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J Interferon Cytokine Res 2002 Dec;22(12):1153-66 Ingested type I interferon: a potential treatment for autoimmunity. Brod SA. Multiple Sclerosis Research Group, Department of Neurology, Graduate School of Biomedical Sciences in Immunology, University of Texas Health Science Center at Houston, Houston, TX 77030. We have proposed a unifying hypothesis of the etiopathogenesis of autoimmunity that defines autoimmunity as a type I interferon (IFN) immunodeficiency syndrome. We have examined toxicity and potential efficacy in three phase I (type 1 diabetes, rheumatoid arthritis, multiple sclerosis) and one phase II clinical trials in multiple sclerosis (MS). In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta cell function in recent onset patients. In a second phase I trial, treatment of rheumatoid arthritis (RA) with ingested IFN-alpha reduced the secretion of interleukin-1 (IL-1), a proinflammatory cytokine. In a third phase I trial in MS, there was a significant decrease in peripheral blood mononuclear cell (PBMC) IL-2 and IFN-gamma production after ingesting IFN-alpha. In a phase II randomized, placebo-controlled, double-blind trial in MS, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. Tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. Ingested IFN-alpha was not toxic in any of these clinical trials. These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. PMID: 12581487 [PubMed - in process] J Neuroimmunol 2003 Jan;134(1-2):128-32 Cytokine profile in patients with multiple sclerosis following vitamin D supplementation. Mahon BD, Gordon SA, Cruz J, Cosman F, Cantorna MT. Graduate Program in Nutrition, Pennsylvania State University, University Park, PA 16802, USA. Multiple sclerosis (MS) patients were randomized, in a double blind design, and placed into either a vitamin D supplemented group or a placebo control group. As expected, serum 25-hydroxyvitamin D levels increased significantly following 6 month vitamin D supplementation (17+/-6 ng/ml at baseline to 28+/-8 ng/ml at 6 months). Vitamin D supplementation also significantly increased serum transforming growth factor (TGF)-beta 1 levels from 230+/-21 pg/ml at baseline to 295+/-40 pg/ml 6 months later. Placebo treatment had no effect on serum TGF-beta 1 levels. Tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-13 were not different following vitamin D supplementation. IL-2 mRNA levels decreased following vitamin D supplementation but the differences did not reach significance. Vitamin D supplementation of MS patients for 6 months was associated with increased vitamin D status and serum TGF-beta 1. Publication Types: ? Clinical Trial ? Randomized Controlled Trial PMID: 12507780 [PubMed - indexed for MEDLINE] Exp Biol Med (Maywood) 2002 Dec;227(11):981-8 Ingested type I interferon: state of the art as treatment for autoimmunity. Brod SA. Multiple Sclerosis Research Group, Department of Neurology, Graduate School of Biomedical Sciences in Immunology, University of Texas Health Science Center at Houston, Houston, Texas 77030, USA. stanley.a.b…@uth.tmc.edu We have proposed a unifying hypothesis of the etiopathogenesis of autoimmunity that defines autoimmunity as a type I interferon (IFN) immunodeficiency syndrome. We have examined toxicity and potential efficacy in three phase I (type 1 diabetes, rheumatoid arthritis, multiple sclerosis) and one phase II clinical trials in multiple sclerosis. In a phase I open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual beta-cell function in recent onset patients. In a second phase I trial, treatment of rheumatoid arthritis with ingested IFN-alpha reduced the secretion of interleukin (IL)-1, a pro-inflammatory cytokine. In a third phase I trial in multiple sclerosis, there was a significant decrease in peripheral blood mononuclear cell IL-2 and IFN-gamma production after ingesting IFN-alpha. In a phase II randomized, placebo-controlled, double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha significantly decreased gadolinium enhancements compared with the placebo group at month 5. Tumor necrosis factor-alpha and IFN-gamma cytokine secretion in the 10,000 IU group at month 5 showed a significant decrease that corresponded with the effect of ingested IFN-alpha on decreasing gadolinium enhancements. Ingested IFN-alpha was not toxic in any of these clinical trials. These studies suggest that ingested IFN-alpha may have a potential role in the treatment of autoimmunity. Publication Types: ? Review ? Review, Tutorial PMID: 12486207 [PubMed - indexed for MEDLINE] J Am Coll Nutr 2002 Dec;21(6):495-505

Response:

"Bob Davidson" <phatb…@shaw.ca> wrote in message

news:YNd9a.392586$sV3.11190473@news3.calgary.shaw.ca… > i have been waiting for an alternative to injecting as i had a bad tumor > necrosis from using betaseron,, if i could get oral interfuron that is shown > to be non toxic, i would give it a try for sure. > bobD

This is Oral "Alpha" interferon.  A known side-effect is muscle waisting.  I know, Id used it on my dog for his cancer.  Its dirt cheap to boot.  But Im sure that itll cost thousands if its used for us MSers.  Its also an anti-viral. Rob – Hide quoted text — Show quoted text -> "Celeste" <celeste…@adelphia.net> wrote in message > news:K4c9a.3238$J51.387422@news1.news.adelphia.net… > > J Interferon Cytokine Res 2002 Dec;22(12):1153-66 > > Ingested type I interferon: a potential treatment for autoimmunity. > > Brod SA. > > Multiple Sclerosis Research Group, Department of Neurology, Graduate > School > > of Biomedical Sciences in Immunology, University of Texas Health Science > > Center at Houston, Houston, TX 77030. > > We have proposed a unifying hypothesis of the etiopathogenesis of > > autoimmunity that defines autoimmunity as a type I interferon (IFN) > > immunodeficiency syndrome. We have examined toxicity and potential > efficacy > > in three phase I (type 1 diabetes, rheumatoid arthritis, multiple > sclerosis) > > and one phase II clinical trials in multiple sclerosis (MS). In a phase I > > open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual > > beta cell function in recent onset patients. In a second phase I trial, > > treatment of rheumatoid arthritis (RA) with ingested IFN-alpha reduced the > > secretion of interleukin-1 (IL-1), a proinflammatory cytokine. In a third > > phase I trial in MS, there was a significant decrease in peripheral blood > > mononuclear cell (PBMC) IL-2 and IFN-gamma production after ingesting > > IFN-alpha. In a phase II randomized, placebo-controlled, double-blind > trial > > in MS, 10,000 IU ingested IFN-alpha significantly decreased gadolinium > > enhancements compared with the placebo group at month 5. Tumor necrosis > > factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU > > group at month 5 showed a significant decrease that corresponded with the > > effect of ingested IFN-alpha on decreasing gadolinium enhancements. > Ingested > > IFN-alpha was not toxic in any of these clinical trials. These studies > > suggest that ingested IFN-alpha may have a potential role in the treatment > > of autoimmunity. > > PMID: 12581487 [PubMed - in process] > > J Neuroimmunol 2003 Jan;134(1-2):128-32 > > Cytokine profile in patients with multiple sclerosis following vitamin D > > supplementation. > > Mahon BD, Gordon SA, Cruz J, Cosman F, Cantorna MT. > > Graduate Program in Nutrition, Pennsylvania State University, University > > Park, PA 16802, USA. > > Multiple sclerosis (MS) patients were randomized, in a double blind > design, > > and placed into either a vitamin D supplemented group or a placebo control > > group. As expected, serum 25-hydroxyvitamin D levels increased > significantly > > following 6 month vitamin D supplementation (17+/-6 ng/ml at baseline to > > 28+/-8 ng/ml at 6 months). Vitamin D supplementation also significantly > > increased serum transforming growth factor (TGF)-beta 1 levels from > 230+/-21 > > pg/ml at baseline to 295+/-40 pg/ml 6 months later. Placebo treatment had > no > > effect on serum TGF-beta 1 levels. Tumor necrosis factor (TNF)-alpha, > > interferon (IFN)-gamma, and interleukin (IL)-13 were not different > following > > vitamin D supplementation. IL-2 mRNA levels decreased following vitamin D > > supplementation but the differences did not reach significance. Vitamin D > > supplementation of MS patients for 6 months was associated with increased > > vitamin D status and serum TGF-beta 1. > > Publication Types: > > ? Clinical Trial > > ? Randomized Controlled Trial > > PMID: 12507780 [PubMed - indexed for MEDLINE] > > Exp Biol Med (Maywood) 2002 Dec;227(11):981-8 > > Ingested type I interferon: state of the art as treatment for > autoimmunity. > > Brod SA. > > Multiple Sclerosis Research Group, Department of Neurology, Graduate > School > > of Biomedical Sciences in Immunology, University of Texas Health Science > > Center at Houston, Houston, Texas 77030, USA. stanley.a.b…@uth.tmc.edu > > We have proposed a unifying hypothesis of the etiopathogenesis of > > autoimmunity that defines autoimmunity as a type I interferon (IFN) > > immunodeficiency syndrome. We have examined toxicity and potential > efficacy > > in three phase I (type 1 diabetes, rheumatoid arthritis, multiple > sclerosis) > > and one phase II clinical trials in multiple sclerosis. In a phase I > > open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual > > beta-cell function in recent onset patients. In a second phase I trial, > > treatment of rheumatoid arthritis with ingested IFN-alpha reduced the > > secretion of interleukin (IL)-1, a pro-inflammatory cytokine. In a third > > phase I trial in multiple sclerosis, there was a significant decrease in > > peripheral blood mononuclear cell IL-2 and IFN-gamma production after > > ingesting IFN-alpha. In a phase II randomized, placebo-controlled, > > double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha > > significantly decreased gadolinium enhancements compared with the placebo > > group at month 5. Tumor necrosis factor-alpha and IFN-gamma cytokine > > secretion in the 10,000 IU group at month 5 showed a significant decrease > > that corresponded with the effect of ingested IFN-alpha on decreasing > > gadolinium enhancements. Ingested IFN-alpha was not toxic in any of these > > clinical trials. These studies suggest that ingested IFN-alpha may have a > > potential role in the treatment of autoimmunity. > > Publication Types: > > ? Review > > ? Review, Tutorial > > PMID: 12486207 [PubMed - indexed for MEDLINE] > > J Am Coll Nutr 2002 Dec;21(6):495-505

Response:

i have been waiting for an alternative to injecting as i had a bad tumor necrosis from using betaseron,, if i could get oral interfuron that is shown to be non toxic, i would give it a try for sure. bobD "Celeste" <celeste…@adelphia.net> wrote in message

news:K4c9a.3238$J51.387422@news1.news.adelphia.net… – Hide quoted text — Show quoted text -> J Interferon Cytokine Res 2002 Dec;22(12):1153-66 > Ingested type I interferon: a potential treatment for autoimmunity. > Brod SA. > Multiple Sclerosis Research Group, Department of Neurology, Graduate School > of Biomedical Sciences in Immunology, University of Texas Health Science > Center at Houston, Houston, TX 77030. > We have proposed a unifying hypothesis of the etiopathogenesis of > autoimmunity that defines autoimmunity as a type I interferon (IFN) > immunodeficiency syndrome. We have examined toxicity and potential efficacy > in three phase I (type 1 diabetes, rheumatoid arthritis, multiple sclerosis) > and one phase II clinical trials in multiple sclerosis (MS). In a phase I > open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual > beta cell function in recent onset patients. In a second phase I trial, > treatment of rheumatoid arthritis (RA) with ingested IFN-alpha reduced the > secretion of interleukin-1 (IL-1), a proinflammatory cytokine. In a third > phase I trial in MS, there was a significant decrease in peripheral blood > mononuclear cell (PBMC) IL-2 and IFN-gamma production after ingesting > IFN-alpha. In a phase II randomized, placebo-controlled, double-blind trial > in MS, 10,000 IU ingested IFN-alpha significantly decreased gadolinium > enhancements compared with the placebo group at month 5. Tumor necrosis > factor-alpha (TNF-alpha) and IFN-gamma cytokine secretion in the 10,000 IU > group at month 5 showed a significant decrease that corresponded with the > effect of ingested IFN-alpha on decreasing gadolinium enhancements. Ingested > IFN-alpha was not toxic in any of these clinical trials. These studies > suggest that ingested IFN-alpha may have a potential role in the treatment > of autoimmunity. > PMID: 12581487 [PubMed - in process] > J Neuroimmunol 2003 Jan;134(1-2):128-32 > Cytokine profile in patients with multiple sclerosis following vitamin D > supplementation. > Mahon BD, Gordon SA, Cruz J, Cosman F, Cantorna MT. > Graduate Program in Nutrition, Pennsylvania State University, University > Park, PA 16802, USA. > Multiple sclerosis (MS) patients were randomized, in a double blind design, > and placed into either a vitamin D supplemented group or a placebo control > group. As expected, serum 25-hydroxyvitamin D levels increased significantly > following 6 month vitamin D supplementation (17+/-6 ng/ml at baseline to > 28+/-8 ng/ml at 6 months). Vitamin D supplementation also significantly > increased serum transforming growth factor (TGF)-beta 1 levels from 230+/-21 > pg/ml at baseline to 295+/-40 pg/ml 6 months later. Placebo treatment had no > effect on serum TGF-beta 1 levels. Tumor necrosis factor (TNF)-alpha, > interferon (IFN)-gamma, and interleukin (IL)-13 were not different following > vitamin D supplementation. IL-2 mRNA levels decreased following vitamin D > supplementation but the differences did not reach significance. Vitamin D > supplementation of MS patients for 6 months was associated with increased > vitamin D status and serum TGF-beta 1. > Publication Types: > ? Clinical Trial > ? Randomized Controlled Trial > PMID: 12507780 [PubMed - indexed for MEDLINE] > Exp Biol Med (Maywood) 2002 Dec;227(11):981-8 > Ingested type I interferon: state of the art as treatment for autoimmunity. > Brod SA. > Multiple Sclerosis Research Group, Department of Neurology, Graduate School > of Biomedical Sciences in Immunology, University of Texas Health Science > Center at Houston, Houston, Texas 77030, USA. stanley.a.b…@uth.tmc.edu > We have proposed a unifying hypothesis of the etiopathogenesis of > autoimmunity that defines autoimmunity as a type I interferon (IFN) > immunodeficiency syndrome. We have examined toxicity and potential efficacy > in three phase I (type 1 diabetes, rheumatoid arthritis, multiple sclerosis) > and one phase II clinical trials in multiple sclerosis. In a phase I > open-label trial in type 1 diabetes, ingested IFN-alpha preserved residual > beta-cell function in recent onset patients. In a second phase I trial, > treatment of rheumatoid arthritis with ingested IFN-alpha reduced the > secretion of interleukin (IL)-1, a pro-inflammatory cytokine. In a third > phase I trial in multiple sclerosis, there was a significant decrease in > peripheral blood mononuclear cell IL-2 and IFN-gamma production after > ingesting IFN-alpha. In a phase II randomized, placebo-controlled, > double-blind trial in multiple sclerosis, 10,000 IU ingested IFN-alpha > significantly decreased gadolinium enhancements compared with the placebo > group at month 5. Tumor necrosis factor-alpha and IFN-gamma cytokine > secretion in the 10,000 IU group at month 5 showed a significant decrease > that corresponded with the effect of ingested IFN-alpha on decreasing > gadolinium enhancements. Ingested IFN-alpha was not toxic in any of these > clinical trials. These studies suggest that ingested IFN-alpha may have a > potential role in the treatment of autoimmunity. > Publication Types: > ? Review > ? Review, Tutorial > PMID: 12486207 [PubMed - indexed for MEDLINE] > J Am Coll Nutr 2002 Dec;21(6):495-505

Response: