Lifetime Morbid Risk Research Articles

Lifetime prevalence, risk, and treatment of mood and anxiety disorders in Qatar's national mental health study.

To estimate lifetime prevalence, risk, and treatment for mental disorders and their correlates in Qatar's general population for the first time. We conducted a national phone survey of 5,195 Qatari and Arab residents in Qatar (2019-2022) using the Composite International Diagnostic Interview Version 3.3 and estimated lifetime mood and anxiety defined diagnoses. Survival-based discrete time models, lifetime morbid risk, and treatment projections were estimated. Lifetime prevalence of any disorder was 28.0% and was associated with younger cohorts, females, and migrants, but lower formal education. Treatment contact in the year of disorder onset were 13.5%. The median delay in receiving treatment was 5years (IQR=2-13). Lifetime treatment among those with a lifetime disorder were 59.9% for non-healthcare and 63.5% for healthcare; it was 68.1% for any anxiety and 80.1% for any mood disorder after 50years of onset.Younger cohorts and later age of onset were significantly predictors of treatment. Lifetime prevalence of mental disorders in Qatar is comparable to other countries. Treatment is significantly delayed and delivered largely in non-healthcare sectors thus the need for increased literacy of mental illness to reduce stigma and improve earlier help-seeking in healthcare settings.

Radiological dose and associated risk due to 210Po in commercial inter-tidal bivalves of southwest (Arabian Sea) coast of India

The activity concentration of 210Po was determined in edible tissues of commercial bivalves on the southwest coast of India. The 210Po activity ranged from 38.3 ± 6.9 Bq kg−1 to 91.2 ± 18.6 Bq kg−1. The annual committed effective dose (ACED) and lifetime carcinogenic risk (LCR) were calculated for different age groups to determine the potential health risk associated with bivalve consumption. The average ACED ranged from 81.5 to 194.1 μSv y−1, with the 10th and 95th percentiles being 68 and 261 μSv y−1, respectively. Lifelong mortality risk (LMTR) values ranged from 1.2 × 10−3 to 2.9 × 10−3, while lifetime morbidity risk (LMBR) values ranged from 1.9 × 10−6 to 4.9 × 10−6. The effective dose was found to be within the UNSCEAR limits.

Lifetime prevalence and age-of-onset distributions of mental disorders in the Saudi National Mental Health Survey.

ObjectivesTo estimate lifetime prevalence of mental disorders in the Saudi National Mental Health Survey (SNMHS).MethodsThe SNMHS is a face‐to‐face community epidemiological survey in a nationally representative household sample of citizens ages 15–65 in the Kingdom of Saudi Arabia (KSA) (n = 4,004). The World Health Organization (WHO) Composite International Diagnostic Interview (CIDI) was used to estimate lifetime prevalence of common DSM‐IV mental disorders.ResultsEstimated lifetime prevalence of any DSM‐IV/CIDI disorder is 34.2% and lifetime morbid risk is 38.0%. Anxiety disorders are by far the most prevalent (23.2%) followed by disruptive behavior (11.2%), mood (9.3%), eating (6.1%), and substance use (4.0%) disorders. Synthetic estimates of cohort effects suggest that prevalence of many disorders has increased in recent cohorts. Onsets typically occur in childhood for a number of anxiety and disruptive behavior disorders and in adolescence or early adulthood for most other disorders, although age‐of‐onset distributions for drug abuse is much later (median age of 31) than in CIDI surveys carried out in other high‐income countries.ConclusionsLifetime mental disorders are highly prevalent in Saudi Arabia and typically have early ages‐of‐onset.

Integrative Analysis of Genomic And Neuroimaging Data Reveal A Genetic-Brain Region Pathway Regulating Schizophrenia

BackgroundSchizophrenia (SCZ) is one of the most chronically disabling psychiatric illnesses with a global median lifetime morbid risk of 7.2/1000 persons. Both genetic and brain region pathways were identified as causal regulating tunnels towards the pathogenesis of SCZ. MethodWe integrated a functional magnetic resonance imaging (fMRI) data set and a brain-gene ResNet (BGR) data set to study the functional pathways through which genes regulate the brain functions associated with SCZ phenotypes. Automated Anatomical Labeling (AAL) based brain connectivity analysis were conducted for fMRI data and a Gene Set Enrichment Analysis (GSEA) and Sub-Network Enrichment Analysis (SNEA) were performed to study the functional profile of the genes associating with these brain regions. Additionally, pathway and network based metrics analysis were proposed to identify the top genes with pathogenesis significance to SCZ. ResultsWe identified 4 SCZ candidate brain regions (P-value<1e-5) using fMRI data alone, which were replicated with the BGR data set. Furthermore, we identified from the BRG data set that the 4 SCZ candidate brain regions were related to 26 SCZ candidate genes. GSEA and SNEA confirmed the observation and demonstrated that 24/26 genes significantly enriched 62 genetic SCZ candidate pathways (P-value<1e-4), 16 of which were related to brain functional development (P-value: 5.5e-13 ~ 5.1e-5). Additionally, pathway and network metrics analysis suggested that 7 genes were top SCZ candidates in terms of both network centrality and functional diversity, including SNAP25, APP, MAPT, APOE, NTRK2, GRM5, and BDNF. ConclusionOur results suggest that integrating both genomic and neuroimaging data could reveal functional genetic-brain region pathways that help in understanding the pathogenic mechanisms of SCZ.

Public perception of the lifetime morbid risk of mental disorders in the United States and associations with public stigma.

PurposeThis study examined the relationship between estimates of the prevalence of mental disorders and mental health stigma. It also examined whether stigma might be more greatly associated with the terms “mental illness,” “mental disorder,” or “mental health condition.”MethodsRespondents (N = 302) on Amazon’s Mechanical Turk completed an online survey designed to measure social distance, which is one variant of stigma. Half of the respondents were informed at the beginning of the survey that the lifetime morbid risk (LMR) of meeting criteria for at least one mental disorder at some point in life was 70–80 %, while the others were asked to provide their own LMR estimates. All respondents were also randomly assigned to view the survey with either the term “mental illness,” “mental disorder,” or “mental health condition.”ResultsHigher LMR estimates (B = −0.030; β = −0.154), having a mental disorder (B = −2.002; β = −0.200), and a history of contact with an individual with a mental disorder (B = −2.812; β = −0.298), each significantly predicted lower desire for social distance. Respondents in the “mental disorder” group endorsed greater desire for social distance. Participants who were informed about LMR at the start of the survey did not score lower on social distance.ConclusionsEstimates for LMR were more than half as predictive of social distance scores as contact with individuals with mental disorders. But anti-stigma interventions may need to do more than inform individuals about the high prevalence of mental disorders in order to be effective.Electronic supplementary materialThe online version of this article (doi:10.1186/s40064-016-2974-y) contains supplementary material, which is available to authorized users.

Psychosis prevalence and physical, metabolic and cognitive co-morbidity: data from the second Australian national survey of psychosis.

There are insufficient data from nationwide surveys on the prevalence of specific psychotic disorders and associated co-morbidities. The 2010 Australian national psychosis survey used a two-phase design to draw a representative sample of adults aged 18-64 years with psychotic disorders in contact with public treatment services from an estimated resident population of 1 464 923 adults. This paper is based on data from 1642 participants with an International Classification of Diseases (ICD)-10 psychotic disorder. Its aim is to present estimates of treated prevalence and lifetime morbid risk of psychosis, and to describe the cognitive, physical health and substance use profiles of participants. The 1-month treated prevalence of psychotic disorders was 3.10 cases per 1000 population aged 18-64 years, not accounting for people solely accessing primary care services; lifetime morbid risk was 3.45 per 1000. Mean premorbid intelligence quotient was approximately 0.5 s.d.s below the population mean; current cognitive ability (measured with a digit symbol coding task) was 1.6 s.d.s below the population mean. For both cognitive tests, higher scores were significantly associated with better independent functioning. The prevalence of the metabolic syndrome was high, affecting 60.8% of participants, and pervasive across diagnostic groups. Of the participants, two-thirds (65.9%) were current smokers, 47.4% were obese and 32.4% were sedentary. Of the participants, half (49.8%) had a lifetime history of alcohol abuse/dependence and 50.8% lifetime cannabis abuse/dependence. Our findings highlight the need for comprehensive, integrative models of recovery to maximize the potential for good health and quality of life for people with psychotic illness.

Neuropsychological deficits in bipolar depression persist after successful antidepressant treatment

BackgroundBipolar disorder is a common disabling illness with a lifetime morbid risk of approximately 4%. Neuropsychological deficits constitute enduring trait-like features in bipolar disorder, are associated with each phase of the illness and persist also in euthymia. Total sleep deprivation (TSD) has been shown to cause rapid and sustained antidepressant effects in bipolar depression and to revert the biased self description and speed of information processing present in these patients. The aim of the study was to assess neuropsychological performances first in a sample of bipolar patients during a depressive episode compared to healthy controls and secondly to investigate if TSD treatment would change cognitive performances. MethodsOne-hundred bipolar patients and 100 healthy controls were evaluated through the Brief Assessment of Cognition in Schizophrenia, 42 patients were assessed before and after TSD treatment. ResultsBipolar patients obtained significantly lower domain scores across the entire battery compared to healthy subjects. Cognitive deficits persisted in each function despite a clinical improvement of depressive symptomatology. LimitationsLimitations of the study include issues such as generalizability, possible undetected past comorbidities, population stratification and ongoing medication. ConclusionsThis is the first study of the effect of TSD treatment on cognitive performance. TSD treatment improved clinical symptoms but not cognitive deficits however bipolar patients did not experience the well known worsening of performance observed in healthy controls after sleep loss.

Twelve-month and lifetime prevalence and lifetime morbid risk of anxiety and mood disorders in the United States.

Estimates of 12-month and lifetime prevalence and of lifetime morbid risk (LMR) of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) anxiety and mood disorders are presented based on US epidemiological surveys among people aged 13+. The presentation is designed for use in the upcoming DSM-5 manual to provide more coherent estimates than would otherwise be available. Prevalence estimates are presented for the age groups proposed by DSM-5 workgroups as the most useful to consider for policy planning purposes. The LMR/12-month prevalence estimates ranked by frequency are as follows: major depressive episode: 29.9%/8.6%; specific phobia: 18.4/12.1%; social phobia: 13.0/7.4%; post-traumatic stress disorder: 10.1/3.7%; generalized anxiety disorder: 9.0/2.0%; separation anxiety disorder: 8.7/1.2%; panic disorder: 6.8%/2.4%; bipolar disorder: 4.1/1.8%; agoraphobia: 3.7/1.7%; obsessive-compulsive disorder: 2.7/1.2. Four broad patterns of results are most noteworthy: first, that the most common (lifetime prevalence/morbid risk) lifetime anxiety-mood disorders in the United States are major depression (16.6/29.9%), specific phobia (15.6/18.4%), and social phobia (10.7/13.0%) and the least common are agoraphobia (2.5/3.7%) and obsessive-compulsive disorder (2.3/2.7%); second, that the anxiety-mood disorders with the earlier median ages-of-onset are phobias and separation anxiety disorder (ages 15-17) and those with the latest are panic disorder, major depression, and generalized anxiety disorder (ages 23-30); third, that LMR is considerably higher than lifetime prevalence for most anxiety-mood disorders, although the magnitude of this difference is much higher for disorders with later than earlier ages-of-onset; and fourth, that the ratio of 12-month to lifetime prevalence, roughly characterizing persistence, varies meaningfully in ways consistent with independent evidence about differential persistence of these disorders.

Schizophrenia: A Concise Overview of Incidence, Prevalence, and Mortality

Recent systematic reviews have encouraged the psychiatric research community to reevaluate the contours of schizophrenia epidemiology. This paper provides a concise overview of three related systematic reviews on the incidence, prevalence, and mortality associated with schizophrenia. The reviews shared key methodological features regarding search strategies, analysis of the distribution of the frequency estimates, and exploration of the influence of key variables (sex, migrant status, urbanicity, secular trend, economic status, and latitude). Contrary to previous interpretations, the incidence of schizophrenia shows prominent variation between sites. The median incidence of schizophrenia was 15.2/100,000 persons, and the central 80% of estimates varied over a fivefold range (7.7-43.0/100,000). The rate ratio for males:females was 1.4:1. Prevalence estimates also show prominent variation. The median lifetime morbid risk for schizophrenia was 7.2/1,000 persons. On the basis of the standardized mortality ratio, people with schizophrenia have a two- to threefold increased risk of dying (median standardized mortality ratio = 2.6 for all-cause mortality), and this differential gap in mortality has increased over recent decades. Compared with native-born individuals, migrants have an increased incidence and prevalence of schizophrenia. Exposures related to urbanicity, economic status, and latitude are also associated with various frequency measures. In conclusion, the epidemiology of schizophrenia is characterized by prominent variability and gradients that can help guide future research.

Analyses of the associations between the genes of 22q11 deletion syndrome and schizophrenia

Schizophrenia is a severe, debilitating mental disorder characterized by profound disturbances of cognition, emotion and social functioning. The lifetime morbid risk is surprisingly uniform at slightly less than 1% across different populations and different cultures. The evidence of genetic risk factors is our strongest clue to the cause of schizophrenia. Linkage and association analyses have identified genes associated with the development of schizophrenia. However, most of the alleles or haplotypes identified thus far have only a weak association or are reported to be population specific. A deletion of 22q11.2 that causes the most common microdeletion syndrome (22q11DS) with an estimated prevalence of 1:2,500-1:4,000 live births may represent one of the greatest known genetic risk factors for schizophrenia. Schizophrenia is a late manifestation in approximately 30% of patients with 22q11.2 deletion, comparable to the risk to offspring of two parents with schizophrenia. Clinical and neuroimaging assessments indicate that 22q11DS-schizophrenia is a neurodevelopmental model of schizophrenia. Recent studies have provided evidence that haploinsufficiency of TBX1 is likely to be responsible for many of the physical features associated with the deletion. Most of the genes in the 22q11 deletion region are conserved together on mouse chromosome 16, enabling the generation of mouse models. Similarities in the cardiovascular and other phenotypes between 22q11DS patients and mouse models can provide important insights into roles of genes in neurobehavioral phenotypes. Because more than one gene in the 22q11DS region is likely to contribute to the marked risk for schizophrenia, further extensive studies are necessary. Analyses of 22q11DS will help clarify the molecular pathogenesis of schizophrenia.

Pathophysiologische Grundlagen der Schizophrenie und deren Relevanz für die Psychopharmakotherapie

Schizophrenia is a severe psychiatric illness with a lifetime morbidity risk of around 1 %. Symptoms include hallucinations, delusions, poverty of thought and emotion and social withdrawal and cognitive deficits. Although newer antipsychotics affecting multiple neurotransmitter receptors facilitate therapy, many patients still do not achieve full response. Despite intensive study, the molecular etiology of schizophrenia remains enigmatic in many ways. The dopamine hypothesis of schizophrenia still plays an important role, although pharmacological studies, brain imaging analyses and genetic research indicate additional dysfunctions of glutamate, GABA and serotonin transmission. This article reviews the pathophysiological background of the disorder, its implications for pharmacological treatment and possible directions for future research.

A systematic review of the prevalence of schizophrenia.

BackgroundUnderstanding the prevalence of schizophrenia has important implications for both health service planning and risk factor epidemiology. The aims of this review are to systematically identify and collate studies describing the prevalence of schizophrenia, to summarize the findings of these studies, and to explore selected factors that may influence prevalence estimates.Methods and FindingsStudies with original data related to the prevalence of schizophrenia (published 1965–2002) were identified via searching electronic databases, reviewing citations, and writing to authors. These studies were divided into “core” studies, “migrant” studies, and studies based on “other special groups.” Between- and within-study filters were applied in order to identify discrete prevalence estimates. Cumulative plots of prevalence estimates were made and the distributions described when the underlying estimates were sorted according to prevalence type (point, period, lifetime, and lifetime morbid risk). Based on combined prevalence estimates, the influence of selected key variables was examined (sex, urbanicity, migrant status, country economic index, and study quality).A total of 1,721 prevalence estimates from 188 studies were identified. These estimates were drawn from 46 countries, and were based on an estimated 154,140 potentially overlapping prevalent cases. We identified 132 core studies, 15 migrant studies, and 41 studies based on other special groups. The median values per 1,000 persons (10%–90% quantiles) for the distributions for point, period, lifetime, and lifetime morbid risk were 4.6 (1.9–10.0), 3.3 (1.3–8.2), 4.0 (1.6–12.1), and 7.2 (3.1–27.1), respectively. Based on combined prevalence estimates, we found no significant difference (a) between males and females, or (b) between urban, rural, and mixed sites. The prevalence of schizophrenia in migrants was higher compared to native-born individuals: the migrant-to-native-born ratio median (10%–90% quantile) was 1.8 (0.9–6.4). When sites were grouped by economic status, prevalence estimates from “least developed” countries were significantly lower than those from both “emerging” and “developed” sites (p = 0.04). Studies that scored higher on a quality score had significantly higher prevalence estimates (p = 0.02).ConclusionsThere is a wealth of data about the prevalence of schizophrenia. These gradients, and the variability found in prevalence estimate distributions, can provide direction for future hypothesis-driven research.

Circadian genes and bipolar disorder

Bipolar disorder (BD) is a chronic, potentially disabling illness with a lifetime morbid risk of approximately 1%. There is substantial evidence for a significant genetic etiology, but gene‐mapping efforts have been hampered by the complex mode of inheritance and the likelihood of multiple genes of small effect. In view of the complexity, it may be instructive to understand the biological bases for pathogenesis. Extensive disruption in circadian function is known to occur among patients in relapse. Therefore, it is plausible that circadian dysfunction underlies pathogenesis. Evidence for such a hypothesis is mounting and is reviewed here. If circadian dysfunction can be established as an ‘endophenotype’ for BD, this may not only enable identification of more homogenous sub‐groups, but may also facilitate genetic analyses. For example, it would be logical to investigate polymorphisms of genes encoding key proteins that mediate circadian rhythms. Association studies that analyzed circadian genes in BD have been initiated and are reviewed. Other avenues for research are also discussed.

A Family Study of Alcohol Dependence

Alcohol dependence tends to aggregate within families. We analyzed data from the family collection of the Collaborative Study on the Genetics of Alcoholism to quantify familial aggregation using several different criterion sets. We also assessed the aggregation of other psychiatric disorders in the same sample to identify areas of possible shared genetic vulnerability. Age-corrected lifetime morbid risk was estimated in adult first-degree relatives of affected probands and control subjects for selected disorders. Diagnostic data were gathered by semistructured interview (the Semi-Structured Assessment for the Genetics of Alcoholism), family history, and medical records. Rates of illness were corrected by validating interview and family history reports against senior clinicians' all sources best estimate diagnoses. Sex, ethnicity, comorbidity, cohort effects, and site of ascertainment were also taken into account. Including data from 8296 relatives of alcoholic probands and 1654 controls, we report lifetime risk rates of 28.8% and 14.4% for DSM-IV alcohol dependence in relatives of probands and controls, respectively; respective rates were 37.0% and 20.5% for the less stringent DSM-III-R alcohol dependence, 20.9% and 9.7% for any DSM-III-R diagnosis of nonalcohol nonnicotine substance dependence, and 8.1% and 5.2% for antisocial personality disorder. Rates of specific substance dependence were markedly increased in relatives of alcohol-dependent probands for cocaine, marijuana, opiates, sedatives, stimulants, and tobacco. Aggregation was also seen for panic disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and major depression. The risk of alcohol dependence in relatives of probands compared with controls is increased about 2-fold. The aggregation of antisocial personality disorder, drug dependence, anxiety disorders, and mood disorders suggests common mechanisms for these disorders and alcohol dependence within some families. These data suggest new phenotypes for molecular genetic studies and alternative strategies for studying the heterogeneity of alcohol dependence.

Mapping genes of complex psychiatric diseases in Daghestan genetic isolates.

Genetic isolates, which provide outstanding opportunities for identification of susceptibility genes for complex diseases, can be classified as primary (having an ancient demographic history in a stable environment) or secondary (having a younger demographic history) Neel [1992: Minority populations: Genetics, demography, and health, pp. 1-13]. Daghestan contains 26 out of 50 indigenous Caucasus ethnicities that have been in existence for hundreds of generations in the same highland region. The ethnic groups are subdivided into numerous primary isolates. The founder effect and gene drift in these primary isolates may have caused aggregation of specific haplotypes with limited numbers of pathogenic alleles and loci in some isolates relative to others. These are expressed as inter-population differences in lifetime prevalence and features of certain complex clinical phenotypes and in patterns of genetic linkage and linkage disequilibrium (LD). Stable highland and ethnic-cultural environments have led to increased penetrance and a reduced number of phenocopies, which typically hamper the identification of any susceptibility genes for complex diseases. Owing to these characteristics of the primary isolates, a comparative linkage study in the primary isolates allows us to define the number of susceptibility genes for any complex disease and to identify the source of variability and non-replication of linkage analysis results. As part of an ongoing study, seven extended schizophrenia and one nonspecific mental retardation kindreds have been ascertained from Daghestan isolates. Lifetime morbid risk for schizophrenia in the isolates varied from 0 to 5%. A genome scan with markers spaced 10 cM apart was carried out on these pedigrees and linkage analysis was performed using descent graph methods, as implemented in Simwalk2. To identify regions containing susceptibility genes within these kindreds, we followed up those regions with non-parametric and parametric linkage analyses, with the choice of genetic model guided by the results obtained in the NPL. While the analyses are ongoing, the most positive findings were made in different isolated pedigrees on chromosomes 17p11, 3q24, and 22q for schizophrenia and on chromosome 12q for nonspecific mental retardation.

Mapping Genes of Complex Disease in Genetic Isolates of Daghestan

Original results of the analysis of genetic linkage between some genomic markers and two complex clinical phenotypes, schizophrenia and mental retardation, in pedigrees from Daghestan genetic isolates are described. Interpopulation differences in the epidemiology of the complex phenotypes were studied and in their genetic linkage was demonstrated. These differences are evidently related to the genetic structure of the isolates determined by their demographic history. The epidemiological index MR characterizing the lifetime morbid risk of schizophrenia varies in the Daghestan isolates studied from 0 to 4.95%, which is almost five times higher than the average worldwide population rate, 1%. Comparative genetic mapping in different isolates permitted determination of the most probable genetic linkages and associations of loci in chromosomal regions 17p11.1–12, 3q13.3, and a locus from 22q with schizophrenia and locus 12q23 with mental retardation. There is evidence that this approach is effective for detailed study of the relationship between the genetic (allele and locus) and clinical heterogeneity of complex diseases, which favors successful identification of the genes determining them. The study of linkage disequilibrium (LD) in genetic isolates of Daghestan ethnic populations (which have a common genetic background) may be an effective methodological approach for revealing the numerous contradictory results of mapping of genes of the same complex disease performed by different researchers in different regions of the world.

Splitting Schizophrenia: Periodic Catatonia–Susceptibility Locus on Chromosome 15q15

The nature of subtypes in schizophrenia and the meaning of heterogeneity in schizophrenia have been considered a principal controversy in psychiatric research. We addressed these issues in periodic catatonia, a clinical entity derived from Leonhard's classification of schizophrenias, in a genomewide linkage scan. Periodic catatonia is characterized by qualitative psychomotor disturbances during acute psychotic outbursts and by long-term outcome. On the basis of our previous findings of a lifetime morbidity risk of 26.9% of periodic catatonia in first-degree relatives, we conducted a genome scan in 12 multiplex pedigrees with 135 individuals, using 356 markers with an average spacing of 11 cM. In nonparametric multipoint linkage analyses (by GENEHUNTER-PLUS), significant evidence for linkage was obtained on chromosome 15q15 (P = 2.6 x 10(-5); nonparametric LOD score [LOD*] 3.57). A further locus on chromosome 22q13 with suggestive evidence for linkage (P = 1.8 x 10(-3); LOD* 1.85) was detected, which indicated genetic heterogeneity. Parametric linkage analysis under an autosomal dominant model (affecteds-only analysis) provided independent confirmation of nonparametric linkage results, with maximum LOD scores 2.75 (recombination fraction [theta].04; two-point analysis) and 2.89 (theta =.029; four-point analysis), at the chromosome 15q candidate region. Splitting the complex group of schizophrenias on the basis of clinical observation and genetic analysis, we identified periodic catatonia as a valid nosological entity. Our findings provide evidence that periodic catatonia is associated with a major disease locus, which maps to chromosome 15q15.

The Prevalence of Schizophrenia in Ireland: Readdressing the Enigma

Consequent to the recent report by Kendler and colleagues in theArchives, 1 Torrey 2 challenges their assertion that there is not a high rate of schizophrenia in the general population in Ireland, while Walsh and Kendler 3 defend their position; curiously, these antagonists fail to note data published previously in theArchivesthat is not only highly relevant to this important, long-standing, and apparently still unresolved controversy, but may also offer some resolution of the impasse. The most recent systematic ( DSM-III-R ) catchment area epidemiological study of both the incidence and the prevalence of schizophrenia in rural Ireland 4 reports overall rates that are entirely unremarkable and fall well within the midrange of values recorded previously on a worldwide basis, eg, a lifetime morbid risk (± SE) of0.7%±0.1% that is virtually identical to the value derived by Walsh and Kendler 3 ; thus, there would appear to be little contemporary evidence

Morbid risk of schizophrenia for relatives of patients with cannabis-associated psychosis

Twenty-three patients admitted with acute psychosis who were cannabis positive on urinary screening were each matched, with respect to sex, with two psychotic controls who screened negatively for all substances. The lifetime morbid risk of psychiatric disorder was estimated among the first degree relatives of cases and controls, using RDC-FH criteria to define diagnoses, and Weinberg's shorter method of age correction. The cases had a significantly greater familial morbid risk of schizophrenia (7.1%) than the controls (0.7%), while the risks of other psychoses, and of non-psychotic conditions were similar. The same pattern of familial risk was evident when the analysis was restricted to patients with DSM-III schizophrenia. The data suggest that the development or recurrence of acute psychosis in the context of cannabis use may be associated with a genetic predisposition to schizophrenia.

Schizophrenia in the Afro-Caribbean Community

Previous studies have shown high rates of schizophrenia among the Afro-Caribbean population in Britain. In order to assess the role of genetic factors in the aetiology of this phenomenon, we have used a standardised family history method (FHRDC) to compare lifetime morbidity risks for first-degree relatives of Afro-Caribbean and white patients with RDC schizophrenia admitted in Central Manchester between 1982 and 1988. Lifetime morbidity risk for parents of Afro-Caribbean subjects was 8.9%, and for parents of white patients 8.4%. For the siblings of black probands, however, the risk was 15.9%, as compared with 1.8% for white siblings (P < 0.05). Among siblings of UK-born Afro-Caribbean probands, morbid risk was even higher at 27.3% (P = 0.001). High rates among siblings of younger Afro-Caribbean patients are consistent with previous reports of a higher incidence in the UK-born. These observations suggest that schizophrenia among Afro-Caribbeans is no less familial than for the remainder of the population, but that the increased frequency of the disorder is due to environmental factors which are most common in the Afro-Caribbean community, and capable of precipitating schizophrenia in those who are genetically predisposed.