Toy preference and parent-infant communication?

I was intrigued to read the findings reported by Anna Sosa [1] who reported that "play with books and traditional toys was superior to play with electronic toys in promoting high-quality communication."

This was a study looking at communication between parents and their infants aged 10-16 months old as a function of toy type, where electronic toys - "3 battery-operated toys with buttons and switches that can be manipulated to produce lights, words, phrases, and songs" - were pitted against 'traditional' toys - "3 nonelectronic toys that also have the potential to teach animal names, colors, and shapes." Those electronic toys were also chosen on the premise that "they are marketed as educational toys that promote language development for children in this age range and are advertised as teaching animal names, colors, and shapes."

Describing results from 26 parent-infant dyads whereby pairs "engaged in 2 15-minute play sessions per toy set over a 3-day period" using electronic toys, non-electronic toys and also books (y'know those paper things), various outcomes were measured including child vocalisations, adult words and conversational turns. As per the opening sentence, toy type did seem to affect communication between parent and child. So: "Play with electronic toys is associated with decreased quantity and quality of language input compared with play with books or traditional toys." The author goes as far to say that set within other research in this area: "both play with traditional toys and book reading can be promoted as language-facilitating activities while play with electronic toys should be discouraged."

Being careful not to fall into any sweeping generalisations about how technology is 'all bad' for child development and beyond, bearing in mind where such discussions have previously led, I have to say that it there may be some important lessons to learn from the Sosa study results. That early years communication between parent and child is increasingly being realised to be pretty important is one part of discussions (see here for more information on the '30 million word gap' for example). That parents are also literally bombarded these days with various edu-toys and other gadgets often making some rather big claims is another aspect. The Sosa results hint that there might be a happy medium to strike between the old and the new when it comes to early play and communication (including reading) and that we should as parents, perhaps be mindful that electronic toys with their lights, sounds and various educational claims might not necessarily trump something a little less flashy. Similar sentiments might also apply to more pathological states too [2].

Music: William Shatner sings er... well, not for the easily offended.

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[1] Sosa AV. Association of the Type of Toy Used During Play With the Quantity and Quality of Parent-Infant Communication. JAMA Pediatrics. 2015. Dec 23.

[2] Christakis DA. Rethinking Attention-Deficit/Hyperactivity Disorder. JAMA Pediatr. 2016 Jan 4:1-2.

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Sosa AV (2015). Association of the Type of Toy Used During Play With the Quantity and Quality of Parent-Infant Communication JAMA Pediatrics : 10.1001/jamapediatrics.2015.3753

Gut dysbiosis in anorexia nervosa

"Collectively, these results clearly indicate the existence of dysbiosis in the gut of AN [anorexia nervosa] patients."

That opening sentence comes from the paper by Chihiro Morita and colleagues [1] (open-access available here) who "compared the fecal microbiota of female patients with AN (n = 25), including restrictive (ANR, n = 14) and binge-eating (ANBP, n = 11) subtypes, with those of age-matched healthy female controls (n = 21)." Stool and blood samples were analysed for various potentially important markers, and some interesting results were forthcoming.

So: "AN patients had significantly lower amounts of total bacteria, C. coccoides group, C. leptum subgroup, B. fragilis, and Streptococcus than age-matched healthy women." Although I am a little wary of zooming in on just one bacterial finding, the suggestion that this relatively small participant group diagnosed with AN showed something akin to a decrease in levels of B. fragilis (Bacteroides fragilis) caught my eye. My reasoning: well, lets just say that research on a certain mouse model applied to another diagnosis frequently discussed on this blog has mentioned B. fragilis before; particularly what happened when this stuff was offered as an oral treatment: "Bacteroides fragilis corrects gut permeability, alters microbial composition, and ameliorates defects in communicative, stereotypic, anxiety-like and sensorimotor behaviors." Now apply all that to the idea that there may be some 'overlap' when it comes to autistic traits and AN (see here) and hopefully I'm not getting too carried away.

One other detail from the Morita study also caught my eye specifically with C-reactive protein (CRP) in mind. We are told that: "The ANR group exhibited significantly lower serum levels of C-reactive protein than the control group." Again accepting the small participant numbers included for study, I was a little surprised that nothing too much was made of this finding in the paper discussion and conclusions. If one assumes that CRP levels might be a rough-and-ready response indicator to something like inflammation, the idea that there may be 'issues' with either systemtic inflammation or the response to inflammation is something than I'd like to see a little more investigation into.

There is a small but growing interest in the possible role of the gut microbiota in relation to AN. Accepting that the issues with food (restriction and in some cases "abnormal eating or purging behaviors") that define the condition are probably going to play some role in the make-up of the gut microbiome, I do think are some interesting routes for future study. That intestinal dysbiosis when present in cases of AN may have some possible psychological repercussions as per the findings reported by Kleiman and colleagues [2] for example, is one area of interest that could lead to some important discussion points.

Oh and whilst we're on the topic of gut bacteria, yes, we might have to redefine what 'the common knowledge' on numbers of bacteria that call us home vs. cells, but don't downplay what important role(s) they play (see here).

Music: Me First and the Gimme Gimmes - Sweet Caroline.

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[1] Morita C. et al. Gut Dysbiosis in Patients with Anorexia Nervosa. PLoS One. 2015 Dec 18;10(12):e0145274.

[2] Kleiman SC. et al. The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology. Psychosom Med. 2015 Nov-Dec;77(9):969-81.

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Morita C, Tsuji H, Hata T, Gondo M, Takakura S, Kawai K, Yoshihara K, Ogata K, Nomoto K, Miyazaki K, & Sudo N (2015). Gut Dysbiosis in Patients with Anorexia Nervosa. PloS one, 10 (12) PMID: 26682545

Pregnancy paracetamol use and the 'hyperactive behavioral phenotype' of autism

"Prenatal use of acetaminophen was associated with an increased risk of ASD [autism spectrum disorder] accompanied by hyperkinetic symptoms..., but not with other ASD cases."

I was rather interested to read that conclusion presented in the study by Zeyan Liew and colleagues [1] talking about how acetaminophen (or paracetamol as it is known here in Blighty) use during pregnancy might have some rather important connections to offspring outcomes specifically with autism and hyperkinetic symptoms in mind.

Interested not only because I've discussed other research talking about how we might need to be a little more cautious about how OTC pain relief such as paracetamol is used in certain circumstances with potential offspring outcomes in mind (see here and see here) but also because it makes reference to a quite specific effect to the "hyperactive behavioral phenotype" of autism. That hyperkinetic behavioural phenotype by the way, plugs into a growing body of peer-reviewed evidence talking about the over-representation of ADHD (attention-deficit hyperactivity disorder) symptoms in relation to [some] autism (see here).

Liew et al "followed 64,322 children and mothers enrolled in the Danish National Birth Cohort (DNBC; 1996–2002) for average 12.7 years to investigate whether acetaminophen use in pregnancy is associated with increased risk of ASD in the offspring." Details about paracetamol use during pregnancy were "collected prospectively from three computer-assisted telephone interviews" and offspring outcomes with labels like autism were compared. This follows a similar methodological template from some of this research team (see here).

Some 1.6% of children included in the analysis were eventually diagnosed with as ASD. Roughly a third of that 1.6% of children were also diagnosed with hyperkinetic disorders (which seems to tally with other independent data analysis [2]). Perhaps unsurprisingly, paracetamol use during pregnancy was pretty widespread in the cohort (~50%) but, despite this, authors detailed something of a potentially important relationship between pregnancy paracetamol use and offspring "ASD accompanied by hyperkinetic symptoms." That there also appeared to be a relationship between length of use of paracetamol and risk of offspring autism with hyperkinetic symptoms, seems to strengthen details of a possible association.

Accepting that this was a study plotting pregnancy medication use and offspring outcomes and hence findings need to be treated with a degree of caution (as with other studies on other medicines), set within the other research talking about paracetamol use during pregnancy I'm coming around the idea that more investigation is required in this area [3]. I could, once again, start talking about how pregnancy paracetamol use might link into childhood asthma symptoms [4] (albeit with some cautions attached [5]) and what that might mean for the behavioural 'associations' noted in some cases of asthma (see here) as a possible angle for future research. I would however temper such musings within the context of autism (see here); although the preliminary suggestion that prenatal exposure to certain drugs used to treat asthma might also affect risk of offspring autism is also interesting [6].

I do like that Liew and colleagues talked about the idea of a specific behavioural phenotype potentially linked to pregnancy paracetamol exposure as providing a guide for more targeted investigation and perhaps to some degree bypassing the need for the sweeping generalisations about 'all autism' (we've had enough of those down the years). I believe there is quite a bit of research traction in this area with the notion of the autisms (see here) in mind.

Music: Elvis Presley - If I Can Dream.

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[1] Liew Z. et al. Maternal use of acetaminophen during pregnancy and risk of autism spectrum disorders in childhood. Autism Research. 2015. Dec 21.

[2] Berenguer-Forner C. et al. Comorbidity of autism spectrum disorder and attention deficit with hyperactivity. A review study. Rev Neurol. 2015 Feb 25;60 Suppl 1:S37-43.

[3] de Fays L. et al. Use of paracetamol during pregnancy and child neurological development. Dev Med Child Neurol. 2015 Aug;57(8):718-24.

[4] Eyers S. et al. Paracetamol in pregnancy and the risk of wheezing in offspring: a systematic review and meta-analysis. Clin Exp Allergy. 2011 Apr;41(4):482-9.

[5] Cheelo M. et al. Paracetamol exposure in pregnancy and early childhood and development of childhood asthma: a systematic review and meta-analysis. Arch Dis Child. 2015 Jan;100(1):81-9.

[6] Gidaya NB. et al. In utero Exposure to β-2-Adrenergic Receptor Agonist Drugs and Risk for Autism Spectrum Disorders. Pediatrics. 2016. 6 Jan.

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Liew Z, Ritz B, Virk J, & Olsen J (2015). Maternal use of acetaminophen during pregnancy and risk of autism spectrum disorders in childhood: A Danish national birth cohort study. Autism research : official journal of the International Society for Autism Research PMID: 26688372

Fish oils for schizophrenia?

Hot on the heels of the peer-reviewed research-based suggestion that fish oil supplementation (high in omega-3 PUFAs) might have some rather important effects pertinent to the transition to full-threshold psychotic disorder for 'young people with an at-risk mental state' (see here), are the results from Tomasz Pawełczyk and colleagues [1].

This time around it was a randomised, placebo-controlled trial "of either 2.2 g/day of n-3 PUFA, or olive oil placebo, with regard to symptom severity in first-episode schizophrenia patients." I might add that we have been expecting these results given the publication of the trial protocol not so long ago [2]. n-3 by the way, refers to omega-3 or rather the Greek lower case character ω or ωμέγα.

Seventy-one participants were randomly assigned to olive oil (placebo) or "1320 mg/day of EPA and 880 mg/day of DHA" and monitored over the course of the 26-week study period. "The primary outcome measure of the clinical evaluation was schizophrenia symptom severity change measured by the Positive and Negative Syndrome Scale (PANSS)."

Results: quite a few changes were noted as a consequence of the fish oil supplementation including that: "A fifty-percent improvement in symptom severity was achieved significantly more frequently in the n-3 PUFA group than in the placebo group." Also: "N-3 PUFA intervention was also associated with an improvement in general psychopathology, measured by means of PANSS... depressive symptoms..., the level of functioning... and clinical global impression." All-in-all, there was quite a bit to see from the use of a humble fish oil supplement in this cohort and hence quite a bit more research is indicated.

A quick survey of the other research literature in this area suggests that the Pawełczyk findings were probably not unexpected. A Cochrane Review ('Cochrane does...') a few years back [3] pointed out that whilst the available literature at that time was not all one-way when it comes to the use of polyunsaturated fatty acids (PUFAs) for people with schizophrenia, there were pockets of evidence suggesting some positive effects might be had from this quite simple intervention. Some but not all subsequent trials have hinted as possible positive effects for some on the schizophrenia spectrum.

If I had to quibble with the Pawełczyk study in any way I might suggest that one has to be slightly cautious about the use of olive oil as a placebo condition. Bearing in mind my not confusing a high fat diet with a ketogenic diet (high fat / low carbohydrate), one has to pause a little to take in the potentially interesting mouse results published by Ann Katrin Kraeuter and colleagues [4] that some media have headlined with "High fat/low carb diet could combat schizophrenia." I personally would like to see the fish oils pitted against a non-fat alternative in clinical study just to be sure.

Music: and what else but goodbye to a legend...

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[1] Pawełczyk T. et al. A randomized controlled study of the efficacy of six-month supplementation with concentrated fish oil rich in omega-3 polyunsaturated fatty acids in first episode schizophrenia. J Psychiatr Res. 2015 Nov 25;73:34-44.

[2] Pawełczyk T. et al. Omega-3 fatty acids in first-episode schizophrenia - a randomized controlled study of efficacy and relapse prevention (OFFER): rationale, design, and methods. BMC Psychiatry. 2015 May 2;15:97.

[3] Joy CB. et al. Polyunsaturated fatty acid supplementation for schizophrenia. Cochrane Database Syst Rev. 2003;(2):CD001257.

[4] Kraeuter AK. et al. Ketogenic diet reverses behavioral abnormalities in an acute NMDA receptor hypofunction model of schizophrenia. Schizophr Res. 2015 Dec;169(1-3):491-3.

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Pawełczyk, T., Grancow-Grabka, M., Kotlicka-Antczak, M., Trafalska, E., & Pawełczyk, A. (2016). A randomized controlled study of the efficacy of six-month supplementation with concentrated fish oil rich in omega-3 polyunsaturated fatty acids in first episode schizophrenia Journal of Psychiatric Research, 73, 34-44 DOI: 10.1016/j.jpsychires.2015.11.013

Serum folate levels in schizophrenia meta-analysed

So: "In conclusion, the present meta-analysis found that folate deficiency is associated to SZ [schizophrenia], and subgroups which did not reach enough statistical power need further investigation in the future."

That was the research bottom line discussed in the paper by Dan Wang and colleagues [1] on a topic that has been of some interest to this blog down the years (see here and see here for example). Folate (folic acid if you will) is a pretty vital nutrient that, among other things, plays an important role in a particular cycle linked to the methylation of DNA. With schizophrenia specifically in mind, there is a body of peer-reviewed evidence emerging suggesting that folate levels might provide some important information about at least some cases bearing in mind the concept of plurality (see here).

Wang et al looked at quite a bit of that research literature on folate and schizophrenia and determined that "decreased serum folate was associated with SZ risk" even when taking into account variables such as when serum folate levels were sampled (i.e. in acute schizophrenia) and "measurement after drugs using in SZ patients." Ergo, science needs to know more about this potentially important association.

As per the various research looking at folate levels in relation to autism (see here for example) one has to tread quite carefully so as not to 'big up' any universal relationship between folate and schizophrenia. That for example, the folate cycle intersects with other potentially important compounds such as homocysteine with schizophrenia in mind (see here) is also something to bear in mind.

Music: Jack Garratt - Breathe Life.

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[1] Wang D. et al. Serum folate levels in schizophrenia: A meta-analysis. Psychiatry Res. 2015 Nov 25. pii: S0165-1781(15)30731-9.

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Wang D, Zhai JX, & Liu DW (2015). Serum folate levels in schizophrenia: A meta-analysis. Psychiatry research PMID: 26652840

Sleep apnoea and autism

Sleep apnoea defined as "a condition where the walls of the throat relax and narrow during sleep, interrupting normal breathing" is not natural fodder for this blog. When however it is mentioned in the context of autism as it was in the paper by Ikuko Hirata and colleagues [1] it becomes a little more relevant; more so when one realises that sleep issues and autism might actually be quite an important topic (see here).

Hirata et al describe the assessment of sleep problems in "965 community and 193 ASD [autism spectrum disorder] preschoolers using the Japanese Sleep Questionnaire for Preschoolers." They noted how various sleep problems were more frequently reported in the the group with autism compared with asymptomatic (not-autism) controls including "obstructive sleep apnea and parasomnias." Further: "ASD preschoolers with sleep problems exhibited more behavioral problems than those without sleep problems"; something perhaps not entirely unexpected.

The comment about obstructive sleep apnoea being more frequently reported in those with autism got me looking into some of the other peer-reviewed material with this 'association' in mind. Not surprisingly, among the vast number of papers making up with the autism research landscape, sleep apnoea receives attention. The case report detailed by Malow and colleagues [2] provides one of the early accounts of sleep apnoea occurring alongside autism. Describing "a 5-year-old female with an autism spectrum disorder" the authors report "improvements in sleep, social communication, attention, repetitive behaviors, and hypersensitivity after adenotonsillectomy for obstructive sleep apnea." Some of the same authors followed up this finding [3] with more general guidance on how "suspected obstructive sleep apnea, should be referred to a sleep specialist" with autism in mind.

When it comes to the question of what factors might be influential in the development of sleep apnoea with autism in mind, there is some science here too. Outside of the typically defined causes of sleep apnoea (see here) papers such as the one by Bowers and colleagues [4] hinted at other potentially important correlates including gestational factors allied to gender. Youssef and colleagues [5] reported a possible connection between serum ferritin levels linked to iron levels and sleep apnoea and autism. Ferritin and iron levels have some history with [some] autism in mind (see here) although I'm a little unsure about the direct connection between this nutrient and sleep apnoea outside of the whole 'periodic limb movement' bit.

Accepting that screening for sleep apnoea is probably not commonplace when it comes to autism, I do believe that there is more science to do on this topic. Without hopefully displaying too much 'lack of knowledge' and making connections where none might exist, I do wonder whether the focus on airways and sleep apnoea might tie into some interesting findings reported a while back on 'bronchoscopic airway anatomy' and autism (see here). That also nasal congestion might be a risk factor for sleep apnoea is potentially relevant to some autism also, specifically where allergy might also be present [6] (see here for my take on this). I don't doubt there will be other factors requiring further investigation too, as once again the idea is to screen not to assume...

Music: Buddy Holly - Everyday.

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[1] Hirata I. et al. Sleep problems are more frequent and associated with problematic behaviors in preschoolers with autism spectrum disorder. Research in Developmental Disabilities.  2016; 49-50: 86-99.

[2] Malow BA. et al. Impact of treating sleep apnea in a child with autism spectrum disorder. Pediatr Neurol. 2006 Apr;34(4):325-8.

[3] Johnson KP. & Malow BA. Sleep in children with autism spectrum disorders. Curr Treat Options Neurol. 2008 Sep;10(5):350-9.

[4] Bowers K. et al. Phenotypic differences in individuals with autism spectrum disorder born preterm and at term gestation. Autism. 2015 Aug;19(6):758-63.

[5] Youssef J. et al. Relationship of serum ferritin levels to sleep fragmentation and periodic limb movements of sleep on polysomnography in autism spectrum disorders. Pediatr Neurol. 2013 Oct;49(4):274-8.

[6] Jyonouchi H. Marked improvement of neuropsychiatric symptoms following control of allergy symptoms with the use of humanized murine anti-IgE antibody (omalizumab) in 2 patients with severely limited expressive language. Allergy Asthma Clin Immunol. 2015 Dec 9;11:38.

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Hirata, I., Mohri, I., Kato-Nishimura, K., Tachibana, M., Kuwada, A., Kagitani-Shimono, K., Ohno, Y., Ozono, K., & Taniike, M. (2016). Sleep problems are more frequent and associated with problematic behaviors in preschoolers with autism spectrum disorder Research in Developmental Disabilities, 49-50, 86-99 DOI: 10.1016/j.ridd.2015.11.002