Epidemiologic studies have reported that the majority of community residents in the United States have experienced posttraumatic stress disorder (PTSD)–level traumatic events, as defined in the ...DSM-IV. Only a small subset of trauma victims develops PTSD (<10%). Increased incidence of other disorders following trauma exposure occurs primarily among trauma victims with PTSD. Female victims of traumatic events are at higher risk for PTSD than male victims are. Direct evidence on the causes of the sex difference in the conditional risk of PTSD is unavailable. The available evidence suggests that the sex difference is not due to (a) the higher occurrence of sexual assault among females, (b) prior traumatic experiences, (c) preexisting depression or anxiety disorder, or (d) sex-related bias in reporting. Observed sex differences in anxiety, neuroticism, and depression, inducing effects of stressful experiences, might provide a theoretical context for further inquiry into the greater vulnerability of females to PTSD.
This paper reviews recent epidemiologic studies of posttraumatic stress disorder (PTSD) in the general population. Estimates of the prevalence of exposure to traumatic events vary with the method ...used to ascertain trauma exposure and the definition of the stressor criterion. Changes in the DSM-IV definition of “stressor” have increased the number of traumatic events experienced in the community that can be used to diagnose PTSD and thus, the number of PTSD cases. Risk factors for PTSD in adults vary across studies. The 3 factors identified as having relatively uniform effects are 1) preexisting psychiatric disorders, 2) a family history of disorders, and 3) childhood trauma. In civilian populations, women are at a higher risk for PTSD than are men, following exposure to traumatic events. Most community residents have experienced 1 or more PTSD-level traumas in their lifetime, but only a few succumb to PTSD. Trauma victims who do not succumb to PTSD are not at an elevated risk for the subsequent onset of major depression or substance use disorders, compared with unexposed persons.
Background: Prenatal problems are among theorized etiologies for child disruptive behavior problems. A key question concerns whether etiological contributors are shared across the broad range of ...disruptive psychopathology or are partially or largely distinct. Method: We examined prenatal smoking exposure and low birth weight as risk factors for attention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) in a population-based longitudinal design from ages 6 to 17 years. Multiple informants were used, with emphasis on parent and teacher report for ADHD, parent-and self-report interview for ODD, and self-report interview for CD, in keeping with evidence about the most valid sources of information for these respective syndromes. Results: The association of prenatal smoking exposure with ADHD was highly confounded by family variables. In contrast, low birth weight independently predicted ADHD, even with family variables statistically controlled. The opposite pattern appeared for ODD and CD. Prenatal smoking exposure but not low birth weight predicted ODD independent of potential confounding variables. Prenatal smoking exposure also predicted CD. The effect on CD was via its effect on ODD. Conclusion: Prenatal smoking exposure may contribute to ODD and via that route to later CD, but does not have a specific association with ADHD in this sample. Findings have implications for distinct etiological contributors to these often comorbid aspects of the disruptive behavior domain. (Contains 4 tables.)
The confluence of sleep/wake cycle and circadian rhythm changes that accompany pubertal development and the social and emotional developmental tasks of adolescence may create a period of substantial ...risk for development of insomnia. Although poor sleep affects cognitive performance and is associated with poor emotional and physical health, epidemiologic studies among adolescents have been limited. In this first epidemiologic study of insomnia defined by Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria in a US sample of adolescents, we estimated lifetime prevalence of insomnia, examined chronicity and onset, and explored the role of pubertal development.
Data come from a random sample of 1014 adolescents who were 13 to 16 years of age, selected from households in a 400000-member health maintenance organization encompassing metropolitan Detroit. Response rate was 71.2%. The main outcome measured was DSM-IV-defined insomnia.
Lifetime prevalence of insomnia was 10.7%. A total of 88% of adolescents with a history of insomnia reported current insomnia. The median age of onset of insomnia was 11. Of those with insomnia, 52.8% had a comorbid psychiatric disorder. In exploratory analyses of insomnia and pubertal development, onset of menses was associated with a 2.75-fold increased risk for insomnia. There was no difference in risk for insomnia among girls before menses onset relative to boys, but a difference emerged after menses onset. In contrast, maturational development was not associated with insomnia in boys.
Insomnia seems to be common and chronic among adolescents. The often found gender difference in risk for insomnia seems to emerge in association with onset of menses.
Only a small minority of trauma victims develops post-traumatic stress disorder (PTSD), suggesting that victims vary in their predispositions to the PTSD response to stressors. It is assumed that the ...role of predispositions in PTSD varies by trauma severity: when stressors are less severe, predispositions play a bigger role. In this study, we test whether the role of intelligence in PTSD varies by trauma severity. Specifically, does low intelligence plays a bigger part among victims of lower magnitude stressors than among victims of extreme stressors?
Data come from a longitudinal study of randomly selected sample in Southeast Michigan (n = 713). IQ was measured at age 6. PTSD was measured at age 17, using the NIMH-DIS for DSM-IV. Stressors were classified as extreme if they involved assaultive violence (e.g. rape, sexual assault, threatened with a weapon); other stressors in the list (e.g. disaster, accidents) were classified as lower magnitude. Assaultive violence victims had experienced assaultive violence plus other event types or only assaultive violence. Victims of other stressors were participants who had never experienced assaultive violence. We compared the influence of age 6 IQ on PTSD among persons exposed to assaultive violence vs. other stressors, using multinomial logistic regression.
Relative risk ratio (RRR) for PTSD associated with a one point drop in age 6 IQ among victims of assaultive violence was 1.04 (95% CI 1.01, 1.06); among victims of other stressors, it was 1.03 (95% CI 0.99, 1.06). A comparison of the two RRRs indicates no significant difference between the two estimates (p = 0.652). IQ does not play a bigger role in PTSD among victims of other stressors than it does among victims of assaultive violence.
Lower IQ exerts an adverse PTSD effect on trauma victims, with no evidence of variability by the severity of trauma they have experienced.
: Information on stress hormones and sleep disturbance in posttraumatic stress disorder (PTSD) is on the basis of clinical samples and samples of other selective populations. Neurobiological studies ...nested in a large epidemiological community sample were recently reported. PTSD was compared with several control groups, defined by exposure and by diagnostic classification on the basis of comorbidity with Major Depression. Key findings were: (a) higher mean catecholamines in persons with PTSD versus controls; (b) no difference in mean cortisol between groups; (c) comorbid PTSD and depression was associated with higher cortisol in women; and (d) polysomnographic studies failed to detect clinically relevant sleep disturbance in PTSD, although an increase in brief arousal from REM was detected. Methodological questions raised by discrepancies between biological findings from epidemiologic versus clinical and other selective samples are discussed.
When smokers were separated by their nicotinic receptor gene variants, those with the low-risk genotype responded equally well to pharmacological treatments, including both nicotine replacement and ...bupropion, and nonpharmacological therapies. Those with the high-risk genotype, as identified by DNA sequencing, responded only to pharmacological treatments. Clinicians advising patients on smoking cessation can suspect genetic risk on the basis of early onset of heavy smoking and direct those smokers specifically to pharmacological treatments.
Objective:Smoking is highly intractable, and the genetic influences on cessation are unclear. Identifying the genetic factors affecting smoking cessation could elucidate the nature of tobacco dependence, enhance risk assessment, and support development of treatment algorithms. This study tested whether variants in the nicotinic receptor gene cluster CHRNA5-CHRNA3-CHRNB4 predict age at smoking cessation and relapse after an attempt to quit smoking.
Method:In a community-based, cross-sectional study (N=5,216) and a randomized comparative effectiveness smoking cessation trial (N=1,073), the authors used Cox proportional hazard models and logistic regression to model the relationships of smoking cessation (self-reported quit age in the community study and point-prevalence abstinence at the end of treatment in the clinical trial) to three common haplotypes in the CHRNA5-CHRNA3-CHRNB4 region defined by rs16969968 and rs680244.
Results:The genetic variants in the CHRNA5-CHRNA3-CHRNB4 region that predict nicotine dependence also predicted a later age at smoking cessation in the community sample. In the smoking cessation trial, haplotype predicted abstinence at end of treatment in individuals receiving placebo but not among individuals receiving active medication. Haplotype interacted with treatment in affecting cessation success.
Conclusions:Smokers with the high-risk haplotype were three times as likely to respond to pharmacologic cessation treatments as were smokers with the low-risk haplotype. The high-risk haplotype increased the risk of cessation failure, and this increased risk was ameliorated by cessation pharmacotherapy. By identifying a high-risk genetic group with heightened response to smoking cessation pharmacotherapy, this work may support the development of personalized cessation treatments.
Background: The DSM-IV two-part definition of posttraumatic stress disorder (PTSD) widened the variety of stressors (A1) and added a subjective component (A2). The effects of the revised stressor ...criterion on estimates of exposure and PTSD in a community sample are evaluated.
Methods: A representative sample of 2181 persons in southeast Michigan were interviewed about lifetime history of traumatic events and PTSD. The evaluation of the revised two-part definition is based on a randomly selected sample of events that represents the total pool of traumatic events experienced in the community.
Results: The enlarged definition of stressors in A1 increased the total number of events that can be used to diagnose PTSD by 59%. The majority of A1 events (76.6%) involved the emotional response in A2. Females were more likely than males to endorse A2 (adjusted odds ratio = 2.66; 95% confidence interval 1.92, 3.71). Of all PTSD cases resulting from the representative sample of events, 38% were attributable to the expansion of qualifying events in A1. The identification of exposures that lead to PTSD were not improved materially by A2 however, events that did not involve A2 rarely resulted in PTSD.
Conclusions: Compared to previous definitions, the wider variety of stressors in A1 markedly increased the number of events experienced in the community that can be used to diagnose PTSD. Furthermore, A2 might be useful as a separate criterion, an acute response necessary for the emergence of PTSD, and might serve as an early screen for identifying a subset of recently exposed persons at virtually no risk for PTSD. The utility of A2 as a screen must be tested prospectively.
Partial PTSD, employed initially in relation to Vietnam veterans, has been recently extended to civilian victims of trauma. We examined the extent to which partial PTSD is distinguishable from full ...DSM-PTSD with respect to level of impairment.
A representative sample of 2181 persons was interviewed by telephone to record lifetime traumatic events and to assess DSM-IV PTSD criteria. Partial PTSD was defined as > or = 1 symptom in each of three symptom groups (criteria B, C and D) and duration of > or = 1 month. Impairment in persons with PTSD and partial PTSD was measured by number of work-related and personal disability days during the 30-day period when the respondent was most upset by the trauma.
Compared to exposed persons with neither PTSD nor partial PTSD, increment in work-loss days associated with PTSD was 11.4 (S.E. =0.6) days and with partial PTSD, 3.3 (S.E. =0.4) days (adjusted for sex, education and employment). Similar disparities were found across other impairment indicators. Persons who fell short of PTSD criteria by one symptom of avoidance and numbing reported an increment of 5.0 (S.E. =0.7) work-loss days, 6.0 fewer than full PTSD. PTSD was associated with excess impairment, controlling for number of symptoms. A significantly lower proportion of persons with partial PTSD than full PTSD experienced symptoms for more than 2 years. A lower proportion of persons with partial PTSD than full PTSD had an etiologic event of high magnitude.
PTSD identifies the most severe trauma victims, who are markedly distinguishable from victims with subthreshold PTSD.
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