"Depression, dysthymia and symptoms of anxiety and post-traumatic stress are associated with extremist sympathies"

It's a particularly poignant time to be writing this post about the findings reported by Kamaldeep Bhui and colleagues [1] on the day that news broke about events in New Zealand (see here). An all-too-familiar story of hate leading to bloodshed helped along by access to weapons; communities are left scared, confused and broken following such acts of depravity.

Although snippets of information about the events leading to the New Zealand murders are still at the time of writing coming to light, the incident is being treated as a terrorist attack. News agencies have converged on the suspect; the life behind such crimes and any possible motives. Discussions will eventually lead to inevitable questions about what motivates someone to kill innocent people under such circumstances and on such a horrific scale, and could such an act have been foreseen and potentially avoided.

The Bhui findings hopefully represent a part of that inquiry as per their focus on trying to "better understand the drivers of radicalisation and extremist attitudes more generally, and the links with symptoms of psychological and mental illnesses." I say the Bhui findings might help, but also reiterate that at the time of writing, we don't know for example, whether 'psychological and mental illness' was part-and-parcel of the motivation for the New Zealand attacks.

The basics: a study based here in Blighty, researchers recruited over 600 adults (18-45 years of age) and asked various questions and for various bits of information. They asked for information about psychiatric variables such as depression (depressive symptoms), dysthymia "(i.e. persistent mild depression, or depressive personality)", personality disorder symptoms and symptoms related to post-traumatic stress disorder (PTSD). We're also told that: "Autism symptoms were measured by using a total score on the Autism Spectrum Quotient (AQ-10), which is reported as having high discriminant validity for those with and without a clinical diagnosis." I'll come back to that sentence shortly. Alongside, participants completed something called the "'SyfoR': Sympathies for Radicalisation" tool. As the name suggests, the instrument is used to gauge sympathies to "(a) committing minor crime, (b) committing violence… in political protests, (c) organising radical terrorist groups, (d) threatening to commit terrorist actions, (e) committing terrorist actions… as a form of political protest, (f) using bombs and (g) using suicide bombs to fight against injustices." Respondents are categorised as sympathisers, condemners or neutral. It appears that Bhui has played an integral part in developing the SyfoR tool.

Results: bearing in mind this was a study of extremist beliefs, not extremist actions, and mental health, researchers observed that: "SVPT [sympathies for violent protest and terrorism] were more common in those with major depression with dysthymia..., symptoms of anxiety... or post-traumatic stress." Perhaps just as important, we are told that: "Autism and personality disorder scores were not associated with SVPT" which kinda ties in with a judgement recently (see here). I say that bearing in mind that the AQ might be picking up quite a bit more than just a possible 'clinical diagnosis' of autism (see here) and reference to the growing research literature on how vulnerability is something to consider when autism is mentioned in several contexts (see here and see here). What else? Well, age played a factor (younger people were more likely to display SVPT) and SVPT was more commonly noted in those who drank, smoked and reported having a previous criminal conviction. Also of important note was the finding that: "SVPT were shown by 15.1% of the White British and 8.1% of the Pakistani groups" taking into account that half of participants were White British and half were of Pakistani heritage.

I don't want to get too carried away with sweeping generalisations stemming from the Bhui results but one can't help but wonder about the potential implications. As the authors opine: "in the absence of links with extremist groups or histories of extremist offending, the presence of mental illnesses may add risk" when it comes to SVPT. Onward: "A more general approach to improving population mental health alongside prevention in specific populations such as those experiencing post-traumatic symptoms and younger people may be helpful." I say all that being very careful not to stigmatise any individual or any group of people.

But there are concerns too. Concerns that for example, with the data suggesting that more and more young people are suffering with mental ill-health (see here) so this *might* potentially tie into some of the Bhui conclusions minus any sweeping generalisations...

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[1] Bhui K. et al. Extremism and common mental illness: cross-sectional community survey of White British and Pakistani men and women living in England. Br J Psychiatry. 2019 Mar 15:1-8.

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"In the milder forms I think it's just a personality variant." Temple Grandin on autism

I draw your attention today to the transcript of an interview (see here) between a Scottish broadcaster, Rona Dougall, and Dr/Prof.Temple Grandin, following Prof. Grandin's recent appearance (Spring 2019) at a conference in Scotland.

The transcript provides readers with quite a lot of insight into Prof. Grandin's views about autism; both from a personal perspective of being diagnosed with autism (and perhaps being one of the most well-known autistic people) and also with reference to some wider discussions about autism.

Alongside the important message that Grandin wants to "see people that learn differently, people that might be labelled with autism getting good jobs" one particular part of the interview stuck out for me: "Rona: How do you define and diagnose autism? Temple: In the milder forms I think it's just a personality variant. In the more severe forms, where the individual remains nonverbal, that is definitely a disability."

I was interested in the notion that 'milder forms' of autism were seen as akin to "a personality variant" by Grandin, whilst more 'severe forms' were labelled "definitely a disability." Interested because, there are some on-going debates in various circles about (a) how one should 'classify' autism from the point of view of how much of an impact symptoms have on daily living, and (b) how the presentation of autistic traits are not solely confined to a diagnosis of autism or autism spectrum disorder (ASD).

On the first point about 'classifying' autism, there is, as I say, debate about how symptoms can variably present and how best to describe the 'differences' between someone diagnosed as being on the autism spectrum who for example, is verbal, is able to navigate the social world to some degree, hold down a job and perhaps raise a family, compared with someone who has no (verbal) language, requires a high level of daily living support and who is likely to need lifelong assistance and support for sometimes simple tasks. Such heterogeneity has been present for many years under the diagnostic label of autism; further compounded by the recent-ish disappearance of Asperger syndrome in current and planned diagnostic texts (see here and see here).

The commonly used terms 'high-functioning' and 'low-functioning' don't seemingly provide the necessary words to differentiate 'levels of autism'; also being perhaps a little demeaning to those they are meant to represent. Outside of the negative connotations of 'low-functioning', one can perhaps see how 'high-functioning' as a term for 'can function' does not always convey the real-life message when it comes to the presentation of autism. I'm thinking specifically about the issue of suicidality and autism for example (see here) and the shocking statistics that continue to emerge. Likewise, to talk about autism in the context of 'severity' comes up against similar obstacles. 'Severe autism' could potentially describe anyone on the autism spectrum during moments of 'meltdown' for example. Indeed, the 'high-functioning' non-severe autistic child who just got handed a school exclusion for having an aggressive meltdown (yes, I said aggression) in class may very well be described as having severe autism in the same way that a 'low-functioning' child screaming and banging their head whilst covering their ears may thus be described. The endpoint in both cases being that autism is significantly and severely affecting both their lives at that point. I firmly believe a lot more thought needs to go into such 'classification' issues (see here) including more mention of the concept of 'profoundness' and perhaps further utilisation of the DSM-5 'support gradings' (see here) which have been installed.

Insofar as the second point covering 'mild' autism as a 'personality variant' and the issue that the label autism does not have exclusive rights to the presentation of autistic traits, another area of interest opens up. I've talked quite a bit on this blog about how autistic features / traits / symptoms are readily seen across a whole variety of different labels (see here and see here) and what this means for the concept of 'self-diagnosis' for example, that is sometimes seen / discussed on social media in particular (see here). Drawing specifically on the presentation of autistic traits in something like borderline personality disorder (BPD) [1] one could very well express an opinion that yes, autism in some cases may well be akin to a personality variant. Such a line of reasoning fits well with the (still emerging) concept of neurodiversity as applied to autism (see here) where autism is viewed as a "natural variation" [2].

But then the questions arise: at what point does autism cease to be a 'personality variant' to then becoming 'definitely a disability'? Is it just based on the acquisition of spoken language? Grandin does mention a few times in the interview about autism "in the milder forms, where the person is fully verbal" so perhaps showing an inclination towards a view that spoken language use is an important measure to differentiate differences vs. disability. But does reliance on spoken language use offer enough to make such a differentiation? Are their other facets of autism (or combinations of facets) which could better reflect any difference vs. disability arguments?

Personally, I'm not inclined to believe that there is a personality variant vs. definite disability debate to be had when it comes to autism. Formal receipt of a diagnosis is based not only on the presentation of autistic features or traits but also that such traits "cause clinically significant impairment in social, occupational, or other important areas of current functioning." If one was to say that some autism is just a personality variation, it could for example, dissipate the meaning of autism and the supports that are required. The risk of 'diluting' an important message about the need for those services and resources to ensure that people across the autism spectrum and their loved ones get the help and support they need to have a good quality of life is not a risk, in my view, worth taking.

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[1] Dell'Osso L. et al. Correlates of autistic traits among patients with borderline personality disorder. Comprehensive Psychiatry. 2018; 83: 7-11.

[2] den Houting J. Neurodiversity: An insider's perspective. Autism. 2019 Feb;23(2):271-273.

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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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Pigeons, meet cat: "The Hans Eysenck affair: Time to correct the scientific record"

I'm heading off-piste with my musings today, drawing your attention to a paper by Anthony Pelosi [1] and an accompanying editorial by David Marks [2] (both open-access) that are likely to 'put the cat among the pigeons' in some quarters (with thanks to Matthew Dalby for bringing the Pelosi study to my Twitter attention). Indeed, the publishing journal - The Journal of Health Psychology - is no stranger to 'cat among the pigeons' discussions, as per their 2017 special edition [3] on the PACE trial "for patients with myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS)." Perhaps interestingly, there is a 'psychosomatic' connection between the topic covered in the Pelosi paper and those critical musings on how to (or perhaps how not to) treat ME/CFS...

The person at the centre of the Pelosi paper is the late Prof. Hans Eysenck; a figure who anyone with the slightest interest in the discipline called psychology would probably have heard of. Personality was one of the major research interests for Eysenck, and in particular, the proposal of dimensions to personality: extroversion/introversion, neuroticism/stability, psychoticism/socialisation. Perhaps not as famously known about, but still influential, were Eysenck's views relating to "his persistent denial of the carcinogenic effects of tobacco." Indeed, his 'alternative view' that "certain personality traits that lead to smoking also increase the risk of developing cancer" is starting to look decidedly 'shaky' in modern times. More so when there is talk of 'funding' and 'sources of funding' potentially complicating the issue.

Pelosi (and Marks) make a case that the time is right for psychology and various other interconnected disciplines to start looking more critically at the collected published work of Eysenck and some of his colleagues. They argue that claims "about the alleged effectiveness of psychotherapy in preventing cancer" or that "behaviour therapy may be useful in prolonging life, as well as in preventing disease" have little place in modern, evidence-based, science and medicine. Pelosi - who has some important history of being slightly critical of some of Eysenck's findings alongside other notable names - also goes one stage further in suggesting that some of the "widely cited studies" published with Eysenck's name attached "have had direct and indirect influences on some people’s smoking and lifestyle choices." Further: "This means that for an unknown and unknowable number of individual men and women, this programme of research has been a contributory factor in premature illness and death." Strong words indeed.

Marks ends his editorial with open letters to the President and Principal of King's College London and the Chief Executive of the British Psychological Society (BPS) calling for further investigation of the points highlighted in the Pelosi paper. Pelosi has seemingly approached the BPS previously on this matter but apparently did not receive a particularly warm reception to his then request for further investigation of some of the science and conclusions made in this area (see here). Whether such a second request - made in the era of social media - will be acted upon differently this time is a 'wait and see' question. All of this taking into account the moves being made to make psychology a more credible science these days...

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[1] Pelosi AJ. Personality and fatal diseases: Revisiting a scientific scandal. Journal of Health Psychology. 2019. Feb 23.

[2] Marks DF. The Hans Eysenck affair: Time to correct the scientific record. Journal of Health Psychology. 2019. Feb 23.

[3] Marks DF. Special issue on the PACE Trial. Journal of Health Psychology. 2017. July 31..

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"Childhood seizures and risk of psychiatric disorders in adolescence and early adulthood"

I want to bring the findings reported by Julie Dreier and colleagues [1] to your attention today and their observation that: "Children with epilepsy and febrile seizures-with and without concomitant epilepsy-are at increased risk of developing a broad range of psychiatric disorders in later life."

Researchers report results based on the examination of one of those ever-so-impressive Scandinavian population registries that have moved science forward in many, many different areas (see here for example). This time around it was the Danish National Patient Register and the inclusion of data from "1 291 679 individuals... born in Denmark and followed up in our population cohort (approximately 15 million person-years)." Over 43,000 individuals showed a history of febrile seizure - "fits that can happen when a child has a fever" - and over 10,000 had epilepsy. Likewise: "83 735 (6%) cohort members were identified with at least one of the psychiatric disorders of interest" including substance abuse disorders, schizophrenia, mood disorder, anxiety, and personality disorder.

Results: "The risk of any psychiatric disorder was raised in individuals with a history of febrile seizures..., epilepsy..., or both disorders." The magnitude of the risk was categorised as statistically significant in terms of elevation but ranged from between a 10-50% increased risk. Further: "Excess risk of psychiatric illness associated with childhood seizures was present across a range of different disorders, most notably schizophrenia but also anxiety and mood disorders." Authors also opine that further research is needed on this topic with regards to mechanisms pertinent to identifying "potential options for prevention."

Although some caution is always required when one variable (epilepsy) is solely correlated with another (history of recorded psychiatric diagnosis), I am interested in the Dreier findings. I'm interested not only because of the *association* being made between a condition that often has life-changing effects on other often life-changing diagnoses but also because this *association* complements other links being made with epilepsy. I speak of the various studies linking epilepsy to diagnostic labels such as autism and attention-deficit hyperactivity disorder (ADHD) of course (see here and see here for examples) whilst pointing out that ADHD and autism are not to be categorised as mental health conditions. Such links between epilepsy and neurodevelopmental diagnoses are all the more interesting because the presence of labels such as autism and ADHD are also known to manifest elevations in other psychiatric diagnoses such as mood disorder, anxiety and schizophrenia (see here and see here and see here for examples). It's not therefore unreasonable to suspect that there may be some 'over-arching' themes when it comes to epilepsy/febrile seizures 'linking' with various developmental and psychiatric diagnoses.

Minus any sweeping generalisations and being careful how I phrase this, one area that requires a lot more investigation is the neurological effect that epilepsy in particular can have. I speak of the idea that seizures can, in some cases, affect the physical nature of the brain [2] and the question of whether such 'damage' might also then affect the presentation of behaviour akin to the signs and symptoms of a neurodevelopmental or psychiatric diagnosis. I know this is not a particularly palatable line of thinking but it does require further scientific exploration. This is also pertinent to the Dreier study focusing in on childhood seizures and by inference, possible effects on the developing brain. Another area of further investigation is whether the presentation of epilepsy or seizures *might* be part-and-parcel of various syndromes also presenting with neurodevelopmental and/or psychiatric features? We do have some examples of this already (see here) and, given that various genetic syndromes are quite regularly being identified day-by-day, it's another area that could yield some important data.

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[1] Dreier JW. et al. Childhood seizures and risk of psychiatric disorders in adolescence and early adulthood: a Danish nationwide cohort study. Lancet Child Adolesc Health. 2018 Dec 6. pii: S2352-4642(18)30351-1.

[2] Bronen RA. et al. The Status of Status: Seizures Are Bad for Your Brain's Health. American Journal of Neuroradiology. 2000; 21: 1782-1783.

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What does the Autism Spectrum Quotient (AQ) actually measure?

"Higher AQ [Autism Spectrum Quotient] scores were associated with higher scores of loneliness, social anxiety, depression, and anxiety, as well as with lower scores of quality of life (QoL)."

Those were some of the key findings reported by Phil Reed and colleagues [1] who used the very popular 'are you autistic?' AQ screening tool to look at the presence of autistic traits "along with depression, anxiety, loneliness, quality of life, and social anxiety" in a University student cohort (N=413).

Finding that among their research population some 8% scored above the cut-offs used by the AQ, researchers also reported those important 'associations' all tied into QofL.

Accepting that I'm probably a little biased when it comes to the 'problematic' use of the AQ as a screening tool for autism (see here and see here), my interpretation of the Reed results plays into the idea that the AQ is certainly picking up something, but exactly what is still the source of some debate (see here). I might for example, point you in the direction of the findings by Kitazoe and colleagues [2] who, based on similar student cohort, talked about "qualitatively different groups" over and above "a single homogeneous group" when it came to high scorers on the AQ.

It is also pretty well accepted that issues such as social anxiety and depression are over-represented when it comes to a diagnosis of autism (see here and see here respectively) and one has to wonder whether the AQ might be tuned into to the features of those labels over and above core autism. Indeed, going back a few years, the findings reported by Kunihira and colleagues [3] kinda signalled as much where personality traits "toward an obsessional personality" were seemingly connected to AQ scores in a non-autistic population as well as "higher depression and anxiety." Such findings might also be 'useful' when it comes to looking at the AQ in the context of eating disorders too [4].

I look forward to seeing more research done on this important topic (something ripe for more University student research projects perhaps).

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[1] Reed P. et al. Loneliness and Social Anxiety Mediate the Relationship between Autism Quotient and Quality of Life in University Students. J Dev Phys Disabil. 2016. Aug 12.

[2] Kitazoe N. et al. Whether the Autism Spectrum Quotient consists of two different subgroups? Cluster analysis of the Autism Spectrum Quotient in general population. Autism. 2016 Apr 30. pii: 1362361316638787.

[3] Kunihira Y. et al. 'Autistic' traits in non-autistic Japanese populations: relationships with personality traits and cognitive ability. J Autism Dev Disord. 2006 May;36(4):553-66.

[4] Mansour S. et al. Emotions mediate the relationship between autistic traits and disordered eating: A new autistic-emotional model for eating pathology. Psychiatry Res. 2016 Aug 8;245:119-126.

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Reed, P., Giles, A., Gavin, M., Carter, N., & Osborne, L. (2016). Loneliness and Social Anxiety Mediate the Relationship between Autism Quotient and Quality of Life in University Students Journal of Developmental and Physical Disabilities DOI: 10.1007/s10882-016-9504-2

Fermented foods and social anxiety?

Stumbling across a headline that reads: 'Study Finds Decreased Social Anxiety Among Young Adults Who Eat Fermented Foods' was bound to pique my blogging interest. When I eventually tracked down the source paper behind the headline I became more and more intrigued as today I bring to your attention the study findings reported by Matthew Hilimire and colleagues [1].

Implementing "a cross-sectional approach to determine whether consumption of fermented foods likely to contain probiotics interacts with neuroticism to predict social anxiety symptoms" researchers asked over 700 students - psychology students - to self-report on "fermented food consumption, neuroticism, and social anxiety." Fermented foods by the way, cover a range of foods "that contain probiotics" including yogurt and sauerkraut (a particular favourite of mine). Researchers also enquired about various other variables such as fruit and vegetable intake and the amount of exercise taken over the past 30 days.

Bearing in mind that this was a study based on self-report and that psychology students might not be entirely representative of the population in general, the results of an "interaction model, controlling for demographics, general consumption of healthful foods, and exercise frequency" did seem to suggest that there may be more to see when it comes fermented food consumption and social anxiety: "Fermented foods should be further investigated as an intervention for social anxiety."

I'm not falling hook, line and sinker for these results - correlation is not the same as causation - despite my continuing interest in the science of psychobacteriomics (my word creation) and the idea that those trillions of wee beasties that inhabit our deepest, darkest [gut] recesses might be doing so much more than just helping to digest food and making the odd nutrient or two. I do however think that we need to dedicate quite a few more resources to the idea that psychology and behaviour might not be solely rooted in the grey-pink matter floating in our skull [2] as recent news articles seem to imply.

Finally, and without wishing to make too many sweeping generalisations from the Hilimire results, I did think about whether such findings may be particularly 'useful' for certain groups of people where social anxiety might be over-represented. Autism is an obvious label given the suggestion that at least a quarter of those on the autism spectrum might also fulfil the diagnostic criteria for social anxiety disorder (see here). That such anxiety might also have knock-on effects to the presentation of more core autism symptoms (see here) is also noteworthy bearing in mind that a diet rich in fermented foods might not be for everyone and that social anxiety with or without autism is bound to be a very complicated process.

We await further research in this area.

Music: The Flaming Lips - Do You Realize??

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[1] Hilimire MR. et al. Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry Res. 2015; 228: 203-208.

[2] Dinan TG. et al. Collective unconscious: how gut microbes shape human behavior. J Psychiatr Res. 2015 Apr;63:1-9.

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Hilimire MR, DeVylder JE, & Forestell CA (2015). Fermented foods, neuroticism, and social anxiety: An interaction model. Psychiatry research, 228 (2), 203-8 PMID: 25998000

Impulsivity and uric acid

A few years back I posted about an interesting body of research on purine metabolism in relation to the autism spectrum disorders (ASDs) and how some work from the likes of Mary Coleman and Ted Page had reported high levels of uric acid to be coincidentally present in cases of ASD.

The gout @ Wikipedia  

As with other research angles, the initial interest in this finding of hyperuricosuria - elevated urinary uric acid - and autism did not seem to last. Just like the dusty research doll that is sulphation (sulfation) and autism, uric acid came to find itself under the autism research bed listening to the tune of 'when somebody loved me'. Sulphation, I might add with autism in mind, has started to see something of a renaissance recently but only a small one (see here).

Enter then an intriguing paper by Angelina Sutin and colleagues* reporting on an association between elevated levels of uric acid and impulsivity as a trait in both human and mice. As per another recent paper which was discussed on this blog on ADHD and solar intensity, the publishing journal was Biological Psychiatry which is fast becoming a real favourite journal of mine. Reading through Dr Sutin's profile page it is interesting to note that she has some interest in how personality might be associated with physical and mental health. Her latest paper therefore continues this interesting theme.

A few details from the Sutin paper are in order:

• This was a study drawing on both human and mouse model data to ascertain whether the findings of elevated uric acid in behavioural and psychiatric conditions "characterized by high impulsivity" might actually be specifically related to the impulsivity trait.
• Human participants (N=6883) derived from two cohorts - SardiNIA and the Baltimore Longitudinal Study of Aging - completed the Revised NEO Personality Inventory which aims to characterise the Big Five personality traits (openness, conscientiousness, extraversion, agreeableness, neuroticism) via self-report.
• They also provided fasting blood samples which were screened for uric acid both at time of schedule completion and at follow-up (some 3-5 years later).
• A second study was also reported looking at the behaviour of mice "urate oxidase null" = bred to show elevations in uric acid, compared with wild-type controls. 
• Results: lots of them, but a few of the more interesting findings included (i) impulsiveness and excitement seeking individuals were more likely to have higher levels of uric acid (albeit mediated by factors such as BMI and smoking which themselves pose some interesting questions), and (ii) "homozygous urate oxidase-deficient mice" (high uric acid) showed a lot more exploratory and "emotional" behaviour. 
• In short, the two experiments reported "supports the hypothesis that impulsivity is associated with higher levels of uric acid".
• Another quote from the paper sums up where this kind of research could potentially lead: "The identification of biological markers of impulsivity may lead to a better understanding of the physiological mechanisms involved in impulsivity and may suggest potential targets for therapeutic intervention".

Very interesting stuff I'm sure you'll agree. Indeed the participant numbers for the human part of the study are certainly impressive and indeed across the two geographically distinct cohorts too, even more impressive.

But with my science-hat on, lets take a step back and point out some important limitations of this work. First and foremost is the assumption that the personality trait impulsivity measured by only one personality inventory is the only potential correlate here, at least among the human participants. It isn't. And indeed one should always be mindful that just because investigators test for something like a personality trait or a specific cognitive skill or even a specific condition/state/disease does not mean they have excluded all other potentially important variables** (indeed if this is even possible). Next is the assumption that self-report responses on a five-point Likert scale are going to be true and honest. No-one can be totally assured of that, particularly if responses are to some of the more less desirable personality traits that we would all like to put to one side. Finally is the interpretation of a mouse model of high uric acid showing the impulsivity trait based on their novelty-seeking and exploratory behaviours during field tests. I've talked mouse models before with autism in mind and how behavioural animal models are always subject to some degree of interpretation until such time that we can talk to the animals (and they talk back).

Having said all that I do find myself still very interested in the Sutin findings in terms of how the work was done, the results obtained and where it could lead. Without giving anything that looks or sounds like medical or clinical advice, one has to wonder (as the authors have done) whether 'adjusting' levels of uric acid might have a knock-on effect on certain behaviours particularly where uric acid might be seen in more behaviourally or psychiatrically defined conditions. I'm not saying everyone should be taking something like allopurinol or anything like that but perhaps further investigation is at least warranted.

Finally, on a similar note to the Sutin study I also recently came across a study by Soto-Insuga and colleagues*** which reported some very preliminary findings from treating iron deficiency in cases of attention-deficit hyperactivity disorder (ADHD). To quote: "Treatment with iron supplements can be an effective alternative to treat patients with ADHD and iron deficiency, especially the inattentive subtype". By 'treatment' I take it to mean that not only were the authors resolving the iron deficiency but also in specific cases of ADHD identified by that inattentive subtype**** they were talking about the management of behavioural symptoms too.

Example evidence that the psychosomatic or somatopsychological relationship should definitely remain near the top of the research agenda?

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* Sutin AR. et al. Impulsivity is associated with uric acid: evidence from humans and mice. Biol Psychiatry. April 2013.

** Cerecero P. et al. Association between serum uric acid levels and cardiovascular risk among university workers from the State of Mexico: a nested case--control study. BMC Public Health 2013; 13: 415.

*** Soto-Insuga V. et al. Role of iron in the treatment of attention deficit-hyperactivity disorder. An Pediatr (Barc). April 2013.

**** Solanto MV. The predominantly inattentive subtype of attention-deficit/hyperactivity disorder. CNS Spectr. 2000; 5: 45-51.

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Sutin AR, Cutler RG, Camandola S, Uda M, Feldman NH, Cucca F, Zonderman AB, Mattson MP, Ferrucci L, Schlessinger D, & Terracciano A (2013). Impulsivity is Associated with Uric Acid: Evidence from Humans and Mice. Biological psychiatry PMID: 23582268