Biomedical subjects

M Tsuang

Publications and source records attributed to M Tsuang.

12 recordsLinked to original sources

PubMed2001

A twin study of generalized anxiety disorder symptoms, panic disorder symptoms and post-traumatic stress disorder in men.

Generalized anxiety disorder (GAD), panic disorder (PD) and post-traumatic stress disorder (PTSD) often co-occur. We investigated whether and to what degree genetic and environmental contributions overlap among symptoms of GAD, symptoms of PD and PTSD. Subjects were 3327 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of GAD symptoms, PD symptoms and PTSD. The liability for GAD symptoms was due to a 37.9% additive genetic contribution common to PD symptoms and PTSD. Liability for PD symptoms was due to a 20.7% additive genetic contribution common to GAD symptoms and PTSD, and a 20.1% additive genetic influence specific to PD symptoms. Additive genetic influences common to symptoms of GAD and PD accounted for 21.3% of the genetic variance in PTSD. Additive genetic influences specific to PTSD accounted for 13.6% of the genetic variance in PTSD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that these disorders each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Adult↗

PubMed2001

A twin study of the association between pathological gambling and antisocial personality disorder.

Many individuals with a history of pathological gambling (PG) also have a history of engaging in antisocial behaviors, and this has often been interpreted as a result of the former causing the latter. In a sample of 7,869 men in 4,497 twin pairs from the Vietnam Era Twin Registry, the authors examined (a) the association between PG and antisocial personality disorder (ASPD), (b) the extent to which PG might be differentially associated with childhood conduct disorder (CD) and adult antisocial behavior (AAB), and (c) the contribution of genetic and environmental factors to the association of PG with ASPD, CD, and AAB. PG was significantly associated with all 3 antisocial behavior disorders, and the association of PG with ASPD, CD, and AAB was predominantly explained by genetic factors. The results of this study suggest that the greater-than-chance co-occurrence of PG and antisocial behavior disorders is partially due to their sharing a common genetic vulnerability. The antisocial behavior observed among many individuals with PG probably cannot be interpreted as being simply a consequence of the PG.

Adult↗

PubMed2001

Traumatic brain injury and schizophrenia in members of schizophrenia and bipolar disorder pedigrees.

OBJECTIVE: Schizophrenia following a traumatic brain injury could be a phenocopy of genetic schizophrenia or the consequence of a gene-environment interaction. Alternatively, traumatic brain injury and schizophrenia could be spuriously associated if those who are predisposed to develop schizophrenia have greater amounts of trauma for other reasons. The authors investigated the relationship between traumatic brain injury and psychiatric diagnoses in a large group of subjects from families with at least two biologically related first-degree relatives with schizophrenia, schizoaffective disorder, or bipolar disorder. METHOD: The Diagnostic Interview for Genetic Studies was used to determine history of traumatic brain injury and diagnosis for 1,275 members of multiplex bipolar disorder pedigrees and 565 members of multiplex schizophrenia pedigrees. RESULTS: Rates of traumatic brain injury were significantly higher for those with a diagnosis of schizophrenia, bipolar disorder, and depression than for those with no mental illness. However, multivariate analysis of within-pedigree data showed that mental illness was related to traumatic brain injury only in the schizophrenia pedigrees. Independent of diagnoses, family members of those with schizophrenia were more likely to have had traumatic brain injury than were members of the bipolar disorder pedigrees. The members of the schizophrenia pedigrees also failed to show the gender difference for traumatic brain injury (more common in men than in women) that was expected and was present in the bipolar disorder pedigrees. Subjects with a schizophrenia diagnosis who were members of the bipolar disorder pedigrees (and thus had less genetic vulnerability to schizophrenia) were less likely to have had traumatic brain injury (4.5%) than were subjects with schizophrenia who were members of the schizophrenia pedigrees (and who had greater genetic vulnerability to schizophrenia) (19.6%). CONCLUSIONS: Members of the schizophrenia pedigrees, even those without a schizophrenia diagnosis, had greater exposure to traumatic brain injury compared to members of the bipolar disorder pedigrees. Within the schizophrenia pedigrees, traumatic brain injury was associated with a greater risk of schizophrenia, consistent with synergistic effects between genetic vulnerability for schizophrenia and traumatic brain injury. Posttraumatic-brain-injury schizophrenia in multiplex schizophrenia pedigrees does not appear to be a phenocopy of the genetic disorder.

Adult↗

PubMed2000

Genetic and environmental influences on posttraumatic stress disorder, alcohol and drug dependence in twin pairs.

We investigated whether and to what degree genetic and environmental contributions overlap among posttraumatic stress disorder (PTSD), alcohol dependence (AD) and drug dependence (DD). Subjects were 3304 monozygotic and dizygotic male-male twin pair members of the Vietnam Era Twin Registry who participated in 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised (DIS-3R). Genetic model fitting was performed to estimate the magnitude of genetic and environmental contributions to the lifetime co-occurrence of DSM-III-R PTSD, AD and DD. The liability for PTSD was partially due to a 15.3% genetic contribution common to AD and DD and 20.0% genetic contribution specific to PTSD. Risk for AD was partially due to a 55.7% genetic contribution common to PTSD and DD. Genetic influences common to PTSD and AD accounted for 25.2% of the total risk for DD. Specific family environmental influence accounted for 33.9% of the total variance in risk for DD. Remaining variance for all three disorders was due to unique environmental factors both common and specific to each phenotype. These results suggest that PTSD, AD and DD each have etiologically distinct components and also have significant genetic and unique environmental contributions in common.

Adult↗

PubMed2000

Impaired verbal memory is associated with impaired motor performance in schizophrenia: relationship to brain structure.

Deficient ability to take advantage of predictable elements in the performance of cognitive tasks has been proposed as an underlying factor for a number of deviances in schizophrenia. In a schizophrenic sample (n=39), we propose and test the view that certain memory and motor anomalies arise because of a compromise in the capacity to take advantage of the redundant (predictable) features of cognitive tasks. Results demonstrate a relationship between reduced capacity to take advantage of predictable features of two different cognitive processing tasks, one verbal memory, and the other motor. Poorer verbal recall on high-redundancy word lists was associated with a reduced ability to produce synchronous finger tapping in response to a high redundancy auditory stimulus, and inversely correlated with formal thought disorder ratings. These relationships, we suggest, reflect a specific and common schizophrenic deficit in the use of redundancies, not attributable to a generalized deficiency in performance. Structural imaging evidence from a subsample of these subjects (n=16) implicates frontal areas as the locus of this cognitive impairment.

Adult↗

PubMed2000

Schizophrenia: genes and environment.

The historical and genetic foundations of our current understanding of schizophrenia are reviewed, as are the present and future directions for research. Genetic epidemiological investigations, including family, twin, and adoption studies have confirmed the contributions of genetic and environmental determinants of schizophrenia. For example, identical twins show average concordance rates of only 50%; rates of 100% would be expected on the basis of genetic equivalence alone. Genetic factors may cause errors in brain development and synaptic connections. A broad range of environmental components may further damage the brain. Biological components may include pregnancy and delivery complications, such as intrauterine fetal hypoxia, infections, and malnutrition. Primarily nonbiological components may include psychosocial stressors, such as residence in an urban area and dysfunctional family communication. It is likely that the environmental factors interact with the genetic liability in a negative manner to produce disorders in the schizophrenic spectrum. Genetic and environmental components of the disorder are examined, as well as their interactions in producing either neurodevelopmental syndromes or schizophrenia itself. The implication of these findings for prevention and treatment are considered.

Brain↗

PubMed2000

Common genetic vulnerability for pathological gambling and alcohol dependence in men.

BACKGROUND: In comparison with alcohol dependence (AD), relatively little is known about the causes of pathological gambling (PG). Given the high rate of comorbidity between PG and AD, knowledge about the causes of AD may be applied to understanding those of PG. METHODS: Subjects were adult male twin pairs from the Vietnam Era Twin Registry. Lifetime histories of PG and AD were assessed by structured psychiatric telephone interview. The validity of a continuum of PG liability was tested to determine whether the causes of subclinical PG, or problem gambling, are quantitatively or qualitatively distinct from those of DSM-III-R PG disorder. Genetic model-fitting methods were used to quantify the extent to which the genetic and environmental risk for PG could be explained by the risk for AD. RESULTS: Tests of the continuity model of PG were all consistent with the hypothesis that subclinical PG and DSM-III-R PG disorder have many, perhaps all, of the same risk factors and thus differ quantitatively rather than qualitatively. Depending on the PG definition, between 12% and 20% of the genetic variation and between 3% and 8% of the nonshared environmental variation in the risk for PG were accounted for by the risk for AD. CONCLUSIONS: Subclinical PG, or problem gambling, may be a milder form of PG, rather than an etiologically distinct syndrome. Risk for AD accounts for a significant but modest proportion of the genetic and environmental risk for subclinical PG and DSM-III-R PG disorder.

Adult↗

PubMed2000

Strategies for improving comorbidity measures based on Medicare and Medicaid claims data.

Claims-based measures of comorbid illness severity have generally relied on the diagnoses listed for a single hospitalization. Unfortunately, such diagnostic information is often limited because patients have not been hospitalized during periods of interest, because of incomplete coding of diagnoses on claims forms, or because listed diagnoses represent complications of the hospitalization rather than pre-existing comorbid conditions. To address these limitations, we developed and tested four comorbidity index scores for patients with breast cancer, each based on different sources of health services claims from Medicare and Medicaid: hospitalization for breast cancer surgery; outpatient care prior to the hospitalization; other inpatient care prior to the hospitalization; and all sources combined. Varying the number and type of sources of diagnostic information yielded only very small improvements in the prediction of mortality at 1 and 3 years. Surprisingly, even simpler measures of comorbidity (crude number of diagnoses) and of prior health care utilization (total days spent in the hospital) performed at least as well in predicting mortality as did the more complex index scores which assigned points and weights for specific conditions. The greatest improvement in explanatory power was observed when another source of clinical information (cancer stage derived from a population-based cancer registry) was used to supplement claims information. Expanding the source of claims diagnoses and focusing on time periods prior to an index hospitalization are insufficient for substantially improving the explanatory power of claims-based comorbidity indices. Other improvements suggested by our results should include: increasing the completeness and accuracy of claims diagnoses; supplementing diagnoses with health care utilization information in claims data; and supplementing claims data with other sources of clinical information.

Aged↗

PubMed1999

Common genetic vulnerability for nicotine and alcohol dependence in men.

BACKGROUND: Nicotine and alcohol dependence often occur together. We examined data from male twin pairs to determine whether there are genetic or environmental influences common to nicotine and alcohol dependence, and, if so, to estimate the magnitude and correlation of these influences. METHODS: Subjects were 3356 male-male twin-pair members of the Vietnam Era Twin Registry who participated in a 1992 telephone administration of the Diagnostic Interview Schedule Version 3 Revised. Genetic model fitting was performed to estimate the magnitude and correlation of genetic and environmental contributions to lifetime nicotine and alcohol dependence. RESULTS: The heritability of nicotine dependence was 60.3% (95% confidence interval [CI], 55.4%-65.2%); that of alcohol dependence, 55.1% (95% CI, 49.7%-60.5%). The best-fitting model for the co-occurrence of lifetime nicotine and alcohol dependence included a substantial genetic correlation between both disorders (r = 0.68; 95% CI, 0.61-0.74) and a modest unique environmental correlation (r = 0.23; 95% CI, 0.14-0.32). CONCLUSIONS: These data suggest a common genetic vulnerability to nicotine and alcohol dependence in men. This common genetic influence may partially explain the clinical and epidemiological observations that alcoholics are often dependent smokers.

Adult↗

PubMed1992

Late-onset atypical psychosis: a case involving neuroleptic drug toxicity and autoimmune serological abnormalities.

Serious or significant neuroleptic toxicity (Kurlan et al. 1984; Lazarus 1985; Levenson 1985; Pearlman 1986) may complicate the diagnosis and management of patients who develop acute medical problems while under treatment with neuroleptics (Levenson and Simpson 1986). We have found that in some cases it is difficult, if not impossible, to determine whether neuroleptics have contributed to the cause of an acute medical illness, or if the occurrence of acute medical problems precipitated the signs of neuroleptic toxicity by altering the disposition or the pharmacologic effects of the drugs.

Autoimmune Diseases↗

PubMed1987

High rate of affective disorders in probands with attention deficit disorder and in their relatives: a controlled family study.

In a controlled family study of attention deficit disorder, data were collected on first-degree relatives of 22 children with attention deficit disorder and 20 normal children. The rate of major affective disorder was significantly higher in the attention deficit disorder probands (32%) and their relatives (27%) than in the normal control subjects (0%) and their relatives (6%). The findings indicate that attention deficit disorder is associated with higher risk for affective disorder and suggest that probands who have both disorders may represent a distinct subgroup.

Adolescent↗

PubMed1975

The Iowa 500: suicide in mania , depression, and schizophrenia.

Long-term (30-to 40-year) follow-up data for 76 manic patients, 182 depressives. 170 schizophrenics, and 109 controls showed that 10 per cent of the schizophrenics, 8.5 percent of the manics, and 10.6 percent of the depressives who were decreased had died by suicide. None of the controls had committed suicide. The authors suggest that suicide is a significant outcome factor in all three of these illnesses and is likely to occur at an earlier age in schizophrenia than in the other illnesses.

Adult↗