Etiology Of Depressive Disorder Research Articles

The role of hypothalamic pituitary-adrenal axis dysfunction in the etiology of depressive disorders

The role of hypothalamic pituitary-adrenal axis dysfunction in the etiology of depressive disorders

Study on the interrelationship between 5-HTTLPR/G-protein β3 subunit (C825T) polymorphisms and depressive disorder

To assess whether the promoter region of the serotonin transporter gene (5-HTTLPR) and G-protein beta3-subunit (GNbeta3 C825T) polymorphisms are associated with depressive disorder and explore the genetic mechanism concerning the pathogenesis of this disorder. The genotypes were determined with polymerase chain reaction and allele-specific restriction enzyme analysis. Patients suffering from depression (n=184) and sex and age-matched controls (n=158) were compared in this study. The frequencies of 5-HTTLPR SS and GNbeta3 825TT genotypes and 5-HTTLPR S and GNbeta3 825T alleles in patients suffering from depression were significantly higher than those in the controls (P<0.01). Combined genotype analysis showed that individuals with both 5-HTTLPR S and GNbeta3 825T alleles (odds ratio=3.25, P=0.002) had a risk of depressive disorder higher than those with 5-HTTLPR S (odds ratio=1.817, P=0.01) or GNbeta3 825T alleles (odds ratio=2.214, P=0.001) alone. These results indicated that the etiology of depressive disorder is associated with 5-HTTLPR and GNbeta3 C825T polymorphisms. Our data also suggests that an interaction effect may exist between the 5-HTTLPR S allele and GNbeta3 825T allele in increasing the risk of depressive disorder.

The role of stress in the onset of depressive disorders. A controlled study in a Spanish clinical sample.

We conducted the present study to evaluate the impact of stressful events on the onset of depressive disorders in a Spanish clinical sample, compared to a control group matched for age, sex, civil status and social class. We compared our results with those of other studies carried out with samples that were both clinically and culturally similar to ours. Fifty depressed patients that were diagnosed with a depressive episode in the 6 months prior to the interview and 50 healthy controls were included in the study. Both groups were compared on the "Life Events and Difficulties Schedule" (LEDS). Of the depressive patients, 68 % compared to only 18 % of the control individuals experienced at least one provoking agent in the 12 months prior to the onset of the symptoms. The risk of developing a depressive disorder was 9.7 % greater in subjects exposed to such provoking agents. Chronic difficulties are equally important to the genesis of depressive disorders as severe life events. No significant differences were seen between the two diagnostic subgroups of depressed patients in the accumulation of severe events, major difficulties or provoking agents. The results support the view that stress is a major factor in the aetiology of depressive disorders. The amount of stress suffered by the patients, however, was less than that found in our healthy sample. Important issues about the model of interaction between stress and depression are discussed.

Maternal depression in three Latin American samples

The purposes of the present study were: 1) to assess the prevalence of depressive symptoms in mothers of young children in two Latin American countries (Costa Rica and Chile), and 2) to identify and compare socio-demographic correlates of depressive symptoms among those women. Information on maternal depression and socio-demographic factors was available for three samples of women (total n = 1256). The samples were drawn from periurban communities that were relatively homogeneous with respect to lower-middle-class status and ethnic origin. Point prevalence of depressive symptomatology was assessed using the Center for Epidemiological Studies - Depression scale in all three samples. Lifetime prevalence of major depressive episodes was assessed in two Costa Rican samples by the Diagnostic Interview Schedule. Finally, episodes of dysphoric mood following childbirth were assessed by interview in the Costa Rican samples. Although the three samples differed on nearly all socio-demographic measures, rates of depression were comparable - 35% to 50% of the mothers had experienced at least one episode of major depression or were experiencing severe dysphoric mood at the time of the evaluation. In addition, one-third of the Costa Rican mothers had experienced dysphoric mood following delivery of a child. The present study indicates that the high prevalence of depression in the mothers of young children is present in developing as well as industrialized countries and represents a major public health hazard. Future cross-cultural studies of maternal depression will require methodologies that are sensitive both to contextual factors in which depressive affect is expressed and individual histories that follow the course and etiology of depressive disorders as a chronic, recurrent illness in women during the childbearing and child-rearing years.

Depression, stress and immunological activation: The role of cytokines in depressive disorders

Traditionally, both stress and depression have been associated with impaired immune function and increased susceptibility to infectious and neoplastic disease. However over the last number of years a large body of evidence suggests that major depression is associated with signs of immunological activation. Moreover it has been suggested that cytokine hypersecretion may be involved in the aetiology of depressive disorders. The present article reviews the evidence from both clinical and experimental studies which implicates immunological activation and particularly hypersecretion of cytokines in the onset and maintenance of depressive illness. Both clinical and experimental studies indicate that stress and depression are associated with increased circulating concentrations of cytokines such as IL-1β, IL-6 and γ-IFN and positive acute phase proteins, and hyperactivity of the HPA-axis. In addition, it has been reported that immunological activation induces “stress-like” behavioural and neurochemical changes in laboratory animals. Although for many years it has been suggested that stress acts a predisposing factor to depressive illness' the precise mechanisms by which stress-induced depressive symptoms occur are not fully understood. Nevertheless, behavioural changes due to stress have often been explained in terms of changes in neurotransmitter function in the brain. In the present article increased cytokine secretion is implicated as a mechanism whereby stress can induce depression.

Clinical guide to depression in children and adolescents

Introduction. Part I: Clinical Manifestations of Depressive Disorders in Children and Adolescents. Clinical manifestations and developmental psychopathology of depression. Epidemiology and etiology of depressive disorders. Neurobiology of depression. Chronobiology of seasonal mood disorders. Relationship between depression and suicidal behavior. Part II: Diagnostic Assessment and Treatment of Depressive Disorders in Children and Adolescents. Standardized approaches to clinical assessment of depression. Dynamic psychotherapy of depression. Group therapy of depression. Cognitive therapy of depression. Pharmacological treatment of major depression. Inpatient treatment of depression. Part III: Bipolar Disorders in Children and Adolescents. Bipolar disorders: natural history, genetic studies, and follow-up. Bipolar disorders: clinical manifestations, differential diagnosis, and treatment. Index.

Animal models of depression reflect changing views on the essence and etiology of depressive disorders in humans

1. 1. Since it is ethically unacceptable to use human subjects to conduct manipulative experimental hypothesis-testing research on major depression, investigators interested in the development, the substrates or the mechanisms of treatment of depressive disorders have turned to observational models with humans or to interactive models with animals. 2. 2. One of the earliest animal models of depression, the infant/mother separation in monkeys, is based on the Freudian notion of the loss-inward directed anger-depression connection. 3. 3. The hypothesis that depression is caused by stress led to the development of numerous animal models of depression based on the behavioral abnormalities induced in animals, usually rats but occasionally other species, by exposure to prolonged or intense stress. 4. 4. The selective therapeutic efficacy of antidepressant drugs suggested the hypothesis that depression is caused by a neurochemical abnormality that is alleviated by chronic exposure to antidepressants. This hypothesis has been refined to state that depressive disorders are caused by genetically based neurochemical dysregulation of neural activity in the limbic system. 5. 5. Models based on the limbic dysfunction hypothesis could be used to explore the specific neural substrates of depression. At present, the rat with limbic dysfunction induced by olfactory bulbectomy appears to fulfill best the requirements for a model of depression. The future development or discovery of a genetic strain of animals that shows comparable behavioral and neurovegetative deficits and similar selective drug responses to those seen in patients with depressive disorder, would make tremendous contributions to the understanding not only of depression but also of the neurobiology of the limbic system.

The fragile self: narcissistic disturbance and the protective function of depression.

The role of self-esteem in the aetiology of depressive disorders is not limited to negative self-evaluations. A broader concept, embracing the experience of the self, is necessary. A developmental model of self-esteem regulation is proposed, derived in part from Mahler's work on separation-individuation in infants and Kohut's work on narcissism. A concept of a 'fragile self' is formulated and developed; the depressive state is seen as protecting this fragile self. The model provides a coherent account of individual differences in proneness to depression (in interaction with environmental factors) which is useful to psychotherapists, yet open to empirical test and research use. The model is discussed in relation to psychological research on depression and implications for clinical practice are outlined.