcaemia" were all in his clinical notes. 
• His psychological development is equally interesting, going from a child who reportedly smiled at 3 weeks (remember he was overdue) and cooed at 5 weeks to a child with "an air of preoccupation and a secret smile".
• Tommy's siblings were not diagnosed with autism but similarly presented with some notable traits. One of the siblings, Peter, was mis-diagnosed with coeliac (celiac) disease though later diagnosed with malabsoprtion in addition to hypomagnesia. He also presented with rapid hair loss aged 16 years. His psychological report mentions quite a lot of attention-seeking behaviour as well as him being prone to depressive episodes and ideations about suicide. 
• Another sibling, Theodore, was described as presenting with hypocalcemia and eventually diagnosed with diabetes. Behaviour was described as 'autistic' at some points in his development, as well as being reported as "hyperactive, disruptive, short in attention span and imitative". 
• All this was set against a family history of ulcerative colitis (UC) (maternal).

I know some people will probably read through all this and perhaps think its all just coincidence. One family history which, in the grand scheme of things, means very little to the millions of cases of autism past, present and future. Indeed also with only one of the brothers formally diagnosed with autism. I have to say however that accepting the heterogeneity present in autism(s), I'm not one of those people. Simply because quite a few elements of the cases described by Money et al have been mentioned in subsequent research literature with autism in mind pointing to some possible connections.

Don't believe me? Well have a look at papers like this one from Mouridsen and colleagues on maternal UC linked to autism*** and this one from Paul Ashwood and Judy Van de Water**** on autoimmunity appearing alongside cases of autism. Indeed Money and colleagues were also seemingly not convinced that these patterns of presentation in the family was merely a random act either, accepting that science is all about probability rather than absolutes. 

I was also drawn to some discussion made in the paper which referenced the work of the late Curt Dohan, he of the gluten-schizophrenia hypothesis. It appears that Money and colleagues might have had some personal communication with Dohan about their results and indeed how Dohan had "reported finding autoimmune antibody formation to brain and gut tissues in patients with schizophrenic-like symptoms and celiac disease". I don't want to make mountains out of molehills but one does wonder whether there might be a link with cases of autism as per the more recent tissue transglutaminase antibodies findings and perhaps even the folate receptor autoantibodies research. Although by no means am I suggesting autism is schizophrenia or vice-versa, we do know that the two conditions have been known to overlap and there's no reason to suspect that biology, genetics and even epigenetics might not also.

I'm going to finish with another quote from the Money paper: "it is quite possible that the patient's progressive withdrawal into autism, after a perhaps auspicious beginning, represents a developmental deterioration dependent on internal autoimmunizing factors rather than psychosocial factors". Sentiments that at least McDougle & Carlezon seem to be taking quite seriously.

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* McDougle CJ. & Carlezon WA. Neuroinflammation and autism: toward mechanisms and treatments. Neuropsychopharmacology. 2013; 38: 241-242.

** Money J. Autism and autoimmune disease: a family study. J Autism Child Schizophr. 1971; 1: 146-160.

*** Mouridesen SE. et al. Autoimmune diseases in parents of children with infantile autism: a case-control study. Dev Med Child Neurol. 2007; 49: 429-432.

**** Ashood P. & Van de Water J. Is autism an autoimmune disease? Autoimmun Rev. 2004; 3: 557-562.

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Money J, Bobrow NA, & Clarke FC (1971). Autism and autoimmune disease: a family study. Journal of autism and childhood schizophrenia, 1 (2), 146-60 PMID: 5172389

Remembering Leo Kanner 30 years on

This is a short post to remember the passing of a man who influenced countless people.

Emeritus Professor of Child Psychiatry, Leo Kanner passed away on 3 April 1981. Thirty years after his death, his name lives on, and his important work still resounds world-wide.

During this years World Autism Awareness Day (2 April), spare a thought for Kanner and perhaps take a little time out to read his original paper. Rest in peace.

Kanner's original autism descriptions

You will find some recurrent themes in this blog. This includes notions of how information can become distorted from the original source over time and the value of corroborating evidence when purporting to make statements of fact.

The first notion in particular may relate to this blog entry; analysing the original clinical descriptions of autism suggested by Dr Leo Kanner in 1943. It is perhaps timely that, in a few days, it will be 30 years since Kanner passed away (3 April 1981); indeed coincidental also that World Autism Awareness Day is on 2nd April (I wonder why they did not make it 3rd April instead?). I digress.

From the outset I want to acknowledge that, whilst Kanner's clinical descriptions form the basis for what we know as autism, I am by no means suggesting that he was the first to 'discover' autism given the many and varied texts from further back in history. Indeed, several other papers have suggested autism to have been present to some extent for many years prior to Kanner; although not labelled as 'autism' at the time (a label which did not exist).

I have always been keenly interested in Kanner's original 1943 paper 'Autistic disturbances of affective contact'. So much so, that my PhD drew heavily on his key clinical descriptions of 11 children who presented with symptoms including: inability to relate to themselves, extreme autistic aloneness, monotonously repetitious, anxiously obsessive desire for the maintenance of sameness and limitation in the variety of spontaneous activity. I have used but a few choice phrases from his text which have echoed down the diagnostic halls ever since.

There are however a few other phrases included in his 1943 text which, for one reason or another, did not quite receive the same subsequent acclaim. There are many reasons why such phrases and descriptions did not 'make the final cut' but I assume most were down to the old adage: a cobbler should stick to his last. Kanner was a Psychiatrist in the 1940s and hence specialised in 'disorders of the mind'. Subsequent interpretations of his text (e.g. DSM) have been undertaken specifically with Psychiatry in mind. Read on and you'll see what I mean.

'Food' (p.244) is mentioned in the 1943 text. Six of the children originally described by Kanner presented with various feeding difficulties; ranging from early vomiting, having to be 'tube-fed' and presenting with 'severe feeding difficulty from the beginning of life'. By early feeding problems I am assuming that this means problems with either mother's milk or the early formula milks (if they were even invented at this point). Six out of eleven cases, that's... er, over 50%. OK, he did not have a control group given that this was a case series description. Yet despite this, have early feeding difficulties ever been included in the diagnostic texts for autism? No, not even as an ancillary risk factor. Not once. Not never (not that I know anyway!). I know a few authors have offered potential explanations for early feeding difficulties in autism relating to the mechanical aspects of feeding and the 'perceptual' side of things. I am not saying that these may not be explanatory of what Kanner was perhaps describing. A few days ago however I blogged about a recent study from Harvard on the likelihood of lactose intolerance in cases of autism. Makes you wonder if today's technology were around during Kanner's tenure, would he be reporting lactose intolerance also?

Another example included in the original text. Kanner discusses the fact that 'several of the children were somewhat clumsy in gait and gross motor performances'. Gait and motor problems have similarly not been included in the diagnostic texts down the years. Unlike feeding problems however, there has been a slow realisation that such issues might be of relevance. It has however taken quite a few years for these elements to be 'realised' in cases of autism. One of the most recent studies being this one on the mechanics of gait in autism which is crying out for further replication.

The point I want to make with this post is that aside from going to the source for evidence, the original descriptions of autism from Kanner contained so much more than just behaviour relating to the triad (or should that be 'dyad'?) of impairments. Kanner did what any good scientist does - he observed and recorded things; not just behaviour but also developmental history and importantly somatic issues (see bottom of page 234).

I appreciate that today Kanner's autism has perhaps been 'subsumed' into this larger spectrum of autistic conditions. I often wonder how many of Kanner's original cohort would be diagnosed with autism, or an autism spectrum disorder, or even Asperger syndrome nowadays (bearing in mind that Hans Asperger did not define his patient group until a year later in 1944, and then light years away in Austria).