The positive effects of 12 weeks of probiotics and vitamin D in chronic schizophrenia?

The findings reported by Amir Ghaderi and colleagues [1] (open-access) provide the blogging fodder today, and the results of a study looking at a "novel combination of vitamin D and probiotic on metabolic and clinical symptoms in chronic schizophrenia." Said probiotic formulation contained "Lactobacillus acidophilus, Bifidobacterium bifidum, Lactobacillus reuteri, and Lactobacillus fermentum (each 2 × 109)" and was delivered over a period of 12 weeks alongside a vitamin D supplement - "50,000 IU vitamin D3 every 2 weeks" - utilising a "randomized, double-blind, placebo-controlled trial" design. We are also told that the trial protocol was "retrospectively registered."

The Ghaderi study wasn't solely focused on what their combined intervention might do for the 'clinical symptoms' of schizophrenia despite this being a prominent part of the results obtained. They also wanted to examine things like "biomarkers of oxidative stress and cardiometabolic risk in chronic schizophrenia." This was done via the measurement of marker compounds pertinent to establishing total antioxidant capacity, total glutathione levels and high-sensitivity C-reactive protein (hs-CRP) among other things.

Results: first things first, vitamin D supplementation raised vitamin D levels in those who received the vitamin D + probiotic supplement. Not exactly an unexpected result I grant you, but important from the point of view that any subsequent findings *could* be linked to those increasing vitamin D levels. Further: "Vitamin D and probiotic co-supplementation was associated with a significant improvement in the general... and total PANSS scores." PANSS stands for the Positive and Negative Syndrome Scale and has some important uses in the context of schizophrenia, and the presentation of positive and negative symptoms. That all being said, the authors also mention how their supplementation combination did not seemingly affect scores on another measure included in the study - the Brief Psychiatric Rating Scale (BPRS) - which kinda demonstrates that vitamin D + probiotics is not a panacea for every aspect of schizophrenia.

Researchers also report on how their combined supplement also *correlated* with a some changes in those oxidative stress and cardiometabolic risk measures included for study in line with other study results (see here). There's quite a bit of data so I won't provide details. Suffice to say that some of them might be 'positively' important to those health inequalities that seem to follow a diagnosis of schizophrenia (see here).

What else? Well, I can't seem to find too much in the way of side-effects details in the Ghaderi paper so I'm assuming that it wasn't a significant issue. The fact that participants in the study were "being hospitalized during the intervention" means that they were, I assume, being monitored with greater assiduity than for example if they were in the community, including looking for potential side-effects.

And with that, and the requirement for further study (see here and see here), I say no more...

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[1] Ghaderi A. et al. Clinical and metabolic response to vitamin D plus probiotic in schizophrenia patients. BMC Psychiatry. 2019; 19:77.

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Yoga therapy and autism: OK but "better trials are required to confirm the positive impact"

I approach the findings reported by HM Vidyashree and colleagues [1] with my typical critical eye but perhaps also with a sense of 'receptivity' to the idea that yoga training *might* be useful for some people diagnosed as being on the autism spectrum. My receptivity is there because: (a) "yoga is a safe and effective way to increase physical activity, especially strength, flexibility and balance" according to the NHS guide to yoga, and (b) putting aside any (non-testable) spirituality or the like associated with yoga use, I'd like to think that some of the aims of and techniques used in yoga are similar to that seen with some of the martial arts. As well as being a fan of the martial arts - Shotokan karate is my particular hobby - certain martial arts already have some quite positive 'history' in the context of autism in the peer-reviewed science arena (see here and see here for examples). We'll see what we'll see...

The Vidyashree paper had the aim: "to investigate the effect of yoga intervention on short-term heart rate variability (HRV) in children with ASD [autism spectrum disorder]." HRV is basically what it describes: "a measure of the variation in time between each heartbeat." That variation is controlled by something called the autonomic nervous system (ANS), which basically regulates various bodily functions typically minus conscious input from ourselves. From what I gather, a low HRV is something to be avoided; as people talk about a higher HRV being linked to better cardiovascular fitness as well as increased resilience to stress (whatever that means). You probably won't be surprised to hear that HRV has been previously talked about with autism in mind [2], albeit with a lot more investigation required (see here).

So: "50 children (38 boys and 12 girls) with ASD were recruited from Swabhimaan Trust, Palavakkam, Chennai." All were diagnosed with an autism spectrum disorder (ASD) and "were grouped into ASD with yoga intervention (n = 25) and ASD without yoga intervention group (n = 25) by simple lottery method." HRV was recorded via an ECG (electrocardiogram) on two occasions, before and after intervention/non-intervention. Said yoga intervention - in 40 minute sessions - was apparently delivered "every day in the morning" over 3 months. That's quite a few sessions...

Results: bearing in mind 10 participants and 5 participants from the yoga and non-yoga groups respectively were excluded from the data analysis side of things, a few details were observed. So: "There is a significant reduction in mean HR [heart rate]... in the ASD children after yoga intervention." As a group, the mean baseline HR for the yoga group was around 90 beats per minute. After intervention, this dropped to under 80 beats per minute. At the same time, the non-yoga group showed an increase in their mean heart rate over the same period. Other results, more technical results, are also included in the Vidyashree paper which I believe translate into measuring HRV [3]. I can't pretend to know all the hows-and-whys of those results, but with a cursory reading of the literature in this area, am willing to go along with the authors' conclusions that results: "showed significant improvement" coinciding with the yoga intervention.

Obviously a lot more study is required in this area before any grand claims about yoga or anything else are made in the context of autism. The Vidyashree results were firmly focused on HRV following yoga and said nothing about how yoga may/may not have affected some of the behavioural profiles associated with autism for example. Likewise, all the stuff about lower HRV being linked to greater resilience to something like stress have not been fully analysed in the context of the current results either. All of this comes alongside the methodological issues that accompany the Vidyashree: an open-trial, yoga vs. no yoga, etc.

But I still remain interested in the potential of something like yoga in many contexts including that related to autism...

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[1] Vidyashree HM. et al. Effect of Yoga Intervention on Short-Term Heart Rate Variability in Children with Autism Spectrum Disorder. Int J Yoga. 2019;12(1):73–77.

[2] Daluwatte C. et al. Atypical pupillary light reflex and heart rate variability in children with autism spectrum disorder. J Autism Dev Disord. 2013 Aug;43(8):1910-25.

[3] Shaffer F. & Ginsberg JP. An Overview of Heart Rate Variability Metrics and Norms. Front Public Health. 2017;5:258. Published 2017 Sep 28.

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The heart and chronic fatigue syndrome

I'll freely admit that I'm no expert when it comes to the biology and physiology of the heart. I know roughly where one should find it in a human body and what it usually does but that's about the sum total of my knowledge. Having said that, such a lack of knowledge has not held me back before from talking about aspects of the heart on this blog (see here)...

I therefore approach the findings reported by Cara Tomas and colleagues [1] with a degree of trepidation such that I don't misrepresent their observations. Importantly because authors reported finding: "an association between reduced cardiac volumes and BNP [brain natriuretic peptide] in CFS [chronic fatigue syndrome]."

The heart and CFS? Well, much like another area of CFS science discussing a possible role for mitochondria (the cell's powerhouse) and some CFS (see here for example), there is good reason to assume that the heart might have some role to play for some. Y'know, the heart - the thing that pumps blood around the body and delivers important things like oxygen and nutrients - could be working sub-optimally in a condition that primarily manifests as fatigue and specifically, post-exertional fatigue and exhaustion (see here).

Indeed, it's worthwhile mentioning that quite a few of the authors on the Tomas paper have previously discussed cardiac issues in the context of CFS [2]. On that previous occasion, they talked about finding evidence to "support the role of cardiovascular physiology as an underpinning problem in those with CFS" on the basis of their finding "an association between reduced cardiac volumes and blood volume in CFS."

This time around BNP was a focus of study; a peptide that is "secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells" and something that is typically elevated in cases of heart failure but can also be present under other clinical circumstances too. Thomas et al defined "a BNP value of >400 pg/mL as being consistent with moderate to severe cardiac disease" in their study based on data from some 42 people diagnosed with CFS and a smaller control group of 10 people who were described as 'sedentary'.

Results: based on analysis for BNP and other cardiac examinations, "BNP levels were significantly higher in the CFS cohort compared with the matched controls." Comparing group mean levels (I think!), the values came in at something like 500 pg/ml for the CFS group compared with about 300 pg/ml for controls. These findings are themselves notable in relation to existing guidance out there when it comes to BNP levels and their meaning in terms of heart health.

Further: "When we compared cardiac volumes (end-diastolic and end-systolic) between those with high BNP levels (BNP >400 pg/mL) and low BNP (<400 pg/mL), there were significantly lower cardiac volumes in those with the higher BNP levels in both end-systolic and end-diastolic volumes." The authors translate this finding in relation to "higher BNP levels are causing a diuresis (or natriuresis) and that this is depleting the plasma/blood volumes and leading to the smaller cardiac volumes."

Of course more investigations are needed in this area. I'd like to see a little more investigation of such BNP findings in the context of using other control groups (including those with diagnosed heart failure) to see where CFS 'ranks' on the basis of other heart tests too. The fact that BNP can be elevated in other conditions too (such as hyperthyroidism) is something else that needs to be analysed a little further [3] in the context that the broad spectrum of CFS might also include a number of other features/diagnoses too.

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[1] Tomas C. et al. Elevated brain natriuretic peptide levels in chronic fatigue syndrome associate with cardiac dysfunction: a case control study. Open Heart 2017; 4: e000697.

[2] Newton JL. et al. Reduced cardiac volumes in chronic fatigue syndrome associate with plasma volume but not length of disease: a cohort study. Open Heart. 2016 Jun 24;3(1):e000381.

[3] Tsai S-H. et al. Interpretation and Use of Natriuretic Peptides in Non-Congestive Heart Failure Settings. Yonsei Medical Journal. 2010;51(2):151-163.

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The physical health of adults with autism

Another short post today opening with the conclusion reached in the paper by Andrew Cashin and colleagues [1]: "From the findings, it can be stated with confidence that people with ASD [autism spectrum disorder] have a high rate of comorbidity and increased risk for chronic disease."

Yes, not new news to many that physical health is generally 'under-rated' when it comes to adult autism (see here and see here for examples). The question remains however: what are we all going to do about it?

Following continued acceptance that a diagnosis of autism might go WELL beyond the presented core behavioural features, how about a few more discussions about the healthcare experiences of those on the spectrum [2] (see here too) as a start and taking things from there, save ending up where another label has (see here) with regards to physical health?

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[1] Cashin A. et al. A scoping review of what is known of the physical health of adults with autism spectrum disorder. J Intellect Disabil. 2016 Sep 13. pii: 1744629516665242.

[2] Raymaker DM. et al. Barriers to healthcare: Instrument development and comparison between autistic adults and adults with and without other disabilities. Autism. 2016 Sep 22. pii: 1362361316661261.

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Cashin A, Buckley T, Trollor JN, & Lennox N (2016). A scoping review of what is known of the physical health of adults with autism spectrum disorder. Journal of intellectual disabilities : JOID PMID: 27623754

Vitamin D deficiency and psychosis

In amongst my various ramblings about how vitamin D - the sunshine vitamin/hormone - might show more than a few connections to conditions/labels outside of just the English disease (see here), I've covered some science on a possible connection with psychosis (see here) and schizophrenia (see here). There are still gaps in terms of the hows and whys of vitamin D insufficiency and deficiency when it comes to this area of psychiatry, but I believe there is enough science in this area to initially warrant screening of vitamin D levels as and when a diagnosis is received. This similarly extends to other labels too (see here and see here).

The paper by Lally and colleagues [1] (open-access) puts a little more scientific flesh on the bones about how vitamin D insufficiency/deficiency might manifest in cases of psychosis, with a particular focus on "increased cardiovascular disease risk factors and in particular metabolic syndrome [MetS]."

With thanks to Brendon Stubbs (one of the authors of the paper) for bringing the findings to my attention, researchers set about looking at "the prevalence of vitamin D deficiency in a cohort of community patients with established psychotic illnesses" (N=324). Given my earlier mention of the 'English disease', the cohort were indeed all living in England and drawn from a larger study initiative. Vitamin D levels were assayed via a chemiluminescence immunoassay based on the examination of serum samples. Various other measures were also included for study around the issue of cardiovascular risk factors including body mass index (BMI), waist circumference, blood pressure, serum cholesterol levels and glucose levels. High sensitivity serum C-reactive protein (HS-CRP) was also included.

Results: "Almost half of the sample (48.8 %, n = 158) were deficient in vitamin D while only 13.9 % (n = 45) had sufficient vitamin D." Ethnicity seemed to play a role in those determinations of deficiency/sufficiency with vitamin D levels generally lower in those who were black African or black Caribbean. Likewise the season of testing showed an effect. When it came to determining whether there was an association between vitamin D status and mental state, researchers reported nothing significant based on the use of the Positive And Negative Syndrome Scale (PANSS) and related measures.

But... there might be quite a bit more to look at when taking into account those cardiovascular disease risk factors and vitamin D levels as the authors reported various significant correlations. So: "those with the highest levels of vitamin D have a lower prevalence of MetS (20.5 %), compared to those in the lowest (39.1 %), second (48.3 %) and third quartile (43.1 %) of vitamin D." Indeed, just about every measure of cardiovascular risk showed an association with measured serum vitamin D levels when controlling for "age, gender, ethnicity and season of 25-OHD blood sampling." The authors also add that: "Those engaging in low intensity physical activity over the week prior to sampling... had significantly lower 25-OHD levels... than those who engaged in moderate or high intensity physical activity."

Teasing apart what might actually be doing what is a difficult task in such studies where various outcome measures might be implicated. The authors do speculate on how for example, their finding of "raised CRP and vitamin D deficiency in established psychosis" might tie into other research on inflammation or inflammatory processes with both variables in mind (see here and see here). Indeed, this might also tie in with calls for further integration of immunopsychiatry with psychotic disorders in mind [2]. But there remains more to do, including the intriguing question: "would the supplementation of vitamin D in psychosis prevent and/or ameliorate cardiovascular and metabolic risk?"

I do have some small points to make about the study that might also require attention in follow-up work, not least the idea that immunoassay for determining functional vitamin D levels might not be the most accurate method [3]. Indeed, the authors make this point in their conclusions. One might also hope that comparisons with other patient groups might offer some further information about how specific the findings are to just psychosis or other psychiatric groupings. If found in a more general sense, the idea that vitamin D is related to variables affecting cardiovascular risk in such groups could make lots and lots of waves.

For now however, this research extends the ideas that: (a) preferential screening for vitamin D might be indicated for this group/label, and (b) the focus on psychiatric presentation should not be made at the expense of somatic presentation. Parity of esteem and all that; or rather just making sure that health inequality does not follow from receipt of a psychiatric label...

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[1] Lally J. et al. Clinical correlates of vitamin D deficiency in established psychosis. BMC Psychiatry. 2016; 16: 76.

[2] Leboyer M. et al. Is it time for immunopsychiatry in psychotic disorders? Psychopharmacology (Berl). 2016 Mar 18.

[3] Yang Y. et al. High-throughput measurement of 25-hydroxyvitamin D by LC-MS/MS with separation of the C3-epimer interference for pediatric populations. Clin Chim Acta. 2016 Feb 15;454:102-6.

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Lally, J., Gardner-Sood, P., Firdosi, M., Iyegbe, C., Stubbs, B., Greenwood, K., Murray, R., Smith, S., Howes, O., & Gaughran, F. (2016). Clinical correlates of vitamin D deficiency in established psychosis BMC Psychiatry, 16 (1) DOI: 10.1186/s12888-016-0780-2

Coenzyme Q10 and NADH supplementation for Chronic Fatigue Syndrome continued

In a previous post on this blog I briefly discussed the research paper from Jesus Castro-Marrero and colleagues [1] suggesting that "oral CoQ10 [Coenzyme Q10] (200 mg/day) plus NADH [nicotinamide adenine dinucleotide (NADH)] (20 mg/day) supplementation" might be something useful for some people diagnosed with Chronic Fatigue Syndrome (CFS).

Enter then a new paper from Castro-Marrero and colleagues [2] (open-access available here) building on the original findings by suggesting that "CoQ10 plus NADH supplementation for 8 weeks is safe and potentially effective in reducing max HR [maximum heart rate] during a cycle ergometer test and also on fatigue in CFS." The max HR by the way, is a measure of cardiovascular function as part of exercise performance. A cycle ergometer test is all about testing parameters such as max HR using a stationary bicycle.

"A proof-of-concept, 8-week, randomized, double-blind, placebo-controlled trial was conducted" whereby either CoQ10 plus NADH was given (n=39) or a placebo (n=34) over the study period. Baseline and end of study max HR was tested alongside self-reported changes to "fatigue, pain and sleep problems" based on scoring using the Fatigue Impact Scale (FIS) among other things.

Based on an intention-to-treat (ITT) analytical strategy, authors reported that: "statistically significant differences were observed in CoQ10 + NADH group during the study, with a reduction in max HR after 8 weeks of treatment compared with baseline max HR." That being said, when comparing max HR from baseline to 8 weeks between the groups (CoQ10+NADH vs placebo), no statistically significant group differences were noted despite a trend towards greater max HR reduction in the experimental group. Insofar as other biological parameters also measured over the course of the study period ("VO2, VCO2, maximal workload, respiratory quotient and arm systolic and diastolic blood pressure") no significant differences were noted between baseline and end of study.

Fatigue scores showed a similar trend in terms of intra- and inter-group comparisons. So, for the CoQ10+NADH group, comparisons between baseline, week 4 and week 8 scores suggested significant reductions in total FIS scores. When it came to comparisons with the placebo group however, no significant differences were reported (indeed, the placebo group also showed a reduction in FIS total scores at least between baseline and week 4). The authors suggest that a lack of study power might have contributed to the lack of significant effects when comparing the experimental and placebo groups.

These are interesting results and from an intra-group perspective (comparing across different testing occasions) suggest that there may be more to see from this preparation on this patient group. Bearing in mind the emphasis on actually looking at physiological parameters such as max HR and as the authors note: "the use of strict inclusion criteria based on 1994 CDC case definition ensures that the participants were appropriately selected and without confounding comorbidities" further research is indicated to further assess such claims and determine specific biological mechanisms pertinent to any effect.

Music: Ike & Tina Turner - River Deep Mountain High.

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[1] Castro-Marrero J. et al. Does oral Coenzyme Q10 plus NADH supplementation improve fatigue and biochemical parameters in Chronic Fatigue Syndrome? Antioxid Redox Signal. 2014 Nov 11.

[2] Castro-Marrero J. et al. Effect of coenzyme Q10 plus nicotinamide adenine dinucleotide supplementation on maximum heart rate after exercise testing in chronic fatigue syndrome - A randomized, controlled, double-blind trial. Clin Nutr. 2015 Jul 17. pii: S0261-5614(15)00189-2.

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Castro-Marrero J, Sáez-Francàs N, Segundo MJ, Calvo N, Faro M, Aliste L, Fernández de Sevilla T, & Alegre J (2015). Effect of coenzyme Q10 plus nicotinamide adenine dinucleotide supplementation on maximum heart rate after exercise testing in chronic fatigue syndrome - A randomized, controlled, double-blind trial. Clinical nutrition (Edinburgh, Scotland) PMID: 26212172

Depression and risk of coronary heart disease

"The results of our meta-analysis suggest that depression is independently associated with a significantly increased risk of CHD [coronary heart disease] and MI [myocardial infarction], which may have implications for CHD etiological research and psychological medicine."

No owners means - no heartbreak!

So said the conclusion of the paper by Yong Gan and colleagues [1] (open-access) and their synthesis of the peer-reviewed literature on the topic of heart health and depression. Granted, such findings are probably not particularly great news to anyone with depression, but as per similar research on health and psychology discussed on this blog (see here), getting the message out is often an important first stage in doing something about mitigating any enhanced risk.

Glancing through some of the previous entries on this blog covering depression - in all its different forms - I realise that this is a topic which has already been raised in a previous entry (see here). In that case based on the study by Amit Shah and colleagues [2] the suggestion was that: "In adults younger than 40 years, depression and history of attempted suicide are significant independent predictors of premature CVD [cardiovascular disease] and IHD [ischemic heart disease] mortality in both sexes." Again, slightly sombre reading.

"Participants with depression, compared with those free of it, experienced a significant
increased risk of 30% for CHD and MI. Furthermore, the association remained significant in
the groups adjusted for potential confounders, such as lifestyle factors and socio-demographic
factors." An important summary from Gan and colleagues highlighting how, whilst their data did point to an increased risk of CHD and MI in relation to depression, one has to be slightly careful in how one communicates the words 'increased risk' and what a 30% risk might translate into in the real world.

Without exceeding the scope of this blog, and in particular my caveats about not giving anything that looks, sounds or smells like medical or clinical advice, I was interested in some discussion by Gan on the potential role of antidepressants to "reduce the risk of development of CHD." They suggested that it may not be as easy as such intervention just impacting on heart health as well as psychological health even though other studies have suggested some beneficial effect [3] to be had from certain antidepressants. I've talked before on this blog about depression and some of the slightly more alternative ways that have been put forward to manage symptoms as per the rise and rise of something like anti-inflammatory strategies for example (see here). If for example, one is to assume that exercise (also included in that post on potential strategies to manage depression) might also be a potentially important tool for at least some types of depression, might it also have some effect to mitigate risk of adverse heart conditions too?

Music to close. When footballers sing.... Glenn & Chris - Diamond Lights (in the 1980s).

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[1] Gan Y. et al. Depression and the risk of coronary heart disease: a meta-analysis of prospective cohort studies. BMC Psychiatry 2014, 14:371

[2] Shah AJ. et al. Depression and history of attempted suicide as risk factors for heart disease mortality in young individuals. Archives of General Psychiatry. 2011: 68: 1135-1142.

[3] Pizzi C. et al. Meta-analysis of selective serotonin reuptake inhibitors in patients with depression and coronary heart disease. Am J Cardiol. 2011 Apr 1;107(7):972-9.

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Gan Y, Gong Y, Tong X, Sun H, Cong Y, Dong X, Wang Y, Xu X, Yin X, Deng J, Li L, Cao S, & Lu Z (2014). Depression and the risk of coronary heart disease: a meta-analysis of prospective cohort studies. BMC psychiatry, 14 (1) PMID: 25540022

Early mortality in mums of children with autism or intellectual disability

I know the paper by Jenny Fairthorne and colleagues [1] (open-access) is probably not the happiest thing to read with their conclusion that: "During the study period, mothers of children with intellectual disability or ASD [autism spectrum disorder] had more than twice the risk of death" but their message is nonetheless an important one.

Based on data derived from "state-wide databases" covering women living in Western Australia who gave birth between 1983 and 2005, researchers detected mums with a child diagnosed with autism and/or intellectual disability (learning disability if you prefer) and cross-referenced findings with "the state mortality registry" providing information on "dates and cause of death by ICD-9 or 10 codes". Various study (case) groups were formed on the basis of offspring diagnosis - intellectual disability (ID) of unknown cause (further separated based on levels of ID), ID of known cause (specifically Down syndrome or other) and a diagnosis of autism spectrum disorder (ASD) with and without ID - and aided analyses.

After some correction for various confounders including maternal age and socio-economic status (SES), from a starting population of some 300,000 mothers, approximately 1% had died before 2011 (the longer follow-up period). To quote: "Twenty-five years after the birth of their index child, the survival rates of mothers of children with no intellectual disability and no ASD were about 98%, followed by 96% for mothers of children with ASD and 95% for mothers of children with intellectual disability." These group difference were significant and led researchers to draw the conclusion: "Mothers from all case groups had an increased risk of death during the study period."

A few other details are also recorded in the Fairthorne study. "Mothers with both a psychiatric disorder and a child with intellectual disability or ASD had about six and a half times the risk of death" was an important finding reported by the authors. When it came to the cause of death, various factors were over-reported in case group mums including cancers, cardiovascular disease and death by misadventure (death due to an unintentional accident, homicide or suicide according to the authors' criteria).

Reiterating that the Fairthorne paper makes for quite uncomfortable reading, there are some potentially important lessons to be learned from the collected data. First and foremost I should stress that the excess percentages of deaths reported during the study period were overall, quite small for the case groups. Whilst there was an excess of deaths over and above that seen in the asymptomatic control group, the data do not suggest that mothers of children with autism or Down syndrome for example, are facing a gigantic excess risk. Risk is risk and influenced by lots of different variables. I say all that with my cold, dispassionate science goggles on, recognising that each death is a mother lost.

That being said, one might make a case for further inspection of maternal (and paternal) health and wellbeing as and when a diagnosis of autism and/or ID is received in one or more offspring. I've covered the topic of parental stress and autism before on this blog (see here) and the [evidence-based] ways and means it might be reduced. Stress is mentioned in the Fairthorne paper as potentially being one factor linking parenting and early mortality although I'd also suggest the concepts of resilience and coping might also require investigation.

Maternal health issues such as a history of psychiatric issues and/or more somatic diagnoses like diabetes and obesity are also covered in the discussion on possible reasons for the added risk in case groups. As per the research suggesting that some of these factors alone or in combination might increase the risk of offspring autism for example (see here), management of said issues should also rank high on the list of monitoring parental wellbeing. Lifestyle issues such as tobacco smoking and poor exercise regimes can also be mitigated if and when required.

Finally, I want to make one further point specifically related to the idea that cancer may feature as one reason for the excess mortality noted in the current study. Late last year (2014) I covered the complicated issue of cancer risk and autism (see here) on the basis of some further 'big data' derived from the Taiwan National Health Insurance database [2]. In amongst the discussions on that post was some mention of a familial history of certain cancers potentially being heightened in cases of autism on the basis of data from Ingudomnukul and colleagues [3]. The Fairthorne data corroborates this view, and further implies screening should perhaps be preferentially extended to mums of children with ID and/or autism. Early detection can save lives.

Mortality and autism is never going to be a great topic to discuss whether based on personal experience or the peer-reviewed evidence base. Linked to the suggestion that a diagnosis of autism - or at least some of the comorbidities which it can carry - for example, might also elevate the risk of early mortality (see here), I believe that it is time to start bigger conversations on how science and society can go about reducing such risk and reducing health inequality. Mothers, like their children, are precious things...

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[1] Fairthorne J. et al. Early Mortality and Primary Causes of Death in Mothers of Children with Intellectual Disability or Autism Spectrum Disorder: A Retrospective Cohort Study. PLoS ONE. 2014; 9(12): e113430.

[2] Chiang H-L. et al. Risk of Cancer in Children, Adolescents, and Young Adults with Autistic Disorder. J Pediatrics. 2014. 18 November.

[3] Ingudomnukul E. et al. Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Horm Behav. 2007 May;51(5):597-604.

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Fairthorne J, Hammond G, Bourke J, Jacoby P, & Leonard H (2014). Early Mortality and Primary Causes of Death in Mothers of Children with Intellectual Disability or Autism Spectrum Disorder: A Retrospective Cohort Study. PloS one, 9 (12) PMID: 25535971

Sedentary behaviours and autism

Standing up is better for your health than sitting down according to the BBC website. As one of those people known to wear a pedometer pretty regularly and generally be quite 'obsessive' about my 10,000 steps per day (or should that be 6000 steps per day [1]), I wasn't surprised by some of the discussions on this topic and how quite a proportion of the population at large could really do with standing up and indeed, moving a little more each day.

 The Ministry... @ Wikipedia 

We are all seemingly bombarded these days with information mixed in with a healthy sprinkling of science suggesting that one needn't be pounding the streets for hours on end in order to get a little bit more healthy. It's all about making sure that we aren't too sedentary and perhaps enjoying a little more of the great outdoors even if at a leisurely pace.

With this in mind, I was very interested to read the paper by Avivia Must and colleagues [2] who upon comparing a small-ish group of children diagnosed with an autism spectrum condition (n=53) with typically developing peers (n=58), found that "children with autism spectrum disorder spent an hour more in sedentary behaviors on weekdays compared to typically developing children". Further Must et al also reported quite a bit of that increase in sedentary behaviour was apportioned to an increase in screen time (TV and computer) and "sedentary behaiour is linked to relative weight status" in the group of children with autism. Think screen time and autism and I think about the work of Micah Mazurek as exemplified by this paper [3] and more recently with the issue of sleep in mind [4].

Some more digging into the various research done on exercise and autism revealed some equally interesting findings. The same authorship group have looked at this issue before as per the article by Bandini and colleagues [5] who suggested based on the same spread of participants (autism, n=53, not-autism, n=58) "moderate and vigorous activity was similar in children with ASD (50.0 minutes/day and typically developing children 57.1 minutes/day)". That being said, the authors did report that children with autism participated in "fewer physical activities and for less time according to parental report" highlighting potential issues with the measurement schedule employed to examine activity levels.

These and other similar research on activity levels and autism perhaps represent the other side of the research coin in terms of the increasing interest in the use of technology to improve quality of life for those on the autism spectrum. The rise and rise of the use of tablet technology for example, whilst often a significant step forward for some on the autism spectrum, not necessarily being great news for levels of physical activity if replacing time that could be used on non-sedentary activities.

The question of whether physical activity might also have some added benefits outside of just physical health has also been looked at. Oriel and colleagues [6] reported that "aerobic exercise prior to classroom activities may improve academic responding in young children with autism spectrum disorder". I'm not for one minute suggesting that every classroom should be installing a treadmill so as to increase 'correct' responses to I assume, questions posed by the teacher. But as I've indicated on a previous post about stress (see here), physical exercise often goes so much further than just improving physical health and that applies to autism too [7]. Other research reviews whilst highlighting a lack of good quality evidence in this area, have nonetheless suggested that exercise participation might have a least some short-term bearing on the presentation of facets of autism also [8].

With all the mind, the question of what kind of activities might increase activity levels in cases of autism in childhood has similarly been examined in autism research circles.

Walking is often a good place to start when it comes to increasing activity levels. The paper by Pitetti and colleagues [9] reported that even for those at the more severe end of the autism spectrum, the implementation of a walking program may well have some important benefits. Correspondingly, I've heard a few people talk about young people and adults with autism (again towards the more severe end of the autism spectrum) who very much enjoy long (sometimes very long) walks in all weathers. One wonders whether they might know more than us about what makes them feel good?

Swimming is another option to consider as per the paper by Fragala-Pinkham and colleagues [10]. Granted their results weren't astounding in terms of fitness outcomes for some participants (although contrasted with previous work of theirs [11]) but one might suggest that anything which increases activity is worthwhile. That and the often life-saving skills that are gained by learning to swim. Indeed, Pan [12] reported on some other potentially important changes noted following implementation of a water exercise swimming program with a small group of children with autism.

And then there are other exercise options to consider. Horseback riding (see here) assuming no fear of such animals and something which has cropped up before on this blog, the various martial arts (see this post) might also be good ways of increasing activity levels and decreasing sedentary behaviours. I suppose it's all about finding something that the individual enjoys.

Recognising that a sedentary lifestyle is not really ideal for anyone, there are perhaps some important lessons to be learned about increasing activity levels among children and adults with autism. Physical activity is an important part of physical health, and as we've seen in relation to schizophrenia, there is an emerging gap appearing in terms of health inequality which includes the issue of physical activity levels. That physical activity levels may also have important knock-on effects for things like bone health (see this post) and possibly exposure to sunshine and that all-important vitamin D (see this post) are also important considerations too.

To close, a song about walking by two brothers who are talking about walking an awfully long way. Oh and for those who were also wondering about the word 'haver', some background can be found here.

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[1] Tudor-Locke C. & Bassett DR Jnr. How many steps/day are enough? Sports Med. 2004: 34: 1-8.

[2] Must A. et al. Comparison of sedentary behaviors between children with autism spectrum disorders and typically developing children. Autism. 2013 Oct 10.

[3] Mazurek MO. & Wenstrup C. Television, video game and social media use among children with ASD and typically developing siblings. J Autism Dev Disord. 2013 Jun;43(6):1258-71.

[4] Engelhardt CR. et al. Media Use and Sleep Among Boys With Autism Spectrum Disorder, ADHD, or Typical Development. Pediatrics. November 2013.

[5] Bandini LG. et al. Comparison of physical activity between children with autism spectrum disorders and typically developing children. Autism. 2013 Jan;17(1):44-54.

[6] Oriel KN. et al. The effects of aerobic exercise on academic engagement in young children with autism spectrum disorder. Pediatr Phys Ther. 2011 Summer;23(2):187-93.

[7] García-Villamisar DA. & Dattilo J. Effects of a leisure programme on quality of life and stress of individuals with ASD. J Intellect Disabil Res. 2010 Jul;54(7):611-9.

[8] Petrus C. et al. Effects of exercise interventions on stereotypic behaviours in children with autism spectrum disorder. Physiother Can. 2008 Spring;60(2):134-45.

[9] Pitetti KH. et al. The efficacy of a 9-month treadmill walking program on the exercise capacity and weight reduction for adolescents with severe autism. J Autism Dev Disord. 2007 Jul;37(6):997-1006.

[10] Fragala-Pinkham MA. et al. Group swimming and aquatic exercise programme for children with autism spectrum disorders: a pilot study. Dev Neurorehabil. 2011;14(4):230-41.

[11] Fragala-Pinkham M. et al. Group aquatic aerobic exercise for children with disabilities. Dev Med Child Neurol. 2008 Nov;50(11):822-7.

[12] Pan CY. Effects of water exercise swimming program on aquatic skills and social behaviors in children with autism spectrum disorders. Autism. 2010 Jan;14(1):9-28.

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Must A, Phillips SM, Curtin C, Anderson SE, Maslin M, Lividini K, & Bandini LG (2013). Comparison of sedentary behaviors between children with autism spectrum disorders and typically developing children. Autism : the international journal of research and practice PMID: 24113339

Schizophrenia and C-reactive protein

Discussions on the various studies hinting at a possible connection between inflammation (however you wish to define this) and autism, at least some of the autisms, have cropped up with increasing frequency on this blog (see here and here). I wouldn't go so far as to say that a causal link has been established yet; as in 'inflammation causes autism', or indeed 'autism cause inflammation' but inflammation. in it's various guises, is certainly one to watch.

Amusing the muses @ Wikipedia 

Outside of autism, and bearing in mind an increasingly vocal research voice suggesting common ground (see here) and connections between autism and other more psychiatrically-defined conditions such as the schizophrenia spectrum (see here), similar work also suggests a possible connection between inflammatory markers and other conditions.

Indeed today's post is dedicated to some of the cumulative work looking at schizophrenia and inflammation, and in particular one of the more reliable markers of inflammation, C-reactive protein (CRP) linked to all manner of health ills (see here for example).

I arrived at this post after reading the paper by Lin and colleagues* and their assertion that subject to much more confirmatory research being required, cases of schizophrenia which were also following a medication regime (antipsychotic meds) seemed more likely to present with elevations in CRP. The medication element to the study reflects some interest in how antipsychotics might be able to affect the CRP measure, bearing in mind the results are still fairly limited in this area (see this paper by Diaz and colleagues**).

The paper by Miller and colleagues*** provides a pretty good summary of the various research undertaken so far on CRP and schizophrenia. They concluded that there was "a 28% prevalence of an elevated CRP level in patients with schizophrenia and related disorders" and onwards quite a strong implication of increased inflammation being associated with schizophrenia. Importantly as per the autism example, this does not necessarily mean that inflammation is causative of schizophrenia or vice-versa.

It is noteworthy that a name which has appeared more than once on this blog has also thrown their research hat into the schizophrenia-CRP arena. Faith Dickerson (with a mention for Robert Yolken too), famous around these parts for her various studies on schizophrenia with the gondii in mind (see here) and a few other potential important associations (see here), also suggested that CRP levels tended to be on the higher side in cases of schizophrenia****. They reported that even after adjusting for various potentially modifying variables such as smoking status (see here) and body mass index (BMI) (see here), CRP levels were elevated in their participants with schizophrenia above and beyond asymptomatic controls and even those diagnosed with bipolar disorder. That bipolar disorder bit has also been explored a little bit more with CRP in mind too*****.

Importantly Dickerson and the other authors included in this mini-review post highlight how elevated CRP outside of any direct connection with either the onset or perpetuation of schizophrenia might place a person at enhanced risk of various health-related issues (see here). Without wishing to sound too morbid, heart health in schizophrenia for example, does not seem to have a great track record as per some previous discussions on this blog (see here). That finding perhaps as part of a greater package of issues with physical health screening and mental illness (see this paper from Barley and colleagues******) and some inequality which appears to be present.

Just before I go, I wonder if it would be worth mentioning a few other potential points of interest which perhaps require some further investigation. I touched upon the topic of homocysteine - the big 'H' - and schizophrenia in a previous post (see here) and also an intersecting area dealing with folate metabolism (see here). Homocysteine, whilst still the topic of some debate, was at one time talked about with issues related to things like cardiovascular health (see this paper by Wald and colleagues*******). Appreciating that humans are very complex creatures and sweeping generalisations about one compound = risk of one disease seem to serve little use, one might choose to enquire whether CRP levels might correlate with homocysteine and whether this clarifies any health-related relationship or not? Something along the lines of this paper but with larger participant numbers and without the interfering variables. Indeed as per another Dickerson paper******** whether CRP plus [insert variable of your choice here] might provide further insights into how CRP levels could even affect some of the facets of schizophrenia itself.

And very, very finally and quickly, I do wonder about the questions raised by Berk and colleagues********* (open-access) bearing in mind no medical advice is given or intended.

To close, are you just living for the weekend?

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* Lin CC. et al. Increased high-sensitivity C-reactive protein levels in Taiwanese schizophrenic patients. Asia Pac Psychiatry. 2013 Jun;5(2):E58-63. doi: 10.1111/appy.12078.

** Diaz FJ. et al. Possible effects of some antipsychotic drugs on C-reactive protein in a drug-naïve psychotic sample. Schizophr Res. 2010 Aug;121(1-3):207-12. doi: 10.1016/j.schres.2010.06.002.

*** Miller BJ. et al. C-Reactive Protein Levels in Schizophrenia. Clin Schizophr Relat Psychoses. 2013 Feb 21:1-22

**** Dickerson F. et al. C-reactive protein is elevated in schizophrenia. Schizophr Res. 2013 Jan;143(1):198-202. doi: 10.1016/j.schres.2012.10.041.

***** Dickerson F. et al. Elevated C-reactive protein and cognitive deficits in individuals with bipolar disorder. J Affect Disord. 2013 May 17. pii: S0165-0327(13)00340-6. doi: 10.1016/j.jad.2013.04.039.

****** Barley E. et al. Interventions to encourage uptake of cancer screening for people with severe mental illness. Cochrane Database Syst Rev. 2013 Jul 16;7:CD009641.

******* Wald DS. et al. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ. 2002 Nov 23;325(7374):1202.

******** Dickerson F. et al. Additive effects of elevated C-reactive protein and exposure to Herpes Simplex Virus type 1 on cognitive impairment in individuals with schizophrenia. Schizophr Res. 2012 Jan;134(1):83-8. doi: 10.1016/j.schres.2011.10.003.

********* Berk M. et al. Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness. BMC Med. 2013 Mar 18;11(1):74.

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Lin CC, Chang CM, Liu CY, & Huang TL (2013). Increased high-sensitivity C-reactive protein levels in Taiwanese schizophrenic patients. Asia-Pacific psychiatry : official journal of the Pacific Rim College of Psychiatrists, 5 (2) PMID: 23857813

The health inequalities of schizophrenia

Heart to heart @ Wikipedia  

Dare I start this post by saying that when it comes to many conditions with a behavioural or cognitive aspect to them, there are some worrying trends emerging from the research literature suggestive of stark differences in both access to healthcare and indeed mortality statistics compared with the general population. Think wandering and elopement with autism in mind as one prime risk factor.

I've touched upon health inequality before with autism spectrum disorders in mind, but on this occasion want to briefly discuss some of the literature with schizophrenia spectrum disorders in mind following yet another revelation of more overlap between the conditions.

The paper which brought me to this post is this one from Paul Kurdyak and colleagues* who reported that people diagnosed with schizophrenia were more likely to die as a result of an acute myocardial infarction (heart attack to you and me) and indeed were less likely to receive the appropriate care (including access to a specialist physician) after such an event. 

The quite shocking figures: individuals with schizophrenia were 56% more likely to die within 30 days of discharge and 50% less likely to receive the appropriate after-event healthcare. One could argue on this basis that schizophrenia and its effects go well beyond the psychiatric symptoms that characterise the condition.

Of course there is already quite a lot of suggestion that schizophrenia and related conditions might place an individual at higher risk of quite a few different conditions. So for example, diabetes - type 2 diabetes - is something which has been on the research radar for a while now as per the study by Schoepf and colleagues**. So too issues with obesity, being overweight and other parts of the so-called metabolic syndrome as per reports like the one from Subashini et al*** covering some of the more usual suspects with heart health risk in mind.

The hows and whys of such an increased prevalence of such conditions are complicated. Certainly the research literature seems to suggest that just having a schizophrenia spectrum disorder might increase the risk of engaging in known lifestyle choices linked to poorer heart health. So smoking tobacco, including being heavy tobacco smokers, seems to be more frequent in cases of schizophrenia as per this study by Zhang and colleagues**** (open-access). Physical inactivity has also been reported to be more common too***** and perhaps even tied into illness duration. Not to also mention a role for food choices****** albeit not necessarily consistently*******. There is however some difficulty in unpicking individual behaviours and factors when assessing overall risk.

Before anyone suggests that I am somehow apportioning 'blame' in listing these lifestyle choices, I think it is also important to highlight other factors as potentially contributing to a heighten risk including that of pharmacotherapy. By saying this I'm not going down the 'pharma-bashing' route despite some quite worrying issues recently discussed reiterating that medicines tend to have quite a few more actions that those just indicated on the insert. No, but certainly some of the medicines used to manage schizophrenia and other conditions have long been linked to certain cardiometabolic issues as per editorials like this one from Remington********. Indeed I have a post scheduled soon talking about antipsychotics and autism following the recent NICE guidance published on adult autism which will discuss this further. Good medicines management seems to be key to mitigating the effects of such risks.

Social factors might also play an important role in the accessing of appropriate healthcare for conditions like schizophrenia. Here in the UK we have something called the NHS (National Health Service) which provides healthcare to everyone "free at the point of use". Not everywhere in the world has such a generous policy however as studies like this one by Khaykin and colleagues********* which suggested that around 7% of their cohort with schizophrenia were medically uninsured all year round.

Although perhaps mixing apples and oranges, when you take into account the high rates of unemployment associated with a diagnosis of schizophrenia, upto 96% according to this study by Perkins & Rinaldi**********, having the financial means to access healthcare in some parts of the world must surely be considered an important factor in determining outcome.

I don't claim to have covered all the literature on health inequality and schizophrenia in this post. Indeed the reasons for the figures cited by Kurdyak are likely to be complex and multiple across different people and different situations. What perhaps such data do suggest however is that looking beyond the immediate and overt presentation of mental 'ill-health' should be a priority where general healthcare is concerned. Realising for example, that ticking boxes on a clinical diagnostic schedule and managing current symptoms of that condition might do little for the long-term health of that individual. Indeed when faced with a life expectancy potentially reduced by the order of 14 years*********** there is most definitely a real issue to be tackled here.

To finish a song about blackbirds by the Beatles.

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* Kurdyak P. et al. High mortality and low access to care following incident acute myocardial infarction in individuals with schizophrenia. Schizophr Res. September 2012.

** Schoepf D. et al. Type-2 diabetes mellitus in schizophrenia: increased prevalence and major risk factor of excess mortality in a naturalistic 7-year follow-up. Eur Psychiatry. 2012; 27: 33-42.

*** Subashini R. et al. Prevalence of diabetes, obesity, and metabolic syndrome in subjects with and without schizophrenia (CURES-104). J Postgrad Med. 2011; 57: 272-277.

**** Zhang XY. et al. Cigarette smoking in male patients with chronic schizophrenia in a Chinese population: prevalence and relationship to clinical phenotypes. PLoS One. 2012; 7: e30937.

***** Vancampfort D. et al. A systematic review of correlates of physical activity in patients with schizophrenia. Acta Psychiatr Scand. 2012; 125: 352-362.

****** McCreadie RG. et al. Diet, smoking and cardiovascular risk in people with schizophrenia: descriptive study. Br J Psychiatry. 2003; 183: 534-539.

******* Henderson DC. et al. Dietary intake profile of patients with schizophrenia. Ann Clin Psychiatry. 2006; 18: 99-105.

******** Remington G. Schizophrenia, antipsychotics, and the metabolic Syndrome: is there a silver lining? Am J Psychiatry. 2006; 163: 1132-1134.

********* Khaykin E. et al. Health insurance coverage among persons with schizophrenia in the United States. Psychiatr Serv. 2010; 61: 830-834.

********** Perkins R. & Rinaldi M. Unemployment rates among patients with long-term mental health problems. The Psychiatrist. 2002; 26: 295-298.

*********** Chang CK. et al. Life expectancy at birth for people with serious mental illness and other major disorders from a secondary mental health care case register in London. PLoS One. 2011; 6: e19590

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Kurdyak P, Vigod S, Calzavara A, & Wodchis WP (2012). High mortality and low access to care following incident acute myocardial infarction in individuals with schizophrenia. Schizophrenia research PMID: 23021899

Interconnectedness: depression and heart disease

Today's topic is slightly off the beaten track when it comes to autism research but some of the themes coming out of the research in question may link back to a few issues discussed previously.

First tulips @ Paul Whiteley 2011

Whilst a term often used as a catch-all for lots of different signs and symptoms, there are a few things to say about depression. First and foremost, depression is a real condition. We all feel down from time to time as a result of lots of different things; work, money, family, football team being relegated, etc. but depression represents something more persistent, all-encompassing and can appear alongside other symptoms. Second, depression appears for many different reasons and is linked to lots of different circumstances. Most people would probably have heard of post-natal depression or the baby blues thought to be tied into the hormonal and chemical changes which occur to new mums after their new arrival has 'left the building'. One example, but there are others. Finally it is pretty well known that depression puts a person at greater risk of developing quite a few different ailments.

Shah and colleagues* recently reported on depression and a history of suicide attempts as being risk factors for cardiovascular disease (CHD) and ischemic heart disease (IHD). Analysing data from over 7500 people, aged 17-39, following up after 15 years as part of the Third National Health and Nutrition Examination Survey and correcting for various lifestyle variables such as smoking and poor diet, the authors reported an increased risk of death associated with CHD and IHD where depression / suicide attempts were historically present. The risk was particularly marked in women; a history of suicide attempts being associated with a 14-fold adjusted risk for IHD. I might add that this is not the first time that an association between depression and heart health outcomes has been reported.

The authors suggested that these findings might be evidence for a physiological effect from depression; so lower heart rate variability, increased stress hormones or inflammation. Indeed on the topic of inflammation, other evidence and commentators have reported some interesting effects relating to depression and inflammatory markers which might tie in. My recent post on the inflammatory consequences of caring might also link to some effect also.

Cumulatively what the research in this area seems to be pointing to is that our psychological health and wellbeing might not only be linked to physiological health but also might be an important driver of risk for quite a few somatic health complaints. Trauma, such as abuse, might also produce a similar effect. There may very well be more peripheral routes from depression to physiological health problems. Without trying to sound like a stuck record, I wonder about the whole gut bacteria angle as potentially being involved also; realising that 'inter-connectedness' is a word that really should be used a lot more with regards to psychology-physiology and health-disease.

* Shah AJ. et al. Depression and history of attempted suicide as risk factors for heart disease mortality in young individuals. Archives of General Psychiatry. 2011: 68: 1135-1142.

Chronic illness and healthcare for autism

Three articles caught my eye today in relation to some recurrent themes on this blog about autism not being protective of other chronic conditions and how some of the most 'disabling' aspects of autism are not necessarily due to the presentation of overt symptoms or comorbidities.

The first paper by Tyler and colleagues* examined risk for several chronic diseases including obesity, high blood pressure and high blood cholesterol levels in autism vs. matched controls. They suggested that hyperlipidemia in particular, set adults with autism aside from controls but importantly noted that anywhere from a fifth to a third of the autistic population surveyed presented with one of the chronic illnesses specified previously. I don't need to say much more about this paper aside from the words 'it's about time'. It has taken long enough for society to realise that conditions such as schizophrenia might place someone at greater risk of some of these issues. Now perhaps autism can benefit from similar health screening.

The next paper by Lai and colleagues ** perhaps ties into several things already discussed on this blog in relation to the effects of unmet health needs. Lai looked at dental health, finding that 12% of parents questioned said their child with autism had unmet dental needs. Even 1 in 10 children who had been to the dentist were reported still to have unmet dental needs. Whilst they suggested that behaviour was one 'barrier' to getting those needs met, they also suggested that unmet dental needs were present across the autism spectrum, implying ability and severity were not deciding factors in this health care 'hole' but possibly also other things like cost. Dental hygiene and health is fast becoming an important variable in several health-related matters. How about oral hygiene and your risk of cardiovascular disease? With autism in mind, I have previously touched upon the need for some sleuthing when trying to determine factors associated with self-injury and aggression.

The final paper by Parellada and colleagues *** is the more 'feel-good' paper reporting not on unmet health needs or risk factors but rather what can be done to make healthcare more accessible to people with autism. I need to find out more about this paper so as to make a more detailed post on it but first impressions are that they were doing a pretty good job in looking not just at autism as a triad (dyad?) of symptoms but rather a more rounded approach encompassing things like nutrition and gastroenterology. Indeed realising that you have a person first and a person 'with autism' second, is a key advancement to removing some of the barriers that a label of autism might bring about and therefore making healthcare accessible to all.

* Tyler CV. et al. Chronic disease risks in young adults with autism spectrum disorder: forewarned is forearmed. Am J Intellect Dev Disabil. September 2011

** Lai B. et al. Unmet dental needs and barriers to dental care among children with autism spectrum disorders. JADD. September 2011

*** Parellada M. et al. Specialty care programme for autism spectrum disorders in an urban population: a case-management model for healthcare delivery in an ASD population. Eur Psychiatry. September 2011