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Familial relationship between mood disorders and alcoholism.

Clinical and epidemiological studies have consistently revealed an association between alcohol use disorders and both bipolar and nonbipolar mood disorders. However, the evidence regarding the nature of these associations is unclear. The familial patterns of alcohol and affective disorders were examined using data from a controlled family study of probands with alcohol and anxiety disorders who were sampled from treatment settings and the community. The substantial degree of comorbidity between mood and anxiety disorders among probands allowed for the examination of comorbidity and familial aggregation of alcohol and mood disorders. The major findings are that (1) alcoholism was associated with bipolar and nonbipolar mood disorders in the relatives; (2) there was a strong degree of familial aggregation of alcohol dependence and both types of mood disorders were observed; and (3) there was no evidence of cross-aggregation (i.e., increase in mood disorders among probands with alcohol dependence, and vice versa) between alcoholism and mood disorders. The independent familial aggregation of bipolar disorder and alcoholism and the finding that the onset of bipolar disorder tended to precede that of alcoholism are compatible with a self-medication hypothesis as the explanation for the frequent co-occurrence of these disorders. In contrast, the independent familial aggregation and the tendency of an earlier onset of alcoholism than that of nonbipolar depression suggest that unipolar mood disorders are frequently secondary to alcoholism.

Adult↗

PubMed2000

Association analysis between mood disorder and monoamine oxidase gene.

To ascertain whether mood disorders, including bipolar and unipolar, are genetically associated with the monoamine oxidase A (MAOA) or monoamine oxidase B (MAOB) gene in the Chinese population, 132 cases of mood disorder and 88 normal controls were genotyped for the MAOA(CA)n, MAOB(GT)n, and MAOB(TG)n loci by the method of amplification fragment length polymorphism. Among 132 cases with mood disorder, eight alleles (size: 112-126 bp) of locus MAOA(CA)n, 12 alleles (size: 168-198 bp) of locus MAOB(GT)n, and nine alleles (size: 195-213 bp) of locus MAOB(TG)n were observed. Comparison of the allele frequency of the three loci showed no difference between mood disorder cases and normal controls on average. When each group was stratified into several subgroups, significant differences were found. On the MAOA(CA)n locus, the frequency of 116 bp allele was higher in the female bipolar disorder cases (0.2581) compared with that in the female unipolar disorder patients (0.1154) (Z=2.15, p<0. 05). On the MAOB(GT)n locus, the frequency of 180 bp allele was higher in bipolar disorder patients (0.1579) than that in normal controls (0.0678) (Z=2.05, p<0.05). The frequency of this allele was even higher in female bipolar disorder patients (0.1719) than that in female normal controls (0.0541). On the MAOB(TG)n locus, the frequency of 205 bp allele was higher in female bipolar disorder patients (0.6406) than that in female normal controls (0.4375) (Z=2. 17, p<0.05). For the unipolar disorder patients, the frequency of this allele was higher in female cases (0.5222) than that in male cases (0.1818) (Z=3.49, p<0.05). As for association studies, significant association between bipolar disorder and MAOB gene was detected. For the 180 bp allele of MAOB(GT)n, the relative risk (RR) of biploar versus normal control was 2.58 (p<0.05), and the RR of female bipolar disorder versus female normal control was 3.63 (p<0. 05). For the 205 bp allele of MAOB(TG)n, the RR of female bipolar disorder versus female normal control was 2.29 (p<0.05). Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:12-14, 2000.

Alleles↗

PubMed2005

Pharmacogenetics in mood disorder.

PURPOSE OF REVIEW: Not all patients with mood disorder respond well to drug treatment. Emerging data suggest that genetic mechanisms could be involved. We searched the literature database and highlighted recent molecular genetic studies pertaining to drug response in mood disorders. RECENT FINDINGS: Recent pharmacogenetic studies in mood disorders have reported generally positive findings supporting the view that genotyping may improve the confidence of prospectively identifying treatment response and adverse outcomes. SUMMARY: The evidence documenting genotype-based response to drug treatment is rapidly expanding. Genes encoding target receptors and signal transduction systems may predict the efficacy of drug therapy in mood disorders. Additional predictors of treatment response in bipolar disorder may include the immediate early genes, mitochondrial genes and epigenetic mechanisms, although some of these studies are still preliminary.

Journal Article↗

PubMed2001

Mood disorders in children and adolescents: psychopharmacological treatment.

Mood disorders are the leading causes of morbidity and mortality in children and adolescence. As a result, many adolescents are treated with psychopharmacologic agents such as antidepressants and mood stabilizers. To date, research into the safety and efficacy of these medications has lagged behind clinical practice. Several controlled trials of antidepressants in this population have recently been completed or are ongoing, yet few controlled trials of mood stabilizers have been conducted. Although acute efficacy of antidepressants is being addressed, many questions remain about pharmacological treatment of early-onset mood disorders. This article will focus on unmet research needs for the psychopharmacologic treatment of child and adolescent mood disorders.

Adolescent↗

PubMed1996

Summary of the DSM-IV mood disorders field trial and issue overview.

The DSM-IV Mood Disorders Field Trial addressed several issues concerning the relationship among major depression, dysthymia, recurrent brief depression, minor depression, and depressive personality disorder. The Mood Disorders Field Trial is a naturalistic, multisite study that investigated the diagnostic criteria for dysthymia, the reliability and validity of longitudinal course modifiers, the nosology of minor and recurrent brief depression, and the relationship between depressive personality disorder and dysthymia. Research on the nosology of chronic depressive disorders will, it is hoped, contribute to a better understanding of pathophysiology, etiology, and treatment. This article presents findings from the Field Trial as well as brief reviews of the other nine articles in this issue.

Adolescent↗

PubMed2005

Association study of neurotrophic tyrosine kinase receptor type 2 (NTRK2) and childhood-onset mood disorders.

Childhood-onset mood disorders (COMD) are often familial, and twin studies of COMD provide compelling evidence that genetic factors are involved. Deficits in neural plasticity have been suggested to underlie the development of depression. The receptor tropomyosin related kinase B (TrkB) and its ligand, brain derived neurotrophic factor (BDNF), play essential roles in neural plasticity, and mRNA expression of both of these genes has been shown to be influenced by stress and chronic antidepressant treatment. In addition, TrkB knock-out mice display inappropriate stress coping mechanisms. Having previously shown that BDNF is associated with COMD, in this study we investigated the gene encoding TrkB, neurotrophic tyrosine kinase, receptor, type 2 (NTRK2) as a susceptibility factor in COMD. We tested for association of NTRK2 with COMD in two independent samples: (a) a case-control sample matched on ethnicity and gender, consisting of 120 cases who met DSM III/IV criteria for major depressive or dysthymic disorder before age 14 or bipolar I/II before the age of 18, and controls, and (b) a family based control sample of 113 families collected in Hungary, identified by a proband between the age of 7 and 14 who met DSM IV criteria for major depressive disorder or bipolar I/II disorder. There was no evidence for an allelic or genotypic association of three polymorphisms of NTRK2 with COMD in the case-control sample. Also, in the family based sample, using the transmission disequilibrium test (TDT), we did not identify any evidence of allelic association for each marker individually or when haplotypes were analyzed. Based on these results, using these three polymorphisms, we do not find support for NTRK2 as a susceptibility gene for COMD.

Age of Onset↗

PubMed1991

Morbidity risk for mood disorders in the families of borderline patients.

We analyzed the familial morbidity risk for mood disorders (MR) and the presence of a family history of alcoholism in a group of 58 patients with DSM-III borderline personality disorder (PD). The MR in the families of borderline subjects was not significantly different from that found in a control group of affective patients with other cluster II PD, or without PD. The MR in the families of borderline subjects who had never developed an affective episode was not significantly different from that found in the families of borderline PD with a history of mood disorders. Borderline subjects with mood disorders had higher rates of alcoholism in their families, mainly among parents. Our results support the hypothesis that borderline PD, even in absence of the codiagnosis of a mood disorder in the subject, may be a predictor of higher familial liability to mood disorders, although it may be more informative for the familial clustering of specific subgroups than for mood disorders as a whole.

Adult↗

PubMed2004

Are mood disorders and obesity related? A review for the mental health professional.

OBJECTIVE: We reviewed evidence regarding a possible relationship between mood disorders and obesity to better inform mental health professionals about their overlap. METHOD: We performed a MEDLINE search of the English-language literature for the years 1966-2003 using the following terms: obesity, overweight, abdominal, central, metabolic syndrome, depression, mania, bipolar disorder, binge eating, morbidity, mortality, cardiovascular, diabetes, cortisol, hypertriglyceridemia, sympathetic, family history, stimulant, sibutramine, antiobesity, antidepressant, topiramate, and zonisamide. We evaluated studies of obesity (and related conditions) in persons with mood disorders and of mood disorders in persons with obesity. We also compared studies of obesity and mood disorders regarding phenomenology, comorbidity, family history, biology, and pharmacologic treatment response. RESULTS: The most rigorous clinical studies suggest that (1). children and adolescents with major depressive disorder may be at increased risk for developing overweight; (2). patients with bipolar disorder may have elevated rates of overweight, obesity, and abdominal obesity; and (3). obese persons seeking weight-loss treatment may have elevated rates of depressive and bipolar disorders. The most rigorous community studies suggest that (1). depression with atypical symptoms in females is significantly more likely to be associated with overweight than depression with typical symptoms; (2). obesity is associated with major depressive disorder in females; and (3). abdominal obesity may be associated with depressive symptoms in females and males; but (4). most overweight and obese persons in the community do not have mood disorders. Studies of phenomenology, comorbidity, family history, biology, and pharmacologic treatment response of mood disorders and obesity show that both conditions share many similarities along all of these indices. CONCLUSION: Although the overlap between mood disorders and obesity may be coincidental, it suggests the two conditions may be related. Clinical and theoretical implications of this overlap are discussed, and further research is called for.

Adolescent↗

PubMed1999

[Genetic association between mood disorder and monoamine oxidase gene].

OBJECTIVE: To ascertain whether the mood disorder (bipolar and unipolar) is genetically associated with genes polymorphisms of MAOA type and MAOB type in the Chinese. METHODS: One hundred and thirty-two cases of Chinese with mood disorder were genotyped for the MAOA(CA)n, MAOB(GT)n and MAOB(TG)n locus using Amp-FLP. RESULTS: Among 132 cases with mood disorder, 8 alleles (size: 112-126 bp) of MAOA(CA)n, 12 alleles (size: 168-198 bp) of MOAB(GT)n and 9 alleles (size: 195-213 bp) of MAOB(TG)n locus were observed. Comparison of the polymorphisms of all alleles in the three locus showed that no significant difference (P > 0.05) was seen in the frequency distribution between cases with mood disorder (bipolar and unipolar) and controls, but the frequency of 180 bp allele for MAOB(GT)n and 250 bp allele for MAOB(TG)n was significantly different (P < 0.05) between the two groups. CONCLUSION: MAO gene (type A and B) is not associated with mood disorder in the Chinese.

Adult↗

PubMed1997

The sensitization hypothesis and importance of psychosensory features in mood disorder: a review.

The sensitization model of mood disorders, articulated 10 years ago, predicts symptoms, course, and treatment response relationships. However, clinical data testing this model have not been reviewed. The authors reviewed all English-language publications characterizing psychosensory features (clinical phenomena hypothesized to reflect temporolimbic sensitization) and the relationship of these features to mood disorder, course, and treatment. They found that 20% to 80% of bipolar and 80% of epileptic patients experience psychosensory phenomena. Although these features do not identify a specific subgroup of mood disorders, their prevalence is highest in schizoaffective bipolar patients. The value of psychosensory features in predicting treatment response or chronicity is unclear.

Humans↗

PubMed2004

Mood disorders in opioid-dependent patients.

AIMS: To assess the rate of current mood disorders in opioid-dependent outpatients. DESIGN: Prevalence study of DSM-IV mood disorders. SETTINGS: Private and government clinics. PARTICIPANTS: Five hundred unpaid opioid-dependent patients who had voluntarily sought treatment. MEASUREMENTS: The Research version of structured clinical interview for DSM-IV Axis I Disorders (SCID-I). RESULTS: The mean age of the subjects (487 men and 13 women) was 33.4 years, ranging from 16 to 67. The majority (68.2%) had private sector job and 13.4% were unemployed. The majority (59.8%) had education at the level of primary, guidance or high school and only 3.8% were illiterate. Three hundred and thirty six (67.2%) subjects were diagnosed as having mood disorders. Of the subjects 274 (54.8%) had substance induced depression, 37 (7.4%) major depression, 14 (2.8%) dysthymia, five (1%) depression due to general medical condition, three (0.6%) cylothymia, three (0.6%) bipolar mood disorder type I. None was diagnosed as having bipolar mood disorder type II. Of the participants 319 (63.8%) reported more than 5 years use of opioid. Of the subjects only 16 (3.2%) reported no episode of abstinence and the majority 484 (96.8%) reported one or more episodes of abstinences. About 4.2% (21) reported less than 1 g/day and the majority 86.4% (432) reported between 1 and 5 g/day current use of opioid. CONCLUSION: Due to high rates of mood disorders in opioid-dependent subjects, psychiatric services should be open and accessible to the patients, especially those who voluntarily seek help and treatment.

Adolescent↗

PubMed2003

Response of cortical metabolic deficits to serotonergic challenge in familial mood disorders.

OBJECTIVE: In subjects with mood disorders, positron emission tomography (PET) with [(18)F]fluorodeoxyglucose has shown prefrontal cortical metabolism deficits, including in a subgenual region in subjects with familial illness. The authors applied a dl-fenfluramine challenge method to study metabolic response in this region to serotonergic challenge in familial major depression. METHOD: The study group consisted of 19 depressed subjects with major depressive disorder or bipolar disorder, all of whom had at least one first-degree relative with history of major depression, and 10 healthy volunteers with similar age and gender distributions. PET images were acquired under placebo and challenge conditions, and volumetric MRI scans were also obtained. Group comparisons of metabolic and volumetric data were performed. Ratings of acute mood change during serotonergic challenge were compared with the imaging data. RESULTS: Within Brodmann's area 32, a glucose metabolism deficit in the depressed subjects on placebo day was observed by voxel-level analysis, but no volumetric deficit was found in the subgenual regions examined. Under challenge, both groups suppressed metabolism similarly. Within the patient group, the correlation between acute mood improvement during challenge and greater metabolic suppression approached significance. CONCLUSIONS: In familial mood disorders, a ventromedial prefrontal cortical deficit in baseline metabolism is not due to altered structural volume, and the response to serotonergic challenge appears predictive of acute mood response. The potential to predict treatment response can be tested by a combined challenge and treatment study.

Adult↗

PubMed2001

Current and lifetime comorbidity of the DSM-IV anxiety and mood disorders in a large clinical sample.

The comorbidity of current and lifetime DSM-IV anxiety and mood disorders was examined in 1,127 outpatients who were assessed with the Anxiety Disorders Interview Schedule for DSM-IV: Lifetime version (ADIS-IV-L). The current and lifetime prevalence of additional Axis I disorders in principal anxiety and mood disorders was found to be 57% and 81%, respectively. The principal diagnostic categories associated with the highest comorbidity rates were mood disorders, posttraumatic stress disorder (PTSD), and generalized anxiety disorder (GAD). A high rate of lifetime comorbidity was found between the anxiety and mood disorders; the lifetime association with mood disorders was particularly strong for PTSD, GAD, obsessive-compulsive disorder, and social phobia. The findings are discussed in regard to their implications for the classification of emotional disorders.

Adolescent↗

PubMed2004

Impact of stressful life events, familial loading and their interaction on the onset of mood disorders: study in a high-risk cohort of adolescent offspring of parents with bipolar disorder.

BACKGROUND: Stressful life events are established as risk factors for the onset of mood disorders, but few studies have investigated their impact on the development of mood disorders in adolescents. AIMS: To study the effect of life events on the development of mood disorders in the offspring of parents with bipolar disorder, with respect to the possibility of a decay effect and modification by familial loading. METHOD: In a high-risk cohort of 140 Dutch adolescent offspring of parents with bipolar disorder, we assessed life events, current and past DSM-IV diagnoses and familial loading. To explore their interaction and impact on mood disorder onset, we constructed four different models and used a multivariate survival analysis with time-dependent covariates. RESULTS: The relationship between life events and mood disorder was described optimally with a model in which the effects of life events gradually decayed by 25% per year. The effect of life event load was not significantly stronger in the case of high familial loading. CONCLUSIONS: Independent of familial loading, life events increase the liability to mood disorders in children of patients with bipolar disorder but the effects slowly diminish with time.

Adolescent↗

PubMed2006

Sleep in mood disorders.

Sleep disturbances are among the most common symptoms in patients who have acute episodes of mood disorders, and patients who have mood disorders exhibit higher rates of sleep disturbances than the general population, even during periods of remission. Insomnia and hypersomnia are associated with an increased risk for the development or recurrence of mood disorders and increased severity of psychiatric symptoms. Sleep electroencephalogram recordings have identified objective abnormalities associated with mood disorders, providing insight into the neurobiologic relationships between mood and sleep. Future studies will continue to investigate this association and potentially improve treatment of sleep and mood disorders.

Brain-Derived Neurotrophic Factor↗

PubMed2005

Bipolar mood disorders among Polish psychiatric outpatients treated for major depression.

BACKGROUND: Significant proportion of patients treated for depression may have various types of bipolar mood disorders. The aim of the study was to assess the frequency of bipolar disorders among outpatients having at least one major depressive episode, treated by 96 psychiatrists, representing all regions of Poland. METHODS: The study included 880 patients (237 male, 643 female), identified to following diagnostic categories: bipolar I, bipolar II, bipolar spectrum disorder and major depressive disorder. RESULTS: Bipolar mood disorders were found in 61.2% of patients studied, bipolar I more frequent in men and bipolar II in women, and bipolar spectrum in 12% of patients. Patients with age ranges 19-49 and 50-65 years did not differ as to the percentage of diagnostic categories. Patients with bipolar mood disorders compared to major depressive disorder had significantly more frequent family history of bipolar disorder, premorbid hyper- or cyclothymic personality, early onset of depression, symptoms of hypersomnia and hyperphagia, psychotic depression, post-partum depression, and treatment-resistant depression. Bipolar spectrum patients had most clinical features similar to classic types of bipolar disorders. LIMITATIONS: Neither structured interview for family history, nor formal criteria for a number of clinical manifestations were used. The population treated by psychiatrists may not be representative and present a subgroup with more severe mood disorders. CONCLUSIONS: Bipolar mood disorders may be very prevalent among depressive outpatients treated by psychiatrists in Poland, which is confirmed by the results of recent studies. Bipolar patients (including bipolar spectrum) significantly differ from major depressive disorder as to numerous clinical features related mostly to depressive episode.

Adult↗

PubMed1995

Meta-analyses of studies of ventricular enlargement and cortical sulcal prominence in mood disorders. Comparisons with controls or patients with schizophrenia.

BACKGROUND: The findings of ventricular enlargement and increased sulcal prominence are well documented in schizophrenia, but the consistency of similar findings in mood disorders is less well appreciated. Reliable documentation of the presence of these structural abnormalities in mood disorders would require a reassessment of their significance for both schizophrenia and mood disorders. In this article, we meta-analytically review the literature on ventricular enlargement and cortical sulcal prominence in patients with mood disorders compared with controls and patients with schizophrenia. METHODS: Four meta-analytic reviews were conducted, two comparing patients with mood disorders with normal controls on ventricular enlargement (meta-analysis 1) or sulcal prominence (meta-analysis 2) and two comparing patients with mood disorders with schizophrenic patients on these same measures (meta-analyses 3 and 4). RESULTS: Meta-analyses 1 and 2 revealed statistically significant (P < .001) moderate composite effect sizes (d) for the comparisons of patients with mood disorders with controls on both ventricular enlargement (d = 0.44) and sulcal prominence (d = 0.42). Meta-analysis 3 further revealed that patients with schizophrenia have significantly greater ventricular enlargement than patients with mood disorders (P = .002), but the effect size was small (d = -0.20). There were too few studies comparing these patient groups on sulcal prominence to support a quantitative meta-analysis. CONCLUSIONS: This review documents the presence of ventricular enlargement and increased sulcal prominence in mood disorders. Patients with mood disorders have less ventricular enlargement than patients with schizophrenia, but this effect is small. These results reinforce previous suggestions of the nonspecificity of structural brain changes in schizophrenia and mood disorders.

Adult↗

PubMed2002

Skating to where the puck is going to be: a plan for clinical trials and translation research in mood disorders.

As part of the National Institute of Mental Health Strategic Plan for Mood Disorders Research effort, the Clinical Trials and Translation Workgroup was asked to define priorities for clinical trials in mood disorders and for research on how best to translate the results of such research to clinical practice settings. Through two face-to-face meetings and a series of conference calls, we established priorities based on the literature to date and what was known about research currently in progress in this area. We defined five areas of priority that cut across developmental stages, while noting that research on adult mood disorders was at a more advanced stage in each of these areas than research on child or geriatric disorders. The five areas of priority are: 1) maximizing the effectiveness and cost-effectiveness of initial (acute) treatments for mood disorders already known to be efficacious in selected populations and settings when they are applied across all populations and care settings; 2) learning what further treatments or services are most likely to reduce symptoms and improve functioning when the first treatment is delivered well, but the mood disorder does not remit or show adequate improvement; 3) learning what treatments or services are most cost-effective in preventing recurrence or relapse and maintaining optimal functioning after a patient's mood disorder has remitted or responded maximally to treatment; 4) developing and validating clinical, psychosocial, biological, or other markers that predict: a) which treatments are most effective, b) course of illness, c) risk of adverse events/tolerability and acceptability for individual patients or well-defined subgroups of patients; 5) developing clinical trial designs and methods that result in lower research costs and greater generalizability earlier in the treatment development and testing process. A rationale for the importance of each of these priorities is provided.

Aged↗