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ScienceWeek
PUBLIC HEALTH: CULTURE AND DEPRESSION
The following points are made by Arthur Kleinman (New Engl. J. Med. 2004 351:951):
1) In many parts of Chinese society, the experience of depression is physical rather than psychological. Many depressed Chinese people do not report feeling sad, but rather express boredom, discomfort, feelings of inner pressure, and symptoms of pain, dizziness, and fatigue. These culturally coded symptoms may confound diagnosis among Chinese immigrants in the US, many of whom find the diagnosis of depression morally unacceptable and experientially meaningless. This cultural pattern changes over time but continues to diverge significantly from the experiences of other groups. The pattern of somatization may be unfamiliar to US clinicians and may further complicate the concept of depression, which, according to biomedicine, can be an emotion, a symptom, or a disease.
2) Depressive feelings are experienced by all people and are a normal component of disappointment and grief. Depression may be a symptom of a mental disorder (such as bipolar disorder, an anxiety disorder, or schizophrenia) or of other medical diseases, ranging from diabetes and thyroid disorders to postviral syndromes. As one of the most prevalent diseases globally and an important cause of disability, depressive disorder is responsible for as many as one of every five visits to primary care doctors; it occurs everywhere and affects members of all ethnic groups. The rates of depression are increasing, and the disorder is nearly twice as common among the poor as among the wealthy.
3) But the way in which depression is confronted, discussed, and managed varies among social worlds, and cultural meanings and practices shape its course. Culture influences the experience of symptoms, the idioms used to report them, decisions about treatment, doctor-patient interactions, the likelihood of outcomes such as suicide, and the practices of professionals. As a result, some conditions are universal and some culturally distinct, but all are meaningful within particular contexts.
4) Among refugees, depressive affect and disorder are common aspects of collective and personal experiences of loss and trauma. Various patterns of somatization are found among depressed patients from many ethnic groups, and even among Latinos. For example, Mexican Americans, Puerto Ricans, and Cuban Americans may report different symptoms. Add differences in sex, age, social class, education, and degree of biculturalism, and the question of cultural influence becomes murky enough to discourage any form of ethnic stereotyping. Inasmuch as black women have lower rates of depression and suicide than white women, and immigrants lower rates of depression than their descendants, some cultural effects may be protective factors rather than risk factors. In a complex, postmodern society like that of the US -- where it is often hard to determine the cultural norm or how experience differs among or within communities -- cultural differences can affect any patient-doctor interaction.
New Engl. J. Med. http://www.nejm.org
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Related Material:
PSYCHOLOGICAL DEPRESSION AND THE SHRINKING HIPPOCAMPUS
The following points are made by Robert M. Sapolsky (Proc. Nat. Acad. Sci. 2001 98:12320):
1) Throughout human history, it has been apparent that few medical maladies are as devastating in their effects as major depression. And since the 1950s, with the advent of the first generation of antidepressant drugs, it has been apparent that depression is a biological disorder. This has generated the tremendous intellectual challenge of how to understand the material, reductive bases of a disease of malignant sadness.
2) Both the tragic components and the intellectual challenge of depression have deepened in the last decade with a series of high-visibility reports that indicate prolonged major depression is associated with atrophy within the central nervous system. Such atrophy is centered in the brain region called the hippocampus [see background material below]. This structure plays a critical role in learning and memory, and the magnitude of the hippocampal volume loss (nearly 20 percent in some reports) helps explain some well-documented cognitive deficits that accompany major depression.
3) These findings of hippocampal atrophy raise immediate questions. First, is it permanent? Tentatively, this appears to be the case, as the atrophy persists for up to decades after the depressions are in remission. Next, does the hippocampal atrophy arise as a result of depression, or does it precede and even predispose toward depression? There is little evidence for the latter, and most researchers tacitly assume that this morphological change is a consequence of the biology underlying the affective (mood) aspects of the disease.
Proc. Nat. Acad. Sci. http://www.pnas.org
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NEUROBIOLOGY: NEUROGENESIS AND CLINICAL DEPRESSION
Notes by ScienceWeek:
The term "depression" as used in clinical psychiatry is a large basket filled with diagnostic ambiguities, historical semantic baggage, and shifting therapeutic fashions. Nevertheless, the clinical syndrome, no matter how foggy its outlines, is real at its core, affects real people, is a major cause of psychological dysfunction, and a major cause of suicide. In the US alone, approximately 200,000 suicide attempts are made each year; 75 people commit suicide every day; suicide accounts for 30 percent of the deaths among university students and is the second leading cause of death among adolescents. What is known is that clinical depression is involved in over half of all attempted suicides, a relation that defines the urgency of research in this area. From the standpoint of clinical neurobiology, the research problem is clear: clinical depression, whatever it may be, is a dysfunctional alteration of behavior, and the task of the clinical neurobiologist is to determine what, if any, dysfunctional alterations of the brain and/or brain dynamics are responsible for the clinical syndrome.
The term "neurogenesis" refers to the generation of new nerve cells. Until a few years ago, neurogenesis was considered to be totally absent in the adult mammalian brain, but neurogenesis has now been identified in certain regions of the brains of several mammalian species, and there is currently much research devoted to relating brain neurogenesis to various brain pathologies.
The following points are made by B.L. Jacobs et al (American Scientist 2000 88:340):
1) The authors point out that many researchers believe that stress is the most significant causal agent (with the possible exception of genetic predisposition) in the etiology of depression. In addition, nerve cells in the hippocampal region of the brain are among the most sensitive to the deleterious effects of stress. Consequently, a stress-induced decrease in neurogenesis in the hippocampus may be an important factor in precipitating episodes of depression. As a corollary, increasing *serotonin-related neurotransmission is apparently the most effective treatment for depression, and such treatment also augments (in animal models) hippocampal neurogenesis. Thus, serotonin-induced increases in neurogenesis might promote recovery from depression. Considering all this, the authors propose that the waxing and waning of neurogenesis in the hippocampus might trigger the precipitation of and recovery from episodes of clinical depression.
2) The relation between stress and hippocampal neurogenesis has been examined in several species. Removing the *adrenal glands of a rat increases neurogenesis in the *dentate gyrus, and this effect can be reversed with the *glucocorticoid hormone corticosterone, which normally is secreted by the adrenal glands. The circulating level of glucocorticoids apparently suppresses the birth of neurons in the dentate gyrus under normal conditions. It has also been demonstrated that systemic administration of corticosterone to normal animals suppresses dentate gyrus neurogenesis. In summary, stress apparently suppresses the rate of dentate-gyrus cell proliferation in adults of a number of species, and it probably does so through increases in brain glucocorticoids.
3) The authors point out that they do not exclude other changes as being important in the etiology and recovery from depression. For example, besides suppressing neurogenesis, increased glucocorticoids might mediate additional direct neuronal effects in various brain structures. Similarly, changes in serotonin neurotransmission might also exert direct effects in various brain structures. The authors suggest that all of these changes, acting in concert, give rise to the complex syndrome of depression.
American Scientist http://www.americanscientist.org
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Notes by ScienceWeek:
serotonin-related neurotransmission: The term "neurotransmission" refers, in general, to the interactions between nerve cells. Serotonin is one of a variety of neurotransmitter substances, i.e., substances involved in the mechanisms of neurotransmission.
adrenal glands: Organs that sit on the tops of the kidneys (one on each kidney). Each adrenal gland has two parts, adrenal cortex and adrenal medulla. The adrenal cortex secretes corticosteroid and androgen hormones; the adrenal medulla makes the hormones epinephrine (adrenalin) and norepinephrine.
dentate gyrus: The term "dentate gyrus" refers to one of the two interlocking gyri (folds) composing the hippocampus.
glucocorticoid hormone corticosterone: See background material below.
ScienceWeek http://scienceweek.com
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