Australian & New Zealand Journal of Psychiatry

Cannabis use is prevalent among people with first episode psychosis and the epidemiology of its use in early psychosis is unclear. We performed a meta-analysis of observational studies to determine; (1) the interval between age at initiation of cannabis use and age at onset of first episode psychosis, (2) the prevalence of cannabis use at time of first episode psychosis, and (3) the odds of continuing cannabis following treatment for first episode psychosis.

Search of electronic databases MEDLINE, EMBASE, PsycINFO, Web of Science and CINAHL for English-language papers using search terms (psychosis OR schizophrenia) AND (cannabis OR marijuana) IN (title OR keyword OR abstract), current to October 2014.

Studies were included if they reported on prevalence of current cannabis use in first episode psychosis cohorts. A total of 37 samples were included for meta-analysis.

Rates of cannabis use in each sample were extracted to determine prevalence estimates. The age at initiation of regular cannabis and age at onset of psychosis were used to determine the length of cannabis use preceding psychosis. Prevalence estimates at first episode psychosis and various time points of follow-up following first episode psychosis were analysed to determine odds ratio of continuing cannabis use. Data synthesis was performed using random-effects meta-analyses.

The pooled estimate for the interval between initiation of regular cannabis use and age at onset of psychosis was 6.3 years (10 samples, standardised mean difference = 1.56, 95% confidence interval = [1.40, 1.72]). The estimated prevalence of cannabis use at first episode psychosis was 33.7% (35 samples, 95% confidence interval = [31%, 39%]). Odds of continued cannabis use between 6 months and 10 years following first episode psychosis was 0.56 (19 samples, 95% confidence interval = [0.40, 0.79]).

Given the sensitivity of individuals with mood disorders to circadian disruption, transmeridian travel would likely be a high-risk endeavour leading to onset or relapses in mood. A systematic review was undertaken to identify the evidence of the impact of transmeridian travel on people with mood disorders.

Databases search included the following: CINAHL, MEDLINE, PsycINFO and manual searching using the keywords jetlag, transmeridian travel, circadian rhythm disruption, mood disorder, bipolar, major depression, seasonal affective disorder, depression, mania and hypomania.

Only three studies were identified that related to transmeridian travel and jetlag in people with mood disorders. There is some suggestion that transmeridian travel does appear to precipitate mood episodes with an increased rate of episodes of depression with westward compared with an increased rate of manic/hypomanic episodes with eastward travel. Individuals with a previous history of mood disorder appear to be more vulnerable if adherence to medication is compromised.

Given the limited evidence that transmeridian travel precipitates mood episodes, this poses difficulties in identifying suitable ways to mitigate the effects of transmeridian travel in mood disorders. However, in the absence of mood-specific guidelines, some guidance can be given based on our current understanding of the relevance of circadian disruption to both jetlag and mood disorders. Further research is required to identify more focused strategies to mitigate the impact of transmeridian travel for individuals with mood disorders.

The results from observation studies on the relationship between coffee intake and risk of depression and the relationship between caffeine consumption and depression remain controversial. We conducted a meta-analysis with a dose–response analysis to quantitatively summarize the evidence about the association between coffee and caffeine intakes and risk of depression.

Relevant articles were identified by researching PubMed, Web of Science, China National Knowledge Infrastructure and WANFANG DATA in English or Chinese from 1 January 1980 to 1 May 2015. Case-control, cohort or cross-sectional studies evaluating coffee or caffeine consumption and depression were included. A random-effects model was used to combine study-specific relative risk and 95% confidence interval. Dose–response relationship was assessed by restricted cubic spline functions.

Data were obtained from 11 observation articles; 330,677 participants from seven studies in seven articles were included in the coffee-depression analysis, while 38,223 participants from eight studies in seven articles were involved in the caffeine-depression analysis. Compared with the lowest level consumption, the pooled relative risk (95% confidence interval) for coffee-depression and caffeine-depression was 0.757 [0.624, 0.917] and 0.721 [0.522, 0.997], respectively. For dose–response analysis, evidence of a linear association was found between coffee consumption and depression, and the risk of depression decreased by 8% (relative risk = 0.92, 95% confidence interval = [0.87, 0.97], p = 0.002) for each cup/day increment in coffee intake; a nonlinear association was found between caffeine consumption and depression, the risk of depression decreased faster and the association became significant when the caffeine consumption was above 68 mg/day and below 509 mg/day.

Coffee and caffeine consumption were significantly associated with decreased risk of depression.

The aim of this study was to identify the prevalence of parent-reported autism spectrum disorder diagnosis in Australia, and examine the developmental profile of children with autism spectrum disorder compared to their peers.

Secondary analyses were undertaken on data from the Longitudinal Study of Australian Children.

Children were recruited at kindergarten (K cohort) and birth (B cohort), and subsequently completed two-yearly ‘waves’ of assessments.

Autism spectrum disorder diagnostic status was ascertained at Wave 4 along with age of diagnosis by parent report. Standardised tools were used to assess children’s quality of life, behaviour, receptive vocabulary and non-verbal intelligence.

Prevalence of autism spectrum disorder was 2.5% (95% confidence interval = [2.0, 3.0]) in the B cohort compared to 1.5% (95% confidence interval = [1.2, 2.0]) in the K cohort. In both cohorts, children with autism spectrum disorder had poorer mean quality of life, emotional-behavioural functioning and receptive vocabulary compared with non-autism spectrum disorder peers, and a higher proportion of children with autism spectrum disorder had problems in these areas. However, between 6% and 9% of children with moderate to severe autism spectrum disorder and 12–20% with mild autism spectrum disorder were not reported to have problems with social interaction.

The prevalence of a parent-reported diagnosis of autism spectrum disorder before age 7 in Australia was higher in the B cohort. Data from future Longitudinal Study of Australian Children waves will clarify whether autism spectrum disorder has been diagnosed earlier in the B cohort or if there is a continued increase in prevalence. Future waves will also provide crucial information about the types and severity of problems experienced during the primary and secondary school years which will assist service planning.

Studies of overall cancer incidence and mortality in psychiatric patients have had mixed results. Some have reported lower than expected cancer incidence or mortality, while others have found no association or an increased risk depending on sample, psychiatric diagnosis, cancer site and methodology. Few studies have compared cancer incidence and mortality using the same population and methodology.

A population-based record-linkage analysis to compare cancer incidence and mortality in psychiatric patients with that for the general Queensland population, using an historical cohort to calculate age- and sex-standardised rate ratios and hazard ratios. Mental health records were linked with cancer registrations and death records from 2002 to 2007.

There were 89,992 new cancer cases, of which 3349 occurred in people with mental illness. Cancer incidence was the same as the general population for most psychiatric disorders. Rates were actually lower for dementia (hazard ratio = 0.77; 95% confidence interval = [0.67, 0.88]) and schizophrenia (hazard ratio = 0.84; 95% confidence interval = [0.72, 0.98]). By contrast, mortality was increased in psychiatric patients (hazard ratio = 2.27; 95% confidence interval = [2.15, 2.39]) with elevated hazard ratios for all the main psychiatric diagnoses.

Lifestyle, such as alcohol or tobacco use, would not explain our findings that people with mental illness are no more likely than the general population to develop cancer but more likely to die of it. Other factors may be the difficulty in differentiating medically explained and unexplained symptoms, greater case fatality or inequity in access to specialist procedures. The study highlights the need for improved cancer screening, detection and intervention in this population.

To evaluate the impact of the National Perinatal Depression Initiative on access to Medicare services for women at risk of perinatal mental illness.

Retrospective cohort study using difference-in-difference analytical methods to quantify the impact of the National Perinatal Depression Initiative policies on Medicare Benefits Schedule mental health usage by Australian women giving birth between 2006 and 2010. A random sample of women of reproductive age enrolled in Medicare who had not given birth where used as controls. The main outcome measures were the proportions of women giving birth each month who accessed a Medicare Benefits Schedule mental health items during the perinatal period (pregnancy through to the end of the first postnatal year) before and after the introduction of the National Perinatal Depression Initiative.

The proportion of women giving birth who accessed at least one mental health item during the perinatal period increased from 88 to 141 per 1000 between 2007 and 2010. The difference-in-difference analysis showed that while there was an overall increase in Medicare Benefits Schedule mental health item access as a result of the National Perinatal Depression Initiative, this did not reach statistical significance. However, the National Perinatal Depression Initiative was found to significantly increase access in subpopulations of women, particularly those aged under 25 and over 34 years living in major cities.

In the 2 years following its introduction, the National Perinatal Depression Initiative was found to have increased access to Medicare funded mental health services in particular groups of women. However, an overall increase across all groups did not reach statistical significance. Further studies are needed to assess the impact of the National Perinatal Depression Initiative on women during childbearing years, including access to tertiary care, the cost-effectiveness of the initiative, and mental health outcomes. It is recommended that new mental health policy initiatives incorporate a planned strategic approach to evaluation, which includes sufficient follow-up to assess the impact of public health strategies.

In humans, depending on dose, blocking the N-methyl-d-aspartate receptor (NMDAR) with ketamine can cause psychomimetic or antidepressant effects. The overall outcome for drugs such as ketamine depends on dose and the number of its available binding sites in the central nervous system, and to understand something of the latter variable we measure NMDAR in the frontal pole, dorsolateral prefrontal, anterior cingulate and parietal cortices from people with schizophrenia, bipolar disorder, major depressive disorders and age/sex matched controls.

We measured levels of NMDARs (using [³H]MK-801 binding) and NMDAR sub-unit mRNAs (GRINs: using in situ hybridisation) as well as post-synaptic density protein 95 (anterior cingulate cortex only; not major depressive disorders: an NMDAR post-synaptic associated protein) in bipolar disorder, schizophrenia and controls.

Compared to controls, levels of NMDAR were lower in the outer laminae of the dorsolateral prefrontal cortex (–17%, p = 0.01) in people with schizophrenia. In bipolar disorder, levels of NMDAR binding (laminae IV–VI; –19%, p < 0.01) and GRIN2C mRNA (laminae I–VI; –27%, p < 0.05) were lower in the anterior cingulate cortex and NMDAR binding was lower in the outer lamina IV of the dorsolateral prefrontal cortex (–19%, p < 0.01). In major depressive disorders, levels of GRIN2D mRNA were higher in frontal pole (+22%, p < 0.05). In suicide completers, levels of GRIN2B mRNA were higher in parietal cortex (+20%, p < 0.01) but lower (–35%, p = 0.02) in dorsolateral prefrontal cortex while post-synaptic density protein 95 was higher (+26%, p < 0.05) in anterior cingulate cortex.

These data suggest that differences in cortical NMDAR expression and post-synaptic density protein 95 are present in psychiatric disorders and suicide completion and may contribute to different responses to ketamine.