Psychological factors psychodynamic theories of depression psychoanalytic theory as postulated by both Freud and Abraham emphasized the connection between mourning and melancholia. The melancholic patient experiences a loss of self esteem with associated helplessness, prominent guilt and self deprecation. According to the theory, these symptoms result from internally directed anger or aggression turned against the self, leading to a depressive experience (kay tasman, 2006). Melanie klein understood depression as involving the expression of aggression toward loved ones. Edward Bibring regarded depression as a phenomenon that sets in when a person becomes aware of the discrepancy between extraordinarily high ideals and the inability to meet those goals. Edith Jacobson saw the state of depression as similar to a powerless, helpless child victimized by a tormenting parent. Silvano Arieti observed that many depressed people have lived their lives for someone else (a principle, an ideal, or an institution, as well as an individual) rather than for themselves. Heinz kohut's conceptualization of depression, derived from his self-psychological theory, rests on the assumption that the developing self has specific needs that must be met by parents to give the child a positive sense of self-esteem and self-cohesion.
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The largest study to date using pet found a marked global reduction in brain 5-HT2 receptor binding (22-27) in various regions (Sheline minyun, 2002). There is an increasing literature using neuroimaging to understand suicidality, particularly essay in depression. Mann (2005) cites several imaging studies suggesting decreased serotonin function in suicidal individuals and decreased activity in associated report areas of the dorsal system involved in emotion regulation, such as the anterior cingulate. A number of regions more specic to suicidality are also highlighted, particularly those that seem to be involved in impulsivity and aggression, such as the right lateral temporal cortex, right frontopolar cortex, and right ventrolateral prefrontal cortex (Goethals., 2005). This literature has as well found structural abnormalities in relevant regions of the dorsal system, particularly the orbitofrontal cortex, which has specically been linked to potential decision making decits that could lead to suicidality. Thus, such data potentially suggest clinically important subtype differentiation in brain function for this symptom (Ingram, 2009). Psychosocial factors stressful life events more often precede first, rather than subsequent, episodes of mood disorders. Some clinicians believe that life events play the primary or principal role in depression; others suggest that life events have only a limited role in the onset and timing of depression. Data indicate that the life event sometimes associated with development of depression is losing a parent before age. The loss of a spouse is the environmental stressor most often associated with the onset of an episode of depression. Another risk factor is unemployment; persons out of work are three times more likely to report symptoms of an episode of major depression than those who are employed (Sadock sadock, 2007).
A number of intracellular changes healthy which involve alterations in cellular second messenger systems and ion channels are postulated to occur in depression. Intracellular changes may involve changes in guanine triphosphate binding proteins, g-proteins on the receptor, cyclic adenosine monophosphate (cAMP) regulation, reduced protein kinase activity and brain derived neurotrophic factor (bdnf). Antidepressants as well as ect increase bdnf and bdnf have been found to increase functioning of serotonin (kay tasman, 2006). Neuroimaging models of depression recent rapid advances in neuroimaging methodology have attempted to relate the phenomenological abnormalities seen in depression to changes in brain structure and function (fu., 2003). There is increasing evidence that depression may be associated with structural brain pathology. Magnetic resonance imaging (MRI) has revealed decreased volume in cortical regions, particularly the frontal cortex, but also in subcortical structures, such as the hippocampus, amygdala, caudate, and putamen (Sheline minyun, 2002). The most widely replicated Positron emission tomography (PET) scanning (PET) finding in depression is decreased anterior brain metabolism, which is generally more pronounced on the left side. In addition, increased glucose metabolism has been observed in several limbic regions (Thase, 2009). Neuroimaging has also helped in the further investigation of the neurochemical deficits in depression.
The most famous hypotheses generated to account for the actual mechanism of the mood disorder focus on regulatory disturbances in the monoamine neurotransmitter systems, particularly that involving norepinephrine and serotonin (5-hydroxytryptamine). It has also been hypothesized that depression is associated with an alteration in the acetylcholine-adrenergic balance and characterized by a relative cholinergic dominance. In addition, there are suggestions that dopamine is functionally decreased in some cases of major depression. Original reports suggesting that patients with endogenous depression experienced either decreased noradrenergic or serotonergic activity now appear to be overly simplistic. All the monoamine neurotransmitter systems are interrelated and subject to compensatory adaptation to perturbation over time (Reus, 2000). Cellular models of depression most current hypotheses of neurotransmitter function in altered mood states have focused on changes in receptor sensitivity and second messenger systems. With a few exceptions long-term antidepressant treatment is associated with reduced you postsynaptic î-adrenergic receptor sensitivity and enhanced postsynaptic serotonergic and cyclic adenosine monophosphate activity (Reus, 2000).
However, studies suggest that other factors also are important (Schiffer, 2008). Actually, it is the tendency to become depressed in response to life events that are inherited (Hirschfield weissman, 2002). Moreover, family and twin studies show a clear genetic component of life events themselves (Kendler karkowski, 1997). Endocrine models of depression, neuroendocrine abnormalities that reflect the neurovegetative signs and symptoms of depression include: first, increased cortisol and corticotrophin-releasing hormone (CRH) secretion, second, an increase in adrenal size, third, a decreased inhibitory response of glucocorticoids to dexamethasone, and fourth, a blunted response. Antidepressant treatment leads to normalization of these pituitary-adrenal abnormalities (Reus, 2008). Thyroid hormone may potentiate both the speed and the efficacy of antidepressant medication (Altshuler., 2001). Furthermore, there also evidence that patient resistant to other treatments may respond to addition of thyroid hormone (Joffe marriott, 2000). Neurochemical models of depression.
Depression : a, review of, literature, omics international
Depression is more common in urban than a rural district (Gill, 2007). Physical illness, having a chronic or severe physical illness is associated with an increased risk for depression. This suggests that the stress associated with a serious or chronic physical illness may act by bringing out an individual's lifetime vulnerability to depression (Joyce, 2003). Etiology of Depressive disorders. The etiology of major depressive the disorder is unknown (Dunner, 2008).
Multiple etiologic factors genetic, biochemical, psychodynamics, and socio-environmental may interact in complex ways to cause major depressive disorder (Loosen shelton, 2011). Genetic models of depression, there is evidence to suggest a genetic basis for the major depression disorder. Occurrences of major depressive episodes are clearly cluster in families. This degree of increased risk is about three to five times that of the normal population. Twin and adoption study is consistent with a genetic contribution to major depressive disorders.
Severe depressive illness in middle age tends to affect hard-working, conventional people with high standards and obsessional traits. Obsessional personalities can find it, particularly difficult to adapt to stress or life changes, as in work or relationships, and this can 'come out' as depression (Gill, 2007). Childhood experiences, early theorizing suggested that the loss of a parent in childhood increased the later risk for major depression. However, many studies have examined this issue; they have inconsistently found it to be a risk factor for adult depression (Tennant, 1988). Childhood sexual abuse has been established as a risk factor for adult major depression (Joyce, 2003).
Rates of depressive illness is lower in the married man than in the single, widowed, or divorced. The protective effects of marriage are less marked in women. Young married women with children have high rates of depression; single women have low rates (Gill, 2007). However, those in a poor marriage with deficient intimacy are at increased risk of depression (Weissman, 1987). Social classes and occupation, people of low socio-economic status (i.e. Low levels of income, employment, and education) are at higher risk of depression (Semple., 2005). While job satisfaction can enhance mental well-being, the workplace can also be a source of stress and depression. However, the consequences of unemployment probably have far changed on mental health. The economic hardship to the unemployed and their families with depression due to long-term unemployment hindering job seeking and re-employment chances, exacerbated by loss of confidence and perceived loss of skills (Strandh, 2001).
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The reasons for the difference are plan hypothesized to involve hormonal differences, the effects of childbirth, and differing on psychosocial stressors for women and for men (Sadock sadock, 2007). Age, major depressive disorder occurs in all cultures and affects all age groups. Depression is common in Childhood and late adult. The mean age of onset is generally in the 30s (Dunner, 2008). Early-onset depression is associated with a higher female to a male ratio than late-onset depression. The incidence of major depressive disorder in old age is lower in both sexes. However, first incidence and prevalence of minor depressive disorder shows the opposite trend (Rihmer angst, 2009). Personality, in younger people, mild depression tends to affect anxious or dependent personalities with poor tolerance of stress.
In Dubai the prevalence of depressive disorders were.7 among women mostly neurotic depression (Ghubash., 1992). About 12-20 of persons experiencing an acute episode develop a chronic depressive syndrome, and up to 15 of patients who have depression for more than one month commit suicide (Reus, 2000). Genetics, there is now substantial evidence that the genetic factors are of major importance as risk factors for vulnerability to major depression. Traditional estimates have put the heritability about 40 (Joyce, 2003). Genetic influences are most marked in patients with more severe forms of depressive disorder and 'biological' symptoms. The morbid risk in first-degree relatives is increased in all studies. This elevation is independent of the effects of environment or upbringing. In fewer severe forms of depression, genetic factors are fewer significant and environmental factors relatively more important (souery., 1997). Gender, major depressive disorder is the twofold greater wghs prevalence in women than in men independent of country or culture.
show substantial variability in the lifetime rates of depression. Lifetime rates are ranging from under 5 percent to 30 percent, but it is widely accepted that the lifetime prevalence is between 10 percent and 20 percent. The 6-month prevalence rate is considered to be between 2 percent and 5 percent based on surveys in several countries (Young., 2010). A cross- sectional who world health survey carried out in 60 countries covering all regions of the world showed a 1-year prevalence of depressive episode.2 percent, with a 95 percent confidence interval.0 percent.5 percent (Moussavi., 2007). The life time prevalence of depression for adults varied from 3 percent in Japan.9 percent in the us, with most countries in the range between 8 percent and 12 percent (Andrade., 2003). The prevalence of major depressive disorder is estimated to be about 2 percent in children (Birmaher., 1996). Estimates of the point prevalence of mdd in adolescence is range from.4 percent.3 percent. Lifetime prevalence rates across adolescence range is from 15 percent to 20 percent (Roberts bishop, 2005).
It is expected to rise to second place, preceded only by cardiovascular disease by 2020 (Thompson, 2007). Depressive disorder has significant potential morbidity and mortality. Suicide is the second leading cause of death in persons aged 20-35 years. Depressive disorder is a major factor in around 50 of these deaths (Semple., 2005). A suicide attempt among the patients with major depressive disorder is associated with the presence and severity of depressive symptoms. Lack of partner, previous suicide attempts and time spent in depression are risk factors of suicide attempts. Reducing the time of depression is a likely preventive measure of suicide (sokero., 2005).
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Print, reference this, published: 23rd March, 2015 16th may, 2017. Depression is one of the most prevailing medical disorders. Depression has been recognized as a distinct pathological entity from early Egyptian times (Reus, 2000). Depression is the most common psychiatric disorders. Each year, more than 100 million people worldwide develop clinical depression (Bjornlund, 2010). During a lifetime, it is estimated that between 8 and 20 of the general population will experience at least one clinically significant episode of depression (Kessler., 1994). Major depression causes report the fourth-highest burden of disease among all medical diseases.