Queensland Center for Mental Health Research

Summer Hill, Australia

Queensland Center for Mental Health Research

Summer Hill, Australia

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Lee B.K.,Drexel University | Lee B.K.,Aj Drexel Autism Institute | McGrath J.J.,University of Queensland | McGrath J.J.,Queensland Center for Mental Health Research
Trends in Molecular Medicine | Year: 2015

Converging evidence from epidemiological, genetic, and animal studies supports the hypothesis that advancing parental age, both of the father and mother, increases the risk of autism spectrum disorders (ASD) in offspring. Paternal age has received considerable attention, with whole-genome sequencing studies linking older fathers to higher rates of de novo mutations and increased risk of ASD. The current evidence suggests that the increased risk of ASD in the offspring of older mothers may be related to mechanisms different from those operating in older fathers. Causal pathways probably involve the interaction of multiple risk factors. Although the etiology of ASD is still poorly understood, studies of parental age provide clues into the genetic and environmental mechanisms that mediate the risk of ASD. © 2014 Elsevier Ltd.


Norman R.E.,University of Queensland | Byambaa M.,University of Queensland | De R.,University of Queensland | Butchart A.,World Health Organization | And 4 more authors.
PLoS Medicine | Year: 2012

Background: Child sexual abuse is considered a modifiable risk factor for mental disorders across the life course. However the long-term consequences of other forms of child maltreatment have not yet been systematically examined. The aim of this study was to summarise the evidence relating to the possible relationship between child physical abuse, emotional abuse, and neglect, and subsequent mental and physical health outcomes. Methods and Findings: A systematic review was conducted using the Medline, EMBASE, and PsycINFO electronic databases up to 26 June 2012. Published cohort, cross-sectional, and case-control studies that examined non-sexual child maltreatment as a risk factor for loss of health were included. All meta-analyses were based on quality-effects models. Out of 285 articles assessed for eligibility, 124 studies satisfied the pre-determined inclusion criteria for meta-analysis. Statistically significant associations were observed between physical abuse, emotional abuse, and neglect and depressive disorders (physical abuse [odds ratio (OR) = 1.54; 95% CI 1.16-2.04], emotional abuse [OR = 3.06; 95% CI 2.43-3.85], and neglect [OR = 2.11; 95% CI 1.61-2.77]); drug use (physical abuse [OR = 1.92; 95% CI 1.67-2.20], emotional abuse [OR = 1.41; 95% CI 1.11-1.79], and neglect [OR = 1.36; 95% CI 1.21-1.54]); suicide attempts (physical abuse [OR = 3.40; 95% CI 2.17-5.32], emotional abuse [OR = 3.37; 95% CI 2.44-4.67], and neglect [OR = 1.95; 95% CI 1.13-3.37]); and sexually transmitted infections and risky sexual behaviour (physical abuse [OR = 1.78; 95% CI 1.50-2.10], emotional abuse [OR = 1.75; 95% CI 1.49-2.04], and neglect [OR = 1.57; 95% CI 1.39-1.78]). Evidence for causality was assessed using Bradford Hill criteria. While suggestive evidence exists for a relationship between maltreatment and chronic diseases and lifestyle risk factors, more research is required to confirm these relationships. Conclusions: This overview of the evidence suggests a causal relationship between non-sexual child maltreatment and a range of mental disorders, drug use, suicide attempts, sexually transmitted infections, and risky sexual behaviour. All forms of child maltreatment should be considered important risks to health with a sizeable impact on major contributors to the burden of disease in all parts of the world. The awareness of the serious long-term consequences of child maltreatment should encourage better identification of those at risk and the development of effective interventions to protect children from violence. Please see later in the article for the Editors' Summary. © 2012 Norman et al.


McGrath J.,Queensland Center for Mental Health Research | McGrath J.,University of Queensland | Brown A.,Columbia University | St Clair D.,University of Aberdeen
Schizophrenia Bulletin | Year: 2011

Adequate prenatal nutrition is essential for optimal brain development. There is a growing body of evidence from epidemiology linking exposure to nutritional deprivation and increased risk of schizophrenia. Based on studies from the Netherlands and China, those exposed to macronutrient deficiencies during famine have an increased risk of schizophrenia. With respect to micronutrients, we focus on 3 candidates where there is biological plausibility for a role in this disorder and at least 1 study of an association with schizophrenia. These nutrients include vitamin D, folic acid, and iron. While the current evidence is incomplete, we discuss the potential implications of these findings for the prevention of schizophrenia. We argue that schizophrenia can draw inspiration from public health interventions related to prenatal nutrition and other outcomes and speculate on relevant factors that bear on the nature, risks, impact, and logistics of various nutritional strategies that may be employed to prevent this disorder. © The Author 2011. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved.


Nielsen R.E.,Aarhus University Hospital | Uggerby A.S.,Aarhus University Hospital | Jensen S.O.W.,Aarhus University Hospital | McGrath J.J.,Queensland Center for Mental Health Research | McGrath J.J.,University of Queensland
Schizophrenia Research | Year: 2013

Objective: The objective of this study is to describe secular trends in the average age of death in patients with schizophrenia and to compare these with the general population. Methods: This is a longitudinal linkage study from 1 January 1980 to 31 December 2010 using the Danish Psychiatric Research Register and the Danish Cause of Death Register. Data were analyzed using descriptive statistics and survival analysis. Results: The average age of death in the schizophrenia population (62.2. years; 95% CI, 61.9-62.5) was lower compared to the general population (73.4. years; 95% CI, 73.4-73.4), P< 0.001. In the general population we found, for men, an average increase in the age of death of 0.28. years (95% CI, 0.27-0.28) per calendar year, and for women an increase in age of death of 0.31. years (95% CI, 0.31-0.32) per calendar year (both P< 0.001). In contrast, age of death decreased in the schizophrenia population: the change in average age of death for males was 0.04. years (95% CI, - 0.09 to 0.00) per calendar year (P< 0.05), and the comparable estimate for females was - 0.05. years (95% CI, - 0.09 to 0.01) per calendar year (P< 0.05). A similar pattern existed after acts of self-harm as cause of death were excluded from the analyses. Patients diagnosed with schizophrenia had an increased mortality rate compared with the general population (hazard ratio, 2.05; 95% CI, 2.01-2.09). Conclusions: On average, patients with schizophrenia die younger than the general population, independent of intentional self-harm as cause of death. © 2013 Elsevier B.V.


Ferrari A.J.,University of Queensland | Ferrari A.J.,Queensland Center for Mental Health Research | Charlson F.J.,University of Queensland | Charlson F.J.,Queensland Center for Mental Health Research | And 8 more authors.
PLoS Medicine | Year: 2013

Background:Depressive disorders were a leading cause of burden in the Global Burden of Disease (GBD) 1990 and 2000 studies. Here, we analyze the burden of depressive disorders in GBD 2010 and present severity proportions, burden by country, region, age, sex, and year, as well as burden of depressive disorders as a risk factor for suicide and ischemic heart disease.Methods and Findings:Burden was calculated for major depressive disorder (MDD) and dysthymia. A systematic review of epidemiological data was conducted. The data were pooled using a Bayesian meta-regression. Disability weights from population survey data quantified the severity of health loss from depressive disorders. These weights were used to calculate years lived with disability (YLDs) and disability adjusted life years (DALYs). Separate DALYs were estimated for suicide and ischemic heart disease attributable to depressive disorders.Depressive disorders were the second leading cause of YLDs in 2010. MDD accounted for 8.2% (5.9%-10.8%) of global YLDs and dysthymia for 1.4% (0.9%-2.0%). Depressive disorders were a leading cause of DALYs even though no mortality was attributed to them as the underlying cause. MDD accounted for 2.5% (1.9%-3.2%) of global DALYs and dysthymia for 0.5% (0.3%-0.6%). There was more regional variation in burden for MDD than for dysthymia; with higher estimates in females, and adults of working age. Whilst burden increased by 37.5% between 1990 and 2010, this was due to population growth and ageing. MDD explained 16 million suicide DALYs and almost 4 million ischemic heart disease DALYs. This attributable burden would increase the overall burden of depressive disorders from 3.0% (2.2%-3.8%) to 3.8% (3.0%-4.7%) of global DALYs.Conclusions:GBD 2010 identified depressive disorders as a leading cause of burden. MDD was also a contributor of burden allocated to suicide and ischemic heart disease. These findings emphasize the importance of including depressive disorders as a public-health priority and implementing cost-effective interventions to reduce its burden.Please see later in the article for the Editors' Summary. © 2013 Ferrari et al.


Mowry B.J.,University of Queensland | Mowry B.J.,Queensland Center for Mental Health Research | Gratten J.,University of Queensland
Molecular Psychiatry | Year: 2013

After decades of halting progress, recent large genome-wide association studies (GWAS) are finally shining light on the genetic architecture of schizophrenia. The picture emerging is one of sobering complexity, involving large numbers of risk alleles across the entire allelic spectrum. The aims of this article are to summarize the key genetic findings to date and to compare and contrast methods for identifying additional risk alleles, including GWAS, targeted genotyping and sequencing. A further aim is to consider the challenges and opportunities involved in determining the functional basis of genetic associations, for instance using functional genomics, cellular models, animal models and imaging genetics. We conclude that diverse approaches will be required to identify and functionally characterize the full spectrum of risk variants for schizophrenia. These efforts should adhere to the stringent standards of statistical association developed for GWAS and are likely to entail very large sample sizes. Nonetheless, now more than any previous time, there are reasons for optimism and the ultimate goal of personalized interventions and therapeutics, although still distant, no longer seems unattainable. © 2013 Macmillan Publishers Limited.


Eyles D.W.,University of Queensland | Eyles D.W.,Queensland Center for Mental Health Research | Liu P.Y.,University of Queensland | Josh P.,University of Queensland | Cui X.,University of Queensland
Neuroscience | Year: 2014

Apart from its role in regulating calcium there is growing evidence that vitamin D is a neuroactive steroid capable of regulating multiple pathways important for both brain development and mature brain function. Vitamin D induces its genomic effects through its nuclear receptor the vitamin D receptor (VDR). Although there is abundant evidence for this receptor's presence in the mammalian brain from studies employing immunohistochemistry, Western blot or quantitative RNA studies there remains some dispute regarding the validity of these studies. In this study we provide unambiguous confirmation for the VDR in adult rodent brain using proteomic techniques. However Western blot experiments show that compared to more classic target organs such as the gut and kidney, VDR expression is quantitatively lower in the brain. In addition we have examined VDR subcellular distribution in the gut, kidney and brain from both embryonic and adult tissues. We show that in all embryonic tissues VDR distribution is mostly nuclear, however by adulthood it appears that at least in the gut and kidney, VDR presence in the plasma membrane is more prominent perhaps reflecting some change in VDR function with the maturation of these tissues. Finally the subcellular distribution of VDR in the embryo did not appear to be altered by vitamin D deficiency indicating that perhaps there are other mechanisms at play in vivo to stabilize this receptor in the absence of its ligand. © 2014.


Baxter A.J.,Queensland Center for Mental Health Research | Baxter A.J.,University of Queensland | Scott K.M.,University of Otago | Vos T.,University of Queensland | And 2 more authors.
Psychological Medicine | Year: 2013

Background The literature describing the global prevalence of anxiety disorders is highly variable. A systematic review and meta-regression were undertaken to estimate the prevalence of anxiety disorders and to identify factors that may influence these estimates. The findings will inform the new Global Burden of Disease study. Method A systematic review identified prevalence studies of anxiety disorders published between 1980 and 2009. Electronic databases, reference lists, review articles and monographs were searched and experts then contacted to identify missing studies. Substantive and methodological factors associated with inter-study variability were identified through meta-regression analyses and the global prevalence of anxiety disorders was calculated adjusting for study methodology. Results The prevalence of anxiety disorders was obtained from 87 studies across 44 countries. Estimates of current prevalence ranged between 0.9% and 28.3% and past-year prevalence between 2.4% and 29.8%. Substantive factors including gender, age, culture, conflict and economic status, and urbanicity accounted for the greatest proportion of variability. Methodological factors in the final multivariate model (prevalence period, number of disorders and diagnostic instrument) explained an additional 13% of variance between studies. The global current prevalence of anxiety disorders adjusted for methodological differences was 7.3% (4.8-10.9%) and ranged from 5.3% (3.5-8.1%) in African cultures to 10.4% (7.0-15.5%) in Euro/Anglo cultures. Conclusions Anxiety disorders are common and the substantive and methodological factors identified here explain much of the variability in prevalence estimates. Specific attention should be paid to cultural differences in responses to survey instruments for anxiety disorders. © 2012 Cambridge University Press.


Gratten J.,University of Queensland | Visscher P.M.,University of Queensland | Mowry B.J.,University of Queensland | Mowry B.J.,Queensland Center for Mental Health Research | Wray N.R.,University of Queensland
Nature Genetics | Year: 2013

Pedigree, linkage and association studies are consistent with heritable variation for complex disease due to the segregation of genetic factors in families and in the population. In contrast, de novo mutations make only minor contributions to heritability estimates for complex traits. Nonetheless, some de novo variants are known to be important in disease etiology. The identification of risk-conferring de novo variants will contribute to the discovery of etiologically relevant genes and pathways and may help in genetic counseling. There is considerable interest in the role of such mutations in complex neuropsychiatric disease, largely driven by new genotyping and sequencing technologies. An important role for large de novo copy number variations has been established. Recently, whole-exome sequencing has been used to extend the investigation of de novo variation to point mutations in protein-coding regions. Here, we consider several challenges for the interpretation of such mutations in the context of their role in neuropsychiatric disease. © 2013 Nature America, Inc. All rights reserved.


Groves N.J.,University of Queensland | McGrath J.J.,University of Queensland | McGrath J.J.,Queensland Center for Mental Health Research | Burne T.H.J.,University of Queensland | Burne T.H.J.,Queensland Center for Mental Health Research
Annual Review of Nutrition | Year: 2014

Vitamin D deficiency is prevalent throughout the world, and growing evidence supports a requirement for optimal vitamin D levels for the healthy developing and adult brain. Vitamin D has important roles in proliferation and differentiation, calcium signaling within the brain, and neurotrophic and neuroprotective actions; it may also alter neurotransmission and synaptic plasticity. Recent experimental studies highlight the impact that vitamin D deficiency has on brain function in health and disease. In addition, results from recent animal studies suggest that vitamin D deficiency during adulthood may exacerbate underlying brain disorders and or worsen recovery from brain stressors. An increasing number of epidemiological studies indicate that vitamin D deficiency is associated with a wide range of neuropsychiatric disorders and neurodegenerative diseases. Vitamin D supplementation is readily available and affordable, and this review highlights the need for further research. Copyright ©2014 by Annual Reviews. All rights reserved.

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