A hypothesis arising from the epidemiology of schizophrenia in Maori

The concept and the epidemiology of schizophrenia have been a focus of research in the mental health field for more than 100 years.

While nosologists have almost always recognized it as a syndrome, rather than a specific disease, the mental health service statistics frequently use the term as though it is a diagnostic entity. Many theories of etiology or pathogenesis have been enthusiastically propounded, often to fall by the wayside as unconfirmed or only as minor contributors to the pathogenesis. Variable genetic predisposition with possibly multiple possible environmental enhancers is the main fallback position. There has been a general consensus that the lifetime incidence of schizophrenia in most populations approaches 1%, but there have been a number of reports of higher rates in ethnic subgroups which have usually been taken to probably reflect particular stressors on those groups.

Until this millennium, the epidemiology of most mental illnesses in New Zealand has been mainly understood by extrapolation from studies undertaken in other countries supplemented by predominantly hospital statistics and qualitative observations or comments. In the last 50 years, a variety of authors have moved from expressing concerns about an apparent underutilization of mental health services by Maori to recognition and quantification of their overrepresentation, at least as reflected in secondary service use. The first community-based study conducted in New Zealand concluded that in only two diagnostic groups, Maori were statistically significantly overrepresented (Browne et al., 2006). One of those categories was substance abuse disorders. That study did not comment on the rates of schizophrenia due to the relative rarity of that disorder in a community-based study. In recent years, two groups of researchers have attempted to quantify the epidemiology of schizophrenia in Maori and non-Maori (Kake et al., 2008; Tapsell et al., 2018). Using quite different research designs, they have demonstrated significantly increased prevalence and incidence of clinical schizophrenia in Maori, when compared with the rest of the New Zealand population. Their reported twofold to threefold increases exceeded the rates which could be attributed to cross-culturally uninformed misdiagnoses. Although good data are not available, there is no evidence that such increased rates of schizophrenia were present in most of last century.

It has been well recognized that amphetamines can produce a mental state mimicking the phenomenological presentation of schizophrenia. The capacity of illicit drugs, particularly methamphetamine and some forms of cannabis, to produce a disorder which resembles schizophrenia in its course and chronicity had been raised in Swedish prospective research published in the Lancet in 1987 and further described with more confidence in the literature (Murray et al., 2016). Accordingly, we now know that some people develop schizophrenia symptoms because of heavy methamphetamine use. With both cannabis derivatives and methamphetamine, the increased risk of later schizophrenic psychosis is dose (frequency and quantity of use) related and the role of genetic susceptibility unconfirmed (Murray et al., 2016).

It is now established that the availability and use of methamphetamines have risen exponentially in New Zealand over the last 10 years. A New Zealand Police Insight Report of April 2018 notes that the numbers arrested and detained while under the influence of methamphetamine increased approximately tenfold from 2010 to 2017. Interestingly, a fivefold increase in amphetamine-related hospital admissions in Australia in the period 2009 to 2015 has also been recently noted by Sara et al. (2018).

The burden of disease due to schizophrenia has been well documented. New Zealand Maori ethnic-related mental health disparities and inequalities have also been frequently publicized. It is important to both Maori and to New Zealand in general that increases in mental morbidity be both understood and remediated.

We propose that the increased burden of schizophrenia in Maori is a consequence of the increased consumption of high-potency cannabis over the last 40 years ¹ and the more recent increase in methamphetamine use. ² This would be consistent with the recent Australian demonstration of the five- to tenfold increase in amphetamine-related admissions (Sara et al., 2018)—the findings of the Te Rau Hinengaro (Browne et al., 2006) and the reports of the general relationship between the use of those illicit substances and the syndrome of schizophrenia.

This hypothesis could be examined and tested by researchers and provide a basis for the planning of preventive and/or therapeutic activities. Longitudinal studies, prospective or even retrospective if appropriate data sources could be found, could examine our hypothesis. These are necessary to clarify the extent to which the observed increases in drug use and schizophrenia are causally related or fellow travelers with some shared etiologic contributors. Understanding such relationships should contribute to the development of helpful national policies or interventions which are very necessary given the burden of this syndrome.