jueves, 8 de abril de 2010
Important links
http://www.personalityresearch.org/papers/allen.html
http://www.enotalone.com/article/8573.html
http://herkules.oulu.fi/isbn9514270215/html/x294.html
http://www.holysmoke.org/sdhok/why-dep.htm
http://www.mentalhelp.net/poc/view_doc.php?type=doc&id=13003&cn=5
http://www.enotalone.com/article/8573.html
http://herkules.oulu.fi/isbn9514270215/html/x294.html
http://www.holysmoke.org/sdhok/why-dep.htm
http://www.mentalhelp.net/poc/view_doc.php?type=doc&id=13003&cn=5
Depression quotes
“I start to feel like I can’t maintain the facade any longer, that I may just start to show through. And I wish I knew what was wrong. Maybe something about how stupid my whole life is. I don’t know. Why does the rest of the world put up with the hypocrisy, the need to put a happy face on sorrow, the need to keep on keeping on?... I don’t know the answer, I know only that I can’t. I don't want any more vicissitudes, I don't want any more of this try, try again stuff. I just want out. I’ve had it. I am so tired. I am twenty and I am already exhausted.”
- Elizabeth Wurtzel
"Depression is nourished by a lifetime of ungrieved and unforgiven hurts”
- Penelope Sweet
- Elizabeth Wurtzel
"Depression is nourished by a lifetime of ungrieved and unforgiven hurts”
- Penelope Sweet
Cognitive Theory of Depression
Beck's main argument was that depression was instituted by one's view of oneself, instead of one having a negative view of oneself due to depression. This has large social implications of how we as a group perceive each other and relate our dissatisfactions with one another. Abela and D'Alessandro's (2002) study on college admissions is a good example of this phenomenon. In their study they found that the student's negative views about their future strongly controlled the interaction between dysfunctional attitudes and the increase in depressed mood. The research clearly backed up Beck's claim that those at risk for depression due to dysfunctional attitudes who did not get into their college of choice then doubted their futures, and these thoughts lead to symptoms of depression. Therefore, the students' self-perceptions became negative after failing to get into college, and many showed signs of depression due to this thinking.
Other aspects of this study did not match up well with Beck. They elaborate: "As for participants' more enduring mood reactions, our findings are incongruent with Beck's...theory.... Therefore, one possible explanation of discrepancies between these studies is that immediately following the occurrence of a negative event, cognitively vulnerable individuals show marked increases in depressed mood. At the same time, the do not yet exhibit increases in other symptoms of depression.... However, in vulnerable individuals…such depressed mood may be to be accompanied by a host of other depressive symptoms.... Their level of depressed mood, however, was simply not more severe than individuals who did not possess dysfunctional attitudes" (Abela & D'Allesandro, 2002, p.122). What occurred is that the requirements, according to Beck, for depressive symptoms were there but they did not occur regardless. Findings like this show that Beck's theory may not be as complete as we would like, and there is likely to be factors which are unaccounted for in play in situations like this.
http://www.personalityresearch.org/papers/allen.html
Other aspects of this study did not match up well with Beck. They elaborate: "As for participants' more enduring mood reactions, our findings are incongruent with Beck's...theory.... Therefore, one possible explanation of discrepancies between these studies is that immediately following the occurrence of a negative event, cognitively vulnerable individuals show marked increases in depressed mood. At the same time, the do not yet exhibit increases in other symptoms of depression.... However, in vulnerable individuals…such depressed mood may be to be accompanied by a host of other depressive symptoms.... Their level of depressed mood, however, was simply not more severe than individuals who did not possess dysfunctional attitudes" (Abela & D'Allesandro, 2002, p.122). What occurred is that the requirements, according to Beck, for depressive symptoms were there but they did not occur regardless. Findings like this show that Beck's theory may not be as complete as we would like, and there is likely to be factors which are unaccounted for in play in situations like this.
http://www.personalityresearch.org/papers/allen.html
Environmental Theory of Depression
Environmental factors, however, may also play a role in depression. When combined with a biochemical or genetic predisposition, life stressors (such as relationship problems, financial difficulties, death of a loved one, or medical illness) may cause the disease to manifest itself.
John (not his real name), 25, was diagnosed with depression for the first time last year when he and his girlfriend ended their three-year relationship. "I couldn't do anything because I was totally absorbed with the whole break-up issue," he says. "It was impossible for me to sleep, and I would wake up at 3 or 4 in the morning and literally shake. And when it was time to wake up, I just couldn't get out of bed."
In addition, substance abuse and side effects from prescription medication may also lead to a depressive episode. And research shows that people battling serious medical conditions are especially prone to depression. According to the U.S. Department of Health and Human Services, those who have had a heart attack, for example, have a 40 percent chance of being depressed.
http://www.enotalone.com/article/8573.html
John (not his real name), 25, was diagnosed with depression for the first time last year when he and his girlfriend ended their three-year relationship. "I couldn't do anything because I was totally absorbed with the whole break-up issue," he says. "It was impossible for me to sleep, and I would wake up at 3 or 4 in the morning and literally shake. And when it was time to wake up, I just couldn't get out of bed."
In addition, substance abuse and side effects from prescription medication may also lead to a depressive episode. And research shows that people battling serious medical conditions are especially prone to depression. According to the U.S. Department of Health and Human Services, those who have had a heart attack, for example, have a 40 percent chance of being depressed.
http://www.enotalone.com/article/8573.html
martes, 23 de marzo de 2010
Biological Theory of Depression
There have been a variety of theories concerning the neurobiologic etiology of depression. The classic biogenic amine theory of depression suggests that a shortage of noradrenalin (NA) and serotonin (5-HT) in the synaptic clefts is the neurobiological basis of depression (Schildkraut 1965, Bunney & Davis 1965, Coppen 1967). Although the serotonin system is still the most widely studied system, there is evidence suggesting that other neurotransmitter systems also play important roles (Barros et al. 2002). It is suggested that instead of being a consequence of a simple decrease in some crucial cerebral transmitter concentrations depression may be the result of a disturbed balance between different regulatory systems and consequent transmitter overactivity in some brain regions (Syvälahti 1994). According to a hypothesis by Harro & Oreland (1996) the neurobiological starting-point of depression lies in the malfunction of the noradrenergic innervation from the locus coeruleus, which, in turn, leads to dysregulation of serotonergic and dopaminergic neurotransmission. A molecular and cellular theory of depression posits that stress-induced vulnerability and the therapeutic action of antidepressant treatments occur via intracellular mechanisms that decrease or increase, respectively, the neurotrophic factors necessary for the survival and function of particular neurons (Duman et al. 1997).
Depression is often accompanied by certain biological alterations, which may well explain the comorbidity of depression and various diseases. The corticosteroid overdrive and noradrenergic hyperactivity present in depression may impair the normal functions of the immune system (Syvälahti 1994). The reports on immune alterations in the context of depression are contradictory, however. According to the meta-analysis of Herbert & Cohen (1993), it seems that such alterations mainly occur in cellular immunity. The association between depression and coronary heart disease, rheumatoid arthritis, and stroke as well as the higher incidence of depression among females have been explained with the macrophage theory of depression, suggesting that excessive secretion of macrophage monokines is the cause of depression (Smith 1991). Many aspects of cellular immunity are activated in depression, including the increased release of proinflammatory cytokines from activated macrophages in the periphery and brain, the excessive synthesis of prostaglandin E2 (PGE2) and nitric oxide (NO), and the increased release of acute-phase proteins from the liver, while there is also evidence of the suppression of natural killer (NK) cell activity, T-lymphocytes, and neutrophils. It is also suggested, that many of these unfavorable changes in immune function involving depression can be normalized with antidepressant treatment. (For a review, see Leonard 2001.)
http://herkules.oulu.fi/isbn9514270215/html/x294.html
Depression is often accompanied by certain biological alterations, which may well explain the comorbidity of depression and various diseases. The corticosteroid overdrive and noradrenergic hyperactivity present in depression may impair the normal functions of the immune system (Syvälahti 1994). The reports on immune alterations in the context of depression are contradictory, however. According to the meta-analysis of Herbert & Cohen (1993), it seems that such alterations mainly occur in cellular immunity. The association between depression and coronary heart disease, rheumatoid arthritis, and stroke as well as the higher incidence of depression among females have been explained with the macrophage theory of depression, suggesting that excessive secretion of macrophage monokines is the cause of depression (Smith 1991). Many aspects of cellular immunity are activated in depression, including the increased release of proinflammatory cytokines from activated macrophages in the periphery and brain, the excessive synthesis of prostaglandin E2 (PGE2) and nitric oxide (NO), and the increased release of acute-phase proteins from the liver, while there is also evidence of the suppression of natural killer (NK) cell activity, T-lymphocytes, and neutrophils. It is also suggested, that many of these unfavorable changes in immune function involving depression can be normalized with antidepressant treatment. (For a review, see Leonard 2001.)
http://herkules.oulu.fi/isbn9514270215/html/x294.html
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