Pregnancy diet and offspring "hyperactivity-inattention symptoms"?

I appreciate that the findings reported by Cédric Galera and colleagues [1] are potentially a little uncomfortable. Their examination of over 1200 mother-child pairs looking at data from food frequency questionnaires during pregnancy and subsequent offspring 'externalising' behaviours into childhood, could be construed as evidence that poor eating habits during the nine months that made us have the ability to translate into childhood issues. Because food choices are seen as just that - 'choices' - the Galera results *could* potentially fall into the same category as other 'choices' that also seemingly affect offspring development in this area (see here for example). I make no value judgements.

Having also bumped into the Galera paper at the same time as seeing a BBC media report observing that "We learn nothing about nutrition, claim medical students", one might further make an argument for the need for much greater education, guidance, support and potentially 'nudging', when it comes to issues such as 'what to eat during pregnancy'. That however, is another discussion for another day.

Anyhow, the science...

Galera et al report findings based on the EDEN mother-child cohort [2], an initiative set up to examine "the relations and potential interactions between maternal exposures and health status during pregnancy, fetal development, health status of the infant at birth and the child’s health and development." It's interesting that the opening words to the Heude [2] description of the initiative mention the name 'Barker', as in the late David Barker, a man who helped popularise the idea that nutrition in the womb (through maternal diet) might have some important *consequences* for offspring in the short- and long-term. Looking at some of the other research produced by the EDEN mother-child cohort (see here), Barker and others may have indeed been on to something.

As well as looking at offspring externalising symptoms such as conduct problems via use of "the Strength and Difficulties Questionnaire at ages 3, 5, and 8 years", authors also looked at "trajectories of hyperactivity-inattention symptoms." This, on the basis that the SDQ does pretty well at discriminating between ADHD and non-ADHD cases [3]. They concluded that, taking into account infant dietary patterns "at age 2 years" and various other potential influencing variables ("maternal stress and depression, gestational diabetes, and socioeconomic variables"), there was something to see with regards to use of a 'high Western diet' and 'low Healthy diet' during pregnancy in relation to offspring developmental outcome. Specifically: "Maternal diet during pregnancy was independently associated with children's hyperactivity-inattention symptoms."

Of course, one needs to be a little bit careful that *association* is not viewed as 'cause-and-effect' based on such observational studies. That also it is downright unethical to put mums-to-be on a 'healthy diet' vs. 'a non-healthy diet' is also a stumbling block to robust investigations in this area; similar to the fact that one wouldn't put mums-to-be on a tobacco smoking vs. a non-smoking intervention.

But the Galera results are not stand-alone in potentially implicating maternal diet as a factor in relation to offspring hyperactivity-inattention [4] and are therefore deserving of some further investigation. I've already mentioned that perhaps more guidance and 'nudges' need to be provided in the area of pregnancy nutrition, and that I assume, would include looking at the cost and convenience of a healthy diet vs. a not-so-healthy diet in the context of a possible *link* between diagnosed attention-deficit hyperactivity disorder (ADHD) and "socioeconomic deprivation" for example (see here). More than that however is the idea that David Barker and others who talked about 'foetal programming' during the pregnancy months as a result of what is in or perhaps not in a maternal diet may have been a lot more accurate than many people would have perhaps imagined...

And on the topic of 'foetal programming', diet might not be the only factor to consider [5]...

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[1] Galera C. et al. Prenatal diet and children's trajectories of hyperactivity-inattention and conduct problems from 3 to 8 years: the EDEN mother-child cohort. J Child Psychol Psychiatry. 2018 Mar 24.

[2] Heude B. et al. Cohort Profile: The EDEN mother-child cohort on the prenatal and early postnatal determinants of child health and development. Int J Epidemiol. 2016 Apr;45(2):353-63.

[3] Algorta GP. et al. Diagnostic efficiency of the SDQ for parents to identify ADHD in the UK: a ROC analysis. Eur Child Adolesc Psychiatry. 2016 Sep;25(9):949-57.

[4] Rijlaarsdam J. et al. Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems. J Child Psychol Psychiatry. 2017 Jan;58(1):19-27.

[5] Andersen SL. et al. Maternal Thyroid Function in Early Pregnancy and Child Neurodevelopmental Disorders: A Danish Nationwide Case-Cohort Study. Thyroid. 2018 Mar 27.

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Bone health and autism continued

It's been a while since I last wrote about the topic of bone health and autism (see here). On that particular occasion, it was the work by Ann Neumeyer and colleagues [1] that provided the blogging fodder and the observation that: "BMD [bone mineral density] is lower in peripubertal boys with ASD [autism spectrum disorder]." BMD is important because of a possible association between lower BMD and risk of fracture or indeed, something more pathological.

Today I continue with this topic as per further work from Neumeyer and colleagues [2] looking to "examine macro- and micronutrient intakes and self-reported physical activity in boys with ASD compared to TDC [typically developing controls] and the relationship of these variables with BMD."

Based on data from nearly 50 boys aged 8-17 years of age (25 diagnosed with ASD and 24 not-autism controls), researchers once again relied on the technique known as dual-energy x-ray absorptiometry (DXA) for the measurement of bone mineral density. Various measures were taken from various parts of the body -"whole body less head, hip, and spine." Alongside, food diaries provided a rough-and-ready measure of food intake, self-reported physical activity (that's self-reported) did what it said on the tin, and fasting levels of 25(OH) vitamin D and calcium were garnered. I'll come back to some of the pros-and-cons of some of these measures shortly.

Results: consistent with the peer-reviewed data that has come before, BMD z scores at the lumbar spine, femoral neck, total hip, and whole body less head were lower in those with autism compared with control participants. A BMD z score by the way, is basically a comparison of BMD with that of standardised data (i.e. an average person of the same sex and age). Added to such results, authors also observed that less calorie intake was present in the ASD group (again compared with controls) and a "lower proportion of ASD participants were categorized as "very physically active" (27% vs 79%; P<0.001)." Interestingly however: "Body mass index and serum vitamin D and calcium levels were similar."

I was rather intrigued by the Neumeyer results. Not least that vitamin D and calcium levels were 'similar' in the autism and control groups. As I've discussed before on this blog, there have been calls for preferential screening for these biological parameters as and when an autism diagnosis is received (see here) in light of other findings (see here). The Neumeyer observations perhaps reflect a wider need for such screening.

The use of self-report as a measure for physical activity, whilst useful, is slightly outdated in these times of actigraphy. Wearable technology to measure activity and rest cycles is cheap and abundant these days and, as I've mentioned on other occasions, really should be the research industry standard. I'm not saying people might not be accurate in reporting their short-term physical activity but...

I do think there are some additional 'where next?' things to consider when it comes to future work looking at BMD and autism. Noting for example, that both dietary and malabsorptive issues seem to be able to influence BMD [3] there are additional parameters to be looked at. Given previous peer-reviewed reports on lactose issues being present in relation to autism (see here), this could feature in future work. Although still possessing the ability to furrow brows in certain quarters, the observation of issues with intestinal permeability ('leaky gut') in relation to some autism (see here) also could be an additional parameter to examine. I daresay also that some initial chatter about a compound called zonulin potentially serving as a 'biomarker of impaired gut barrier function' in relation to some autism (see here) might also be revealing. And then there is the important issue of epilepsy / seizure disorder often being comorbid with autism (see here), and how certain [important] intervention measures for said issues might affect parameters such as vitamin D (see here) and what that might mean for long-term bone health...

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[1] Neumeyer AM. et al. Bone density in peripubertal boys with autism spectrum disorders. J Autism Dev Disord. 2013 Jul;43(7):1623-9.

[2] Neumeyer AM. et al. Nutrition and Bone Density in Boys with Autism Spectrum Disorder. J Acad Nutr Diet. 2018 Feb 3. pii: S2212-2672(17)31749-5.

[3] Di Stefano M. et al. Lactose malabsorption and intolerance and peak bone mass. Gastroenterology. 2002 Jun;122(7):1793-9.

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Mediterranean-style diet + fish oils = better diet quality and mental health in depression

"This is one of the first randomized controlled trials to show that healthy dietary changes are achievable and, supplemented with fish oil, can improve mental health in people with depression."

So said the findings reported by Natalie Parletta and colleagues [1] reporting results from a randomised-controlled trial investigating "the impacts of a Mediterranean-style diet intervention for mental health and quality of life (QoL) in people with depression."

Their study, called "HELFIMED (Healthy Eating for Life with a Mediterranean-style diet) Mood Study", drew on various data derived from a starting population of some 180 participants randomised to receive a Mediterranean diet plus fish oil (MedDiet) or a control social group who - "attended fortnightly social groups (e.g. sharing holiday stories, playing games, doing personality tests, watching a movie with discussion, book club)." The focus on 'social' noted in the control group was designed to "control for the social component of the cooking workshops that can help to improve depressive symptoms" used by the experimental (dietary) group. Having said that, I can't ever recall 'doing personality tests' as being something I've ever encountered in any social groups/outings down the years but hey-ho! We are also told that: "Assessments at baseline, 3 and 6 months included mental health, quality of life (QoL) and dietary questionnaires, and blood samples for erythrocyte fatty acid analysis" covering both groups over the intervention period.

Results: bearing in mind the numbers of completers at 3- and 6-months were quite a bit down on the starting numbers, a few important details were observed. So: "Compared to the social group, the MedDiet group reported significantly greater increase in their total Mediterranean diet score from baseline to 3 months... along with a significantly greater increase in consumption of vegetables, fruit, wholegrain foods, nuts and legumes, significantly lower consumption of unhealthy snacks and meat/chicken, and a greater diversity of vegetables." It appeared that quite a bit of 'nutrition education' and cooking classes et al seemed to do the trick in increasing the nutritional quality of participants food intake in this arm of the trial. Importantly too: "These dietary changes were maintained at 6 months" when intervention wasn't as intense as that given in the first 3-months.

Also: "Both the MedDiet and the social group reported significantly improved mental health on all outcome measures (DASS, PANAS, and AQoL-8D subscales) over 3 months (all P < 0.001) except for the AQoL-8D pain value." The authors speculate that this could be "attributed to the social component of the study as both groups were exposed to group workshops (either cooking or social group)." In other words, loneliness and/or lack of social support are important features when it comes to mental health in relation to depression (see here).

But... "Compared to the social group, the MedDiet group reported significantly greater improvement in their DASS depression score... and AQoL-8D mental health score over 3 months." The authors observed that transition to a Mediterranean diet plus fish oil supplement seemed to provide some value-added benefits when it came to self-reported depression scores. Whether it was the dietary change or the fish oil supplementation is not really clear from the data but the findings do invite further investigation.

Allowing for the fact that there were 'limitations' to this study (use of self-report, high attrition rate, single blind study design) I think it's fair to say that moves towards getting those with depression to eat healthier is a win-win situation on the basis of what the peer-reviewed evidence seems to point to [2]. Adding to the results of other similar trials in this area (see here) and there is a picture building up that alongside the physical health benefits a good diet (good insofar as containing fruit, vegetables, nuts, etc) can bring, there may be psychological benefits too [3]. It's not just about diet however, as the Parletta results show, but diet does seem to be quite a useful add-on.

The fish oil supplementing side of things is something else that requires some further investigation. I note that I've already covered other work by authors of this most recent study before on this blog with regards to their investigation on fatty acids and autism among other things (see here). In relation to depression (clinical depression), there is also evidence suggesting that certain types of fatty acid supplementation do seem to be able to act on presented symptoms (see here and see here) for some people at least. The problem, as I've mentioned in this study, is teasing apart fish oil/fatty acid supplements from the role played by the dietary changes.

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[1] Parletta N. et al. A Mediterranean-style dietary intervention supplemented with fish oil improves diet quality and mental health in people with depression: A randomized controlled trial (HELFIMED). Nutr Neurosci. 2017 Dec 7:1-14.

[2] Fowles ER. et al. Stress, Depression, Social Support, and Eating Habits Reduce Diet Quality in the First Trimester in Low-Income Women: A Pilot Study. Journal of the Academy of Nutrition and Dietetics. 2012; 112: 1619-1625.

[3] Opie RS. et al. Dietary recommendations for the prevention of depression. Nutr Neurosci. 2017 Apr;20(3):161-171.

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MoBa does... maternal pregnancy iodine intake and offspring ADHD symptoms and diagnosis

Yet another 'MoBa does...' post today, reflecting data derived from the Norwegian Mother and Child Cohort Study and the findings reported by Marianne Hope Abel and colleagues [1] (open-access available here).

Maternal pregnancy iodine intake (both calculated from food sources and also as a supplement) was the starting variable, where responses to "a food frequency questionnaire (FFQ)" provided researchers with enough data to categorise mums-to-be in terms of their iodine intake. Iodine, by the way, is something of an important nutrient from many biological reasons; not least for optimal thyroid function. During pregnancy, suitable iodine levels are also seemingly required to ensure that the developing child is able to reach their full potential (see here).. seemingly.

Alongside, researchers also looked at both children diagnosed with attention-deficit hyperactivity disorder (ADHD) and "maternal report of child ADHD symptoms at eight years of age" on the basis of other data talking about "a negative impact on child behavior problems when mothers had inadequate iodine intake from food and initiated use of supplemental iodine in the first trimester of pregnancy." Keep in mind that last part about supplemental use during early pregnancy...

So, including some 77,000 mother-child pairs where "for 27,945 there were data on maternally reported ADHD scores when the child was aged eight years", what did the researchers find?

"Iodine from food was significantly associated with maternally reported child ADHD symptoms at eight years of age... but not with risk of child ADHD diagnosis." Authors expanded on this observing that the 'inattention' side of ADHD symptoms, derived from a questionnaire covered in independent research [2], was the driving force behind the connection being made, not the hyperactivity subscale. They also noted that "maternal iodine intake of less than ~200 µg/day" seemed to be the crucial cut-off point when it came to those maternal reports of ADHD symptoms.

But... I'm sure it can't have escaped your attention that although maternal reports of offspring ADHD symptoms - indeed, inattention - *correlated* with maternal iodine intake, there was little to see when it came to "risk of specialist-diagnosed ADHD in the child." Indeed, the authors also note that they found "no evidence of any beneficial effect of supplemental iodine in pregnancy" and even that "initiating iodine supplement use within the first trimester in mothers with inadequate iodine intake from food (<EAR) was associated with both an increased risk of ADHD diagnosis and higher ADHD symptom score at eight years of age."

Science is [almost] never clear-cut in the conclusions it arrives at and the Abel results just add to that sentiment. Given that this authorship group seemingly having a considerable research interest in all-things iodine and health, I'm assuming that these latest results were quite the talking point. Certainly, just a little bit different from their other recent publication on this topic [3] that concluded: "Maternal iodine intake below the Estimated Average Requirement during pregnancy was associated with symptoms of child language delay, behavior problems, and reduced fine motor skills at 3 y of age" but perhaps not with the supplementation angle in mind: "results showed no evidence of a protective effect of iodine supplementation during pregnancy."

I don't know what and how much to make of the findings as they stand, aside from suggesting that other recent findings [4] also questioning the value of daily iodine supplementation "in mildly iodine-deficient pregnant women" perhaps add to the discussions in this area. MoBA represents a great resource in these days of population science, so one can't blame the findings on a lack of "large sample size, prospective design, extensive collection of data, and the possibility of linking the cohort to national registries." It could, therefore, well be that talk on iodine supplementation during early pregnancy perhaps needs a lot more science behind it before anyone makes any grand, sweeping claims about its usefulness...

To close, in case you're wondering about the photo included in this post, it's all part of the Public Health England 'celebrations' for 100 years of public health marketing (see here).

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[1] Abel MH. et al. Maternal Iodine Intake and Offspring Attention-Deficit/Hyperactivity Disorder: Results from a Large Prospective Cohort Study. Nutrients. 2017 Nov 13;9(11). pii: E1239.

[2] Silva RR. et al. A rating scale for disruptive behavior disorders, based on the DSM-IV item pool. Psychiatr Q. 2005 Winter;76(4):327-39.

[3] Abel MH. et al. Suboptimal Maternal Iodine Intake Is Associated with Impaired Child Neurodevelopment at 3 Years of Age in the Norwegian Mother and Child Cohort Study. J Nutr. 2017 Jul;147(7):1314-1324.

[4] Gowachirapant S. et al. Effect of iodine supplementation in pregnant women on child neurodevelopment: a randomised, double-blind, placebo-controlled trial. Lancet Diabetes Endocrinol. 2017 Nov;5(11):853-863.

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Obesity and overweight in autism meta-analysed

So: "The meta-analysis showed a significant association between obesity and ASD [autism spectrum disorder]. However, no significant association was identified between overweight and ASD."

Those were the conclusions reached by Zhen Zheng and colleagues [1] (open-access) who surveyed the pertinent peer-reviewed science literature up to November 2016 on the topic of the prevalence of overweight and obesity in relation to the autism spectrum (see here).

Including some 15 studies in their meta-analysis mix "encompassing 49,937,078 participants and 1,045,538 individuals with ASD" authors observed a connection between obesity and autism (a body mass index - BMI - between 30 and 39 for obesity and 40 and over for severely obese) but not being overweight. Among the many analyses undertaken by the authors, we are told that "the sensitivity analysis showed that removing any study did not change the final results, suggesting that our findings were robust."

Zheng et al have covered many bases when it comes to the interpretation of their findings. Feeding and eating issues potentially making "healthy dietary interventions less effective"... check (see here). Physical activity levels and 'sedentary activities'... check (see here). Potential side-effects of medication - antipsychotic medication in particular - check (see here). Also: "some individuals with ASD have been reported to have 16p11.2 or 11p14.1 microdeletions, which encompass genes related to obesity susceptibility." Yup, some genetic conditions that manifest autism also place that person at a greater risk for weight issues, either directly or peripherally.

Minus any sweeping generalisations, there are some obvious implications from such results. Obesity places a person at some heightened risk for various adverse health outcomes and potentially, early mortality outside of other, more socially-defined adversities. Prevention and treatment are key. Yes, facets of autism may make intervention slightly more complicated than perhaps noted in not-autism populations but that does not mean that one should not try to impact on the variables that lead someone down a pathway to obesity. And such intervention should be multi-faceted and perhaps also take into account a role for comorbidity that seemingly follows autism (see here)...

Oh, and probably relevant to today's posting, the scientific support for the old "healthy at every size" notion is dwindling...

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[1] Zheng Z. et al. Association among obesity, overweight and autism spectrum disorder: a systematic review and meta-analysis. Sci Rep. 2017 Sep 15;7(1):11697.

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Food neophobia and autistic traits (or at least AQ defined autistic traits)

I was rather interested in the findings reported by Lorenzo Stafford and colleagues [1] suggesting "a positive association between food neophobia and the magnitude of autistic traits." Food neophobia is a fear of eating new or unfamiliar foods, and is something that most parents will have encountered at some point in their child/children's lives. With autism in mind, this type of issue is seemingly not uncommon in amongst various other food-related symptoms that can also be present.

Looking at the "broader aspects of autistic traits" and specifically whether a non-autistic (not diagnosed with autism) population showed any connection between their scores on the Autism Spectrum Quotient (AQ) and their scores on the Food Neophobia Scale (FNS), authors set about their study. They also examined whether olfactory sensitivity - "an olfactory threshold test for a food related odour" - might also show an effect in any relationship.

As per the opening paragraph to this entry, authors reported something of a relationship between AQ scores and FNS scores. Importantly, olfactory sensitivity did not seem to link in with AQ scores, suggesting that the link with food neophobia was not necessarily because of enhanced food odour perception for example. At least in this cohort.

This is potentially important work. Bearing in mind the quite small participant group (N=50), the reliance on "student participants" (not always the most representative of groups) as a non-clinical group and the assumption that AQ is actually measuring just the traits of autism (see here), the findings carry some interest. If there is indeed a connection between autistic traits and food neophobia, one could quite sensibly ask whether intervention(s) to ameliorate or reduce certain autistic traits might have some important knock-on effects for aspects of problematic food-related behaviours in relation to autism. Y'know, similar to the idea offered by other independent studies suggesting for example, that anxiety in the context of autism might be influenced by core traits (such as RRBs [restricted and repetitive behaviours]) and the implications thereof. Further investigations are implied.

And for those who might not fully understand just what food-related issues can mean in the context of autism...

Music to close: Harder, Better, Faster, Stronger.

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[1] Stafford KD. et al. Autistic traits associated with food neophobia but not olfactory sensitivity. Appetite. 2017. June 3.

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The strengthening relationship between eating disorders and ADHD

The results from Loretta Sala and colleagues [1] confirms a recent trend in research circles observing a potentially important relationship between various types of eating disorder and the presence of traits/behaviours consistent with a diagnosis of attention-deficit hyperactivity disorder (ADHD).

It's something that has been covered on this blog previously (see here) and represents an extension to the idea that the presentation of autistic traits might not be the only relevant comorbidity when it comes to eating disorders (ED) (see here).

Sala et al report results based on a sample of some 70 female inpatients "all with longstanding histories of eating disorder (ED)." Various scales and instruments were used to assess both ED and ADHD traits/symptoms including the "presence of a diagnosis of ADHD." Accepting the rather nebulous term ED, participants were divided up into specific groups based on the type of eating disorder present: anorexia nervosa restricting type (AN-R), anorexia nervosa binge-eating/purging type (AN-BP) and bulimia nervosa (BN).

Results suggested that ADHD comorbidity is not necessarily an uncommon feature among quite a few cases of ED: "13 patients reported comorbidity with ADHD; three in the AN-R subtype, nine in the AN-BP and one in the BN." Findings also suggested that further research efforts might need to be directed into how ADHD traits/symptoms correlates with other features in cases of ED; specifically in relation to scores on the EAT-40 and the presence of anxiety as measured by the Hamilton scales for Anxiety (HAM-A).

It can only be a good thing that science and clinical practice is beginning to understand that various behavioural/psychiatric labels are rarely observed in isolation to other comorbidity. Not only does this offer potential new avenues for screening/prevention/treatment (see here for one example) but could also provide some much-needed clues as to why conditions such as ED might come about and indeed, who might be particularly at risk for such conditions.

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[1] Sala L. et al. Attention-deficit/hyperactivity disorder symptoms and psychological comorbidity in eating disorder patients. Eat Weight Disord. 2017 May 22.

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Sala L, Martinotti G, Carenti ML, Romo L, Oumaya M, Pham-Scottez A, Rouillon F, Gorwood P, & Janiri L (2017). Attention-deficit/hyperactivity disorder symptoms and psychological comorbidity in eating disorder patients. Eating and weight disorders : EWD PMID: 28534123

Depression, SMILES and Modified Mediterranean diet (advice)

SMILES in the title of this post refers to the SMILES trial - Supporting the Modification of lifestyle In Lowered Emotional States - and results recently published by Felice Jacka and colleagues [1] (open-access) pertinent to the idea that "dietary improvement" might be something to consider when a diagnosis of major depressive episode (MDE) is received.

Having previously published their study protocol [2], researchers set about looking at whether under "single blind, randomised controlled" conditions, the application of advice pertinent to a diet - the 'ModiMedDiet' - focused on increasing diet quality along Mediterranean diet lines, might be useful for those diagnosed with MDE. The results (which had already been revealed before peer-reviewed publication) said 'yes', such an intervention might be something to consider based on scoring of the Montgomery–Åsberg Depression Rating Scale (MADRS) after 3 months of "individual nutritional consulting sessions delivered by a clinical dietician."

Looking at two groups, those randomly allocated to dietary advice/intervention (n=31 completing) and those allocated to a control condition (social support) (n=25 completing), researchers noted improvements in the MADRS scores more frequently in the diet intervention group. To quote: "At 12 weeks, 32.3% (n = 10) of the dietary support group and 8.0% (n = 2) of the social support control group achieved remission criteria of a score less than 10 on the MADRS." Similar differences were also noted on other study schedules: the Hospital Anxiety and Depression Scale (HADS)-depression subscale.

Caveats? Well as a seasoned veteran of research looking at how dietary intervention for labels generally thought to be outside of the somatic domain can go, I can testify to the limitations attached to this kind of work associated with a lack of double-blindedness and issues associated with dietary compliance. This was also a study providing dietary support and so was not necessarily making study controlled meals for each participant over the course of the study (lessons from other recent research show that advice and prompts can only go so far in dietary studies). The authors also note that they "recruited participants on the basis of existing ‘poor’ quality diet" and how "this may limit the generalisability of our findings to the wider population of individuals with depression." An important point indeed.

But this study represents important work and provides yet more evidence that 'nutritional medicine' should perhaps be part of mainstream psychiatry (see here). You can um-and-ah about whether 'food is medicine' and all that jazz (have you never heard of pharmacognosy?) but I'm firmly with the idea that what we eat might, on occasion and for some people, have some pretty profound implications for things other than our physical health and that includes depression (included in several forms)...

To close, a note to any would-be ageing karateka, middle-aged hips tend to take a little more time to get used to perfecting yoko geri kekomi (pass the ibuprofen please). But practice does (eventually) make perfect...

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[1] Jacka F. et al. A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial). BMC Medicine. 2017; 15: 23.

[2] O'Neil A. et al. A randomised, controlled trial of a dietary intervention for adults with major depression (the “SMILES” trial): study protocol. BMC Psychiatry. 2013; 13: 114.

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Jacka, F., O’Neil, A., Opie, R., Itsiopoulos, C., Cotton, S., Mohebbi, M., Castle, D., Dash, S., Mihalopoulos, C., Chatterton, M., Brazionis, L., Dean, O., Hodge, A., & Berk, M. (2017). A randomised controlled trial of dietary improvement for adults with major depression (the ‘SMILES’ trial) BMC Medicine, 15 (1) DOI: 10.1186/s12916-017-0791-y

ADHD, obesity and bariatric surgery?

"The findings suggest that a considerable number of patients before and after bariatric surgery screened positive for ADHD [attention-deficit hyperactivity disorder]. It can be hypothesized that some core ADHD symptoms improve after surgery."

Bariatric surgery, where several surgical options are available to aid weight loss in those who present with 'dangerous' obesity, was the topic of the paper by Nielsen and colleagues [1] (open-access available here) who set out to compare "pre- and post-bariatric surgery patients using the internationally used Conners' Adult ADHD Rating Scale (CAARS™) to screen for ADHD" among other measures. The authors came up with some interesting details. They reported that the rate of 'probably ADHD' (defined using the CAARS and also the Wender Utah Rating Scale Short Version (WURS-k) cut-off scores) were 8.3% in their pre-surgery sample (n=120) and 6.3% in their post-surgery sample (n=128).

When looking at the behavioural profiles of those pre- and post-surgery, there were some not entirely unexpected differences when it came to items related to depression and eating-related psychopathology - both scoring lower in the post-surgery participants. But also those post-surgery reported some potentially important information in relation to generally better attention and memory compared to pre-surgery participants. I was intrigued by the authors explanation of this: "The finding of a better attention and memory function in the post-surgery sample is in line with the results of longitudinal studies demonstrating improvements in cognitive functioning following bariatric surgery." Further: "It is reasonable to assume that postoperative cognitive improvement in attention and memory might have impacted the self-report on the respective CAARS subscale." Does this imply that bariatric surgery might act as some kind of nootropic for [some of] those with obesity?

In these days of ADHD being 'linked' to obesity (see here), the Nielsen results fit nicely. Alongside the idea that weight loss surgery might link into improved cognitive functioning and onwards, impacting on facets of ADHD I'd have to question what the biological mechanism(s) might be. Does the restriction of food intake as a consequence of surgery indicate a role for food in some cognitive processes? Does such surgery potentially impact on the trillions of wee beasties that populate our gut and then onwards exert an effect of cognitive processes? There are several questions that still need answering...

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[1] Nielsen F. et al. Attention Deficit Hyperactivity Disorder Prevalence and Correlates Pre- and Post-Bariatric Surgery: A Comparative Cross-Sectional Study. Obes Facts. 2017 Jan 20;10(1):1-11.

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Nielsen F, Georgiadou E, Bartsch M, Langenberg S, Müller A, & de Zwaan M (2017). Attention Deficit Hyperactivity Disorder Prevalence and Correlates Pre- and Post-Bariatric Surgery: A Comparative Cross-Sectional Study. Obesity facts, 10 (1), 1-11 PMID: 28103594

Urban neighbourhood, food and risk of psychosis?

It's another research mash-up today as I bring to your attention two papers talking about potential correlates associated with psychosis and/or psychotic symptoms.

First up are the findings reported by Joanne Newbury and colleagues [1] (open-access here) who observed that urban residency and certain factors associated with urban residency might link into a higher risk of childhood psychotic symptoms. A second paper by Tomasz Pawełczyk and colleagues [2] provides some further food for thought and the suggestion that "dietary patterns of PUFA [polyunsaturated fatty acids] consumption may play a role in the conversion to psychosis of HR [ultra high-risk] individuals."

Newbury et al report findings from the Environmental Risk (E-Risk) Longitudinal Twin Study and specifically the idea of "whether specific features of urban neighborhoods increase children's risk for psychotic symptoms." Aside from finding a potential association between urban residency at aged 5 and aged 12 and psychotic symptoms at aged 12, researchers also suggested that: "Low social cohesion, together with crime victimization in the neighborhood explained nearly a quarter of the association between urbanicity and childhood psychotic symptoms after considering family-level confounders."

Pawełczyk et al continued a research theme suggesting that what we do or do not eat might have implications for some with regards to transition to psychosis (see here). Focusing specifically on a group of HR individuals, they looked at the diet of those who did and did not transition into psychosis. They reported: "C-HR [converted into psychosis] individuals reported significantly higher consumption of n-6 fatty acids (linoleic acid, LA and arachidonic acid, AA) in comparison with individuals who did not develop psychosis (NC-HR)."

Although not seemingly covering the same factors when it comes to psychosis/psychotic symptoms, one of the things that I thought might also unite both these findings is food. Yes, Pawełczyk et al already talk about food (albeit based on the warts and all use of "a validated Food-Frequency Questionnaire") but the Newbury paper might also include a food element insofar as what types of food might be more readily available and eaten in urban vs. not-so-urban environments.

Bearing in mind that sweeping generalisations about food availability and importantly, what types of food are available depending on where one lives, are not required, I would like to suggest that spatial patterning of say, supermarkets vs. fast food outlets might be something that could potentially unite results. The paper by Lamichhane and colleagues [3] for example found that: "the availability of supermarkets and fast food outlets differed significantly by neighborhood characteristics; neighborhoods with supermarkets and with fast food outlets were significantly higher in socio-economic status." Research looking at the causes and/or drivers of obesity have tended to predominate in the area of how neighbourhood might influence eating patterns [4] but similar modelling could be done with more psychiatric outcomes in mind. Indeed to quote Newbury et al: "Neighborhood-level physical exposures such as noise, light, and air pollution, as well as exposure to viral infections warrant research in relation to early psychotic symptoms." Who says that food should not also be included?

I don't want to gloss over just how complicated the factors might be bringing someone to clinically relevant psychotic symptoms nor to say that food is somehow the 'missing' element for all cases. But it's not outside of the realms of possibility that in these days of nutritional psychiatry, food might exert an important effect for some people and food availability (certain food availability) could be one factor contributing to the idea that where you live might affect your risk of psychosis...

And if that wasn't enough speculating, how about sweeping generalisations about maternal smoking habits and prenatal nicotine exposure as a risk factor for psychosis+ [5] as something else potentially linked to urban living?

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[1] Newbury J. et al. Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophr Bull. 2016 May 6. pii: sbw052.

[2] Pawełczyk T. et al. The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals. Prostaglandins Leukot Essent Fatty Acids. 2016 May;108:30-7.

[3] Lamichhane AP. et al. Spatial patterning of supermarkets and fast food outlets with respect to neighborhood characteristics. Health & place. 2013;23:10.1016/j.healthplace.2013.07.002.

[4] Macdonald L. et al. Neighbourhood fast food environment and area deprivation—substitution or concentration? Appetite. 2007; 49: 251-254.

[5] Niemelä S. et al. Prenatal Nicotine Exposure and Risk of Schizophrenia Among Offspring in a National Birth Cohort. American Journal of Psychiatry. 2016. May 24.

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Pawełczyk, T., Trafalska, E., Kotlicka-Antczak, M., & Pawełczyk, A. (2016). The association between polyunsaturated fatty acid consumption and the transition to psychosis in ultra-high risk individuals Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA), 108, 30-37 DOI: 10.1016/j.plefa.2016.03.010




Newbury J, Arseneault L, Caspi A, Moffitt TE, Odgers CL, & Fisher HL (2016). Why are Children in Urban Neighborhoods at Increased Risk for Psychotic Symptoms? Findings From a UK Longitudinal Cohort Study. Schizophrenia bulletin PMID: 27153864

Bacterial origin and transferability of depression?

The paper by Zheng and colleagues [1] caught my eye recently and the interesting ideas that "dysbiosis of the gut microbiome may have a causal role in the development of depressive-like behaviors" and "transplantation of GF [germ-free] mice with ‘depression microbiota’ derived from MDD [major depressive disorder] patients resulted in depression-like behaviors compared with colonization with ‘healthy microbiota’ derived from healthy control individuals."

Bearing in mind the focus on mice not people in these results, it's not necessarily new news that the trillions of bacteria that call our gut home might be doing so much more than just helping to digest food and producing the odd vitamin or two. I've covered the concept a few times on this blog (see here for example) and how the so-called gut-microbiota-brain axis is gaining some scientific ground [2].

Whilst there are still quite a few more investigations to do in this area, this is not the first time that elements of the gut microbiome have been implicated in a complex condition like depression (see here) including how certain routinely available medicines might also show some involvement (see here). Zheng et al elaborate on some of the types of bacteria that might play a role in their results - "the gut microbiotic compositions of MDD patients and healthy controls were significantly different with MDD patients characterized by significant changes in the relative abundance of Firmicutes, Actinobacteria and Bacteroidetes" - but I think we have to be a little cautious about casting 'blame' just yet. The gut houses quite a lot more than just bacteria y'know and it's not outside the realms of possibility that elements of the gut virome for example, might also be able to exert some effect.

The idea of potential 'transferability' or transmission of depression [3] as a function of gut bacteria or other elements also gathers ground based on the Zheng findings. Accepting that familial transmission of depression is not an entirely new concept, the idea that genetic and other non-genetic factors might be complimented by sharing a similar gut microbial profile is a tantalising idea. Not least also because there is the prospect of 'changing' the gut microbiome [4] and potentially impacting on the the presentation of at least some 'types' of depression [5] alongside various other conditions. I say this also with the understanding that depression is a complicated condition and that various other 'biological' factors might also play an important role in presentation (see here and see here)...

But this is interesting work.

Music - and yet again, The Gimme Gimmes with I will survive...

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[1] Zheng P. et al. Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism. Molecular Psychiatry. 2016. April 12.

[2] Rogers GB. et al. From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Molecular Psychiatry. 2016. April 19.

[3] Canli T. Reconceptualizing major depressive disorder as an infectious disease. Biology of Mood & Anxiety Disorders. 2014;4:10.

[4] Evrensel A, Ceylan ME. The Gut-Brain Axis: The Missing Link in Depression. Clinical Psychopharmacology and Neuroscience. 2015;13(3):239-244.

[5] Dinan TG. et al. Psychobiotics: a novel class of psychotropic. Biol Psychiatry. 2013 Nov 15;74(10):720-6.

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Zheng, P., Zeng, B., Zhou, C., Liu, M., Fang, Z., Xu, X., Zeng, L., Chen, J., Fan, S., Du, X., Zhang, X., Yang, D., Yang, Y., Meng, H., Li, W., Melgiri, N., Licinio, J., Wei, H., & Xie, P. (2016). Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism Molecular Psychiatry DOI: 10.1038/mp.2016.44

#Breadgate and nutritional psychiatry

The review paper by Paola Bressan & Peter Kramer [1] (open-access) titled: 'Bread and Other Edible Agents of Mental Disease' has been getting a few people a little hot under the collar recently. With it's own Twitter hashtag #breadgate it looks like the idea that certain foods might have something of a bearing on "human behaviour and mental health" has not been received particularly well. I might add that this not the first time that such ideas have been entertained (see here) but there was no such outcry on previous occasions...

As anyone who drops by this blog might know, I'm quite interested in the idea that what we eat and how it's metabolised might have some important implications for SOME people in terms of not just their physical health but also other facets covering behaviour and cognition. I've also talked about it in the peer-reviewed domain quite a bit too using conditions such as phenylketonuria (PKU) as a template. In their latest paper, Bressan & Kramer discuss the quite long-running idea that [some] cereal grains, the starting material for foods like bread, might have some interesting physiological effects that could have a bearing on mental health and wellbeing.

I should at this point mention that I was invited to peer-review the Bressan / Kramer article. I accepted (given my research in this area) and as well as providing a review also let the editor and authors know that my view whilst as unbiased as possible did come alongside a few conflicts of interest (COIs) such as the book that graces the edge of this blog. The journal editor accepted this fact and my comments alongside those of a far more notable researcher were included in the peer-review process.

The Bressan / Kramer paper presents quite a thorough overview of the research looking at food and psychiatry. The language is quite stark in places as words like 'defect' and 'derangement' are included in the text (something that I queried during peer-review) and with a sub-heading titled 'Diet as a Cure' the authors are pretty forth-right in their interpretation of the available peer-reviewed evidence. I would be perhaps less strong in any claims made but ho-hum. I might add that this is not the first time that this authorship team have talked about big hypotheses...

Without seeming like I am springing to the defence of the Bressan / Kramer paper I have decided to list a few previous blog entries that I've written about other relevant texts in the peer-reviewed domain that add something to the discussions in this area. I'm sure that Bressan / Kramer if they have heard about the 'discussions' around their paper are able to defend their writings and so I'm not doing this to somehow cover their backs. I do however think it is important to talk about this topic and this is as good an opportunity as any...

So:

Brain and gut in autism: a historical perspective
For many years now, diet and [some] autism has been discussed. The work of the late Curt Dohan was the leader in this emerging field and his suggestion that [some] schizophrenia might have a dietary component. Before you ask it, no, no-one has ever said that diets devoid of gluten and casein are some sort of cure-all for all autism... they're not. But that does not mean there might be 'best responders' to this type of intervention (see here) in terms of their effect on some behaviours linked to autism. The mechanism for any effect from diet could also be multi-fold (see here).

Psychotic symptoms managed by a gluten-free diet?
Yes. it's a case report, but there are quite a few of them in the peer-reviewed literature talking about dietary manipulations seemingly affecting often quite severe psychiatric presentation. There are more controlled trials too if you want to have a look...

More gluten sensitivity and schizophrenia
The immune system seems to be in the ascendancy when it comes to psychiatry these days (see here also) and diet has been mentioned as an influencing variable on immune function...

Gluten free diet adherence reduces depression in coeliac disease
Building on the idea that coeliac disease - that archetypal autoimmune condition where gluten is the baddie - might have quite a few more 'presentations' than just the physical, there is some emerging peer-reviewed evidence to suggest that adherence to a gluten-free diet might have multiple benefits for certain groups.

Just what is 'non-coeliac gluten sensitivity'?
The idea that outside of coeliac disease there may be a spectrum of 'gluten-related ills' is not a new one. There are still gaps in the research literature and in particular, whether non-coeliac gluten sensitivity (NCGS) might intersect with certain behavioural and/or psychiatric labels but...

Schizophrenia and milk
With the focus also on milk, or rather the casein protein that is also said to produce peptide metabolites that might not be a millions miles away from various opioid-like compounds like to gluten digestion (hence the name casomorphins), I've included reference to the David Niebuhr et al paper too titled: 'Association between bovine casein antibody and and new onset schizophrenia among US military personnel'. Correlation is not causation but this and other data are interesting.

Intestinal permeability: an emerging scientific area (also with autism in mind)
Gluten 'punching holes in the gut' is mentioned in some of the discussion about the Bressan / Kramer paper and with it the words 'leaky gut' make an appearance. As per my ramblings on some of the peer-reviewed science in this area, there is emerging evidence for this concept in relation to specific conditions including the fantastic paper by Laura de Magistris and colleagues [3] citing food as having a potentially modifying effect.

These are just a selection of the entries that I've written on this blog covering the topic of nutritional psychiatry (see here) but there are more. Accepting that "mental disease" (authors term not mine) covers quite a lot of ground and even within the various labels we have a lot of heterogeneity (see here for example) I would suggest that more research is required into how diet might influence behaviour and psychiatry. The paper by Dash et al [3] similarly titled: 'Diet and common mental disorders; the imperative to translate evidence into action' recently published (in the same family of journals) reiterates that there is more to do in this area including the identification of potential 'best responders' to this type of approach. Diet again, is not put forward as a cure-all for every single label/condition, but that doesn't mean it might not be useful to look at it for some.

I know there is still quite a lot of hostility to the idea that what we eat (or don't eat) might have a bearing on something other than physical health. I'm not advocating for any universal 'change your diet to this' approach to manage mental health issues but I do believe that there is enough peer-reviewed science out there to merit some further sensible discussions on the topic...

Music to close, and what else but Toast... a little bit of toast.

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[1] Bressan P. & Kramer P. Bread and Other Edible Agents of Mental Disease. Front Hum Neurosci. 2016 Mar 29;10:130.

[2] de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.

[3] Dash SR. et al. Diet and common mental disorders; the imperative to translate evidence into action. Front. Public Health | doi: 10.3389/fpubh.2016.00081.

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Bressan P, & Kramer P (2016). Bread and Other Edible Agents of Mental Disease. Frontiers in human neuroscience, 10 PMID: 27065833

Autism in phenylketonuria (PKU)

"Autism has been reported in untreated patients with phenylketonuria."

Indeed it has, as the paper by Sameh Khemir and colleagues [1] revisits something of a long known about association whereby the archetypal inborn error of metabolism that is phenylketonuria (PKU) has been linked to the presentation of autism or autistic traits [2].

Looking at 18 participants diagnosed with PKU, Khemir et al "report their clinical, biochemical and molecular peculiarities" (authors words not mine) and how 15 of the 18 presented with autism as per assessment with "The Childhood Autism Rating Scale and the Autism Diagnostic Interview-Revised." Following some molecular biological analysis specifically with the "phenylalanine hydroxylase gene" in mind (a key player in PKU), the authors reported on various potentially important issues but "no correlation between autism and mutations affecting the phenylalanine hydroxylase gene."

I have a lot of time for PKU on this blog. Not only because PKU represents one of the best examples of how certain foods for some can affect development and onwards mental health (see here) but also because some of the other intervention options for PKU (outside of low phenyalanine diet) might hold some promise for some autism too (see here). Indeed, the idea that tetrahydrobiopterin (BH4) - an important cofactor for phenyalanine hydroxylase and related aromatic amino acid hydroxylase enzymes - might be quite good at helping to mop up excess phenylalanine and other compounds continues to find favour in some autism research circles. Dare I also mention the effects of BH4 on tryptophan and 5-HTP as potentially being relevant to some autism too? (see here)

In many parts of the world, the advent of the newborn screening program (built on the genius of people like Robert Guthrie and others) has all but eradicated untreated PKU and perhaps impacted on the number of people presenting with autism too. There remain however, challenges in certain areas of the globe, where people are not so fortunate to have such screening measures in place. Indeed, Khemir and colleagues report their results based in Tunisia and Algeria; other geographically related areas might also benefit from the implementation of such screening practices [3].    

Just before I go, there is one last comment to make on something discussed by Khemir and colleagues: "age of diet onset was the determining factor in autistic symptoms' evolution." Diet, as I've mentioned, refers to the low phenylalanine (low protein) diet commonly used to manage PKU. It appears that there might be more to see in terms of how long PKU goes untreated and the progression of autistic traits similar to other descriptions, particularly the findings reported by Baieli and colleagues [4]: "None out of 62 patients with classic PKU diagnosed early met criteria for autism. In the group of 35 patients diagnosed late, two boys (5.71%) ages 16 and 13 years fulfilled the diagnostic criteria for autism."

Diet potentially affecting the presentation of autism eh? I'll be coming to the paper by Oyarzabal and colleagues [5] soon enough built on some related research...

Music: Led Zeppelin - Rock And Roll.

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[1] Khemir S. et al. Autism in Phenylketonuria Patients: From Clinical Presentation to Molecular Defects. J Child Neurol. 2016 Jan 12. pii: 0883073815623636.

[2] Miladi N. et al. Phenylketonuria: an underlying etiology of autistic syndrome. A case report. J Child Neurol. 1992 Jan;7(1):22-3.

[3] Saad K. et al. ADHD, autism and neuroradiological complications among phenylketonuric children in Upper Egypt. Acta Neurol Belg. 2015 Dec;115(4):657-63.

[4] Baieli S. et al. Autism and phenylketonuria. J Autism Dev Disord. 2003 Apr;33(2):201-4.

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

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Khemir S, Halayem S, Azzouz H, Siala H, Ferchichi M, Guedria A, Bedoui A, Abdelhak S, Messaoud T, Tebib N, Belhaj A, & Kaabachi N (2016). Autism in Phenylketonuria Patients: From Clinical Presentation to Molecular Defects. Journal of child neurology PMID: 26759449

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

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