- For Patients
- Introduction to the Marshall Protocol
- Length of the MP
- Immunopathology
- Managing immunopathology
- Food and drink
- Light restriction
- Vitamin D metabolite calculator - get feedback on vitamin D results
- Therapeutic probe - best method for determining MP suitability
- Starting the Marshall Protocol
- Resources for patients
- Marshall Protocol summary
- Palliative vs. curative treatments
- Patient interviews on Bacteriality
- Non-MP treatments
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- Science behind immunopathology
- Science behind olmesartan (Benicar)
- Safety of olmesartan
- Resources for physicians
- Vitamin D metabolite calculator - get feedback on vitamin D results
- Therapeutic probe - best method for determining MP suitability
- Physicians' concerns about the MP
- Notice for emergency medical personnel
- The Pathogenesis
- Publications and presentations
- Science behind Marshall Pathogenesis
- Microbes in the human body
- Successive infection and variability in disease
- Autoimmune theory of disease
- Science behind vitamin D
- Metabolism of vitamin D and the VDR
- Th1 Spectrum Disorder - how chronic inflammatory diseases are related
- Transmission of bacteria and onset of chronic disease
- Evolutionary perspective on disease
- Incidence and prevalence of disease
- Evidence that chronic disease is caused by pathogens
- Diseases
- Foundation
- Related Sites
Differences
This shows you the differences between two versions of the page.
| Both sides previous revisionPrevious revisionNext revision | Previous revisionNext revisionBoth sides next revision | ||
| home:starting:physician:reluctant [04.29.2019] – [Read more] sallieq | home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq | ||
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| - | Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.(in rat)(({{pubmed> | + | Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.[in rat](({{pubmed> |
| Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (({{pubmed> | Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (({{pubmed> | ||
| Line 209: | Line 209: | ||
| - | 6 mg/kg olmesartan reduces the inflammatory process and bone loss in rats (({{pubmed> | + | 6 mg/kg olmesartan reduces the inflammatory process and bone loss [in rats] (({{pubmed> |
| + | |||
| + | Olmesartan at a dose of 10 mg/kg prevented the mucosal damage and inflammation associated with 5-FU-induced OM, increasing granulation and tissue repair. [in hamsters] (({{pubmed> | ||
| Line 272: | Line 274: | ||
| the volume of larger atherosclerotic plaques (({{pubmed> | the volume of larger atherosclerotic plaques (({{pubmed> | ||
| + | Observations suggest a positive role in a potentially lower rate of coronary atheroma progression through the administration of olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris. | ||
| + | |||
| + | This study showed that olmesartan reduces angiotensin II and aldosterone levels more effectively than azilsartan. | ||
| improvement of Plasma Biomarkers after switching stroke patients from other Angiotensin II Type I Receptor Blockers to Olmesartan (({{pubmed> | improvement of Plasma Biomarkers after switching stroke patients from other Angiotensin II Type I Receptor Blockers to Olmesartan (({{pubmed> | ||
home/starting/physician/reluctant.txt · Last modified: 09.14.2022 by 127.0.0.1
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