Treating ADHD: better school results, less risk of crime and better sleep?

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I had already written and scheduled in this blog post before an important - very important - headline appeared on the BBC News website: "ADHD [attention-deficit hyperactivity disorder] testing after 'impulsive crime' arrests should be mandatory, MPs say." The news piece covered, amongst other things, some of the peer-reviewed research findings suggesting that a diagnosis of ADHD appears to place someone at various enhanced risk for adverse life outcomes. And that potentially includes offending behaviour and prison time.

So...

Today's post is a bit of a mash-up insofar as bringing together three pieces of independent peer-reviewed research pertinent to the important idea of managing or 'treating' ADHD when it arises. I appreciate that not many people would want their nearest-and-dearest 'medicated' for example in the long-term. But when it comes to something like ADHD the case is indeed growing strong for how pharmacological intervention in particular, could literally be a life-saver for some (see here)...

The papers: first there are the findings reported by Andreas Jangmo and colleagues [1] who "analyzed school performance in students with ADHD compared to students without ADHD, and the association between pharmacological treatment of ADHD and school performance." This continues a research theme (see here). The second paper is that from Christina Mohr-Jensen and colleagues [2] which looked at "the risk of long-term conviction and incarceration associated with childhood attention-deficit/hyperactivity disorder (ADHD), and to identify risk and protective factors including associations with active treatment with ADHD medication." Again, this is a topic that has previously received quite a bit of study before (see here). Finally, I'd like to bring the paper by Stephen Becker and colleagues [3] to the blogging table, investigating whether "sleep duration is causally linked to sleepiness, inattention, and behavioral functioning in adolescents with ADHD." The answer: yes, yes it was, in line with other independent research (see here). And that potentially opens the door to intervention (see here).

Minus any sweeping generalisations from me or anyone else, the net result of these studies suggest that intervention for ADHD - primarily pharmacotherapy along the lines of what is currently indicated for ADHD - seems to have an important positive effect for many people diagnosed with ADHD. Some examples of this in action:

• School performance and ADHD: "ADHD was associated with substantially lower school performance independent of socioeconomic background factors." But the good news: "Treatment with ADHD medication for 3 months was positively associated with all primary outcomes" including higher grades and improving access to education. Such data was derived from a total sample size in the hundreds of thousands.
• Crime and ADHD: "Out of n=4,231 individuals with ADHD, n=1,355 (32.0%) had received at least one conviction compared to n=3,059 (15.6%) of the n=19,595 participants without ADHD." But... "The crime rates increased with the number of associated risks but were reduced during periods of taking ADHD medication."
• Sleep and ADHD: "Compared to the extended sleep week, parents reported more inattentive and oppositional symptoms during the restricted sleep week." The Becker study did not specifically talk about the use of intervention for sleep issues in the context of ADHD but it wouldn't be a giant leap to look at 'options' for improving sleep parameters in that context (and what knock-on effects this might have for behaviour).

Caveats? Well, correlation is not the same as causation, so even despite the 'strong' connections noted across these various studies mentioning ADHD, one cannot rule out other confounding variables playing a role. There's also the issue of balancing efficacy and safety to consider as and when any form of pharmacotherapy is introduced, something that is still being looked at with for example, methylphenidate and ADHD (paediatric ADHD) in mind [4]. I'm also minded to suggest that more fundamental work on the basis for ADHD should continue, alongside examination of the hows-and-whys of certain medicines *working* in the context of the biology of ADHD too. That, and an acceptance that medication might be but one tool in the arsenal (see here and see here and see here) to help prevent ADHD from negatively affecting a person's life and/or life chances.

But still the combined results are important. And they may well be important to those who don't quite reach all the thresholds for ADHD as a diagnosis [5] too... 

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[1] Jangmo A. et al. Attention-Deficit/Hyperactivity Disorder, School Performance, and Effect of Medication. J Am Acad Child Adolesc Psychiatry. 2019 Feb 1. pii: S0890-8567(19)30059-0.

[2] Mohr-Jensen C. et al. Attention-Deficit/Hyperactivity Disorder in Childhood and Adolescence and the Risk of Crime in Young Adulthood in a Danish Nationwide Study. J Am Acad Child Adolesc Psychiatry. 2019 Feb 11. pii: S0890-8567(19)30105-4.

[3] Becker SP. et al. Shortened Sleep Duration Causes Sleepiness, Inattention, and Oppositionality in Adolescents With ADHD: Findings From a Crossover Sleep Restriction/Extension Study. J Am Acad Child Adolesc Psychiatry. 2018 Nov 1. pii: S0890-8567(18)31914-2.

[4] Inglis SK. et al. Prospective observational study protocol to investigate long-term adverse effects of methylphenidate in children and adolescents with ADHD: the Attention Deficit Hyperactivity Disorder Drugs Use Chronic Effects (ADDUCE) study. BMJ Open. 2016;6(4):e010433.

[5] Kirova AM. et al. Are subsyndromal manifestations of attention deficit hyperactivity disorder morbid in children? A systematic qualitative review of the literature with meta-analysis. Psychiatry Res. 2019 Feb 3;274:75-90.

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"The MMR Vaccine Is Not Associated With Risk for Autism"

The quote heading this rather long post - "The MMR [measles, mumps and rubella] Vaccine Is Not Associated With Risk for Autism" - comes from a patient summary covering the the findings reported by Anders Hviid and colleagues [1].

Hviid et al utilised some of those oh-so-useful Scandinavian population registries to provide support for the hypothesis that "MMR vaccination does not increase the risk for autism, does not trigger autism in susceptible children, and is not associated with clustering of autism cases after vaccination." As per some media reporting of the study (see here), such a finding comes at a time when cases of measles in particular, are on the rise (see here) in various parts of the developing and developed world (see here) as a possible/probable consequence of specific viewpoints around vaccination (see here).

The Hviid data, as important as it is, is nothing new in terms of research that has been done on the topic of childhood vaccination and autism risk (see here). Indeed, the author is no stranger to this area of the autism research 'scene' as per other population-based cohort studies looking at "whether vaccination with a thimerosal-containing vaccine is associated with development of autism" [2]. The answer on that peer-reviewed research occasion was probably not: "results do not support a causal relationship between childhood vaccination with thimerosal-containing vaccines and development of autistic-spectrum disorders." The authors have also previously looked specifically at the MMR vaccine and autism risk too [3] albeit with caveats, some of which they addressed in this more recent investigation...

The basics this time around: look through the registry data of some 650,000 children "born in Denmark from 1999 through 31 December 2010, with follow-up from 1 year of age and through 31 August 2013." Collect and collate various information - use of "MMR and other childhood vaccinations, autism diagnoses, sibling history of autism" - and undertake some statistical analysis pertinent to the question of "whether autism developed in children who got the MMR vaccine compared with those who did not during the follow-up period." Researchers also included various potential confounders in their statistical analyses: "maternal age, paternal age, smoking during pregnancy, method of delivery, preterm birth, 5-minute Apgar score, low birthweight, and head circumference."

As per the opening paragraph, the results did not detect any link: "Comparing MMR-vaccinated with MMR-unvaccinated children yielded a fully adjusted autism hazard ratio of 0.93 (95% CI, 0.85 to 1.02)." This based on data where around 95% of the population received the vaccine (around 31,000 were classed as 'MMR-unvaccinated') and 1% (n=6,517) of the total population were diagnosed with autism. A few other observations were also noted by Hviid and colleagues: "The highest risk for autism was conferred by being a boy..., being born in a late birth cohort (2008-2010...), having no early childhood vaccinations..., and having siblings with autism at study entry." Such observations have some important links to other independent findings; for example, children with a sibling already diagnosed with autism are more likely to be diagnosed with autism (see here) and children who did not receive the MMR vaccine were actually slightly more likely to be diagnosed with autism than those who were vaccinated (a trend particularly noted in girls I believe). That last result might tie into other independent findings too (see here).

As with any research study, there were limitations attached to the Hviid investigation. So: "No individual medical chart review was performed" meaning that registry data, as strong as it is, is not the same as "medical records or direct examination of the children by research staff." The use of such population registries across a wide variety of different research topics (see here and see here for examples) carries the same limitation. I'm also minded to mention that population registry data is good for ascertaining population trends, but tends to say little about rare events. Individual issues can sometimes get lost in the statistical noise [4]. The focus of the Hviid study was also specifically on the MMR vaccine. Although not completely au-fait with the vaccination schedule in Denmark (see here) the data say little about the use of other vaccinations, their timing, and any connection (or not) to autism. And finally, I might quibble with the idea that Hviid et al looked at 'susceptible groups' on the basis of the variables they included in their 'autism risk score'. 'Smoking during pregnancy' for example has shown little to no association with autism (see here and see here) (something we can't say when it comes to offspring risk of ADHD for example). Other variables such a maternal metabolic syndrome signs and symptoms during pregnancy (see here) or maternal vitamin supplementation during pregnancy (see here) might have provided some stronger indications of autism risk/susceptibility. And then there's the recent results from Xie and colleagues [5] to also consider...

Still, the Hviid data provide further pretty powerful evidence disproving any population-wide link between MMR vaccine receipt and autism risk. The big question is whether such results, added to quite a lot of other science on this topic, are actually going to make any difference to something like vaccination rates against diseases like measles?

As per an editorial [6] accompanying the Hviid paper we live in an age where scientific data seems to have 'limited persuasive value' for some people and where the concept of 'risk' is often not well understood. The editorial authors also opine that "an alternative explanation of the perceived phenomenon should be provided" which is something else rather important. Not least because some parents, right or wrong, are still adamant that their child had a reaction to one or more of their childhood vaccinations (see here and see here). Autism research has tended to shy away from looking at this specific scenario (see here) thus leaving it unchallenged. Perhaps therefore the time is right for some brave researcher to study those children who were reported to have allegedly undergone a reaction to vaccination and see if anything is significantly 'different' about them on a behavioural and/or biological level? Whether indeed an alternative explanation could be provided for their clinical regression including the influence of variables immediately after the vaccination event [7]?

And as for the message about ensuring children (and adults, particularly vulnerable adults) are vaccinated and protected against diseases, I once again turn to the writings of Roald Dahl, and how measles devastated his family (see here) and what vaccination would have meant to his daughter. A powerful personal message that perhaps needs to be used a little more often alongside the dissemination (and translation) of scientific data to promote the benefits of vaccination to individuals and populations alike...

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[1] Hviid A. et al. Measles, Mumps, Rubella Vaccination and Autism: A Nationwide Cohort Study. Ann Intern Med. 2019 Mar 5.

[2] Hviid A. et al. Association between thimerosal-containing vaccine and autism. JAMA. 2003 Oct 1;290(13):1763-6.

[3] Madsen KM. et al. A population-based study of measles, mumps, and rubella vaccination and autism. N Engl J Med. 2002 Nov 7;347(19):1477-82.

[4] Poling JS. et al. Developmental regression and mitochondrial dysfunction in a child with autism. J Child Neurol. 2006 Feb;21(2):170-2.

[5] Xie S. et al. Family History of Mental and Neurological Disorders and Risk of Autism. JAMA Network Open. 2019; 2: e190154.

[6] Omer SB. & Yildirim I. Further Evidence of MMR Vaccine Safety: Scientific and Communications Considerations. Ann Intern Med. 2019 Mar 5.

[7] Schultz ST. et al. Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Autism. 2008 May;12(3):293-307.

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Childhood lead (Pb) exposure and "greater psychopathology across the life course"

I've talked about the effects of lead (Pb) on cognition, behaviour and psychology before on this blog (see here and see here for examples). A (heavy) metal with no confirmed biological function, lead represents something that pretty much everyone should be avoiding exposure to, despite it still being used in everything from roofing materials to batteries. The findings reported by Aaron Reuben and colleagues [1] add further to the 'avoid lead' sentiments, and specifically how: "Childhood lead exposure may have long-term consequences for adult mental health and personality."

The aim of the Reuben paper was to conduct "the longest and largest psychiatric follow-up to date in a cohort of adults who were lead exposed and lead tested as children." Participants and their data came from "the Dunedin Multidisciplinary Health and Development Study, a longitudinal investigation of health and behavior in a birth cohort." This study specifically drew on data from over 500 Dunedin study members who were tested for lead exposure around age 11 years and were followed up until their late 30s. A range of psychometric measures were employed in adulthood to complement participants' blood lead test results during childhood, including "(1) repeated clinical interviews assessing psychopathology symptoms across adulthood up to 38 years of age; (2) comprehensive, dimensional measures of psychopathology that account for severity, comorbidity, and reoccurrence; and (3) a broad measure of adult personality (Big Five Personality Inventory)... that did not rely on self-report." Importantly, researchers relied on a sample where "the extent of children's exposure to lead was unrelated to their socioeconomic origins."

Results: most of the cohort (over 90%) had tested blood lead levels above the 5 μg/dL level that the US CDC currently describes as a "reference value for clinical attention." This threshold value replaced the 10 μg/dL level that used to be thought to be important. Indeed within the Reuben cohort: "The mean (SD) blood lead level was 11.08 (4.96) μg/dL."

Researchers also observed that: "After adjusting for covariates, each 5-μg/dL increase in childhood BLL was associated with a 1.34-point increase... in general psychopathology." Covariates included "family socioeconomic status, maternal IQ, and family history of mental illness." This seemingly dose-dependent relationship looked to be quite important.

Onward: "study members with higher BLLs [blood lead levels] at 11 years of age were viewed in adulthood by their informants as more neurotic..., less agreeable..., and less conscientious" than those with lower levels. Personality it seems *might* also be affected by childhood lead exposure (at least partially). These and other factors lead Reuben et al to conclude that: "the association between lead exposure and psychopathology may begin to manifest broadly well before adulthood" and "early-life lead exposure in the era of leaded gasoline experienced by individuals who are currently adults may have contributed to subtle, lifelong differences in emotion and behavior that are detectable at least up to 38 years of age."

I know there are caveats to this type of observational work - "there was only one time point of lead testing" - and even controlling for some potential covariates does not mean that the total spread of covariates has been covered in this study. Personally, I'm not overly enthused by the whole personality types bit either; particularly in light of further revelations about some of the historical proponents of such an idea (see here). But taken as part of a wider series of research on lead exposure and psychopathology, the Reuben work is in line with other results on how an environmental factor can seemingly affect both development and psychopathology. And minus any sweeping generalisations about psychopathology and crime, the so-called 'lead-crime hypothesis' under the guise of biosocial criminology for example, doesn't exactly suffer as a result of the Reuben findings...

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[1] Reuben A. et al. Association of Childhood Lead Exposure With Adult Personality Traits and Lifelong Mental Health. JAMA Psychiatry. 2019. Jan 23.

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'Stimming' and autism: an insiders perspective

"Autistic adults highlighted the importance of stimming as an adaptive mechanism that helps them to soothe or communicate intense emotions or thoughts and thus objected to treatment that aims to eliminate the behaviour."

So said the findings reported by Steven Kapp and colleagues [1] (open-access available here) who analysed the viewpoints of around 30 autistic adults (or adults with autism if you prefer) on the topic of self-stimulatory behaviour 'reclaimed' as stimming. Said participants aged between 21 and 56 years old, were recruited "through residential homes specialising in housing autistic adults, a training centre for autistic adults and existing networks." All were formally diagnosed with autism; something that might be particularly important when it comes to the specific patterns of behaviour under study (see here).

Before proceeding, a question: What is stimming? Well, I found one particularly good article describing stimming (see here) as something that "somebody is doing... to give themselves sensory input." In clinical terms, stimming falls under the category of repetitive behaviours, and covers quite a wide array of presentations ranging from flicking fingers in front of the eyes, to more pronounced body movements such as rocking, jumping or walking on tiptoes (see here) and lots more in-between. The source website describing stimming that I just highlighted also lists "banging one’s head on the floor" as a stim; something I'll come on to shortly.

"Autistic people have become increasingly mobilised and vocal in defence of stimming" is an important starting point raised in the Kapp paper, as some "believe that stims may serve as coping mechanisms, thus opposing attempts to eliminate non-injurious forms of stimming." Not surprisingly accompanying such sentiments, Kapp et al identified a couple of primary themes garnered from their interviews of said study participants: "stimming as (1) a self-regulatory mechanism and (2) lacking in social acceptance, but can become accepted through understanding." Important stuff.

There are a couple of 'issues' that interrupt the important messages presented by Kapp, as 'psychobabble' seemingly creeps into some of the text. For example: "Several participants internalised the stigmatisation of stimming, with ambivalent attitudes despite recognising the utility of their stims." Internalised stigma? What exactly does that mean and how was it objectively tested for? As I said psychobabble. I also note that there is a hint of a socio-political side to the Kapp paper, as per quotes like the findings "suggest that many autistic adults agree with the neurodiversity movement’s opposition to eliminating all forms of stimming across all contexts (e.g. traditional uses of early intensive behavioural intervention) and desire for society to accept non-harmful forms of stimming." This in the context that some people on the autism spectrum have for example, voiced concerns about the use of techniques such as applied behavioural analysis (ABA) in the context of autism, and the accusation that "they basically condition them like Pavlov’s dogs to stop stimming." I'm not so sure that every single occasion when ABA or other intensive behavioural intervention is used in the context of autism is quite that forthright in their aims and objectives (i.e. stopping all stimming), but ho-hum. And whist I've mentioned the concept of neurodiversity, well, let's just say that such a movement is still seemingly very much in its infancy on lots of different matters (see here).

What else? Well in amongst the various good points raised in defence of stimming, another side to such behaviour is also discussed in the Kapp paper: harms. So: "Participants gave several examples of stimming behaviours that caused physical harm to themselves (with no evidence of intentional self-injury), which they did not find helpful, regardless of social context." It's important that this side of stimming is discussed as per my previous mention of head-banging. I say this also because stimming might not just solely be a self-stimulatory behaviour but rather also reflective of various other processes too [2] including "stimming caused by uncontrollable thoughts." If one for example assumes that stress and anxiety (something which may be a lot more 'core' to autism than hitherto reported) are part-and-parcel of some stimming behaviours used on some occasions, the logical next step is to ask what is being done to address something like anxiety as a possible trigger. Again minus any psychobabble, there are further studies that could be undertaken (see here). And as for the notion that there is "potential evidence of the spread of the movement through the report of teaching oneself how to stim via online resources" well, let's just say that someone, somewhere making such 'online resources' probably doesn't have a great understanding of the wide (wide!) complexity surrounding stimming...

The Kapp paper provides an important [autistic] perspective on stimming. It suggest that as part of a core feature of autism, stimming should not always be viewed as a 'negative thing' provided that it does not harm or significantly interfere with a person's quality of life or that of others. As per the possibility of an 'anxiety link' to some stimming, one also needs to recognise that the presence of stimming might be reflective of some unmet need and make any possible (reasonable) adjustments. And if you happen to see someone rocking or flapping their hands in a public place, don't stare, don't snigger, and as long as they don't seem to be in distress or causing any distress, just let them be...

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[1] Kapp SK. et al. 'People should be allowed to do what they like': Autistic adults' views and experiences of stimming. Autism. 2019 Feb 28:1362361319829628.

[2] Cunningham AB. & Schreibman L. Stereotypy in Autism: The Importance of Function. Res Autism Spectr Disord. 2008;2(3):469-479.

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"Ashleigh's vision problems were misdiagnosed as autism"

The quote titling this post - "Ashleigh's vision problems were misdiagnosed as autism" - comes from a TV programme that was picked up by the BBC news website recently.

It continues a theme in recent times showing examples where autism has been seemingly 'misdiagnosed' (see here and see here) at the cost of other recognised medical conditions being present. Such misdiagnoses have many potential implications; not least for the various trends in some quarters to 'self-diagnose' autism or self-identify as autistic without any formal assessment seemingly being undertaken (see here and see here).

So what was the misdiagnosed condition this time around? Well, it's potentially an important one because is covers a topic rather salient to autism: vision and the processing of visual (sensory) information (see here for example). To quote: "After being misdiagnosed with Asperger syndrome, Ashleigh later found out that her behavioural problems actually came from Cerebral Visual Impairment (CVI)." When describing CVI, the key point I get from the descriptive literature is that vision is not just about the eyes but also what the brain does to/with the visual information collected through the eyes.

Aside from the label 'Asperger syndrome' disappearing from diagnostic texts and discussions for various reasons (see here and see here), a quick glance at some of the information on CVI reveals that the potential misdiagnosis of autism when CVI was present is not something entirely new (see here). To quote from the RNIB (Royal National Institute for the Blind) website here in Blighty: "Many of the standard special needs assessments generally fail to identify children with CVI. If anything there is a danger that they may be misdiagnosed as possibly having autistic spectrum condition, due to some of the characteristics being shared. Not being able to maintain eye contact or respond to facial expressions, may be due to poor contrast sensitivity or to the part of the brain that recognises facial expressions being impaired." They don't however discount the idea that CVI and autism can co-occur - "Of course CVI and autism can co-exist" - something that an expert I mentioned this study to confirmed and something noted in the peer-reviewed science literature [1] too. But misdiagnosis is also a potential risk.

I'm not going to say too much more on this topic aside from reiterating an oft-mentioned phrase on this blog: the diagnosis of autism should be a starting point for further investigations and not the finishing line. I appreciate that to many people - individuals and their parents/caregivers - the time and effort spent actually getting and going through assessment and diagnosis of autism feels like it should be the finishing line (see here). But please, don't stop there. Keep questioning and importantly, keep screening, and screening for lots of different things. As per the example of Ashleigh, there may be lots more to see (pardon the pun) and in some cases, potentially novel and important 'intervention' avenues to consider to improve quality of life [2]...

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[1] Bosch DG. et al. Cerebral visual impairment, autism, and pancreatitis associated with a 9 Mbp deletion on 10p12. Clin Dysmorphol. 2015 Jan;24(1):34-7.

[2] Bartel T. Mystery solved: Our son's autism and extreme self-injury is genetic and treatable. Am J Med Genet A. 2017 May;173(5):1190-1193.

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On gut bacteria and depression

I'm kinda standing on the shoulders of giants with this post talking about the findings reported by Mireia Valles-Colomer and colleagues [1]. An editorial published in Nature [2] to coincide with the publication of the Valles-Colomer paper says just about everything that needs to be said on this research, which observed that: "Gut–brain module analysis of faecal metagenomes identified the microbial synthesis potential of the dopamine metabolite 3,4-dihydroxyphenylacetic acid as correlating positively with mental quality of life and indicated a potential role of microbial γ-aminobutyric acid production in depression." Yes folks, the idea that "microorganisms in the human gut could influence the brain" is moving from 'wild idea' to "wise pursuit".

The sequencing of DNA from donor stool samples as part of the Flemish Gut Flora Project ('You too are a walking bacteria colony' is the strap line) was the starting point for the Valles-Colomer study; stool samples provided by over 1000 participants. Researchers also accessed data on both self-reported and "physician-diagnosed depression" and set to work looking for any potentially important correlates between bacteria and psychology. The words "with validation in independent data sets (ntotal = 1,070)" are also (importantly) mentioned in the Valles-Colomer paper. Oh, and they also "mined the data to generate a catalogue describing the microbiota’s capacity to produce or degrade molecules that can interact with the human nervous system."

Results: "Butyrate-producing Faecalibacterium and Coprococcus bacteria were consistently associated with higher quality of life indicators." There's that word again: butyrate and yet more positive publicity for this compound (see here) and it's standing reaching almost 'bacterial sainthood'. Researchers also observed that two groups of bacteria were also reduced in those with depression: Coprococcus and Dialister alongside observing that this finding held "even after correcting for the confounding effects of antidepressants [use]." And then there was that 3,4-dihydroxyphenylacetic acid, also called DOPAC, finding, a metabolite of the neurotransmitter dopamine. I have actually mentioned DOPAC before on this blog (see here) in relation to what happens when rats are subjected to 'early immune stimulation' [2]. I don't think there is much overlap between that rat study and the Valles-Colomer paper (that rat paper was looking at DOPAC levels in brain tissue for example) but the suggestion from the authors that DOPAC levels were "correlating positively with mental quality of life" requires quite a bit more investigation.

Caveats? Well, out of their initial 1054 participant cohort, only 121 participants had "GP-reported depression." About half of these participants were taking antidepressants for their depression, the others weren't. The participant numbers aren't exactly tremendous for this portion of the study. Similar to something mentioned in other research (see here), I'm also minded to suggest that future research might perhaps consider looking at multiple stool samples taken over different occasions for the same person. This would perhaps establish whether gut bacterial populations are stable and whether that stability translates into stability of something like depressive symptoms too. I am likewise cautious that we don't jump ahead of ourselves here in terms of important issues like cause-and-effect and for example; whether there may be other important 'influencers' of gut bacteria when it comes to depression (see here and see here).

Lots more study is required on the suggestion of a gut bacterial *link* to depression [3], including that focused on the mechanics of any relationship (e.g. any involvement of the vagus nerve). If the link is further established, there are a number of potentially important implications: the possibility of a 'bacterial transferability hypothesis of [some] depression' (see here), intervention options focused on redressing balance in bacterial colonies (see here) and what such findings might do for the whole 'gut-brain axis' idea.

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[1] Valles-Colomer M. et al. The neuroactive potential of the human gut microbiota in quality of life and depression. Nature Microbiology. 2019. Feb 4.

[2] Editorial. Links between gut microbes and depression strengthened. Nature. 2019. Feb 4.

[3] Cheung SG. et al. Systematic Review of Gut Microbiota and Major Depression. Front Psychiatry. 2019;10:34.

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