Hi, all.
It has been known for quite a few years that in ME/CFS, there is often a deficiency of intracellular magnesium in the tissue cells. The best test for this is the EXAtest offered by Intracellular Diagnostics, Inc., in Oregon. People try various treatments to raise the intracellular magnesium level, including Epsom salt baths, injections with magnesium sulfate, magnesium oil applied to the skin, and oral magnesium supplements, and it has seemed to be difficult to raise the intracellular magnesium level and keep it up.
Another essential nutrient that I often find to be low when I analyze urine organic acids tests for PWMEs is vitamin B6 (and sometimes also B2, which is necessary to convert B6 into its active form, P5P). I think that the reason B6 (and maybe B2) tend to be low in ME/CFS is that P5P is very important in amino acids metabolism, enabling conversion of one amino acid into another, and this is necessary for feeding some of them into the Krebs cycle to be burned for energy. PWMEs burn amino acids at a higher rate than normal, because glutathione depletion puts a partial block in the Krebs cycle early on, and that inhibits the utilization of carbs and fats as fuel, according to my hypothesis.
I'm writing this post to point out that I think there is a connection between these two deficiencies, such that a B6 (or B2) deficiency will cause lowered intracellular magnesium.
Here's some history behind this issue: When the late Dr. Bernie Rimland started what became the Autism Research Foundation back in the 60s, he asked parents of autistic children what treatments they had found helpful for their children. Several replied that vitamin B6 was helpful, and Bernie started recommending it. He then received a phone call from the controversial pioneering nutritionist Adelle Davis, who told him that it is important to take magnesium with B6, because they work together in the metabolism. He started suggesting that to the autism parents, and significantly better results were found for this combination than when either of them was taken alone.
Since I heard Bernie tell this story at a DAN! conference several years ago, I've wondered what this connection is in the biochemistry. I've never seen it spelled out anywhere. And since we have found that autism and ME/CFS share much of the same pathophysiology, I've wondered how this might apply to ME/CFS.
Well, yesterday I think I came up with the connection. I was working on a case in which the person has high P5P in the blood, but appears to be unable to remove the phosphate group so that the pyridoxal can enter the cells to be rephosphorylated and utilized as P5P in its normal roles in the biochemistry. His urine organic acids panel showed lots of evidence of deficiency of P5P activity. But it also showed evidence of severe magnesium deficiency, even though he was getting magnesium injections. It occurred to me that perhaps intracellular P5P is needed to transport magnesium into the cells.
The mechanisms involved in the transport of magnesium have not been completely figured out by researchers yet, but I located a study published in 1981 (abstract below) in which vitamin B6 supplementation was found to raise the intracellular magnesium levels in the red blood cells. Since additional magnesium was not given, this indicates that vitamin B6 is important in the transport of magnesium into cells. Since vitamin B2 is necessary to form P5P (the active form of B6) from vitamin B6, I think that a deficiency in B2 would also impact intracellular magnesium.
I'm posting this to let PWMEs know of the importance of this connection.
Best regards,
Rich
Ann Clin Lab Sci. 1981 Jul-Aug;11(4):333-6.
Effect of vitamin B-6 on plasma and red blood cell magnesium levels in premenopausal women.
Abraham GE, Schwartz UD, Lubran MM.
Abstract
The effect of 100 mg of vitamin B6 twice a day on plasma and red blood cell (RBC) magnesium was evaluated in nine premenopausal subjects during the period of one month. According to reported normal ranges for plasma and RBC magnesium (1.7 to 2.3 and 4.7 to 7.0, mg per dl, respectively), three subjects had low plasma magnesium, and all subjects had low RBC magnesium during the control period. Following vitamin B6 administration, the mean plasma and RBC magnesium levels were significantly elevated, with a doubling of RBC levels after four weeks of therapy. These results support the postulate that vitamin B6 plays a fundamental role in the active transport of minerals across cell membranes.
PMID: 7271227
It has been known for quite a few years that in ME/CFS, there is often a deficiency of intracellular magnesium in the tissue cells. The best test for this is the EXAtest offered by Intracellular Diagnostics, Inc., in Oregon. People try various treatments to raise the intracellular magnesium level, including Epsom salt baths, injections with magnesium sulfate, magnesium oil applied to the skin, and oral magnesium supplements, and it has seemed to be difficult to raise the intracellular magnesium level and keep it up.
Another essential nutrient that I often find to be low when I analyze urine organic acids tests for PWMEs is vitamin B6 (and sometimes also B2, which is necessary to convert B6 into its active form, P5P). I think that the reason B6 (and maybe B2) tend to be low in ME/CFS is that P5P is very important in amino acids metabolism, enabling conversion of one amino acid into another, and this is necessary for feeding some of them into the Krebs cycle to be burned for energy. PWMEs burn amino acids at a higher rate than normal, because glutathione depletion puts a partial block in the Krebs cycle early on, and that inhibits the utilization of carbs and fats as fuel, according to my hypothesis.
I'm writing this post to point out that I think there is a connection between these two deficiencies, such that a B6 (or B2) deficiency will cause lowered intracellular magnesium.
Here's some history behind this issue: When the late Dr. Bernie Rimland started what became the Autism Research Foundation back in the 60s, he asked parents of autistic children what treatments they had found helpful for their children. Several replied that vitamin B6 was helpful, and Bernie started recommending it. He then received a phone call from the controversial pioneering nutritionist Adelle Davis, who told him that it is important to take magnesium with B6, because they work together in the metabolism. He started suggesting that to the autism parents, and significantly better results were found for this combination than when either of them was taken alone.
Since I heard Bernie tell this story at a DAN! conference several years ago, I've wondered what this connection is in the biochemistry. I've never seen it spelled out anywhere. And since we have found that autism and ME/CFS share much of the same pathophysiology, I've wondered how this might apply to ME/CFS.
Well, yesterday I think I came up with the connection. I was working on a case in which the person has high P5P in the blood, but appears to be unable to remove the phosphate group so that the pyridoxal can enter the cells to be rephosphorylated and utilized as P5P in its normal roles in the biochemistry. His urine organic acids panel showed lots of evidence of deficiency of P5P activity. But it also showed evidence of severe magnesium deficiency, even though he was getting magnesium injections. It occurred to me that perhaps intracellular P5P is needed to transport magnesium into the cells.
The mechanisms involved in the transport of magnesium have not been completely figured out by researchers yet, but I located a study published in 1981 (abstract below) in which vitamin B6 supplementation was found to raise the intracellular magnesium levels in the red blood cells. Since additional magnesium was not given, this indicates that vitamin B6 is important in the transport of magnesium into cells. Since vitamin B2 is necessary to form P5P (the active form of B6) from vitamin B6, I think that a deficiency in B2 would also impact intracellular magnesium.
I'm posting this to let PWMEs know of the importance of this connection.
Best regards,
Rich
Ann Clin Lab Sci. 1981 Jul-Aug;11(4):333-6.
Effect of vitamin B-6 on plasma and red blood cell magnesium levels in premenopausal women.
Abraham GE, Schwartz UD, Lubran MM.
Abstract
The effect of 100 mg of vitamin B6 twice a day on plasma and red blood cell (RBC) magnesium was evaluated in nine premenopausal subjects during the period of one month. According to reported normal ranges for plasma and RBC magnesium (1.7 to 2.3 and 4.7 to 7.0, mg per dl, respectively), three subjects had low plasma magnesium, and all subjects had low RBC magnesium during the control period. Following vitamin B6 administration, the mean plasma and RBC magnesium levels were significantly elevated, with a doubling of RBC levels after four weeks of therapy. These results support the postulate that vitamin B6 plays a fundamental role in the active transport of minerals across cell membranes.
PMID: 7271227
