Genetic and environmental influences on sleep quality in middle-aged men: a twin study.

Poor sleep quality is a risk factor for a number of cognitive and physiological age-related disorders. Identifying factors underlying sleep quality are important in understanding the etiology of these age-related health disorders. We investigated the extent to which genes and the environment contribute to subjective sleep quality in middle-aged male twins using the classical twin design. We used the Pittsburgh Sleep Quality Index to measure sleep quality in 1218 middle-aged twin men from the Vietnam Era Twin Study of Aging (mean age = 55.4 years; range 51-60; 339 monozygotic twin pairs, 257 dizygotic twin pairs, 26 unpaired twins). The mean PSQI global score was 5.6 [SD = 3.6; range 0-20]. Based on univariate twin models, 34% of variability in the global PSQI score was due to additive genetic effects (heritability) and 66% was attributed to individual-specific environmental factors. Common environment did not contribute to the variability. Similarly, the heritability of poor sleep-a dichotomous measure based on the cut-off of global PSQI>5-was 31%, with no contribution of the common environment. Heritability of six of the seven PSQI component scores (subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, and daytime dysfunction) ranged from 0.15 to 0.31, whereas no genetic influences contributed to the use of sleeping medication. Additive genetic influences contribute to approximately one-third of the variability of global subjective sleep quality. Our results in middle-aged men constitute a first step towards examination of the genetic relationship between sleep and other facets of aging.

Gene-environment interaction of ApoE genotype and combat exposure on PTSD.

Factors determining who develops PTSD following trauma are not well understood. The €4 allele of the apolipoprotein E (apoE) gene is associated with dementia and unfavorable outcome following brain insult. PTSD is also associated with dementia. Given evidence that psychological trauma adversely affects the brain, we hypothesized that the apoE genotype moderates effects of psychological trauma on PTSD pathogenesis. To investigate the moderation of the relationship between PTSD symptoms and combat exposure, we used 172 participants with combat trauma sustained during the Vietnam War. PTSD symptoms were the dependent variable and number of combat experiences, apoE genotype, and the combat experiences × apoE genotype interaction were predictors. We also examined the outcome of a diagnosis of PTSD (n = 39) versus no PTSD diagnosis (n = 131). The combat × apoE genotype interaction was significant for both PTSD symptoms (P = .014) and PTSD diagnosis (P = .009). ApoE genotype moderates the relationship between combat exposure and PTSD symptoms. Although the pathophysiology of PTSD is not well understood, the €4 allele is related to reduced resilience of the brain to insult. Our results are consistent with the €4 allele influencing the effects of psychological trauma on the brain, thereby affecting the risk of PTSD.

Context binding in schizophrenia: effects of clinical symptomatology and item content.

Impairments in source monitoring have been widely reported in schizophrenia, with patients typically misattributing self-generated items to external sources. Some studies have reported that patients with more severe positive symptoms (notably hallucinations) exhibit a greater impairment on these tasks, although findings are not uniformly positive. The emotional content of the items to be remembered also may affect subsequent retrieval, with some studies suggesting a greater misattribution bias for affectively-laden material. Recently, it has been proposed that schizophrenic patients have a fundamental deficit in binding different contextual elements together in memory. The effect of clinical symptomatology and item content on source monitoring and context binding has yet to be examined in a single study. Twenty-one patients with schizophrenia and 21 healthy control subjects completed a task wherein memory for affective and neutral word pairs was assessed in conjunction with memory for both source and temporal information. Schizophrenic patients performed more poorly than controls overall, and tended to exhibit a more fractionated retrieval of word pairs across all levels of affective valence. Current intellectual level and overall verbal memory performance were significantly correlated with context binding performance for positive and neutral word pairs. Clinical symptomatology was unrelated to source monitoring performance. The results of this pilot study provide tentative support for the notion that schizophrenia is associated with an impairment in combining contextual cues together to form a coherent memory of an event, irrespective of the affective valence of the material. Clinical symptomatology bore no significant relationship to source memory performance.

Factor analysis of neurocognitive tests in a large sample of schizophrenic probands, their siblings, and healthy controls.

Large batteries of neuropsychological tests are typically necessary to identify cognitive deficits in schizophrenia and routinely examine multiple cognitive processes, with many tests often yielding more than one measure of interest. This study investigates the feasibility of a partial solution to the problem of multiple comparisons: the use of factor analysis to reduce the number of phenotypic variables and to better understand the underlying cognitive architecture in schizophrenia. Using a principle components analysis followed by a varimax rotation, we identified factor structures for schizophrenic patients (n=99), their unaffected siblings (n=167), and control subjects (n=131), both separately and as a composite group. Exploratory factor analysis of the full sample yielded a 7-factor model that included verbal memory, working memory, visual memory, IQ/speed/fluency, executive function, attention and digit span. A confirmatory factor analysis (CFA) with maximum likelihood estimation revealed that the 7-factor model fit observed data from the three groups adequately. Since we identified a factor structure representative of all groups that reduced 24 original variables to 7 variables of interest, factor analysis was useful in reducing the complexity of large batteries of cognitive measures to more manageable numbers of phenotypic variables. Furthermore, these findings provide the first confirmation that cognitive structure is comparable in family members of schizophrenia patients, as well as in patients themselves and controls.

Smoking cessation in people with schizophrenia.

OBJECTIVE: High rates of smoking and nicotine dependence have a profoundly negative impact on the health and well being of individuals with schizophrenia. Treating smoking is a critical step in improving the health and quality of life of people affected by this illness. This paper reviews the literature on smoking cessation interventions in schizophrenia and discusses potential barriers to effective treatment with this population. METHODS: The criteria used to select studies for inclusion were: (1) Sample included 50% or more individuals with schizophrenia spectrum diagnosis (SSD); (2) Some individual or group intervention for smoking cessation was provided; and (3) Some smoking-related outcome variable was measured (self-reported smoking, breath carbon monoxide, etc). RESULTS: Both pharmacologic and psychosocial smoking cessation treatments have been found to be useful in helping individuals with schizophrenia reduce and quit smoking in the short term. Few interventions have been found to be effective in promoting smoking abstinence in the long term. CONCLUSIONS: Intervention development must include strategies to overcome barriers to smoking cessation that are most relevant to individuals with schizophrenia and focus on translating short term gains into long term abstinence.