Nicholas B. Allen
University of Oregon
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Featured researches published by Nicholas B. Allen.
Psychology and Aging | 1997
Peter M. Lewinsohn; John R. Seeley; Robert Roberts; Nicholas B. Allen
The efficacy of the Center for Epidemiologic Studies Depression Scale (CES-D) as a screener for clinical depression was examined in a sample of 1,005 community-residing adults (age range = 50-96). Presence of a depressive disorder was determined by diagnostic interview. Analyses revealed that neither age, gender, cognitive impairment, functional impairment, physical disease, nor social desirability had a significant negative effect on the psychometric properties or screening efficacy of the CES-D. These results indicate that there was no significant degradation in the ability of the CES-D to screen for depression among community-residing elderly adults. This conclusion must be tempered by the fact that the sample did not include participants with the more disabling forms of cognitive or functional impairment and physical illness.
Cognitive Therapy and Research | 2008
Richard Chambers; Barbara Chuen Yee Lo; Nicholas B. Allen
To evaluate the impact of an intensive period of mindfulness meditation training on cognitive and affective function, a non-clinical group of 20 novice meditators were tested before and after participation in a 10-day intensive mindfulness meditation retreat. They were evaluated with self-report scales measuring mindfulness, rumination and affect, as well as performance tasks assessing working memory, sustained attention, and attention switching. Results indicated that those completing the mindfulness training demonstrated significant improvements in self-reported mindfulness, depressive symptoms, rumination, and performance measures of working memory and sustained attention, relative to a comparison group who did not undergo any meditation training. This study suggests future directions for the elucidation of the critical processes that underlie the therapeutic benefits of mindfulness-based interventions.
The Lancet | 2016
Ali H. Mokdad; Mohammad H. Forouzanfar; Farah Daoud; Arwa A. Mokdad; Charbel El Bcheraoui; Maziar Moradi-Lakeh; Hmwe H Kyu; Ryan M. Barber; Joseph A. Wagner; Kelly Cercy; Hannah Kravitz; Megan Coggeshall; Adrienne Chew; Kevin F. O'Rourke; Caitlyn Steiner; Marwa Tuffaha; Raghid Charara; Essam Abdullah Al-Ghamdi; Yaser A. Adi; Rima Afifi; Hanan Alahmadi; Fadia AlBuhairan; Nicholas B. Allen; Mohammad A. AlMazroa; Abdulwahab A. Al-Nehmi; Zulfa AlRayess; Monika Arora; Peter Azzopardi; Carmen Barroso; Mohammed Omar Basulaiman
BACKGROUND Young peoples health has emerged as a neglected yet pressing issue in global development. Changing patterns of young peoples health have the potential to undermine future population health as well as global economic development unless timely and effective strategies are put into place. We report the past, present, and anticipated burden of disease in young people aged 10-24 years from 1990 to 2013 using data on mortality, disability, injuries, and health risk factors. METHODS The Global Burden of Disease Study 2013 (GBD 2013) includes annual assessments for 188 countries from 1990 to 2013, covering 306 diseases and injuries, 1233 sequelae, and 79 risk factors. We used the comparative risk assessment approach to assess how much of the burden of disease reported in a given year can be attributed to past exposure to a risk. We estimated attributable burden by comparing observed health outcomes with those that would have been observed if an alternative or counterfactual level of exposure had occurred in the past. We applied the same method to previous years to allow comparisons from 1990 to 2013. We cross-tabulated the quantiles of disability-adjusted life-years (DALYs) by quintiles of DALYs annual increase from 1990 to 2013 to show rates of DALYs increase by burden. We used the GBD 2013 hierarchy of causes that organises 306 diseases and injuries into four levels of classification. Level one distinguishes three broad categories: first, communicable, maternal, neonatal, and nutritional disorders; second, non-communicable diseases; and third, injuries. Level two has 21 mutually exclusive and collectively exhaustive categories, level three has 163 categories, and level four has 254 categories. FINDINGS The leading causes of death in 2013 for young people aged 10-14 years were HIV/AIDS, road injuries, and drowning (25·2%), whereas transport injuries were the leading cause of death for ages 15-19 years (14·2%) and 20-24 years (15·6%). Maternal disorders were the highest cause of death for young women aged 20-24 years (17·1%) and the fourth highest for girls aged 15-19 years (11·5%) in 2013. Unsafe sex as a risk factor for DALYs increased from the 13th rank to the second for both sexes aged 15-19 years from 1990 to 2013. Alcohol misuse was the highest risk factor for DALYs (7·0% overall, 10·5% for males, and 2·7% for females) for young people aged 20-24 years, whereas drug use accounted for 2·7% (3·3% for males and 2·0% for females). The contribution of risk factors varied between and within countries. For example, for ages 20-24 years, drug use was highest in Qatar and accounted for 4·9% of DALYs, followed by 4·8% in the United Arab Emirates, whereas alcohol use was highest in Russia and accounted for 21·4%, followed by 21·0% in Belarus. Alcohol accounted for 9·0% (ranging from 4·2% in Hong Kong to 11·3% in Shandong) in China and 11·6% (ranging from 10·1% in Aguascalientes to 14·9% in Chihuahua) of DALYs in Mexico for young people aged 20-24 years. Alcohol and drug use in those aged 10-24 years had an annual rate of change of >1·0% from 1990 to 2013 and accounted for more than 3·1% of DALYs. INTERPRETATION Our findings call for increased efforts to improve health and reduce the burden of disease and risks for diseases in later life in young people. Moreover, because of the large variations between countries in risks and burden, a global approach to improve health during this important period of life will fail unless the particularities of each country are taken into account. Finally, our results call for a strategy to overcome the financial and technical barriers to adequately capture young peoples health risk factors and their determinants in health information systems. FUNDING Bill & Melinda Gates Foundation.
Journal of Abnormal Psychology | 1998
Peter M. Lewinsohn; Ian H. Gotlib; Mark Lewinsohn; John R. Seeley; Nicholas B. Allen
Gender differences in anxiety were examined in a large sample of adolescents that included 1,079 who had never met criteria for any disorder, 95 who had recovered from an anxiety disorder, and 47 who had a current anxiety disorder. Participants were examined on a wide array of psychosocial measures. There was a preponderance of females among current and recovered anxiety disorder cases, but not among those who had never experienced an anxiety disorder. The female preponderance emerges early in life, and retrospective data indicate that at age 6, females are already twice as likely to have experienced an anxiety disorder than are males. Psychosocial variables that were correlated with both anxiety and gender were identified. Statistically controlling for these variables did not eliminate the gender differences in prevalence or anxiety symptom means.
BMC Medicine | 2013
Michael Berk; Lana J. Williams; Felice N. Jacka; Adrienne O’Neil; Julie A. Pasco; Steven Moylan; Nicholas B. Allen; Amanda L. Stuart; Amie C. Hayley; Michelle L. Byrne; Michael Maes
BackgroundWe now know that depression is associated with a chronic, low-grade inflammatory response and activation of cell-mediated immunity, as well as activation of the compensatory anti-inflammatory reflex system. It is similarly accompanied by increased oxidative and nitrosative stress (O&NS), which contribute to neuroprogression in the disorder. The obvious question this poses is ‘what is the source of this chronic low-grade inflammation?’DiscussionThis review explores the role of inflammation and oxidative and nitrosative stress as possible mediators of known environmental risk factors in depression, and discusses potential implications of these findings. A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.SummaryThe identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression. Critically, most of these factors are plastic, and potentially amenable to therapeutic and preventative interventions. Most, but not all, of the above mentioned sources of inflammation may play a role in other psychiatric disorders, such as bipolar disorder, schizophrenia, autism and post-traumatic stress disorder.
Journal of Affective Disorders | 2009
Valentina Lorenzetti; Nicholas B. Allen; Alex Fornito; Murat Yücel
BACKGROUND While there is evidence to suggest that major depressive disorder (MDD) is associated with structural brain abnormalities, the precise nature of these abnormalities remains unclear. AIMS To review recent structural magnetic resonance imaging (MRI) research findings in MDD while considering the potential influence of key clinical and demographic variables. METHOD A selective review of all T1-weighted structural MRI studies published between 2000 and 2007 in adult samples of MDD patients. RESULTS Volumetric reductions of the hippocampus, basal ganglia and OFC and SGPFC are consistently found in MDD patients, with more persistent forms of MDD (e.g., multiple episodes or repeated relapses, longer illness duration) being associated with greater impact on regional brain volumes. Gender, medication, stage of illness, and family history all affect the nature of the findings in a regionally specific manner. LIMITATIONS Overall, differences between the samples in factors such as illness severity, medication, gender and family history of mental illness makes difficult to identify their confounding effects on the observed neuroanatomical changes. Also, the tracing protocols used for particular brain regions were different amongst the reviewed studies, making difficult to compare their findings. CONCLUSIONS The data support the notion that MDD involves pathological alterations of limbic and cortical structures, and that they are generally more apparent in patients with more severe or persistent forms of the illness.
Psychological Bulletin | 2003
Nicholas B. Allen; Paul B. Badcock
The authors hypothesize that depressed states evolved to minimize risk in social interactions in which individuals perceive that the ratio of their social value to others, and their social burden on others, is at a critically low level. When this ratio reaches a point where social value and social burden are approaching equivalence, the individual is in danger of exclusion from social contexts that, over the course of evolution, have been critical to fitness. Many features of depressed states can be understood in relation to mechanisms that reduce social risk in such circumstances, including (a) hyper-sensitivity to signals of social threat from others, (b) sending signals to others that reduce social risks, and (c) inhibiting risk-seeking (e.g., confident, acquisitive) behaviors. These features are discussed in terms of psychosocial and neurobiological research on depressive phenomena.
Neuroscience & Biobehavioral Reviews | 2008
Christopher G. Davey; Murat Yücel; Nicholas B. Allen
Adolescent development is accompanied by the emergence of a population-wide increase in vulnerability to depression that is maintained through adulthood. We provide a model for understanding how this vulnerability to depression arises, and why depression is so often precipitated by social rejection or loss of status during this phase. There is substantial remodeling and maturation of the dopaminergic reward system and the prefrontal cortex during adolescence, that coincides with the adolescent entering the complex world of adult peer and romantic relationships, where the rewards that can be obtained (feelings such as belonging, romantic love, status and agency) are abstract and temporally distant from the proximal context. Development of the prefrontal cortex makes it possible to pursue such complex and distal rewards, which are, however, tenuous and more readily frustrated than more immediate rewards. We hypothesize that when these distant rewards are frustrated they suppress the reward system, and that when such suppression is extensive and occurs for long enough, the clinical picture that results is one of depression.
Biological Psychiatry | 1999
Nicholas B. Allen; John Trinder; Catherine Brennan
BACKGROUND Modulation of the startle reflex by affective foreground stimuli was investigated in a group receiving inpatient treatment for major depressive episodes (n = 14) and an age and gender matched nondepressed group (n = 14). METHODS Participants viewed 27 pleasant, neutral, and unpleasant pictures chosen from the International Affective Picture System. Acoustic startle probes were presented during picture viewing, and participants also rated the affective qualities of the pictures. RESULTS While ratings of the pictures were largely similar between the depressed and nondepressed groups, they displayed dissimilar patterns of startle modulation. In the nondepressed group, blinks elicited during unpleasant pictures were significantly larger than during pleasant pictures, whereas the depressed group failed to show this effect. Analyses, which separated the depressed participants into moderate and severe groups based on Beck Depression Inventory scores, revealed that while the moderately depressed group also showed a normal pattern of startle modulation, the severely depressed showed potentiated startles during the pleasant pictures. CONCLUSIONS These preliminary results suggest that severely depressed patients may respond to some pleasant stimuli as if they are aversive, possibly because such stimuli are seen as signals of frustrative nonreward.
Psychological Science | 2010
Peter Kuppens; Nicholas B. Allen; Lisa Sheeber
In this article, we examine the concept of emotional inertia as a fundamental property of the emotion dynamics that characterize psychological maladjustment. Emotional inertia refers to the degree to which emotional states are resistant to change. Because psychological maladjustment has been associated with both emotional underreactivity and ineffective emotion-regulation skills, we hypothesized that its overall emotion dynamics would be characterized by high levels of inertia. We provide evidence from two naturalistic studies that, using different methods, showed that the emotional fluctuations of individuals who exhibited low self-esteem (Study 1) and depression (Study 2) were characterized by higher levels of inertia in both positive and negative emotions than the emotional fluctuations of people who did not exhibit low self-esteem and depression. We also discuss the usefulness of the concept of emotional inertia as a hallmark of maladaptive emotion dynamics.