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Severe depression treatment resistant, side effects for prescription drugs - Within Minutes

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Epidemiology of major depressive disorder: results from the National Epidemiologic Survey on Alcoholism and Related Conditions.
Not only is there a dose-response relationship between BMI and a number of inflammatory markers, but also there is an array of inflammatory mediators that are released by fat cells, including the inflammatory cytokines tumor necrosis factor (TNF)-?, and interleukin (IL)-6 as well as the chemokine monocyte chemoattractant protein-1, which is a potent attractant for macrophages that accumulate in fatty tissue and sustain inflammatory responses.10 Childhood maltreatment has also been associated with increased markers of inflammation in depression, under resting conditions, and following stress. Depression may be considered resistant to treatment when at least two trials with antidepressants from different pharmacologic classes (adequate in dose, duration, and compliance) fail to produce a significant clinical improvement. Evidence regarding psychotherapy and pharmacotherapy has recently been enhanced by results from the STAR*D (Sequenced Treatment Alternatives to Relieve Depression) study, a seven-year randomized controlled trial (RCT) that evaluated medication switching and augmentation in 3,671 outpatients with unipolar depression.11 Citalopram (Celexa) was the initial treatment (20 mg daily, titrated to 60 mg daily if needed). Papakostas, MD is Director of Treatment-Resistant Depression Studies in the Department of Psychiatry at Massachusetts General Hospital and Associate Professor of Psychiatry at Harvard Medical School in Boston.
Describe the clinical factors associated with treatment non-response and how these factors correlate with inflammation. A significant percentage of patients with TRD exhibit increased markers of inflammation, and clinical factors that are linked with treatment nonresponse are associated with inflammation. Data show a dose-response relationship between BMI and TRD—the higher the BMI, the lower the response rate.4 Early life stress is also associated with poor treatment outcome.

Evidence regarding the effectiveness of psychotherapy for treatment-resistant depression is limited.
Ongoing cognitive behavior therapy (CBT) and frequent follow-up with the physician may encourage adherence during the early stages of treatment. The data indicate that treatment resistance may be in part a function of activation of inflammatory pathways.
These findings provide powerful evidence that inhibition of inflammation or its downstream effects on mood may open up a host of new approaches to treatment for depression, especially for patients with TRD. The clinical factors that may alert the clinician to which patients are most likely to exhibit increased inflammatory biomarkers and risk for treatment resistance include obesity, childhood maltreatment, bipolar disorder, and comorbid medical illness (Figure 1). Cytokine effects on these biological processes thus conspire to sabotage and circumvent the mechanism of action of conventional antidepressants, leading to treatment resistance.
In general, patients who require more treatment steps have higher relapse rates, and fewer than one half of patients achieve sustained remission. Electroconvulsive therapy is effective as short-term therapy of treatment-resistant depression.

There is no good-quality evidence that vagal nerve stimulation is an effective treatment for this condition. MAOIs are associated with serious side effects (hypertensive crisis) and require dietary restriction; these drugs should generally be reserved for patients who do not respond to other treatments. Depression is a common condition in the United States, with 12-month and lifetime prevalence rates of approximately 5 and 13 percent, respectively.1 The mean age of onset is 30 years, and there is a higher prevalence in women, whites, and Native Americans. Other evidence suggests that augmentation of second-generation antidepressants or TCAs with pindolol, lithium, or methylphenidate (Ritalin) is not effective for treatment-refractory depression.22,23ELECTROCONVULSIVE THERAPYElectroconvulsive therapy is used primarily for treatment-resistant depression, although it may be used in high-risk cases of severe or psychotic depression, or when pharmacotherapy is contraindicated or not tolerated. Cognitive impairment may be inversely related to treatment effectiveness (greater with bilateral and high-dose therapy).22VAGAL NERVE STIMULATION AND OTHER THERAPIESVagal nerve stimulation refers to electrical stimulation of the cervical portion of the left vagus nerve. This treatment was approved in 2005 for treatment-resistant depression (inadequate response to at least four antidepressant drugs).

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