Dr. Gordon

[Guest guest]

Note: this is from another group but very interesting so passing it along

There is no question infections are part of CV and, in fact, all chronic diseases had SOME infection contributing to the clinical picture. The idea in this report of prophylactic antibiotics has been tried and always fails for many reasons. ACS 200 is an approach that works against all infections but no acquired resistance to it has been shown with any significant downside. No Argyria has ever been reported with this form of ADVANCED CELLULAR SILVER, which has been shown to kill all pathogens – fungal, viral and microbial even Lyme.Garry F. Gordon MD,DO,MD(H)President, Gordon Research Institutewww.gordonresearch.comhttp://www.medscape.com/viewarticle/714413Exploring the Links Between Infectious Disease and Cardiovascular DiseaseMarilyn W. Edmunds, PhD, CRNP; Laurie Scudder, MS, NPPosted: 01/15/2010Links Between Infectious Diseases and Cardiovascular Disease: A Growing Body of EvidenceCurry K, Lawson LJ Nurse Pract. 2009;5:733-741Article SummaryCardiovascular disease (CVD) is the leading cause of death in industrialized nations. It is widely acknowledged that a systemic inflammatory process is involved in atherogenesis leading to CVD. Several types of microbes have been implicated as causative agents in acquired CVD. This article reviews current and emerging knowledge about the links between specific microorganisms and cardiac vessel and other vascular damage.Inflammatory markers such as C-reactive protein, fibrinogen, tumor necrosis factor alpha, and others can be used to measure systemic inflammation and risk for CVD. Patients with autoimmune diseases characterized by chronic systemic inflammation, such as rheumatoid arthritis and systemic lupus erythematosus, demonstrate a significantly increased risk for CVD. Spirochetes Borrelia burgdorferi (Lyme disease) and Treponema pallidum (syphilis), and flagellated bacteria such as streptococci have well-recognized atherosclerotic potential. Additional studies are beginning to shed light on the possible role played by other bacterial and viral illnesses in the later development of atherosclerosis or other cardiovascular damage.Periodontal disease. Early studies indicated that patients with poor dental health were 1.3 to 1.7 times more likely to experience myocardial infarction than patients with good dental health. Various mechanisms have been explored in an attempt to explain this relationship. Periodontal disease involves inflammation and infection of the supportive structures of the teeth, including soft tissue and bone. Periodontal disease becomes established when plaque accumulation on the teeth induces an inflammatory response. Most adults in the United States have a mild form of periodontal disease, but 20% to 30% of adults have more severe forms. The main mechanism postulated in the subsequent development of CVD is that the chronic local infection characteristic of periodontitis increases the levels of systemic inflammatory chemicals. The increased presence of these inflammatory mediators promotes atherosclerosis. Periodontal disease may be an independent or contributing risk factor for CVD. Not all studies have found a causal link, and further studies are needed to determine the extent of the relationship and whether outcomes are improved through preventive dental care.Chlamydia pneumoniae. C pneumoniae is a very common respiratory pathogen. About 50% of adults in the United States have been infected with C pneumoniae by age 20 and re-infection is common, because the organism is ubiquitous. Although a causative role has not been firmly established, C pneumoniae has been detected in atherosclerotic plaques.Helicobacter pylori. H pylori is a known causal agent of several gastrointestinal diseases and has also been implicated in ischemic heart disease. It is speculated that H pylori may act directly on atherosclerotic plaques because studies have found its DNA in arterial plaque. Another thought is that H pylori infection has indirect effects related to chronic inflammation, and long-term inflammation raises circulating cytokine levels. Thus, H pylori might serve as a trigger for the inflammatory cascade. Other studies suggest that H pylori may induce platelet aggregation and thereby play a role in the acute phase of ischemic heart disease.Virus-related CVD. Several viruses have been shown to affect the heart. These include the adenoviruses, sackie viruses, hepatitis A virus, and herpes simplex viruses. The adenoviruses can cause myocarditis but do not appear to have a role in CVD. The sackie B viruses are known to cause myocarditis, but the relationship to CVD is unconfirmed. Hepatitis A virus might contribute to CVD by eliciting a chronic inflammatory response. Herpes simplex virus 1 and herpes simplex virus 2 have been found in human atherosclerotic plaque. Studies of cytomegalovirus have shown that it has both positive and negative associations with coronary artery disease.The role of antibiotics in prevention and treatment. A number of clinical trials have been undertaken to determine whether antibiotics might play a role in the primary prevention of cardiac events or in secondary prevention once a cardiac events has occurred. The early studies in humans seemed to indicate that prophylactic antibiotics might lead to reductions in secondary cardiovascular events in patients with stable coronary heart disease and those with acute coronary syndrome.Primary and secondary prevention. Multiple complex processes are involved in the development of CVD. Currently, no specific guidelines exist for general preventive measures related to infectious diseases as a specific causal factor for CVD. Indeed, some authors still debate the sequence of events and question whether chronic inflammation might predispose some individuals to infection rather than vice versa.ViewpointGiven the lack of clarity linking infectious disease as a causative factor in CVD, clinicians should also consider what would be the cost of giving antibiotics prophylactically to individuals, and whether the increased antibiotic resistance and adverse drug reactions would be worth the chance of reducing cardiovascular disease. The current take-away lessons from this new area of research seem few. Good dental hygiene, particularly prior to surgery, might be the only thing conclusively agreed upon to date.

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[Guest guest]

I think silver is a wonderful product, but when asked, I

always say to use it for ear/nose/throat applications, and particularly for use

with a nebulizer, which makes it a very powerful and economical assist to

anything in the lungs. The reasoning being that we don’t really

know what silver will bind to in the salty internal environment, but being anti

inflammatory, phlegm (the main thing we notice from the immune system having a

response in the lungs), and having such obvious and immediate relief for

bronchial situations, it takes a large load off the immune system so it can

concentrate on other things.

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