Marnie
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Member # 773
posted
It looks like Bb is using NFkB to survive...to keep lyme chronic. NFkB is a "tiny messenger".
This triggers TNF alpha...inflammation.
Ongoing inflammation = disaster.
I found a fairly easy to understand link (if you have a hard time understanding...skip to the "dots"):
"All of these events, cumulatively known as ``oxidative stress,'' lead to increased production of free radicals inside the cell,
with the *activation* of tiny messengers called transcription factors such as AP-1 and nuclear factor kappa B, or NfkB for short.
When NfkB detects oxidative stress, it translocates to the nucleus of the cell, which contains the DNA (which in turn contains the master instructions of the cell).
NfkB attaches to a portion of the DNA and instructs the cell to make inflammatory chemicals such as interleukins 1 and 6 and tumor necrosis factor, types of cytokines (intercellular chemical messenger proteins released by white blood cells as well as other cells) that create further inflammation and damage.
(Dots here)
* When NfkB is activated in skin cells along with another transcription factor called AP-1, it can lead to wrinkles in the skin.
(Sounds like aging!)
* When NfkB is activated in the brain, it can lead to Alzheimer's disease, and activated in other organs it can lead to cancer.
* When NfkB is activated in the pancreas, it can lead to the destruction of the B-cells of the pancreas, which are the sole source of insulin, resulting in diabetes.
* NfkB blocks the ability to utilize insulin effectively, which leads to the storage of body fat, causing us to gain weight and have great difficulty shedding the pounds.
With NF-kB activated, even thin animals develop insulin resistance and diabetes as though they were obese. Perhaps more importantly, with NF-kB inhibited, obese animals do not develop insulin resistance or diabetes.
Bb doesn't want insulin (acidic), it wants a lot of sugar (fructose)...and other nutrients.
INactivating NFkB (as well as utilizing melatonin - indoles to trigger bicarbonate release) is now a very, very hot subject in cancer research!
Cancer ONLY happens in an acidic environment.
Cancer also follows the glycolysis pathway. This has been known for YEARS. And some cancers (breast - estrogen comes from cholesterol) and prostate (testosterone also comes from cholesterol) are linked, like Bb, to both pathways...the glycolysis pathway AND the cholesterol pathway.
Okay...Mg can and does INactivate both of these pathways simultaneously.
But...remember, there is always another way to skin a cat....
To INactivate NFkB, these nutrients look to play a part:
Vitamin E (the RIGHT KIND and with a meal)
L-Tyrosine
Black Raspberry extracts
Zinc...but Bb looks to be using this...(preventing us from using it). Zinc is not gone, merely displaced.
NAC...precursor to glutathione...which is thought to inhibit NFkB
Lipoic acid...part of a product called Juvenon (NAC, ALA, biotin)
= Juvenon is looking mighty good! Yea, Prof. Bruce Ames!!!
Higher levels of Mg - 'cause LOW levels ACTIVATE NFkB
High NFkB is inversely correlated with the hemaglobin level
Insulin (acidic)...Bb prefers sugar to insulin..but ongoing insulin not possible, not health, glucagon steps in to downregulate it ie., halt its production.
But FIRST...PROBIOTICS...LOTS. Before meals with a full glass of water.
Because...
Healing always starts in the gut. We have to be able to absorb (and make) the nutrients our body needs to fight.
[ 15. July 2006, 10:00 PM: Message edited by: Marnie ]
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Now I'll bookmark this one also! Ya know... now I won't feel so dumb today. I'm even checking the flip flops before I leave the house.
I do bookmark a lot of your posts in hopes of one day I'll get it.
Thanks again, Stella Marie
-------------------- Stella Marie Posts: 694 | From US | Registered: Apr 2005
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northstar
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posted
Indoles =indole-3-carbinol? This is in the brassica family (cruciferous vegetables): broccoli, cabbage, kale, brussels spouts, bok choy, cauliflower.
Solaray has an "indole-3-carbinol with cruciferous vegetables" capsule, each having one serving. So, if one missed a days serving, one could take this instead.
black raspberry? are you referring to ellagic acid products?
Weill has a good Vit. E, with mixed tocopherols and tocotrienols.
Can you tell I just returned from the health/vitamin store?
Gasping, as I swiped the card...... Northstar
[ 16. July 2006, 02:13 PM: Message edited by: northstar ]
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northstar
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posted
Marnie,
When you say high hemoglobin....... does that also include ferritin? I have high hemog., but low ferritin (sp?).
Northstar
Posts: 1331 | From hither and yonder | Registered: Sep 2005
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posted
Marnie, Excellent!!! This is close to the holy grail. You are pulling this all together for us!!
A few questions...
1) For Choline, what is a good source? 2) ASA/salicylates...does this mean asprin? 3)Reguarding the cholesterol Pathway, does Bb infections favor excess cholesterol?
Thanks, Ernie
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johnnyb
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Ooooh Oooohh! I can answer #1.
Lecithin is good source of Choline, and it is safe. Marnie posted something before on how isolated Choline can be harmful in large quantities, but in Lecithin, it is quite safe. Lecithin can be bought at any vitamin / health food store.
- JB
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Marnie
Frequent Contributor (5K+ posts)
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posted
Choline...lecithin (phosphorus + choline)...I personally like Carlson's which I keep in the fridge. It's cheap...how's that for a switch?! Find the ODA...optimal dietary allowance, not RDA.
ASA...yes...aspirin.
Bb looks to have a cholesterol outer cell wall.
This is the basis of Benicar...lower cholesterol.
*Inhibit* HMG CoA reductase...an enzyme. Halt angiogenesis II. Mg does this too...cheaper and safer. If going the Rx route, be SURE to supp. with CoQ10. They KNOW this is depleted via the cholesterol lowering drugs and are supposed to be adding it, but...
HMG CoA reductase triggers VLDL (very low density lipoproteins) released from the liver. We want to stop this.
Now...we can't do without cholesterol. We get it 2 ways...from our foods or we make it. We can still get enough from our foods, but chose the fats carefully...the good ones.
Northstar...you listed some super nutritious foods...we should all eat like that...ah, well...I live in the real world too, but I try...make soup from "scratch", etc. Occasionally splurge on organic produce, etc., but I cheat other ways...
Yes...my bill at the nutrition store to restore our son's health (salmonella infection) has been astronomical. I can "identify"!
"The serum ferritin test is ordered to see how much iron your body has stored for future use. Reduced serum ferritin concentration is the most useful test for diagnosis of iron deficiency.[1]
As the body iron stores decrease so does the serum ferritin. A serum ferritin concentration below 12 ug/L is virtually diagnostic of absent iron stores.
On the other hand, a normal serum ferritin concentration does not confirm the presence of storage iron, because serum ferritin concentration may be increased independently of body iron by infection, inflammation, liver disease, malignancy, and other conditions.[2]
The goal of therapy in individuals with iron deficiency Anemia is not only to repair the Anemia, but also to replenish the iron stores. Sustained treatment for a period of 6 to 12 months after correction of the Anemia will be necessary.
The Hemoglobin concentration begins to increase after the first week and is usually normal within 6 weeks. Microcytosis may take as long as 4 months to resolve completely. The serum ferritin concentration remains below 12 ug/L until the Anemia is corrected and then gradually rises as storage iron is replenished.
References: ========== 1. Goddard AF, McIntyre AS, Scott BB: Guidelines for the management of iron deficiency anaemia. British Society of Gastroenterology. Gut 46(suppl 3-4):IV1, 2000. 2. Cook J: The nutritional assessment of iron status. Arch Latinoam Nutr 49:11S, 1999. _________________ Dr. Tamer Fouad, MB, BCh, MSc. Physician Specialist; Medical Oncology, Internal Medicine."
Definitions of microcytosis on the Web:
the overabundance of cells that are smaller than normal in size
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5dana8
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Thanks marnie
This is awesome! I can actually understand this.
Does anyone know a natural replacement for asprin/ibuprofen? My stomach hasn't allowed my to take these.
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Marnie
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posted
More coming that is mind-blowing...I'm working as fast as possible. Will post later.
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northstar
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posted
Pantethine , a derivative of vit B5, is reported to raise levels of CoEnzyme A. (it is used with equal amounts of pantothenic acid, another form of B5). According to the Jarrow's label, this is supposed to help with lipid metabolism.
For some reason, it is part of an anti-candida protocol.
Would this be a way to the same goal? i.e. higher coenzyme A?
Northstar
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Thanks Marnie. In case you are interested, just wanted to add that Metagenics makes products that modulate the NFKb pathway...Kaprex, Kaprex AI (for autoimmune) and Insinase. I've had great results with Kaprex AI. More information is on their website if you are interested.
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Marnie
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posted
That would not be my choice.
Zinc is toxic in high doses. It might be there, just "displaced".
Selenium...no prob.
Amino acids...which ones?
Herbal formula...what?
Where's Mg?
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
a. The degranulated mastocyte releases various substances, mainly histimine
b. Ca2+ and Mg2+ competition appears to regulate secretion of histamine by the mastocytes
i. Ca2+ ion stimulates secretion of histamine
ii. Mg2+ ion inhibits the secretion
5. Disorders in immunity and allergy-like symptoms have been described in Mg deficiency
Highly recommend skimming the above website to gain an "appreciation" of this critical mineral.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Marnie, regarding cholesterol, let me ask the question a different way. Do people with Lyme tend to have high cholesterol?
Is there a process that Lyme is affecting that changes our normal processing/production of cholesterol?
The reason I ask, is because my cholesterol is high, yet my diet is low in cholesterol rich foods. This is not logical, just asking to see if Lyme could be the villian. Thanks, Ernie
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i,too, would like an answer to the above question. I have asked this one before, but never gotten a clear reply.
Has anyone's LLMD given them a possible explanation? or can one of the researchers explain their hypothesis??
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1) What is a toxic dose of zinc? Should I get my levels tested? Can you test for the displaced zinc? Since Zinc is important in immune pathways, how do I know whether to avoid it or supplemen with it? Each tab of Kaprex AI has 5 mg. I know the RDI is 12-15 and am getting minimal in food through my diet.
2)Thanks for the info on Mg. I agree it is very important. I don't think they can put everything in a formula costwise. But I do supplement. How much do you recommend per day? I take 1200-1800mg/day. I immediately felt better once I started this. Do you think i need to supplement with Ca also? I get 1500-2000 mg in my multi, and a good amount through diet.
3)I didn't see anything claiming amino acids...
4)The herbal formula is "Luduxin" - Reduced Iso Alpha Acids (has been shown to modulate the kinase pathways) to modulate eicosanoid balance.
Since this formula modulates the GSK3 kinase pathway, and thus Nfkb and the inflammatory cascade, why wouldn't it be good to take? Is it just the zinc? If supplemented with Mg is it okay?
Thanks!
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Marnie
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Member # 773
posted
In another post I have explained...in a non technical way...that yes indeed...Bb is triggering/following the cholesterol pathway as well as the glycolysis pathway.
Bb wants VLDL...very low density lipoproteins released from the liver. These are like LDL...the "lousy" cholesterol.
This is the basis of Mg and drugs to lower cholesterol release from the liver.
If going the Rx route, be SURE to supp. with CoQ10!
We have to have SOME cholesterol! We can get enough by consuming (eating) the GOOD fats. We can stop "excess" production in our liver.
Re: Zinc...I just don't know. I really wish I did! Maybe...but to play it safe...just stick with what is already in most vitamin-mineral formulas such as Pharmanex. I wouldn't take ``extra'' or significantly above that which is already in that daily supp.
[ 24. July 2006, 10:20 PM: Message edited by: Marnie ]
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marnie, thanks for repeating info that i know i've seen before. sometimes we just need to see the same stuff repeated over and over and then a "light bulb" moment happens. I find this to be true when I'm learning something I've never seen/understood before.
I appreciate your patience.
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lymeHerx001
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what a great synchronisity marnie. I had on NPR the other day (national public radio) and they had on an indian doctor that said the reason thin indians are getting type one diabetes is because of cellular debris and waste. It was being triggered in the pancreas. The medical community has ignored this they continue to push drugs.
Well not exactlly what you posted but close enough for me to make a corrilation.
Posts: 2905 | From New England | Registered: Sep 2004
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quote:Originally posted by Marnie: Bb looks to have a cholesterol outer cell wall.
This is the basis of Benicar...lower cholesterol.
*Inhibit* HMG CoA reductase...an enzyme. Halt angiogenesis II. Mg does this too...cheaper and safer.
quote:Originally posted by Marnie: The basis of the "M" protocol ie., Benicar...is to stop this production...to INactivate an enzyme called HMG CoA reductase.
This information is inaccurate because Statins (spelled: S-T-A-T-I-N) drugs act to inhibit cholesterol synthesis by inhibiting HMG-CoA reductase.
The Marshall Protocol, however, does NOT rely on the use of any statin drugs, and it never has. The backbone of the Marshall Protocol is a sartan drug (spelled: S-A-R-T-A-N) called Olmesartan or Benicar. It is an ARB, which stands for angiotensin II receptor blocker.
Please note that Benicar's action has nothing to do with the cholesterol pathway and HMG-CoA reductase. It is in a completely different class of drugs, which is NOT even remotely related to the statins, which are the HMG-CoA reductase inhibitors, to which you are referring in your posts.
I believe your confusion about these two distinct classes of drugs stems from the fact that statins and sartans are sometimes combined in mainstream medicine when a patient has both high blood pressure and high cholesterol.
Sankyo, the company that makes Benicar, which is a s-a-r-t-a-n drug (used to lower blood pressure), also makes a popular s-t-a-t-i-n drug (used to lower cholesterol). Although the similar spelling, ``statin'' versus ``sartan'', is very confusing, the two drugs are very different. One is designed to lower cholesterol, the other is designed to lower blood pressure. They are not at all related to one another.
I don't think the majority of the Lymenet members are familiar enough with either of those two drug classes to be able to catch those mistakes easily, but continuing to lump those two very different drugs together in your posts as if they are one and the same is completely inaccurate. I feel just awful for always being the one to point this out, but this is such a huge mistake that it would be far more inappropriate if I stood by and said nothing.
That is the official website for the protocol that gave my husband and me our lives back. www.marshallprotocol.com They have a plethora of valuable information on Benicar and its use in the MP (Marshall Protocol). Having done plenty of magnesium by IV, IM as well as oral, I can personally testify to the fact that there is no comparison between magnesium and the MP - absolutely none at all... especially when one realizes that the comparisons, which have been stated here, hinge upon confusion between two very different drugs, and do NOT accurately refer to any medications that are, or have ever been, a part of the MP.
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Marnie
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posted
Benicar...
Benicar controls high blood pressure. It works
by blocking the effect of a hormone called angiotensin II.
* Olmesartan is in a class of drugs called angiotensin II receptor antagonists. Olmesartan prevents the constriction (narrowing) of blood vessels (veins and arteries). * Olmesartan is used to treat hypertension (high blood pressure). * Olmesartan may also be used for purposes other than those listed in this medication guide.
Biochem Biophys Res Commun. 2002 Feb 8;290(5):1529-34.
Angiotensin II reduces macrophage cholesterol efflux: a role for the AT-1 receptor but not for the ABC1 transporter.
???
Apr 13 (Reuters Health) - Treatment with the blood pressure drug olmesartan (sold as Benicar) effectively prevents migraine in patients with high blood pressure (hypertension) or pre-hypertension, a study hints.
Olmesartan belongs to a class of drugs called angiotensin II receptor blockers (ARBs). SOURCE: Headache March, 2006.
Angiotensin II Receptor Blockers (ARBs) ARBs are generally used as an alternate therapy to ACE inhibitors when ACE inhibitors cause side effects (for example, coughing).
While ACE inhibitors block the production of Angiotensin II,
these drugs serve as a blockade to Angiotensin II receptors, preventing it from constricting blood vessels.
Journal of the American College of Nutrition, Vol. 23, No. 5, 501S-505S (2004) Published by the American College of Nutrition Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals Andrea Rosanoff, PhD and Mildred S. Seelig, MD Independent Scholar, Pohoa, Hawaii (A.R.) Department of Physiology and Pharmacology, State University of New York, Downstate Medical Center, Brooklyn (M.S.)
Address reprint requests to: Mildred S. Seelig, MD, Department of Physiology and Pharmacology, State University of New York, Downstate Medical Center, Brooklyn, NY 11203. E-mail: [email protected]
Since Mg2+-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg2+ on lipoproteins with those of the statin drugs is warranted.
Formation of cholesterol in blood, as well as of cholesterol required in hormone synthesis, and membrane maintenance, is achieved in a series of enzymatic reactions that convert HMG-CoA to cholesterol.
The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA.
The statins and Mg inhibit that enzyme.
Large trials have consistently shown that statins, taken by subjects with high LDL-cholesterol (LDL-C) values, lower its blood levels 35 to 65%.
They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality.
These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation, Mg has effects that parallel those of statins.
For example, the enzyme that deactivates HMG-CoA Reductase requires Mg, making Mg a Reductase controller rather than inhibitor.
Mg is also necessary for the activity of lecithin cholesterol acyl transferase (LCAT), which lowers LDL-C and triglyceride levels and raises HDL-C levels.
Desaturase is another Mg-dependent enzyme involved in lipid metabolism which statins do not directly affect. Desaturase catalyzes the first step in conversion of essential fatty acids (omega-3 linoleic acid and omega-6 linolenic acid) into prostaglandins, important in cardiovascular and overall health. Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker.
More recent work shows that Mg also acts as a statin. Key words: enzymes: HMG-CoA Reductase, LCAT, desaturase, statins, magnesium, dyslipidemia: LDL-C, HDL-C, TG, heart, arteries
� Severity of Hyperlipidemia Does Not Affect Antiatherosclerotic Effect of an Angiotensin II Receptor Antagonist in Apolipoprotein E-deficient Pharmacology and Molecular Biology Research Laboratories, Sankyo Co, Ltd, Tokyo, Japan.
The purpose of this study was to clarify whether severity of hyperlipidemia affects the antiatherosclerotic effect of angiotensin II receptor blockers (ARBs).
The effect of olmesartan medoxomil, an ARB, on atherosclerotic lesion was examined in apolipoprotein E-deficient (ApoEKO) mice fed a normal diet (ND) or a high-fat-supplemented diet (FD) for 25 weeks.
ApoEKO mice have high plasma cholesterol levels, which were further increased by feeding of an FD.
Both the atherosclerotic lesion area of the aortic luminal surface and the atherosclerotic lesion thickness in the aortic valves were significantly greater in the FD mice than in the ND mice.
Olmesartan medoxomil did not affect the plasma cholesterol levels in either the ND or FD ApoEKO mice;
however,
***it reduced effectively both the atherosclerotic lesion surface area and the lesion thickness even in FD ApoEKO mice. ***
(My note here...wow...Benicar reduces the lesion surface area and thickness - of the plaques!)
It is concluded that the antiatherosclerotic effect of ARBs is not weakened by the high plasma cholesterol level, suggesting the usefulness of ARBs in the treatment of atherosclerosis,
even in a situation in which the plasma cholesterol level is not fully controlled.
PMID: 16810077
Are not these plaques LDL???!!!!!!!!!!!!
There have been very few studies to examine how angiotensin II (AII) affects lipid metabolism.
We examined the roles of AII type 1 and type 2 receptors (AT1R and AT2R) in cholesterol metabolism in rats fed either normal chow or high-fructose diets.
METHODS AND RESULTS: AII (100 ng/kg per min) or vehicle (saline) was continuously infused through an osmotic mini-pump to normal chow-fed or 60% fructose-fed rats for 2 weeks.
AII infusion markedly elevated both the systolic and diastolic blood pressure in the two animal groups. AII did not affect the plasma total cholesterol (TC) in the chow-fed rats.
In the AII-infused rats treated with olmesartan medoxomil,
an AT1R blocker, we were interested to observe
significant decreases in plasma TC and non-high-density lipoprotein (HDL)-cholesterol (C) (TC minus HDL-C), and liver cholesterol content were also decreased.
Simultaneous infusion of AII and PD123319, an AT2R blocker, markedly increased non-HDL-C and hepatic cholesterol. The infusion of CGP42112A, an AT2R agonist, decreased non-HDL-C by 30% in normal rats.
The AII infusion led to significant elevations in TC and non-HDL-C
in the fructose-fed rats,
and olmesartan treatment completely rectified this AII-induced hypercholesterolemia.
CONCLUSIONS: These results suggest that the AII receptors exert opposing effects on the plasma cholesterol level; that is, AT1R increases plasma cholesterol while AT2R decreases it.
Fructose feeding may selectively augment the action of AT1R and thereby enhance the increase in plasma cholesterol levels in response to AII infusion.
PMID: 16331107
A quantal perceptive model of brain function has been postulated by several groups. Reiki-like healing practices in seizure disorder (ILAE classification - II E - generalized seizures - tonic clonic), involving transfer of life force or low level of electromagnetic force (EMF) from the healer to the recipient patient, may act via quantal perceptive mechanisms.
Increased synthesis of an endogenous membrane Na+-K+ ATPase inhibitor digoxin and a related tyrosine / tryptophan transport defect has been demonstrated in refractory seizure disorder (ILAE classification - II E - generalized seizures - tonic clonic).
Reiki-like healing practices in refractory epilepsy results in a reduction in seizure frequency. Reiki-like healing practices produce membrane stabilization and stimulation of membrane Na+-K+ ATPase activity by quantal perception of low levels of EMF
(VERY IMPORTANT):
The consequent intracellular hypermagnesemia inhibits HMG CoA reductase activity and digoxin synthesis resulting in
the alteration of the neutral amino acid transport (tryptophan / tyrosine) defect. ***
A hypothalamic digoxin-mediated quantal perception model of brain function is proposed. The phenomena of biological transmutation and consequent hypermagnesemia occurring in the resultant neuronal quantal state is also discussed.
How to cite this article:Kumar RA, Kurup PA. Changes in the isoprenoid pathway with transcendental meditation and Reiki healing practices in seizure disorder . Neurol India 2003;51:211-214
I posted some connections re: tyrosine this morning!
P.S. I have edited my post above which were my words. However, I will not alter the words cut and pasted from research which clearly stated:
"The AII infusion led to significant elevations in TC and non-HDL-C
in the fructose-fed rats,
and olmesartan treatment completely rectified this AII-induced hypercholesterolemia."
Sometimes drugs behave in ways we don't "expect" them to.
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posted
I believe we will see much more research examining the anti inflammatory effects of Olmesartan (Benicar) and other ARBs in the future. There has already been increased interest in that area. Dr. Marshall's most recent work with molecular modeling shows that ARBs, including Benicar, modulate the activation of VDR, PPAR gamma and CCR2b.
In reference to the citation you quoted, an effect on PPAR gamma could explain the decreased the lesion surface area and the decreased thickness of the plaques while the plasma cholesterol levels remained unchanged in the experiment. This effect would be independent of its action on the renin-angiotensin system.
Angiotensin II and, as a result ARBs (angiotensin receptor blockers), probably will be shown to have a limited (small) role in lipid metabolism. ARBs have also been shown to reduce fatty streaks and lipid deposition in the cardiovascular system, but that does not indicate that these actions are a result of any action on HMG-CoA reductase. In the case of another ARB with an effect on lipid metabolism, this has been attributed to a partial activation of PPAR gamma.
I do understand your comparison of magnesium to the statin drugs (HMG-CoA reductase - cholesterol lowering drugs) and I have no objection to that. At a matter of fact, I agree with you. My only real concern is when you continue to post inaccurate and misleading information about Benicar and the Marshall Protocol. It is hard not to object when you constantly refer to Benicar as a statin drug and when you state emphatically that its efficacy is due to an effect on HMG-CoA reductase. I can't help but feel that it is careless and unfair. However, if you insist on continuing to portray it as such, at least I know that I have made several attempts privately and publicly to ask you to make those corrections.
The best source for accurate information about the Marshall Protocol and Benicar is: www.marshallprotocol.com I am not affiliated with that site; however, my husband and I do credit it with our recovery from late-stage Lyme and co-infections.
edited to correct a spelling mistake.
Posts: 487 | From USA | Registered: Feb 2002
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
The enzyme HMG CoA reductase looks to release VLDL (very low density cholesterol) from the liver.
This appears to be INactivated by Mg and statin drugs.
"More recent work shows that Mg also acts as a statin."
You said, "My only real concern is when you continue to post inaccurate and misleading information about Benicar and the Marshall Protocol. It is hard not to object when you constantly refer to Benicar as a statin drug and
when you state emphatically that its efficacy is
due to an effect on HMG-CoA reductase."
EXCUSE me but...!!!
Does Benicar not BLOCK a HMG CoA reductase RECEPTOR thus "effecting" HMG CoA reductase by preventing it from working? Yea...it has an effect on HMG CoA reductase. It stops appears to stop it from attaching to the receptor - or specifically a part of it.
And... I stated... I corrected my post!!!
So...your comment,
"My only real concern is when you continue to post inaccurate and misleading information about Benicar and the Marshall Protocol."
Was uncalled for. I corrected my post.
FYI...I never mentioned his name!
The various drug companies make similar drugs and are in competition with one another. And NO drug company can market a NUTRIENT that can effectively INactivate HMG CoA reductase and one that has MULTIPLE functions including being needed to make healthy antibodies.
For those who may be reading this and who are not familiar with his "protocol", it is important that you know this person is NOT a medical doctor, but is very, very, very computer "savy".
From the Department of Medical Biochemistry, Ehime University School of Medicine, Japan.
Angiotensin II has been shown to contribute to the pathogenesis of insulin resistance; however, the mechanism is not well understood. The present study was undertaken
to investigate the potential effect of an angiotensin II type-1 (AT1) receptor blocker, valsartan, to improve insulin resistance
and to explore the signaling basis of cross-talk of the AT1 receptor- and insulin-mediated signaling in type 2 diabetic KK-Ay mice. Treatment of KK-Ay mice with valsartan at a dose of 1 mg/kg per day, which did not influence systolic blood pressure, significantly increased insulin-mediated 2-[3H]deoxy-D-glucose (2-[3H]DG) uptake into skeletal muscle and
attenuated the increase in plasma glucose concentration after a glucose load and plasma concentrations of glucose and insulin.
In contrast, insulin-mediated 2-[3H]DG uptake into skeletal muscle was not influenced in AT2 receptor null mice, and an AT2 receptor blocker, PD123319, did not affect 2-[3H]DG uptake and superoxide production in skeletal muscle of KK-Ay mice. Moreover, we observed that valsartan treatment exaggerated the insulin-induced phosphorylation of IRS-1, the association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3 kinase (PI 3-K), PI 3-K activity, and translocation of GLUT4 to the plasma membrane.
***It also reduced tumor necrosis factor- (TNF- ) expression and superoxide production in skeletal muscle of KK-Ay mice.
Specific AT1 receptor blockade increases insulin sensitivity and glucose uptake in skeletal muscle of KK-Ay mice via stimulating the insulin signaling cascade and consequent enhancement of GLUT4 translocation to the plasma membrane.
*********
Any drug or nutrient that can dilate the blood vessels, improve insulin sensitivity (brain cells need glycogen) and reduces TNF alpha (inflammation)...the immune system TH1 pathway...and reduced superoxide production...making a pathogen much more susceptible to killing by hydroxyl radicals...
Well....duh.
As a pharmacist, Francis Marshall had access to this info.
I wonder where Robert E. Lee (psychology teacher at Black Hawk college in a little town - Moline- in Illinois???) enters in the picture?
[ 27. July 2006, 01:46 AM: Message edited by: Marnie ]
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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quote:Originally posted by Marnie: EXCUSE me but...!!!
Does Benicar not BLOCK a HMG CoA reductase RECEPTOR thus "effecting" HMG CoA reductase by preventing it from working? Yea...it has an effect on HMG CoA reductase. It stops appears to stop it from attaching to the receptor - or specifically a part of it.
And... I stated... I corrected my post!!!
No. Benicar neither blocks nor inhibits the HMG-CoA reductase receptor the way the statins do. HMG-CoA reductase still works in the presence of Benicar. It is an angiotensin receptor blocker - angiotensin is downstream of the HMG-CoA-mevalonate pathway and mevalonate is downstream of HMG-CoA reductase. In the case of statins, when you competitively inhibit HMG-CoA reductase, you also downregulate AT1 (angiotensin II type 1 receptor), but ARBs (Benicar = sartan) don't work on that same pathway. ARBs block the actual activation of Angiotensin II AT1 receptors.
It might help to think of it this way, if an ARB such as Benicar inactivated or inhibited HMG-CoA reductase, it would not be necessary to combine a sartan = ARB with a statin= HMG-CoA reductase inhibitor for the purposes of controlling cholesterol via the HMG-CoA reductase inhibition in combination therapies where you want to control blood pressure and cholesterol. If you were correct, one could control blood pressure and cholesterol with the same ARB, and the popular combined therapies, which combine ARBs and statins, wouldn't be necessary. However, since ARBs don't effectively control cholesterol, combined therapies are widely used.
I'm sorry that I didn't notice your corrections under this topic. We had a family emergency and I lost track of the internet with the exception of researching my Dad's medical emergency. Any prayers are welcome and would be appreciated.
Posts: 487 | From USA | Registered: Feb 2002
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Which came first the chicken or the egg? Plaques are forming, vessels are narrowing and hardening.
I believe stop the plaques (LDL accumulation) from forming and the vessels can then expand (and perhaps then the antibodies can REACH the infected cells). Put the brakes on the cholesterol pathway.
Vessels can't expand if they are clogged. Viagra and sudden blindness is an example.
Unclog them. High dose statins(with CoQ10) or Mg OR Mg + statins. Put the brakes on the cholesterol pathway.
"Increasing evidence has revealed that endothelial cells play an important role in the pathogenesis of development and progression of atherosclerosis.
Endothelial dysfunction induces disruption of the balance between vasoconstrictive factors and vasodilatory factors secreted from endothelial cells.
Among these factors, NO and angiotensin II are especially important factors, and have been shown to exert various direct effects on the endothelial functions that are closely related to the pathogenesis of atherosclerosis.
Endothelial dysfunction induces
decreased NO bioactivity
and increased angiotensin II expression,
which increase oxidative stress and expression of adhesion molecules, cytokines, and chemokines.
These conditions mediate inflammation, proliferation, and thrombogenesis in vessel wall and promote atherosclerotic lesions.
On the other hand, therapies that improve endothelial dysfunction, such as administration of HMG-CoA reductase inhibitors or angiotensin converting inhibitors, have been demonstrated to reduce cardiovascular events and strokes.
In this article, we focus on NO and angiotensin II and describe their roles in the pathogenesis of atherosclerosis.
P.S. Hope your dad is okay! Privately (!) ask a nurse who she/he thinks is the best doctor and then ask your dad's attending doctor if that doctor could be consulted for a second opinion.
The nurses are not supposed to "recommend" doctors, but will list several they feel are good. Listen carefully to the first few names they "volunteer".
You could ask, "If it were your father, which doctor would YOU like your father to be seen by?"
Things never dull in this household either. My son-in-law had his small Miata totalled last week. Air bags saved his life. Someone turned in front of him.
[ 20. August 2006, 02:36 PM: Message edited by: Marnie ]
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Update - Doc got Dad in with ID specialist who identified Rickettsia and West Nile Virus. Either alone would have been difficult, but both together, well... you can imagine. It has been quite a battle - & just when our family thought we were completely through with vector-borne pathogens,too.
I'm glad to hear the airbags saved your son, but I'm so sorry that y'all have been through something so traumatic and frightening. Hugs to both of you.
Posts: 487 | From USA | Registered: Feb 2002
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Lecithin is good source of Choline, and it is safe. Marnie posted something before on how isolated Choline can be harmful in large quantities, but in Lecithin, it is quite safe. Lecithin can be bought at any vitamin / health food store.
Marnie, is this true? Do you think that pure Phosphatidylcholine like Phoschol is bad for us? Why would Patricia Kane use it then for her Lyme Tx? She uses it orally and IV as Lipostabil.
-------------------- You're only a failure when you stop trying. Posts: 945 | From U.S | Registered: Oct 2004
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-------------------- You're only a failure when you stop trying. Posts: 945 | From U.S | Registered: Oct 2004
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
It takes DAYS for our bodies to make perfect "fitting" antibodies to rid bacterial infections. (It also takes enough Mg and Ca to make healthy antibodies.)
In the meantime...I believed the body recognized a very major toxic pathogen attack and responded accordingly.
Up went inflammation...lots.
The body went into an immediate PROTECTIVE mode.
Here are some of the ways TNF alpha PROTECTS US!!!
(11) TNF alpha has many jobs. In fact, it is protective and beneficial.
3. ``one mechanism of action of TNF-alpha ...on thyroid FRTL-5 cells is to inhibit calcium entry.'' PMID: 10092616
4. ``is actually a potent modulator of neurotransmitter interaction.'' hdlighthouse.org/see/immune/tnf.htm
5. ``the body does use tumor necrosis factor-alpha (TNF-alpha) to acutely fight infections. If patients are showing any sign of infectious disease, drugs such as Enbrel (that inhibit the effects of TNF-alpha) are temporarily discontinued.'' www.lef.org/protocols/prtcl-128a.shtml
6. ``After noticing that exposure to the naturally occurring compound TNF-alpha (Tumor Necrosis Factor-alpha) killed malfunctioning immune cells...'' www.diabetesincontrol.com/issue166/item1.shtml
7. ``generally the level of TNF increases with aging. Lactic acid and unsaturated fats and hypoxia stimulate increased formation of TNF. Estrogen increases production of nitric oxide systemically, and nitric oxide can stimulate TNF formation. When oxygen and the correct nutrients are available, the hypermetabolism produced by TNF could be reparative (K. Fukushima, et al., 1999), rather than destructive.''
(Original website would not link. Above website says the same.)
8. ``TNF-a is a molecule responsible for activating and proliferating cells of the immune system as well as protecting the body from abnormal cell growth.'' (same source as #7)
9. ``Activity of TNF-a is associated with inflammation, cytotoxicity (destruction of abnormal cells) antiviral activity, and the proliferation of immune cells.'' (same source as #7)
10. ``modulate cell proliferation and cellular calcium homeostasis.''
(If you go to the above website, please note the mention of spingolipid metabolites and keep this in mind: syhingomyelinase is Mg dependent)
PMID: 9195931
11. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody'' PMID: 12522038
12. ``The increased *bone resorption* may be due to an increase in TNF-alpha'' PMID: 14704297
13. ``no detrimental effects on normal neurons and can protect neurons when present in neuronal cultures during in vitro ischaemia...Once TNF's removed, neuroprotection is lost.''
14. ``TNF- a also causes production of sphingosine which can directly block the release of calcium from the sarcoplasmic reticulum and therefore depress cardiac contraction.''
15. ``suppression of insulin action in the liver resulting from TNF-alpha mediated suppression of tyrosine phosphorylation'' Gastroenterology 2004; 126: 840-848,917-919
(Keep in mind insulin ACTIVATES PFK which Bb is dependent on.)
16. ``Total elimination of the TNF-a cytokine apparently creates a less hostile immune environment...Although `Chronic-lyme' is a lympopenic disease, chronic lyme patients do not usually form sarcoid granuloma.
Borrelia burgdorferi appears to be a pathogen with insufficient lympopenic activity to proliferate sarcoid granulomas on its own. However, together with other pathogens, it is frequently found as a component of sarcoid inflammation.''
17. ``the level of TNF-alpha directly or indirectly regulates the production of borreliacidal antibody'' PMID: 12522038
18. ``Polymerase chain reaction analysis indicated a protection rate of 95% in mice receiving tumor necrosis factor (TNF)-alpha.'' PMID: 8537658
19. These results are in line with previous experiments using cells of the adaptive immune response, indicating that strong T helper type 1 (Th1) proinflammatory responses might be associated with a successful resolution of Lyme disease. PMID: 15958074
What is the underlying CAUSE of the increase in TNF-alpha?
1. "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
It appears: (1)Mg ++ charge levels drop -> increase in Ca ++ charge (not good) -> stimulates TNF alpha -> angiotensin II)
2. ``In severely Mg deficient rodents, it was found that there were greatly increased plasma concentrations of inflammatory cytokines.'' www.mgwater.com/clmd.shtml
3. ``Severe Mg deficiency changed mineral homeostasis, induced membrane damage, increased lipid peroxidation and cytokine concentrations and reduced immunocompetence.'' PMID: 9558736
4. ``During the progression of Mg deficiency in a rodent model, we have observed dramatic increases in serum level of inflammatory cytokines.'' PMID: 1384353
5. ``Bone loss induced by dietary magnesium reduction to 10% of the nutrient requirements in rats is associated with increased release of supstance P and tumor necrosis factor-alpha.'' J Nutr. 2004 Jan;134(1): 79-85
6. ``Visual defects are common in surviving preterm infants. Increased levels of harmful neurochemical mediators that have been reported in these conditions include oxygen free radicals, excitatory amino acids, tumor necrosis factor-alpha (TNF-a) and in thromboxane A2 (TXA2) which are aggravated in magnesium deficiency and
7. ``An increased production of nitric oxide and of various inflammatory peptides - such as substance P, CGRP, and VIP - is observed in Mg-deficient rats.'' http://www.mgwater.com/dur30.shtml
8. ``Magnesium (Mg) plays an essential role in fundamental cellular reactions and the importance of the immuno-inflammatory processes in the pathology of Mg deficiency...A significant increase in TNF alpha plasma level was observed in Mg-deficient rats compared to rats fed the control diet.'' PMID: 9989243
9. ``Patients with multiple EM lesions had greater symptom scores and higher serum levels of IFN-alpha, TNF-alpha and IL2 than patients with solitary EM. PMID: 12928420
Why does Mg levels drop i.e. why is it pulled from storage (it is locked onto ATP), likely from the liver?
For many, many reasons, but primarily because Mg INactivates PFK and HMG CoA reductase...the enzymes that control the glycolysis and cholesterol pathways...the pathways Bb takes.
The kidneys regulate the acid-base balance and will try to keep the level of Mg at a certain point. They do this within a 2 hour time frame, so timing is critical. It is important to sustain a SLIGHTLY high(ish) level of Mg (and B 6) in your system for as many hours a day as possible.
Normally our lactobacillus make B6 for us. If we don't destroy them with abx.
Vitamin E is a critical antioxidant to help protect the liver and pancreas and brain which are impacted as Bb ferments sugar -> ethanol. Choline and phosphorus (combo = lecithin) is also very important (to keep bile salts "thinned") since we KNOW it is choline Bb is after and is taking from us -> "fatty liver" and impacting the neurotransmitter, acetylcholine.
A LOT of nutrients are impacted. As I have said before, this is a nutritional nightmare.
Rebalancing isn't easy!
We need cholesterol from GOOD fats that we EAT. We have to stop VLDL production in the liver which is the OTHER way we get cholesterol...and is what Bb is triggering.
High levels of the "good" cholesterol, HDL is very very important.
Our bodies do NOT make mistakes! I believe it is looking for back-up routes...many.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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I continue to be amazed at your knowledge and so glad you are here! I have to read these posts in very small doses due to brain fog and appreciate any synopsis that anyone gives.
I often look to the end to see what the suggestions are because i can't spend my brain energy on reading the research.
Is that ibuprofen in addition to asa as a NFkB blocker?
Posts: 460 | From Illinois | Registered: Aug 2005
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