Saturday, 23 May 2015

Psychological morbidity of coeliac disease

"Anxiety, depression and fatigue are common complaints in patients with untreated celiac disease and contribute to lower quality of life."

That was one of the conclusions reached in the paper by Fabiana Zingone and colleagues [1] (open-access available here) following their review of the research literature "on psychological morbidity of celiac disease." Celiac (coeliac) disease (CD), by the way, is the autoimmune condition classically treated via the use of a gluten-free diet (GFD). Readers might wish to peruse my training post on the condition for some further background information about some of the known 'hows and whys' (see here) as well as other posts on what we don't know about CD (see here) (hint: quite a bit).

The Zingone paper is open-access so it doesn't require any grand discussions from me at this point. "Our search of the available literature suggests that CD has a considerable psychological impact" is another way the authors discuss their findings and I for one, would not argue with such sentiments on potential extraintestinal manifestations of the condition. Importantly, they make a distinction between whether such 'psychological impact' may directly derive from having the disease itself or other reasons potentially relating "to the patient’s subjective perception of the disorder and of the GFD used to treat it."

I was also taken by some of the 'clinical implications' listed by the authors when it comes to the 'considerable psychological impact' including that: (1) "GFD improves quality of life (QoL) in symptomatic patients, but not always in asymptomatic patients", (2) "Anxiety and depression may affect dietary adherence and QoL" and (3) "Fatigue is sometimes the unique symptom at CD presentation."

Point (1) taps into the idea of a better cost-benefit profile from the use of a GFD when people actually see such a diet improving their health and wellbeing. As per other rumblings on this blog, I might also suggest that this effect extends into some of the asymptomatic group too (see here). Point (2) raises an important issue that potential psychological effects associated with CD might have important implications for things like sticking to the diet. I wonder if that also includes those slightly outside of the classical presentation of CD too? Point (3) on fatigue as a possible 'unique' symptom of CD takes me back to a distant post titled 'gluten relations' and the idea that screening for CD or even the broader non-coeliac gluten sensitivity (NCGS) might be indicated in a few 'fatigue-linked' conditions including cases of chronic fatigue syndrome / myalgic encephalomyelitis (CFS / ME) (sorry, SEID). By saying that I'm not making any value judgements about SEID simply being CD or vice-versa, merely that within the spectrum of fatigue-manifesting conditions, one might find one or two surprising results [2] as you might in other conditions too [3].

Yet after all that, mass screening for CD is still not indicated? [4]

Music: Muse - Plug In Baby.

----------

[1] Zingone F. et al. Psychological morbidity of celiac disease: A review of the literature. United European Gastroenterol J. 2015 Apr;3(2):136-45.

[2] Isasi C. et al. Fibromyalgia and chronic fatigue syndrome caused by non-celiac gluten sensitivity. Reumatol Clin. 2015 Jan-Feb;11(1):56-7.

[3] Gadoth A. et al. Transglutaminase 6 Antibodies in the Serum of Patients With Amyotrophic Lateral Sclerosis. JAMA Neurol. 2015. April 13.

[4] Ludvigsson JF. et al. Screening for celiac disease in the general population and in high-risk groups. United European Gastroenterol J. 2015 Apr;3(2):106-20.

----------

ResearchBlogging.org Zingone F, Swift GL, Card TR, Sanders DS, Ludvigsson JF, & Bai JC (2015). Psychological morbidity of celiac disease: A review of the literature. United European gastroenterology journal, 3 (2), 136-45 PMID: 25922673

Friday, 22 May 2015

Early Start Denver Model (ESDM) and autism: 2 year outcomes

"These results provide evidence that gains from early intensive intervention are maintained 2 years later. Notably, core autism symptoms improved in the ESDM [Early Start Denver Model] group over the follow-up period relative to the COM [community-intervention-as-usual] group."

Those were some of the conclusions reported in amongst the potentially very important results from Annette Estes and colleagues [1] looking at "the sustained effects of early intervention" following previous studies [2] specifically looking at the ESDM for children with an autism spectrum disorder (ASD). ESDM by the way, is a behavioural intervention model that draws on elements of Applied Behaviour Analysis (ABA) and is based on 'a relationship-focused developmental model'.

Authors reported that when examining follow-up data for some 39 children aged 6 previously included in a trial of ESDM, those that received intervention (compared to those in receipt of 'treatment as usual') "demonstrated improved core autism symptoms and adaptive behavior." These findings were present despite no significant group differences in intellectual functioning between ESDM and COM participants. Perhaps also important were the discussions that: "The two groups received equivalent intervention hours during the original study, but the ESDM group received fewer hours during the follow-up period."

As I've hinted before on this blog, parent-led interventions when it comes to autism have historically been met with varying degrees of success when experimentally tested (see here). By saying this, I'm not trying to poo-poo such efforts; merely that discussions about how early intervention for autism is the gold standard are all well and good, but exactly what form that early intervention takes has yet to be authoritatively decided bearing in mind the pluralisation of the label (see here). In more recent times, we have seen some slightly more optimistic results appearing with specific interventions in mind, as per previous preliminary results based on very, very early implementation of something like ESDM (see here) and the use of ABA possibly linked to those 'optimal outcomers' (see here). But there is still a lot more to do in this area of research before any big promises are made.

Insofar as the idea that intensive efforts in the early years might pay more cost-effective dividends as time goes on, I'm sure that a few eyes and ears will have been grabbed [3] by such a sentiment in these times of continued austerity and resources being squeezed. As I suggested in a previous post (see here) on the idea that parent training might be superior over parent education [4] when it comes to facets of autism, such squeezes to finances/resources might not necessarily translate great experimental results into great real-world outcomes without some blue-sky thinking about how such programmes can be delivered mindful of costs. Estes et al seem to suggest that 'early and intensive' might be eventually able to give way to 'less and sustained'.

One last thing: I'm minded to take readers back to the post I wrote concerning the paper by Barnevik Olsson and colleagues [5] and the idea that 'tackling' core autism symptoms is a noble cause but that one has to be mindful of all of the other comorbidity that can follow a diagnosis and can seriously impact on behaviour and development. What perhaps I would like to see a lot more of in lots of areas of intervention with autism in mind, is how said program/tool/schedule also impacts on comorbid features and whether those variables should be the more important factors related to outcome. Sort of like what has been talked about the dietary intervention and autism in mind...

Music: Paul McCartney & Wings - Live And Let Die.

----------

[1] Estes A. et al. Long-Term Outcomes of Early Intervention in 6-Year-Old Children With Autism Spectrum Disorder. J Am Acad Child Adolesc Psychiatry. 2015. April 28.

[2] Dawson G. et al. Randomized, controlled trial of an intervention for toddlers with autism: the Early Start Denver Model. Pediatrics. 2010 Jan;125(1):e17-23.

[3] Penner M. et al. Cost-Effectiveness Analysis Comparing Pre-diagnosis Autism Spectrum Disorder (ASD)-Targeted Intervention with Ontario's Autism Intervention Program. J Autism Dev Disord. 2015 May 5.

[4] Bearss K. et al. Effect of parent training vs parent education on behavioral problems in children with autism spectrum disorder: a randomized clinical trial. JAMA. 2015 Apr 21;313(15):1524-33.

[5] Barnevik Olsson M. et al. “Recovery” from the diagnosis of autism – and then?  Neuropsychiatric Disease and Treatment. 2015. 11: 999-1005.

----------

ResearchBlogging.org Annette Estes, Jeffrey Munson, Sally J. Rogers, Jessica Greenson, Jamie Winter, & Geraldine Dawson (2015). Long-Term Outcomes of Early Intervention in 6-Year-Old Children With Autism Spectrum Disorder J Am Acad Child Adolesc Psychiatry : 10.1016/j.jaac.2015.04.005

Thursday, 21 May 2015

Respiratory illness and schizophrenia

"Schizophrenia is associated with impaired lung function and increased risk for pneumonia, COPD [Chronic obstructive pulmonary disease] and chronic bronchitis."

That was the primary conclusion reached in the paper by Krista Partti and colleagues [1] who aimed to "compare the respiratory health of people with psychosis with that of the general population." Their findings, based on data from "a nationally representative sample of 8028 adult Finns" (Finns as in inhabitants of Finland) involved collected data on the frequency of respiratory disease/symptoms as well as measuring lung function via the technique known as spirometry. Tobacco smoking or exposure to smoking, one of the primary causes of respiratory illness in the general population, was "quantified with serum cotinine levels."

"Participants with schizophrenia and other non-affective psychoses had significantly lower lung function values compared with the general population, and the association remained significant for schizophrenia after adjustment for smoking and other potential confounders." Indeed, as per the opening sentence to this post, authors reported some pretty elevated odds ratios (ORs) for various respiratory illnesses related to a diagnosis of schizophrenia compared with asymptomatic controls.

This is not the first time that respiratory diseases have been reported as potentially being more frequently diagnosed in cases of schizophrenia. Schoepf and colleagues [2] reported that in their cohort of those diagnosed with schizophrenia, various physical comorbidity were detected including COPD. As a predictor of "general hospital mortality" both COPD and bronchitis were included in the list of diseases. Other studies have arrived at similar conclusions [3] including data derived from the 'big data' producer that is Taiwan as per the findings from Hsu and colleagues [4].

As per the NHS Choices entry on COPD: "The main cause of COPD is smoking." Tobacco smoking is reported to be more frequently present in cases of schizophrenia [5] albeit with the need for some caution when it comes to making sweeping statements about the overlap [6]. It's therefore not beyond the realms of possibility that smoking habits may very well have a primary role in the association reported by Partti et al particularly in light of their findings on cotinine levels.

That being said, and acknowledging that smoking cessation programmes may be lifesavers for people with schizophrenia as they are for the rest of the population, I'm interested in whether there may be other factors at work when it comes to lung function and schizophrenia. Airway physiology, for example, might be something to consider, particularly in light of other findings when it comes to autism covered previously on this blog (see here). I'm not trying to downplay lifestyle factors [7], just sayin' that we need to cover all the potential bases including looking at whether familial transmission might also be a factor to consider [8].

Music: Song 2 by Blur.

----------

[1] Partti K. et al. Lung function and respiratory diseases in people with psychosis: population-based study. Br J Psychiatry. 2015 Apr 9.

[2] Schoepf D. et al. Physical comorbidity and its relevance on mortality in schizophrenia: a naturalistic 12-year follow-up in general hospital admissions. Eur Arch Psychiatry Clin Neurosci. 2014 Feb;264(1):3-28.

[3] Hendrie HC. et al. Health outcomes and cost of care among older adults with schizophrenia: a 10-year study using medical records across the continuum of care. Am J Geriatr Psychiatry. 2014 May;22(5):427-36.

[4] Hsu JH. et al. Increased risk of chronic obstructive pulmonary disease in patients with schizophrenia: a population-based study. Psychosomatics. 2013 Jul-Aug;54(4):345-51.

[5] Kelly C. & McCreadie R. Cigarette smoking and schizophrenia. BJPsych Advances. 2000; 6.

[6] Chapman S. et al. Citation bias in reported smoking prevalence in people with schizophrenia. Aust N Z J Psychiatry. 2009 Mar;43(3):277-82.

[7] Filik R. et al. The cardiovascular and respiratory health of people with schizophrenia. Acta Psychiatr Scand. 2006 Apr;113(4):298-305.

[8] Zöller  B. et al. Familial transmission of chronic obstructive pulmonary disease in adoptees: a Swedish nationwide family study. BMJ Open 2015;5:e007310 doi:10.1136/bmjopen-2014-007310

----------

ResearchBlogging.org Partti K, Vasankari T, Kanervisto M, Perälä J, Saarni SI, Jousilahti P, Lönnqvist J, & Suvisaari J (2015). Lung function and respiratory diseases in people with psychosis: population-based study. The British journal of psychiatry : the journal of mental science PMID: 25858177

Wednesday, 20 May 2015

Severe obesity pre-pregnancy and offspring developmental outcome

"Children whose mothers were severely obese before pregnancy had increased risk for adverse developmental outcomes."

That was the conclusion reached in the paper by Heejoo Jo and colleagues [1] based on results derived from the Infant Feeding Practices Study II (IFPS II) "a US nationally distributed longitudinal study of maternal health and infant health and feeding practices." Said data included information on "maternal prepregnancy BMI [body mass index] and child psychosocial development in 1311 mother–child pairs." Child development was measured in a number of ways including scores on the Strengths and Difficulties Questionnaire and other indications of diagnoses linked to child development.

Various results are presented including the suggestion that mothers with a prepregnancy BMI above 35 - classed as obese II and III - were potentially quite a bit more likely to have a child presenting with various "emotional symptoms" or "psychosocial difficulties" compared with those children of mothers with a more typical weight (BMI 18.5–24.9). When it came to specific developmental diagnoses, the children of obese mothers as a group were also at greater risk of receipt of a label of attention-deficit hyperactivity disorder (ADHD) and/or autism spectrum disorder (ASD) or developmental delay too. Importantly the authors note that: "Adjustment for potential causal pathway factors including pregnancy weight gain, gestational diabetes, breastfeeding duration, postpartum depression, and child’s birth weight did not substantially affect most estimates."

Without wishing to blame or stigmatise, the finding that maternal prepregnancy BMI might be a specific risk factor for offspring receipt of a diagnosis of ASD or developmental delay "(aOR [adjusted odds ratio] 3.13; 95% CI, 1.10–8.94)" is what grabbed my attention. Harking back to previous posts on this blog (see here) specifically discussing the paper by Paula Krakowiak and colleagues [2] (open-access), it is not necessarily new news that issues with maternal weight/BMI and it's association with various metabolic conditions, might place offspring at some increased risk of subsequent autism or ASD. This includes the increasingly strong evidence pointing towards gestational diabetes - an outcome associated with elevated maternal weight - as potentially increasing the risk of offspring autism (see here).

Allowing for the fact that there may be lots of interfering pregnancy variables influencing the risk of autism [3] (see here), some perhaps working synergistically, there are perhaps some important public health messages to take from the Jo paper and other peer-reviewed studies [4]. Weight loss is one modifiable option that might be considered following this body of data; although as per important recommendations: "If you are very overweight and pregnant, don't try to lose weight during your pregnancy, as this may not be safe." There is also still some debate about the best way to achieve weight loss (before pregnancy) as has been played out recently with headlines such as 'Exercise 'not key to obesity fight'' on the back of the editorial by Malhotra et al and not being able to 'outrun a bad diet'. I might add that the simple 'calories in - energy out' formula might also not be as useful as one might first think (see here).

The issue of risk factors for autism is a complicated and often emotive topic when periods such as pregnancy are thrown into the mix. I've covered lots of research on them down the years of this blog and although I've tried to handle them as sensitively as possible, there is always the risk that correlation/association might be viewed as 'blame'. Blame is certainly something that I've not intended in summarising such research and hopefully not interpreted that way by readers. Wearing the objective goggles of science, I would champion continued research on the possible mechanisms behind obesity and specific issues such as gestational diabetes when it comes to offspring outcomes, simply because they may provide important clues as to the underlying nature of at least some autism as well as other conditions [5]. I'd also suggest that when it comes to the topic of parental weight and something like offspring autism, one also might need to take into account other potentially important correlations too (see here).

Music: David Bowie - Starman.

----------

[1] H Jo. et al. Maternal Prepregnancy Body Mass Index and Child Psychosocial Development at 6 Years of Age. Pediatrics. 2015. April 27.

[2] Krakowiak P. et al. Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders. Pediatrics. 2012;129(5):e1121-e1128.

[3] Walker CK. et al. Preeclampsia, placental insufficiency, and autism spectrum disorder or developmental delay. JAMA Pediatr. 2015 Feb;169(2):154-62.

[4] Reynolds LC. et al. Maternal obesity and increased risk for autism and developmental delay among very preterm infants. J Perinatol. 2014 Sep;34(9):688-92.

[5] Hussen HI. et al. Maternal overweight and obesity are associated with increased risk of type 1 diabetes in offspring of parents without diabetes regardless of ethnicity. Diabetologia, April 2015.

----------

ResearchBlogging.org Jo, H., Schieve, L., Sharma, A., Hinkle, S., Li, R., & Lind, J. (2015). Maternal Prepregnancy Body Mass Index and Child Psychosocial Development at 6 Years of Age PEDIATRICS, 135 (5) DOI: 10.1542/peds.2014-3058

Tuesday, 19 May 2015

Social anxiety affecting autism intervention outcome?

"Anxiety is an unpleasant state of inner turmoil" according to one definition. In other descriptions, words such as 'worry' and 'dread' are used (see here) describing how beyond the typical feelings of apprehension about a new situation for example, anxiety can turn into something altogether more serious and life-disrupting for some.

There are various types of anxiety disorder (see here) to consider, but for the purposes of this post I'm going to focus on social anxiety disorder in the context of autism and how the results from Melanie Pellecchia and colleagues [1] suggest we should be dedicating quite a few more resources to studying and ameliorating this important issue.

"This study examined the extent to which clinical and demographic characteristics predicted outcome for children with autism spectrum disorder." That was the starting point for the Pellecchia study looking at how child characteristics including the presentation of autism and other comorbidities might affect outcome following a school-based behavioural intervention. Drawing on data from an initial sample of over 150 pupils with autism, authors concluded that: "age and the presence of symptoms associated with social anxiety, such as social avoidance and social fearfulness, as measured through the Child Symptom Inventory-4, were associated with differences in outcome." Further: "The findings regarding the role of social anxiety are new and have important implications for treatment."

I'll chime in here and say that social anxiety in relation to autism is by no means a 'new ' concept as per other mentions on this blog (see here and see here for example). Indeed, anxiety appearing in the context of autism or autistic traits (see here) is something that many people have recognised as being potentially central to the more disabling features for quite a few on those on the autism spectrum. That and an 'intolerance of uncertainty' to borrow an important phrase [2]. The novelty from the Pellecchia data comes from the idea that the presentation of social anxiety alongside paediatric autism might well have some important effects on intervention outcome.

It's an interesting idea that when it comes to intervention for autism, the presentation of core autism symptoms might not be the major hurdle to 'treatment' success or positive outcome. I'm not sure how relevant it might be to this discussion, but I have talked previously on this blog about how one or two intervention ideas put forward for autism are probably not affecting core symptoms but rather peripheral or comorbid presentations. It strikes me that a question requiring some answers is whether targeting issues like social or other forms of anxiety when comorbid, might similarly affect the core presentation of autism? How about targeting other potential manifestations of anxiety presenting as more somatic features too?

And just in case you needed telling, issues such as anxiety are not some 'flash in the pan' thing when it comes to quite a few cases of autism [3]. Indeed, the implication being that even into adulthood, moves to curb anxiety-related issues might potentially have some very positive effects on the presentation of autism and onwards improvements in quality of life. The flip-side to all that being that anxiety, when unremitting, might have some far-reaching implications [4]...

----------

[1] Pellecchia M. et al. Child characteristics associated with outcome for children with autism in a school-based behavioral intervention. Autism. 2015. April 24.

[2] Boulter C. et al. Intolerance of uncertainty as a framework for understanding anxiety in children and adolescents with autism spectrum disorders. J Autism Dev Disord. 2014 Jun;44(6):1391-402.

[3] Gotham K. et al. Depressive and anxiety symptom trajectories from school age through young adulthood in samples with autism spectrum disorder and developmental delay. J Am Acad Child Adolesc Psychiatry. 2015 May;54(5):369-376.e3.

[4] Verhoeven JE. et al. Anxiety disorders and accelerated cellular ageing. Br J Psychiatry. 2015. May 1.

----------

ResearchBlogging.org Pellecchia, M., Connell, J., Kerns, C., Xie, M., Marcus, S., & Mandell, D. (2015). Child characteristics associated with outcome for children with autism in a school-based behavioral intervention Autism DOI: 10.1177/1362361315577518

Monday, 18 May 2015

Pregnancy vitamin D levels and offspring ADHD

"Higher maternal circulating levels of 25(OH)D3 in pregnancy are associated with lower risk of developing ADHD [attention deficit hyperactivity disorder]-like symptoms in childhood."

Eva Morales and colleagues [1] came to that conclusion in their study - prospective study - looking at how estimated pregnancy vitamin D levels might have impacted on teacher-assessed ADHD-like symptoms in offspring when aged between 4 and 5 years old. Based on participants involved in the INMA project looking at how various environmental issues during pregnancy and into early infancy might impact on the 'physical, social and intellectual development' of children, researchers looked at over 1600 mother-child pairs. 25-hydroxyvitamin D3 [25(OH)D3] levels were assayed for in pregnant women at 13 weeks gestation and offspring children were subsequently assessed for ADHD-like behaviours a few years later.

Not only was a correlation reported between increasing vitamin D levels during pregnancy and lower levels of ADHD-type behaviours to be reported in young children, authors also: "found an association of increasing maternal 25(OH)D3 with a lower risk of ADHD DSM-IV... and ICD-10 hyperkinetic disorder in children" albeit with statistics (confidence intervals) implying caution in the interpretation of results.

Accepting that correlation is not the same as causation and that a whole host of factors probably affect the presence of ADHD-type behaviours in children, these are interesting results. I've covered vitamin D quite a few times on this blog (see here) and how widespread the correlations seem to be between a lack of the sunshine vitamin and a whole range of diagnoses and labels. Of particular note, are the various studies looking at vitamin D and autism; specifically the findings from Fernell and colleagues [2] (covered in this post) who suggested that low vitamin D levels in the very earliest days might "act as a risk factor for ASD [autism spectrum disorder]" albeit with caveats. Yet more research has appeared in recent days with autism in mind [3].

Back to ADHD and vitamin D has also started to make something of a research appearance in recent times. Bener and Kamal [4] (covered in this post) in amongst their various data, suggested that "vitamin D deficiency was higher in ADHD children" than in controls. Other studies have suggested similar things [5]. That being said, there is still quite a bit more research to do in this area as per the rather less significant findings reported by Strøm and colleagues [6] looking at pregnancy levels of vitamin D and various "offspring neurodevelopmental outcomes." The idea that Strøm et al also assayed for pregnancy vitamin D levels over and above vitamin D levels directly in kids is comparable to the methods reported by Morales and colleagues.

ADHD like many (all?) other diagnoses currently based on behavioural observations alone is a complicated entity. The Morales results, whilst interesting, are probably not the only issue pertinent to ADHD (or do I start to pluralise that label too) as per the recent results reported by Alhraiwil et al [7] and their suggestion that: "male gender, previous psychiatric illness in the family, vitamin D deficiency, poor school performance, sleep problems, and nocturnal enuresis" might all show some effect when it comes to ADHD. I might also add that the rise and rise of evidence talking about a possible connection between physical complaints such as asthma and ADHD (see here) should also not be ignored as part of any bigger picture.

But the idea of a connection between vitamin D and ADHD is a tantalising one added to a growing nutritional element (see here). Bearing in mind my caveat about no medical or clinical advice given or intended, such an association also begs some further questions about the value of supplementation (see here)...

Music and just in case you ain't seen it: Taylor Swift - Bad Blood ft. Kendrick Lamar. Kiai!!

----------

[1] Morales E. et al. Vitamin D in Pregnancy and Attention Deficit Hyperactivity Disorder-like Symptoms in Childhood. Epidemiology. Epidemiology. 2015 Apr 10.

[2] Fernell E. et al. Autism spectrum disorder and low vitamin D at birth: a sibling control study. Molecular Autism. 2015; 6: 3.

[3] Saad K. et al. Vitamin D status in autism spectrum disorders and the efficacy of vitamin D supplementation in autistic children. Nutritional Neuroscience. 2015. 15 April.

[4] Bener A. & Kamal M. Predict attention deficit hyperactivity disorder? Evidence -based medicine. Glob J Health Sci. 2013 Nov 27;6(2):47-57.

[5] Goksugur SB. et al. Vitamin D status in children with attention-deficit-hyperactivity disorder. Pediatr Int. 2014 Aug;56(4):515-9.

[6] Strøm H. et al. Vitamin D measured in maternal serum and offspring neurodevelopmental outcomes: a prospective study with long-term follow-up. Ann Nutr Metab. 2014;64(3-4):254-61.

[7] Alhraiwil NJ. et al. Systematic review of the epidemiology of attention deficit hyperactivity disorder in Arab countries. Neurosciences (Riyadh). 2015 Apr;20(2):137-44.

----------

ResearchBlogging.org Morales E, Julvez J, Torrent M, Ballester F, Rodríguez-Bernal CL, Andiarena A, Vegas O, Castilla AM, Rodriguez-Dehli C, Tardón A, & Sunyer J (2015). Vitamin D in Pregnancy and Attention Deficit Hyperactivity Disorder-like Symptoms in Childhood. Epidemiology (Cambridge, Mass.) PMID: 25867115

Saturday, 16 May 2015

Poverty affects autism + ADHD?

A brief post for you today to bring to your attention the paper by Eirini Flouri and colleagues [1] who suggested that although socio-economic disadvantage (SED) was probably not a risk factor for autism spectrum disorder (ASD) and attention-deficit hyperactivity disorder (ADHD) when comorbid, "it was associated with elevated emotional problems among children with ASD + ADHD."

Based on data derived from "209 children with ASD who took part in the UK's Millennium Cohort Study", an initiative that has appeared on this blog before (see here), researchers examined developmental trajectories across ages 3, 5 and 7 years. Aside from observing a possible detrimental effect from SED on aspects of ASD + ADHD, they also reported that ASD + ADHD seemed to be associated with a consistently 'high trajectory' when it came to conduct issues compared with those with ASD only.

Continuing the ideas that (a) autism appearing alongside ADHD (or should that be the other way around) is not an uncommon situation (see here), and (b) said association potentially increases the risk of various other issues coming about (see here), the suggestion that SED might impact on the presentation of autism + ADHD is an important one. Other work from this group [2] had hinted that family poverty may be one factor "associated with broad and specific (emotional and conduct problems) psychopathology" in the context of autism. I say this acknowledging that poverty has a range of effects when it comes to autism including the potential timing of diagnosis [3].

Other, independent work, has not been so quick to drop the idea that poverty and deprivation may be a risk factor for autism [4] or at least, referral rates for autism (and on more than one occasion [5]) so I'd perhaps be a little guarded about removing this aspect from the autism + ADHD grouping altogether at the present time. The next question then needs to be how, in these times of continued austerity, can society deliver something that might mitigate the impact of autism + ADHD?

Music: Morrissey - Everyday Is Like Sunday.

----------

[1] Flouri E. et al. Poverty and the Growth of Emotional and Conduct Problems in Children with Autism With and Without Comorbid ADHD. J Autism Dev Disord. 2015 Apr 25.

[2] Midouhas E. et al. Psychopathology trajectories of children with autism spectrum disorder: the role of family poverty and parenting. J Am Acad Child Adolesc Psychiatry. 2013 Oct;52(10):1057-1065.e1.

[3] Mandell DS. et al. Age of diagnosis among Medicaid-enrolled children with autism, 2001-2004. Psychiatr Serv. 2010 Aug;61(8):822-9.

[4] Campbell M. et al. Autism in Glasgow: cumulative incidence and the effects of referral age, deprivation and geographical location. Child Care Health Dev. 2013 Sep;39(5):688-94.

[5] Li X. et al. Neighborhood deprivation and childhood autism: a nationwide study from Sweden. J Psychiatr Res. 2014 Jun;53:187-92.

----------

ResearchBlogging.org Flouri E, Midouhas E, Charman T, & Sarmadi Z (2015). Poverty and the Growth of Emotional and Conduct Problems in Children with Autism With and Without Comorbid ADHD. Journal of autism and developmental disorders PMID: 25911306