Tracking the next pandemic: Avian Flu Talk |
Evidence Based Alternative Treatments for H5N1 |
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Jhetta
Valued Member Joined: March 28 2006 Status: Offline Points: 1272 |
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Posted: May 23 2006 at 9:37pm |
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http://www.med-owl.com/herbal-antivirals/tiki-index.php?page=H5N1+Avian+Flu
Somewhat backed by research
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I would say their research is flawed.
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Jhetta
Valued Member Joined: March 28 2006 Status: Offline Points: 1272 |
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I have decided against using any Elderberry products bases on the "limited info" I have found showing they could increase inflammatory cytokines.
Here is a link that to an animation that explains how H5N1 induces a Cytokins Storm.
Comment in: The effect of herbal remedies on the production of human inflammatory and anti-inflammatory cytokines. Barak V, Birkenfeld S, Halperin T, Kalickman I. Immunology Laboratory for Tumor Diagnosis, Department of Oncology, Hadassah University Hospital, Jerusalem, Israel. barak845@yahoo.com BACKGROUND: Some herbal remedies are sold as food additives and are believed to have immune-enhancing properties. OBJECTIVES: To study the effect of five herbal remedies--Sambucol Black Elderberry Extract, Sambucol Active Defense Formula and Sambucol for Kids (with known antiviral properties), Protec and Chizukit N (containing propolis and Echinacea, claimed to be immune enhancers)--on the production of cytokines, one of the main components of the immune system. METHODS: The production of four inflammatory cytokines (interleukin-1 beta, tumor necrosis factor alpha, and IL-6 and IL-8) and one anti-inflammatory cytokine (IL-10) was tested using blood-derived monocytes from 12 healthy donors. RESULTS: The Sambucol preparations increased the production of five cytokines (1.3-6.2 fold) compared to the control. Protec induced only a moderate production of IL-8 (1.6 fold) and IL-10 (2.3 fold) while Chizukit N caused only a moderate increase in IL-10 production (1.4 fold). Both Protec and Chizukit N caused moderate decreases in IL-1 beta, TNF alpha and IL-6 production. Lipopolysaccharide, a known activator of monocytes, induced the highest levels of cytokine production (3.6-10.7 fold). CONCLUSIONS: The three Sambucol formulations activate the healthy immune system by increasing inflammatory and anti-inflammatory cytokines production, while the effect of Protec and Chizukit N is much less. Sambucol could therefore have immunostimulatory properties when administered to patients suffering from influenza (as shown before), or immunodepressed cancer or AIDS patients who are receiving chemotherapy or other treatments. PMID: 12455180 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16283933&query_hl=15&itool=pubmed_docsum
Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells. Chan MC, Cheung CY, Chui WH, Tsao SW, Nicholls JM, Chan YO, Chan RW, Long HT, Poon LL, Guan Y, Peiris JS. Department of Microbiology, The University of Hong Kong, Queen Mary Hospital, Hong Kong Special Administrative Region of China. mchan@hkucc.hku.hk BACKGROUND: Fatal human respiratory disease associated with influenza A subtype H5N1 has been documented in Hong Kong, and more recently in Vietnam, Thailand and Cambodia. We previously demonstrated that patients with H5N1 disease had unusually high serum levels of IP-10 (interferon-gamma-inducible protein-10). Furthermore, when compared with human influenza virus subtype H1N1, the H5N1 viruses in 1997 (A/Hong Kong/483/97) (H5N1/97) were more potent inducers of pro-inflammatory cytokines (e.g. tumor necrosis factor-a) and chemokines (e.g. IP-10) from primary human macrophages in vitro, which suggests that cytokines dysregulation may play a role in pathogenesis of H5N1 disease. Since respiratory epithelial cells are the primary target cell for replication of influenza viruses, it is pertinent to investigate the cytokine induction profile of H5N1 viruses in these cells. METHODS: We used quantitative RT-PCR and ELISA to compare the profile of cytokine and chemokine gene expression induced by H5N1 viruses A/HK/483/97 (H5N1/97), A/Vietnam/1194/04 and A/Vietnam/3046/04 (both H5N1/04) with that of human H1N1 virus in human primary alveolar and bronchial epithelial cells in vitro. RESULTS: We demonstrated that in comparison to human H1N1 viruses, H5N1/97 and H5N1/04 viruses were more potent inducers of IP-10, interferon beta, RANTES (regulated on activation, normal T cell expressed and secreted) and interleukin 6 (IL-6) in primary human alveolar and bronchial epithelial cells in vitro. Recent H5N1 viruses from Vietnam (H5N1/04) appeared to be even more potent at inducing IP-10 than H5N1/97 virus. CONCLUSION: The H5N1/97 and H5N1/04 subtype influenza A viruses are more potent inducers of proinflammatory cytokines and chemokines in primary human respiratory epithelial cells than subtype H1N1 virus. We suggest that this hyper-induction of cytokines may be relevant to the pathogenesis of human H5N1 disease. PMID: 16283933 [PubMed - indexed for MEDLINE] |
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Jhetta
Valued Member Joined: March 28 2006 Status: Offline Points: 1272 |
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Note: No supporting evidence
A nutritional supplement formula for influenza A (H5N1) infection in humans.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16624496&query_hl=15&itool=pubmed_docsum
Friel H, Lederman H. 32 Paradise Road, Northampton, MA 01060, USA. By early February 2006, the World Health Organization had reported 165 human cases of H5N1 influenza since December 2003, with 88 fatalities. However, the avian H5N1 influenza virus apparently is not yet efficiently transmitted between humans. Though a near-term possibility of a global H5N1 influenza pandemic remains, currently there is no vaccine or anti-viral drug that is proven to be safe and effective in preventing or treating H5N1 influenza in humans. There is thus a compelling public interest in developing alternative prophylaxis and treatment strategies for H5N1 influenza, which would need to address the complex pathogenesis of H5N1 influenza that is responsible for its apparently unusually high virulence. The authors present here a significant body of medical and scientific evidence to support the prophylactic use of a carefully designed nutritional supplement formulation that may antagonize the major pathogenic processes of H5N1 influenza in humans. Through several independently-mediated mechanisms, the formulations may: (a) degrade H5N1 virulence by directly affecting the virus itself, (b) inhibit H5N1 viral replication by maintaining cellular redox equilibrium in host cells, (c) inhibit H5N1 replication by a blockade of the nuclear-cytoplasmic translocation of the viral ribonucleoproteins and reduced expression of late viral proteins related to the inhibition of protein kinase C activity and its dependent pathways, (d) down-regulate activation and proliferation of proinflammatory cytokines in respiratory epithelial cells and macrophages that are implicated in the pathogenesis of H5N1 influenza, and (e) protect the lungs and other vital organs from virus- and cytokine-induced oxidative stress by supplying and maintaining sufficient levels of exogenous and endogenous antioxidants. Key mediators in these processes include selenium, vitamin E, NAC/glutathione, resveratrol, and quercetin. Taken prophylactically, and throughout the duration and recovery of an H5N1 infection, the nutritional supplement formula may aid humans infected with H5N1 influenza to survive with a reduced likelihood of major complications, and may provide a relatively low-cost strategy for individuals as well as government, public-health, medical, health-insurance, and corporate organizations to prepare more prudently for an H5N1 pandemic. Some evidence also indicates that the supplement formulation may be effective as an adjunctive to H5N1 vaccine and anti-viral treatments, and should be tested as such. PMID: 16624496 [PubMed - as supplied by publisher] |
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This is NOT and endorsement of the use of this herb.
Macrophages. Alveolar macrophages are the principal immune-effector cells in the lung and are primarily responsible for protecting the lung against infectious microorganisms, inhaled foreign substances, and tumor cells. They are increased during tissue inflammation. In a large sample of volunteers, habitual marijuana smokers had twice as many alveolar macrophages as nonsmokers, and smokers of both marijuana and tobacco had twice as many again.11 Marijuana smoking also reduced the ability of alveolar macrophages to kill fungi, such as Candida albicans;3 pathogenic bacteria, such as Staphylococcus aureus; and tumor target cells. The reduction in ability to destroy fungal organisms was similar to that seen in tobacco smokers. The inability to kill pathogenic bacteria was not seen in tobacco smokers.10 Furthermore, marijuana smoking depressed production of proinflammatory cytokines, such as TNF-I and IL-6, but not of immunosuppressive cytokines.10 Cytokines are important regulators of macrophage function, so this marijuana-related decrease in inflammatory cytokine production might be a mechanism whereby marijuana smokers are less able to destroy fungal and bacterial organisms, as well as tumor cells.
The inability of alveolar macrophages from
habitual marijuana smokers without apparent disease to destroy fungi,
bacteria, and tumor cells and to release proinflammatory cytokines,
suggests that marijuana might be an immunosuppressant with clinically
significant effects on host defense. Therefore, the risks of smoking
marijuana should be seriously weighed before recommending its use in
any patient with preexisting immune deficits--including AIDS patients,
cancer patients, and those receiving immunosuppressive therapies (for
example, transplant or cancer patients). any comments? |
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Jhetta
Valued Member Joined: March 28 2006 Status: Offline Points: 1272 |
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New evidence of cytokine storm in avian flu cases
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