The field of psychoneuroimmunology has witnessed an explosion of empirical findings during the last two decades. Research has documented the mechanisms through which stressful emotions alter white blood cell function. Stress diminishes white blood cell response to viral infected cells and to cancer cells. Moreover, vaccination is less effective in those who are stressed and wounds heal less readily in those who are stressed. While stress decreases the activity of some white blood cells, stress does not compromise the function of all types of white blood cells. Indeed, some types of autoimmune disease, which involve particular subsets of white blood cells, are exacerbated by stress. The literature documents the efficacy of talk-therapy interventions in altering immune system parameters and enhancing the body's ability to combat disease. The literature also documents the impact of the chronic stress of poverty on immune system function.
Eleven studies that addressed the question of reuptake-blocker antidepressant prophylaxis are examined. In all the studies, there was a higher incidence of depression recurrence in the antidepressant-discontinued group than in the antidepressant-maintained group. Although the findings from these studies are consistent with the explanation of the efficacy of antidepressant prophylaxis, an alternative explanation is that the findings demonstrate antidepressant drug withdrawal. Factors consistent with the antidepressant withdrawal explanation are discussed. A research design allowing for a definitive test of prophylaxis is proffered.
Research has established that psychological states can affect the immune system. This article discusses the psychological states associated with enhanced immune system functioning and those associated with suppressed immune functioning. Studies of psychological and behavioral interventions to boost the immune systems of people who are HIV positive, including people with AIDS, are reviewed. Suggestions are made for group interventions to enhance psychological states associated with better immune system function.
This paper reviews both the evidence that supports the characterization of depression as an inflammatory disorder and the different biochemical mechanisms that have been postulated for the connection between inflammation and depression. This association offers credible explanation for the short term efficacy of antidepressants, which have short term anti-inflammatory effects. Evidence for those anti-inflammatory effects is discussed. Evidence of the contrary long-term effects of antidepressants, which increase rather than decrease inflammation, is also reviewed. It is argued that this increase in inflammation would predict an increase in chronicity among depressed patients that have been treated with antidepressants drugs, which has been noted in the literature. A brief discussion of alternatives for decreasing inflammation, some of which have demonstrated efficacy in ameliorating depression, is presented.
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