scholarly journals Childhood maltreatment and adult medical morbidity in mood disorders: comparison of unipolar depression with bipolar disorder

2018 ◽  
Vol 213 (5) ◽  
pp. 645-653 ◽  
Author(s):  
Georgina M. Hosang ◽  
Helen L. Fisher ◽  
Karen Hodgson ◽  
Barbara Maughan ◽  
Anne E. Farmer

BackgroundThe medical burden in mood disorders is high; various factors are thought to drive this pattern. Little research has examined the role of childhood maltreatment and its effects on medical morbidity in adulthood among people with unipolar depression and bipolar disorder.AimsThis is the first study to explore the association between childhood maltreatment and medical morbidity in bipolar disorder and in unipolar depression, and examine whether the impact of abuse and neglect are distinct or combined.MethodThe participants consisted of 354 psychiatrically healthy controls, 248 participants with recurrent unipolar depression and 72 with bipolar disorder. Participants completed the Childhood Trauma Questionnaire and received a validated medical history interview.ResultsAny type of childhood maltreatment, child abuse and child neglect were significantly associated with the medical burden in bipolar disorder, but not unipolar depression or for controls. These associations worked in a dose–response fashion where participants with bipolar disorder with a history of two or more types of childhood maltreatment had the highest odds of having a medical illness relative to those without such history or those who reported one form. No such significant dose–response patterns were detected for participants with unipolar depression or controls.ConclusionsThese findings suggest that childhood maltreatment may play a stronger role in the development of medical illnesses in individuals with bipolar disorder relative to those with unipolar depression. Individuals who had been maltreated with a mood disorder, especially bipolar disorder may benefit most from prevention and intervention efforts surrounding physical health.Declaration of interestNone.

Author(s):  
Georgina M. Hosang ◽  
Helen L. Fisher ◽  
Rudolf Uher ◽  
Sarah Cohen-Woods ◽  
Barbara Maughan ◽  
...  

2011 ◽  
Vol 26 (S2) ◽  
pp. 813-813
Author(s):  
A. Schosser ◽  
M.Y. Ng ◽  
A.W. Butler ◽  
S. Cohen-Woods ◽  
N. Craddock ◽  
...  

Catechol-O-methyltransferase (COMT) has a central role in brain dopamine, noradrenalin and adrenalin signaling, and has been suggested to be involved in the pathogenesis and pharmacological treatment of affective disorders. The functional single nucleotide polymorphism (SNP) in exon 4 (Val158Met, rs4680) influences the COMT enzyme activity. The Val158Met polymorphism is a commonly studied variant in psychiatric genetics, and initial studies in schizophrenia and bipolar disorder presented evidence for association with the Met allele. In unipolar depression, while some of the investigations point at an association between the Met/Met genotype and others have found a link between the Val/Val genotype and depression, most of the studies cannot detect any difference in Val158Met allele frequency between depressed individuals and controls.In the present study, we further elucidated the impact of COMT polymorphisms including the Val158Met in MDD. We investigated 1,250 subjects with DSM-IV and/or ICD-10 diagnosis of major depression (MDD), and 1,589 control subjects from UK. A total of 24 SNPs spanning the COMT gene were successfully genotyped using the Illumina HumaHap610-Quad Beadchip (22 SNPs), SNPlex™ genotyping system (1 SNP), and Sequenom MassARRAY® iPLEX Gold (1 SNP). Statistical analyses were implemented using PASW Statistics18, FINETTI (http://ihg.gsf.de/cgi-bin/hw/hwa1.pl), UNPHASED version 3.0.10 program and Haploview 4.0 program.Neither single-marker nor haplotypic association was found with the functional Val158Met polymorphism or with any of the other SNPs genotyped. Our findings do not provide evidence that COMT plays a role in MDD or that this gene explains part of the genetic overlap with bipolar disorder.


2017 ◽  
Author(s):  
Hasan A Baloch ◽  
Jair C. Soares

Affective disorders are among the most common disorders in psychiatry. They are generally classified according to the persistence and extent of symptoms and by the polarity of these symptoms. The two poles of the affective spectrum are mania and depression. Bipolar disorder is characterized by the presence of the mania or hypomania and often depression. Unipolar depression is defined by depression in the absence of a lifetime history of mania or hypomania. These differences are not merely categorical but have important implications for the prognosis and treatment of these conditions. Bipolar disorder, for example, is better treated using mood-stabilizing medication, whereas unipolar depression responds optimally to antidepressant medications. In addition, prognostically, unipolar depression may sometimes be limited to one episode in a lifetime, whereas bipolar disorder is typically a lifelong condition. The course of both conditions, however, is often chronic, and frequently patients can present with unipolar depression only to later develop manic symptoms. A thorough understanding of both conditions is therefore required to treat patients presenting with affective symptomatology. This chapter discusses the epidemiology, etiology and genetics, pathogenesis, diagnosis, and treatment of unipolar depression and bipolar disorder. Figures illustrate gray matter differences with lithium use and the bipolar spectrum. Tables list the pharmacokinetics of commonly used antidepressants and medications commonly used in the treatment of bipolar disorder. This review contains 2 figures, 2 tables, and 136 references.


1994 ◽  
Vol 40 (2) ◽  
pp. 303-308 ◽  
Author(s):  
B J Carroll

Abstract Manic depressive illness (bipolar disorder) is the mood disorder classically considered to have a strong biological basis. During manic depressive cycles, patients show dramatic fluctuations of mood, energy, activity, information processing, and behaviors. Theories of brain function and mood disorders must deal with the case of bipolar disorder, not simply unipolar depression. Shifts in the nosologic concepts of how manic depression is related to other mood disorders are discussed in this overview, and the renewed adoption of the Kraepelinian "spectrum" concept is recommended. The variable clinical presentations of manic depressive illness are emphasized. New genetic mechanisms that must be considered as candidate factors in relation to this phenotypic heterogeneity are discussed. Finally, the correlation of clinical symptom clusters with brain systems is considered in the context of a three-component model of manic depression.


2010 ◽  
Author(s):  
Hasan A Baloch ◽  
Jair C. Soares

Affective disorders are among the most common disorders in psychiatry. They are generally classified according to the persistence and extent of symptoms and by the polarity of these symptoms. The two poles of the affective spectrum are mania and depression. Bipolar disorder is characterized by the presence of the mania or hypomania and often depression. Unipolar depression is defined by depression in the absence of a lifetime history of mania or hypomania. These differences are not merely categorical but have important implications for the prognosis and treatment of these conditions. Bipolar disorder, for example, is better treated using mood-stabilizing medication, whereas unipolar depression responds optimally to antidepressant medications. In addition, prognostically, unipolar depression may sometimes be limited to one episode in a lifetime, whereas bipolar disorder is typically a lifelong condition. The course of both conditions, however, is often chronic, and frequently patients can present with unipolar depression only to later develop manic symptoms. A thorough understanding of both conditions is therefore required to treat patients presenting with affective symptomatology. This chapter discusses the epidemiology, etiology and genetics, pathogenesis, diagnosis, and treatment of unipolar depression and bipolar disorder. Figures illustrate gray matter differences with lithium use and the bipolar spectrum. Tables list the pharmacokinetics of commonly used antidepressants and medications commonly used in the treatment of bipolar disorder. This review contains 2 figures, 2 tables, and 135 references.


2008 ◽  
Vol 10 (2) ◽  
pp. 251-255 ◽  

Research designed to examine the relationship between creativity and mental illnesses must confront multiple challenges. What is the optimal sample to study? How should creativity be defined? What is the most appropriate comparison group? Only a limited number of studies have examined highly creative individuals using personal interviews and a noncreative comparison group. The majority of these have examined writers. The preponderance of the evidence suggests that in these creative individuals the rate of mood disorder is high, and that both bipolar disorder and unipolar depression are quite common. Clinicians who treat creative individuals with mood disorders must also confront a variety of challenges, including the fear that treatment may diminish creativity. In the case of bipolar disorder, however, it is likely that reducing severe manic episodes may actually enhance creativity in many individuals.


2021 ◽  
pp. 1-14
Author(s):  
Laia Marques-Feixa ◽  
Helena Palma-Gudiel ◽  
Soledad Romero ◽  
Jorge Moya-Higueras ◽  
Marta Rapado-Castro ◽  
...  

Abstract Background This study investigates the impact of childhood maltreatment (CM) on hypothalamic–pituitary–adrenal (HPA)-axis functioning and on anxiety perception. Moreover, the influence of CM severity and frequency was also explored. Methods In total, 187 participants aged 7–17 were assessed for CM history using validated questionnaires and ad hoc interviews to be classified according to the criteria of the Tool for Assessing the Severity of Situations in which Children are Vulnerable (TASSCV). Psychopathology was ascertained using the K-SADS-PL5. To assess HPA-axis functioning, salivary cortisol samples were collected throughout a normal day and during an acute psychosocial stressor, the Trier Social Stress Test for children (TSST-C). Subjective anxiety was evaluated using STAI/-C. Results Youth with a CM history had higher overall diurnal cortisol levels (p = 0.001), blunted cortisol response to acute psychosocial stress (p = 0.002) and greater perceived anxiety (p = 0.003), than those without CM. Specifically, participants exposed to moderate/severe or often/frequent CM showed the greater diurnal cortisol output (pseverity = 0.002; pfrequency = 0.003), and blunted cortisol response during the TSST-C (pseverity = 0.006; pfrequency = 0.008). Meanwhile, youth with low CM severity/frequency exhibited a similar cortisol response to those without CM. However, perceived anxiety was higher in those exposed to CM (p < 0.001), regardless of its severity/frequency. Conclusions Disturbances in HPA-axis functioning are already evident early after CM exposure, while psychological and physiological responses to an acute stressor are dissociated in youth exposed to CM. The dose–response relationship described in this paper highlights the need to comprehensively evaluate CM so that vulnerable children can be identified and assigned to proper interventions.


2021 ◽  
Vol 23 (11) ◽  
Author(s):  
Christine Kuehner ◽  
Sibel Nayman

Abstract Purpose of Review In contrast to premenstrual dysphoric disorder (PMDD), premenstrual exacerbations (PMEs) of ongoing mood disorders are understudied. The aim of this review is to describe diagnostic issues, epidemiology, underlying mechanisms, and treatment for PME in unipolar depression and bipolar disorder, and to discuss clinical and research implications. Recent Findings Community-based and clinical studies estimate that in women with mood disorders around 60% report PME, while some women with bipolar disorder also show symptom exacerbations around ovulation. In general, PME predicts a more severe illness course and an increased burden. While heightened sensitivity to fluctuations of sex hormone levels across the menstrual cycle appears to contribute to PME and PMDD, the overlap of their underlying biological mechanisms remains unclear. Beneficial treatments for PMDD show less or no efficacy in PME. Pharmacological treatments for PME in mood disorders predominantly seem to profit from adjustable augmentation of treatment dosages during the luteal phase for the underlying disorder. However, the evidence is sparse and mainly based on earlier small studies and case reports. Summary Previous research is mainly limited by the lack of a clear differentiation between PME and PMDD comorbidity with mood disorders. More systematic research with uniformly defined and prospectively assessed subgroups of PME in larger epidemiological and clinical samples is needed to receive reliable prevalence estimates and information on the clinical impact of PME of mood disorders, and to uncover underlying mechanisms. In addition, larger randomized controlled trials are warranted to identify efficacious pharmacological and psychotherapeutic treatments for affected women.


2003 ◽  
Vol 15 (6) ◽  
pp. 368-380 ◽  
Author(s):  
E. Serap Monkul ◽  
Gin S. Malhi ◽  
Jair C. Soares

Background:Mood disorders are related to considerable morbidity and mortality, and although there is little doubt that they are brain-based disorders, their neural correlates still remain elusive. A neuro-anatomic model of mood regulation comprising the prefrontal cortex, amygdala-hippocampus complex, thalamus, basal ganglia, and connections among these areas has been proposed.Objective:We reviewed the evidence for regional brain abnormalities in bipolar disorder, and attempted to integrate available findings into a comprehensive pathophysiological model of illness.Methods:A computerized Medline Ovid search was conducted for the period 1966–2002, and complemented by a manual search of bibliographical references from recent reviews. Articles meeting specified criteria were included.Results:Hyperintense lesions in cortical and subcortical regions are the most consistently reported and widely studied structural abnormalities. Smaller prefrontal cortical volume is a common finding in bipolar disorder and unipolar depression. Enlarged amygdala (in bipolar disorder) and smaller hippocampus (in unipolar depression) have been reported by several groups. Decreased volumes (in unipolar depression) and increased or unaltered volumes (in bipolar disorder) of striatal structures have been reported.Conclusions:Bipolar and unipolar mood disorders are associated with detectable structural brain abnormalities. The histopathology underlying such anatomical changes remains to be elucidated. To reach more definitive conclusions about neuroanatomical changes that take place during the course of mood disorders, prospective longitudinal studies are needed. Also, integration with functional imaging is necessary in order to elucidate the relevance of identified structural abnormalities.


2012 ◽  
Vol 201 (6) ◽  
pp. 458-465 ◽  
Author(s):  
Georgina M. Hosang ◽  
Ania Korszun ◽  
Lisa Jones ◽  
Ian Jones ◽  
Peter McGuffin ◽  
...  

BackgroundLittle is known about the impact of different types of stressful events (for example divorcev.bereavement) on unipolar depression compared with bipolar disorder. Inconsistencies exist concerning the association between independent events (beyond an individual's control, such as bereavement) and bipolar disorder.AimsTo examine the role of specific, independent and dependent events in mood disorders.MethodLife-event information was collected from 512 people with bipolar disorder, 1448 people with unipolar depression and over 600 controls.ResultsVarious events were associated with unipolar depression and bipolar disorder, but some event specificity was detected. For example, financial crisis was more strongly related to bipolar disorder rather than unipolar depression. Independent events were only related to unipolar depression and not bipolar disorder.ConclusionsThe events that were linked to bipolar disorder and unipolar depression were similar. Independent events were not associated with bipolar episodes, suggesting that life stress may be a consequence of, rather than a trigger for, bipolar episodes.


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