Re: No danger at all
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This is a reply to # 1,874,806
Re: No danger at all
You're in over your head. Here is a paper describing how SSRI's improve NK cell function in HIV. Most psychiatric drugs work by modulating the immune system in one way or another. The mechanism of action of psychiatric drugs is purposefully misleading by the drug companies. The whole psychiatric disease theory is a joke, most brain and behavioral problems are most likely the result of persistent ongoing infections.
Saying that meditation can cure every single variety of these infections that manifest as "psychiatric" diseases is nonsense.
I do think that meditation may cure mild to moderate depression, as well as other illnesses. It will also help a lot in times that it does not cure. But that doesn't mean it is good for every single thing out there. Geez, be open minded. You are the close minded one, I don't see how you don't understand that.
Evans DL, Lynch KG, Benton T, Dubé B, Gettes DR, Tustin NB, Lai JP, Metzger D, Douglas SD.
Department of Psychiatry, Joseph J. Stokes Research Institute of The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania, USA. psych@mail.med.upenn.edu
Abstract
BACKGROUND: Natural killer (NK) cells play an important role in innate immunity and are involved in the host defense against human immunodeficiency virus (HIV) infection. This study examines the potential role of three underlying regulatory systems that have been under investigation in central nervous system research as well as immune and viral research: serotonin, neurokinin, and glucocorticoid systems. METHODS: Fifty-one HIV-seropositive subjects were recruited to achieve a representative sample of depressed and nondepressed women. The effects of a selective serotonin reuptake inhibitor (SSRI), a substance P (SP) antagonist, and a glucocorticoid antagonist on NK cell function were assessed in a series of ex vivo experiments of peripheral blood mononuclear cells from each HIV-seropositive subject. RESULTS: Natural killer cell cytolytic activity was significantly increased by the SSRI citalopram and by the substance P antagonist CP-96345 relative to control conditions; the glucocorticoid antagonist, RU486, showed no effect on NK cytotoxicity. Our results suggest that the effects of the three agents did not differ as a function of depression. CONCLUSIONS: Our findings provide evidence that NK cell function in HIV infection may be enhanced by serotonin reuptake inhibition and by substance P antagonism. It remains to be determined if HIV-related impairment in not only NK cytolytic activity but also NK noncytolytic activity can be improved by an SSRI or an SP antagonist. Clinical studies are warranted to address these questions and the potential roles of serotonergic agents and SP antagonists in improving NK cell immunity, delaying HIV disease progression, and extending survival with HIV infection.
PMID: 17945197
Based on my research and opinion, IL-4 is more directly implicated as problematic in human Lyme infection than IL-10. Thus, even if it stimulates IL-10 production, suppression of IL-4 by SSRI's may have a net positive impact:
QUOTE
Psychiatry Res. 2000 Nov 20;96(3):255-66.
Effects of repeated fluoxetine and citalopram administration on cytokine release in C57BL/6 mice.
Kubera M, Simbirtsev A, Mathison R, Maes M.
Department of Endocrinology, Institute of Pharmacology, Polish Academy of Sciences, Smêtna 12, 31-343 Kraków, Poland.
Abstract
This study examines the effects of repeated administration of the selective serotonin reuptake inhibitors (SSRIs), fluoxetine and citalopram (10 mg/kg, i.p.), on immunoreactivity in C57BL/6 mice. Immune functions were evaluated by the ability of splenocytes to reduce a tetrazolium salt to formazan (MTT test), to proliferate, and to produce cytokines, including interleukin (IL)-1, IL-2, IL-4, IL-6, IL-10 and interferon gamma (IFN gamma). Citalopram administered for 1, 2 and 4 weeks stimulates the proliferative activity of splenocytes and suppresses their ability to secrete the anti-inflammatory cytokine IL-4. Fluoxetine administration for 1 and 2 weeks, but not 4 weeks, stimulates the proliferative activity of splenocytes, whereas a 4-week administration of fluoxetine suppresses the secretion of IL-4. Four weeks of prolonged administration of citalopram and fluoxetine induces a significant increase in the production of IL-6 and IL-10, a cytokine with immunosuppressive and anti-inflammatory activities. The results show that, in C57BL/6 mice, the immunomodulatory effects of SSRIs depend on the SSRI used and the duration of administration.
PMID: 11084221
Effects of repeated fluoxetine and citalopram administration on cytokine release in C57BL/6 mice.
Kubera M, Simbirtsev A, Mathison R, Maes M.
Department of Endocrinology, Institute of Pharmacology, Polish Academy of Sciences, Smêtna 12, 31-343 Kraków, Poland.
Abstract
This study examines the effects of repeated administration of the selective serotonin reuptake inhibitors (SSRIs), fluoxetine and citalopram (10 mg/kg, i.p.), on immunoreactivity in C57BL/6 mice. Immune functions were evaluated by the ability of splenocytes to reduce a tetrazolium salt to formazan (MTT test), to proliferate, and to produce cytokines, including interleukin (IL)-1, IL-2, IL-4, IL-6, IL-10 and interferon gamma (IFN gamma). Citalopram administered for 1, 2 and 4 weeks stimulates the proliferative activity of splenocytes and suppresses their ability to secrete the anti-inflammatory cytokine IL-4. Fluoxetine administration for 1 and 2 weeks, but not 4 weeks, stimulates the proliferative activity of splenocytes, whereas a 4-week administration of fluoxetine suppresses the secretion of IL-4. Four weeks of prolonged administration of citalopram and fluoxetine induces a significant increase in the production of IL-6 and IL-10, a cytokine with immunosuppressive and anti-inflammatory activities. The results show that, in C57BL/6 mice, the immunomodulatory effects of SSRIs depend on the SSRI used and the duration of administration.
PMID: 11084221
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