Tuesday, 21 November 2017

"Spending constraints" a.k.a austerity and a mortality gap?

I try not to be too political on this blog given the focus on peer-reviewed science and my notable lack of political interest or motivation. It is however difficult to completely separate science and politics from each other given the world that we live in. A world that still commonly uses the term 'austerity' quite a few years after 'the crisis', alongside a realisation that behind headlines on the continued drive(s) towards 'fiscal security' and 'balancing the books' there are inevitably going to be winners and losers.

The paper by Jonathan Watkins and colleagues [1] highlights some of the extreme 'not winners' potentially stemming from the "relative constraints in public expenditure on healthcare (PEH) and social care (PES)" here in Blighty over recent years. They concluded that: "Spending constraints between 2010 and 2014 were associated with an estimated 45 368 (95% CI 34 530 to 56 206) higher than expected number of deaths compared with pre-2010 trends." Further, that if current trends continue in relation to funding "approximately 150 000 additional deaths may arise between 2015 and 2020." Cue the sharp intake of breath as words such as 'economic murder' have been banded around in the popular press discussing this research (see here).

I'm not going to go into all the details of the Watkins findings on this occasion. The data for the study was derived from various public databases in relation to population mortality, spending on health and social care and related variables. I don't doubt that as per other debates on the 'weekend effect' for example, different people with different mindsets might arrive at different conclusions based on such data. 'Lies, damn lies and statistics' is a phrase that springs to mind. With my very rudimentary reading and understanding of the Watkins data, I can't however see any obvious flaws in their methods or logic behind their results; aside that is from remembering that correlation does not always equal causation. Others have voiced similar sentiments (see here).

"By setting, deaths at care homes and at home contributed most to the observed ‘mortality gap’, while hospital mortality was lower than expected." The authors specifically attribute such data to the gap between spending on social care vs. spending on health care; also noting that "the recent drive to move patients with poor prognoses and who have reached their ceiling of care away from the hospital environment to care homes or their own homes may have contributed to this." One interpretation of this is that those who are elderly and/or vulnerable placed outside of the hospital environment are perhaps disproportionately being burdened with the effects of austerity.  And one possible solution? Well: "Our study suggests that the number of NHS-qualified nurses is the strongest tested mediator of the relationships between spending, and care home and home mortality." One solution but not the only solution.

With a UK budget announcement set for later this week, I wonder if the Watkins findings might figure in relation to the suggestion that "a cumulative spending increase of approximately £25.3 billion would be required to close this gap across health and social care by 2020/2021, equating to around £6.3 billion annually." Yes, those are some quite staggering sums of money, but at the end of day what is to be valued more: balancing the books or plugging quite a significant mortality gap? (and even some of our elected officials seem to be interested in this debate).

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[1] Watkins J. et al. Effects of health and social care spending constraints on mortality in England: a time trend analysis. BMJ Open 2017;7:e017722.

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Monday, 20 November 2017

"the importance of considering how autism acceptance could contribute to mental health in autism"

The quote heading this post comes from the findings reported by Eilidh Cage and colleagues [1] (open-access) who sought to examine how "experiences and perceptions of autism acceptance could impact on the mental health of autistic adults."

Using an on-line survey "to test the relationship between perceived autism acceptance and mental health (specifically, depression, anxiety and stress)" findings are reported based on responses from over 110 people diagnosed as on the autism spectrum. I say 'diagnosed as on the autism spectrum' but as with any internet survey, there is always a degree of 'trust' that autism diagnoses are being reported faithfully just as it is with other labels that were under study: "a high proportion of participants reported additional diagnoses." Indeed, I also note that "11 participants reported that they did not currently have a formal diagnosis of autism" and were still included in some of the analyses...

No mind, the authors sought to 'quantify' autism acceptance given no measure currently exists by asking various questions including "whether they felt that society (specified as the general public, made up of people who did not personally know them) generally accepted them, with “yes”, “no”, “sometimes” and “prefer not to say” as response options." Responses were also sought to statements such as "over the past week, I have felt accepted by society as an autistic person/person with autism" and onward "perceptions of autism acceptance from different sources." This was complemented by responses to the Depression, Anxiety and Stress Scale (DASS-21).

Results: "depression was predicted by autism acceptance from external sources (society, family and friends) and personal acceptance" but anxiety was not seemingly *linked* to autism acceptance. Drilling down further into their results, researchers observed that "greater personal autism acceptance predicted lower depressive symptoms" indicating that variables such as self-esteem might mediate any risk of presenting with depressive signs and symptoms [2] (see here for my take). This is something that perhaps tallies with other research talking about autistic traits and wellbeing [3].

The author has also written a piece for The Conversation on her research study (see here).

I'm not quite sure why the ever-fluffy psychological concept of 'Theory of Mind' (ToM) needed to be introduced into the Cage paper given that no measure of ToM was actually included in the study. A quick search of other published research from these authors reveals that ToM is a feature there too [4]. The authors talk about how "Theory of Mind ability may impact on perceptions of autism acceptance" but I'm not so sure that this is particularly important. It's kinda like suggesting that society is completely autism aware and accepting/accommodating but those on the spectrum 'don't seem to understand it' as a result of any ToM issues, which is of course, a nonsense. ToM also still requires a bit more investigation into what it actually means and covers (see here) including the idea that issues with ToM might themselves be 'impaired' as a result of something like depression (see here). I'd also point out that quite a few other over-represented diagnoses potentially appearing alongside autism also seem to present with ToM issues [5] too...

"There is still a long way to go in understanding and tackling the high prevalence of mental health difficulties in autism, but we believe that the social model approach is a useful and positive lens through which mental health outcomes could be improved." That was the conclusion reached by authors on the basis of their findings. I would agree that there is still a long way to go on the topic of mental health and autism and the social model approach - "disability is caused by the way society is organised, rather than by a person’s impairment or difference" - is an option for further research of this kind. But I would also caution that one needs to balance such a perspective with others too (see here), and accept that the organisation of society is not always the most disabling aspect of a person's disability, particularly when it comes to something like depressive symptoms. Indeed, to say that depressive symptoms accompanying autism might merely be a facet of a 'lack of acceptance' or a lack of understanding from society or the individual themselves, risks plunging autism back into some pretty dark times (see here) and is likely to conflict with various other views. From a clinical point of view, it ignores some very serious research on the wide spectrum that is depression potentially present for all-manner of different reasons, being relevant to the equally wide spectrum that is autism (see here for a discussion on how depression might actually be something rather more fundamental to some autism over just being 'comorbidity'). At worst, it may even delay or put people off from seeking timely recognised treatments when depression becomes 'clinical', which could be a rather dangerous path to start down (see here).

Having said all that, I don't however think too many people would argue with the idea that personal perception(s) whether positive or negative are likely to impact on a person's mental (and physical?) health and wellbeing. If one is constantly feeling like an 'outsider' or excluded or feels that ones needs are not being met, added to a possible history of being bullied or loneliness or indeed, with other clinical labels also potentially being present for example, one is likely to build up a mindset appropriate to such a situation which probably includes some advanced risk for depressive signs and symptoms. From that point of view, much more needs to be done to look at the ways and means of impacting those personal perceptions; possibly taking into account other relevant research which has some [evidence-based] suggestions on things like societal inclusion and increasing access to it (see here) for those who want this option, alongside other complementary strategies where some [peer-reviewed] evidence is present (see here) and continues to be produced (Google the 'HUNT Cohort Study' to see what I mean). I say all this reiterating that something like chronic loneliness can very much be a major contributor to issues like depression.

I also understand the calls to make society more autism-accepting which I think most people would support as being pertinent across the ENTIRE autism spectrum (see here). I'm however, a little unsure of the real-life plan and details of the plan attempting to achieve this goal; particularly in the current climate when even getting a timely diagnosis seems to be an uphill struggle and when also many on the autism spectrum are seemingly left to fend for themselves post-diagnosis. Society it seems, is getting much more autism aware (for good or bad based on current media portrayals for example) but not necessarily getting more autism accommodating nor necessarily putting important words into actions. Indeed, one could argue that other societal factors like unemployment and financial hardship readily experience by those with autism are probably as, if not more, important to their experiences of something like depression yet little appears to be done to improve such issues for the vast majority...

As for the "experiences of “camouflaging” [that] could relate to higher rates of depression" also mentioned in the Cage article, I have quite a lot of time for this area of autism research (see here). Particularly the idea that camouflaging is not necessarily an all-female pursuit in the context of autism (see here) and how truly energy-sapping it can be for many, many people on the spectrum...

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[1] Cage E. et al. Experiences of Autism Acceptance and Mental Health in Autistic Adults. J Autism Dev Disord. 2017. Oct 25.

[2] McCauley JB. et al. Self-Esteem, Internalizing Symptoms, and Theory of Mind in Youth With Autism Spectrum Disorder. J Clin Child Adolesc Psychol. 2017 Oct 19:1-12.

[3] Rodgers JD. et al. Brief Report: Personality Mediates the Relationship between Autism Quotient and Well-Being: A Conceptual Replication using Self-Report. J Autism Dev Disord. 2017 Sep 16.

[4] Cage E. et al. Reputation management: evidence for ability but reduced propensity in autism. Autism Res. 2013 Oct;6(5):433-42.

[5] Wang Y-Y. et al. Theory of mind impairment and its clinical correlates in patients with schizophrenia, major depressive disorder and bipolar disorder. Schizophrenia Res. 2017. Nov 7.

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Saturday, 18 November 2017

Probiotics degrading gluten peptides - part 4

Here we go again. Probiotics degrading gluten peptides part 4 adds to previous posts on this topic (see part 1 here, part 2 here and part 3 here).

The difference this time around? People. People actually eating a a test meal containing gluten - "a porridge containing 0.5 g gluten" - and being given a potential gluten-degrading preparation - "Aspergillus niger-derived prolyl endoprotease (AN-PEP)" - or a placebo whilst their gastric and duodenal content was sampled for gluten concentrations over a 3-hour period after. So described the results published by Julia König and colleagues [1] continuing a research theme from this group [2].

AN-PEP was the product under the research spotlight following some previous scientific findings [3] suggesting that unlike various other digestive enzyme supplements, this stuff showed some pretty good actions/effects on immunogenic gluten peptides. Following a "randomized placebo-controlled crossover study" design, researchers followed 16 participants "with self-reported gluten sensitivity" (but not coeliac disease or wheat allergy) across 3 test days when on each day either a high dose of AN-PEP was given, or a low dose of AN-PEP was given or a placebo was given. Details of the high and low doses included: "The low dose tablets provided 83300 Protease Picomol International (PPI), and the high dose 166700 PPI of AN-PEP enzyme (1 PPI is the amount of enzyme that releases one picomole of p-nitroaniline per second under defined assay conditions)."

This was quite an invasive study as researchers had to gain access to parts of the gastrointestinal (GI) tract of participants and so: "Subjects attended each test day after an overnight fast, and a multi-lumen nasoduodenal catheter was placed with one lumen tip in the gastric antrum and one lumen tip 15 cm lower in the duodenum." It was then a case of drawing off stomach and duodenal samples and analysing for gluten content. Further: "success of AN-PEP in degrading gluten was defined as at least 50% gluten degradation compared to placebo, calculated as area under the curve (AUC) over 180 min."

Results: "It actually works" was a quote from one of the authors of the paper in previous media attention of this study before peer-reviewed publication. "In the stomach, gluten levels were reduced from 176.9 to 22.0 in the high dose and to 25.4 μg × min/ml in the low dose. In the duodenum, gluten levels were reduced from 14.1 in the placebo to 6.3 in the high dose and to 7.4 μg × min/ml in the low dose." AN-PEP appeared to be doing its designated job. Importantly too: "No severe adverse events were reported" over the course of the study period.

Scientific replication is the name of the game following the König results. Replication with larger sample numbers and also potentially looking at whether such a preparation might be useful for those diagnosed with something like coeliac disease or other accepted immune-related pathology linked to gluten consumption. I say that acknowledging that a gluten-free diet is the best that science and medicine currently has for the management of coeliac disease. The authors also note that they "did not perform a double-blinded placebo-controlled gluten challenge as sometimes suggested to confirm the diagnosis of gluten sensitivity" in their participants. This kinda intersects with the continuing discussions about what non-coeliac gluten/wheat sensitivity actually is (see here).

"In conclusion, our study showed that the AN-PEP enzyme is effective in degrading small amounts of gluten as part of a complex meal in the stomach. Even though the use of AN-PEP is not intended to replace a gluten-free diet in gluten-related disorders, it appears to be effective as a digestive aid protecting against the unintentional intake of gluten." I can't argue with that and look forward to seeing more on this topic in future.

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[1] König J. et al. Randomized clinical trial: Effective gluten degradation by Aspergillus niger-derived enzyme in a complex meal setting. Sci Rep. 2017 Oct 12;7(1):13100.

[2] Salden BN. et al. Randomised clinical study: Aspergillus niger-derived enzyme digests gluten in the stomach of healthy volunteers. Aliment Pharmacol Ther. 2015 Aug;42(3):273-85.

[3] Janssen G. et al. Ineffective degradation of immunogenic gluten epitopes by currently available digestive enzyme supplements. PLoS One. 2015 Jun 1;10(6):e0128065.

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Friday, 17 November 2017

On iron and vitamin D and autism

"This study suggests that deficiency of iron and Vitamin D as well as anemia were more common in autistic compared to control children."

'This study' refers to the findings reported by Abdulbari Bener and colleagues [1] (open-access available here) who set out to "investigate iron deficiency anemia and Vitamin D deficiency among autism children" in Qatar, a part of the world not renowned for its 'lack of sunshine' (a source material for the production of vitamin D).

Looking at some 300 children diagnosed with an autism spectrum disorder (ASD) and an equal number of controls, not-autism controls "who visited the primary health-care centers", researchers concluded that as a group, those with autism were more likely to present with low serum iron levels (and various related measures) and further that: "Vitamin D deficiency was considerably more common among autistic children." The authors provide some background details on what constitutes vitamin D deficiency and other 'levels': "Participants were classified into four categories: (1) severe Vitamin D deficiency, 25OHD <10 ng/ml; (2) moderate deficiency, 25OHD 10–19 ng/ml; (3) mild deficiency, 25OHD 20–29 ng/ml; and normal/optimal level is between 30 and 80 ng/ml."

When attempting to ascertain what factors might be important to the autism vs. not-autism participants, researchers reported that: "serum iron deficiency, serum calcium levels, serum Vitamin D levels; ferritin, reduced physical activity; child order, body mass index percentiles, and parental consanguinity can all be considered strong predictors and major factors associated with autism spectrum disorders." I might add that consanguinity defined as "unions between couples who share at least one common ancestor" is perhaps something more 'culturally-relevant' to autism in certain countries and societies [2] but not necessarily widely applicable...

What's more to say about the Bener findings? Well, given that issues with iron (see here) and issues with vitamin D (see here) are no strangers to the autism research landscape, there is little novelty in the conclusions reached even if being "the first report on an establishing level of iron deficiency in children with autism in Qatar and in Arabian Gulf Countries." The implication is again that preferential screening and treatment of such issues should be offered when a diagnosis of autism is received, save any further health inequalities arising. Whether or not treating something like iron deficiency and/or vitamin D issues will impact on behavioural presentation (see here) is perhaps an issue for another day. I say this bearing in mind the sentiments expressed in the recent paper by Philippe Autier and colleagues [3] examining the collected data on vitamin D supplementation "on non-skeletal disorders" and results seemingly "strengthening the hypothesis that low vitamin D status is a consequence of ill health, rather than its cause."

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[1] Bener A. et al. Iron and vitamin D levels among autism spectrum disorders children. Ann Afr Med. 2017 Oct-Dec;16(4):186-191.

[2] Mahajnah M. et al. Clinical characteristics of autism spectrum disorder in Israel: impact of ethnic and social diversities. Biomed Res Int. 2015;2015:962093.

[3] Autier P. et al. Effect of vitamin D supplementation on non-skeletal disorders: a systematic review of meta-analyses and randomised trials. Lancet Diabetes Endocrinol. 2017 Oct 25. pii: S2213-8587(17)30357-1.

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Thursday, 16 November 2017

Sleep and gut issues in autism: a clinically relevant subtype?

"Autistic children with gastrointestinal or/and sleep problems may represent clinically relevant subtypes of ASD [autism spectrum disorder], for which targeted treatments may be needed."

That was one of the conclusions reached by Xiao-Lei Yang and colleagues [1] looking at an interesting combination of symptoms/conditions that have featured before on this blog (see here and see here): gastrointestinal (GI) and sleep issues with autism in mind.

Surveying around 170 children diagnosed with an autism spectrum disorder (ASD) and a similar number of "healthy children" (authors words, most definitely not mine), researchers sought to estimate the prevalence of GI and sleep issues among their cohort(s). Perhaps unsurprisingly "GI and sleep problems were prevalent in Chinese ASD children." Interestingly too: "ASD children with GI symptoms reported more severe ASD core symptoms than others." Those with sleeping issues also showed "lower performance in daily living skills, social cognition, social communication and intellectual development" than the children with ASD who did not present with sleeping issues.

The implications of such observations? Several. Not least that when one talks about GI issues  - whether functional or more pathological - being over-represented in relation to autism, one has some confidence that such 'over-representation' seems to cross different ethnicities and different countries and is not just derived from or based on Western research findings. This adds further weight to the notion that at least some types/phenotypes of autism may have a significant bowel-related component to them for whatever reason(s).

Next, the suggestion that children with autism who also present with GI symptoms might present with a more 'severe ASD core symptoms' profile provides some truly tantalising clinical and research opportunities. Not least that said bowel symptoms might be able to affect some aspects of behaviour and onward the question: what happens when bowel symptoms are effectively treated? I know such sentiments are not necessarily welcomed in some quarters ('autism symptoms are lifelong and immutable' so the saying goes) but for others, particularly those suffering with bowel symptoms (yes, I did say suffering), there are some potentially interesting consequences following intervention. Assuming also that pain and discomfort are key parts of 'suffering' from bowel issues in autism as they are when present in not-autism, we arrive at a situation whereby certain autistic traits may be at least 'heightened' when pain is present. Such a proposition is not necessarily new news to the peer-reviewed autism research (see here and see here). And if one was to assume that something like 'inflammation' might be part and parcel of said GI issues and pain in relation to autism, we arrive at yet another testable hypothesis (see here)...

Finally, sleep issues in relation to the autism spectrum. What's more to say? They are pretty prevalent throughout children and adults on the autism spectrum and probably contribute to the various 'quality of life' disparities that have been shown in relation to autism (see here). There are things that can be 'tried' in relation to intervention (see here and see here for examples) but by no means is there some 'magic wand' that helps every single sleep issue for every single person. The idea that sleep issues, like GI issues, might also impact on certain behavioural aspects linked to autism is probably not unexpected but I would like to see a lot more research done in this area before any grand sweeping generalisations are made. Not least recognising that certain over-represented behavioural comorbidity such as attention-deficit hyperactivity disorder (ADHD) is rising through the sleep research ranks (see here) and what that might mean for autistic traits in these ESSENCE-like times...

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[1] Yang X-L. et al. Are Gastrointestinal and Sleep Problems Associated with Behavioral Symptoms of Autism Spectrum Disorder? Psychiatry Research. 2017. Oct 24.

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Wednesday, 15 November 2017

Loneliness --> low self-esteem ---> depression?

It was the findings reported by James McCauley and colleagues [1] that prompted today's post. Working on the basis that "there have been few comprehensive investigations of self-esteem in children and adolescents with autism spectrum disorder (ASD)" researchers set out "to assess how youth with ASD rate their self-esteem compared to age-matched TYP [typically developing] youth." Further, how levels of self-esteem (or not) might onward influence "internalizing psychopathology", the fancy phrase for issues such as depression and anxiety.

I don't typically go for grand theories and sweeping generalisations on this blog, particularly when referencing the very large and very diverse autism spectrum. I've not moved over to the 'dark side' of generalisation in this post but am particularly interested in the some of the *associations* talked about my McCauley et al.

Specifically how: "youth with ASD rated their self-esteem significantly lower than did TYP youth" and how self-esteem was "strongly related to depression." Add in the findings reported by Micah Mazurek [2] who observed that "loneliness was associated with increased depression and anxiety and decreased life satisfaction and self-esteem" and some potentially important processes emerge as per the equation titling this post: Loneliness --> low self-esteem ---> depression?

McCauley and colleagues do also talk about how Theory of Mind (ToM) also showed some possible *associations* to elements of their results but I'm not really minded to go into this part of their findings with any great detail. It's not that I don't believe that ToM might not be an issue for some on the autism spectrum, but rather as other results have suggested [3], questions still remain about what ToM actually means and whether other issues (i.e. alexithymia) might predominate in relation to some autism [4] (where the stress is on 'some').

I don't doubt that there are several other important elements potentially influencing things like self-esteem in relation to autism and how it can lead to issues such as depression (see here). Further studies are needed on this topic, including drawing on the autism-not-specifically-mentioned research literature [5]. But insofar as the simplistic relationship set out in the post, there is an obvious area ripe for intervention: loneliness. And on that point, there are options available (see here) if and when desired; accepting that not everyone wants (or needs) lots of people around them all of the time. This perhaps is also where the online world (in moderation) can also come into it's own [6] (I repeat 'in moderation').

Finally, I'll be coming to the findings reported by Cage and colleagues [7] in the not-too-distant-future talking about how "personal acceptance significantly predicted depression" in the context of autism and what role self-esteem might play here too (minus too much psychological fluff and ToM chatter)...

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[1] McCauley JB. et al. Self-Esteem, Internalizing Symptoms, and Theory of Mind in Youth With Autism Spectrum Disorder. J Clin Child Adolesc Psychol. 2017 Oct 19:1-12.

[2] Mazurek MO. Loneliness, friendship, and well-being in adults with autism spectrum disorders. Autism. 2014 Apr;18(3):223-32.

[3] Oakley BF. et al. Theory of mind is not theory of emotion: A cautionary note on the Reading the Mind in the Eyes Test. J Abnorm Psychol. 2016 Aug;125(6):818-23.

[4] Trevisan DA. et al. Alexithymia, but not autism spectrum disorder, may be related to the production of emotional facial expressions. Mol Autism. 2016 Nov 11;7:46.

[5] Sowislo JF. & Orth U. Does low self-esteem predict depression and anxiety? A meta-analysis of longitudinal studies. Psychol Bull. 2013 Jan;139(1):213-240.

[6] Sundberg M. Online gaming, loneliness and friendships among adolescents and adults with ASD. Computers in Human Behavior. 2017. Nov 1.

[7] Cage E. et al. Experiences of Autism Acceptance and Mental Health in Autistic Adults. J Autism Dev Disord. 2017 Oct 25.

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Tuesday, 14 November 2017

Breastfeeding and autism meta-analysed

"This meta-analysis provides evidence that breastfeeding (exclusively or including additional supplements) may protect against ASD [autism spectrum disorder]. Prospective longitudinal research is required to disentangle the complex relationships and to explore potential pathophysiological mechanisms."

So said the systematic review and meta-analysis published by Ping-Tao Tseng and colleagues [1] covering a [complicated] topic that has been discussed on this blog before (see here). I should mention that I was part of the 'and colleagues' bit to this latest paper; something that will in no way interfere with my hopefully critical musings on this latest publication.

Bearing in mind "a controversial relationship between ASD and breastfeeding" that exists in the peer-reviewed literature and the strong requirement not to make new mums feel bad just because they don't want to or can't breastfeed, the aim of the meta-analysing game was to synthesise the collected research literature into something like a coherent 'where we're at' statement. Seven studies out of a possible 20 were included for review, together including nearly 1500 children diagnosed with ASD and nearly 1200 not-diagnosed-with-autism controls.

Results: "Cumulatively, children with ASD, either in the form of clinical diagnosis or self-report, were significantly less likely to have been breastfed than children without ASD." I should add that 'self-report' refers to parents reporting on their child receiving a diagnosis of autism but not necessarily being independently confirmed by researchers or medical records. The strength of the association/effect was not to be sniffed at; with results even holding up when taking into account those "who were breastfed with additional supplementation."

Another important quote: "one should note the observational nature of these preliminary findings, whereby causation can clearly not be determined." What this means is that whilst variable A (breastfeeding) and variable B (autism or ASD) might be *associated* it is nigh on impossible to definitively say whether variable A *causes* or *protects against* variable B on the basis of the studies analysed. I might also suggest that the call for 'prospective longitudinal research' is also not likely to provide a definitive answer any time soon either, when taking into account how many other variables might be associated with risk of offspring autism and indeed, the plurality of the label and some related discussions on that topic (see here and see here). It's also noteworthy that autism rarely exists in some sort of diagnostic vacuum (see here) and how breastfeeding trends might be important there too [2] thus complicating any 'causative' picture.

Still, the Tseng results do provide some further information about this issue and a reiteration of the value of breastfeeding for many different reasons. Other studies have arrived at a similar conclusion insofar as the impact that breastfeeding *might* have on 'autistic traits' [3]; again, with more research to do.

Mechanisms of effect? Well, once again we're faced with a 'we don't know yet' scenario. Tseng et al speculated on various possible factors linked to breastfeeding and breast milk 'ingredients' that may be important (neurotrophic factors, oxytocin, fatty acid constitution, casomorphins) and could conceivably impact on risk of offspring autism. I'm also minded to add in the idea that the early presentation of autism in the first months of life [for some] could also potentially affect breastfeeding patterns; perhaps making breastfeeding practices more difficult and/or contributing to the early cessation of breastfeeding in some cases. Relevant mechanisms are likely to be complicated.

I appreciate that not everyone is going to be enthralled with this study or topic - no, it doesn't say that a lack of breastfeeding causes all autism - particularly when words like "protect against ASD" are also included in the text. All I can say is that we faithfully looked at the existing peer-reviewed research available to us in this area and went where the data instructed us to do so without fear or favour...

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[1] Tseng P-T. et al. Maternal breastfeeding and autism spectrum disorder in children: A systematic review and meta-analysis. Nutritional Neuroscience. 2017. Oct 18.

[2] Bar S. et al. Long-term neurodevelopmental benefits of breastfeeding. Curr Opin Pediatr. 2016 Aug;28(4):559-66.

[3] Boucher O. et al. Association between breastfeeding duration and cognitive development, autistic traits and ADHD symptoms: a multicenter study in Spain. Pediatr Res. 2017 Mar;81(3):434-442.

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