Summary:
It is currently unclear what causes the chronic inflammation within atherosclerotic plaques (at least to ignorant doctors).
One emerging paradigm suggests that infection with bacteria and/or viruses can contribute to the pathogenesis of atherosclerosis either via direct infection of vascular cells or via the indirect effects of cytokines or acute phase proteins induced by infection at non-vascular sites (I believe this is much less significant).
This paradigm has been supported by multiple epidemiological studies that have established positive associations between the risk of cardiovascular disease morbidity and mortality and markers of infection.
It has also been supported by experimental studies showing an acceleration of the development of atherosclerosis following infection of hyperlipidaemic animal models.
There are now a large number of different infectious agents that have been linked with an increased risk of cardiovascular disease. These include (in order of priority):
Chlamydia pneumoniae,
Porphyromonas gingivalis,
Helicobacter pylori,
influenza A virus,
hepatitis C virus,
cytomegalovirus, and
human immunodeficiency virus.
Not listed here are spirochetes from a tick bite or periodontal disease, rickettsial infections (Rocky Mountain spotted fever), and toxoplasma gondii.
However, there are significant differences in the strength of the data supporting their association with cardiovascular disease pathogenesis.
In some cases, the infectious agents are found within the plaques, and viable organisms can be isolated, suggesting a direct effect.
and
Electron and immunoelectron-microscopic studies of tissues from affected AD brain regions identified chlamydial elementary and reticulate bodies, but similar examinations of nonAD brains were negative for the bacterium.
Culture studies of a subset of affected AD brain tissues for C. pneumoniae were strongly positive, while identically performed analyses of non-AD brain tissues were negative. Reverse transcription (RT)-PCR assays using RNA from affected AD brain areas confirmed transcripts from two important C. pneumoniae genes were present in those samples but not in controls.
Immunohistochemical examination of AD brains, but not those of controls, identified C. pneumoniae within pericytes, microglia, and astroglia. Further immunolabelling studies confirmed the organisms’ intracellular presence primarily in areas of neuropathology in the AD brain.
Thus, C. pneumoniae is present, viable, and transcriptionally active in areas of neuropathology in the AD brain, possibly suggesting that infection with the organism is a risk factor for late-onset AD.
Here is a link to Dr. Balin's talk on our blog and rumble channel.
Recent observations showed that bacteria, including spirochetes, contain amyloidogenic proteins. Abeta deposition and tau phosphorylation can also be induced in or in vivo following exposure to bacteria or LPS. Bacteria or their poorly degradable debris are powerful inflammatory cytokine inducers, activate complement, affect vascular permeability, generate nitric oxide and free radicals, induce apoptosis and are amyloidogenic. All these processes are involved in the pathogenesis of AD.
Back to the main article summary....
In other cases, the association is entirely based on biomarkers. In the following review, we evaluate the strength of the data for individual or groups of pathogens with regard to atherosclerosis pathogenesis and their potential contribution by direct or indirect mechanisms and discuss whether the established associations are supportive of the infectious disease paradigm.
We also discuss the failure of antibiotic trials and the question of persistent infection.
Lewis: This is a very important concept. You cannot treat "chronic" using "acute" protocols!
Several factors must be considered critically in interpreting the failed trials that suggest infection's role should not be dismissed.
First, the difficulty in treating chronic chlamydial infections is well-documented for both C. trachomatis and C. psittaci (175, 176, 185). These difficulties are due to the developmental cycle of Chlamydia in which the infectious but metabolically inactive form (the elementary body) is not susceptible to antibiotics, and the intracellular replicating form (the reticulate body) can establish persistence. In the persistent state, the developmental cycle is arrested, and the organisms are not susceptible to antibiotics.
Moreover, various antibiotics can induce chlamydial persistence in cell culture (185). In a continuous cell culture model of C. pneumoniae infection, in which aberrant forms characteristic of persistence have been described, prolonged treatment with azithromycin, clarithromycin, or levofloxacin failed to eliminate infection (186).
Lewis comment: with azithromycin, clarithromycin, or levofloxacin - NOTE THE WORD "OR," NOT "AND." Robust studies show that antibiotic combinations, along with risk mitigations, do lower C. pneumoniae.
Unfortunately, there is no clearly defined diagnostic marker of persistent infection.
Lewis comment: Yes, there is a diagnostic marker - or markers: IgG antibody titers for the organism(s) and evaluation of the white blood cell counts with emphasis on neutrophils % and the NLR.
Another key concept within this article:
Evaluations of atherosclerotic plaques from HIV-infected individuals at autopsy revealed extensive lipid deposition and calcification (158),
Lewis: HIV is highly studied. The medical literature supports the same process with these other infectious species. What is that process?
Calcification (hardening) of the vessels occurs because the organisms use (and poop!) calcium.
Lipids are highly concentrated to repair damaged tissue. That is why I have written several blogs on phospholipids. These form the cell membrane structure. With these infections come damaged and destroyed cells that must be rebuilt - thus, the lipids in the area. And the actual cholesterol molecule is the most important repair molecule.
Subcutaneous immunization with Hp-HSP60 or antibiotic treatments significantly reduced atherosclerosis (79).
New Findings: We are seeing a reduction in some of these stealth pathogens with a combination of the Brownstein Protocol and Mega IGG 2000.
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I recommend everyone consider taking mega igg 2000 based on these initial results.
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The test results above truly signify a solid solution. I agree with the Brownstein protocol. I recently implemented high dosages of vitamin A every month. However, I am not sure if I would benefit from taking MegalgG2000. My WBC results are low, the opposite of the person above, but here are some of my lab results…
WBC 3.6
Neutrophils (Absolute) 2.3
Sedimentation Rate 2
Fibrinogen Activity 338