Maternal prenatal vitamin use and reduced risk of offspring autism recurrence

Question: "Is maternal use of prenatal vitamins associated with decreased risk for autism recurrence in siblings of children with autism spectrum disorder?" Answer: "Maternal prenatal vitamin intake during the first month of pregnancy may reduce ASD [autism spectrum disorder] recurrence in siblings of children with ASD in high-risk families." So that looks like a 'very possibly' then.

That was the long-and-short of the findings reported by Rebecca Schmidt and colleagues [1]. Some notable names are included on the authorship list of the Schmidt paper who are no strangers to the idea that maternal prenatal vitamin use may very well impact on offspring risk of autism or ASD (see here and see here for examples).

The Schmidt study on this occasion relied on data from the MARBLES (Markers of Autism Risk in Babies: Learning Early Signs) study, an important longitudinal initiative originally designed to investigate "possible pre-natal and post-partum biological and environmental exposures and risk factors that may contribute to the development of autism." Yes, you read that right, that's 'biological and environmental' exposures and risk factors (see here)...

In this "prospective cohort study" younger brothers and sisters deemed to be at high-risk of autism (N=241) by virtue of their older sibling having been diagnosed with autism were the target participant group. Said group were followed from 6 months to around about their third birthday and developmentally assessed. Mums of the children were also asked about their vitamin use during pregnancy via interview. All the collected data was crunched and results presented.

"The prevalence of ASD was 14.1% (18) in children whose mothers took prenatal vitamins in the first month of pregnancy compared with 32.7% (37) in children whose mothers did not take prenatal vitamins during that time." As you can see, that is quite a stark [statistically significant] difference between the groups bearing in mind that around 25% of the total cohort were eventually diagnosed with autism (or at least met thresholds for a diagnosis based on the use of a gold-standard instrument). Authors also add that prenatal vitamin use did not seemingly impact on "other nontypical development" which included various other developmental 'outcomes'. They also reported that: "Children in the former maternal prenatal vitamin group also had statistically significantly lower autism symptom severity... and higher cognitive scores." This implies that even if such vitamin use did not 'halt' a/the pathway to an autism diagnosis in some, it might well have affected the presentation of their autism in terms of symptoms and intellectual functions (see here).

So an important question: what were the nutrients being supplemented that seemed to show such an effect? Well, as per that other previous research from Schmidt et al folic acid popped up again, as well as another important nutrient, iron (Fe) which she's also been previously interested in (see here).

As per some 'expert reaction' to the study (see here) there is a need for further research in this area before any sweeping generalisations are made. Ideally, I'd like to see Schmidt or others go further into the whole folate metabolism bit applied to autism (see here and see here) and what that means for supplementation levels in mums-to-be where offspring autism recurrence risk is potentially high. Indeed, whether folic acid is actually the ideal supplement for some pregnant mums (see here) is another potential route of investigation on the basis of what has previously turned up in 'some autism' (see here). By saying all that, I want to make it clear that I'm not giving anything that looks, sounds or smells like medical or clinical advice on this or any topic. The Schmidt findings also potentially tie into another area of autism research looking at the inter-pregnancy interval (IPI) with autism in mind (see here and see here). This, on the basis that words like 'depletion of micronutrients' have been banded around as being one possible explanation for the elevated risk of offspring autism correlating with a short IPI. Again, more study is indicated.

I try not to get too excited about new findings when it comes to autism because, inevitably, many end up falling by the wayside or being over-hyped. Given however the history of peer-reviewed science on the topic of pregnancy nutrition and risk of offspring autism, I'm inclined to think that there may be something quite special in the Schmidt findings and what directions they could eventually take with regards to both research and policy. Certainly when I read another study talking about siblings at 'high-risk' for autism, I'll be looking to see whether pregnancy nutrition has been considered as a potentially modifying variable...

28 February 2019: An addition. So, here I am talking about prenatal vitamin use and offspring autism risk and lo-and-behold, someone has just published a meta-analysis and systematic review of this topic [2]. The conclusion: "the likelihood of ASD in offspring whose mothers used multivitamin supplements during the prenatal period was significantly reduced compared with that in offspring of mothers without such supplementation."

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[1] Schmidt RJ. et al. Association of Maternal Prenatal Vitamin Use With Risk for Autism Spectrum Disorder Recurrence in Young Siblings. JAMA Psychiatry. 2019. Feb 27.

[2] Guo B-Q. et al. Maternal multivitamin supplementation is associated with a reduced risk of autism spectrum disorder in children: A systematic review and meta-analysis. Nutrition Research. 2019. Feb 24.

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"Omega-3 polyunsaturated fatty acid treatment for anxiety might be effective in clinical settings"

Today I present the findings of yet another systematic review and meta-analysis as per the publication from Kuan-Pin Su and colleagues [1] that concluded: "omega-3 PUFAs [polyunsaturated fatty acids] might help to reduce the symptoms of clinical anxiety." A finding that may have some quite profound implications for lots and lots of different diagnoses/conditions/labels where anxiety seems to be particularly over-represented and life-draining (see here and see here for examples).

So, the starting hypothesis was that "omega-3 PUFAs might have anxiolytic effects in patients with significant anxiety- and fear-related symptoms." Various studies, both in animals and humans, have implicated fatty acids in 'emotional states', particularly the so-called 'good fatty acids' including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The authors reported that "there have been no systematic reviews of this topic to date" so decided to remedy the situation.

Trawling through various repositories and databases of peer-reviewed science, they searched for relevant science on the topic of fatty acid supplementation and anxiety measurement. From little over a hundred possible science articles, they whittled the numbers down to 19 studies including over 1200 participants "with omega-3 PUFA treatment (mean age, 43.7 years; mean female proportion, 55.0%; mean omega-3 PUFA dosage, 1605.7 mg/d)" and "1037 participants without omega-3 PUFA treatment (mean age, 40.6 years; mean female proportion, 55.0%)." Taking into account that some studies (most) included a placebo element to their design, different dosages and formulations of PUFAs were used and that various different tools and schedules were used to 'measure anxiety', there were some boiled-down messages to emerge.

First: "The overall findings revealed modest anxiolytic effects of omega-3 PUFAs in individuals with various neuropsychiatric or major physical illnesses." That's not to say that every study was 'positive' in terms of PUFA effects on anxiety, but generally speaking the evidence tended to side more with an effect rather than no effect. Second, dose and formulation seemed to matter: "Participants treated with a daily dose of 2000 mg or more of omega-3 PUFAs showed a significantly greater association of treatment with reduced anxiety symptoms." Third: "the association of omega-3 PUFA treatment with reduced anxiety symptoms was significantly stronger in subgroups with specific clinical diagnoses than in subgroups without specific clinical conditions." So the effect of PUFA supplementation was stronger in those with a clinical diagnosis of something like anxiety than those who didn't have one.

Downsides? Well, there are of course limitations to the data included in the Su study; for example, "the significant heterogeneity among the included studies... with potential influence by some outlier studies" and these should not be underestimated. I'm also minded to bring in the [still emerging] issue that meta-analyses are only as good as the data that they are based on (see here and see here for examples). And I'd also mention that side-effects are something not discussed too heavily in the Su study but one shouldn't assume that just because we're talking about a fish oil so this is somehow side-effect free for everyone...

Given the low cost of fatty acid supplements and their wide, very wide, availability, the Su results provide some pretty good support to suggest that 'giving it a go' could be an option for at least some people diagnosed with an anxiety disorder. Please don't however take that as me giving anyone medical or clinical advice; I'm merely following what the results say and the media coverage that has followed (see here).

And since we're on the topic of food and mood, I note the recent meta-analysis from Camille Lassale and colleagues [2] suggesting that "adhering to a healthy diet, in particular a traditional Mediterranean diet, or avoiding a pro-inflammatory diet appears to confer some protection against depression in observational studies" has been garnering news headlines (see here). These studies combined suggest that diet might have an important effect of mood and well being. Now, where have I heard that before (see here)...?

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[1] Su K-P. et al. Association of Use of Omega-3 Polyunsaturated Fatty Acids With Changes in Severity of Anxiety Symptoms. JAMA Network Open. 2018;1(5):e182327.

[2] Lassale C. et al. Healthy dietary indices and risk of depressive outcomes: a systematic review and meta-analysis of observational studies. Molecular Psychiatry. 2018. Sept 26.

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Pregnancy diet and offspring "hyperactivity-inattention symptoms"?

I appreciate that the findings reported by Cédric Galera and colleagues [1] are potentially a little uncomfortable. Their examination of over 1200 mother-child pairs looking at data from food frequency questionnaires during pregnancy and subsequent offspring 'externalising' behaviours into childhood, could be construed as evidence that poor eating habits during the nine months that made us have the ability to translate into childhood issues. Because food choices are seen as just that - 'choices' - the Galera results *could* potentially fall into the same category as other 'choices' that also seemingly affect offspring development in this area (see here for example). I make no value judgements.

Having also bumped into the Galera paper at the same time as seeing a BBC media report observing that "We learn nothing about nutrition, claim medical students", one might further make an argument for the need for much greater education, guidance, support and potentially 'nudging', when it comes to issues such as 'what to eat during pregnancy'. That however, is another discussion for another day.

Anyhow, the science...

Galera et al report findings based on the EDEN mother-child cohort [2], an initiative set up to examine "the relations and potential interactions between maternal exposures and health status during pregnancy, fetal development, health status of the infant at birth and the child’s health and development." It's interesting that the opening words to the Heude [2] description of the initiative mention the name 'Barker', as in the late David Barker, a man who helped popularise the idea that nutrition in the womb (through maternal diet) might have some important *consequences* for offspring in the short- and long-term. Looking at some of the other research produced by the EDEN mother-child cohort (see here), Barker and others may have indeed been on to something.

As well as looking at offspring externalising symptoms such as conduct problems via use of "the Strength and Difficulties Questionnaire at ages 3, 5, and 8 years", authors also looked at "trajectories of hyperactivity-inattention symptoms." This, on the basis that the SDQ does pretty well at discriminating between ADHD and non-ADHD cases [3]. They concluded that, taking into account infant dietary patterns "at age 2 years" and various other potential influencing variables ("maternal stress and depression, gestational diabetes, and socioeconomic variables"), there was something to see with regards to use of a 'high Western diet' and 'low Healthy diet' during pregnancy in relation to offspring developmental outcome. Specifically: "Maternal diet during pregnancy was independently associated with children's hyperactivity-inattention symptoms."

Of course, one needs to be a little bit careful that *association* is not viewed as 'cause-and-effect' based on such observational studies. That also it is downright unethical to put mums-to-be on a 'healthy diet' vs. 'a non-healthy diet' is also a stumbling block to robust investigations in this area; similar to the fact that one wouldn't put mums-to-be on a tobacco smoking vs. a non-smoking intervention.

But the Galera results are not stand-alone in potentially implicating maternal diet as a factor in relation to offspring hyperactivity-inattention [4] and are therefore deserving of some further investigation. I've already mentioned that perhaps more guidance and 'nudges' need to be provided in the area of pregnancy nutrition, and that I assume, would include looking at the cost and convenience of a healthy diet vs. a not-so-healthy diet in the context of a possible *link* between diagnosed attention-deficit hyperactivity disorder (ADHD) and "socioeconomic deprivation" for example (see here). More than that however is the idea that David Barker and others who talked about 'foetal programming' during the pregnancy months as a result of what is in or perhaps not in a maternal diet may have been a lot more accurate than many people would have perhaps imagined...

And on the topic of 'foetal programming', diet might not be the only factor to consider [5]...

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[1] Galera C. et al. Prenatal diet and children's trajectories of hyperactivity-inattention and conduct problems from 3 to 8 years: the EDEN mother-child cohort. J Child Psychol Psychiatry. 2018 Mar 24.

[2] Heude B. et al. Cohort Profile: The EDEN mother-child cohort on the prenatal and early postnatal determinants of child health and development. Int J Epidemiol. 2016 Apr;45(2):353-63.

[3] Algorta GP. et al. Diagnostic efficiency of the SDQ for parents to identify ADHD in the UK: a ROC analysis. Eur Child Adolesc Psychiatry. 2016 Sep;25(9):949-57.

[4] Rijlaarsdam J. et al. Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems. J Child Psychol Psychiatry. 2017 Jan;58(1):19-27.

[5] Andersen SL. et al. Maternal Thyroid Function in Early Pregnancy and Child Neurodevelopmental Disorders: A Danish Nationwide Case-Cohort Study. Thyroid. 2018 Mar 27.

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Vitamin-mineral mix for ADHD part 2

"Although direct benefit for core ADHD [attention-deficit hyperactivity disorder] symptoms was modest, with mixed findings across raters, the low rate of adverse effects and the benefits reported across multiple areas of functioning indicate micronutrients may be a favourable option for some children, particularly those with both ADHD and emotional dysregulation."

So said the findings reported by Julia Rucklidge and colleagues [1] posting results from their "fully blinded randomized controlled trial" of micronutrients in the context of childhood ADHD. Said study is similar to other research from this authorship group that has been previously covered on this blog (see here). The trial protocol (prospectively registered!) can be seen here and provides further details of the micronutrients in question, study design and various outcome measures employed.

Medication-free children diagnosed with ADHD were assigned to either the micronutrient formulation or placebo for 10 weeks. This was not a study for faint-hearted when it came to pill swallowing as up to 12 capsules a day were required to taken over the course of the study period. Then: "Data were collected from clinicians, parents, participants and teachers across a range of measures assessing ADHD symptoms, general functioning and impairment, mood, aggression and emotional regulation."

Results: well as per the opening sentence to this post, there were some important differences noted across the vitamin-mineral supplement group compared with the placebo arm of the trial. But: "No group differences were identified on clinician, parent and teacher ratings of overall ADHD symptoms." It appeared instead that specific aspects of ADHD presentation and more general issues such as aggression were seemingly affected by the micronutrient supplementation but effects were not necessarily just in universal terms of ADHD.

There are a few other important details to add to this post. First: "no group differences in adverse events and no serious adverse events identified" so taking a vitamin-mineral supplement in the context of paediatric ADHD over 10 weeks is a relatively safe affair we are told. I wouldn't have thought anything different to be honest. Bear also in mind that those diagnosed with ADHD may be at greater risk of vitamin deficiencies according to other research (see here) so there may have been a clinical need here also. Second, vitamin and mineral supplements are pretty widely available for many different age groups so getting hold of them is not likely to be a problem. Looking at the specific formulation used, it appears however that an important class of nutrient(s) are missing: essential fatty acids. I could be wrong, but given the quite large body of peer-reviewed research talking about specific fatty acid supplementation in the context of ADHD (see here) one might have expected to have seen this in the formulation used?

There is apparently more to come from this research initiative so I'll probably be posting a part 3 to complement this and the previous post on this topic. As part of the whole 'nutritional medicine as mainstream in psychiatry' ethos (see here) and bearing in mind the range of adverse outcomes over-represented when it comes to a diagnosis of ADHD (see here for example) I'd like to think that relatively simple and affordable moves to manage [some aspects of some] ADHD involving nutritional tools (see here also) are going to continue to be on the research agenda for some time yet.

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[1] Rucklidge JJ. et al. Vitamin-mineral treatment improves aggression and emotional regulation in children with ADHD: a fully blinded, randomized, placebo-controlled trial. J Child Psychol Psychiatry. 2017 Oct 2.

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Treating violence in schizophrenia with fish oils?

"Violent schizophrenia patients treated with fish oil (360mg DHA+540mg EPA) demonstrated a decrease in violence."

That was the primary conclusion arrived at in the study results by Yi Qiao and colleagues [1] suggesting that some aspects of nutrition may very well have implications for extremes of behaviour in the context of psychiatric diagnoses. The ClinicalTrials.gov entry for this study can be seen here.

DHA - Docosahexaenoic acid - and EPA - Eicosapentaenoic acid - are categorised as omega-3 fatty acids. In this research instance, Qiao et al divided up their "Fifty inpatients meeting ICD-10 criteria for schizophrenia" such that roughly half received a fish oil for 12 weeks and half received a placebo. I should add that this 'inpatient' group also scored significantly on the Modified Overt Aggression Scale (MOAS) at baseline.

Results: well, fish oil use did not seem to make any significant difference to some of the [positive and negative] signs and symptoms of schizophrenia compared with placebo use. But as per the opening sentence to this post, there did seem to be something significant to see when it came to follow-up of violent behaviour alongside the use of fish oils.

These are interesting findings. My first thoughts on reading the Qiao results harked back to previous work looking at the use of nutrition in the context of a prison population by Bernard Gesch and colleagues [2]. That research concluded that: "Antisocial behaviour in prisons, including violence, are reduced by vitamins, minerals and essential fatty acids" where EPA and DHA were part of the supplement provided under "double-blind, placebo-controlled, randomised trial" conditions; albeit in smaller doses that those used by Qiao and colleagues.

The Qiao results are also not the first time that fish oil use for violence in the context of schizophrenia have been talked about in the peer-reviewed science domain [3]. With the understanding that violence accompanying schizophrenia is probably going to be as complex as violence outside of schizophrenia, such promising results require some further replication and a little more data on possible hows-and-whys. The low cost, pretty favourable safety profile and reports of other potential health benefits associated with fish oil use however, suggest that such an intervention could easily be incorporated into treatment plan for many people fitting a similar profile to those described by Qiao and colleagues.

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[1] Qiao Y. et al. Effects of Omega-3 in the treatment of violent schizophrenia patients. Schizophr Res. 2017 Aug 19. pii: S0920-9964(17)30501-7.

[2] Gesch CB. et al. Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. Randomised, placebo-controlled trial. Br J Psychiatry. 2002 Jul;181:22-8.

[3] Légaré N. et al. Omega-3 and violence in schizophrenia. Schizophrenia Res. 2007; 96: 269.

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Herbal medicines 'for' ADHD systematically reviewed

The paper by Dennis Anheyer and colleagues [1] (open-access available here) is offered up for your reading consumption today, and the results of a review of the available published science - "Only randomized controlled trails (RCT)" (authors' spelling mistake not mine) - looking at the use of herbal medicines for the treatment/management of attention-deficit hyperactivity disorder (ADHD).

OK I know some people read the term 'herbal medicine' and automatically think 'woo'. If I instead use the term 'pharmacognosy' to denote how plants and herbs are the starting material for quite a few active ingredients included in various medicines (and related products!), you can perhaps see that a little more scientific respect is required for our cumulative flora. Respect and caution I should perhaps say...

Anheyer et al boiled the literature on this topic down into 9 studies fulfilling their eligibility criteria, covering a variety of herbal medicines. These included: Melissa officinalis, Valeriana officinalis, Passiflora incarnata, evening primrose oil, Gingko biloba, Pycnogenol and St. John’s Wort.  They concluded that based on their examination of the collected literature "no concrete recommendations for use can be made so far."

But that's not to say that there weren't some potentially encouraging 'green shoots' to be seen in the literature reviewed. The "potential efficacy of pine bark extract [pycnogenol] in the therapy of ADHD" was mentioned, as the 'bark with bite' (see here) got something of a thumbs-up (or at least, not a thumbs down). Researchers also suggested that: "Low evidence could be found for Melissa officinalis, Valeriana officinalis and Passiflora incarnata" as part of a mixture (compound herbal preparation) indicating that more research might be indicated.

It's also worth pointing out that within the studies examined by Anheyer and colleagues, the safety profiles of the herbal medicines used were typically good in relation to reported side-effects over the duration of their study. Only one 'serious event' was recorded as far as I can see when it came to the use of evening primrose oil and a participant who "developed severe diarrhea" (although even this event may not have been directly due to the remedy given).

Where next I thought I heard you ask? Well, assuming one can get around any issues with the term 'herbal medicine' I'd like to think that further investigations could be attempted on some of the more favourable herbal medicines identified in this and other reviews [2] and what the active ingredients and relevant biological processes might be. Allied to the increasingly important data on how something like certain fatty acids might be an intervention option for some with ADHD (see here), there is potentially still much we can learn from applying the science of pharmacognosy to a label like ADHD.

But, as I've said before, treat your herbal medicines (and other nutritional supplements) as what they are - medicines - and just be careful [3] particularly when other medicines might also be administered at the same time.

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[1] Anheyer D. et al. Herbal medicines in children with attention deficit hyperactivity disorder (ADHD): A systematic review. Complement Ther Med. 2017 Feb;30:14-23.

[2] Sarris J. et al. Complementary medicines (herbal and nutritional products) in the treatment of Attention Deficit Hyperactivity Disorder (ADHD): a systematic review of the evidence. Complement Ther Med. 2011 Aug;19(4):216-27.

[3] Mouly S. et al. Is the clinical relevance of drug-food and drug-herb interactions limited to grapefruit juice and Saint-John's Wort? Pharmacol Res. 2016 Sep 28. pii: S1043-6618(16)30991-4.

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Anheyer D, Lauche R, Schumann D, Dobos G, & Cramer H (2017). Herbal medicines in children with attention deficit hyperactivity disorder (ADHD): A systematic review. Complementary therapies in medicine, 30, 14-23 PMID: 28137522

On dietary and nutritional therapies for ME/CFS

ME/CFS in case you don't already know refers to Myalgic Encephalomyelitis / Chronic Fatigue Syndrome and, according to the findings reported by Nadia Campagnolo and colleagues [1], is in need of quite a bit more scientific investigation when it comes to the application of dietary changes and nutritional supplements to potentially alter the course of the condition(s).

Surveying the peer-reviewed literature "from 1994 to May 2016" the authors looked for peer-reviewed studies where "CFS/ME patients modified their diet or supplemented their habitual diet on patient-centred outcomes (fatigue, quality of life, physical activity and/or psychological wellbeing)." They found 17 studies that included 14 different interventions. Unfortunately they concluded that: "Many studies did not show therapeutic benefit on CFS/ME" alongside the observation that the methodological quality of the research in this areas 'could do better'.

But it was not all research doom-and-gloom as some approaches seemed to show promise: "Improvements in fatigue were observed for nicotinamide adenine dinucleotide hydride (NADH), probiotics, high cocoa polyphenol rich chocolate, and a combination of NADH and coenzyme Q10." Without wishing to toot my blogging trumpet, some of these approaches have been discussed before on this blog (Coenzyme Q10 and NADH supplementation for Chronic Fatigue Syndrome? and Coenzyme Q10 and NADH supplementation for Chronic Fatigue Syndrome continued) and beyond that, the target organ of something like the use of probiotics for CFS has made an appearance more than once too (see here for example). I might also add that just outside of the search dates used by Campagnolo et al was the suggestion that issues with a staple foodstuff - cows milk - might be over-represented in cases of CFS (see here) and that a milk-free diet could be useful [2] for some at least. By saying all that, I'm not giving any medical or clinical advice...

As science starts to move further away from the the biopsychosocial (BPS) model of CFS/ME (see here) and starts looking at genetics, biology and somatic disease processes with regards to the various presentations included under the banner of ME/CFS (see here) I foresee some interesting developments further down the line. Granted, dietary and nutritional approaches to CFS/ME are probably not considered 'mainstream' in terms of management strategies but that does not mean they aren't important or at least important in the context of a diagnosis of ME/CFS seemingly being protective of nothing. Central to any future studies in this or any related area is the idea that there may be lots going on under the 'plural' diagnostic umbrella of ME/CFS (see here). Indeed, something that even the PACE trial is starting to take on board [3].

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[1] Campagnolo N. et al. Dietary and nutrition interventions for the therapeutic treatment of chronic fatigue syndrome/myalgic encephalomyelitis: a systematic review. J Hum Nutr Diet. 2017 Jan 22.

[2] Rowe PC. et al. Cow's milk protein intolerance in adolescents and young adults with chronic fatigue syndrome. Acta Paediatr. 2016 Sep;105(9):e412-8.

[3] Williams TE. et al. Heterogeneity in chronic fatigue syndrome - empirically defined subgroups from the PACE trial. Psychol Med. 2017 Jan 23:1-12.

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Campagnolo N, Johnston S, Collatz A, Staines D, & Marshall-Gradisnik S (2017). Dietary and nutrition interventions for the therapeutic treatment of chronic fatigue syndrome/myalgic encephalomyelitis: a systematic review. Journal of human nutrition and dietetics : the official journal of the British Dietetic Association PMID: 28111818

Autism and visual impairment reviewed

Of the various autism science journals out there in peer-reviewed (La-La!) land, one journal in particular is really starting to grow on me: [The] Review Journal of Autism and Developmental Disorders.

I like this journal because it is basically systematic review and meta-analysis heaven when it comes to the quite voluminous autism research literature and seems to publish some real gems (see here for example).

Another paper from this journal caught my eye recently by Maggie Butchart and colleagues [1] (open-access) synthesising the collected research on "the prevalence of visual impairments in children and adults with Autism Spectrum Disorder (ASD), and the similar behavioural traits associated with both visual impairment and autism." Affiliated with the RNIB - Royal National Institute of Blind People - Scotland among other groups, the authors trawled the research literature looking at reported visual impairments in relation to the autism spectrum and provide quite a nice overview of 'where we're at' with regards to "papers published from 2000-2015."

The paper is open-access but a few comments are required bearing in mind my relative lack of knowledge on the complexities of visual impairments.

First: "Collating the evidence from six of the seven prevalence studies suggests a refractive error rate in the childhood ASD population studied at 22.9–32.7%, which is comparable with general childhood refractive error rates in 6–7 year olds at 29%, and 32.3% in 12–13 year olds." What this means is that a diagnosis of autism does not protect against the presence of refractive errors ('when the shape of the eye prevents light from focusing directly on the retina').

Second: "Estimates of childhood strabismus in the UK is 1.5 to 5.3%... but in the evidence collated in this review, the incidence of strabismus amongst autistic participants is higher at 8.3%." Strabismus, where the eyes don't align properly, seems to be a little bit more prevalent when it comes to autism compared with general population statistics. This is a topic that I've talked about before on this blog in relation to correcting such an issue with autism in mind (see here).

Finally: "There were no studies examining ophthalmic conditions and adult autistic populations who are more at risk of age-related visual impairments." Bearing in mind the search parameters included in the Butchart paper, I'm kinda dismayed that this is the current state of affairs. You'd have thought with all the money and resources being thrown into autism research that someone, somewhere might have thought more about eye health in adults with autism? Eye-tracking, reading the mind in the eyes test... the word 'eye' or 'eyes' is prominent in autism research but just not in relation to eye health it seems. And bear in mind that issues with eye health probably will affect the results of some of those autism 'eye' studies.

Eye or vision issues related to autism have often been a topic of discussion on this blog (see here and see here for examples) and so I'm glad that someone has finally brought a review of this area into the peer-reviewed arena. Screening is important; even if some of those on the autism spectrum may not always be by first sight (pardon the pun) particularly amenable to taking part in an eye exam - adjustments can and should be made.

And finally consider this: "Undiagnosed visual impairment is likely to severely impact quality of life. There is a need therefore for education and training that equip autism support practitioners with the awareness and skills to identify potential visual impairment, to refer individuals to optometry professionals if necessary, and to make necessary adjustments to service environments and support practices for individuals identified as having a visual impairment." Not much more to say really is there aside from 'make it so'.

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[1] Butchart M. et al. Autism and Visual Impairment: a Review of the Literature. Review Journal of Autism and Developmental Disorders. 2017. Jan 5.

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Butchart, M., Long, J., Brown, M., McMillan, A., Bain, J., & Karatzias, T. (2017). Autism and Visual Impairment: a Review of the Literature Review Journal of Autism and Developmental Disorders DOI: 10.1007/s40489-016-0101-1

A prenatal 'unhealthy' diet and offspring ADHD?

'Scientists study link between unhealthy pregnancy diet and ADHD' went one media headline covering the paper by Jolien Rijlaarsdam and colleagues [1].

The name of the research game was again to draw on data derived from ALSPAC (Avon Longitudinal Study of Parents and Children) (yes, again) to look-see "the degree to which prenatal high-fat and -sugar diet might relate to ADHD [attention-deficit hyperactivity disorder] symptoms via IGF2 DNA methylation for early-onset persistent (EOP) versus low CP [conduct problems] youth." In other words: "Experts examine how a diet high in fat and sugar could alter baby’s DNA in a way that might cause behavioural problems."

To do this meant looking at around 80 youth presenting with early-onset conduct problems compared with around 80 youths who didn't have the same magnitude of issues. Data on maternal nutrition captured for the two groups (ALSPAC did a lot of data collecting!) was cross-referenced with group status and also epigenetic - methylation - status of the insulin-like growth factor 2 gene (IGF2). IGF2 is a gene that seems to be pretty active during the nine months that made us but less so as we enter the big, wide world. As the name suggests it seems to have a 'growth' role which is probably why issues with this gene have also been associated with the development of a number of cancers.

Results: "Prenatal ‘unhealthy diet’ was positively associated with IGF2 methylation at birth for both the EOP and low CP youth." Minus any 'blame', such results suggest that maternal diet might be important for the developing child. I know this is it not exactly a shock, but in these days of more and more research and clinical focus on the special time called pregnancy, the idea that particular epigenetic changes might come from a chosen diet is a potentially important one.

Further: "For EOP only: (a) higher IGF2 methylation predicted ADHD symptoms; and (b) prenatal ‘unhealthy diet’ was associated with higher ADHD symptoms indirectly via higher IGF2 methylation." The higher IGF2 methylation - higher ADHD symptoms is an interesting association. Methylation - the addition of a methyl group - is normally taken to mean gene silencing suggesting that a malfunction of the the IGF2 gene and/or lower levels of its protein product might have some important implications. At this point I might add that whilst there is a bit of a research gap when it comes to IGF2 and behaviour specifically linked to ADHD, there is some interesting animal research looking at mice engineered to show low levels of the protein product in terms of behaviours such as anxiety [2] alongside "a role for the placenta in long-term programming of emotional behaviour." Cutting edge stuff to be sure.

"At present, this is not a study that would change my clinical practice, but if intervention studies resulting from this work show nutritional support in pregnancy can have an effect then we should take any opportunity we can to help." That was one comment from a physician discussing the results of the Rijlaarsdam study that I would agree with. The fact that the study focuses on just one gene in amongst the thousands potentially linked to conduct problems and ADHD is something to bear in mind.

Set however within the context that food can seemingly also affect behaviour and psychiatry as well as physiology (see here for example) I'd like to think that more studies on nutrition during pregnancy would be forthcoming and quickly on this important topic.

To close, thanks to Gene for the laughter...

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[1] Rijlaarsdam J. et al. Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems. J Child Psychol Psychiatry. 2016 Aug 18.

[2] Mikaelsson MA. et al. Placental programming of anxiety in adulthood revealed by Igf2-null models. Nat Commun. 2013;4:2311.

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Rijlaarsdam J, Cecil CA, Walton E, Mesirow MS, Relton CL, Gaunt TR, McArdle W, & Barker ED (2016). Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems. Journal of child psychology and psychiatry, and allied disciplines PMID: 27535767

Add-on nutraceuticals for depression?

It came as no surprise to me that the systematic review and meta-analysis article by Jerome Sarris and colleagues [1] found what it did in relation to the use of [certain] adjunctive (add-on) nutraceuticals alongside antidepressants to reduce depressive symptoms: some of them might actually be clinically useful.

With no medical or clinical advice given or intended, the authors report that "adjunctive use of SAMe, methylfolate, omega-3, and vitamin D with antidepressants" might be something to consider "for improving inadequate response to antidepressants." Dr Sarris was one among many authors who contributed to the 'personal view' paper titled: 'Nutritional medicine as mainstream in psychiatry' [2] which was also covered a while back on this blog (see here). This latest addition to that and other opinions [3] which covered the peer-reviewed literature on a variety of nutrients also found something of a mixed bag of results for various other compounds including the aromatic amino acid tryptophan, zinc, folic acid and vitamin C.

Quite a bit more science needs to be done in this area, not least around the hows and whys that the various preparations might exert some effect. Vitamin D has of course been covered quite a bit on this blog in relation to something like depression (see here for example) so that particular nutraceutical might already have a research head start compared to others. I'm also minded to suggest that the involvement of something like SAMe (S-adenosylmethionine) as an add-on treatment might also imply a role for epigenetic variables in relation to at least some depression [4]. And then there is the question of who might be best responders to such nutraceutical use which implies heterogeneity and possible plural depressions...

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[1] Sarris J. et al. Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses. American Journal of Psychiatry. 2016. April 26.

[2] Sarris J. et al. Nutritional medicine as mainstream in psychiatry. Lancet Psychiatry. 2015 Mar;2(3):271-4.

[3] Sarris J. et al. International Society for Nutritional Psychiatry Research consensus position statement: nutritional medicine in modern psychiatry. World Psychiatry. 2015 Oct;14(3):370-1.

[4] McGowan PO. & Kato T. Epigenetics in mood disorders. Environ Health Prev Med. 2008 Jan;13(1):16-24.

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Sarris J, Murphy J, Mischoulon D, Papakostas GI, Fava M, Berk M, & Ng CH (2016). Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses. The American journal of psychiatry PMID: 27113121

#Breadgate and nutritional psychiatry

The review paper by Paola Bressan & Peter Kramer [1] (open-access) titled: 'Bread and Other Edible Agents of Mental Disease' has been getting a few people a little hot under the collar recently. With it's own Twitter hashtag #breadgate it looks like the idea that certain foods might have something of a bearing on "human behaviour and mental health" has not been received particularly well. I might add that this not the first time that such ideas have been entertained (see here) but there was no such outcry on previous occasions...

As anyone who drops by this blog might know, I'm quite interested in the idea that what we eat and how it's metabolised might have some important implications for SOME people in terms of not just their physical health but also other facets covering behaviour and cognition. I've also talked about it in the peer-reviewed domain quite a bit too using conditions such as phenylketonuria (PKU) as a template. In their latest paper, Bressan & Kramer discuss the quite long-running idea that [some] cereal grains, the starting material for foods like bread, might have some interesting physiological effects that could have a bearing on mental health and wellbeing.

I should at this point mention that I was invited to peer-review the Bressan / Kramer article. I accepted (given my research in this area) and as well as providing a review also let the editor and authors know that my view whilst as unbiased as possible did come alongside a few conflicts of interest (COIs) such as the book that graces the edge of this blog. The journal editor accepted this fact and my comments alongside those of a far more notable researcher were included in the peer-review process.

The Bressan / Kramer paper presents quite a thorough overview of the research looking at food and psychiatry. The language is quite stark in places as words like 'defect' and 'derangement' are included in the text (something that I queried during peer-review) and with a sub-heading titled 'Diet as a Cure' the authors are pretty forth-right in their interpretation of the available peer-reviewed evidence. I would be perhaps less strong in any claims made but ho-hum. I might add that this is not the first time that this authorship team have talked about big hypotheses...

Without seeming like I am springing to the defence of the Bressan / Kramer paper I have decided to list a few previous blog entries that I've written about other relevant texts in the peer-reviewed domain that add something to the discussions in this area. I'm sure that Bressan / Kramer if they have heard about the 'discussions' around their paper are able to defend their writings and so I'm not doing this to somehow cover their backs. I do however think it is important to talk about this topic and this is as good an opportunity as any...

So:

Brain and gut in autism: a historical perspective
For many years now, diet and [some] autism has been discussed. The work of the late Curt Dohan was the leader in this emerging field and his suggestion that [some] schizophrenia might have a dietary component. Before you ask it, no, no-one has ever said that diets devoid of gluten and casein are some sort of cure-all for all autism... they're not. But that does not mean there might be 'best responders' to this type of intervention (see here) in terms of their effect on some behaviours linked to autism. The mechanism for any effect from diet could also be multi-fold (see here).

Psychotic symptoms managed by a gluten-free diet?
Yes. it's a case report, but there are quite a few of them in the peer-reviewed literature talking about dietary manipulations seemingly affecting often quite severe psychiatric presentation. There are more controlled trials too if you want to have a look...

More gluten sensitivity and schizophrenia
The immune system seems to be in the ascendancy when it comes to psychiatry these days (see here also) and diet has been mentioned as an influencing variable on immune function...

Gluten free diet adherence reduces depression in coeliac disease
Building on the idea that coeliac disease - that archetypal autoimmune condition where gluten is the baddie - might have quite a few more 'presentations' than just the physical, there is some emerging peer-reviewed evidence to suggest that adherence to a gluten-free diet might have multiple benefits for certain groups.

Just what is 'non-coeliac gluten sensitivity'?
The idea that outside of coeliac disease there may be a spectrum of 'gluten-related ills' is not a new one. There are still gaps in the research literature and in particular, whether non-coeliac gluten sensitivity (NCGS) might intersect with certain behavioural and/or psychiatric labels but...

Schizophrenia and milk
With the focus also on milk, or rather the casein protein that is also said to produce peptide metabolites that might not be a millions miles away from various opioid-like compounds like to gluten digestion (hence the name casomorphins), I've included reference to the David Niebuhr et al paper too titled: 'Association between bovine casein antibody and and new onset schizophrenia among US military personnel'. Correlation is not causation but this and other data are interesting.

Intestinal permeability: an emerging scientific area (also with autism in mind)
Gluten 'punching holes in the gut' is mentioned in some of the discussion about the Bressan / Kramer paper and with it the words 'leaky gut' make an appearance. As per my ramblings on some of the peer-reviewed science in this area, there is emerging evidence for this concept in relation to specific conditions including the fantastic paper by Laura de Magistris and colleagues [3] citing food as having a potentially modifying effect.

These are just a selection of the entries that I've written on this blog covering the topic of nutritional psychiatry (see here) but there are more. Accepting that "mental disease" (authors term not mine) covers quite a lot of ground and even within the various labels we have a lot of heterogeneity (see here for example) I would suggest that more research is required into how diet might influence behaviour and psychiatry. The paper by Dash et al [3] similarly titled: 'Diet and common mental disorders; the imperative to translate evidence into action' recently published (in the same family of journals) reiterates that there is more to do in this area including the identification of potential 'best responders' to this type of approach. Diet again, is not put forward as a cure-all for every single label/condition, but that doesn't mean it might not be useful to look at it for some.

I know there is still quite a lot of hostility to the idea that what we eat (or don't eat) might have a bearing on something other than physical health. I'm not advocating for any universal 'change your diet to this' approach to manage mental health issues but I do believe that there is enough peer-reviewed science out there to merit some further sensible discussions on the topic...

Music to close, and what else but Toast... a little bit of toast.

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[1] Bressan P. & Kramer P. Bread and Other Edible Agents of Mental Disease. Front Hum Neurosci. 2016 Mar 29;10:130.

[2] de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.

[3] Dash SR. et al. Diet and common mental disorders; the imperative to translate evidence into action. Front. Public Health | doi: 10.3389/fpubh.2016.00081.

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Bressan P, & Kramer P (2016). Bread and Other Edible Agents of Mental Disease. Frontiers in human neuroscience, 10 PMID: 27065833

Scurvy and autism continued

"Scurvy as a Manifestation of Food Selectivity in Children with Autism" read the title of the paper by Nina Ma and colleagues [1] continuing a topic of some interest to this blog regarding the need for more research and practical focus on nutritional insufficiency and deficiency when it comes to the label of autism (see here for example).

As per other occasions when scurvy - a condition linked to a deficiency of vitamin C - has been talked about in the context of autism (see here), the Ma paper continues an all-too familiar theme of how "a long-standing history of food selectivity" when it comes to at least some autism, can have some pretty serious onward health implications (see here). Alongside reporting on how "an elaborate panel of tests and procedures were undertaken before the diagnosis of scurvy was made" in seven children, all of whom had a developmental disorder, Ma et al highlight how vitamin C treatment "led to rapid recovery of symptoms." Without doing a Linus Pauling special on the wonders of vitamin C (accepting that in some respects he might not have been too far off the mark) I would draw your attention to some very preliminary work looking at vitamin C supplementation (sorry, ascorbic acid) with autism in mind [2].

That none of the children included in the Ma study "were supplemented with a multivitamin" at the time of their clinical evaluation is also relevant, especially in light of some rather sweeping generalisations made about other autism research on the use of dietary/nutritional supplementation and autism (see here). Certainly, what this and other related research suggests is that (a) a diagnosis of autism may indeed place someone at risk of certain dietary or nutritional issues and (b) appropriate screening should be in place to mitigate any potential health effects from such dietary-related problems. Oh, and just in case you were wondering, the horror that is a gluten- and casein-free (GFCF) diet when done correctly, is probably not to blame for cases of scurvy in relation to autism (see here)...

Music: Nothing But Thieves - Trip Switch.

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[1] Ma NS. et al. Brief Report: Scurvy as a Manifestation of Food Selectivity in Children with Autism. J Autism Dev Disord. 2015 Nov 21.

[2] Dolske MC. et al. A preliminary trial of ascorbic acid as supplemental therapy for autism. Prog Neuropsychopharmacol Biol Psychiatry. 1993 Sep;17(5):765-74.

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Ma NS, Thompson C, & Weston S (2015). Brief Report: Scurvy as a Manifestation of Food Selectivity in Children with Autism. Journal of autism and developmental disorders PMID: 26590972

Is a GFCF diet for autism inherently unhealthy? (part 2)

Consider today's entry as a sort of continuation of a previous post looking at the 'horror' that is a gluten-free, casein-free (GFCF) diet for autism (see here).

This time around I'm bringing the paper by Salvador Marí-Bauset and colleagues [1] to your attention and the idea that things might not necessarily be all bad when it comes to the use of a GFCF diet in terms of nutritional quality nor anthropometric values. Indeed, subject to the correct dietetic input, that there may be some important food exchanges going on when a diet devoid of gluten and casein is instigated specifically where an autism diagnosis is mentioned.

I realise that not everyone is as enthusiastic about how food might impact on behaviour and development with at least some autism in mind as I am, but science is coming around to the idea that what we eat (or not) might have some important influences on our being (see here). Appreciating that the GFCF diet is also probably not for everyone [2] (see here also), there continues to be some 'appetite' for such an approach for at least some autism [3]. It is therefore important to understand a little more about what might be the positives and negatives to following such a restrictive dietary regime.

Marí-Bauset et al report results for some 20 children with autism following a GFCF diet compared with 85 "on a regular diet in Valencia (Spain)." This follows a scheme of work from this authorship group looking at various aspects of nutrition when applied to autism [4]. Upon analysing 3-day food diaries, researchers concluded that: "Those on the GFCF diet had a lower weight, body mass index, and total energy, pantothenic acid, calcium, phosphorus and sodium intake." Further however, the GFCF group had: "a higher intake of fiber, legumes, and vegetables" and something of a more favourable fat intake profile that non-GFCF dieters. That last point also ties into other work from the authors [5].

As per the part 1 entry on the nutritional and health related aspects to a GFCF diet for autism (here it is again) there are some details in the Marí-Bauset data that perhaps require some clinical input. I'm thinking specifically about the lower calcium intake in this case, bearing in mind calcium and autism is a very complicated issue (see here) and some continued questioning about the more general link between calcium intake and bone health. The idea that those following a GFCF diet might also present with a lower weight and body mass index (BMI) is also interesting; particularly in light of quite a lot of the chatter in this area focusing on elevated weight and the health effects that can have with autism in mind (see here). I might add that I am in no way endorsing a GFCF diet (or any other diet) for weight loss or management; that's not my job.

The slightly more positive idea that those following a GFCF diet might have a better intake of vegetables and legumes probably also tied into a higher intake of fibre is important. I've previously talked about where the extremes of a limited diet can lead when it comes to [some] autism (see here). Although supplementation has its place in terms of as and when specific deficiencies are present and identified (see here) I think most people would agree that consumption of foodstuffs like fruit and vegetables probably do a better job of supplying nutritional needs than a pill (most of the time). In that respect, one might assume that those on a GFCF diet with more favourable vegetable consumption profile, might be slightly less prone to certain deficiencies. As per other research in this area, we would need a little more biological testing to be sure (see here). The specific idea that fibre intake was higher for the GFCF group is also an important point if one considers fibre to be an essential component when it comes to gastrointestinal (GI) motility, again, as has been specifically mentioned with autism in mind (see here).

In short, and with more research required, the horror that is a GFCF diet for autism might actually with the right clinical input, not be so horrible...

Music: Lily Allen - The Fear.

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[1] Marí-Bauset S. et al. Nutritional Impact of a Gluten-Free Casein-Free Diet in Children with Autism Spectrum Disorder. J Autism Dev Disord. 2015 Oct 1.

[2] Buie T. The relationship of autism and gluten. Clin Ther. 2013 May;35(5):578-83.

[3] Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. 2015 Aug;74(3):202-7.

[4] Marí-Bauset S. et al. Nutritional status of children with autism spectrum disorders (ASDs): a case-control study. J Autism Dev Disord. 2015 Jan;45(1):203-12.

[5] Marí-Bauset S. et al. Fat intake in children with autism spectrum disorder in the Mediterranean region (Valencia, Spain). Nutr Neurosci. 2015 May 28.

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Marí-Bauset S, Llopis-González A, Zazpe I, Marí-Sanchis A, & Suárez-Varela MM (2015). Nutritional Impact of a Gluten-Free Casein-Free Diet in Children with Autism Spectrum Disorder. Journal of autism and developmental disorders PMID: 26428353

Maternal obesity and offspring autism meta-analysed

So: "The meta-analysis results support an increased risk of autism spectrum disorder in children of women who were obese during pregnancy. However, further study is warranted to confirm these results."

That was the conclusion reached by Ya-Min Li and colleagues [1] looking at the collected peer-reviewed data currently available on how maternal weight might impact on offspring neurodevelopmental outcomes. Without wishing to blame or stigmatise (this is a blog based on the examination of cold, objective, peer-reviewed science) such results are not altogether unexpected based on instances where maternal weight might impact on offspring autism risk have been discussed (see here).

There are caveats to ideas of such an association. Not least that observational studies for example, often provide little information on 'cause and effect'. That not every child born to a mum who is overweight and/or obese develops autism should also be kept firmly in mind, as should the idea that overweight and/or obesity can sometimes sit with other comorbidity as part of the 'metabolic syndrome' so potentially introducing other variables into any association (see here). I might add that an array of other factors cross obesity and autism risk areas, not least mothers' nutritional status before and during pregnancy for example (see here).

That all being said, there is more science to do in this area. Thinking back to other discussions on data about how father's weight might also influence offspring autism risk (see here) and the idea of foetal programming [2] based to a large extent on the writings of the late David Barker, one gets some ideas of where science might want to start heading in continuing this line of inquiry.

Music: Keane - Everybody's Changing.

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[1] Li YM. et al. Association Between Maternal Obesity and Autism Spectrum Disorder in Offspring: A Meta-analysis. J Autism Dev Disord. 2015 Aug 9.

[2] Lau C. & Rogers JM. Embryonic and fetal programming of physiological disorders in adulthood. Birth Defects Res C Embryo Today. 2004 Dec;72(4):300-12.

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Li YM, Ou JJ, Liu L, Zhang D, Zhao JP, & Tang SY (2015). Association Between Maternal Obesity and Autism Spectrum Disorder in Offspring: A Meta-analysis. Journal of autism and developmental disorders PMID: 26254893

Dietary supplementation and autism (and the horror of a GFCF diet)

As perhaps expected, the results reported by Patricia Stewart and colleagues [1] suggesting that: "Few children with ASD [autism spectrum disorder] need most of the micronutrients they are commonly given as supplements, which often leads to excess intake" has generated some interesting media headlines given their mention of the words "gluten/casein-free diet (GFCF)".

A case in point is an article titled: 'Autism Diets' Do Not Provide Children With Adequate Supplementation, Can Lead To Overuse which aside from making little sense (do not provide children with adequate supplementation?) seems to be using the Stewart paper to take pot shots at the mention that GFCF diets have some research (yes, peer-reviewed research) history with autism in mind. Bearing in mind that I have something of an interest in this area, I'm gonna go through some of the findings reported by Stewart et al with a slightly different mindset albeit based on the science to hand.

Drawing on participants with autism (N=288) recruited via the Autism Speaks Autism Treatment Network (ATN) researchers set about examining "dietary supplement use and micronutrient intake in children with ASD." This was accomplished by analysing data from 3-day diet/supplement records "relative to GFCF diet status."

There were a few important results to mention following analysis of [trained] caregiver food/supplement diaries for children based on the reported data and other write-up of the findings:

• Overall, children with ASD were consuming similar amounts of micronutrients as children without ASD. "They also had the same deficits in vitamins D, E, calcium, potassium, and choline as the general pediatric population." I'll come back to some of the details of this shortly.
• Children receiving GFCF diets (~20%) had similar micronutrient intake to those not following a GFCF diet. Indeed: "Children on the GFCF diet consumed more magnesium and vitamin E" and "Children on this diet were more adequately supplemented with vitamin D." These findings hark back to other research suggestions that the 'horror' that is a GFCF diet might not be as poor in nutrition as some people might imagine (see here). I might add that if readers look elsewhere on this blog, you might notice that yours truly has written a book about how a GFCF diet can be implemented safely and nutritiously without the requirement for high levels of supplementation when it comes to autism (sorry for the blatant self-publicity).
• "Dietary supplements, especially multivitamin/minerals, were used by 56% of children with ASD." Using a GFCF diet seemed to be associated with greater supplement use (78% vs 56%) compared with those not following such a diet. I assume this is because of the perception that a GFCF diet is 'nutritionally inadequate' when it comes to important minerals such as calcium for example. That being said: "Calcium supplementation was equally inadequate in those on and off the diet." This is interesting and perhaps relevant to other work on diet, calcium, bone health and autism (see here).
• "Despite different eating behaviors, children with ASD received much of their needed micronutrients from food consumption." The authors suggest that this might have something to do with the various food fortification strategies in place these days, but likewise "may also be responsible for the overconsumption of certain nutrients by children with ASD."
• "Even when supplements are used, careful attention should be given to adequacy of vitamin D and calcium intake." Coming back to the idea that deficiencies noted in this sample of children with autism are not so dissimilar from that seen in the general population, the suggestion that issues such as vitamin D deficiency or insufficiency might be over-represented when it comes to autism continues an emerging research theme (see here).

There are some important points to take from the Stewart paper bearing in mind that 3-day food / supplement diaries are really only providing a snapshot of food / supplement intake and say nothing about the biological levels of various nutrients when it comes to autism. As per the numerous entries on this blog about where eating habits can go wrong with autism in mind (see here) and what happens when vitamin/mineral supplementation in autism is put to the double-blind test (see here) I'd be slightly guarded about drawing too many sweeping conclusions from the new data.

"In clinical practice, each patient needs to be individually assessed for potential nutritional deficiencies or excess." So says Dr Stewart in the press release accompanying the study. I'd be minded to agree with that sentiment given the idea of plurality in autism (see here) and the potential for various biochemistry that can follow a diagnosis (see here and see here) potentially impacting on food and feeding habits. As I've said many times before, receipt of the label of 'autism' or 'autism spectrum disorder' should be a starting point for quite a bit more clinical inspection and not the finishing line...

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[1] Stewart PA. et al. Dietary Supplementation in Children with Autism Spectrum Disorders: Common, Insufficient, and Excessive. Journal of the Academy of Nutrition and Dietetics. 2015. June 4.

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Patricia A. Stewart, Susan L. Hyman, Brianne L. Schmidt, Eric A. Macklin, Ann Reynolds, Cynthia R. Johnson, S. Jill James, & Patricia Manning-Courtney (2015). Dietary Supplementation in Children with Autism Spectrum Disorders: Common, Insufficient, and Excessive Journal of the Academy of Nutrition and Dietetics