Posts Tagged ‘anxiety’
Genetic factors that are associated with fears appear to change as children and adolescents age, with some familial factors declining in importance over time while other genetic risk factors arise in adolescence and adulthood, according to a new report .
The nature of common fears changes during childhood and adolescent development, according to background information in the article. Two hypotheses have been proposed regarding genetic risk factors for these fears. “The ‘developmentally stable’ hypothesis predicts that a single set of genetic risk factors impacts the level of fears at age 8 years and these same genes constitute the only genetic influences on fear-proneness throughout development,” the authors write. “By contrast, the ‘developmentally dynamic’ hypothesis predicts that genetic effects on fear-proneness will vary over time.”
Kenneth S. Kendler, M.D., of the Virginia Commonwealth University School of Medicine, Richmond, and colleagues studied 2,490 twins born in Sweden between 1985 and 1986. The twins were assessed for their level of fear four times: at age 8 to 9 by a questionnaire mailed to parents, at ages 13 to 14 and 16 to 17 with questionnaires mailed to twins and parents and at age 19 to 20 with questionnaires only to the twins.
Fears naturally divided into three categories: situational fears (such as fear of closed spaces, flying or the dark), animal fears (including rats, dogs and snakes) and blood or injury fears (fears of dentists, injections and blood). Overall, genetic factors influenced all three types of fears, but did not remain stable over time. “We identified one set of genetic risk factors that act in childhood and have a steep decline in influence with age,” the authors write. “Furthermore, we see evidence for new sets of genetic risk factors ‘coming on line’ in early adolescence, late adolescence and early adulthood.”
As the twins aged, the effects of their shared environment on their fears diminished and the influence of their individual environment increased. “This is an expected pattern given that adolescence is a time of declining influence of the home environment as individuals spend less time with family and progressively make their own world, spending more time with friends,” the authors write.
Further research is needed to determine the exact mechanisms by which genetics influences fears, they note–for example, if genes influence mental processes such as sensitivity to disgust or are more closely linked to changes in neurobiology, including alterations in the brain circuits through which fear is processed.
Arch Gen Psychiatry. 2008;65(4):421-429.
A Longitudinal Twin Study of Fears From Middle Childhood to Early Adulthood: Evidence for a Developmentally Dynamic Genome
Kenneth S. Kendler; Charles O. Gardner; Peter Annas; Michael C. Neale; Lindon J. Eaves; Paul Lichtenstein
Context While the nature of common fears changes over development, we do not know whether genetic effects on fear-proneness are developmentally stable or developmentally dynamic.
Objective To determine the temporal pattern of genetic and environmental effects on the level of intensity of common fears.
Design Prospective, 4-wave longitudinal twin study. Structural modeling was performed with Mx.
Setting General community.
Participants Two thousand four hundred ninety twins and their parents from the Swedish Twin Study of Child and Adolescent Development.
Main Outcome Measure The level of parent- and/or self-reported fears obtained at ages 8 to 9, 13 to 14, 16 to 17, and 19 to 20 years.
Results Thirteen questionnaire items formed 3 distinct fear factors: situational, animal, and blood/injury. For all 3 fears, the best-fit model revealed developmentally dynamic effects and, in particular, evidence for both genetic attenuation and innovation. That is, genetic factors influencing fear intensity at age 8 to 9 years decline substantially in importance over time. Furthermore, new sets of genetic risk factors impacting fear intensity “come on line” in early adolescence, late adolescence, and early adulthood. As the twins aged, the influence of the shared environment declined and unique environment increased. No sex effects were found for situational fears while for animal and blood/injury fears, genetic factors in males and females were correlated but not identical. Shared environmental factors were both more important and more stable for animal fears than for situational or blood/injury fears.
Conclusions Genetic effects on fear are developmentally dynamic from middle childhood to young adulthood. As children age, familial-environmental influences on fears decline in importance.
This Month in Archives of General Psychiatry
Arch Gen Psychiatry. 2008;65(4):373.
Inherited variations in the amount of an innate anxiety-reducing molecule help explain why some people can withstand stress better than others, according to a new study led by researchers at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health (NIH).
“Stress response is an important variable in vulnerability to alcohol dependence and other addictions, as well as other psychiatric disorders,” noted NIAAA Director Ting-Kai Li, M.D. “This finding could help us understand individuals’ initial vulnerability to these disorders.”
Scientists led by David Goldman, M. D., chief of the NIAAA Laboratory of Neurogenetics, identified gene variants that affect the expression of a signaling molecule called neuropeptide Y (NPY). Found in brain and many other tissues, NPY regulates diverse functions, including appetite, weight, and emotional responses.
“NPY is induced by stress and its release reduces anxiety,” said Dr. Goldman. “Previous studies have shown that genetic factors play an important role in mood and anxiety disorders. In this study, we sought to determine if genetic variants of NPY might contribute to the maladaptive stress responses that often underlie these disorders.” A report of the findings appears online today in Nature.
Analyses of human tissue samples led by researchers at NIAAA identified several NPY gene variants. Collaborations with NIH-supported scientists at the University of Michigan, University of Pittsburgh, University of Helsinki, University of Miami, University of Maryland, the University of California at San Diego, and Yale University, showed that these variants result in a range of different effects including altered levels of NPY in brain and other tissues, and differences in emotion and emotion-induced responses of the brain.
The researchers evaluated the NPY gene variants’ effects on brain responses to stress and emotion. Using functional brain imaging, they found that individuals with the variant that yielded the lowest level of NPY reacted with heightened emotionality to images of threatening facial expressions. “Metabolic activity in brain regions involved in emotional processing increased when these individuals were presented with the threatening images,” explained Dr. Goldman.
In another brain imaging experiment, people with the low level NPY variant were found to have a diminished ability to tolerate moderate levels of sustained muscular pain. Previous studies had shown that NPY’s behavioral effects are mediated through interactions with opioid compounds produced by the body to help suppress pain, stress, and anxiety. “As shown by brain imaging of opioid function, these individuals released less opioid neurotransmitter in response to muscle discomfort than did individuals with higher levels of NPY,” said Dr. Goldman. “Their emotional response to pain was also higher, showing the close tie between emotionality and resilience to pain and other negative stimuli.”
In a preliminary finding, the low level NPY gene variant was found to be more common than other variants among a small sample of individuals with anxiety disorders. The researchers also found that low level NPY expression was linked to high levels of trait anxiety. “Trait anxiety is an indication of an individual’s level of emotionality or worry under ordinary circumstances,” explained Dr. Goldman.
The researchers conclude that these converging findings are consistent with NPY’s role as an anxiety-reducing peptide and help explain inter-individual variation in resiliency to stress. “This inherited functional variation could also open up new avenues of research for other human characteristics, such as appetite and metabolism, which are also modulated by NPY,” said Dr. Goldman.
 Laboratory of Neurogenetics, NIAAA, NIH, Bethesda, Maryland 20892, USA  These authors contributed equally to this work.
Understanding inter-individual differences in stress response requires the explanation of genetic influences at multiple phenotypic levels, including complex behaviours and the metabolic responses of brain regions to emotional stimuli. Neuropeptide Y (NPY) is anxiolytic and its release is induced by stress. NPY is abundantly expressed in regions of the limbic system that are implicated in arousal and in the assignment of emotional valences to stimuli and memories. Here we show that haplotype-driven NPY expression predicts brain responses to emotional and stress challenges and also inversely correlates with trait anxiety. NPY haplotypes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY. Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency as assessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain regions. A single nucleotide polymorphism (SNP rs16147) located in the promoter region alters NPY expression in vitro and seems to account for more than half of the variation in expression in vivo. These convergent findings are consistent with the function of NPY as an anxiolytic peptide and help to explain inter-individual variation in resiliency to stress, a risk factor for many diseases.
Doctors may one day be able to control alcohol addiction by manipulating the molecular events in the brain that underlie anxiety associated with alcohol withdrawal, researchers at the University of Illinois at Chicago College of Medicine and the Jesse Brown VA Medical Center report in the March 5 issue of the Journal of Neuroscience.
“The association of anxiety with increased alcohol use is a key factor in the initiation and maintenance of alcohol addition,” says Dr. Subhash Pandey, UIC professor of psychiatry and director of neuroscience alcoholism research, the lead author of the study.
Previous research has shown that people with inherently high levels of anxiety are at an increased risk of becoming alcoholics. In addition, withdrawal of alcohol in chronic users is often accompanied by extreme anxiety.
“Alcoholics may feel a need to continue to drink alcohol in an attempt to self-medicate to reduce their anxiety and other unpleasant withdrawal symptoms,” said Pandey.
Pandey and his colleagues have discovered the molecular basis for the link between anxiety and alcohol addiction, which may help in identifying new therapeutic strategies for the treatment of alcohol addiction.
The researchers found that a protein within neurons in the amygdala — the area of the brain associated with emotion and anxiety — controls the development of alcohol withdrawal symptoms and drinking behaviors in laboratory animals by changing the shape of the neurons. This change in shape affects the communication between neurons, leading to changes in behavior.
Neurons communicate by sending signals through branches called dendritic spines. The researchers found that short-term alcohol exposure increased the number of dendritic spines in certain regions of the amygdala, producing anti-anxiety effects. Alcohol-dependent animals eventually developed a tolerance to the anxiety-lowering effects of alcohol.
The researchers traced the anti-anxiety effect to the production of a particular protein, Arc, in response to a nerve growth factor called BDNF that is stimulated by alcohol exposure. BDNF is vital in the functioning and maintenance of neurons.
When alcohol was withheld from animals that had been chronically exposed, they developed high anxiety. Levels of BDNF and Arc — and the number of dendritic spines — were decreased in the amygdala. But the researchers were able to eliminate the anxiety in the alcohol-dependent animals by restoring BDNF and Arc to normal levels.
Pandey suggested that an initial easing of anxiety may encourage people to begin to use alcohol, while for chronic users, a lack of alcohol provokes high anxiety, creating a need to continue drinking to feel normal.
The researchers blocked Arc production in normal rats by injecting a complementary sequence to Arc gene DNA into the central amygdala. They found that when levels of Arc in the central amygdala were lowered, the spines decreased and anxiety and alcohol consumption increased. When levels of Arc were returned to normal three days post-injection, anxiety and alcohol consumption also returned to normal. In a previous study, researchers found that lowering BDNF in amygdala promoted anxiety and alcohol drinking.
“This is the first direct evidence of the molecular processes occurring in the neurons that is responsible for the co-morbidity of anxiety and alcoholism, which we believe plays a major role in the addictive nature of alcohol,” said Pandey.
“This offers the possibility of new therapeutic target — BDNF-Arc signaling and associated dendritic spines in the amygdala — or new drug development.”
“These observations by Dr. Pandey’s research group provide an insight into the link between alcohol and anxiety and could be used to identify new targets for developing medications that alleviate withdrawal-induced anxiety and potentially modify a motivation for drinking,” said Antonio Noronha, director of neuroscience and behavior research at the National Institute on Alcohol Abuse and Alcoholism.
J. Neurosci. 2008 28: 2589-2600; doi:10.1523/JNEUROSCI.4752-07.2008
Effector Immediate-Early Gene Arc in the Amygdala Plays a Critical Role in Alcoholism
Subhash C. Pandey, Huaibo Zhang, Rajesh Ugale, Anand Prakash, Tiejun Xu, and Kaushik Misra
The immediate early gene, activity-regulated cytoskeleton-associated protein (Arc), has been implicated in synaptic plasticity. However, the role of Arc in alcoholism is unknown. Here, we report that the anxiolytic effects of acute ethanol were associated with increased brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (trkB) expression, increased phosphorylation of extracellular signal-regulated kinases 1/2 (Erk1/2), Elk-1, and cAMP responsive element-binding protein (CREB), increased Arc expression, and increased dendritic spine density (DSD) in both the central amygdala (CeA) and medial amygdala (MeA) but not in the basolateral amygdala (BLA) of rats. Conversely, the anxiogenic effects of withdrawal after long-term ethanol exposure were associated with decreased BDNF and trkB expression, decreased phosphorylation of Erk1/2, Elk-1, and CREB, decreased Arc expression, and decreased DSD in both the CeA and MeA but not in the BLA of rats. We also showed that BDNF infusion into the CeA normalized phosphorylation of Erk1/2, Elk-1, and CREB, and normalized Arc expression, thereby protecting against the onset of ethanol withdrawal-related anxiety. We further demonstrated that arresting Arc expression in the CeA decreased DSD, thereby increasing anxiety-like and alcohol-drinking behaviors in control rats. These results revealed that BDNF–Arc signaling and the associated DSD in the CeA, and possibly in the MeA, may be involved in the molecular processes of alcohol dependence and comorbidity of anxiety and alcohol-drinking behaviors.
Very young rat brains process memories of fear differently than more mature ones, new research indicates. The work significantly advances scientific understanding of when and how fear is stored and unlearned, and introduces new thinking on the implications of fear experience early in life.
“This important paper raises questions that are the ‘tip of the iceberg’ related to the very complex series of events that occur as we learn to fear something. In the real world, we become fearful, extinguish that fear, reacquire it at another time, and then conquer it yet again,” says John Krystal, MD, of Yale University and director of the clinical neuroscience division of the VA National Center for Post-Traumatic Stress Disorder. “Typically, we think about long-term, negative impact of fear learning, such as lifelong problems with anxiety. But this work highlights an avenue for adapting to early stresses that apparently can occur only early in life: to erase a learned fear from memory.” Krystal was not affiliated with the research.
Study co-authors Jee Hyun Kim and Rick Richardson, PhD, of the University of New South Wales in Sydney, homed in on the amygdala, using anesthesia to temporarily inactivate it and therefore isolate its role. The amygdala is critical for emotional learning and plays a central role in dulling the memory of a fear.
Kim and Richardson trained rats that were 16 and 23 days old–the human equivalent of children and budding adolescents–to associate a specific sound with a mild shock to the foot. After subsequent training, when the sound was not followed by a shock, the animals’ fearful reaction to hearing the sound faded. Technically, this is known as “extinction,” and depended on the function of the amygdala.
In a second round of training, the researchers reintroduced the fear and tried to re-extinguish it. This time around, they found, only the older rats were able to do so without the amygdala.
The researchers concluded that the age at which the initial extinction training occurred was critical to whether or not the rats’ fear faded the second time independently of the amygdala. The authors suggest that in the very young, it is primarily the amygdala that extinguishes fearful memories, but that mechanisms independent of the amygdala develop later.
This raises the possibility that fears unlearned at an early enough age are, in fact, erased. As brains develop, however, and related structures near the amygdala mature, these structures take on a greater role. Thus, fear in adolescence and later in life may not be erased, but instead be, for example, inhibited by a process of overlaying neutral memories on top of the initial fear reaction. The initial memory could still exist and be called on again.
“Extinction in the young brain might forever erase early traumatic learning–but accepting this hypothesis will have to wait for more research,” says Mark Bouton, PhD, of the University of Vermont, who did not participate in the esearch. “What might change as the brain develops is where and how fear learning and extinction are stored and how they can be retrieved.”J Neurosci. 2008 Feb 6;28(6):1282-90.
School of Psychology, The University of New South Wales, Sydney 2052, Australia. email@example.com
It is well accepted that fear extinction does not cause erasure of the original conditioned stimulus (CS)-unconditioned stimulus association in the adult rat because the extinguished fear often returns (e.g., renewal and reinstatement). Furthermore, extinction is NMDA and GABA dependent, showing that extinction involves new inhibitory learning. We have recently observed each of these extinction-related phenomena in 24-d-old but not in 17-d-old rats. These results suggest that different neural processes mediate extinction early in development. However, the neural processes underlying extinction in the developing rat are unknown. Therefore, the present study investigated amygdala involvement in extinction and reextinction during development. In experiment 1, temporary inactivation of the amygdala (using bupivacaine, a sodium channel modulator) during extinction training impaired extinction of conditioned fear in 17- and 24-d-old rats. In experiment 2, 17- and 24-d-old rats were conditioned, extinguished, and then reconditioned to the same CS. After reconditioning, the CS was reextinguished; at this time, some rats at each age had their amygdala temporarily inactivated. Reextinction was amygdala independent in 24-d-old rats, as previously shown in adult rats. However, reextinction was still amygdala dependent in 17-d-old rats. In Experiment 3, the age at conditioning, reconditioning, reextinction, and test was held constant, but the age of initial extinction varied across groups; reextinction was found to be amygdala independent if initial extinction occurred at 24 d of age but amygdala dependent if it occurred at 17 d of age. Consistent with previous findings, these results show that there are fundamental differences in the neural mechanisms of fear extinction across development.
Psychiatrists remain divided as to how to define and classify the mood and anxiety disorders, the most common mental disorders. Committees across the globe are currently pondering how best to carve nature at its anxious joints for the fifth version of the Diagnostic and Statistical Manual (DSM-V), the “gold standard” reference book for psychiatrists. Only recently has the process of refining the diagnostic system been informed by high quality longitudinal data.
Ian Colman, Ph.D., the lead author, notes, “”Rarely have classification systems in psychiatry considered the nature of symptoms of depression and anxiety over time; however research into trajectories of alcohol abuse and antisocial behaviour shows that accounting for symptoms over time may help in better understanding causes and outcomes of these disorders.” Colman and colleagues at the University of Cambridge in England and the Medical Research Council National Survey of Health and Development (now called the MRC Unit for Lifelong Health and Ageing), using fundamental ideas about the life-course origins of common mental illnesses, statistical techniques for handling large quantities of longitudinal information and one of the longest running cohort studies in the world, were able to analyze data by grouping people according to their symptoms of anxiety and depression over a 40-year period.
The researchers were able to identify six courses of mental health, ranging from those with repeated severe symptoms to those in good mental health, while others fluctuated in between. Dr. Colman adds, “The usefulness of characterizing people by their experience over time became evident when we investigated markers of early development, and found that those with poorer mental health over time were more likely to be smaller at birth and tended to reach developmental milestones later than those with good mental health.”
John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, comments, “The study by Colman and colleagues suggests that children with low weight during infancy or slight developmental delays may be at greater risk for developing depression. How does this risk work? After all, it is extremely unlikely that adults bear emotional scars from very subtle delays in their standing or walking.”
The authors explain that their findings support a proposed “fetal programming” model for depression and anxiety, which posits that prenatal stress may result in permanent maladaptive changes to the developing fetal brain. Particularly notable was the fact that differences with regards to early development were apparent not only for those with severe problems with mental health, but also for those with mild to moderate symptoms of depression and anxiety over time. Dr. Krystal adds that it may also be “that genes that are involved in shaping the development of the brain and the emergence of particular behaviors during infancy also influence the development of brain circuits that influence the risk for depression later in life.”
The authors hope that this rich-data/whole life approach may foster insights into the causes of brief versus persistent and early vs late onset disease processes, and eventually identify underlying mechanisms responsible for such different life course outcomes in mental ill-health.
Biol Psychiatry. 2007 Dec 1;62(11):1265-71. Epub 2007 Aug 9.
Department of Psychiatry, University of Cambridge, Addenbrooke’s Hospital, Cambridge, UK.
BACKGROUND: Little is known about long-term profiles of depressive and anxious symptomatology over the life course and about the developmental determinants of different trajectories. The objective of this study was to identify a novel typology of symptoms of depression and anxiety over the life course and examine its neurodevelopmental antecedents in an epidemiological sample. METHODS: A longitudinal latent variable analysis was conducted on measures of anxious and depressive symptoms at ages 13, 15, 36, 43, and 53 years among 4627 members of the Medical Research Council National Survey of Health & Development (the British 1946 birth cohort). Early life predictors of class membership were studied with ordinal logistic regression. RESULTS: We identified six distinct profiles up to age 53: absence of symptoms (44.8% of sample); repeated moderate symptoms (33.6%); adult-onset moderate symptoms (11.3%); adolescent symptoms with good adult outcome (5.8%); adult-onset severe symptoms (2.9%); and repeated severe symptoms over the life course (1.7%). Heavier babies had lower likelihood of depressive and anxious symptoms (odds ratio [OR] = .92; 95% confidence interval [CI] .85-.99), whereas delay in first standing (OR = 1.19; 95% CI 1.11-1.28) and walking (OR = 1.22; 95% CI 1.14-1.31) was associated with subsequent higher likelihood of symptoms, controlling for social circumstances and stressful life events during childhood. CONCLUSIONS: There was evidence of distinct profiles of depressive and anxious symptomatology over the life course and associations with markers of neurodevelopment. This suggests very early factors are associated with long-term experience of symptoms of depression and anxiety.
Almost half of pre-hurricane residents of New Orleans and one-fourth of those living in other affected areas had evidence of an anxiety or mood disorder five to seven months following Hurricane Katrina, according to a new article.
“Hurricane Katrina was the worst natural disaster in the United States in the past 75 years, creating a disaster region as large as Great Britain, killing more than 1,000 people, uprooting 500,000 others and causing more than $100 billion in damage,” the authors write as background information in the article. “This vast devastation would lead us to expect a high prevalence of mental illness among people who lived through Katrina.”
Sandro Galea, M.D., Dr. P.H., of the University of Michigan School of Public Health, Ann Arbor, and colleagues surveyed 1,043 residents who had been living in affected areas of Louisiana, Alabama and Mississippi before Hurricane Katrina. The telephone survey was conducted between Jan. 19 and March 31, 2006, five to seven months after the storm. Participants were asked about stressors related to the hurricane and screened for symptoms of mood and anxiety disorders–which include depression, panic disorders and post-traumatic stress disorder (PTSD)–within 30 days of the interview.
A total of 31.2 percent of the participants had an anxiety-mood disorder, including 49.1 percent of the New Orleans metropolitan area residents and 26.4 percent of the other participants. Among all participants, 16.3 percent had PTSD; this included 30.3 percent of New Orleans residents and 12.5 percent of the others. Individuals who were younger than age 60, female, did not graduate college, had a low family income or were unmarried or unemployed before the hurricane were more likely to have anxiety-mood disorders, and those who were Hispanic or other minorities excluding blacks had lower rates of these conditions.
“The vast majority of respondents both in the New Orleans metro (91.9 percent) and in the remainder of the sample (81.7 percent) reported experiencing at least one of the 10 categories of hurricane-related stressors,” including the death of a loved one, robbery, injury or property loss, the authors write. Among New Orleans residents, the extent of exposure to these stressors was more strongly related to anxiety-mood disorders than among residents of other areas. While New Orleans residents were most likely to develop anxiety-mood disorders following physical illness or injury and physical adversity, the rest of the participants were more likely to develop such a disorder following property loss.
The rate of anxiety and mood disorders in New Orleans residents was higher than that typically found in studies of mental illness following natural disasters in the United States, while the rate among the other respondents was roughly equivalent, the authors note. In addition, they conclude, “evidence that avoidable stressors associated with the slow government response to Hurricane Katrina (e.g., physical adversity) had important implications for the mental health of people who lived through Katrina argues strongly for the importance of efficient provision of practical and logistical assistance in future disasters, not only on humanitarian grounds, but also as a way to minimize the adverse mental health effects of disasters.”
Arch Gen Psychiatry. 2007;64(12):1427-1434.
Exposure to Hurricane-Related Stressors and Mental Illness After Hurricane Katrina
Sandro Galea, MD, DrPH; Chris R. Brewin, PhD; Michael Gruber, MA; Russell T. Jones, PhD; Daniel W. King, PhD; Lynda A. King, PhD; Richard J. McNally, PhD; Robert J. Ursano, MD; Maria Petukhova, PhD; Ronald C. Kessler, PhD
Context Uncertainty exists about the prevalence, severity, and correlates of mental disorders among people exposed to Hurricane Katrina.
Objective To estimate the prevalence and associations between DSM-IV anxiety-mood disorders and hurricane-related stressors separately among prehurricane residents of the New Orleans metropolitan area and the remainder of the areas in Alabama, Louisiana, and Mississippi affected by Katrina.
Design Community survey.
Setting and Participants A probability sample of 1043 English-speaking prehurricane residents of the areas affected by Hurricane Katrina was administered via telephone survey between January 19 and March 31, 2006. The survey assessed hurricane-related stressors and screened for 30-day DSM-IV anxiety-mood disorders.
Main Outcome Measures The K6 screening scale of anxiety-mood disorders and the Trauma Screening Questionnaire scale for posttraumatic stress disorder (PTSD), both calibrated against blinded structured clinical reappraisal interviews to approximate the 30-day prevalence of DSM-IV disorders.
Results Prehurricane residents of the New Orleans metropolitan area were estimated to have a 49.1% 30-day prevalence of any DSM-IV anxiety-mood disorder (30.3% estimated prevalence of PTSD) compared with 26.4% (12.5% PTSD) in the remainder of the sample. The vast majority of respondents reported exposure to hurricane-related stressors. Extent of stressor exposure was more strongly related to the outcomes in the New Orleans metropolitan area subsample than the remainder of the sample. The stressors most strongly related to these outcomes were physical illness/injury and physical adversity in the New Orleans metropolitan area subsample and property loss in the remainder of the sample. Sociodemographic correlates were not explained either by differential exposure or reactivity to hurricane-related stressors.
Conclusions The high prevalence of DSM-IV anxiety-mood disorders, the strong associations of hurricane-related stressors with these outcomes, and the independence of sociodemographics from stressors argue that the practical problems associated with ongoing stressors are widespread and must be addressed to reduce the prevalence of mental disorders in this population.