posted
I just bought some Manganese Asporotate due to my running out of magnesium citrate recently. I couldn't find any magnesium citrate at Wild Oats which was a surprise, because it's a huge health food store.
But, since I have the Manganese (30 mg per one cap), could I use that in place of magnesium in a pinch?
I have an order in for magnesium but it's not here yet.
I usually take 800 mg magnesium in divided doses every day.
Mostly, health food stores, I'm finding, have a combination of Calcium-magnesium together, and I've always taken my calcium separately.
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
How about a nice handful of almonds?
Seriously...I had to search, since my knowledge of Mn is extremely limited.
Hummm...curious.
"For example, in India, where they don't have as much osteoporosis in certain areas and where they do get fed properly, they have 10 times the manganese intake we do. I like to look at building bones and minerals as a chain.
The chain is only as strong as its weakest link. Say you have a chain that is 100 links long. Well, 50 of them are calcium, 40 of them are magnesium, then you have five or six for zinc, a few for manganese, a few for copper, and one or two for boron.
You can see that if any single mineral is deficient, the whole chain is no good. Even with everything else being perfectly fine. That's why if you don't have enough calcium the chain won't be very good either. You need everything in conjunction, and emphasizing just calcium alone is not the full picture.
Dr. Andersen: What about manganese for injuries? A lot of the companies that support the chiropractic profession have injury formulas that contain quite a bit of manganese. Should DCs continue to recommend manganese for healing?
Dr. Bucci: I think it's a very good idea because manganese is involved in running the enzymes that make proteoglycans and they must be synthesized before any collagen can. They're the real framework.
Dr. Andersen: Is there a best form of manganese?
Dr. Bucci: The manganese ascorbate is probably the best because manganese is similar to iron. Therefore, vitamin C will improve its uptake and that is well studied.
Dr. Andersen: What about manganese sulfate? That seems to be the most popular form in the supplements.
Dr. Bucci: That's probably one of the worst. Early research showed that manganese helps produce proteoglycans which are sulfated, so they (nutrition companies) figure they can give manganese and sulfate.
However, the absorption or manganese sulfate is poor. It's kind of like ferrous sulfate. It interacts with calcium, fiber, and iron adversely. Manganese chelates do not have these interactions.
Dr. Andersen: How much manganese would you recommend for a whiplash or disc patient? Are manganese ascorbate and sulfate dosed the same way?
Dr. Bucci: I think you need to take a good 10 mg a day of manganese from manganese ascorbate, or probably 50 to 100 mg a day of manganese sulfate.
Dr. Andersen: Are there any contraindications to manganese? I have read that people who work in manganese mines have an increased risk factor for getting Parkinson's disease. Have you heard that?
Dr. Bucci: Yes, but that is only for different valences of manganese like hexavalents and pentavalents. So, manganese has many chemical charges. Those other types of non-nutrient manganese are the ones causing that environmental exposure. The divalent manganese has never been shown to cause that problem. http://www.chiroweb.com/archives/13/13/12.html
Mg citrate is avail. everywhere (grocery stores, drug stores).It comes as a liquid in bottles for about $1.18. It is used as a prep for bowel x-rays.
Use an insulin syringe, minus the needle. Some pharmacists will give you one, others will charge 25 cents. Since kids meds are hard to measure, an insulin syringe (1ml) comes in handy.
1 ml = 58mg of magnesium citrate.
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I guess I can subsitute Mn for a while anyway. I don't take the liquid magnesium, just 4 200 mg tabs every day. Just didn't know I was so low on it and had to rush out for more. Bubblehead, that's me today!
posted
You might want to check that. My LLMD insisted that I NOT take any manganese since it feeds the Borrelia.
He suggested that I do take magnesium, but he said never, ever take manganese because the Borrelia is dependent upon it for its metabolic functions. Borrelia utilizes manganese instead of iron.
posted
Well, Bb supposedly loves magnesium also. So are we better off not taking it even though we desperately need it?
Do pathogens take in minerals directly from our GI tract as we swallow them, or do they have to wait until the nutrients get taken up into our cells? Or is it both ways? Because the little boogeres are both inside and outside our cells
I haven't read any articles that demonstrate Borrelia utilizes magnesium in their metabolic pathway. It's my understanding that it utilizes a manganese dependent pathway.
I think we use more magnesium as a result of the disease process. Magnesium deficiency can impair immune response and it is common with so many chronic diseases. Given the demonstrable role for magnesium, I would continue to supplement magnesium. In my personal experience, it really helps, so I take a lot. As a matter of fact, ILADS and my doctor both recommend it in their treatment guidelines. (Thank you Marnie for the important magnesium reminders.)
It is so good to have someone back up what they say in writing. A lot of don't do's are just heresay that get passed around. They don't really have any basis to them.
One Dr did a hair analysis on me 3 yrs ago and said that I needed to start taking manganese supplements. I told him that I already did because of a back problem. He said that I wasn't absobing it, and to triple it. Lucky for me that I never did. This was before I knew that I had lyme. I think that I will just rely on trace minerals for it from now on.
I'm neither Marnie, nor am I a doctor, so I don't feel comfortable telling you what you should or should not take,other than my doctor states clearly NOT to take manganese for the reasons stated above.
I am happy to share with you the products that we use. Note, I do NOT sell any of these, and I am NOT affiliated with them in any way.
My husband's LLMD suggested we use Nature's Sunshine Magnesium Complex. It was one of the many supplements used in the Samento Study. I bought mine from the naturopath who worked with the study, but later I found it at my corner health food store. This site lists the ingredients on the label: http://www.healthy-sunshine.com/magnesium-complex.htm
It contains a combination of magnesium citrate and magnesium malate, because these are considered to be very bioavailable. I have bought other similar tablet products through Source Naturals, Allergy Research and Solaray in the past.
We liked the Nature's Sunshine formula so much that if we hadn't found it nearby, we would have started ordering it. We also use the slow release magnesium that Dr. B recommends. When we can't find Dr.B's recommended magnesium, we occasionally use Slow-Mag in place of it.
We are fond of the Nature's Sunshine Magnesium Complex for other reasons. This product is a capsule filled with powder. The naturopath taught me to open it up, and hold the contents under my tongue with a couple of tablespoons of naturally sparkling mineral water. I was so surprised to find how well it worked sublingually.
I had another doctor in the past that had given me magnesium shots and IVs with magnesium. This seemed almost as effective as the shots did. I believe the NP also mentioned that Dr. C (TX) was involved in helping NS to develop certain products that met his strict standards for the Samento Study.
The naturopath taught me to monitor my urine pH. This has really helped. I've learned that I'm almost always acidic when I'm having a lot of inflammatory symptoms. I used the pH chart and sticks as suggested. My husband and I have both discovered that we can bring Herx, and Lyme rage symptoms under control quickly by taking a magnesium or two sublingually for quick absorption.
We also use glutathione capsules sublingually this way to help with Herxing and detox.
I have always been cautioned to take my magnesium and other vitamins containing minerals away from my antibiotics. They interfere with certain antibiotics such as Minocin, Zithromax, etc. Usually the information printed with the antibiotics will include a warning.
I hope this helps until Marnie can come along with more information.
[This message has been edited by Lonestartick (edited 27 February 2005).]
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Microbiologist, Dr. Gary Kaiser, has clearly stated that Bb uses Mg in its enzyme reactions.
In Romania, at a cancer hospital, they treated 2 lyme patients with Mg AND abx. and cured the disease. They found an astonishing (early on) drop in 2 lyme patient's Mg levels. Do the math. Look at their level before and after treatment to determine the % loss.
But, yes...Bb uses MANY of our nutrients besides Mg. However, the loss of this MAJOR nutrient (an ELECTROLYTE) is devastating...and is KEY to healing.
It takes Mg and Ca to make HEALTHY antibodies...our OWN highly targeted "antibiotics" to knock off this pathogen.
Without enough Mg...eventually you will not be able to hold onto Ca or K. A Magnesium deficiency disrupts the Na-K pump. (Ca and K will rise at first, before being depleted - or lowered to a certain level -before the body goes on a hunt for OTHER metals/minerals to use..the bad guys..Al an Hg).
1. Mg is needed to make ATP - sparks of energy - for every cell, every second. 2. Mg is needed to make PROTEINS...immunoglobulins (antibodies included). Hormones and enzymes are proteins. 3. Mg controls OVER 350 enzymes. Read the above again. 4. Mg is capable of DNA REPAIR.
Go to the "mdschoice" website mentioined in my updated nutshell post to learn about Mg.
Restore the balance.
This is all documented with links in my updated nutshell post. You will have to cut, paste, and drop it into a MS word file. print it out, and read it many times before it "clicks" and you understand what is going on.
An Italian, named Valletta, has a U.S. patent, titled: "Magnesium for autoimmune". He used Mg pyrophosphate and sublingual B6 (IV doses at first and timing is CRITICAL)to cure RA, ulcerative colitis and invasive bowel cancer. Cancer, like lyme, follows the glycolysis pathway...very unhealthy for us.
Yes...of course Mn (not Mg) is toxic at too high a level for too long (welders). And too much Ca will further deplete Mg levels. It has to do with their "reactive" level. Lithium is the most reactive of the metals, next is potassium...there are lists on the internet...reactivity of the minerals.
Substituting one mineral for another doesn't get to the ROOT of the problem.It's been tried. Gold shots for arthritis, for example. It helps for awhile, but eventually catches up.
You can't take B vitamins (acidic) and hope to cure scurvy (which is a vitamin C - weak acid - deficiency).
Yes, the salt (Na) and high dose Vitamin C(weak acid, so high doses are needed) will help to knock out the pathogen because this combo produces hydrogen, but you have to get that hydrogen INTO the cells. And while this will destroy the pathogen, you will continue to have lyme symptoms BECAUSE your Mg level is far too low. You will continue to be at risk for many other diseases...diabetes and cancer for starters.
CoQ10 carries hydrogen INTO the cells...but to MAKE CoQ10 (when we exercise, RDA unknown)...takes B6 which needs *additional Mg.
Then the cells can't STAY acidic when those hydrogens get into the cells and combine with free oxygen radicals -> H202, hydrogen peroxide, a weak acid.
If the cells remain acidic, they will die and... in 20 min. Bb will go into a cyst form.
We need the ENZYME, catalase, to break down H2O2 into H20 and O. This is happening inside our cells very, very fast, constantly. For evey TWO hydrogens we get into the cells, we get rid of ONE damaging free oxygen radical. Obviously we need a lot of hydrogen going into the cells...constantly...to stay healthy.
Curious, I didn't know Mn fit "in between" Ca and Mg in the reactivity.
We are very "electromagnetic" and so are the pathogens. The nutrients have electrical charges.
Acids have a negative charge. Lots of them combine with a little (usually) mineral - or glycogen (both have a positive charge)! - to make hydrogen.
The body will use the most "reactive" mineral first...Calcium before magnesium. They "compete". They will "chelate" the minerals below them on the reactivity list.
The jury's out...re: titanium dioxide in many slow Mg supplements and in many abxs. To my knowledge, we don't need titanium...
P.S. In case you're wondering what some of the other nutrient requirements of Bb are...go to the following and read a sentence that begins, "Because of their larger diameter, borreliae are more"
Could you please post the full scientific article to which you are referring. I am very interested in it.
In the meantime, Posey an Gheradidni proved that Borrelia burgdoferi does not use iron, unlike most other bacteria. This was published in Science, June 2000. They went on to conclude that Borrelia uses manganese for all of its enzymatic functions. This is the science my doctor was relying on when he advised me not to take manganese.
"All of the metalloproteins in Borrelia burgdorferi, the causative agent of Lyme disease, use manganese and iron is not required (Posey and Gherardini, 2000)"
Keep in mind, Manganese and Magnesium are NOT interchangable in all bacterial pathways. For instance, Treponema pallidum, the spirochetal cause of Syphilis, uses the regulatory protein troR. Unlike some other metal-dependent regulatory proteins, TroR is NOT activated by all divalent metals. It is ONLY activated by manganese. Treponema pallidum does NOT use magnesium, and it is highly doubtful that borrelia does, given current scientific evidence that suggests it uses manganese-dependent enzymes for its metabolic pathways. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10485921
You may be confused. Magnesium deficiency in a patient, and a positive response to magnesium supplementation does NOT mean the Borrelia bacteria itself is capable of utilizing magnesium for its enzymatic pathways. I will gladly concede this point if you can post sufficient peer reviewed literature to the contrary. Currently it goes against information I have found on PubMed and in peer-reviewed sources. Telling a patient to substitute manganese for magnesium could be harmful in this case.
This is NOT to state that magnesium is not important. Marnie's research substantiates the important role magnesium plays in our body's immune response, and in so many of our body's other functions.
[This message has been edited by Lonestartick (edited 28 February 2005).]
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Lonestartick...
You said above,
"Telling a patient to substitute manganese for magnesium could be harmful in this case."
I never told her to substitue Mn for Mg. To imply that I did, is a personal attack.
I merely posted "cut and paste" information regarding these minerals. She is an intelligent woman capable of making her own choices.
But I'm really, really upset...Dr. K's website has been altered.
This is what it said:
"Hemophilus influenzaea, however, have receptors for human lactoferrin and transferrin and can utilize iron bound to these compounds. Borrelia bergdorferi is a bacterium that doesn't even use iron as a cofactor for enzyme reactions. It instead uses magnesium.''
This is what it NOW says:
``Some bacteria such as Neisseria gonorrhoeae, Neisseria meningitidis, and Hemophilus influenzaea, however, have receptors for human lactoferrin and transferrin and can utilize iron bound to these compounds. Borrelia burgdorferi is a bacterium that doesn't even use iron as a cofactor for enzyme reactions. It instead uses manganese.''
Not only did he change magnesium to manganese, he corrected his misspelling of burgdorferi from bergdorferi...which I pointed out in my original nutshell post!!!
I am not that good of a speller... ``Hemophilus influenzaea''...and as many will note in my original Updated Nutshell post...when I cut and pasted that information, Dr. Kaiser had misspelled bergforferi. I pointed this out! Notice the ``e''. I had NOT misspelled it. This website has been changed!!!
This makes me really, really upset!
Do you think information doesn't ``disappear'' or isn't changed?...
``Discussion: This case illustrates that Lyme disease-associated demyelinating polyneuropathy may be treated with IVIG.
The potential use of IVIG in this population is based on its efficacy in those with acute demyelinating neuropathy of alternative etiologies. Conclusion: IVIG can be considered as a treatment option for demyelinating polyneuropathy associated with Lyme disease.'' PMID: 13680780
The above link no longer works which is very puzzling since it was a ``cut and paste'' on my part. If whoever is reading this has access to a hard copy of this journal, I urge that person to find it and copy it. The Sept. 2003 issue of that journal may be found in hospital or medical school libraries.
My updated Nutshell post contains the entire Romanian abstract with the link at the bottom...compliments of George Eby...he provided the link for me.
Here is the Romanian abstract from a CANCER hospital once AGAIN:
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. http://coldcure.com/html/2003-mag-abstracts.pfd Takes 2 minutes to download. Scroll down to page 79. Pay very close attention to the % decrease in the Mg levels initially. They are astounding!
Borrelia Burgdorferi, the lyme spirochete's DNA... "and likely contacts the essential Mg(2+) cation via a water molecule" PMID: 12015149 "a 51 kDa MgtE magnesium transporter protein" (Type in this sentence into PubMed to bring up the following abstract): FEMS Microbiol Lett. 1996 Dec 15;145(3):309-14.
Identification and mapping of a chromosomal gene cluster of Borrelia burgdorferi containing genes expressed in vivo. Aron L, Toth C, Godfrey HP, Cabello FC. Department of Microbiology and Immunology, New York Medical College, Valhalla 10595, USA.
Bb is PFK dependent:
The structure of the 60 kDa PYROPHOSPHATE (PP(i))-dependent phosphofructokinase (PFK) from Borrelia burgdorferi...
PMID: 12015149
(Documentation)"We hypothesize that extracellular Mg2+ regulates PFK and glycolysis in these neoplastic cells not by entering the cytosol but by a specific interaction with the plasma membrane."
PMID: 1832860 [PubMed - indexed for MEDLINE]
Some cell types have H+ pumps which are driven by pyrophosphate.
Magnesium ions are required for pyrophosphate release. In fact, none of the partial reactions specified in Fig. 1 can be observed in the absence of magnesium ions. http://content.febsjournal.org/cgi/content/full/269/21/5264 (look below figure 6)
CoQ10 Deficiency caused by lack of other vitamins (like Vitamin B6) the body needs to manufacture CoQ10. If CoQ10 is deficient, nerve cells in the brain and elsewhere may not have the ability to withstand the overstimulation caused by excess glutamate. http://www.msgtruth.org/why.htm.
It is very important to give magnesium along with B6 because B6 requires extra magnesium to be effective, and thus may cause a deficiency. http://www.autism.org/vitaminb6.html.
COQ10 regulates the ATP -generating capabilities as an electron carrier. Recent studies have shown that it transports protons for the proton gradient used to drive oxidative phosphorylation.
Hard breathing, aerobic exercise, increases oxidative phosphorylation to make ATP which may boost our immune by virtue of reducing PFK and dependent pathogens.
In addition:
``The body makes most of its own CoQ10. Physical exercise increases the body's CoQ10 supply. The remainder of CoQ10 necessary for the body is obtained from dietary sources.'' http://www.akins.com/hh/co_q10.htm
Borrelia Clinical Manifestations Once the relapsing-fever borreliae have entered the host, they cause a generalized infection, apparent after an incubation period of approximately 1 week (Fig. 35-4). The onset of the disease, which is associated with numerous spirochetes in the blood is abrupt, with fever, headache, and muscle pain that persists for 4 to 10 days, followed by an afebrile period of 5 to 6 days correlated with the absence of spirochetemia. Usually, a single relapse occurs in louse-borne relapsing fever.
The clinical features of relapsing fever, other than its recurrent pattern, are not diagnostic. The mortality in untreated epidemic relapsing fever can be higher than 40 percent, and myocarditis probably is the most common cause of death. The tick-borne relapsing fever is similar to the louse-borne disease, but is less severe (mortality, 0 to 8 percent), and several relapses of decreasing intensity are commonly experienced. Structure, Classification, and Antigenic Types Borrelia has morphologic characteristics similar to those of Leptospira, except that cells average 0.2 to 0.5 �m by 4 to 18 �m and have fewer coils (Fig. 35-5). Seven to twenty periplasmic flagella originate at each end and overlap at the center of the cell. In contrast to the Leptospira peptidoglycan, that of Borrelia contains ornithine rather than diaminopimelic acid. Basal bodies of periplasmic flagella of borreliae resemble those in Gram-positive bacteria. Because of their larger diameter, borreliae are more readily stained with aniline dyes than are other spirochetes.
***Their lipid components are unusual in that they include cholesterol; this substance has been found in only one other bacterial genus, Mycoplasma. The nutritional requirements of the borreliae are more complex than those of leptospires. Glucose, amino acids, long-chain fatty acids, N-acetylglucosamine, and several vitamins are some of their required organic nutrients. The borreliae are microaerophilic organisms. Borrelia hermsii has a generation time of 12 hours when cultivated in artificial media at 35�C compared with only 6 to 10 hours in the mouse. http://gsbs.utmb.edu/microbook/ch035.htm
(Cholesterol is PROTEIN - and ALL proteins need Mg to be made according to the mdschoice website which explains the functions of Mg to doctors - PLUS a fat.) See where the above - last paragraph says, ``Their lipid components are unusual in that they include cholesterol.''?
"According to the chemiosmotic hypothesis, the free energy released during electron transport is used to pump PROTONS from the cell into the periplasmic space of gram-negative bacteria and, in the case of gram-positive bacteria, between the cytoplasmic membrane and cell wall. As a result [H+]out> [H+]in resulting in a sharp concentration gradient of protons across the membrane and since there is a tendency for protons to flow into the cell to equalize concentration.This is referred to as the protonmotive force (pmf) and is due to the difference in pH and electrical charge across the membrane. The membrane is said to be in an "energized state". http://216.239.51.100/search?q=cache:RqDVXbqqPNoC:home.cc.umanitoba.ca/~oresniki/210/LEC27-01.pdf+gram+negative+bacteria+electrical+charge&hl=en&ie=UTF-8
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
Quick...before this patent disappears:
In 2001, an Italian, by the name of Valletta got a U.S. patent - # 6,248,368. It is titled: Magnesium for autoimmune. Valletta used Mg pyrophosphate and sub. B6 to cure RA, ulcerative colitis and INVASIVE CANCER in 6 months time. The turning point is 3 months (perhaps because of the AVERAGE normal cell lifespan?). It is the TIMING that is absolutely critical! Higher levels must be maintained for several hours per day, due in part to our body's constant attempt to regulate the acid-base balance (kidneys) perhaps.
``Lupin Ap4A hydrolase has particularly high sequence identity with the Ap4A hydrolase encoded by ialA, one of two genes associated with the ability of Bartonella bacilliformis to invade and survive as a parasite of human erythrocytes [4].
Many years ago, the ``Universal Remedy'' was in the Merck manual. It was Mg oxide, tannic acid and activated charcoal. Problem is...we can't duplicate tannic acid.
Why are we using Mg peroxide solutions in ``clothing'' now? Think about this.
Activated charcoal TRAPS pathogens, but it didn't/doesn't destroy them.
We were curing many diseases a long time ago using Mg chloride. We used IV Na-bicarb to cure dogs of neuro babesia in Germany in the 1970s. Think about that implication!
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treepatrol
Honored Contributor (10K+ posts)
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Marnie posted But I'm really, really upset...Dr. K's website has been altered.
Theres something really fishy about this disease Drs changing stuff to journals floating around the connections and also CDC
Changing stuff or elimanating there previous stuff WAY to much slight of hand going on.
Its like the Government knows something that we dont?
I sincerely did not mean to attack you. I'm sorry that I made you feel that way and that I misread your post to mean that you were suggesting manganese supplementation. Like so many here, I have really valued your information. That's why I asked you for the reference. That's also why I immediately went back to edit my post to state that I did not mean to state that magnesium was not important.
I quite imagine that K changed his website simply to reflect current knowledge. Science is always evolving and it has really taken off as a result of genomics. Prior to gene sequencing, much of this has been a mystery. These advances are so new that they can take a while to be assimilated. (That's why I wasn't sure if you knew something that I didn't about Bb's use of magnesium.) I was curious because I have studied this organism until I am cross-eyed, and I couldn't find it anywhere. All I've ever been able to find were references to manganese.
It makes sense that this knowledge has evolved now that the mechanisms of specific metal-dependent regulatory proteins are becoming understood. I do NOT think the fact that the information changed recently points to a conspiracy: I think it just means our understanding is evolving and that the processes are complicated.
It's hard to keep up when the current knowledge contradicts what we've learned in recent years. That's why I reference things. It gives me a way to track the evolution of my understanding so that I can see how ideas and concepts evolve.
I think of science as a quest for truth and knowledge. It's a journey, not a destination. My understanding of Borrelia is ever changing. I'm addicted to learning about it, but I barely keep up.
It came as quite a shock to me too when I first learned Bb uses manganese. I like to imagine that there were some rather surprised scientists out there as well.
It says: ``All of the metalloproteins in Borrelia burgdorferi, the causative agent of Lyme disease, use manganese and iron is not required (Posey and Gherardini, 2000).''
However, given the following...this is curious:
``B. Burgdorferi is an obligate parasite throughout its natural life cycle and has limited metabolic capabilities. As a result, it can be propagated in vitro only in a complex, undefined growth medium known as BSK.'' www.nature.com/cgi-taf/DynaPage.taf?file=/ nrmicro/journal/v3/n2/full/nrmicro1086_fs.html&filetype=pdf
The new kid on the block is Borrelia Burgdorferi (Bb) and some of us have looked at it for a long time as possibly the bug that opens the door for all the other infections to enter the system. Lyme disease has become a buzzword in the alternative medical field. Since none of the recommended treatments are specific to either one of the microbes, we can never assume that we really know what we treated once a patient has recovered.
Microbiologist Gitte Jensen, PhD had shown, that the older we get, the more foreign DNA is attached to our own DNA. Somewhere along the line pathogenic microbes invade the host's DNA and become a permanent part of it. Since we use only 2% of our DNA, it may not be a problem. In fact, it may make us who we finally become. It may also cause a number of symptoms and chronic illness. Genius Guenther Enderlein's discoveries take us off the hook: if one microbe can change into another given the right environment, why bother to find out, who we are infected with?
The book ''Lab 257'' suggests that Bb is a an escaped man-made US military bio-warfare organism (just like myoplasma incognitus and HHV 6). Other authors suggest that different subtypes of Borrelia which cause illness in humans, such as B. afzelii and B.garinii have probably existed longer than B.burgdorferi and occur naturally (1, 2) and have been with us for a long time, maybe centuries or more.
Neurologist Prof. J.Faust MD, PhD of the Albert-Ludwig University in Freiburg, Germany (3) related many neurological and psychiatric illnesses to spirochete infections as early as the 1960s. He was so skilled in his clinical knowledge that he could - only based on clinical neurological symptoms - accurately predict which valley in the Black Forest the infected patient was from! This clearly was a time before Bb - showing that non-syphilis spirochete infections were around earlier then the famous Bb outbreak in Connecticut in the mid seventies. It also makes a strong statement to the fact how easily these creatures may mutate and adapt to local conditions. It may however validate the findings published in ``Lab 257'': Tuebingen, the place where German/US warfare spirochete expert Traub was continuing his spirochete experiments in the early 50s, is situated in the Black Forest also. Were these spirochetes genuine or have they escaped from a university laboratory?
And
There has been much speculation, why Lyme disease seems to be increasingly common. The book ``Lab 257''is an investigative report on the issues involved. The insects which are the vectors for these microbes thrive in warmer climates. I have no doubt, that to a large degree the greenhouse effect is responsible and will be confronting us with the onslaught of more and more aggressive microbes. The partial pressure of oxygen on the earth at sea level has decreased from 30% 150 years ago to 19% today. The oxygen producing algae in the oceans are dying.
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treepatrol
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up for marnie
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``B. Burgdorferi is an obligate parasite throughout its natural life cycle and has limited metabolic capabilities. As a result, it can be propagated in vitro only in a complex, undefined growth medium known as BSK.'' www.nature.com/cgi-taf/DynaPage.taf?file=/ nrmicro/journal/v3/n2/full/nrmicro1086_fs.html&filetype=pdf
Odd...if Bb needs Mn...how can it grow in the above mediums?
Please be careful what you are comparing when referring to growth mediums. You are incorrect in your assumptions because of the following.
BSK = rabbit serum BSKII = medium lacking rabbit serum. BSKH = has both bovine serum and modified rabbit serum
B. burgdorferi can be cultivated in vitro by using an enriched artificial medium, named Barbour-Stoenner-Kelly medium BSK), supplemented with serum
BSK- Unlike Treponema pallidum, Borrelia burgdorferi can be cultivated in vitro. However, the bacterium is fastidious and requires a very complex growth medium. The medium used to grow Borrelia burgdorferi is called Barbour-Stoenner-Kelly (BSK) medium.
It contains over thirteen ingredients in a rabbit serum base. Borrelia burgdorferi has an optimal temperature for growth of 32 C, in a microaerobic environment. Even under optimal conditions, the generation time is slow, about 10-12 hours.
Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi P. Scott Alban1, Paul W. Johnson2 and David R. Nelson1 Department of Biochemistry, Microbiology, and Molecular Genetics1, and Electron Microscope Facility2, University of Rhode Island, Kingston, RI 02881, USA Author for correspondence: David R. Nelson. Tel: +1 401 874 5902. Fax: +1 401 874 2202. e-mail: [email protected] It has been demonstrated previously that motile Borrelia burgdorferi cells transform into non-motile cyst-forms when incubated for several weeks in BSKII (a complex medium) lacking rabbit serum. B. burgdorferi cells cannot synthesize fatty acids de novo and serum is thought to provide a source of fatty acids and lipids. When B. burgdorferi cells were serum-starved in defined RPMI medium, ~90% of the cells formed spherical cysts within 48 h. Cyst formation was inhibited by tetracycline. Cyst opening and recovery of vegetative cells was rapidly induced by the addition of either BSKII or rabbit serum. The percentage of viable cells recovered from cysts ranged from 2�9% to 52�5%. Viability was inversely proportional to cyst age. Protein synthesis by B. burgdorferi during serum starvation was examined by labelling cells with Tran35S-Label and analysing the labelled proteins by two-dimensional gel electrophoresis and fluorography. The synthesis of over 20 proteins was induced during serum starvation. Western blots of proteins from vegetative cells and cysts probed with sera from either B. burgdorferi-infected humans or monkeys revealed that several cyst proteins were antigenic. These data suggest that cells of B. burgdorferi, although possessing a small genome and extremely limited biosynthetic capabilities, rapidly respond to conditions of serum starvation by inducing changes in protein synthesis and cell morphology. This study may help explain how cells of B. burgdorferi can survive periods of nutrient deprivation in different hosts and host tissues. Keywords: Borrelia burgdorferi, spirochaete, serum starvation, cysts, Lyme disease Abbreviations: CSF, cerebrospinal fluid; MPN, most probable number; SSP, serum starvation protein
Marnie, in the above abstract it says, "It has been demonstrated previously that motile Borrelia burgdorferi cells transform into non-motile cyst-forms when incubated for several weeks in BSKII (a complex medium) lacking rabbit serum." I gather that the genetic expressions of Bb in various culture media and their ability to convert to starvation forms have to do with their inability to synthesize fatty acids.
Odd...if Bb needs Mn...how can it grow in the above mediums?
Marnie, you cited a comparison of BSKH and BSKII. There is a difference between BSK, BSKII and BSKH. These are apples and oranges. BSK, BSKII and BSKH are not the same thing.
BSKH growth medium is BSKII that has been modified to contain bovine serum also.Pollack et al. (19) described the standardization of a modified version of BSKII, designated BSKH, in which the composition of BSKII medium was further modified to contain bovine serum albumin (BSA) and rabbit serum that were prescreened for optimal B. burgdorferi growth-supporting characteristics. BSKH medium has since become commercially available (Sigma Chemical Co., St. Louis, Mo.)
Again, I gather that the genetic expressions of Bb in various culture media and their ability to convert to starvation forms have to do with their inability to synthesize fatty acids.
There is a reason why these changes are often referred to as "serum starvation forms."
[This message has been edited by Lonestartick (edited 02 March 2005).]
This is a case where we cannot ignore the scientific research just to cling to a belief system that defies current research. You need to reevaluate your findings in light of science that is current, not outdated.
Everything I have stated is based on knowledge from The Borrelia burgdorferi Genome Project and other Genome research. I am not merely guessing.
As I stated before, when I was very clearly referring to Treponema Pallidum, the cause of Syphilis, I referred to that organism to illustrate an important point about selective pathways.I said,
``Keep in mind, Manganese and Magnesium are NOT interchangable in all bacterial pathways. For instance, Treponema pallidum, the spirochetal cause of Syphilis, uses the regulatory protein troR. Unlike some other metal-dependent regulatory proteins, TroR is NOT activated by all divalent metals. It is ONLY activated by manganese. Treponema pallidum does NOT use magnesium, and it is highly doubtful that borrelia does, given current scientific evidence that suggests it uses manganese-dependent enzymes for its metabolic pathways.''
I was very clearly referring to Treponema Pallidum, the cause of Syphilis because this illustrates clearly the point that not all metal-dependent regulatory pathways are activated by all divalent metals. Some are activated only by a specific metal. In this case, it is magnesium.
I see no need to continue to debate you further. Cling to your beliefs if they make you comfortable, but do not continue to mislead people about Borrelia loving magnesium or using magnesium when that is unsubstantiated and contradicts current scientific evidence.
Even Dr. Kaiser has seen the need to change the information on his website to state that Bb uses manganese in light of current science. You might ask Gary Kaiser him why he changed the information on his website.
Interestingly, new experimental and genomic sequence data suggest that some micro-organisms may have no requirement for Fe, having evolved metabolic and survival strategies that can be accommodated by Mn. For example, the Lyme disease pathogen Borrelia burgdorferi appears to have an obligate requirement for Mn (Posey & Gherardini, 2000 )
"Substitution of manganese for iron is also important in the bacterial pathogen Borrelia burgdorferi, the causative agent of Lyme disease. The B. burgdorferi genome project has revealed the absence of iron-containing membrane proteins and annotated genes encoding proteins such as superoxide dismutase that are predicted to contain manganese rather than iron (97). The absence of iron and iron-containing proteins is proposed to allow B. burgdorferi to survive in a host that restricts iron, an action that normally limits microbial growth and thus prevents infection. In this way, the B. burgdorferi genome may have evolved by eliminating the requirement for what is usually an essential element."
[This message has been edited by Lonestartick (edited 02 March 2005).]
Why do you keep refering to SYPHILIS (above info.)?
"Here are current sites that are quoting/citing this information. It is not anecdotal, but is becoming widely accepted. It is based on genomic sequencing, not guessing." http://pubs.acs.org/cen/80th/manganese.html
The above is info. on manganese...sort of a history lesson.
The following sites you lead to all refer to Posey, Gherardini single research:
(Sorry, but when a professor said, it is an enzyme or protein that destroys Bb and protects the Western fence lizard...and he didn't do the "BASICS" before boiling the lizard's blood...I tend to be very skeptical of ALL research, unless it is substantiated by others.)
Since you seem to have a tremendous genetic knowledge, why does Bb have the following?:
Borrelia Burgdorferi, the lyme spirochete's DNA...
"a 51 kDa MgtE magnesium transporter protein" (Type in this sentence into PubMed to bring up the following abstract): FEMS Microbiol Lett. 1996 Dec 15;145(3):309-14.
Identification and mapping of a chromosomal gene cluster of Borrelia burgdorferi containing genes expressed in vivo. Aron L, Toth C, Godfrey HP, Cabello FC. Department of Microbiology and Immunology, New York Medical College, Valhalla 10595, USA.
"and likely contacts the essential Mg(2+) cation via a water molecule" PMID: 12015149
Cholesterol is a protein and a fat. Mg is needed to make proteins...all of them (mdschoice website...until that one changes). Borreliae have lipid components that include cholesterol (as does Mycoplasma).
More later. Gotta run. Will address the BSK discussion. Isn't it curious about gelatin?
Have you personally had your intracellular minerals tested? Was your Mn significantly low? Are you supplementing with this also, to restore the balance?
Once more, we have known for a long time...years...prior to geonome testing that Bb didn't need iron. That comes as no surprise.
[This message has been edited by Marnie (edited 03 March 2005).]
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Marnie, I see no reason to debate you further. I might only suggest you ask your Gary Kaiser why he changed the information on his website to state, ``Borrelia burgdorferi is a bacterium that doesn't even use iron as a cofactor for enzyme reactions. It instead uses manganese.''
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
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I find it very odd that this morning, I cannot access the following information (2 posts) that I posted above (they were cut and pasted):
``B. Burgdorferi is an obligate parasite throughout its natural life cycle and has limited metabolic capabilities. As a result, it can be propagated in vitro only in a complex, undefined growth medium known as BSK.'' www.nature.com/cgi-taf/DynaPage.taf?file=/ nrmicro/journal/v3/n2/full/nrmicro1086_fs.html&filetype=pdf
And since our discussion, Dr. K's website was changed.
You imply (below) that I do not know that BSK/BSKII/BSKH/RPMI medium have differences in nutrients:
You said: ``Please be careful what you are comparing when referring to growth mediums. You are incorrect in your assumptions because of the following.
BSK = rabbit serum BSKII = medium lacking rabbit serum. BSKH = has both bovine serum and modified rabbit serum''
I'm dropping this again for others to interpret:
``Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi P. Scott Alban1, Paul W. Johnson2 and David R. Nelson1
Department of Biochemistry, Microbiology, and Molecular Genetics1, and Electron Microscope Facility2, University of Rhode Island, Kingston, RI 02881, USA Author for correspondence: David R. Nelson. Tel: +1 401 874 5902. Fax: +1 401 874 2202. e-mail: [email protected]
It has been demonstrated previously that motile Borrelia burgdorferi cells transform into non-motile cyst-forms when incubated for several weeks in BSKII (a complex medium) lacking rabbit serum.
B. burgdorferi cells cannot synthesize fatty acids de novo and serum is thought to provide a source of fatty acids and lipids.
When B. burgdorferi cells were serum-starved in defined RPMI medium, ~90% of the cells formed spherical cysts within 48 h.
Cyst formation was inhibited by tetracycline.
Cyst opening and recovery of vegetative cells was rapidly induced by the addition of either BSKII or rabbit serum.
The percentage of viable cells recovered from cysts ranged from 2�9% to 52�5%. Viability was inversely proportional to cyst age. Protein synthesis by B. burgdorferi during serum starvation was examined by labelling cells with Tran35S-Label and analysing the labelled proteins by two-dimensional gel electrophoresis and fluorography.
The synthesis of over 20 proteins was induced during serum starvation. Western blots of proteins from vegetative cells and cysts probed with sera from either B. burgdorferi-infected humans or monkeys revealed that several cyst proteins were antigenic.
These data suggest that cells of B. burgdorferi, although possessing a small genome and extremely limited biosynthetic capabilities, rapidly respond to conditions of serum starvation by inducing changes in protein synthesis and cell morphology. This study may help explain how cells of B. burgdorferi can survive periods of nutrient deprivation in different hosts and host tissues.
In BSKII medium, Bb transforms into cysts after several weeks. (Use up the nutrients?)
In RPMI medium, Bb goes into cyst form within 48 hours.
But if the dormant cysts in RPMI are given EITHER, I repeat, EITHER, BSKII OR, I repeat, OR...rabbit serum, then they open and recover. We need to read the above abstract very, very carefully.
It would appear that something in both BSKII and/or in rabbit serum that supplies the nutrients to Bb.
The nutrient requirements of the pathogens are not one, or two...but many! As an example, the pathways for energy production for V. cholerae as shown in a diagram in Nature, Vol 406, 3 August 2000 are astounding. I would suspect Bb's pathways to make energy would be equally complex.
However, that said, it is obvious from the Romanian abstract that our Mg levels drop significantly, very fast. The loss of Mg has a HUGH impact on the body. It would appear from the following abstract - ***please note the date (!), that there is indeed a Bb-Mg connection.
Furthermore, it is known that we have to have Mg (and Ca) to make healthy antibodies and the fab portion of the antibody specific to lyme is damaged, but restored when Ca and Mg levels are restored (pubmed abstract - documented).
Structure (Camb). 2002 May;10(5):659-71. Related Articles, Links
The structure of a pyrophosphate-dependent phosphofructokinase from the Lyme disease spirochete Borrelia burgdorferi.
Moore SA, Ronimus RS, Roberson RS, Morgan HW.
Institute of Molecular Biosciences and Allan Wilson Centre for Molecular Ecology and Evolution, Massey University, Palmerston North, New Zealand. [email protected]
The structure of the 60 kDa pyrophosphate (PP(i))-dependent phosphofructokinase (PFK) from Borrelia burgdorferi has been solved and refined (R(free) = 0.243) at 2.55 A resolution. The domain structure of eubacterial ATP-dependent PFKs is conserved in B. burgdorferi PFK, and there are three large insertions relative to E. coli PFK, including a helical domain containing a hairpin structure that interacts with the active site. Asp177, conserved in all PP(i) PFKs, negates the binding of the alpha-phosphate group of ATP and likely contacts the essential Mg(2+) cation via a water molecule. Asn181 blocks the binding of the adenine moiety of ATP. Lys203 hydrogen bonds to a sulfate anion that likely mimics PP(i) substrate binding.
PMID: 12015149 [PubMed - indexed for MEDLINE]
An older abstract said much the same:
FEMS Microbiol Lett. 1996 Dec 15;145(3):309-14. Related Articles, Links
Identification and mapping of a chromosomal gene cluster of Borrelia burgdorferi containing genes expressed in vivo.
Aron L, Toth C, Godfrey HP, Cabello FC.
Department of Microbiology and Immunology, New York Medical College, Valhalla 10595, USA.
A clone containing a 6.4 kb Borrelia burgdorferi chromosomal DNA insert reacted only with sera from patients with Lyme disease and not with any normal human or rabbit sera. Restriction enzyme analysis indicated that this DNA fragment was located on the B. burgdorferi chromosomal map between rpoB and p22A; its direction of transcription was towards p22A. Sequence analysis suggests that LA006 encodes six proteins: three previously described immunodominant lipoproteins of the 39 kDa Bmp protein family, BmpA, BmpB and BmpC; *** a 51 kDa MgtE magnesium transporter protein; a 16 kDa protein kinase C inhibitor; and a 56 kDa protein with similarity to an uncharacterized Escherichia coli chromosomal open reading frame.
PMID: 8978084
``Substitution of manganese for iron is also important in the bacterial pathogen Borrelia burgdorferi, the causative agent of Lyme disease. The B. burgdorferi genome project has revealed the absence of iron-containing membrane proteins and annotated genes encoding proteins such as superoxide dismutase that are *predicted to contain manganese rather than iron (97). The absence of iron and iron-containing proteins is proposed to allow B. burgdorferi to survive in a host that restricts iron, an action that normally limits microbial growth and thus prevents infection. In this way, the B. burgdorferi genome may have evolved by eliminating the requirement for what is usually an essential element. `` http://aem.asm.org/cgi/content/full/70/2/647
It would seem it is a protective measure:
``Intracellular Mn2+ may directly protect against the damaging effects of H2O2 (Kehres et et al., 2000 ).
(Normally H2O2 is capable of destroying many kinds of pathogens.)
Mn 2+ is an essential COFACTOR for many enzymes. But Mg CONTROLS over 350 enzymes. Once again, enzymes and hormones are proteins and according to the mdschoice website (which explains the functions of Mg)...Mg is needed to make all proteins...so Mg would have to be available to make the enzyme and Mn serves as a cofactor of that particular enzyme.
I wish I had access to the following (perhaps you do?):
Mn2+ uptake in bacteria can be inhibited by uncouplers (Silver & Lusk, 1987
Silver, S. & Lusk, J. E. (1987). Bacterial magnesium, manganese and zinc transport. In Ion Transport in Prokaryotes , pp. 165-180. Edited by B. P. Rosen & S. Silver. London:Academic Press.
What uncouplers?
And more from Silver...
Work by Silver and colleagues has shown that CorA-like Mg2+ uptake systems are present in E. coli, Bacillus subtilis, and Rhodobacter capsulatus (6, 11, 12). Using both genomic Southern blot analysis and PCR followed by Southern blot analysis, we showed that corA or a similar gene was present in a wide variety of gram-negative and gram-positive bacteria (14); these results suggest that CorA forms the dominant Mg2+ transport system of the domain Bacteria.
Recently, several complete microbial genomic sequences have become available including examples within both the Bacteria and the domain Archaea. A CorA homolog has been shown to be present in all of these sequences to date except for those for Mycoplasma genitalium, Mycoplasma pneumoniae, and Borrelia burgdorferi, confirming the ubiquity of this class of Mg2+ transporter.
*However, comparison of these CorA-like proteins suggests that the major sequence conservation is within the second and third transmembrane domains (8, 13). The question therefore arises whether this sequence conservation reflects a functional similarity. We tested this possibility by comparing the Mg2+ transport properties of the putative CorA homolog of the archaeon Methanococcus jannaschii (MJ-CorA) and the S. typhimurium CorA (ST-CorA).
Our previous data demonstrated the ubiquity of corA-like genes in virtually all gram-positive and gram-negative bacterial species tested (14). Thus, we suggest that a CorA-like Mg2+ transporter is the major constitutive Mg2+ uptake system of both the Bacteria and the Archaea. It remains to be seen whether similar proteins will be found in eukaryotes. http://jb.asm.org/cgi/content/full/180/10/2788#B14
You stated:
``You need to reevaluate your findings in light of science that is current, not outdated.''
P&G's research, in 2000, is a key component of our understanding of Bb. However, Moore SA, Ronimus RS, Roberson RS, Morgan HW's research in *2002 is equally important...as we piece together an understand of how this Bb manages to survive in us.
You said the following:
``Treponema pallidum does NOT use magnesium, and it is highly doubtful that borrelia does, given current scientific evidence that suggests it uses manganese-dependent enzymes for its metabolic pathways.''
Insulin carries Mg into the cells. However, insulin activates PFK...an enzyme Bb is dependent on. It can be INactivated by glucagons.
Human DC have been reported to phagocytose Borrelia burgdorferi (36) and Mycobacterium tuberculosis (37), influenza (60), and measles (61) viruses and the protozoans Trypanosoma cruzi (39) and L. donovani (38).
``PFK1 can be INHIBITED by H, ATP, glucagons , citrates, and H2O2 and PFK2(liver) is inhibited by glucagons and epinephrine. They are ACTIVATED by insulin.'' http://www.mcw.edu/student/mcwsa/files/biochem22.doc
Glucagon is from islet Alpha cells, is stimulated by hypoglycemia, amino acids, growth hormone and both sympathetic and parasympathetic stimulation. Glucagon release is inhibited by glucose, insulin and somatostatin.
Glucagon is a major catabolic ***hormone, acting primarily on the liver to stimulate glycogenolysis and glyconeogenesis, and inhibit glycogenesis and glycolysis, overall increasing hepatic glucose output and ketone body formation.
In both type 1 and Type 2 diabetes are accompanied by glucagons excess, which may be partly due to insulin deficiency and partly to failure of the diabetic Alpha cell to be suppressed by hyperglycemia. The hyper glucagonaemia may be the cause of insulin resistance in diabetic patients. http://www.diabetesforum.net/eng_glucagon_gut.htm
The body tries to find many alternative pathways to fight Lyme disease because our own highly targeted antibodies have been damaged.
??? Is the following significant:
YhaM. The YhaM protein has recently been identified as an Mn2+-dependent 3'-to-5' exonuclease, active on both RNA and single-stranded DNA (180). It was purified from a B. subtilis strain lacking PNPase and RNase R, and its amino acid sequence, and hence its gene, was identified by mass spectroscopy analysis. YhaM has a molecular mass of 35.5 kDa. It is also active in the presence of Co2+ but ***inactive in the presence of Mg2+ ions. http://mmbr.asm.org/cgi/content/full/67/2/157
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manganese and magnesium are different unrelated elements.
Manganese is number 25 on periodic table of elements, Magnesium is 12.
Manganese cannot substitute for magnesium just because their names are similar. Its like saying that you ran out of Hydrogen so you'll substitute Helium. Hydrogen's symbol is H and Helium He. They are completely different elements with different atomic structures and therefore different reactivities.
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
FEBS Lett. 1983 Sep 19;161(2):247-50. Related Articles, Links
Magnesium as a natural substitute for manganese in concanavalin A and other lectins.
Young NM.
Addition of magnesium to apo-concanavalin A in the presence of calcium was shown by ultraviolet difference spectroscopy to generate a holoprotein spectroscopically identical to the MnCa-holoprotein. The MgCa- and MnCa-forms bound equally strongly to Sephadex G-75.
In kinetic experiments, the binding of Mg2+ was much slower than Mn2+ binding; Kd for Mg2+ was estimated as 7.4 mM. The combined Mg2+ and Mn2+ contents of 10 lectins specific for D-galactose or N-acetyl-D-galactosamine were each close to one atom per subunit, suggesting occupancy of the Mn2+ site by Mg2+ is common in plant lectins.
PMID: 6617878 [PubMed - indexed for MEDLINE]
Concentrations of manganese are found in the mitrochondria of the pituitary, liver, pancreas, kidneys, and bone and is deemed essential for the synthesis of a number of enzymes.
Manganese has the unusual ability of being able to substitute for magnesium in many biochemical processes. It is involved in the synthesis of the neurotransmitter dopamine and is used in the treatment of neuologic disorders.
It also appears to be instrumental in the development of normal bone structure, particularly the growth at the ends of bones where new formation takes place. In addition, some nutritionists have noted a relationship between a deficiency in manganese and that of ear noises and diminished hearing. http://www.innvista.com/health/nutrition/minerals/manganes.htm
Manganese deficiency in crops is the most common micronutrient problem in Michigan. The micronutrient manganese should not be confused with magnesium, a secondary nutrient. Manganese is mainly absorbed by plants in the Mn++ ionic form. Manganese may substitute for magnesium by activating certain phosphate- transferring enzymes, which in turn affect many metabolic processes. A high manganese concentration may induce iron deficiency in plants. http://www.msue.msu.edu/msue/imp/modf1/05209705.html
It is well known that manganese can compete for crucial enzyme activation sites with magnesium. So if magnesium is in short supply, manganese can substitute for magnesium at the active site; subsequently causing a failure to catalyse the activation of various crucial enzymes required for healthy metabolism.
Such is the case for glutamine synthetase, where a delicate balance of magnesium and manganese is required for activating this vital enzyme's function along the pathway which breaks down glutamate into glutamine in the brain.
If the enzyme fails due to a high loading of manganese and depletion of magnesium in the tissues, then highly neuro-toxic levels of glutamate will accumulate in the brain leading to a progressive neuro-degeneration.
A pathogenic acceleration of the ageing process ensues; a which lies at the heart of so many neuro-degenerative conditions such as Motor Neurone disease, Alzheimer's disease and Parkinson's disease, CJD. - where individual genetic susceptibility factors dictate the class of neuro-degenerative disease which you get at the end of the day. www.markpurdey.com/articles_endearth_5.htm
Manganese deficiency is unlikely but the effects of it are likely to be on the skin and bones primarily. The rareness of deficiency may be due to the fact that magnesium can readily substitute for manganese in many reactions when the latter is not available 8 http://www.portfolio.mvm.ed.ac.uk/studentwebs/session2/group29/mangnut.htm
Need more?
Simple question...if the pathogens that cause syphilis and lyme disease don't use Mg...why do they have a protein to transport Magnesium?
Once again...the pathogens use MANY of our nutrients...many.
Sneaky Bb apparently uses Mn to avoid damage from H2O2.
It is a Mg deficiency that I am most concerned about because Mg is needed to make ATP, controls most of the enzymes, is needed to make healthy antibodies (along with Ca)...our own route to destroying the pathogen... and is capable of DNA REPAIR.
[This message has been edited by Marnie (edited 05 March 2005).]
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