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Trevor G Marshall, PhD, Director, Autoimmunity Research Foundation Thousand Oaks, California
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The authors' statement "furthermore, C pneumoniae, or at least its DNA, is probably carried from the respiratory tract to atherosclerotic lesions by peripheral blood mononuclear cells" is effectively a statement that these bacteria possess an adaptation by which they can overcome phagocytosis. The mechanism by which these bacterium survive in phagocytes, both mature and immature, is key to their survival, and by corollary, to killing them. We too have been trying to understand and kill these intra-phagocytic bacteria, and have been having success. That success comes from two breakthoughs
As we have reported previously[1],[2],[3],[4], we have had success applying the above two pragma when assisting physicians who are treating patients with a variety of chronic disease diagnoses. Patients are recovering from chronic disease including, inter alia, Sarcoidosis, Pulmonary hypertension, Hypertension, Hashimoto's Thyroiditis and Diabetes Type 2. Patients recover after 12-36 months of treatment using antibiotics which symbiotically inhibit protein synthesis by the bacterial 70S Ribosome, along with Angiotensin Receptor Blockade, and control of the synthesis of the secosteroid immune-stimulant 1,25-dihydroxyvitamin-D. It is our experience that no single antibiotic from those cited in this editorial, namely Rifampin, Azithromycin, Gatifloxacin or Clarithromycin has any effect on the intra-phagocytic bacteria causing the diseases we have studied. However, a regime involving control of the two key hormones and inhibition of the 70S Ribosome with judicious use of combinations of Demeclocycline, Minocycline, Azithromycin and Clindamycin is showing itself capable of working miracles against chronic disease. We have not specifically studied Atherosclerosis, although we have shown that patients' general cardiac health returns at the same time as their other chronic diagnoses go into remission.
Competing interests: None declared |
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Jawad M Khan, Specialist Registrar in Cardiology City Hospital, Birmingham, B18 7QH, Timothy J Watson
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The relationship between inflammation, infection and coronary atherosclerosis is complex. Our understanding of this relationship is in it’s infancy, i.e. we are at the beginning of the road and not the end! Markers of inflammation identify subjects who are at high risk of coronary heart disease and acute coronary events (1). However, whether cardiovascular disease is an infectious disease is less clear. A number of infectious agents have been implicated including Helicobacter pylori and Cytomegalovirus, but Chlamydia pneumoniae is by far the most extensively investigated. A number of studies have shown short term benefit from the use of macrolide antibiotics in patients presenting with acute coronary syndromes (2,3). However, these benefits have not been translated to longer term studies, reflecting the multifactorial aetiology of atherosclerosis. Whether the benefits of macrolides are due to their anti- inflammatory properties or due to their anti-chlamydial effects is not clear. If the link between Chlamydia pneumoniae, or other infective agent, and atheroma were confirmed then it would have a substantial effect on antibiotic use. However, inappropriate use of antibiotics would be detrimental in terms of the development of antibiotic resistance. Whether infectious agents are causal or consequential to atheroma, or simply innocent bystanders, needs to be evaluated further and is fertile ground for future research. 1. Ridker PM. On evolutionary biology, inflammation, infection, and the causes of atherosclerosis. Circulation. 2002; 105: 2–4. 2. Gupta S, Leatham EW, Carrington D, et al. Elevated Chlamydia pneumoniae antibodies, cardiovascular events, and azithromycin in male survivors of myocardial infarction. Circulation. 1997; 96: 404-407. 3. Gurfinkel E, Bozovich G, Beck E, et al. Treatment with the antibiotic roxithromycin in patients with acute non-Q-wave coronary syndromes. The final report of the ROXIS Study. Eur Heart J. 1999; 20: 121 -127. Competing interests: None declared |
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Nadaraja Bathirunathan, Visiting Professor Dept.Transfusion Medicine, MGR Medical University, Chennai India
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Microorganisms are probably one of the important agents initiating the atherosclerotic lesion.However we have very little information on when and under what conditions this occurs, to effectively use antibiotics to control cardiovascular disease. There is no reason to consider Chlamydiae pneumoniae as the only etiological agent for this condition.Coliforms,endotoxin or any other inflammatory agent in the local environment can initiate the atherosclerotic plaque, and having initiated need not necessarily continue to remain there for the process to evolve. The antibiotic era has brought us so much of improvement in health and longevity and I beleive antibiotics made a multifactorial contribution to health Competing interests: None declared |
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