"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
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