I made a mistake a long time ago in my original updated nutshell post...I thought low Mg triggered Calcium influx, triggered angiotensin II, triggered TNF alpha (which I thought was alkaline. It is not.).
The correction follows:
Low Mg triggers calcium influx triggers TNF alpha (protein, neg charge) and TNF alpha triggers angiotensin ( a hormone, protein also).
Now we KNOW that statin drugs (Benicar high doses...kidney caution) OR Magnesium INactivate an enzyme, HMG-CoA reductase which puts the brakes on cholesterol formation in the liver at step #1.
Okay...why would the body want to trigger antiotensin?
Angiotensin is a hormore, a very potent vasoconstrictor.
Why does our body want vasoconstriction to happen?
Good:
Well...vasoconstriction ensures that blood pressure stays high enough to perfuse the kidneys and brain. (But this can damage the heart.)
Bad:
Vasoconstriction caused by angiotensin II triggers the adrenals to release aldosterone effecting the kidneys which results in sodium and water retention to maintain normal BP and cardiac output. (But if the system doesn't down-regulate, the person develops hypertension, high BP).
Bad:
Persistent vasoconstriction caused by angiotensin leads to target-organ damage such as heart failure and chronic kidney disease. Elevated LDL (an "associated" disorder) alter the permeability of vascular endothelial cell membranes, which allows monocytes to adhere to the endothelial cell membranes and migrate under the surface. The monocytes accumulate lipids and become foam cells, which eventually form the fatty streaks of atherosclerosis. If the endothelium becomes distorted and breaks, platelets are attracted to the damaged areas.
Bad:
An abundance of vasoconstrictors leads to hypertrophy of vascular smooth muscle and vascular remodeling.
Good and bad:
Nitric oxide, secreted by endothelial cells, is a potent vasodialtor that normally stops the damage, but hypertension, nicotine use and excessive INSULIN levels (triggered by an increase in glucose levels), inhibit the release of NO. That prevents blood vessel dilation, and the damage continues, eventually affecting target organs.
Good:
Vasoconstriction assures that the brain gets enough nutrients. The blood flow to the brain must remain constant as the neurons are intolerant of ischemia (not enough oxygen).
Low levels of oxygen trigger vasoconstriction; high levels promote vasodilation.
Good and bad:
Vasoconstriction of veins returns blood to the heart -> raises CO -> raises BP. But the blood is then pumped to the lungs to pick up more oxygen.
So why, once again, does our body want more angiotensin released?
"Angiotensin II inhibits acetylcholine release from human temporal cortex: implications for congnition." PMID 2337775.
Ohhhhhhhhh. Let's block acetylcholine release..."starve" the pathogen which needs acetylCoA?
Soo...back to the beginning:
Low Mg -> calcium influx ->TNF alpha -> angiotensin -> inhibition of acetylcholine release.
If Mg levels were restored...this whole process should be able to be stopped.
Acetylcholine causes vasodilation when, and only when, the endothelium is functioning normally. It causes vasoconstriction when the endothelium is removed or damaged.
Soooo...what do we do? We give Magnesium OR statin drugs ie. Benicar (careful of permanent kidney damage) to BLOCK angiotensin II thus allowing more acetylcholine release and we are cured...if the kidneys can handle it. (If not...bypass them...temporarily...dialysis machine?)
That's the key...supply the body with the nutrients this pathogen is taking from us...supply enough for ourselves (and the pathogen) to heal.
This is once again not unlike what researchers discovered about how to treat the SARS virus:
"Penninger and colleagues report in Monday's issue of Nature Medicine that, working in mice, they found that angiotensin-converting enzyme 2 (ACE2) is a crucial receptor for the SARS virus.
The result is disruption of the body's protective renin-angiotensin system, leading to respiratory distress syndrome as fluids seep into the air sacks. The renin-angiotensin system uses enzymes to regulate sodium balance, fluid volume and blood pressure.
SARS was first identified in 2003, originating in China and spreading rapidly to Asia, Canada and elsewhere. It killed nearly 800 people and disrupted travel, economics and even some scientific meetings.
The researchers found that the SARS virus binds to the ACE2, Penninger said in a telephone interview.
If disabling ACE2 allowed lung damage to occur, the researchers wondered whether providing more of the enzyme would help. They created more ACE2 and infused it into the mice. The result was to protect mice from the lung failure effects of SARS.
It was effective in two ways, Penninger said.
First, ACE2 combined with the virus and prevented it from binding to normal cells. Also, the enzyme protected the mice from acute lung failure.
"We of course need to extend these findings in mice now to humans," Penninger said. "Yet in essence, SARS pointed us to a protein that may help millions of people affected with a previously untreatable disease."
A commentary by John Nicholls and Malik Peiris of the University of Hong Kong said the findings indicate that the potential therapeutic value of ACE2 and angiotensin 2 receptor inhibitors for acute lung injury will be a productive field for investigation.
But Peiris and Nicholls, who were not part of Penninger's team, said there are differences in the way SARS binds with human ACE2 and ACE2 in mice.
The research was funded by the Austrian Academy of Sciences, Austrian National Bank, Marie Curie Fellowship of the European Union, Beijing Committee of Science and Technology, National Natural Science Foundation of China, Joincare Corporation, Canadian Institutes of Health Research, Canada Foundation for Innovation and the German Research Council."
On the Net:
Nature Medicine: http://www.nature.com/naturemedicine
Always keep in mind...Mg is capable of stimulating DNA REPAIR.
M.
Now...anticipating your question...how much Mg is needed:
Enough to make healthy antibodies(along with Ca), to make the hormones, to make and control the enzymes...esp. the enzymes that control glycolysis and the cholesterol pathway and the antioxidant enzymes, enough to make (along with other nutrients) the neurotransmitters...
And once the infection is gone...enough to continue to stimulate DNA REPAIR.
We need HELP. We need the medical community to recognize the value of the nutrients.
But will they?
[This message has been edited by Marnie (edited 27 August 2005).]