Early Autism and Developmental Disabilities Monitoring says autism prevalence is still rising...

"The overall ASD [autism spectrum disorder] prevalence was 13.4 per 1,000 children aged 4 years in 2010, 15.3 in 2012, and 17.0 in 2014 for Early ADDM [Autism and Developmental Disabilities Monitoring] sites with data for the specific years."

So said the surveillance summary published by Deborah Christensen and colleagues [1]. Those of you who follow the US ADDM initiative (see here) will already know about the aims of this "group of programs funded by the CDC" looking at the (estimated) autism numbers, changes to the numbers and the impact of the numbers on various communities. Through initiatives like the ADDM, we already know that the estimated prevalence of autism in 8-year olds living in the United States is round about 1 in 59 (see here) and that the estimate continues to grow for pretty much every surveillance year examined. We are also starting to find out about how the change to DSM-5 from DSM-IV is likely to/not to impact on future figures (see here). And hopefully, at some point, we might have some further data on what happens to autism past childhood (see here) from such an initiative.

The Christensen paper adds another tier to the knowledge being acquired as per their analysis of the (estimated) prevalence rate of autism in 4 year olds "whose parents or guardians lived within designated sites." Those sites were: Arizona, Colorado, Missouri, New Jersey, North Carolina, Utah, and Wisconsin. The Early ADDM initiative does not cover the same area as its big brother/sister ADDM but "is conducted in two phases using the same methods and project staff members as the ADDM Network." Those phases include first "reviewing and abstracting data from children’s records, including comprehensive evaluations performed by community professionals" and then a second phase involving "a review of the abstracted evaluations by trained clinicians using a standardized case definition and method." DSM-IV criteria covers most of the time points examined but: "For 2014 only, prevalence estimates based on surveillance case definitions according to DSM-IV-TR and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) were compared."

Results: as per the opening sentence of this post, the overall (estimated) autism prevalence across all sites for autism in 4 year olds was on the increase between 2010 and 2014. That's not to say that there weren't differences between the various sites - New Jersey, a favourite autism prevalence site (see here) showed the highest prevalence: 19.7, 22.1, and 28.4 per 1,000 for 2010, 2012 and 2014 respectively - but overall the prevalence rate was increasing not decreasing.

There were a number of other important points raised in the Christensen findings. So: "Among four sites with ≥60% data on cognitive test scores (Arizona, New Jersey, North Carolina, and Utah), the frequency of co-occurring intellectual disabilities was significantly higher among children aged 4 years than among those aged 8 years for each site in each surveillance year except Arizona in 2010." I don't think I need to say much more about that. Also: "The overall prevalence estimate using a DSM-IV-TR case definition was approximately 20% higher than the prevalence estimate based on DSM-5 criteria." Again, I don't think too much more discussion is needed on this point aside from saying that for 4-year olds, the switch to DSM-5 might have made more of a difference than for 8-year olds. Indeed in comparison to the Wiggins data [2] based on 8-year olds where "46.0% children met both DSM-IV-TR and DSM-5 surveillance status, 44.0% met neither the DSM-IV-TR nor DSM-5 surveillance status, 4.0% met DSM-IV-TR status, but not DSM-5 status, and 6.0% met DSM-5 status, but not DSM-IV-TR status of ASD" the Christensen data showed something a little different: "Among 1,237 children who met the surveillance case definition for either DSM-IV-TR or DSM-5, 974 (78.7%) met both case definitions, 234 (18.9%) met the DSM-IV-TR but not the DSM-5 case definition, and 29 (2.3%) met the DSM-5 but not the DSM-IV-TR case definition." Perhaps more study is required on the diagnostic changes?

What's more to say? Well, one of the authors - Walter Zahorodny - kinda said it all in a media comment: "There’s no letup. I really don’t understand why the rate is going up in this way." So maybe the next question, a question that really should have been examined a long, long time ago, needs to be 'Why?' rather than just a continual chain of studies saying autism prevalence is increasing...

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[1] Christensen DL. et al. Prevalence and Characteristics of Autism Spectrum Disorder Among Children Aged 4 Years - Early Autism and Developmental Disabilities Monitoring Network, Seven Sites, United States, 2010, 2012, and 2014. MMWR Surveill Summ. 2019 Apr 12;68(2):1-19.

[2] Wiggins L. et al. Comparison of autism spectrum disorder surveillance status based on two different diagnostic schemes: Findings from the Metropolitan Atlanta Developmental Disabilities Surveillance Program, 2012. PLoS ONE. 2018; 13(11): e0208079.

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One more time... (roughly) 1 in 40 children with parent-reported autism in the US

Consider this short post an extension of another recent entry on this blog talking about new data observing that the estimated autism prevalence rate (parent-reported) is around 1 in 40 children in the United States (US) (see here). That entry was based on the paper by Michael Kogan and colleagues [1] and their examination of data "using the 2016 National Survey of Children's Health (NSCH)" initiative.

Enter then another piece of research published little over a week after the Kogan study from Guifeng Xu and colleagues [2] which concluded that: "In a large, nationwide, population-based study, the estimated prevalence of ever-diagnosed ASD [autism spectrum disorder] was 2.79% among US children in 2016." In case you were wondering, 2.79% or 2.8% roughly translates as 1 in 36 children. Xu and colleagues, I might add, are no strangers to prevalence studies on childhood neurodevelopmental disorders (see here and see here).

Both these studies have attracted some media attention (see here and see here) mainly because they show a prevalence rate quite a bit higher than the recent CDC (estimated) autism prevalence figures - 1 in 59 8-year olds - published earlier this year (2018) (see here). Those media reports also seem to make quite a big deal of the 'parent-reported' nature of the figures (both derived from the NSCH initiative). As I mentioned in my last discussion of the Kogan paper, a quote from the lead author Michael Kogan is important in the context of those parent-report 'issues' that some people seem to have: "We know that in terms of having a major condition like autism, parents are usually pretty good reporters compared to medical records." Indeed they are.

Other details to add? Well, the Xu paper also reported on "state-level prevalence of ASD in the United States." They observed variations in the reported prevalence of autism (ASD) across the different states: "The state-level prevalence varied from 1.54% (95% CI, 0.60-2.48) in Texas to 4.88% (95% CI, 2.72-7.05) in Florida." Little explanation is given about such a discrepancy in their paper and so further research is implied.

Also: "Among those who had ever been diagnosed as having ASD, 92.79% (95% CI, 90.19-95.39) reported currently having ASD." This is interesting. Allowing for the fact that the diagnosis of autism or ASD is often more of an art form than a scientific endeavour, I did wonder whether the loss of about 8% of children who were previously diagnosed with autism but did not report currently having autism might overlap with the 9% figure with regards to the term 'optimal outcome' (see here). Y'know, the ever-growing body of peer-reviewed research that seems to suggest that for some people, a diagnosis of autism is not necessarily 'lifelong' (see here) (even if 'optimal outcome' is not necessarily the best phrase to use). Again, further research is implied.

For now however, we can conclude that there is : "a relatively high prevalence of ASD among US children" mirroring that in other parts of the world (see here for example). We really need to be asking questions like 'why?' and also 'are the relevant mechanisms in place to ensure that money, resources and services are directed towards this growing population?'

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[1] Kogan MD. et al. The Prevalence of Parent-Reported Autism Spectrum Disorder Among US Children. Pediatrics. 2018 Nov 26. pii: e20174161.

[2] Xu G. et al. Prevalence and Treatment Patterns of Autism Spectrum Disorder in the United States, 2016. JAMA Pediatrics. 2018. Dec 3.

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8 in 1000 babies born with foetal alcohol spectrum disorder

The results of the systematic review and meta-analysis published by Shannon Lange and colleagues [1] make for important reading with their conclusion that the global prevalence of foetal alcohol spectrum disorder (FASD) is estimated to be around 8 in 1000 live births. The accompanying editorial by Albert Chudley [2] rightly talks about 'high time for action' on the basis of such figures, particularly because FASD is a largely preventable condition and specific groups of people and specific geographical regions seem to carry elevated risk(s) when it comes to offspring FASD and so can be targeted for additional support.

Looking at the collected data from 24 studies examining the prevalence of FASD - a condition whereby babies exposed to alcohol in the womb present with specific morphological features and accompanying behavioural / cognitive issues - researchers concluded that around 7.7 per 1000 live births presented with FASD. They reported that 76 counties (of 187 countries providing data) showed an estimated prevalence rate for offspring FASD above 1% of total births. South Africa came top with over 1 in 10 births being estimated to present with FASD. Croatia, Ireland, Italy and Belarus filled the other top 5 hotspots for FASD with estimated prevalence rates between 3-5% of births derived from various methods.

'Special populations' are also mentioned in the Lange paper. Specifically: "the prevalence of FASD among special populations was 15.6 to 24.6 times higher among aboriginal populations... 5.2 to 67.7 times higher among children in care... 30.3 times higher in a correctional population... 23.7 times higher in a population with low socioeconomic status... and 18.5 times higher among a population in psychiatric care compared with the global prevalence among children and youth in the general population." One might argue that at least for some of these at-risk populations, issues such as binge drinking habits combined with an elevated risk of unplanned pregnancy [3] could lie at the root of the estimates detailed by Lange et al. I say that minus any sweeping generalisation but in light of the scientific 'facts' detailed in the latest review paper.

I note that some of the media around the Lange findings (see here) have already mentioned about some of the behavioural manifestations of FASD 'crossing over' with diagnoses such as attention-deficit hyperactivity disorder (ADHD) and autism. I would perhaps draw your attention to a previous blogging occasion when I discussed some of the research specifically looking at any overlap between autism and FASD (see here) and how one needs to be quite careful not to overplay any would-be links despite some data on possible overlap [4] (this paper was also from Lange).

Then to the specifics of the hows-and-whys of alcohol exposure in-utero causing FASD and whether effects might somehow be mitigated. Alcohol (ethanol) is a known teratogen [5] so effects are likely to be numerous in terms of how it affects the developing foetus. I note that the word 'epigenetics' has entered the vocabulary when it comes to possible mechanisms of effect(s) and that would suggest that at some point there may be ways and means of mitigating the effects of alcohol consumption at critical periods during pregnancy. At some point.

For now the message from Lange and colleagues is clear: FASD is not an uncommon finding in many different countries and different populations, and remains largely preventable. Abstinence from alcohol is advised before and during that special time (see here). And just in case anyone thinks I'm only zooming in on mums-to-be, dads might also heed similar advice at critical periods too.

Straight Edge from Minor Threat seems an appropriate song to conclude this post given what the song title means (veganism and the non-use of prescription medicines are optional extras I might add)...

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[1] Lange S. et al. Global Prevalence of Fetal Alcohol Spectrum Disorder Among Children and Youth. JAMA Pediatrics. 2017. Aug 21.

[2] Chudley AE. Fetal Alcohol Spectrum Disorder—High Rates, High Needs, High Time for Action. JAMA Pediatrics. 2017. Aug 21.

[3] Font-Ribera L. et al. Socioeconomic Inequalities in Unintended Pregnancy and Abortion Decision. Journal of Urban Health. 2008;85(1):125-135.

[4] Lange S. et al. Prevalence of Externalizing Disorders and Autism Spectrum Disorder among Children with Fetal Alcohol Spectrum Disorder: Systematic Review and Meta-analysis. Biochem Cell Biol. 2017 May 18.

[5] Randall CL. Alcohol as a teratogen: a decade of research in review. Alcohol Alcohol Suppl. 1987;1:125-32.

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Autism research in Jamaica

For the past couple of years I've been tracking some rather interesting publications coming out of data from Jamaica on the topic of autism / autism spectrum disorder (ASD) specifically looking at the possible overlap between genes and various environmental factors. I thought now would be a good time to bring this collection of papers to the blogging table and summarise their findings based on the analysis of data collected from The Jamaican Autism study. The fact that their latest research foray mentions some of the genetics of glutathione [2] with autism in mind is very interesting in light of some other findings in this area (see here). There's more on this shortly.

You're not Absolem. I'm Absolem. Stupid girl.

So:

Study 1: Maternal and paternal age are jointly associated with childhood autism in Jamaica [2].
Higher parental age - both mother and father age - seemed to be associated with a diagnosis of autism/ASD in offspring. Higher maternal age in particular, survived further statistical analysis as being a potentially important factor. This is a topic which has cropped up in autism research circles before (see here).

Study 2: Seafood consumption and blood mercury concentrations in Jamaican children with and without autism spectrum disorders [3].
"Our findings do not support an association between blood mercury concentrations measured in Jamaican children 2–8 years of age and ASD case status." Such a conclusion was based on the analysis of blood mercury concentrations between ASD cases and a control group, and took into account important factors such as seafood consumption bearing in mind what is known about such a foodstuff and environmental exposures (see here).

Study 3: The role of drinking water sources, consumption of vegetables and seafood in relation to blood arsenic concentrations of Jamaican children with and without Autism Spectrum Disorders [4].
Blood arsenic levels were the focal point of this study, and a familiar conclusion to the previous study: "Our results do not support an association between postnatal total blood arsenic measured in Jamaican children 2-8 years of age and ASD case status." Again the consumption of certain foodstuffs seemed to be important correlates related to any elevated levels of arsenic detected.

Study 4: Role of fruits, grains, and seafood consumption in blood cadmium concentrations of Jamaican children with and without Autism Spectrum Disorder [5].
Cadmium levels this time around, and again: "we did not find any significant differences between ASD cases and typically developing (TD) controls with respect to the 75th percentile of blood cadmium concentrations." Food (yes again) seemed to be a good correlate linked to differences in blood cadmium levels.

Study 5: Blood manganese concentrations in Jamaican children with and without autism spectrum disorders [6].
Manganese, and wait for it... "Our results do not indicate a relationship between postnatal BMC [blood manganese concentrations] and ASD case status of Jamaican children ages 2–8 years."

Study 6: Blood Lead Concentrations in Jamaican Children with and without Autism Spectrum Disorder [7].
Lead (Pb), a favourite topic of this blog, was the metal of choice when it came to analysis to see if there was any connection between the stuff and autism. Er,... "Our results do not support an association between postnatal blood lead concentration measured in Jamaican children 2–8 years of age and ASD case status."

I think you can see the trend coming out of this data examining samples of children living in Jamaica with and without autism. Perhaps just as important are the various discussions about the ways and means that participants might have been exposed to these various metals and how one needs to be aware of how food in particular, could be a significant source of exposure. This perhaps puts a new slant on previous studies which have suggested an increased body burden of certain metals to be associated with autism (see here) and the question of whether dietary sources of such metals have adequately been taken into account. Don't get me wrong, I'm still very keen to see more 'metallomics' applied to autism research (see here), perhaps just controlling for a few more potentially important confounders.

The Jamaican Autism study also provides quite a nice template for setting up further geographically distinct initiatives to compare and contrast with/against. I note for example that the recent study from Hodgson and colleagues [8] looking at autism in Oman (itself the topic of quite a few peer-reviewed publications) suggested some rather different results for their cohort: "Mercury levels were markedly elevated in the hair of autistic subjects vs. control subjects" albeit based on hair analysis not blood. With the previous caveat about confounders in operation, one wonders whether there may be more to see across different countries particular when bringing into play the potential importance of that glutathione connection which has also previously received some mention in the Jamaican autism studies [9].

And then some music. Jamaica and music, mmm... One Love.

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[1] Rahbar MH. et al. nteraction between GSTT1 and GSTP1 allele variants as a risk modulating-factor for autism spectrum disorders. Research in Autism Spectrum Disorders. 2015; 12: 1-9.

[2] Rahbar MH. et al. Maternal and paternal age are jointly associated with childhood autism in Jamaica. J Autism Dev Disord. 2012 Sep;42(9):1928-38.

[3] Rahbar MH. et al. Seafood consumption and blood mercury concentrations in Jamaican children with and without autism spectrum disorders. Neurotox Res. 2013 Jan;23(1):22-38.

[4] Rahbar MH. et al. The role of drinking water sources, consumption of vegetables and seafood in relation to blood arsenic concentrations of Jamaican children with and without Autism Spectrum Disorders. Sci Total Environ. 2012 Sep 1;433:362-70.

[5] Rahbar MH. et al. Role of fruits, grains, and seafood consumption in blood cadmium concentrations of Jamaican children with and without Autism Spectrum Disorder. Res Autism Spectr Disord. 2014 Sep 1;8(9):1134-1145.

[6] Rahbar MH. et al. Blood manganese concentrations in Jamaican children with and without autism spectrum disorders. Environ Health. 2014 Aug 23;13:69.

[7] Rahbar MH. et al. Blood Lead Concentrations in Jamaican Children with and without Autism Spectrum Disorder. Int J Environ Res Public Health. 2014 Dec 23;12(1):83-105.

[8] Hodgson NW. et al. Decreased glutathione and elevated hair mercury levels are associated with nutritional deficiency-based autism in Oman. Exp Biol Med (Maywood). 2014 Jun;239(6):697-706.

[9] Rahbar MH. et al. Role of metabolic genes in blood arsenic concentrations of Jamaican children with and without autism spectrum disorder. Int J Environ Res Public Health. 2014 Aug 6;11(8):7874-95.

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Rahbar MH, Samms-Vaughan M, Loveland KA, Pearson DA, Bressler J, Chen Z, Ardjomand-Hessabi M, Shakespeare-Pellington S, Grove ML, Beecher C, Bloom K, & Boerwinkle E (2012). Maternal and paternal age are jointly associated with childhood autism in Jamaica. Journal of autism and developmental disorders, 42 (9), 1928-38 PMID: 22230961

Autism in the Somali population in Minneapolis

I see that the report from Amy Hewitt and colleagues* (open-access) providing results from The Minneapolis Somali Autism Spectrum Disorder Prevalence Project has been published and has started to generate some media interest (see here).

Gondereshe @ Warya @ Wikipedia 

The long-and-short if it was that based on some concerns that children of Somali origin seemed to be over-represented when it came to a diagnosis of an autism spectrum condition, otherwise known as 'otismo' among some in the Somali community, the research wheels were set in motion in the City of Minneapolis to see if there were indeed disparities in the numbers of children presenting with autism. The project was "expanded" above and beyond just asking about prevalence of autism in Somali children vs. non-Somali children to importantly include other questions; not least: "Were children with ASD and of Somali descent more likely to have intellectual disability than children with ASD who were not of Somali descent?" I was particularly interested in the intellectual disability (ID) issue in light of other research suggesting that there may indeed be an over-representation of ID alongside autism in migrant children from countries of the African continent or with a low 'human development index' (see here and more recently here).

Without trying to simply plagiarise the Hewitt report, there are a few key findings worthy of comment.

• Bearing in mind how researchers collected information about autism - screening and reviewing health records - from a total population numbering above 12,000 7-9 year olds in 2010, the autism prevalence rate in Minneapolis was estimated to be 1 in 48 children. This figure covered all children irrespective of any ethnicity differences.
• Specifically looking at children of Somali origin, 31 children out of a total of 1007 children were judged to be on the autism spectrum equating to a prevalence of 1 in 32 children. Nearly half of the Somali children identified as being on the autism spectrum were done so via inspection of a combination of school and health records (48%).
• Within the range of other ethnic groupings examined, 120 out of a total of 4,336 white children were also judged to be on the autism spectrum, making a prevalence estimate of 1 in 36 children.
• Just as important, all the Somali children with autism were reported to have some degree of ID (this being ascertained as an IQ level below 70).
• The average age at diagnosis for Somali children was 5.3 years, exceeding all other ethnic groups and above the overall mean age at diagnosis of 4.9 years.

There's not too much more to add to those factoids aside from the need for quite a bit more research into this area given the data indicating that almost 1 child in every classroom aged between 7-9 years old will potentially present as being on the autism spectrum. The fact that Somali children, and indeed white children, presented with prevalence estimates of autism above that of other ethnic groups potentially offers some clues as to where research might next head in terms of genetics, epigenetics and even environmental differences tied into such categorisations. I've speculated before about the possibility of something like a vitamin D link** given the differences in sun exposure between Somalia and the City of Minneapolis, but I dare say the whole thing is going to be a lot more complicated than just this one potential precipitating factor.

It's also interesting to note that the Hewitt report includes some mention of 'interventions' for autism, and quite prominently, the use of 'dietary and nutritional interventions'. Although the authors are right to be wary and sceptical of the effectiveness of any 'universal' intervention for autism (sorry the autisms), it got me wondering whether this was given such prominence specifically because of the chatter about such an intervention including the horror that is a GFCF diet, or whether there may be some differences in the effectiveness of such interventions with an ethnic slant? I might add I'm not talking about 'eating right for your blood type' or anything like that but there is always the example of ethnicity and lactose intolerance and its potential link to cases of autism for example. Food for thought anyway.

Whatever your interpretation of the Hewitt report, there are important practical lessons to be learned in terms of screening, diagnosis and the provision of services for those children diagnosed with autism whether of Somali origin or any other ethnic group. And once again, parents of children with autism were a primary driving force behind getting this research done and bringing it into the public arena...

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* Hewitt A, Gulaid A, Hamre K, Esler A, Punyko J, Reichle J. & Reiff M. (2013). Minneapolis Somali autism spectrum disorder prevalence project: Community report 2013. Minneapolis, MN: University of Minnesota,  Institute on Community Integration, Research and Training Center on Community Living

** Fernell E. et al. Serum levels of 25-hydroxyvitamin D in mothers of Swedish and of Somali origin who have children with and without autism. Acta Paediatr. 2010 May;99(5):743-7. 

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Fernell E, Barnevik-Olsson M, Bågenholm G, Gillberg C, Gustafsson S, & Sääf M (2010). Serum levels of 25-hydroxyvitamin D in mothers of Swedish and of Somali origin who have children with and without autism. Acta paediatrica (Oslo, Norway : 1992), 99 (5), 743-7 PMID: 20219032

Ironing out iron and autism

I'm a little bit puzzled when it comes to iron and autism.  In one of my earliest posts on this blog I talked about iron deficiency and autism, and how at that point there was some suggestion that there may be issues with iron availability in cases of autism and what remedial measures might be indicated.

Opposites attract? @ Wikipedia  

As with just about everything in autism research, things are never so straight forward though. With the recent paper from Reynolds and colleagues* (open-access) published as part of the Pediatrics special on autism we are advised that their data "do not support previous reports that children with ASD are at greater risk for ID [iron deficiency] than the general population".

A few details about the Reynolds study:

• Iron status and intake data were collected for 222 participants of the Autism Treatment Network Diet and Nutrition Study. Coincidentally, this initiative might also be reporting on vitamin D status in autism quite soon, so one to watch there also in light of other sunshine vitamin interest with autism in mind.
• Low iron stores indicated by serum ferritin levels <12mcg/L were present in 8% of their study cohort (18/218). Low transferrin saturation (TS) (defined as <10%) was present in 6% (12/199) bearing in mind some gaps in the testing regime in some important individual participants. Anaemia (UK spelling) was present in 7 participants (3%).
• The authors discuss some limitations of their findings including the possibility that accompanying inflammation might influence results, and the fact that they did not look at measures such as C-reactive protein (CRP) in their cohort (see this previous post). 

The message from Reynolds et al is that iron is a vital part of biochemical functioning - they mention tyrosine hydroxylase but I would be minded to also point out its role in a related enzyme tryptophan hydroxylase - and with autism in mind, how we need to be quite careful how we interpret any iron results.

I wouldn't argue with that but just before you start muttering to yourself that iron might be another research dead-end for autism, have a peek at the quite recent study from Hergüner and colleagues** whose estimates of iron deficiency (24%) and anaemia (15%) in their cohort of children with autism were a little bit different from Reynolds.

Again, a few points to mention about the Hergüner et al research:

• Sorry that I can't link to the full-text paper but this was a study of 116 children diagnosed with DSM-IV autism (aged 3-16 years). 
• As per the authorship group, participants were all Turkish in residency (and I assume origin), and various serum levels of iron and related measures were analysed.
• The figures for iron deficiency and anaemia were quite different from those reported by Reynolds; indeed when participants were divided up into under-6s (n=37) and 6 and overs (n=79), iron deficiency was more prevalent in the younger aged group.
• The authors conclude: "results of this study suggest that serum ferritin levels should be measured in every case with autism as a part of routine investigation".

I was intrigued at the disparity between these data (and others***) bearing in mind the different geographic and ethnic populations studied and the various interfering variables affecting results including sample size. Reynolds and colleagues are very forthcoming in mentioning how their results show so much difference from the other studies mentioned but are not altogether clear as to why there is such difference aside from noting that iron deficiency seems to be generally on the decrease in countries such as the United States and indeed worldwide. Factors such as fortification, guidance on not introducing cows milk too early and even delayed cord clamping**** probably all contributing to the decline.

I don't have anything further to add to this explanation by the way, aside from always being rather interested in results which don't follow the majority trend, and indeed whether this could imply some specific population/ethnic differences in risk among autism worldwide. It would be rather useful to have more up-to-date information from non-US parts of the world to work with including food diaries as per what Reynolds used to establish dietary iron intake. That and whether issues such as those pertaining to things like malabsorption may show some effect which might lead down some interesting paths...

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* Reynolds A. et al. Iron status in children with autism spectrum disorder. Pediatrics. 2012; 130 Suppl 2:S154-S159.

** Hergüner S. et al. Ferritin and iron levels in children with autistic disorder. Eur J Pediatr. 2012; 171: 143-146.

*** Latif A. et al. Iron deficiency in autism and Asperger syndrome. Autism. 2002; 6: 103-114.

**** Andersson O. et al. Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. BMJ. 2011; 343: d7157.

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Reynolds A, Krebs NF, Stewart PA, Austin H, Johnson SL, Withrow N, Molloy C, James SJ, Johnson C, Clemons T, Schmidt B, & Hyman SL (2012). Iron status in children with autism spectrum disorder. Pediatrics, 130 Suppl 2 PMID: 23118246

The geography of autism: urban or rural?

A short sentence in the abstract to a paper by Kiani and colleagues* caught my attention recently. The paper reported on the distribution of autism spectrum and other conditions in the UK according to defined designations of geographical location. In other words, whether there were any differences in reported rates according to whether people were living in a rural or an urban area. The authors suggested that among their sample (N=2713), autism spectrum disorders in particular, were more common in people living in rural areas.

I was interested in this work for several reasons. Quite a few years ago an undergraduate psychology student - 'Big bad BB' (you know who you are) - came and did some work with us involving pin-mapping where people with autism and related conditions resided on a large map of the UK. I need to track down the results which were published as conference proceedings to check but I faintly remember some interesting 'trends' emerging from this data not entirely dissimilar from the current paper.

Of course there could be lots of reasons to account for the reported results. Socio-economic status, where people work, or just a wish for a bit of quiet and tranquillity are a few factors. Those of you who regularly read this and my other blog might also pick up a bit of interest in the 'chemical world' around us, and in particular the various descriptions of exposure patterns and relative risk of lots of things. Suffice to say that when I think about rural areas and countryside, apart from rolling hills and cows and sheep chewing the cud, I unfortunately also tend to think 'pesticides'.

I'm not on this occasion going to get too alarmist based on the findings of the current paper. Trawling back through the research archives, the data is fairly mixed when it comes to asking the question 'where do you live' with regards to autism. This paper based on Taiwanese data suggested that residing in rural parts was actually less likely to get you an autism diagnosis than being an urban dweller but there again, rural Taiwan might not be the same as rural England or rural elsewhere. Data from Western nations do point to 'urbanisation' as being a potential contributory factor in the increasing numbers being diagnosed with autism. Remember freeways (motorways in England) and autism? Bear also in mind that (a) where you currently live is not necessarily the same as where were you born or where your parents lived before you were born and (b) very few people tend to live in city centres, at least here in the UK; more often than not you get a doughnut effect in terms of residence being outside of a hollow built-up city centre.

That all being said I'm not ready to discount the current results as an artifact or fluke just yet. The study by Roberts and colleagues** published a few years back which suggested that pregnant women living close to sprayed fields had a six-fold increase in later offspring diagnosis of autism comes to mind. Having done a little bit of reading on the persistence and potential effects of things like pesticides, it is perhaps unwise to rule out any 'environmental' factor in relation to autism, at least some cases of autism, just yet. Certainly here in the UK, the potential health implications of pesticide exposure seems to still be on the research menu as per this study description by Galea and colleagues***. We await their findings.

[Update 15/02/12: Found the pin-mapping data we undertook. A poster presentation 'UK Autism Demographics' Budd, B. 2000: Autism: perspectives on progress. University of Durham. pp.207-214. Yes, proportionally more people with autism living in rural areas based on analysis of 784 people with autism in the UK (1996-2000)].

* Kiani R. et al. Urban–rural differences in the nature and prevalence of mental ill-health in adults with intellectual disabilities. Journal of Intellectual Disability Research. February 2012.
DOI: 10.1111/j.1365-2788.2011.01523.x

** Robert E. et al. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley. Environmental Health Perspectives. 2007; 115: 1482-1489.
DOI: 10.1289/ehp.10168

*** Galea KS. et al. Biological monitoring of pesticide exposures in residents living near agricultural land. BMC Public Health. November 2011.
DOI: 10.1186/1471-2458-11-856