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Supplemental material, sj-docx-1-jop-10.1177_02698811231182012 for The New Zealand drug harms ranking study: A multi-criteria decision analysis by Rose Crossin, Lana Cleland, Chris Wilkins, Marta Rychert, Simon Adamson, Tuari Potiki, Adam C Pomerleau, Blair MacDonald, Dwaine Faletanoai, Fiona Hutton, Geoff Noller, Ian Lambie, Jane L Sheridan, Jason George, Kali Mercier, Kristen Maynard, Louise Leonard, Patricia Walsh, Rhys Ponton, Sue Bagshaw, Suresh Muthukumaraswamy, Tracey McIntosh, Edward Poot, Paul Gordon, Patrick Sharry, David Nutt and Joseph Boden in Journal of Psychopharmacology

Supplemental material, sj-docx-1-jop-10.1177_02698811231182012 for The New Zealand drug harms ranking study: A multi-criteria decision analysis by Rose Crossin, Lana Cleland, Chris Wilkins, Marta Rychert, Simon Adamson, Tuari Potiki, Adam C Pomerleau, Blair MacDonald, Dwaine Faletanoai, Fiona Hutton, Geoff Noller, Ian Lambie, Jane L Sheridan, Jason George, Kali Mercier, Kristen Maynard, Louise Leonard, Patricia Walsh, Rhys Ponton, Sue Bagshaw, Suresh Muthukumaraswamy, Tracey McIntosh, Edward Poot, Paul Gordon, Patrick Sharry, David Nutt and Joseph Boden in Journal of Psychopharmacology

Acute alcohol use is a proximal risk factor for suicide. However, the proportion of suicide deaths involving acute alcohol use has not been quantified in New Zealand. We sought to quantify and characterise the association between acute alcohol use and suicide.Data for all suicides (≥15 years) between July 2007 and December 2020 were drawn from the National Coronial Information System. Acute alcohol use was defined as blood alcohol concentration (BAC)50mg/100mL. Logistic regression was used to compare characteristics between suicide deaths with and without acute alcohol use.Twenty-six point six percent of suicide deaths involved acute alcohol use. No difference in the association was found by sex (male AOR: 0.87 (95%CI: 0.74,1.02)). Ethnicity differences were identified (Māori AOR: 1.20 (95%CI: 1.01,1.42), Pacific AOR: 1.46 (95%CI: 1.10,2.00)). Those aged 15-54 years had similar risks of suicide involving acute alcohol use, with a lower association in older age groups.Acute alcohol use was identified in approximately one quarter of suicides, with stronger associations in those of Māori and Pasifika ethnicity, and those aged55 years. Acute alcohol use is a significant but modifiable risk factor for suicide in New Zealand.

Supplemental material, sj-docx-1-anp-10.1177_00048674221138499 for The long-term impacts of the Canterbury earthquakes on the mental health of the Christchurch Health and Development Study cohort by Ben Beaglehole, Joseph M Boden, Caroline Bell, Roger T Mulder, Bhubaneswor Dhakal and L John Horwood in Australian & New Zealand Journal of Psychiatry

Supplemental material, sj-docx-1-anp-10.1177_00048674211064183 for The association between alcohol use disorder and suicidal ideation in a New Zealand birth cohort by Rose Crossin, Lana Cleland, Geraldine FH McLeod, Annette Beautrais, Katrina Witt and Joseph M Boden in Australian & New Zealand Journal of Psychiatry

BackgroundVariation in liability to cannabis use disorder has a strong genetic component (estimated twin and family heritability about 50-70%) and is associated with negative outcomes, including increased risk of psychopathology. The aim of the study was to conduct a large genome-wide association study (GWAS) to identify novel genetic variants associated with cannabis use disorder.MethodsTo conduct this GWAS meta-analysis of cannabis use disorder and identify associations with genetic loci, we used samples from the Psychiatric Genomics Consortium Substance Use Disorders working group, iPSYCH, and deCODE (20 916 case samples, 363 116 control samples in total), contrasting cannabis use disorder cases with controls. To examine the genetic overlap between cannabis use disorder and 22 traits of interest (chosen because of previously published phenotypic correlations [eg, psychiatric disorders] or hypothesised associations [eg, chronotype] with cannabis use disorder), we used linkage disequilibrium score regression to calculate genetic correlations.FindingsWe identified two genome-wide significant loci: a novel chromosome 7 locus (FOXP2, lead single-nucleotide polymorphism [SNP] rs7783012; odds ratio [OR] 1·11, 95% CI 1·07-1·15, p=1·84 × 10-9) and the previously identified chromosome 8 locus (near CHRNA2 and EPHX2, lead SNP rs4732724; OR 0·89, 95% CI 0·86-0·93, p=6·46 × 10-9). Cannabis use disorder and cannabis use were genetically correlated (rg 0·50, p=1·50 × 10-21), but they showed significantly different genetic correlations with 12 of the 22 traits we tested, suggesting at least partially different genetic underpinnings of cannabis use and cannabis use disorder. Cannabis use disorder was positively genetically correlated with other psychopathology, including ADHD, major depression, and schizophrenia.InterpretationThese findings support the theory that cannabis use disorder has shared genetic liability with other psychopathology, and there is a distinction between genetic liability to cannabis use and cannabis use disorder.FundingNational Institute of Mental Health; National Institute on Alcohol Abuse and Alcoholism; National Institute on Drug Abuse; Center for Genomics and Personalized Medicine and the Centre for Integrative Sequencing; The European Commission, Horizon 2020; National Institute of Child Health and Human Development; Health Research Council of New Zealand; National Institute on Aging; Wellcome Trust Case Control Consortium; UK Research and Innovation Medical Research Council (UKRI MRC); The Brain & Behavior Research Foundation; National Institute on Deafness and Other Communication Disorders; Substance Abuse and Mental Health Services Administration (SAMHSA); National Institute of Biomedical Imaging and Bioengineering; National Health and Medical Research Council (NHMRC) Australia; Tobacco-Related Disease Research Program of the University of California; Families for Borderline Personality Disorder Research (Beth and Rob Elliott) 2018 NARSAD Young Investigator Grant; The National Child Health Research Foundation (Cure Kids); The Canterbury Medical Research Foundation; The New Zealand Lottery Grants Board; The University of Otago; The Carney Centre for Pharmacogenomics; The James Hume Bequest Fund; National Institutes of Health: Genes, Environment and Health Initiative; National Institutes of Health; National Cancer Institute; The William T Grant Foundation; Australian Research Council; The Virginia Tobacco Settlement Foundation; The VISN 1 and VISN 4 Mental Illness Research, Education, and Clinical Centers of the US Department of Veterans Affairs; The 5th Framework Programme (FP-5) GenomEUtwin Project; The Lundbeck Foundation; NIH-funded Shared Instrumentation Grant S10RR025141; Clinical Translational Sciences Award grants; National Institute of Neurological Disorders and Stroke; National Heart, Lung, and Blood Institute; National Institute of General Medical Sciences.

Supplemental material, EASAVALMHAPO_supplement_260320 for Alcohol use in adolescents and adult psychopathology and social outcomes: Findings from a 35-year cohort study by Joseph Boden, Sarah Blair and Giles Newton-Howes in Australian & New Zealand Journal of Psychiatry

Cannabis use is of increasing public health interest globally. Here we examined the effect of heavy cannabis use, with and without tobacco, on genome-wide DNA methylation in a longitudinal birth cohort (Christchurch Health and Development Study, CHDS). A total of 48 heavy cannabis users were selected from the CHDS cohort, on the basis of their adult exposure to cannabis and tobacco, and DNA methylation assessed from whole blood samples, collected at approximately age 28. Methylation in heavy cannabis users was assessed, relative to non-users (n = 48 controls) via the Illumina Infinium® MethylationEPIC BeadChip. We found the most differentially methylated sites in cannabis with tobacco users were in the AHRR and F2RL3 genes, replicating previous studies on the effects of tobacco. Cannabis-only users had no evidence of differential methylation in these genes, or at any other loci at the epigenome-wide significance level (P −7). However, there were 521 sites differentially methylated at P TMEM190, MUC3L, CDC20 and SP9). We conclude that the effects of cannabis use on the mature human blood methylome differ from, and are less pronounced than, the effects of tobacco use, and that larger sample sizes are required to investigate this further.

BACKGROUND: Studies involving clinically recruited samples show that genetic liability to schizophrenia overlaps with that for several psychiatric disorders including bipolar disorder, major depression and, in a population study, anxiety disorder and negative symptoms in adolescence.AimsWe examined whether, at a population level, association between schizophrenia liability and anxiety disorders continues into adulthood, for specific anxiety disorders and as a group. We explored in an epidemiologically based cohort the nature of adult psychopathology sharing liability to schizophrenia. METHOD: Schizophrenia polygenic risk scores (PRSs) were calculated for 590 European-descent individuals from the Christchurch Health and Development Study. Logistic regression was used to examine associations between schizophrenia PRS and four anxiety disorders (social phobia, specific phobia, panic disorder and generalised anxiety disorder), schizophrenia/schizophreniform disorder, manic/hypomanic episode, alcohol dependence, major depression, and - using linear regression - total number of anxiety disorders. A novel population-level association with hypomania was tested in a UK birth cohort (Avon Longitudinal Study of Parents and Children). RESULTS: Schizophrenia PRS was associated with total number of anxiety disorders and with generalised anxiety disorder and panic disorder. We show a novel population-level association between schizophrenia PRS and manic/hypomanic episode. CONCLUSIONS: The relationship between schizophrenia liability and anxiety disorders is not restricted to psychopathology in adolescence but is present in adulthood and specifically linked to generalised anxiety disorder and panic disorder. We suggest that the association between schizophrenia liability and hypomanic/manic episodes found in clinical samples may not be due to bias.Declarations of interestNone.

BackgroundGenetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche.MethodsA secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (ResultsTwo loci were genome-wide significant in the typical-onset AN GWAS. Heritability estimates (single nucleotide polymorphism–h2) were 0.01–0.04 for age of onset, 0.16–0.25 for early-onset AN, and 0.17–0.25 for typical-onset AN. Early- and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age of onset and early-onset AN estimated from independent GWASs significantly predicted age of onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and early-onset AN.ConclusionsOur results provide evidence consistent with a common variant genetic basis for age of onset and implicate biological pathways regulating menarche and reproduction. Background: Genetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche. Methods: A secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (2) were 0.01–0.04 for age of onset, 0.16–0.25 for early-onset AN, and 0.17–0.25 for typical-onset AN. Early- and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age of onset and early-onset AN estimated from independent GWASs significantly predicted age of onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and early-onset AN. Conclusions: Our results provide evidence consistent with a common variant genetic basis for age of onset and implicate biological pathways regulating menarche and reproduction.