Saturday, 13 February 2016

Big names coming around to 'neuroinflammation' and autism?

I won't keep you too long today as I bring the paper by Adam Young and colleagues [1] (open-access available here) to your attention and some discussions around the concept of inflammation and autism. To quote: "An emerging focus of research into the aetiology of ASC [autism spectrum condition] has suggested neuroinflammation as one candidate underlying [the] biological model."

Including one Simon Baron-Cohen on the authorship list, I have to say that I was impressed to see this quite comprehensive review of the peer-reviewed literature covering "the mechanisms that may underlie neuroinflammation and the evidence at genetic and protein levels for each of these mechanisms." The authors concluded that whilst there are some important gaps to be filled in the research literature in this area - "the greatest area of weakness in the field is that in general, the findings tend to be from individual studies and rarely are these replicated" - to mention 'inflammation' and 'autism' in the same sentence is no longer 'crazy talk'.

I've discussed quite a bit about inflammation and autism on this blog down the years. Personally, I've seen and read enough (peer-reviewed) papers on the topic to form an opinion that for at least some on the autism spectrum ('autisms' people, autisms) there is an overwhelming case for much more detailed investigation in this area. If you don't believe me, well, take a look at some of the science and form your own opinion (see here and see here for example). And when I say that some of the genetics of 'some' autism might also implicate inflammation and inflammatory processes too (see here), there appears to be something for everyone in the field.

One area that I would like to see more study on (aside from what science can potentially do when inflammation runs amok) is inspection of the interplay between genetic and biological factors pertinent to inflammation/inflammatory processes and behaviour and psychology. We've already had some hints down the years about how inflammation might 'affect' things like social cognitive processing (see here) including mention of a concept not unfamiliar to Prof. Baron-Cohen - Theory of Mind (ToM) - and potentially pertinent to autism. I'd like to see much more investigation on whether for example, cyclical patterns of inflammation might correspond to some of the cyclical patterns of behaviour noted in some on the spectrum. This set against the idea that some of the contents of the medicine cabinet already applied to some cases of autism might have some relevant actions on facets of immune function overlapping with inflammation and inflammatory processes (see here). Much more research is indicated.

Oh, and since we are on the topic of neuroinflammation and autism, I'd also suggest you having a look at the recent review from Janet Kern and colleagues [2] (open-access) too. They've also included some important mention of anti-NMDA-receptor encephalitis and autism (see here) which I'm particularly interested in...

Music: Me First and the Gimme Gimmes - My Heart Will Go On. Please, give the song a chance...

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[1] Young AM. et al. From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Mol Autism. 2016 Jan 20;7:9.

[2] Kern J. et al. Relevance of Neuroinflammation and Encephalitis in Autism. Front Cell Neurosci. 2016 Jan 19;9:519.

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ResearchBlogging.org Young AM, Chakrabarti B, Roberts D, Lai MC, Suckling J, & Baron-Cohen S (2016). From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Molecular autism, 7 PMID: 26793298

Friday, 12 February 2016

Mitochondrial response to BCKDK-deficiency and 'some' autism

I'll admit to being pretty fascinated by the Branched Chain α-Keto acid Dehydrogenase Kinase (BCKDK) gene. As per previous blog entries about this gene (see here and see here) and the important biological step it plays in the metabolism of the branched-chain amino acids (BCAAs), at least one 'form' of autism might be particularly sensitive to issues with it [1]. I take it you've heard of the idea that the autisms (plural) might be a better description of autism? If you haven't, here is a peer-reviewed take on it [2]...

I'm happy to report that science continues to study this gene; its biology and it's associations with "a novel dietary-treatable form of autism" as per the findings reported by Oyarzabal and colleagues [3]. The focus of the Oyarzabal paper was to study the "mitochondrial response to the BCKDK-deficiency" potentially brought about for example, when there are issues with the BCKDK gene given its links to the mitochondria matrix. This work also takes on particular relevance given the idea that mitochondrial issues - mitochondria: the powerhouse of cells - might not be something entirely new to at least some autism (see here for example).

Anyhow, fibroblasts were the starting material and the measurement of "bioenergetics, ultra-structural and dynamics parameters" of fibroblasts from those who had BCKDK-deficiency. Although not totally au-fait with all the science included in the paper, the authors report results on: "a general bioenergetics depletion that could affect the mitochondrial dynamics and cell fate." They even reported complementary findings following a: "Knockdown of BCKDK gene in control fibroblasts" and mention of some findings relevant to maple syrup urine disease (MSUD) in light of the involvement of the BCAAs there. In short: "All these data gives us a clue to understand the positive dietary response to an overload of branched-chain amino acids."

This is an exciting area of autism research pertinent to the idea that (a) there may be various types of autism characterised by various different genetic and biological factors being involved, and (b) the possibility that at least some autism might stem from one or more inborn errors of metabolism is gaining ground (see here) and hence might be potentially 'treatable'. For that last point I'm minded to take you back to a recent post on phenylketonuria and autism (see here) and some more recent [peer-reviewed] research talking about 'Succinic Semialdehyde Dehydrogenase Deficiency Presenting as Autism Spectrum Disorder' [4]. Dare I even present the idea of carnitine issues falling into this area?

Screening for such inborn errors of metabolism seems to be the important conclusion; screening not assuming nor guessing nor making grand generalisations. Just screening.

Music: the glorious music accompanying the film Interstellar has to be the one for today in light of new discoveries in recent days...

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[1] Novarino G. et al. Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy. Science. 2012 Oct 19;338(6105):394-7.

[2] Poot M. Towards identification of individual etiologies by resolving genomic and biological conundrums in patients with autism spectrum disorders. Mol Syndromol. 2013 Jun;4(5):213-26.

[3] Oyarzabal A. et al. Mitochondrial response to the BCKDK-deficiency: Some clues to understand the positive dietary response in this form of autism. Biochim Biophys Acta. 2016 Jan 22. pii: S0925-4439(16)30003-5.

[4] Gogou M. et al. Succinic Semialdehyde Dehydrogenase Deficiency Presenting as Autism Spectrum Disorder. Indian J Pediatr. 2016 Jan 25.

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ResearchBlogging.org Oyarzabal A, Bravo-Alonso I, Sánchez-Aragó M, Rejas MT, Merinero B, García-Cazorla A, Artuch R, Ugarte M, & Rodríguez-Pombo P (2016). Mitochondrial response to the BCKDK-deficiency: Some clues to understand the positive dietary response in this form of autism. Biochimica et biophysica acta PMID: 26809120

Thursday, 11 February 2016

2% of UK 16-year olds with chronic fatigue [syndrome]?

"CFS [chronic fatigue syndrome] affected 1.9% of 16-year-olds in a UK birth cohort and was positively associated with higher family adversity. Gender was a risk factor at age 16 years but not at age 13 years or in 16-year-olds without high levels of depressive symptoms."

So said the findings reported by Simon Collin and colleagues [1] which also gained some media interest as per an entry on the BBC news website for example (see here). Based on data generated by the Children of the 90s research initiative (ALSPAC to you and me), researchers looked to estimate the prevalence of the condition in some 5,700 youth participants.

I say looked to 'estimate the prevalence' of CFS but I don't think they formally screened/assessed for the condition on this occasion; rather sending out questionnaires to parents and youth regarding "unexplained disabling fatigue lasting ≥6 months." As per the introduction of SEID (see here) to CFS (and ME) such questioning addresses one aspect of CFS but not necessarily all. One also has to be slightly careful about spreading the label too liberally [2] so as not to dilute what CFS means to many, many people and potentially including many presentations under the current banner [3]. I'll say something further about this shortly.

Authors reported an overall prevalence of chronic fatigue of ~2% in their cohort. This figure fell somewhat when "excluding children with high levels of depressive symptoms" to something like 0.6%. Further, when also looking at data "obtained from the National Pupil Database" and cross-linking it to findings, they found that authorised school absences were higher for those with CFS. This follows previous work from this research group already covered on this blog (see here). Finally, the authors talk about how being female and "family adversity" seemed to be more frequently associated with chronic fatigue. As far as I can ascertain however, no other measure (biological or genetic) was included in the study as it stands.

Set within the context of 2015 seeing a real ramping up of research into CFS/ME (see here) and some rather public discussions on what may (or may not) be the best way to manage/treat the condition (see here), the Collin findings are an interesting addition to the research base. As per the accompanying press release, the idea that family adversity - that "included poor housing, financial difficulties and a lack of practical and/or emotional support for the mother" - seemed to play something of a role in the findings goes some way to "dispelling the commonly held view that CFS is a 'middle-class' illness or 'yuppie-flu'." The same authors have also talked about other factors linked to adolescent fatigue in other publications [4] but I'm minded to be a little careful around suggested ideas like "children whose mothers experience anxiety and/or depression between pregnancy and child's age 6 years have an increased risk of developing chronic disabling fatigue in early adolescence." I think many people have had quite enough of hearing about 'psychosomatic explanations' of CFS/ME (see here) and would perhaps prefer further concentration on more pertinent biological and/or genetic processes. I'd also like to see the term 'yuppie flu' stricken from any text where CFS/ME is also mentioned.

Significantly more resources need to be put into looking at CFS/ME (including identification [5]) and what can be done to alleviate the condition particularly when one sees how much it can affect a person (see here and see here) and those around them. As per my previous ramblings on the topic (see here and see here) I'm pretty firmly sold on the idea that whilst psychology will (inevitably) be affected by a diagnosis, targeting the underlying genetics [6] and biology of the condition is the way forward (see here for example) mindful that there probably is no universal one-size-fits-all intervention for this 'spectral' condition.

Just before I go, I do want to return to that point about what exactly comes under the banner of CFS/ME based on the Collin study findings and some other goings on. As per the example detailed by Jason et al [3], one has to be a little cautious about what one includes under labels such as SEID. To quote: "many individuals from major depressive disorder illness groups as well as other medical illnesses were categorized as having SEID" based on the lack of exclusionary criteria applied to this new label. I kinda get the impression that set within the viewpoint of CFS/ME being a 'psychological condition' still unfortunately prevalent in some quarters, conflating certain depressive illnesses with CFS/ME could be used to serve an important purpose when it comes to things like presenting certain intervention options above others. At the very least, it provides a handy distraction from looking at more objective biological information potentially pertinent to at least some of this patient group. We need to be very careful...

I foresee 2016 as being another important year for CFS/ME and yes, I will be blogging about the recent Roberts study on mortality statistics and CFS/ME soon enough...

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[1] Collin SM. et al. Chronic Fatigue Syndrome at Age 16 Years. Pediatrics. 2016 Jan 25. pii: peds.2015-3434.

[2] Friedberg F. et al. Prolonged fatigue in Ukraine and the United States: Prevalence and risk factors. Fatigue. 2015;3(1):33-46.

[3] Jason LA. et al. Unintended Consequences of not Specifying Exclusionary Illnesses for Systemic Exertion Intolerance Disease. Diagnostics (Basel). 2015 Jun 23;5(2):272-86.

[4] Collin SM. et al. Maternal and childhood psychological factors predict chronic disabling fatigue at age 13 years. J Adolesc Health. 2015 Feb;56(2):181-7.

[5] Collin SM. et al. Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME) is different in children compared to in adults: a study of UK and Dutch clinical cohorts. BMJ Open. 2015 Oct 28;5(10):e008830.

[6] Schlauch KA. et al. Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome. Translational Psychiatry. 2016; 6: e730.

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ResearchBlogging.org Collin, S., Norris, T., Nuevo, R., Tilling, K., Joinson, C., Sterne, J., & Crawley, E. (2016). Chronic Fatigue Syndrome at Age 16 Years PEDIATRICS, 137 (2), 1-10 DOI: 10.1542/peds.2015-3434

Wednesday, 10 February 2016

Autism and the 'female camouflage effect'

Two papers provide some blogging fodder today. The first is from Agnieszka Rynkiewicz and colleagues [1] (open-access available here) who introduces a concept that many people with an interest in autism might have considered: a 'female camouflage effect' in autism. The second paper is by C Ellie Wilson and colleagues [2] and continues the idea that sex/gender differences present in autism might have some important implications for diagnostic evaluation.

Both these papers entertain the idea that although the history of autism has been very 'male-dominated' in light of the sex ratio for the label for example (see here), science and clinical practice is coming round to the idea that there may be important sex/gender differences in the presentation of core issues (see here) that might mean quite a few females have been 'over-looked' or 'under-identified' when it comes to autism. It's of increasing interest.

Rynkiewicz et al set about to present "an innovative computerized technique to objectively evaluate the non-verbal modality of communication (gestures) during two demonstration tasks of ADOS-2 (Autism Diagnostic Observation Schedule, Second Edition)." ADOS, by the way, is one of the gold-standard assessment instruments designed with autism in mind (see here). As part of their really interesting report on "automated coding of non-verbal mode of communication (gestures)" and computation of a "Gesture Index (GI)" they compared results from boys and girls ("high-functioning" as they describe them) and whether "females with autism had a higher GI compared to males with autism."

After data were crunched and the like, the authors concluded that: "High-functioning females with autism might present better on non-verbal (gestures) mode of communication than boys with autism." Further: "This may be because they are effective at camouflaging other diagnostic features." Potentially very important information indeed.

The second paper by Wilson et al continues the theme that sex/gender might have a part to play on the manifestation of autism and onwards diagnostic evaluation. With the aim of reporting "sex differences in clinical outcomes for 1244 adults (935 males and 309 females) referred for autism spectrum disorder assessment", researchers found among other things that: "Males had significantly more repetitive behaviours/restricted interests than females." Onwards: "The sexes may present with different manifestations of the autism spectrum disorder phenotype and differences vary by diagnostic subtype."

Variation in the presentation of repetitive and/or restricted behaviours/interests by sex has been talked about in the peer-reviewed research before [3]. As part of a wider suggestion of a specific female phenotype of autism potentially emerging (see here) (being careful with those generalisations) I'd like to think that a greater awareness of such issues could notably enhance the whole diagnostic system especially for females. Indeed, one area that I think would substantially benefit from a little more inspection of a potential 'female camouflage effect' in autism is that of the 'diagnosis' (although not formally noted in standardised texts) of pathological demand avoidance (PDA). At least one person has talked about female autism and the overlap with PDA (see here) and I'm minded to suggest that they might be on to something rather important.

Oh, and since I'm on the topic of sex/gender and autism, I'm minded to bring in the paper by Katarzyna Chawarska and colleagues [4] talking about infant 'at-risk for autism' girls and social attention potentially pertinent to discussions on any female camouflage effect...

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[1] Rynkiewicz A. et al. An investigation of the 'female camouflage effect' in autism using a computerized ADOS-2 and a test of sex/gender differences. Mol Autism. 2016 Jan 21;7:10.

[2] Wilson CE. et al. Does sex influence the diagnostic evaluation of autism spectrum disorder in adults? Autism. 2016. Jan 22.

[3] Van Wijngaarden-Cremers PJ. et al. Gender and age differences in the core triad of impairments in autism spectrum disorders: a systematic review and meta-analysis. J Autism Dev Disord. 2014 Mar;44(3):627-35.

[4] Chawarska K. et al. Enhanced Social Attention in Female Infant Siblings at Risk for Autism. Journal of the American Academy of Child & Adolescent Psychiatry. 2015. Dec 17.

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ResearchBlogging.org Rynkiewicz, A., Schuller, B., Marchi, E., Piana, S., Camurri, A., Lassalle, A., & Baron-Cohen, S. (2016). An investigation of the ‘female camouflage effect’ in autism using a computerized ADOS-2 and a test of sex/gender differences Molecular Autism, 7 (1) DOI: 10.1186/s13229-016-0073-0




ResearchBlogging.org Wilson CE, Murphy CM, McAlonan G, Robertson DM, Spain D, Hayward H, Woodhouse E, Deeley PQ, Gillan N, Ohlsen JC, Zinkstok J, Stoencheva V, Faulkner J, Yildiran H, Bell V, Hammond N, Craig MC, & Murphy DG (2016). Does sex influence the diagnostic evaluation of autism spectrum disorder in adults? Autism : the international journal of research and practice PMID: 26802113

Tuesday, 9 February 2016

Decreased brain levels of vitamin B12 in autism

I have to thank Dr Malav Trivedi for bringing my attention to some recent findings reported by Yiting Zhang and colleagues (including Malav) [1] (open-access) suggesting that: "levels of vitamin B12, especially its MeCbl [methylcobalamin] form, decrease with age in frontal cortex of control human subjects."

Further, researchers reported: "abnormally lower total Cbl [cobalamin] and MeCbl levels in subjects with autism and schizophrenia, as compared to age-matched controls." Some media on the findings can also be read here.

Working from the lab of Dr Richard Deth (quite a familiar name to this blog), researchers initially analysed a most precious sample medium (postmortem brain samples) obtained from various biobanks and including various patient groups. So alongside samples from 12 children with autism were samples from 9 people diagnosed with schizophrenia and some 43 'controls' with ages ranging between 19 weeks old and 80 years old. "Changes in Cbl species were compared with the status of methylation and antioxidant pathway metabolites" accompanied by data derived from a knock-out mouse model: "the influence of decreased GSH [glutathione] production on brain Cbl levels was evaluated in glutamate-cysteine ligase modulatory subunit knockout (GCLM-KO) mice in which GSH synthesis was impaired, leading to a brain GSH level decrease of 60–70%."

Looking at postmortem frontal cortex brain samples, researchers reported that finding on levels of vitamin B12 - particularly the MeCbl vitamer -  decreasing with age. Bearing in mind the relatively small participant numbers included, the idea that lower brain tissue levels of total cobalamin and methylcobalamin were also present (almost unanimously) in the autism and schizophrenia groups could be important. I might at this point direct readers to previous discussions on vitamin B12 and autism on this blog (see here) including the research idea of supplementing (see here) with no medical advice given or intended.

There are a few other details worth pointing out from the Zhang findings. Analysis of thiols in brain samples across the autism vs control group revealed some potentially interesting data. So, methionine levels were quite a bit lower in the autism group [significantly lower] as were levels of "the methyl donor S-adenosylmethionine (SAM)." Both these compounds form an important part of the whole 'methylation of DNA' process (see here) among other things.

Glutathione, a compound that has seen its fair share of speculation with autism in mind (see here), was also on the research menu in the Zhang study. Interestingly and again bearing mind the small participant numbers, brain levels of this stuff were lower in the autism group as a whole but not significantly so when compared to controls. This finding might map on to other brain studies with autism in mind (see here). Likewise, cysteine (another potentially relevant compound to some autism) produced a similar finding.

I would encourage readers to take some time looking at the Zhang paper. In conjunction with other results reporting on some important elements to the emerging story (see here) I believe there are further studies to be done applicable to the notion that: "impaired methylation may be a critical pathological component" for at least some autism (see here). Indeed, other research papers have also discussed this issue [2]. The idea that studies about human ageing may likewise be informative to autism (and schizophrenia) research also carries quite a lot of traction too.

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[1] Zhang Y. et al. Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia. PLoS One. 2016 Jan 22;11(1):e0146797.

[2] Keil KP. & Lein PJ. DNA methylation: a mechanism linking environmental chemical exposures to risk of autism spectrum disorders? Environmental Epigenetics. 2016; 1-15.

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ResearchBlogging.org Zhang Y, Hodgson NW, Trivedi MS, Abdolmaleky HM, Fournier M, Cuenod M, Do KQ, & Deth RC (2016). Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia. PloS one, 11 (1) PMID: 26799654

Monday, 8 February 2016

"People with ASD had lower odds of employment in the community"

The title of this quite brief post refers to an important finding detailed by Derek Nord and colleagues [1] who, when analysing data from the "2008–09 National Core Indicators Adult Consumer Survey", concluded that there were some important inequalities when it came to employment rates for those diagnosed on the autism spectrum.

Employment rates and work opportunities for people diagnosed with an autism spectrum disorder (ASD) is a hot topic at the moment. The Nord findings build upon report after report published in the peer-reviewed domain and beyond basically telling everyone what was already quite widely known: "despite their capacity and willingness to work, [people with autism / autistic people] face significant disadvantages in the labour market." [2] Like many others, I am happy to see that things are [slowly] changing insofar as increasingly more resources being put into highlighting this issue and most importantly, the translation of talk into action. But such change is not happening everywhere for everyone and, as if to prove a point...

Appreciating that the autism spectrum includes a whole tapestry of skills and disabilities that might affect both the ability and desire to seek employment (and no, not everyone with autism automatically wants to work in IT or engineering), there is still quite a lot more to do in this area. Things like making the job application and interview a little more 'friendly' is a good start (see here) and also not assuming that getting someone a job is the end of the process [3] no matter how many 'feel good' boxes this might tick. Indeed, I'm particularly interested in the factors that are linked to the sustainability of employment and how making the workplace 'work' for people on the autism spectrum might be a key part of the benefits employment can bring to the person themselves, their family and society in general.

Now, about making the labour market also 'work' for parents of children with autism too (see here)...

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[1] Nord DK. et al. Employment in the community for people with and without autism: A comparative analysis. Research in Autism Spectrum Disorders. 2016; 24: 11-16.

[2] Baldwin S. et al. Employment activities and experiences of adults with high-functioning autism and Asperger’s Disorder. J Autism Dev Disord. 2014 Oct;44(10):2440-9.

[3] Holwerda A. et al. Predictors of sustainable work participation of young adults with developmental disorders. Res Dev Disabil. 2013 Sep;34(9):2753-63.

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ResearchBlogging.org Nord, D., Stancliffe, R., Nye-Lengerman, K., & Hewitt, A. (2016). Employment in the community for people with and without autism: A comparative analysis Research in Autism Spectrum Disorders, 24, 11-16 DOI: 10.1016/j.rasd.2015.12.013

Saturday, 6 February 2016

Sleep as a target of antibiotic use in chronic fatigue syndrome?

"The primary finding from the study was evidence of an improvement in several objective sleep parameters in participants in whom the increased colonization of lactic acid producing organisms was resolved after antibiotic treatment."

Those were the words written by Melinda Jackson and colleagues [1] (open-access) who, during an open-label trial, looked at whether administration of an antibiotic (erythromycin 400 mg) over the course of 6 days might have some important effects on elements of sleep in a patient group diagnosed with chronic fatigue syndrome (CFS). Yes, sleep did seem to be [positively] affected was the finding. The suggested mode of action of antibiotic administration was linked to colonisation "with gram-positive faecal Streptococcus (determined by stool analysis and suggestive of abnormal gut functioning)" onwards to the idea that the those trillions of wee beasties that inhabit us all might show some specific connection to elements in cases of CFS.

From an initial study population of 70 recruited for study, data for 22 participants (who completed the trial and met study inclusion criteria) were reported on. Those 22 all had "increased colonization of Streptococcus sp. (defined as >3×105 cfu/g of faecal sample)" as a pre-requisite to taking part in the trial based on the results of a "faecal microbiota analysis (FMA)." Actigraphy and sleep diaries were kept for a week before antibiotic use, during use and for 8 days after. Various facets of CFS symptoms were also examined during points of the study.

Bearing in mind some 'malfunctions' affecting actigraphy results, the authors describe some interesting findings. First and foremost, is the idea that not everyone who took erythromycin showed the same profile (behavioural or biochemical). The authors talk about "responders" to the intervention (music to my ears) on the basis that: "Thirteen of the patients showed a reduction in Streptococcus counts after treatment, whereas four patients showed an increase level of Streptococcus and four patients had no change at the end of the trial." Outside of the idea that there may be some significant individual variation in the effects of antibiotics on gut flora (remembering the idea of 'swallowing a grenade'), questions abound as to why some people did not seem to be so affected by this strain of antibiotics whilst others did. Further: "While 13 participants showed a reduction in Streptococcus only 7 of these had a significant change as defined by a percentage distribution post-therapy of less than 6% of Streptococcus after antibiotic treatment." Mmm, indeed.

Second, and linked back to the idea of 'responders' and 'non-responders' on the basis of microbiological results are the findings that there were: "more improvement in actigraphic sleep with treatment in responders compared to non-responders from baseline to post-treatment 2." Indeed, we are told that responders tended to increase their total sleep time by about 40 minutes between baseline and end of study, whereas: "non-responders slept an average of 15 min less from baseline to post-treatment 2."

Finally, and quite importantly: "No significant change in any of the subjective measures was observed between baseline and the two follow-up points for responders versus non-responders." The subjective measures in question were linked to things like self-reported fatigue, mood and the such like. The authors have suggested that there may be some 'correlation' between a subscale on 'vigour' and "Streptococcus viable count" but when you're talking about 7 participants as your responder group, one has to be mighty careful of making too many sweeping generalisations.

Although this is a preliminary study, I'd like to think that the Jackson findings might eventually be worked up into a larger, more methodologically sound research agenda encompassing a placebo arm and the like. We know for example, that sleep patterns can be affected by CFS and that at least subjective measures of sleep may affect the presentation of elements of CFS [2]. That children and adolescents with CFS may be particularly vulnerable to sleep disturbances [3] is an area in specific need of further investigation. Moves therefore to improve sleep measures in CFS are perhaps to be welcomed mindful of the idea that persistent use of antibiotics is not exactly a great long-term strategy particularly in these days of growing antibiotic resistance. I could offer a possible alternative to antibiotic use that has been initially tried with CFS in mind (see here) but again, more research is indicated first and perhaps also some PR! Still, the focus on the gut microbiota and CFS/ME continues at a pace (er, maybe a should rephrase that) and with the promise of much, much more to come.

I'll also be talking about the paper by Collin and colleagues in the not-too-distant future so watch this space...

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[1] Jackson ML. et al. Sleep quality and the treatment of intestinal microbiota imbalance in Chronic Fatigue Syndrome: A pilot study. Sleep Sci. 2015 Nov;8(3):124-33.

[2] Russell C. et al. Subjective But Not Actigraphy-Defined Sleep Predicts Next-Day Fatigue in Chronic Fatigue Syndrome: A Prospective Daily Diary Study. Sleep. 2015 Dec 22. pii: sp-00453-15.

[3] Snodgrass K. et al. Sleep Disturbances in Pediatric Chronic Fatigue Syndrome: A Review of Current Research. J Clin Sleep Med. 2015 Jul 15;11(7):757-64.

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ResearchBlogging.org Jackson ML, Butt H, Ball M, Lewis DP, & Bruck D (2015). Sleep quality and the treatment of intestinal microbiota imbalance in Chronic Fatigue Syndrome: A pilot study. Sleep Science (Sao Paulo, Brazil), 8 (3), 124-33 PMID: 26779319