ADHD in the prison population: a second micropost

"The results indicate that 41 % of the prisoners met the diagnostic criteria for ADHD [attention-deficit hyperactivity disorder] in childhood and continued to meet criteria for ADHD as adults."

So said the study results from Romana Farooq and colleagues [1] continuing a theme of how ADHD may very well have some important associations with the prison population (see here). This time around surveying "both childhood and adult ADHD symptoms using the Barkley Adult ADHD Rating Scale-IV" among 69 female prisoners, Farooq et al ventured down an important research path covering how ADHD manifests in women.

A few other important details are mentioned in their paper including how "young female prisoners (aged 18-25) were significantly more likely to report symptoms of ADHD than older prisoners" and "Prisoners who reported symptoms of ADHD also reported high levels of impairment associated with these symptoms."

Avoiding any sweeping generalisations about ADHD and incarceration, there continues to be some potentially important lessons to be learned from such research. That tackling ADHD as and when it presents in childhood might be an important goal is one of them (see here) save any heightened risk of future adverse consequences. More preferential screening for conditions like ADHD in the prison population might also be a good idea also. I might also forward the suggestion (yet again) that when it comes to the management of ADHD-related symptoms specifically in the prison environment, there may be important lessons we can learn from papers such as the one from Bernard Gesch and colleagues [2] set in the context of work from Julia Rucklidge et al (see here) and the importance of nutrition to behaviour...

Music: New Order - Tutti Frutti.

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[1] Farooq R. et al. Prevalence of adult ADHD in an all-female prison unit. Atten Defic Hyperact Disord. 2015 Dec 9.

[2] Gesch CB. et al. Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners. Randomised, placebo-controlled trial. Br J Psychiatry. 2002 Jul;181:22-8.

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Farooq, R., Emerson, L., Keoghan, S., & Adamou, M. (2015). Prevalence of adult ADHD in an all-female prison unit ADHD Attention Deficit and Hyperactivity Disorders DOI: 10.1007/s12402-015-0186-x

Early intervention before autism diagnosis

Santa is approaching so I don't want to keep you too long today. I just thought you might want to briefly cast your eye over the paper by Sonia Monteiro and colleagues [1] and their findings that: "most children are receiving early intervention services before their diagnostic ASD [autism spectrum disorder] evaluations, particularly if an ASD diagnosis is confirmed."

Set within the context of some rather disturbing reports about children (and adults) sometimes waiting a very, very long time for their assessments, the current findings suggest that in the US at least, some education and healthcare providers might have cottoned on to the fact that early intervention is an important part of managing autism in childhood and such early intervention services shouldn't necessarily wait until formal diagnosis is received.

Perhaps also allied to the Monteiro findings is another paper in the same journal by Christensen and colleagues [2] who, when looking at "ASD prevalence and characteristics among 4-year-old children in 5 of 11 sites participating in the 2010 Autism and Developmental Disabilities Monitoring Network" found that the prevalence of ASD in 4 years "was 30% lower than 8-year-old ASD prevalence." As per an associated commentary [3]: "This finding points to a gap between current knowledge of early manifestations of ASD and our ability to use such knowledge to detect and record ASD symptoms in preschoolers." I might add that given issues such as regression being linked to cases of autism (see here) one has to be mindful of the idea that not all autism might present in the earliest years of life (see here for another example). I'd also suggest that there might be alternative explanations for the finding that 4-year old prevalence of autism was lower than 8-year old prevalence...

Cumulatively what these papers highlight is that there is still some way to go insofar as accurate screening and diagnosis of early days autism (see here) and even when screening points to more thorough assessment for autism, various obstacles remain to get this accomplished in a timely manner. The saving grace being that some educational and healthcare providers think screening positive is enough to facilitate some kind of interventional involvement; at least in some parts of the world.

And with that I send you Seasons Greetings and Happy Christmas complete with archetypal Christmas song (please do try not to end up in the drunk tank this festive period).

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[1] Monteiro SA. et al. Early Intervention Before Autism Diagnosis in Children Referred to a Regional Autism Clinic. J Dev Behav Pediatr. 2015 Dec 1.

[2] Christensen DL. et al. Prevalence and Characteristics of Autism Spectrum Disorder Among 4-Year-Old Children in the Autism and Developmental Disabilities Monitoring Network. J Dev Behav Pediatr. 2015 Dec 9.

[3] Robins DL. Prevalence Counts: Commentary on "Prevalence and Characteristics of Autism Spectrum Disorder Among 4-Year-Old Children in the Autism and Developmental Disabilities Monitoring Network". J Dev Behav Pediatr. 2015 Dec 9.

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Monteiro SA, Dempsey J, Broton S, Berry L, Goin-Kochel RP, & Voigt RG (2015). Early Intervention Before Autism Diagnosis in Children Referred to a Regional Autism Clinic. Journal of developmental and behavioral pediatrics : JDBP PMID: 26647354

Prevalence of schizophrenia in China up: was Dohan (partially) right?

"The prevalence of schizophrenia in China has more than doubled between 1990 and 2010, with rates being particularly high in the most developed areas of modern China."

So said the study results from Chan and colleagues [1] reviewing the collected peer-reviewed "epidemiological studies of schizophrenia in mainland China published between 1990 and 2010."

Taking into account data from 42 eligible trials covering some "2 284 957 persons, with 10 506 diagnosed with schizophrenia" researchers applied some statistical wizardry "to estimate the probability of case of schizophrenia ("prevalence") by type of residency in different years."

The figures make for interesting read as the estimated lifetime prevalence rate of schizophrenia steadily rose between 1990, 2000 and 2010. Further: "In 1990 there were 3.09 (2.87-3.32) million people in China affected with schizophrenia during their lifetime. The number of cases rose to 7.16 (6.57-7.75) million in 2010, a 132% increase, while the total population increased by 18%." As per my opening sentence, area of residence in terms of industrialisation and urbanisation also seemed to exert something of an effect. I might add that this data also seems to have appeared in another publication [2] (open-access).

I have no doubt that the reasons behind the increase in cases of schizophrenia in China are likely to be numerous and complex. To say that there may be just one factor universally contributing to every case of schizophrenia in China would be a fool-hardy thing to state in these days of plural labels (including 'the schizophrenias') and multi-factorial explanations of how someone arrives at such a diagnosis. That screening and assessment facilities have no doubt changed over the course of 20 years in China is also worth mentioning.

I do however want to forward one idea that perhaps requires a little bit more investigation as potentially being pertinent to the increase in prevalence rates: food, and specifically, the idea that gluten consumption may have played a role as per the ideas of the late Curt Dohan. Quite a good overview of 'Dohan's hypothesis' can be read here by Dr Emily Deans from the Evolutionary Psychiatry blog. He basically suggested that where grain (and milk) consumption were rare, so schizophrenia tended to be rare. Conversely, where populations started to take on board grain (and milk) as a staple food, so admission rates for schizophrenia increased. Dohan produced quite a few papers discussing this hypothesis including this one [3] including the idea that foods containing gluten and casein can produce exorphins akin to certain opiates.

I've always been interested in this work given my research affinity to the idea that certain foods might have some important 'effects' on certain behaviours or diagnostic labels covering certain behaviours [4]. That ideas about gluten and casein potentially being important to 'some' autism [5] have generally emerged from the discussions in schizophrenia perhaps highlights how central Dohan has been given also the tangled history that schizophrenia and autism have at times shared.

In recent times, there has been more interest in Dohan's hypothesis and the idea that some people diagnosed with schizophrenia (or on the schizophrenia spectrum) may demonstrate specific genetic and biological issues associated with gluten and casein. I've blogged about it a few times including the idea of immunological gluten 'sensitivity' in schizophrenia (see here and see here), a possible role for food and gastrointestinal (GI) inflammation in cases (see here) allied to a possible role for milk antibodies in relation to potentially predicting the development of schizophrenia (see here). All of this set in the context of some growing interest in food and nutrition within psychiatry (see here). Such research has met with some criticism down the years but more and more the peer-reviewed evidence is highlighting how things like immune function and the concept of inflammation do seem to be important to various psychiatric labels.

Some of the elements discussed by Dohan and others seem to make sense in the context of schizophrenia and China. The idea of "rates being particularly high in the most developed areas of modern China" might imply that food and the types of food eaten in more developed areas may be slightly different from those in less developed (more traditional) areas of the country. In the context of milk consumption and given the important biology associated with milk consumption in China (quite a high proportion of the population are deemed lactose intolerant), one might also envisage some connection.

I'm not saying that a complex condition like schizophrenia is all down to food within the data coming out of China. What I am saying is that one might entertain the idea that as part of suite of potentially important variables, what someone is eating may have some bearing on their psychiatric health and wellbeing and hence potentially be amenable to change...

Music: Descendents - Everything Sucks. Dedicated to Kylo Ren and, as one of my brood observed when watching the latest Star Wars film, the fact that he is rather an angry man throughout. I'd like to think in subsequent films we might see a 'lighter' side to ole' Ben...

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[1] Chan KY. et al. Prevalence of schizophrenia in China between 1990 and 2010. J Glob Health. 2015 Jun;5(1):010410.

[2] Chan KY. et al. Urbanization and the prevalence of schizophrenia in China between 1990 and 2010. World Psychiatry. 2015;14(2):251-252.

[3] Dohan FC. Genetic hypothesis of idiopathic schizophrenia: its exorphin connection. Schizophr Bull. 1988;14(4):489-94.

[4] Whiteley P. et al. Gluten- and casein-free dietary intervention for autism spectrum conditions. Front Hum Neurosci. 2013 Jan 4;6:344.

[5] Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets?  Proc Nutr Soc. 2015 Aug;74(3):202-7.

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Chan KY, Zhao FF, Meng S, Demaio AR, Reed C, Theodoratou E, Campbell H, Wang W, Rudan I, & Global Health Epidemiology Reference Group (GHERG) (2015). Prevalence of schizophrenia in China between 1990 and 2010. Journal of global health, 5 (1) PMID: 26649171

Allergy symptoms affecting autistic symptoms?

I have quite a bit of time for Harumi Jyonouchi on this blog (see here and see here for example). Not only has Dr Jyonouchi got an eye for some potentially important biological issues associated with at least some cases of autism, she also seems to recognise that behavioural symptoms often seem to go hand-in-hand with other more somatic features as per her work taking gastrointestinal (GI) symptoms into account for example [1].

Another, more recent paper from Dr Jyonouchi caught my eye [2], specifically talking about how "clinicians need to be aware of profound effects of allergy rhinitis on neuropsychiatric symptoms in individuals with limited expressive language." This conclusion comes on the basis of her reporting on two cases - "one with ASD [autism spectrum disorder] and the other with developmental delay, congenital deafness, and other multiple congenital anomalies" - attending a pediatric allergy/immunology clinic for "non-IgE mediated food allergy" and "delayed type food allergy around 4–5 years of age" respectively. In both cases treatment was made using "the second line allergy treatment, omalizmab" (also known as omalizumab), a humanised monoclonal antibody that "inhibits binding of IgE to the IgE receptor expressed on effector cells... and blocks allergen induced immune responses." Normally indicated for patients with 'convincing' IgE-mediated asthma (at least here in Blighty), both children were offered this treatment when first line allergy medications (steroid nasal inhalers, a leukotriene receptor antagonist, and topical ophthalmic solutions for ocular allergy) did not seem to be as effective as they should. Some quite surprising effects are detailed as and when omalizumab was started including a "marked attenuation of their problematic neuropsychiatric symptoms and subsequent improvement in the cognitive development, once respiratory allergy symptoms were under control."

For the child (male, 10 years old) diagnosed with autism, Dr Jyonouchi includes some scores based on the Aberrant Behavior Checklist (ABC) subscales illustrating how correlating with the use of omalizumab, several areas of functioning seemed to improve. Also: "Unfortunately, interruption of omalizmab treatment due to delay in insurance approval, following changes in his insurance coverage, resulted in worsening of his behavioral symptoms in 2015 at 16 years of age. This was again resolved after resuming omalizmab treatment."

Although case reports are particularly interesting in the context of the N=1 with autism in mind (see here) and provide some useful starting points for future research, one has to be slightly cautious in generalising such findings to the larger body of people on the autism spectrum. As I've said many times before on this blog, the growing moves towards pluralising autism (see here) represents one of the more enlightened changes in autism research circles. What this means is that what might be a useful intervention for one person on the autism spectrum, might not necessarily translate to others or all.

That being said, I do find the suggestion of a connection between allergy symptoms and autistic and related symptoms to be a tantalising one. I've previously discussed the idea that allergy and autism (and attention-deficit hyperactivity disorder, ADHD) might eventually show some rather surprising links based on what has been seen in the peer-reviewed science domain (see here and see here) and continues to be discussed [3]. The hints from that research were that more needs to be done and specifically, what happens when allergy and related symptoms are 'treated'; something which the latest Jyonouchi paper has seemingly started to take more seriously.

Music: Weezer - Thank God for Girls.

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[1] Jyonouchi H. et al. Dysregulated innate immune responses in young children with autism spectrum disorders: their relationship to gastrointestinal symptoms and dietary intervention. Neuropsychobiology. 2005;51(2):77-85.

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

[3] Miyazaki C. et al. Allergies in Children with Autism Spectrum Disorder: a Systematic Review and Meta-analysis. Review Journal of Autism and Developmental Disorders. 2015; 2: 374-401.

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Jyonouchi, H. (2015). Marked improvement of neuropsychiatric symptoms following control of allergy symptoms with the use of humanized murine anti-IgE antibody (omalizumab) in 2 patients with severely limited expressive language Allergy, Asthma & Clinical Immunology, 11 (1) DOI: 10.1186/s13223-015-0105-x

Maternal pregnancy CRP levels and offspring autistic traits

Elevated levels of inflammatory markers present during pregnancy have been linked to quite a few labels and diagnoses down the years. Schizophrenia is a prime example as per various peer-reviewed science with that label in mind (see here). There is still quite a bit more research to do in these days of plural schizophrenias (see here) but the intersection between immune function and psychiatry is a growing area of interest.

Autism is another label that has been talked about with elevated gestational inflammatory markers in mind (see here). CRP or C-reactive protein has tended to be a focus for many studies despite other pentraxins potentially also showing some effect (see here). It is therefore with autism in mind that today I'm discussing the paper by Natasja Koks and colleagues [1] and the suggestion that: "the association between elevated levels of maternal CRP in pregnancy and autistic traits in children is confounded by maternal health-related and socioeconomic factors."

Based initially on measured levels of pregnancy CRP before 18 weeks gestation in quite a large group of mums-to-be based in the Netherlands (N=4165), researchers also collected parental reports of offspring at 6 years of age "using the Social Responsiveness Scale, and the Pervasive Developmental Problem scale." They reported that compared to a reference group: "elevated levels of CRP (>7.8 mg/L) in pregnant women were associated with higher Social Responsiveness Scale scores in children." The Social Responsiveness Scales (SRS) by the way has found some favour in terms of screening for autistic-like traits and symptoms as per other research (see here).

But... things were not so straight-forward when it came to the relationship between pregnancy CRP levels as a marker of inflammation and 6-year old SRS scores as a marker of autistic traits. So: "the effect was strongly attenuated after adjustment for several socioeconomic factors and in particular by maternal health-related factors including body mass index." Further the authors reported "no relation between maternal CRP levels and pervasive developmental problem." In other words, simplistic notions that 'more inflammation during pregnancy = more autistic traits in offspring' might need to be tempered to a degree. Anyone who has followed the autism research scene down the years will not be surprised at such sentiments.

One obviously has to be a little guarded when it comes to studies such as this where variables stretching back into the important nine months that made us are 'correlated' with measures quite a few years later. As per similar work with an autism research slant looking at such widely-spaced apart variables (see here) there may be a multitude of other important variables and factors to consider.

"Further studies are needed to explore whether other maternal inflammatory markers during pregnancy, as a response to maternal inflammation, are associated with the development of autistic traits in the offspring." Going back to my previous discussions about CRP being only one of several potential inflammatory markers that might need to be explored (including the various cytokines that have cropped up over the years) I'd be minded to suggest that there is good sense in looking at a wider selection of immune related compounds when it comes to the question of immune mediation being potentially linked to at least some offspring autism or the presentation of autistic traits. Alongside ideas that acute inflammation might have some interesting links to things like social cognitive processing (see here) and that within the vast heterogeneity of autism, there may be cases where infection stands out as a possible aetiological factor (see here) there are plenty of avenues to be explored by science in this area.

Music: San Diego - Hinds.

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[1] Koks N. et al. Maternal C-Reactive Protein Concentration in Early Pregnancy and Child Autistic Traits in the General Population. Paediatric and Perinatal Epidemiology. 2015. Dec 3.

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Koks, N., Ghassabian, A., Greaves-Lord, K., Hofman, A., Jaddoe, V., Verhulst, F., & Tiemeier, H. (2016). Maternal C-Reactive Protein Concentration in Early Pregnancy and Child Autistic Traits in the General Population Paediatric and Perinatal Epidemiology DOI: 10.1111/ppe.12261

The ties that bind? Comorbidity and autism (again)

"It was found that 92.9% of participants presented with a family history of autoimmune disease."

That was one of the headline findings reported in the paper by Arlene Mannion & Geraldine Leader [1] who conducted a follow-up study to previous work [2] looking at the important issue of comorbidity and autism with a specific focus on whether "comorbid symptoms changed over time."

Fifty-six children and adolescents diagnosed with DSM-IV autism spectrum disorder (ASD) participated in their study, drawn from a previous cohort of 89 involved in previous research by these authors. A range of measures were included for study including a focus on sleep and functional bowel issues.

When it came to describing this smaller cohort two years after their original research participation, examination of current comorbid diagnoses alongside ASD showed a worrying trend insofar as rates of epilepsy, attention-deficit hyperactivity disorder (ADHD) and anxiety disorder. An additional 5 children/young adults presented with ADHD at this second time of study for example. Three participants also presented with an anxiety disorder this time around. These are perhaps not unexpected findings (see here and see here).

Drilling down further into the presented data, a few other trends are present:

• Sleep issues were prevalent. Nearly 80% of participants showed signs of a sleep problem "classified as a score of 41 or more on the CSHQ [Children's Sleep Habits Questionnaire]."
• Gastrointestinal (GI) symptoms, as measured on the Gastrointestinal Symptom Inventory from the ATN, were also notable in this cohort. Nearly three-quarters of participants presented with at least on GI symptom within the last 3 months. A smaller group (7%) presented with 5 GI symptoms recently. GI symptoms also persisted in over 80% of participants during the 2-year period before this follow-up study.
• GI and sleep issues also seemed to go hand-in-hand. Almost two-thirds of the cohort "presented with both sleep problems and gastrointestinal symptoms" as evidenced when specific GI symptoms were analysed (bloating, nausea, abdominal pains, diarrhoea and constipation).
• Researchers also questioned about family medical history as well as participants. Alongside the figure already presented about familial autoimmune disease, various other "psychological, developmental or medical disorder" were noted.
• Osteoarthritis, psoriasis and hypothyroidism (Hashimoto's thyroiditis) were the most common familial autoimmune conditions described in this cohort. Mention is however also made about Crohn's disease (n=9) and coeliac disease (n=4) too.

Obviously one has to keep in mind a few salient points before getting to carried away with this information. The participant numbers on the first occasion (N=89) and this time around (N=56) are quite small. The authors also note that the use of "parental report" might also be considered a limitation; balancing that however by making reference to the Phillip Gorrindo paper [3] covered in previous posts (see here) on how: "Parents were sensitive to the existence, although not necessarily the nature, of GID [gastrointestinal dysfunction]".

That all being said, the trends reported by Mannion & Leader are consistent with previous peer-reviewed data on the issue of comorbidity and autism. Sleep problems are pretty widespread (see here) as are functional bowel issues (see here). Indeed, even more pathological bowel issues seem to be 'over-represented' when it comes to a diagnosis of autism (see here). That the two issues might be somehow 'joined together' has also been previously raised in the research literature (see here).

The reports on certain familial health conditions being associated with cases of autism is also not new news. I've long speculated about the role of familial autoimmune conditions and autism on this blog (see here and see here) on the back of research spanning several decades (see here). Talk specifically of a connection between the skin condition psoriasis and autism is included (see here) as is the idea that both inflammatory bowel conditions (see here) and more food-related bowel states (see here) might in some families, show a connection to autism. Much more study is implied including a focus on the N=1 [4].

The idea that autoimmune disease specifically affecting the thyroid might also be a route of further scientific inquiry with autism in mind is something of real interest in light of quite a bit of other research in this area (see here and see here). As I've mentioned in previous posts, the idea that familial autoimmune disease affecting the thyroid might also be related to the onset of presentation of offspring autism [5] is a research topic crying out for further replication. The possibility of an association also opens up a number of other avenues for study based on the idea that autoimmune features might reflect one or more 'types' of autism (see here) or indeed, linked to one or more of the common comorbidities occurring alongside autism (see here and see here). Speculations are potentially aplenty in this area (see here) so we need more hard data.

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[1] Mannion A. & Leader G. An investigation of comorbid psychological disorders, sleep problems, gastrointestinal symptoms and epilepsy in children and adolescents with autism spectrum disorder: A two year follow-up. Research in Autism Spectrum Disorders. 2016; 22: 20-33.

[2] Mannion A. et al. An investigation of comorbid psychological disorders, sleep problems, gastrointestinal symptoms and epilepsy in children and adolescents with autism spectrum disorder: A two year follow-up. Research in Autism Spectrum Disorders. 2013; 7: 35-42.

[3] Gorrindo P. et al. Gastrointestinal Dysfunction in Autism: Parental Report, Clinical Evaluation, & Associated Factors. Autism Research. 2012;5(2):101-108.

[4] Genuis SJ. & Bouchard TP. Celiac disease presenting as autism. J Child Neurol. 2010 Jan;25(1):114-9.

[5] Molloy CA. et al. Familial autoimmune thyroid disease as a risk factor for regression in children with Autism Spectrum Disorder: a CPEA Study. J Autism Dev Disord. 2006 Apr;36(3):317-24.

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Mannion, A., & Leader, G. (2016). An investigation of comorbid psychological disorders, sleep problems, gastrointestinal symptoms and epilepsy in children and adolescents with autism spectrum disorder: A two year follow-up Research in Autism Spectrum Disorders, 22, 20-33 DOI: 10.1016/j.rasd.2015.11.002