PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-13 (13)
 

Clipboard (0)
None

Select a Filter Below

Journals
more »
Year of Publication
Document Types
1.  Shared intermediate phenotypes for schizophrenia and bipolar disorder: neuroanatomical features of subtypes distinguished by executive dysfunction 
Background
Shared genetic vulnerability for schizophrenia and bipolar disorder may be associated with common neuroanatomical features. In view of the evidence for working memory dysfunction as a candidate intermediate phenotype for both disorders, we explored neuroanatomical distinctions between subtypes defined according to working memory (n-back task) performance.
Methods
We analyzed T1-weighted MRI scans for patients with schizophrenia-spectrum disorder, bipolar-I disorder (BD-I) and healthy controls. The VBM8 toolbox was used to assess differences in grey and white matter volume across traditional diagnostic groups (schizophrenia v. BD-I). Subsequently, groups were defined as “executively spared” (ES) based on the achievement of greater than 50% accuracy in the 2-back task performance (comparable to performance in the control group) or “executively deficit” (ED) based on the achievement of less than 50% accuracy.
Results
Our study included 40 patients with schizophrenia-spectrum disorders, 30 patients with BD-I and 34 controls. Both the schizophrenia and BD-I groups showed grey matter volume reductions relative to the control group, but not relative to each other. The ED subtype (n = 32 [10 BD-I, 22 schizophrenia]) showed grey matter volume reductions in the bilateral superior and medial frontal gyri, right inferior opercular gyri and hippocampus relative to controls. The ES subtype (n = 38 [20 BD-I, 18 schizophrenia]) showed grey matter volume reductions in the right precuneus and left superior and medial orbital frontal gyri relative to controls. The ED subtype showed grey matter volume reduction in the right inferior frontal and precentral gyri relative to the ES subtype. There were no significant differences in white matter volume in any group comparisons.
Limitations
This analysis was limited by small sample sizes. Further, insufficient numbers were available to assess a control-deficit comparison group. We were unable to assess the effects of mood stabilizer dose on brain structure.
Conclusion
Neuroanatomical commonalities are evident among patients with schizophrenia-spectrum disorders and BD-I with working memory deficits. Reduced inferior frontal lobe volume may mediate cognitive deficits shared across the psychosis–mood spectrum.
doi:10.1503/jpn.130283
PMCID: PMC4275333  PMID: 25268788
2.  The International Society for Bipolar Disorders (ISBD) Task Force Report on Antidepressant Use in Bipolar Disorders 
The American journal of psychiatry  2013;170(11):1249-1262.
Objective
The risk-benefit profile of antidepressant medications in bipolar disorder is controversial. When conclusive evidence is lacking, expert consensus can guide treatment decisions. The International Society for Bipolar Disorders (ISBD) convened a task force to seek consensus recommendations on the use of antidepressants in bipolar disorders.
Method
An expert task force iteratively developed consensus through serial consensus-based revisions using the Delphi method. Initial survey items were based on systematic review of the literature. Subsequent surveys included new or reworded items and items that needed to be rerated. This process resulted in the final ISBD Task Force clinical recommendations on antidepressant use in bipolar disorder.
Results
There is striking incongruity between the wide use of and the weak evidence base for the efficacy and safety of antidepressant drugs in bipolar disorder. Few well-designed, long-term trials of prophylactic benefits have been conducted, and there is insufficient evidence for treatment benefits with antidepressants combined with mood stabilizers. A major concern is the risk for mood switch to hypomania, mania, and mixed states. Integrating the evidence and the experience of the task force members, a consensus was reached on 12 statements on the use of antidepressants in bipolar disorder.
Conclusions
Because of limited data, the task force could not make broad statements endorsing antidepressant use but acknowledged that individual bipolar patients may benefit from antidepressants. Regarding safety, serotonin reuptake inhibitors and bupropion may have lower rates of manic switch than tricyclic and tetracyclic antidepressants and norepinephrine-serotonin reuptake inhibitors. The frequency and severity of antidepressant-associated mood elevations appear to be greater in bipolar I than bipolar II disorder. Hence, in bipolar I patients antidepressants should be prescribed only as an adjunct to mood-stabilizing medications.
doi:10.1176/appi.ajp.2013.13020185
PMCID: PMC4091043  PMID: 24030475
3.  Neuroplasticity in Depressed Individuals Compared with Healthy Controls 
Neuropsychopharmacology  2013;38(11):2101-2108.
Several lines of evidence suggest that neuroplasticity is impaired in depression. This study aimed to compare neuroplasticity in 23 subjects with DSM-IV major depressive episode and 23 age- and gender-matched healthy controls, using an objective test that is independent of subject effort and motivation. Neuroplasticity was assessed in the motor cortex using a brain stimulation paradigm known as paired associative stimulation (PAS), which induces transient changes in motor cortical function. Motor cortical excitability was assessed before and after PAS using single-pulse transcranial magnetic stimulation (TMS) to induce motor evoked potentials (MEPs) in a hand muscle. After PAS, MEP amplitudes significantly increased in healthy controls compared with depressed subjects (P=0.002). The functional significance of motor cortical changes was assessed using a motor learning task—a computerized version of the rotor pursuit task. Healthy controls also performed better on motor learning (P=0.02). BDNF blood levels and genotype were assayed to determine any relationship with motor cortical plasticity. However, PAS results did not correlate with motor learning, nor appear to be related to BDNF measures. The significance of these findings is that it provides one of the first direct demonstrations of reduced neuroplasticity in depressed subjects, using an objective test.
doi:10.1038/npp.2013.126
PMCID: PMC3773676  PMID: 23676792
Depression; Unipolar/Bipolar; Learning & Memory; major depressive disorder; motor cortex; Neurophysiology; neuroplasticity; paired associative stimulation; Plasticity; transcranial magnetic stimulation; neuroplasticity; major depressive disorder; transcranial magnetic stimulation; paired associative stimulation; motor cortex; motor learning
4.  Mutations in SLC20A2 are a major cause of familial idiopathic basal ganglia calcification 
Neurogenetics  2013;14(1):11-22.
Familial idiopathic basal ganglia calcification (IBGC) or Fahr’s disease is a rare neurodegenerative disorder characterized by calcium deposits in the basal ganglia and other brain regions, which is associated with neuropsychiatric and motor symptoms. Familial IBGC is genetically heterogeneous and typically transmitted in an autosomal dominant fashion. We performed a mutational analysis of SLC20A2, the first gene found to cause IBGC, to assess its genetic contribution to familial IBGC. We recruited 218 subjects from 29 IBGC-affected families of varied ancestry and collected medical history, neurological exam, and head CT scans to characterize each patient’s disease status. We screened our patient cohort for mutations in SLC20A2. Twelve novel (nonsense, deletions, missense, and splice site) potentially pathogenic variants, one synonymous variant, and one previously reported mutation were identified in 13 families. Variants predicted to be deleterious cosegregated with disease in five families. Three families showed nonsegregation with clinical disease of such variants, but retrospective review of clinical and neuroimaging data strongly suggested previous misclassification. Overall, mutations in SLC20A2 account for as many as 41 % of our familial IBGC cases. Our screen in a large series expands the catalog of SLC20A2 mutations identified to date and demonstrates that mutations in SLC20A2 are a major cause of familial IBGC. Non-perfect segregation patterns of predicted deleterious variants highlight the challenges of phenotypic assessment in this condition with highly variable clinical presentation.
doi:10.1007/s10048-012-0349-2
PMCID: PMC4023541  PMID: 23334463
Basal ganglia calcification; Fahr’s; Genetics; Sequencing; Mutations
5.  Characterisation of Genetic Variation in ST8SIA2 and Its Interaction Region in NCAM1 in Patients with Bipolar Disorder 
PLoS ONE  2014;9(3):e92556.
Alpha-2,8-sialyltransferase 2 (ST8SIA2) is an enzyme responsible for the transfer of polysialic acid (PSA) to glycoproteins, principally the neuronal cell adhesion molecule (NCAM1), and is involved in neuronal plasticity. Variants within ST8SIA2 have previously shown association with bipolar disorder, schizophrenia and autism. In addition, altered PSA-NCAM expression in brains of patients with schizophrenia or bipolar disorder indicates a functional dysregulation of glycosylation in mental illness. To explore the role of sequence variation affecting PSA-NCAM formation, we conducted a targeted re-sequencing study of a ∼100 kb region – including the entire ST8SIA2 gene and its region of interaction with NCAM1 – in 48 Caucasian cases with bipolar disorder using the Roche 454 platform. We identified over 400 DNA variants, including 47 putative novel variants not described in dbSNP. Validation of a subset of variants via Sequenom showed high reliability of Roche 454 genotype calls (97% genotype concordance, with 80% of novel variants independently verified). We did not observe major loss-of-function mutations that would affect PSA-NCAM formation, either by ablating ST8SIA2 function or by affecting the ability of NCAM1 to be glycosylated. However, we identified 13 SNPs in the UTRs of ST8SIA2, a synonymous coding SNP in exon 5 (rs2305561, P207P) and many additional non-coding variants that may influence splicing or regulation of ST8SIA2 expression. We calculated nucleotide diversity within ST8SIA2 on specific haplotypes, finding that the diversity on the specific “risk” and “protective” haplotypes was lower than other non-disease-associated haplotypes, suggesting that putative functional variation may have arisen on a spectrum of haplotypes. We have identified common and novel variants (rs11074064, rs722645, 15∶92961050) that exist on a spectrum of haplotypes, yet are plausible candidates for conferring the effect of risk and protective haplotypes via multiple enhancer elements. A Galaxy workflow/pipeline for sequence analysis used herein is available at: https://main.g2.bx.psu.edu/u/a-shaw-neura/p/next-generation-resources.
doi:10.1371/journal.pone.0092556
PMCID: PMC3961385  PMID: 24651862
6.  Common Variant at 16p11.2 Conferring Risk of Psychosis 
Steinberg, Stacy | de Jong, Simone | Mattheisen, Manuel | Costas, Javier | Demontis, Ditte | Jamain, Stéphane | Pietiläinen, Olli P H | Lin, Kuang | Papiol, Sergi | Huttenlocher, Johanna | Sigurdsson, Engilbert | Vassos, Evangelos | Giegling, Ina | Breuer, René | Fraser, Gillian | Walker, Nicholas | Melle, Ingrid | Djurovic, Srdjan | Agartz, Ingrid | Tuulio-Henriksson, Annamari | Suvisaari, Jaana | Lönnqvist, Jouko | Paunio, Tiina | Olsen, Line | Hansen, Thomas | Ingason, Andres | Pirinen, Matti | Strengman, Eric | Hougaard, David M | Ørntoft, Torben | Didriksen, Michael | Hollegaard, Mads V | Nordentoft, Merete | Abramova, Lilia | Kaleda, Vasily | Arrojo, Manuel | Sanjuán, Julio | Arango, Celso | Etain, Bruno | Bellivier, Frank | Méary, Alexandre | Schürhoff, Franck | Szoke, Andrei | Ribolsi, Michele | Magni, Valentina | Siracusano, Alberto | Sperling, Swetlana | Rossner, Moritz | Christiansen, Claus | Kiemeney, Lambertus A | Franke, Barbara | van den Berg, Leonard H | Veldink, Jan | Curran, Sarah | Bolton, Patrick | Poot, Martin | Staal, Wouter | Rehnstrom, Karola | Kilpinen, Helena | Freitag, Christine M | Meyer, Jobst | Magnusson, Pall | Saemundsen, Evald | Martsenkovsky, Igor | Bikshaieva, Iana | Martsenkovska, Inna | Vashchenko, Olesya | Raleva, Marija | Paketchieva, Kamka | Stefanovski, Branislav | Durmishi, Naser | Milovancevic, Milica Pejovic | Tosevski, Dusica Lecic | Silagadze, Teimuraz | Naneishvili, Nino | Mikeladze, Nina | Surguladze, Simon | Vincent, John B | Farmer, Anne | Mitchell, Philip B | Wright, Adam | Schofield, Peter R | Fullerton, Janice M | Montgomery, Grant W | Martin, Nicholas G | Rubino, I Alex | van Winkel, Ruud | Kenis, Gunter | De Hert, Marc | Réthelyi, János M | Bitter, István | Terenius, Lars | Jönsson, Erik G | Bakker, Steven | van Os, Jim | Jablensky, Assen | Leboyer, Marion | Bramon, Elvira | Powell, John | Murray, Robin | Corvin, Aiden | Gill, Michael | Morris, Derek | O’Neill, F Anthony | Kendler, Ken | Riley, Brien | Craddock, Nick | Owen, Michael J | O’Donovan, Michael C | Thorsteinsdottir, Unnur | Kong, Augustine | Ehrenreich, Hannelore | Carracedo, Angel | Golimbet, Vera | Andreassen, Ole A | Børglum, Anders D | Mors, Ole | Mortensen, Preben B | Werge, Thomas | Ophoff, Roel A | Nöthen, Markus M | Rietschel, Marcella | Cichon, Sven | Ruggeri, Mirella | Tosato, Sarah | Palotie, Aarno | St Clair, David | Rujescu, Dan | Collier, David A | Stefansson, Hreinn | Stefansson, Kari
Molecular psychiatry  2012;19(1):10.1038/mp.2012.157.
Epidemiological and genetic data support the notion that schizophrenia and bipolar disorder share genetic risk factors. In our previous genome-wide association (GWA) study, meta-analysis and follow-up (totaling as many as 18,206 cases and 42,536 controls), we identified four loci showing genome-wide significant association with schizophrenia. Here we consider a mixed schizophrenia and bipolar disorder (psychosis) phenotype (addition of 7,469 bipolar disorder cases, 1,535 schizophrenia cases, 333 other psychosis cases, 808 unaffected family members and 46,160 controls). Combined analysis reveals a novel variant at 16p11.2 showing genome-wide significant association (rs4583255[T], OR = 1.08, P = 6.6 × 10−11). The new variant is located within a 593 kb region that substantially increases risk of psychosis when duplicated. In line with the association of the duplication with reduced body mass index (BMI), rs4583255[T] is also associated with lower BMI (P = 0.0039 in the public GIANT consortium dataset; P = 0.00047 in 22,651 additional Icelanders).
doi:10.1038/mp.2012.157
PMCID: PMC3872086  PMID: 23164818
schizophrenia; bipolar disorder; association; 16p11.2; cross-disorder
7.  Cluster randomized controlled trial of a psycho-educational intervention for people with a family history of depression for use in general practice 
BMC Psychiatry  2013;13:325.
Background
The strongest risk factor for depression is having a family history of the condition. Many individuals with a family history of depression are concerned about their personal risk for depression and report unmet educational and psychological support needs. No supportive and/or educational interventions are currently available that target this group of individuals. In this study we will develop and evaluate the first online psycho-educational intervention targeted to individuals with a family history of depression. Genetic risk information and evidence-rated information on preventive strategies for depression will be provided to such individuals in a general practice setting. The intervention will also incorporate a risk assessment tool. The content and delivery of the intervention will be pilot-tested.
Methods/design
The proposed intervention will be evaluated in the general practitioner (GPs) setting, using a cluster randomized controlled trial. GP practices will be randomized to provide either access to the online, targeted psycho-educational intervention or brief generic information about depression (control) to eligible patients. Eligibility criteria include having at least one first-degree relative with either major depressive disorder (MDD) or bipolar disorder (BD). The primary outcome measure is 'intention to adopt, or actual adoption of, risk-reducing strategies’. Secondary outcome measures include: depression symptoms, perceived stigma of depression, knowledge of risk factors for development of depression and risk-reducing strategies, and perceived risk of developing depression or having a recurrence of family history. Over the course of the study, participants will complete online questionnaires at three time points: at baseline, and two weeks and six months after receiving the intervention or control condition.
Discussion
This novel psycho-educational intervention will provide individuals with a family history of depression with information on evidence-based strategies for the prevention of depression, thus, we hypothesize, enabling them to make appropriate lifestyle choices and implement behaviors designed to reduce their risk for depression. The online psycho-educational intervention will also provide a model for similar interventions aimed at individuals at increased familial risk for other psychiatric disorders.
Trial registration
The study is registered with the Australian and New Zealand Clinical Trials Group (Registration no: ACTRN12613000402741).
doi:10.1186/1471-244X-13-325
PMCID: PMC3897985  PMID: 24289740
Family history; Major depressive disorder; Bipolar disorder; Online intervention; Psycho-education; Prevention
8.  Assessment of Response to Lithium Maintenance Treatment in Bipolar Disorder: A Consortium on Lithium Genetics (ConLiGen) Report 
Manchia, Mirko | Adli, Mazda | Akula, Nirmala | Ardau, Raffaella | Aubry, Jean-Michel | Backlund, Lena | Banzato, Claudio EM. | Baune, Bernhard T. | Bellivier, Frank | Bengesser, Susanne | Biernacka, Joanna M. | Brichant-Petitjean, Clara | Bui, Elise | Calkin, Cynthia V. | Cheng, Andrew Tai Ann | Chillotti, Caterina | Cichon, Sven | Clark, Scott | Czerski, Piotr M. | Dantas, Clarissa | Zompo, Maria Del | DePaulo, J. Raymond | Detera-Wadleigh, Sevilla D. | Etain, Bruno | Falkai, Peter | Frisén, Louise | Frye, Mark A. | Fullerton, Jan | Gard, Sébastien | Garnham, Julie | Goes, Fernando S. | Grof, Paul | Gruber, Oliver | Hashimoto, Ryota | Hauser, Joanna | Heilbronner, Urs | Hoban, Rebecca | Hou, Liping | Jamain, Stéphane | Kahn, Jean-Pierre | Kassem, Layla | Kato, Tadafumi | Kelsoe, John R. | Kittel-Schneider, Sarah | Kliwicki, Sebastian | Kuo, Po-Hsiu | Kusumi, Ichiro | Laje, Gonzalo | Lavebratt, Catharina | Leboyer, Marion | Leckband, Susan G. | López Jaramillo, Carlos A. | Maj, Mario | Malafosse, Alain | Martinsson, Lina | Masui, Takuya | Mitchell, Philip B. | Mondimore, Frank | Monteleone, Palmiero | Nallet, Audrey | Neuner, Maria | Novák, Tomás | O’Donovan, Claire | Ösby, Urban | Ozaki, Norio | Perlis, Roy H. | Pfennig, Andrea | Potash, James B. | Reich-Erkelenz, Daniela | Reif, Andreas | Reininghaus, Eva | Richardson, Sara | Rouleau, Guy A. | Rybakowski, Janusz K. | Schalling, Martin | Schofield, Peter R. | Schubert, Oliver K. | Schweizer, Barbara | Seemüller, Florian | Grigoroiu-Serbanescu, Maria | Severino, Giovanni | Seymour, Lisa R. | Slaney, Claire | Smoller, Jordan W. | Squassina, Alessio | Stamm, Thomas | Steele, Jo | Stopkova, Pavla | Tighe, Sarah K. | Tortorella, Alfonso | Turecki, Gustavo | Wray, Naomi R. | Wright, Adam | Zandi, Peter P. | Zilles, David | Bauer, Michael | Rietschel, Marcella | McMahon, Francis J. | Schulze, Thomas G. | Alda, Martin
PLoS ONE  2013;8(6):e65636.
Objective
The assessment of response to lithium maintenance treatment in bipolar disorder (BD) is complicated by variable length of treatment, unpredictable clinical course, and often inconsistent compliance. Prospective and retrospective methods of assessment of lithium response have been proposed in the literature. In this study we report the key phenotypic measures of the “Retrospective Criteria of Long-Term Treatment Response in Research Subjects with Bipolar Disorder” scale currently used in the Consortium on Lithium Genetics (ConLiGen) study.
Materials and Methods
Twenty-nine ConLiGen sites took part in a two-stage case-vignette rating procedure to examine inter-rater agreement [Kappa (κ)] and reliability [intra-class correlation coefficient (ICC)] of lithium response. Annotated first-round vignettes and rating guidelines were circulated to expert research clinicians for training purposes between the two stages. Further, we analyzed the distributional properties of the treatment response scores available for 1,308 patients using mixture modeling.
Results
Substantial and moderate agreement was shown across sites in the first and second sets of vignettes (κ = 0.66 and κ = 0.54, respectively), without significant improvement from training. However, definition of response using the A score as a quantitative trait and selecting cases with B criteria of 4 or less showed an improvement between the two stages (ICC1 = 0.71 and ICC2 = 0.75, respectively). Mixture modeling of score distribution indicated three subpopulations (full responders, partial responders, non responders).
Conclusions
We identified two definitions of lithium response, one dichotomous and the other continuous, with moderate to substantial inter-rater agreement and reliability. Accurate phenotypic measurement of lithium response is crucial for the ongoing ConLiGen pharmacogenomic study.
doi:10.1371/journal.pone.0065636
PMCID: PMC3686769  PMID: 23840348
9.  Adaptive Associations between Social Cognition and Emotion Regulation are Absent in Schizophrenia and Bipolar Disorder 
Schizophrenia (SZ) and bipolar disorder (BD) are associated with impairments in facial emotion perception and Theory of Mind (ToM). These social cognitive skills deficits may be related to a reduced capacity to effectively regulate one’s own emotions according to the social context. We therefore set out to examine the relationship between social cognitive abilities and the use of cognitive strategies for regulating negative emotion in SZ and BD. Participants were 56 SZ, 33 BD, and 58 healthy controls (HC) who completed the Ekman 60-faces test of facial emotion recognition; a sub-set of these participants also completed The Awareness of Social Inference Test (TASIT) and the Cognitive Emotion Regulation Questionnaire (CERQ). SZ participants demonstrated impairments in emotion perception on both the Ekman and the TASIT Emotion Evaluation tests relative to BD and HC. While both SZ and BD patients showed ToM deficits (i.e., perception of sarcasm and lie) compared to HC, SZ patients demonstrated significantly greater ToM impairment compared to BD. There were also distinct patterns of cognitive strategies used to regulate emotion in both patient groups: those with SZ were more likely to engage in catastrophizing and rumination, while BD subjects were more likely to blame themselves and were less likely to engage in positive reappraisal, relative to HC. In addition, those with SZ were more likely to blame others compared to BD. Associations between social cognition and affect regulation were revealed for HC only: TASIT performance was negatively associated with more frequent use of rumination, catastrophizing, and blaming others, such that more frequent use of maladaptive cognitive emotion regulation strategies was associated with poor social cognitive performance. These associations were not present in either patient group. However, both SZ and BD patients demonstrated poor ToM performance and aberrant use of emotion regulation strategies consistent with previous studies. SZ also showed basic emotion recognition deficits relative to BD and HC. That there were no associations between social cognition and the capacity to self-regulate negative emotion in SZ and BD (in the context of poor social cognition and maladaptive regulatory strategies) suggests that dysfunction in fronto-limbic brain networks may underpin both social cognitive deficits and the use of maladaptive cognitive strategies in these disorders, albeit by potentially different routes.
doi:10.3389/fpsyg.2012.00607
PMCID: PMC3573888  PMID: 23423878
social cognition; emotion; cognitive emotion regulation; schizophrenia; bipolar disorder
10.  A consensus statement for safety monitoring guidelines of treatments for major depressive disorder 
Objective
This paper aims to present an overview of screening and safety considerations for the treatment of clinical depressive disorders and make recommendations for safety monitoring.
Method
Data were sourced by a literature search using MEDLINE and a manual search of scientific journals to identify relevant articles. Draft guidelines were prepared and serially revised in an iterative manner until all co-authors gave final approval of content.
Results
Screening and monitoring can detect medical causes of depression. Specific adverse effects associated with antidepressant treatments may be reduced or identified earlier by baseline screening and agent-specific monitoring after commencing treatment.
Conclusion
The adoption of safety monitoring guidelines when treating clinical depression is likely to improve overall physical health status and treatment outcome. It is important to implement these guidelines in the routine management of clinical depression.
doi:10.3109/00048674.2011.595686
PMCID: PMC3190838  PMID: 21888608
11.  Public interest in predictive genetic testing, including direct-to-consumer testing, for susceptibility to major depression: preliminary findings 
The past decade has seen rapid advances in the identification of associations between candidate genes and a range of common multifactorial disorders. This paper evaluates public attitudes towards the complexity of genetic risk prediction in psychiatry involving susceptibility genes, uncertain penetrance and gene–environment interactions on which successful molecular-based mental health interventions will depend. A qualitative approach was taken to enable the exploration of the views of the public. Four structured focus groups were conducted with a total of 36 participants. The majority of participants indicated interest in having a genetic test for susceptibility to major depression, if it was available. Having a family history of mental illness was cited as a major reason. After discussion of perceived positive and negative implications of predictive genetic testing, nine of 24 participants initially interested in having such a test changed their mind. Fear of genetic discrimination and privacy issues predominantly influenced change of attitude. All participants still interested in having a predictive genetic test for risk for depression reported they would only do so through trusted medical professionals. Participants were unanimously against direct-to-consumer genetic testing marketed through the Internet, although some would consider it if there was suitable protection against discrimination. The study highlights the importance of general practitioner and public education about psychiatric genetics, and the availability of appropriate treatment and support services prior to implementation of future predictive genetic testing services.
doi:10.1038/ejhg.2009.138
PMCID: PMC2987161  PMID: 19690586
predictive genetic testing; psychiatric genetics; major depression; direct-to-consumer genetic testing; public opinion; mental health
13.  Association between antidepressant prescribing and suicide in Australia, 1991-2000: trend analysis 
BMJ : British Medical Journal  2003;326(7397):1008.
Objective
To examine the association between trends in antidepressant prescribing and suicide rates in Australia for 1991-2000.
Design
Analysis of databases of suicide and rates of antidepressant prescribing according to age and sex.
Setting
Australian Bureau of Statistics data, sales data from the Australian pharmaceutical industry, prescribing data in general practice.
Subjects
Men and women aged 15 years and over in 10 year age groups.
Main outcome measures
Trends in suicide rates and trends in antidepressant prescribing. Association measured by Spearman's rank correlations.
Results
While overall national rates of suicide did not fall significantly, incidence decreased in older men and women and increased in younger adults. In both men (rs=−0.91; P<0.01) and women (rs=−0.76; P<0.05) the higher the exposure to antidepressants the larger the decline in rate of suicide.
Conclusions
Changes in suicide rates and exposure to antidepressants in Australia for 1991-2000 are significantly associated. This effect is most apparent in older age groups, in which rates of suicide decreased substantially in association with exposure to antidepressants. The increase in antidepressant prescribing may be a proxy marker for improved overall management of depression. If so, increased prescribing of selective serotonin reuptake inhibitors in general practice may have produced a quantifiable benefit in population mental health.
What is already known on this topicThere has been a substantial increase in antidepressant prescribing by general practitioners in Australia since the introduction of selective serotoin reuptake inhibitors in the early 1990sPrevious studies have indicated an association between increased antidepressant prescribing and reduced suicide rateWhat this study addsIn Australia the rate of suicide fell in older people, the age group most heavily exposed to antidepressantsMost antidepressants are now prescribed by general practitionersThe association may indicate the improved treatment of depression by general practitioners
PMCID: PMC154757  PMID: 12742921

Results 1-13 (13)