We now know that CP (Chlamydophila pneumoniae) can persist intracellularly in a cryptic and arrested state, that cannot be cultured, is immunologically muted, and becomes resistant to antibiotics.
By 2011, there was 1635 published research on CP as a mechanism of heart disease. Since nothing much can be done to treat CP that lodged inside the wall of the blood vessel the interest and new ideas to treat is not developed. However, chelation therapy has the understood mechanism to bind metal ion.
Atherosclerosis is Successfully Treated with EDTA Chelation Therapy
intravenous EDTA chelation therapy was recently shown to be of marked benefit in atherosclerotic heart disease, which suggests a new approach to CP research.
The reversal of atherosclerosis observed long after finished intensive treatment renders the mechanism of action by EDTA chelation requires more research to understand the mechanism. It is theorized in this paper that benefit from EDTA results from an action against CP.
CP as a cause of atherosclerosis can at least partially be explained by metallo-proteins that are created or upregulated by CP.
A $30 million, NIH funded clinical trial of intravenous EDTA chelation therapy has shown success in treatment of atherosclerotic cardiovascular disease. [5,6] In that “Trial to Assess Chelation Therapy (TACT),” the composite primary endpoint was death, reinfarction, stroke, coronary revascularization, or hospitalization for angina.
In that “Trial to Assess Chelation Therapy (TACT),” the composite primary endpoint was death, reinfarction, stroke, coronary revascularization, or hospitalization for angina. A total of 1,708 post-myocardial infarction patients who were 50 years or older received 55,222 infusions of either disodium EDTA or placebo, with a median follow-up of 55 months.
A total of 1,708 post-myocardial infarction patients who were 50 years or older received 55,222 infusions of either disodium EDTA or placebo, with a median follow-up of 55 months.
Doubtful that Removal of Xenobiotic Metals is the EDTA Mechanism
The currently favored explanation for benefit in atherosclerosis is by removal of xenobiotic metallic toxins (toxic heavy metals). Provoked excretion of toxic metals following chelation is no greater in healthy control subjects, when compared with patients suffering atherosclerotic cardiovascular disease.
All metals are potentially toxic, even essential nutrients. Essential nutritional metals also become toxic when maldistributed within the body (i.e., intracellular calcium or sodium). There commonly exists a narrow margin between optimal and toxic levels for metals. A two or three fold increase can be toxic.
The Table below is taken from data published in the TEXTBOOK ON EDTA CHELATION THERAPY,  showing that EDTA chelation has a much greater impact on a number of essential nutritional metals, compared with known toxins.. These data suggest that chelation of essential nutritional elements might be more important for benefit from EDTA than action on toxic, xenobiotic metals.
Chlamydia as a Cause of Cardiovascular Disease
Many published studies have linked CP to atherosclerosis.[1-4]
90% or more of the adult population eventually become infected with CP. The incidence of infection Increases with age, parallel to the age-related incidence of atherosclerosis.
Evidence exists that CP remains in the body for decades, perhaps throughout life, in a low-grade inflammatory but the partially dormant state, much like Varicella virus.
Although classified as a bacterium, CP has many characteristics of a virus. It is an obligate, aerobic, intracellular, gram negative organism with a unique growth cycle of multiple stages.
Like a virus, CP hijacks the energy metabolism of host cells for survival and replication.
The initial acute phase of CP infection commonly lasts only a week or two, and is mainly respiratory. It can be relatively mild or even unsuspected, following which the organism migrates throughout the body in monocytes (macrophages). It then hibernates, as inert, cryptic, and immunologically attenuated intracellular inclusions. These inclusions are persistent and remain potentially infective if reactivated. They hide away for decades, possibly a lifetime, as chronic, low-grade, lingering infections. Traditional risk factors for atherosclerosis may trigger reactivation. Atherosclerosis develops slowly, perhaps as host responses to sustained low-grade infection and inflammation.
EDTA Chelation Has Anti-Chlamydia Properties
The slow, chronic, long-term, multiphasic, and variable nature of intravascular CP prevents the use of Koch’s postulates, despite the infectious nature of this disease. Traits of CP leading to atherosclerosis require the presence of metal cofactors, that can be bound and inactivated by EDTA.
Anti-Chlamydia properties of EDTA could reduce plaque turbulence and size, and stabilize plaque against disruption.
CP most often enters the body through the lungs. Smoking inhibits lung defenses increasing the risk of CP. Perhaps that is a reason why smoking is a risk factor for atherosclerosis.
EDTA removes calcium from plaque, which might make CP inclusions more vulnerable to host defenses, in addition to increasing lumen diameter.
CP needs iron for survival. Atherosclerosis is associated with increased iron levels. EDTA strongly chelates iron. The Chlamydia growth cycle can be disrupted by iron chelation, using deferoxamine, an iron chelator.  EDTA is also a strong iron chelator.
EDTA chelation therapy requires many slow, infusions, lasting hours, with 30 or more infusions, requiring several months to achieve good benefit. Full improvement takes several more months following the last infusion. Any proposed mechanism of action must take this delay into consideration. If effects of CP are reduced, full healing of infected tissues could require such time.
Although EDTA remains mostly extracellular, a powerful extracellular-to-intracellular diffusion gradient is created during the infusion.
Bits and pieces to Think About
- CP is speculated to initiate inflammatory scarring of artery walls, which could evolve into plaque.
- CP induces macrophages to become the type of foam cells associated with plaque formation.
- CP causes lipid accumulations as found in plaque.
- CP is lipophilic.
- CP oxidizes LDL cholesterol.
- CP releases a variety of metalloproteins that can disrupt tissues.
- CP may facilitate plaque rupture.
- CP releases inflammatory “shock proteins” and a cytokine cascade that can disrupt host tissues.
- CP is believed by some investigators to trigger a coagulation cascade, causing local hypercoagulability and thrombosis.
- CP growth cycles have been reported to be inhibited by statin drugs, unrelated to cholesterol.
- CP upregulates production of metallo-proteinases in atheromas increasing the risk of plaque rupture.
- CP disrupts apoptosis of smooth muscle cells in vascular walls.
- CP has been reported to cause thinning of fibrous caps on plaque facilitating rupture.
- CP can cause tissue calcification and fibrosis as found in plaques. It is further speculated that Chlamydia-specific bacteriophage activity might genetically alter the host expression of this organism.
Chlamydia Research is Needed Relative To Effects of EDTA
It is hoped that microbiologists will find a way to investigate this theory further.
Miscellaneous Background Information
CP has been implicated in many other chronic or autoimmune diseases, which could explain why so many different conditions have been reported anecdotally to improve following EDTA chelation therapy.