The ROOT of the problem is the fact that Bb seriously depletes magnesium and this spirals out of control. This metalloprotease (Bb) uses Mg in its enzyme reactions as stated by microbiologist, Dr. Gary Kaiser.
Furthermore, according to the recent research out of Romania, it appears to SIGNIFICANTLY reduce the avail. amt. of Mg very fast. The % decrease is astounding.
Restoring the normal level of Mg while giving abx. did cure the 2 Romanian patients (see abstract under "If this doesn't convince you". Why? Lots of reasons, but here is a "technical" explanation:
"To justify this prediction you have to scan back to the factors which effect the rate of the reaction, there it says at a higher concentration of an Acid there is more Hydrogen ions amiable to react with the Magnesium atoms than at a lower concentration.
This can be summed up simply in that at a higher concentration there is more Hydrogen ions present so more collisions occur therefore reaction takes less time."
http://www.coursework.info/i/67.html
By giving (acidic) abx. ALONG with a significant amt. of Mg. -> hydrogen.
"Magnesium helps the body convert vitamin D--which the body needs to take advantage of bone-strengthening calcium--into a form that it can use efficiently. By contributing to increased bone density, the mineral may help stall the onset of the debilitating, bone-thinning disease known as osteoporosis."
http://www.wholehealthmd.
com/refshelf/substances_
view/1,1525,890,00.html
Not enough Mg to convert vit D perhaps.
Scott, you did not respond to this abstract, why?
: J Hypertens. 1993 May;11(5):551-8. Related Articles, Links
The effect of angiotensin II on platelet intracellular free magnesium and calcium ionic concentrations in essential hypertension.
Touyz RM, Schiffrin EL.
Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.
OBJECTIVE: To assess the effects of angiotensin II on intracellular free Mg2+ and Ca2+ concentrations in platelets from normotensive and hypertensive subjects.
DESIGN AND METHODS: Seventeen normotensive, 25 untreated hypertensive and 18 treated hypertensive patients were studied. Intracellular Mg2+ concentrations were measured with the fluorescent dye mag-fura-2-acetyoxymethylester (AM) and intracellular Ca2+ concentrations with the fluorescent dye fura-2AM under basal conditions and after stimulation by angiotensin II, saralasin (angiotensin II antagonist), arginine vasopressin and endothelin-1.
The effects of increased extracellular Mg2+ concentrations on intracellular Mg2+ and Ca2+ concentrations were also determined.
RESULTS: The intracellular basal Ca2+ concentration was significantly higher in the untreated hypertensives compared with the normotensives and treated hypertensive subjects (150 +/- 14 nmol/l versus 120 +/- 17 nmol/l for normotensives and 124 +/- 8 nmol/l for treated hypertensives).
The basal intracellular Mg2+ concentration was significantly lower in the untreated hypertensive compared to the normotensive and treated hypertensive groups (0.37 +/- 0.08 mumol/l versus 0.58 +/- 0.09 mumol/l for normotensives and 0.52 +/- 0.11 mumol/l for treated hypertensives). In the hypertensive groups, inverse correlations were found between intracellular Ca2+ and intracellular Mg2+ concentrations (r = -0.44, P < 0.05) and between intracellular Mg2+ and diastolic blood pressure (r = -0.35, P < 0.05), while a positive correlation was found between intracellular Ca2+ and systolic blood pressure (r = 0.41, P < 0.05).
Exposure of the platelets to 1 nmol/l angiotensin II significantly increased intracellular Ca2+ and significantly decreased intracellular Mg2+ concentrations in all three groups. The angiotensin II-evoked effect on intracellular Ca2+ was exaggerated in the untreated hypertensives and blunted in the treated patients (basal versus stimulated: 150 +/- 14 versus 217 +/- 20 nmol/l in untreated hypertensives; 124 +/- 8 versus 140 +/- 10 nmol/l in treated hypertensives).
Saralasin (0.1 mumol/l) abolished the effects of angiotensin. Arginine vasopressin (1 mumol/l) increased the intracellular Ca2+ concentration, whereas endothelin-1 (1 nmol/l) had no significant effect on either intracellular Ca2+ or intracellular Mg2+.
Increasing extracellular Mg2+ concentrations led to significant reductions in intracellular Ca2+ concentrations in all groups and a significant elevation of the intracellular Mg2+ concentration in the untreated hypertensive patients only.
CONCLUSIONS: These data demonstrate a relationship between angiotensin II and intracellular magnesium and calcium. In hypertension, angiotensin II-stimulated calcium responses may be related to simultaneously decreased intracellular magnesium concentrations.
PMID: 8390527