Lifetime Prevalence of Recurrent and Persistent Depression: A Scoping Review of Epidemiological Studies.

Age at Onset or Late‐Life Depression: A Research Agenda Report of a MacArthur Foundation‐NIMH Workshop

Practical Geriatrics: Clinically Significant Nonmajor Geriatric Depression

BackgroundData on the long‐term poststroke depression trajectories and their determinants are limited. This study aims to estimate the 5‐year course of poststroke depression and identify risk factors for recurrent and persistent depression.MethodsData were from the South London Stroke Register (1997–2022). Depression was defined as a subscale score >7 on the Hospital Anxiety and Depression Scale at 3 months and annually up to 5 years. Participants with >2 assessments of depression were included. Multinomial logistic regression examined associations between baseline factors, changes in function, and recurrent or persistent depression.ResultsThe analysis comprised 1724 participants (mean age, 65.5 years; men, 55.9%, White race, 65.2%). Of these, 1067 (61.9%) were not depressed at any time point. Among those with depression at some time point, 125 (19.0%) had transient depression, 231 (35.2%) had recurrent depression, and 301 (45.8%) had persistent depression. Patients with moderate to severe stroke (adjusted odds ratio, 1.81 [95% CI, 1.25–2.61]) or physical disability (adjusted odds ratio, 1.59 [95% CI, 1.12–2.26]) were more likely to develop recurrent depression, while patients with cognitive impairment (adjusted odds ratio, 2.09 [95% CI, 1.44–3.05]) or prestroke depression (adjusted odds ratio, 2.67 [95% CI, 1.60–4.47]) were at increased likelihood of having persistent depression. Patients exhibiting a decline in physical ability at 3 months were more likely to experience depression with poor progression (recurrent or persistent depression), independent of the initial severity of physical disability.ConclusionsRecurrent depression was associated with moderate to severe stroke or disability, whereas persistent depression was linked to prestroke depression or cognitive impairment. Progressive worsening disability was associated with recurrent or persistent depression, regardless of initial severity.

Older adults with insomnia have a high risk of incident and recurrent depression. Depression prevention is urgently needed, and such efforts have been neglected for older adults. To examine whether treatment of insomnia disorder with cognitive behavioral therapy for insomnia (CBT-I) compared with an active comparator condition, sleep education therapy (SET), prevents major depressive disorder in older adults. This assessor-blinded, parallel-group, single-site randomized clinical trial assessed a community-based sample of 431 people and enrolled 291 adults 60 years or older with insomnia disorder who had no major depression or major health events in past year. Study recruitment was performed from July 1, 2012, to April 30, 2015. The trial protocol was modified to extend follow-up from 24 to 36 months, with follow-up completion in July 2018. Data analysis was performed from March 1, 2019, to March 30, 2020. Participants were randomized to 2 months of CBT-I (n = 156) or SET (n = 135). The primary outcome was time to incident major depressive disorder as diagnosed by interview and Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) criteria. Secondary outcome was sustained remission of insomnia disorder before depression event or duration of follow-up. Among 291 randomized participants (mean [SD] age, 70.1 [6.7] years; 168 [57.7%] female; 7 [2.4%] Asian, 32 [11.0%] Black, 3 [1.0%] Pacific Islander, 241 [82.8%] White, 6 [2.1%] multiracial, and 2 [0.7%] unknown), 156 were randomized to CBT-I and 135 to SET. A total of 140 participants (89.7%) completed CBT-I and 130 (96.3%) participants completed SET (χ2 = 4.9, P = .03), with 114 (73.1%) completing 24 months of follow-up in the CBT-I group and 117 (86.7%) in the SET group (χ2 = 8.4, P = .004). After protocol modification, 92 (59.0%) of the CBT-I participants and 86 (63.7%) of the SET participants agreed to extended follow-up (χ2 = 0.7, P = .41), with 81 (51.9%) of the CBT-I participants and 77 (57.0%) of the SET group completing 36 months of follow-up (χ2 = 0.8; P = .39). Incident or recurrent major depression occurred in 19 participants (12.2%) in the CBT-I group and in 35 participants (25.9%) in the SET group, with an overall benefit (hazard ratio, 0.51; 95%, CI 0.29-0.88; P = .02) consistent across subgroups. Remission of insomnia disorder continuously sustained before depression event or during follow-up was more likely in CBT-I participants (41 [26.3%]) compared with the SET participants (26 [19.3%], P = .03). Those in the CBT-I group with sustained remission of insomnia disorder had an 82.6% decreased likelihood of depression (hazard ratio, 0.17; 95%, CI 0.04-0.73; P = .02) compared with those in the SET group without sustained remission of insomnia disorder. The findings of this randomized clinical trial indicate that treatment of insomnia with CBT-I has an overall benefit in the prevention of incident and recurrent major depression in older adults with insomnia disorder. Community-level screening for insomnia concerns in older adults and wide delivery of CBT-I-based treatment for insomnia could substantially advance public health efforts to treat insomnia and prevent depression in this vulnerable older adult population. ClinicalTrials.gov Identifier: NCT01641263.

Two recent meta-analyses reported a high prevalence of both anxiety and depression in patients with alopecia areata (AA), as well as a positive association of AA with anxiety and depression, without distinguishing between disorders and symptoms. Yet, depression and anxiety can manifest either as symptoms identified in questionnaires or as specific diagnoses defined by Diagnostic and Statistical Manual of Mental Disorders (Fifth Edition) or International Statistical Classification of Diseases and Related Health Problems, Tenth Revision criteria. To perform a large meta-analysis separating the prevalence of depressive and anxiety disorders from that of depressive and anxiety symptoms in patients with AA. PubMed, ScienceDirect, the Cochrane Library, Embase, and PsycINFO databases were searched from inception through August 1, 2020. Studies that contained data on the prevalence of depressive or anxiety disorders or symptoms were included. The Meta-analysis of Observational Studies in Epidemiology (MOOSE) reporting guidelines were used. Pooled prevalence was calculated with a random effects model meta-analysis that took into account between- and within-study variability. Meta-regressions were used to study the association between variations in prevalence and study characteristics. The prevalence of depressive and anxiety disorders and symptoms in patients with AA. Thirty-seven articles (29 on depression and 26 on anxiety) that met the inclusion criteria were identified. By distinguishing between disorders and symptoms, the prevalence of both depressive disorders (9%) and unspecified anxiety disorders (13%) in patients with AA was shown to be greater than that in the general population. The prevalence and odds ratio (OR) of depressive disorders (prevalence, 9%; OR, 1.38) and anxiety disorders of which each category had been specifically studied (prevalence, 7%-17%; OR, 1.51-1.69) were markedly lower than that of depressive symptoms (prevalence, 37%; OR, 2.70) and anxiety symptoms (prevalence, 34%; OR, 3.07). Meta-regressions showed that variations in prevalence were mainly associated with methodological differences between studies. In this systematic review and meta-analysis, the separate analyses showed that 7% to 17% of patients with AA had depressive or anxiety disorders that require psychiatric care, including specific medication. Additionally, more than one-third of patients had symptoms that are warning signs and that need monitoring because they can develop into disorders.

Lifetime prevalence of brief recurrent depression (results from a community survey)

Back to table of contents Previous article Next article Clinical & Research NewsFull AccessGene Links Early Death, Early DepressionJoan Arehart-TreichelJoan Arehart-TreichelSearch for more papers by this authorPublished Online:15 Aug 2003https://doi.org/10.1176/pn.38.16.0013When major depression strikes a person at age 25 or younger and then recurs, chances are good that it has a strong genetic input, research has shown.Now 19 genetic regions have been identified that seem to play a role in this kind of depression.The finding comes from George Zubenko, M.D., Ph.D., a professor of psychiatry at the University of Pittsburgh School of Medicine, and his colleagues. Their research is in press with the American Journal of Medical Genetics.The focus of the study was 1,323 subjects consisting of 81 persons who had experienced early-onset, recurrent major depression and their 407 first-degree relatives and 835 extended relatives.The researchers used a technique called linkage analysis to hunt for depression-causing genes in these subjects. Linkage analysis is a statistical technique that explores whether the transmission of a particular piece of DNA is associated with the transmission of a trait of interest—say depression—to a statistically significant degree, that is, at a rate greater than would be expected by chance alone.Zubenko and his colleagues found 19 different regions of genetic material that could be linked with early-onset, recurrent major depression to a statistically significant degree. The regions were on chromosomes 1, 2, 5, 8, 10, 11, 15, 18, and 19 and the X chromosome.The genetic region that was linked to early-onset, recurrent major depression to the most significant degree was on chromosome 2 and contained a gene called CREB1. The gene makes a protein called CREB. The protein CREB in turn is a lynchpin in a variety of cell-signaling pathways that regulate the downstream expression of genes that participate in many important cellular processes. For instance, CREB regulates the expression of genes that make neurotransmitter receptors.It is also possible that the 19 genetic regions linked with early-onset, recurrent major depression have some control over human longevity, because deceased family members of the families studied were found to have died on average eight years earlier than people in the general population. In fact, over 40 percent died before age 65.One might expect that many of these family members died at earlier ages because they were extremely depressed and committed suicide. “But the fact is,” Zubenko told Psychiatric News, “that whether people got depressed or not didn’t seem to matter in these families. Those individuals who never got depressed died just as early as did those who were depressed.”Further, most of the premature deaths were due not to suicide, but to natural causes such as heart disease, cancer, and stroke. So putting all these pieces together, they suggest that there is something else shared in those families besides an elevated rate of depression that is contributing to the accelerated death rate. “And we speculate that it might be some of the genes that are segregating in these families and that were detected because they contribute to depression,” Zubenko said.Indeed, one of the depression genes that might be shortening lifespan could be the one on chromosome 2 that makes the protein CREB. The reason? “CREB is an important regulatory protein that is expressed ubiquitously in all human tissues,” Zubenko explained. “In fact, it is expressed in a wide range of species, so it has been a ubiquitously conserved protein throughout evolution.”Thus, if a person inherits an abnormal form of CREB, it might not only be able to trigger depression but also a host of bodily illnesses that could lead to premature death.When Psychiatric News asked Zubenko whether any other researchers have confirmed these findings, he replied: “This is the first genome-wide survey for susceptibility genes for depression. And it only took us about 15 years to do this. So I wouldn’t be too disappointed if we didn’t get to see a replication quickly. However, one part of our results has also been found by another group of researchers—the association of genetic markers in the region of CREB with early-onset, recurrent depression.”The study was funded by the National Institutes of Health and U.S. Public Health Service.An abstract of the study, “Genome-Wide Linkage Survey for Genetic Loci That Influence the Development of Depressive Disorders in Families With Recurrent, Early-Onset Major Depression,” will be posted on the Web at www.interscience.wiley.com/jpages/0148-7299 after publication. ▪ ISSUES NewArchived

To explore clinical and treatment-response variability in late-onset vs early-onset non-bipolar, non-psychotic major depression. We grouped patients from a late-life depression treatment study according to illness-course characteristics: those with early-onset, recurrent depression (n = 59), late-onset, recurrent depression (n = 27), and late-onset, single-episode depression (n = 95). Early-onset was defined as having a first lifetime episode of major depression at age 59 or earlier; late-onset was defined as having a first episode of major depression at age 60 or later. We characterized the three groups of patients with respect to baseline demographic, neuropsychological, and clinical characteristics, use of augmentation pharmacotherapy to achieve response, and treatment outcomes. Rates of response, remission, relapse, and termination were similar in all three groups; however, patients with late-onset, recurrent major depression took longer to respond to treatment than those with late-onset, single-episode depression (12 weeks vs 8 weeks) and had more cognitive and functional impairment. Additionally, patients with recurrent depression (whether early or late) were more likely to require pharmacotherapy augmentation to achieve response than patients with a single lifetime episode. Late-onset, recurrent depression takes longer to respond to treatment than late-onset single-episode depression and is more strongly associated with cognitive and functional impairment. Further study of biological, neuropsychologic, and psychosocial correlates of late-onset, recurrent depression is needed.

Special Report: Bipolar Disorder II—Frequently Neglected, Misdiagnosed

Reactivity toward daily events: Intraindividual variability and change in recurrent depression – A measurement burst study

Diabetes and Mental Health

Community-based mental health studies have revealed that the point prevalence of depressive disorders in the elderly population of the world varies between 10% and 20%, depending on cultural situations. A retrospective study based on analysis of various study reports was conducted, to determine the median prevalence rates of depressive disorders in the elderly population of India and various other countries in the world. All the studies that constituted the sample were conducted between 1955 and 2005. Included are only community-based, cross-sectional surveys and some prospective studies that had not excluded depression at baseline. These studies were conducted on a homogenous community of the elderly population in the world, who were selected by a simple random sampling technique. After applying the inclusion and exclusion criteria on published and indexed articles, 74 original research studies that surveyed a total of 487 275 elderly individuals, in the age group of 60 years and above, residing in various parts of the world, were included for the final analysis. The median prevalence rate and its corresponding interquartile range were calculated. The chi-square test and chi-square for linear trend were applied. A P value of <.05 was considered as statistically significant. The median prevalence rate of depressive disorders in the world for the elderly population was determined to be 10.3% (interquartile range [IQR], 4.7%-16.0%). The median prevalence rate of depression among the elderly Indian population was determined to be 21.9% (IQR, 11.6%–31.1%). Although there was a significant decrease in the trend of world prevalence of geriatric depression, it was significantly higher among Indians, in recent years, than the rest of the world.

Residual memory dysfunction in recurrent major depressive disorder—A longitudinal study from Juntendo University Mood Disorder Project

Minor physical anomalies in women with recurrent unipolar depression

Hypomania Associated With Adjunctive Aripiprazole in an Elder Female With Recurrent Major Depressive Disorder