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home:othertreatments:antibacterials:highdose [03.06.2011] – external edit 127.0.0.1 | home:othertreatments:antibacterials:highdose [09.14.2022] (current) – external edit 127.0.0.1 | ||
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The absence of inflammation is undoubtedly one of the principal reasons why patients report feeling better on high-dose antibiotics. It is also why the guidelines for the Marshall Protocol recommend doses of antibiotics low enough to avoid the problem of uninterrupted immunosuppression. The presence of a sustained immunopathological response is evidence that the MP uses antibiotics in such a way that it does not suppress the immune system. | The absence of inflammation is undoubtedly one of the principal reasons why patients report feeling better on high-dose antibiotics. It is also why the guidelines for the Marshall Protocol recommend doses of antibiotics low enough to avoid the problem of uninterrupted immunosuppression. The presence of a sustained immunopathological response is evidence that the MP uses antibiotics in such a way that it does not suppress the immune system. | ||
- | Note that formulations which keep antibiotic concentrations at artificially high concentrations such as extended-release minocycline(({{pubmed> | + | Note that formulations which keep antibiotic concentrations at artificially high concentrations such as extended-release minocycline(({{pmid> |
==== Mechanisms of immunosuppression ==== | ==== Mechanisms of immunosuppression ==== | ||
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Moreover, pre-exposure to agents that selectively inhibit protein synthesis (30S or 50S subunit inhibitors) or DNA metabolism (DNA gyrase) mitigated subsequent tPMP-1 [an antimicrobial peptide] induced killing of an otherwise susceptible //S. aureus// strain in vitro. | Moreover, pre-exposure to agents that selectively inhibit protein synthesis (30S or 50S subunit inhibitors) or DNA metabolism (DNA gyrase) mitigated subsequent tPMP-1 [an antimicrobial peptide] induced killing of an otherwise susceptible //S. aureus// strain in vitro. | ||
- | // | + | // |
</ | </ | ||
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< | < | ||
- | [[http:// | + | [[https:// |
* **Activation of the PXR Nuclear Receptor** – Minocycline [[home: | * **Activation of the PXR Nuclear Receptor** – Minocycline [[home: | ||
==== Curing disease by reducing inflammation? | ==== Curing disease by reducing inflammation? | ||
- | The immunosuppressive properties of antibiotics have been long known. Labro states that the tetracycline family of antibiotics – four of which are a part of the MP's guidelines – are desirable because they inhibit " | + | The immunosuppressive properties of antibiotics have been long known. Labro states that the tetracycline family of antibiotics – four of which are a part of the MP's guidelines – are desirable because they inhibit " |
To that end, most researchers have assumed, consistent with the autoimmune theory of disease, that using antibiotics to reduce immune activity would improve disease. | To that end, most researchers have assumed, consistent with the autoimmune theory of disease, that using antibiotics to reduce immune activity would improve disease. | ||
- | On the basis of this understanding, | + | On the basis of this understanding, |
- | One study compared the use of hydroxychloroquine (Plaquenil) to minocycline in early seropositive rheumatoid arthritis patients.(({{pubmed> | + | One study compared the use of hydroxychloroquine (Plaquenil) to minocycline in early seropositive rheumatoid arthritis patients.(({{pmid> |
Indeed, a number of studies have been able to demonstrate the " | Indeed, a number of studies have been able to demonstrate the " | ||
- | One telling study looking at tetracycline' | + | One telling study looking at tetracycline' |
< | < | ||
- | **//M.T. Labro//** (({{pubmed> | + | **//M.T. Labro//** (({{pmid> |
- | Earlier on in the paper, Labro concludes that when it comes to treating inflammatory diseases, immunosuppression is " | + | Earlier on in the paper, Labro concludes that when it comes to treating inflammatory diseases, immunosuppression is " |
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===== High-dose clarithomycin is ineffective ===== | ===== High-dose clarithomycin is ineffective ===== | ||
- | In a 2006 trial appearing in //BMJ// (nicknamed the CLARICOL trial), 13,702 patients with a history of myocardial infarction or angina pectoria (chest pain) were given two weeks' treatment with clarithromycin 500 mg/day or matching placebo. Mortality was significantly higher in the clarithromycin arm as a result of significantly higher cardiovascular mortality. The authors concluded: "Short term clarithromycin in patients with stable coronary heart disease may cause significantly higher cardiovascular mortality. The long term safety of clarithromycin in patients with stable ischaemic heart disease should be examined." | + | In a 2006 trial appearing in //BMJ// (nicknamed the CLARICOL trial), 13,702 patients with a history of myocardial infarction or angina pectoria (chest pain) were given two weeks' treatment with clarithromycin 500 mg/day or matching placebo. Mortality was significantly higher in the clarithromycin arm as a result of significantly higher cardiovascular mortality. The authors concluded: "Short term clarithromycin in patients with stable coronary heart disease may cause significantly higher cardiovascular mortality. The long term safety of clarithromycin in patients with stable ischaemic heart disease should be examined." |
These results are consistent with the explanation that immunosuppressive therapies exacerbate inflammatory diseases. | These results are consistent with the explanation that immunosuppressive therapies exacerbate inflammatory diseases. | ||
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- | Fallon //et al// treated patients diagnosed with Lyme disease with intravenous ceftriaxone (Rocephin) for a period of 24 weeks.(({{pubmed> | + | Fallon //et al// treated patients diagnosed with Lyme disease with intravenous ceftriaxone (Rocephin) for a period of 24 weeks.(({{pmid> |
< | < | ||
- | //**B.A. Fallon,** et al.// (({{pubmed> | + | //**B.A. Fallon,** et al.// (({{pmid> |
The study also revealed that more than one quarter of antibiotic-treated patients had significant adverse effects necessitating treatment termination. | The study also revealed that more than one quarter of antibiotic-treated patients had significant adverse effects necessitating treatment termination. | ||
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< | < | ||
- | //**John J. Halperin MD**// (({{pubmed> | + | //**John J. Halperin MD**// (({{pmid> |
- | Other controlled trials have found no improvement in treatment outcome when the length of the study was extended.(({{pubmed> | + | Other controlled trials have found no improvement in treatment outcome when the length of the study was extended.(({{pmid> |
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< | < | ||
- | //**Ken L.**, [[http:// | + | //**Ken L.**, [[https:// |
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===== Read more ===== | ===== Read more ===== | ||
- | * [[http:// | + | * [[https:// |
- | {{tag>antibiotics}} | + | {{tag>Other_medication}} |
+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
- | EDIT | + | |
*Legacy content | *Legacy content | ||
* f271 | * f271 | ||
- | ===== References ===== | + | |
+ | < | ||
+ | |||
+ | topof page | ||
+ | Abstract | ||
+ | |||
+ | Antibiotics have been used effectively as a means to treat bacterial infections in humans and animals for over half a century. However, through their use, lasting alterations are being made to a mutualistic relationship that has taken millennia to evolve: the relationship between the host and its microbiota. Host–microbiota interactions are dynamic; therefore, changes in the microbiota as a consequence of antibiotic treatment can result in the dysregulation of host immune homeostasis and an increased susceptibility to disease. A better understanding of both the changes in the microbiota as a result of antibiotic treatment and the consequential changes in host immune homeostasis is imperative, so that these effects can be mitigated. | ||
+ | </ | ||
+ | ===== References =====</ |