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Time for a repeat.
Lyme disease and magnesium deficiency
V. CRISTEA - Department of Immunopathology, Medical Clinic III, "Iuliu Hatieganu" University of Medicine and Pharmacy, MONICA CRIAN - Department of Immunology, "Ion Chiricu" Oncological Institute, Cluj-Napoca, Romania
During the period April 2001 - January 2003, we had under observation two cases, in which the presence of both IgM and IgG antibodies to Borrelia burgdorferi was serologically confirmed at high titers.
In both cases, clinical manifestations were similar: shivering, fever, headache, articular and right hypochondrium pain, and objectively - tachycardia and erythema migrans - these elements being important for the formulation of Lyme disease suspicion.
Humoral tests showed: significantly increased ESR, leukocytosis with PMN predominance, intensely positive PCR (for B. Burgdorferi DNA)
and significant magnesium deficiency (1.20 mEq/L, 1.33 mEq/L, respectively).
A large spectrum of antibiotics with both oral and parenteral administration has been so far used in the treatment of Lyme borreliosis. Among the most frequently used are tetracyclines, betalactamides and cephalosporins.
The decision to initiate antibiotic therapy can be difficu1t because in the majority of the cases acute infection is self-limited. Asymptomatic patients, in whom laboratory examinations sustain the diagnosis of Lyme disease, should be treated in order to prevent rnfection dissemination.
Since in the first case antibiotic therapy alone
did not lead to the expected results, magnesium derivatives ***were also associated**.
In both cases, following combined therapy, symptomatology significantly improved at 14 days, and laboratory examinations were restored to normal values after 6-8 weeks - disappearance of IgM to B. Burgdorferi and significantly increased magnesemia (1.74 mEq/L, 1.72 mEq/L, respectively)
We believe that in certain diseases, Mg deficiency can cause a decrease in immune response.
The appearance of recurrences, which are frequently reported in the literature, in spite of adequate antibiotic therapy, could represent an argument for this.
This is why the use of Mg derivatrves in therapy can represent an immunostimulating factor. The peculiarities of the cases are the following:
1. Patients had in addition to fever, articular pain and erythema migrans, Mg deficiency
2. The supplementation of therapy with Mg derrvatives had an immediate beneficial effect that was maintained in time.
As a conclusion at this stage, we consider that in the acute phase of Lyme borreliosis there is a significant Mg consumption and the introduction in therapy of such preparations is recommended and beneficial."
The "cure" for lyme appears to be 2 fold:
Destroy the pathogen AND restore Mg levels which are very very low (do the math).
Abx + MgCl
"Electromagnetic" therapies + MgCl
Benicar(?) + MgCl
Mg (and Ca) restored the "health of our own antibody to Bb's OspB:
Characterization of the physiological requirements for the bactericidal effects of a monoclonal antibody to OspB of Borrelia burgdorferi by confocal microscopy.
The bactericidal effect of Fab-CB2 is not dependent on the induction of spirochetal proteases but is dependent on the presence of Ca2+ and Mg2+.
Supplementation of Ca2(+)- and Mg2(+)-free medium with these cations ***restored the bactericidal effects of Fab-CB2.***
The mechanism by which a Fab fragment of an antibody destroys a bacterium directly may represent a novel form of antibody-organism interaction.
See the need to increase Ca (block it's exit i.e., close the TRPM8 channel) AND increase Mg.
A ``novel form of antibody-organism interaction?'' I don't THINK so!
E. Required by immunological process.
Magnesium, immunity, and allergy: Mg is required for several steps of immunological reactions
1. Lymphoblastic transformation, a prerequisite of secretion of antibodies by lymphoblasts, requires Ca2+ and Mg2+
2. Mg is required for synthesis of proteins, immunoglobulins included
3. Antibody-induced complement activation is Mg dependent
4. The antigen-immunoglobulin-complement reaction induces degranulation of the mastocyte