Guest guest Posted June 5, 2006 Report Posted June 5, 2006 I have only a few studies, but this one on rats is pretty convincing. (Please note that my tendon pain was not like muscle or nerve twitching.) http://www.prostatitis.org/quinolonejoints.html Antimicrobial Agents and Chemotherapy, February 2000, p. 261-266, Vol. 44, No. 2 Ultrastructure of Achilles Tendons of Rats Treated with Ofloxacin and Fed a Normal or Magnesium-Deficient Diet Mehdi Shakibaei, 1Kerstin Pfister, 2 Rudolf Schwabe, 2 JÝrgen Vormann,3 and Ralf Stahlmann 2 ,* Institute of Anatomy, 1Institute of Clinical Pharmacology and Toxicology, 2and Institute of Molecular Biology and Biochemistry, 3 lin Medical Center, Freie Universität Berlin, 14195 Berlin, Germany ABSTRACT Fluoroquinolones can cause tendinitis and tendon rupture. However, toxicological as well as clinical information on quinolone-induced tendopathy is scarce. We performed extensive electron microscopic studies with Achilles tendon specimens from ofloxacin-treated rats. The drug was given at a dose of 1,200 mg/kg (body weight) orally. Juvenile Wistar rats received one or three oral doses each of 1,200 mg of ofloxacin/kg (body weight)/day. Three days after treatment, the tenocytes of their Achilles tendons showed degenerative alterations, such as multiple vacuoles and vesicles in the cytoplasm that had developed due to swellings and dilatations of cell organelles. Other indications of cell degradation were the occurrence of cell debris and cell detachment from the extracellular matrix accompanied by a loss of cell-matrix interaction. The tenocytes of juvenile Wistar rats that had been treated at day 36 with a single oral dose of 1,200 mg of ofloxacin/kg (body weight) and sacrificed either 3 or 6 months later exhibited similar degenerative alterations. The number of degenerative alterations of tenocytes after ofloxacin treatment was considerably higher in rats that had received a magnesium-deficient diet than in rats with normal magnesium status. Of the adult rats that had been treated once, 5 times, and 10 times with ofloxacin and killed 1 day later, only those with the 10-times treatment showed a significantly increased number of degeneratively altered tenocytes. In summary, effects observed in tendons show similar pathological features as described earlier in cartilage, indicating that quinolone-induced arthropathy and quinolone-induced tendopathy probably are different clinical manifestations of the same toxic effect on cellular components of connective tissue structures. And Dr. Cohen on treating quinolone problems: Alternative Possibilities Magnesium in doses of 400-1000 mg/day may be useful for reducing neuropathic pain or muscle spasms in some people. Feedback from quinolone sufferers about magnesium has been mixed. The U.S. recommended daily amount of magnesium is 320 mg for women and 400 mg for men. Use of higher dosages should always be done with the supervision of a healthcare practitioner. Seniors, people with kidney disorders, and those taking medications for cardiovascular or neurological disorders should have medical supervision even for RDA doses of magnesium. Interestingly, Dr. Flockhart also recommends magnesium for quinolone reactions. Dr. Flockhart recommends low doses of milk of magnesia (1 or 2 teaspoons twice-daily), to be taken for several months. His theory is that because of the affinity of minerals for quinolone antibiotics, magnesium might help leech some remaining fluoroquinolone molecules from the tissues. I am not a fan of milk of magnesia, which is a laxative. If the goal is to absorb magnesium in order to get it into the tissues, chelated magnesium (e.g., magnesium aspartate, magnesium glycinate) or a magnesium solution (e.g., magnesium chloride) are absorbed better than milk of magnesium or cheap magnesium supplements. It has also been suggested that magnesium could be used with calcium and other minerals. The fact is, no one knows. There's little solid science, so it is trial and error. (For more information on magnesium, please go to the other magnesium sections of this website.) B-vitamins have been reported to reduce tingling. Pyrodoxine (vitamin B6) and pantethine (a derivative of pantothenic acid) have been reported to improve some types of nerve pain. One person wrote to me that high doses of lecithin had helped with memory problems. This is not farfetched. Lecithin contains several substances essential for normal nerve functioning. One of these is phosphatidylcholine. For anxiety or agitation, or to increase GABA in the nervous system, many alternative doctors recommend taking GABA, which is an amino acid. GABA has some similar qualities to Valium and Xanax, and it may be helpful for anxiety, nervousness, or insomnia. Too much GABA can cause sedation. Inositol is also used for treating anxiety. There are several alternative methods for reducing inflammation. Omega-3 fatty acids (fish or flax oils) increase the anti-inflammatory prostaglandins (PGE3) in cell membranes. GLA, found in primrose or borage seed oil, increases PGE1, which is also anti-inflammatory. Studies have shown that high doses of omega-3 fatty acids and of GLA reduce the pain of arthritis. This method takes time, several months, because it requires a rebalancing of the prostaglandins in the membranes of trillions of cells, but the ultimate reduction in inflammation is better, in my experience, than with prescription anti-inflammatory drugs. Omega-3 fatty acids and GLA are just two of many alternative methods for reducing inflammation. If you are interested in alternative supplement and diet possibilities, I would suggest consulting with a knowledgeable alternative practitioner. Many doctors have adopted alternative methods because they became dissatisfied with the drug-oriented mindset of mainstream medicine. In my experience, alternative doctors are much more receptive to patients' concerns about medication side effects. Good alternative practitioners are also far more knowledgeable about the biochemical systems of the body. They have tests to measure people's levels of fatty acids, amino acid, antioxidants, minerals (including toxic minerals), and many other factors that may explain why some people are more vulnerable to certain diseases or reactions. Good alternative doctors are knowledgeable about magnesium and other minerals, GABA, omega-3 fatty acids, and many other human-compatible therapies. For example, alternative practitioners use alpha lipoic acid for treating neuropathies. Alpha lipoic acid has long been used in Europe, and there is a considerable medical literature on this substance. Few mainstream doctors are aware of alpha lipoic acid, magnesium, or the other natural remedies I have discussed above. I cannot say that alternative doctors have the answer to quinolone reactions. I can only say that it is another option worth considering. If you run out of options with your mainstream doctors and would like to consult with an alternative practitioner, ask your friends whom they have seen and recommend. Half of the population has consulted with an alternative practitioner at one time or another. You can also find practitioners via the websites of the American College for the Advancement of Medicine (www.ACAM.org) or the American Holistic Medical Association (www.AHMA.org). One caveat: many alternative practitioners do not accept insurance and many of their tests are not covered by health insurance plans. Another caveat: different alternative practitioners use different methods; ask questions, ask for written information; many offices will send brochures or other information about practitioners' methods. In Summary Fluoroquinolone-linked reactions are nasty. These reactions vary from minor to extremely serious. Some are disabling. Recovery varies from individual to individual, with some reactions resolving quickly and others lasting years. As far as I know, none of the companies that manufacture quinolones has attempted to study how to help people sustaining severe quinolone reactions. The manufacturers seem content to list tendon ruptures or neuropathies when the FDA finally demands it, while ignoring the thousands of people who are suffering. To me, this is unconscionable. Then again, if you have looked at my website, you know that for many years I have been concerned about the failure of the drug industry to adequately ensure drug safety. If you have not already done so, please submit a Medwatch report to the FDA about your quinolone reactions. The FDA moves slowly, but with enough reports and pressure from patients (and some doctors, hopefully), the FDA will examine a problem. Filing a Medwatch report is easy to do at: www.fda.gov/medwatch/report/consumer/consumer.htm <http://www.fda.gov/medwatch/report/consumer/consumer.h> .. Or call 800-FDA-1088). I regret that I cannot provide you with more specific, proven treatment options for these terrible reactions. I hope that some of the suggestions above are helpful or at least provide ideas that stimulate other possibilities. Whether you have a mild, moderate, or severe reaction to a quinolone, I hope that your condition resolves soon. Sincerely, Jay S. Cohen, M.D. Quote
Guest guest Posted June 5, 2006 Report Posted June 5, 2006 , I am not able to access the link given to the article. Carolehttp://www.exatest.com/PDF%20Files/15.%20Chronic%20Fatigue%20Syndrome%20.PDF Quote
Guest guest Posted June 5, 2006 Report Posted June 5, 2006 I also had a lot of eye twitching which stopped with magnesium supplementation. It works really fast, too. The strange thing is, magnesium did not show up depleted on my Spectracell testing, so apparently there's plenty in my blood, but it isn't necessarily getting absorbed into my tissue. penny <usenethod@...> wrote: a do you have any refs/elaboration on quinolone tendon damage possibly being at least in part a function of Mg status?I used to have muscle twitches (1000s/day) that would completely stop immediately (for a month or so) whenever I recieved an intravenous Meyers cocktail, which I understand contains alot of Mg. This phenomenon *may not* represent correction of Mg deficiency, as it could also be that my Mg status was perfectly fine, but that the presence of *super-normal* Mg was somehow able to stop the twitching. Nevertheless, I think correction of Mg deficiency has a much greater ring of plausibility.At that point in my history, oral Mg did not affect my twitches discernably. After much strong abx treatment got rid of most of my illness, I now have only a dozen twitches a day, and these are suppressed as long as I take ~200 mg of oral Mg a couple times a week. Thus, if in fact I did have Mg deficiency in the past, it might well be that my Mg status remains marginal at present.I finally looked into intracellular Mg status in CFS. Pubmed yields various findings on red cell Mg. This JCFS paper claims (p 17) that red cell Mg testing may not be valid, and gives 2 refs on that which I may or may not look up sometime. The same paper cites unpublished claims that CFSers are Mg deficient according to a different assay. (Without further info I cannot assume that unpublished results have high validity.) Retention of Mg after IV loading seems to be the gold standard test according to this JCFS paper. http://www.exatest.com/PDF%20Files/15.%20Chronic%20Fatigue%20Syndrome%20.PDFAlso interesting re that gold standard is this rather confusing pubmed abstract, and the one after:97 patients (25 per cent males, ages ranging from 14 to 73 years, median 38 years) with complaints of chronic fatigue (chronic fatigue syndrome, fibromyalgia or/and spasmophilia) have been enrolled in a prospective study to evaluate the Mg status and the dietary intake of Mg. An IV loading test (performed following the Ryzen protocol) showed a Mg deficit in 44 patients. After Mg supplementation in 24 patients, the loading test showed a significant decrease (p = 0.0018) in Mg retention. Mean values of serum Mg, red blood cell Mg and magnesuria showed no significant difference between patients with or without Mg deficiency. No association was found between Mg deficiency, CFS or FM. However serum Mg level was significantly lower in the patients with spasmophilia than in the other patients.PMID: 9513929 [PubMed - indexed for MEDLINE] Red blood cell magnesium concentrations were measured in samples from 89 patients who fulfilled the diagnostic criteria for chronic fatigue syndrome and the results compared to those found in an age and sex matched group selected from the normal population. No significant difference was found. Six patients were further investigated using a magnesium loading test to determine if there was any evidence of magnesium deficiency associated with this disorder. None was found. There is therefore no indication for the use of magnesium therapy in the management of this condition.PMID: 7832571 [PubMed - indexed for MEDLINE] Further papers on Mg status in CFS/etc, and further work on the validity of the Mg lodaing/retention assay, are here:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed_pubmed & from_uid=9513929 Quote
Guest guest Posted June 5, 2006 Report Posted June 5, 2006 I also had a lot of eye twitching which stopped with magnesium supplementation. It works really fast, too. The strange thing is, magnesium did not show up depleted on my Spectracell testing, so apparently there's plenty in my blood, but it isn't necessarily getting absorbed into my tissue. penny <usenethod@...> wrote: a do you have any refs/elaboration on quinolone tendon damage possibly being at least in part a function of Mg status?I used to have muscle twitches (1000s/day) that would completely stop immediately (for a month or so) whenever I recieved an intravenous Meyers cocktail, which I understand contains alot of Mg. This phenomenon *may not* represent correction of Mg deficiency, as it could also be that my Mg status was perfectly fine, but that the presence of *super-normal* Mg was somehow able to stop the twitching. Nevertheless, I think correction of Mg deficiency has a much greater ring of plausibility.At that point in my history, oral Mg did not affect my twitches discernably. After much strong abx treatment got rid of most of my illness, I now have only a dozen twitches a day, and these are suppressed as long as I take ~200 mg of oral Mg a couple times a week. Thus, if in fact I did have Mg deficiency in the past, it might well be that my Mg status remains marginal at present.I finally looked into intracellular Mg status in CFS. Pubmed yields various findings on red cell Mg. This JCFS paper claims (p 17) that red cell Mg testing may not be valid, and gives 2 refs on that which I may or may not look up sometime. The same paper cites unpublished claims that CFSers are Mg deficient according to a different assay. (Without further info I cannot assume that unpublished results have high validity.) Retention of Mg after IV loading seems to be the gold standard test according to this JCFS paper. http://www.exatest.com/PDF%20Files/15.%20Chronic%20Fatigue%20Syndrome%20.PDFAlso interesting re that gold standard is this rather confusing pubmed abstract, and the one after:97 patients (25 per cent males, ages ranging from 14 to 73 years, median 38 years) with complaints of chronic fatigue (chronic fatigue syndrome, fibromyalgia or/and spasmophilia) have been enrolled in a prospective study to evaluate the Mg status and the dietary intake of Mg. An IV loading test (performed following the Ryzen protocol) showed a Mg deficit in 44 patients. After Mg supplementation in 24 patients, the loading test showed a significant decrease (p = 0.0018) in Mg retention. Mean values of serum Mg, red blood cell Mg and magnesuria showed no significant difference between patients with or without Mg deficiency. No association was found between Mg deficiency, CFS or FM. However serum Mg level was significantly lower in the patients with spasmophilia than in the other patients.PMID: 9513929 [PubMed - indexed for MEDLINE] Red blood cell magnesium concentrations were measured in samples from 89 patients who fulfilled the diagnostic criteria for chronic fatigue syndrome and the results compared to those found in an age and sex matched group selected from the normal population. No significant difference was found. Six patients were further investigated using a magnesium loading test to determine if there was any evidence of magnesium deficiency associated with this disorder. None was found. There is therefore no indication for the use of magnesium therapy in the management of this condition.PMID: 7832571 [PubMed - indexed for MEDLINE] Further papers on Mg status in CFS/etc, and further work on the validity of the Mg lodaing/retention assay, are here:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Display & dopt=pubmed_pubmed & from_uid=9513929 Quote
Guest guest Posted June 6, 2006 Report Posted June 6, 2006 a - thanks, awesome. Carole - that link still works for me. I'm running Microsoft Explorer 6.0. The files a pdf; can your setup read other .pdf's? Penny - apparantly at least some believe that blood Mg is not at all indicative of cellular Mg status. Quote
Guest guest Posted June 6, 2006 Report Posted June 6, 2006 , I tried it again and it works. Thanks ! Carole > > a - thanks, awesome. > > Carole - that link still works for me. I'm running Microsoft Explorer > 6.0. The files a pdf; can your setup read other .pdf's? > > Penny - apparantly at least some believe that blood Mg is not at all > indicative of cellular Mg status. > Quote
Guest guest Posted June 6, 2006 Report Posted June 6, 2006 a The amounts used in the study 1200mg per kilo is like 10,000 times more quinolone than a normal human gets.I certainly believe that they kill a ton of bacteria in there path and annoy a ton more so you really can't say what toxins are being expressed that may harm body systems.I feel strongly that when you get resistance, easily achieved, and you find cipro resistance you really have got some pissed off bugs IMO.I actually used heaps more cipro second and third time around and yet the first time was a disaster a week or two after the initial treatment the infection came back with a vengeance and cipro didn't touch it.So I feel if you respect the infections and don't play with them your going to be a happier camper and the fact that quinolones don't feature in true disease- repair of skeletal systems- it ain't a choice of drug to even contemplate on it's own. > > I have only a few studies, but this one on rats is pretty convincing. > (Please note that my tendon pain was not like muscle or nerve twitching.) > > > > > > http://www.prostatitis.org/quinolonejoints.html > > > > Antimicrobial Agents and Chemotherapy, February 2000, p. 261-266, Vol. > > 44, No. 2 Ultrastructure of Achilles Tendons of Rats Treated with Ofloxacin > and Fed a Normal or Magnesium-Deficient Diet Mehdi Shakibaei, 1Kerstin > Pfister, 2 Rudolf Schwabe, 2 JÝrgen Vormann,3 and Ralf Stahlmann 2 ,* > Institute of Anatomy, 1Institute of Clinical Pharmacology and Toxicology, > 2and Institute of Molecular Biology and Biochemistry, 3 lin > Medical Center, Freie Universität Berlin, 14195 Berlin, Germany > > > > ABSTRACT > > > > Fluoroquinolones can cause tendinitis and tendon rupture. However, > toxicological as well as clinical information on quinolone-induced > tendopathy is scarce. We performed extensive electron microscopic studies > with Achilles tendon specimens from ofloxacin-treated rats. The drug was > given at a dose of 1,200 mg/kg (body weight) orally. Juvenile Wistar rats > received one or three oral doses each of 1,200 mg of ofloxacin/kg (body > weight)/day. > > > > Three days after treatment, the tenocytes of their Achilles tendons showed > degenerative alterations, such as multiple vacuoles and vesicles in the > cytoplasm that had developed due to swellings and dilatations of cell > organelles. Other indications of cell degradation were the occurrence of > cell debris and cell detachment from the extracellular matrix accompanied by > a loss of cell-matrix interaction. > > > > The tenocytes of juvenile Wistar rats that had been treated at day 36 with a > single oral dose of 1,200 mg of ofloxacin/kg (body weight) and sacrificed > either 3 or 6 months later exhibited similar degenerative alterations. The > number of degenerative alterations of tenocytes after ofloxacin treatment > was considerably higher in rats that had received a magnesium- deficient diet > than in rats with normal magnesium status. Of the adult rats that had been > treated once, 5 times, and 10 times with ofloxacin and killed 1 day later, > only those with the 10-times treatment showed a significantly increased > number of degeneratively altered tenocytes. In summary, effects observed in > tendons show similar pathological features as described earlier in > cartilage, indicating that quinolone-induced arthropathy and > quinolone-induced tendopathy probably are different clinical manifestations > of the same toxic effect on cellular components of connective tissue > structures. > > > > And Dr. Cohen on treating quinolone problems: > > > > Alternative Possibilities > Magnesium in doses of 400-1000 mg/day may be useful for reducing > neuropathic pain or muscle spasms in some people. Feedback from quinolone > sufferers about magnesium has been mixed. The U.S. recommended daily amount > of magnesium is 320 mg for women and 400 mg for men. Use of higher dosages > should always be done with the supervision of a healthcare practitioner. > Seniors, people with kidney disorders, and those taking medications for > cardiovascular or neurological disorders should have medical supervision > even for RDA doses of magnesium. Interestingly, Dr. Flockhart also > recommends magnesium for quinolone reactions. Dr. Flockhart recommends low > doses of milk of magnesia (1 or 2 teaspoons twice-daily), to be taken for > several months. His theory is that because of the affinity of minerals for > quinolone antibiotics, magnesium might help leech some remaining > fluoroquinolone molecules from the tissues. > > I am not a fan of milk of magnesia, which is a laxative. If the goal is > to absorb magnesium in order to get it into the tissues, chelated magnesium > (e.g., magnesium aspartate, magnesium glycinate) or a magnesium solution > (e.g., magnesium chloride) are absorbed better than milk of magnesium or > cheap magnesium supplements. It has also been suggested that magnesium > could be used with calcium and other minerals. The fact is, no one knows. > There's little solid science, so it is trial and error. (For more > information on magnesium, please go to the other magnesium sections of this > website.) > > B-vitamins have been reported to reduce tingling. Pyrodoxine (vitamin > B6) and pantethine (a derivative of pantothenic acid) have been reported to > improve some types of nerve pain. One person wrote to me that high doses of > lecithin had helped with memory problems. This is not farfetched. Lecithin > contains several substances essential for normal nerve functioning. One of > these is phosphatidylcholine. > > For anxiety or agitation, or to increase GABA in the nervous system, > many alternative doctors recommend taking GABA, which is an amino acid. > GABA has some similar qualities to Valium and Xanax, and it may be helpful > for anxiety, nervousness, or insomnia. Too much GABA can cause sedation. > Inositol is also used for treating anxiety. > > There are several alternative methods for reducing inflammation. > Omega-3 fatty acids (fish or flax oils) increase the anti- inflammatory > prostaglandins (PGE3) in cell membranes. GLA, found in primrose or borage > seed oil, increases PGE1, which is also anti-inflammatory. Studies have > shown that high doses of omega-3 fatty acids and of GLA reduce the pain of > arthritis. This method takes time, several months, because it requires a > rebalancing of the prostaglandins in the membranes of trillions of cells, > but the ultimate reduction in inflammation is better, in my experience, than > with prescription anti-inflammatory drugs. Omega-3 fatty acids and GLA are > just two of many alternative methods for reducing inflammation. > > If you are interested in alternative supplement and diet possibilities, > I would suggest consulting with a knowledgeable alternative practitioner. > Many doctors have adopted alternative methods because they became > dissatisfied with the drug-oriented mindset of mainstream medicine. In my > experience, alternative doctors are much more receptive to patients' > concerns about medication side effects. Good alternative practitioners are > also far more knowledgeable about the biochemical systems of the body. They > have tests to measure people's levels of fatty acids, amino acid, > antioxidants, minerals (including toxic minerals), and many other factors > that may explain why some people are more vulnerable to certain diseases or > reactions. Good alternative doctors are knowledgeable about magnesium and > other minerals, GABA, omega-3 fatty acids, and many other human- compatible > therapies. For example, alternative practitioners use alpha lipoic acid for > treating neuropathies. Alpha lipoic acid has long been used in Europe, and > there is a considerable medical literature on this substance. Few > mainstream doctors are aware of alpha lipoic acid, magnesium, or the other > natural remedies I have discussed above. I cannot say that alternative > doctors have the answer to quinolone reactions. I can only say that it is > another option worth considering. > > If you run out of options with your mainstream doctors and would like to > consult with an alternative practitioner, ask your friends whom they have > seen and recommend. Half of the population has consulted with an > alternative practitioner at one time or another. You can also find > practitioners via the websites of the American College for the Advancement > of Medicine (www.ACAM.org) or the American Holistic Medical Association > (www.AHMA.org). One caveat: many alternative practitioners do not accept > insurance and many of their tests are not covered by health insurance plans. > Another caveat: different alternative practitioners use different methods; > ask questions, ask for written information; many offices will send brochures > or other information about practitioners' methods. > > In Summary > Fluoroquinolone-linked reactions are nasty. These reactions vary from > minor to extremely serious. Some are disabling. Recovery varies from > individual to individual, with some reactions resolving quickly and others > lasting years. As far as I know, none of the companies that manufacture > quinolones has attempted to study how to help people sustaining severe > quinolone reactions. The manufacturers seem content to list tendon ruptures > or neuropathies when the FDA finally demands it, while ignoring the > thousands of people who are suffering. To me, this is unconscionable. Then > again, if you have looked at my website, you know that for many years I have > been concerned about the failure of the drug industry to adequately ensure > drug safety. > > If you have not already done so, please submit a Medwatch report to the > FDA about your quinolone reactions. The FDA moves slowly, but with enough > reports and pressure from patients (and some doctors, hopefully), the FDA > will examine a problem. Filing a Medwatch report is easy to do at: > www.fda.gov/medwatch/report/consumer/consumer.htm > <http://www.fda.gov/medwatch/report/consumer/consumer.h> . Or call > 800-FDA-1088). > > I regret that I cannot provide you with more specific, proven treatment > options for these terrible reactions. I hope that some of the suggestions > above are helpful or at least provide ideas that stimulate other > possibilities. Whether you have a mild, moderate, or severe reaction to a > quinolone, I hope that your condition resolves soon. > > Sincerely, > > Jay S. Cohen, M.D. > > > > > > > > > > a do you have any refs/elaboration on quinolone tendon damage > possibly being at least in part a function of Mg status? > > I used to have muscle twitches (1000s/day) that would completely stop > immediately (for a month or so) whenever I recieved an intravenous > Meyers cocktail, which I understand contains alot of Mg. This > phenomenon *may not* represent correction of Mg deficiency, as it > could also be that my Mg status was perfectly fine, but that the > presence of *super-normal* Mg was somehow able to stop the twitching. > Nevertheless, I think correction of Mg deficiency has a much greater > ring of plausibility. > > At that point in my history, oral Mg did not affect my twitches > discernably. After much strong abx treatment got rid of most of my > illness, I now have only a dozen twitches a day, and these are > suppressed as long as I take ~200 mg of oral Mg a couple times a > week. Thus, if in fact I did have Mg deficiency in the past, it might > well be that my Mg status remains marginal at present. > > I finally looked into intracellular Mg status in CFS. Pubmed yields > various findings on red cell Mg. This JCFS paper claims (p 17) that > red cell Mg testing may not be valid, and gives 2 refs on that which > I may or may not look up sometime. The same paper cites unpublished > claims that CFSers are Mg deficient according to a different assay. > (Without further info I cannot assume that unpublished results have > high validity.) Retention of Mg after IV loading seems to be the gold > standard test according to this JCFS paper. > > http://www.exatest.com/PDF%20Files/15.%20Chronic%20Fatigue% 20Syndrome% > <http://www.exatest.com/PDF%20Files/15.%20Chronic%20Fatigue% 20Syndrome%25> > 20.PDF > > Also interesting re that gold standard is this rather confusing > pubmed abstract, and the one after: > > 97 patients (25 per cent males, ages ranging from 14 to 73 years, > median 38 years) with complaints of chronic fatigue (chronic fatigue > syndrome, fibromyalgia or/and spasmophilia) have been enrolled in a > prospective study to evaluate the Mg status and the dietary intake of > Mg. An IV loading test (performed following the Ryzen protocol) > showed a Mg deficit in 44 patients. After Mg supplementation in 24 > patients, the loading test showed a significant decrease (p = 0.0018) > in Mg retention. Mean values of serum Mg, red blood cell Mg and > magnesuria showed no significant difference between patients with or > without Mg deficiency. No association was found between Mg > deficiency, CFS or FM. However serum Mg level was significantly lower > in the patients with spasmophilia than in the other patients. > PMID: 9513929 [PubMed - indexed for MEDLINE] > > > Red blood cell magnesium concentrations were measured in samples from > 89 patients who fulfilled the diagnostic criteria for chronic fatigue > syndrome and the results compared to those found in an age and sex > matched group selected from the normal population. No significant > difference was found. Six patients were further investigated using a > magnesium loading test to determine if there was any evidence of > magnesium deficiency associated with this disorder. None was found. > There is therefore no indication for the use of magnesium therapy in > the management of this condition. > PMID: 7832571 [PubMed - indexed for MEDLINE] > > > Further papers on Mg status in CFS/etc, and further work on the > validity of the Mg lodaing/retention assay, are here: > > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? > db=pubmed & cmd=Display & dopt=pubmed_pubmed & from_uid=9513929 > > > > > _____ > Quote
Guest guest Posted June 6, 2006 Report Posted June 6, 2006 Yes- I'm one of the people who think blood levels of magnesium(mg) do not reflect cellular status. Barb > > > > a - thanks, awesome. > > > > Carole - that link still works for me. I'm running Microsoft > Explorer > > 6.0. The files a pdf; can your setup read other .pdf's? > > > > Penny - apparantly at least some believe that blood Mg is not at all > > indicative of cellular Mg status. > > > Quote
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