Exatest interpretation guide

From [www.exatest.com]

MAGNESIUM -
DESIRABLE INTRACELLULAR REFERENCE RANGE:
33.9-40mEq/l

Adequate intracellular magnesium is essential to normal tissue and organ function. Next to potassium it is the most abundant cation in cells and tissues. Measurement of intracellular levels with the EXA test is vital to maintain and treat many medical syndromes. Serum levels, RBCs and lymphocytes do not adequately reflect cell or tissue levels of magnesium. Magnesium modulates tissue transport of calcium and potassium ions and participates in hundreds of enzyme systems including formation of high-energy compounds such as ATP. All physiological activity, secretion, bone formation, cardiac and neuromuscular activity is affected by magnesium in tissues. Optimal tissue levels of magnesium prevent cardiac irregularities and tend to maintain lower blood pressure. Magnesium concentrations in optimal ranges indicate possible lowered risk factor for hypertension, angina, arrhythmias and vascular spasm.
RDA for MAGNESIUM IS 350-400 mg

LOW MAGNESIUM
Determination of low tissue magnesium using the EXA test is vital to the objective treatment of depleted patients. Magnesium loss affects normal tissue and organ function while modulating transport of potassium, calcium, and phosphorus within tissues. Causative factors of Mg deficiency include diabetes, use of diuretics and digitalis, excessive stress, exercise, malabsorption, poor diet, alcoholism, and heavy metal poisoning. LOW magnesium has been associated with EKG and cardiac abnormalities, fibrillation, vascular and muscle spasms. Correlations with migraine headaches, asthma, eclampsia, PMS, and chronic fatigue syndrome are abundant in the medical literature. Low magnesium is seen in cardiac failure and prolonged QT syndrome. Neurological disorders, panic attacks and nerve irritability have been associated with low tissue magnesium levels.

HIGH MAGNESIUM
Since the kidneys excrete excess magnesium, it is rare to find tissue levels, which exceed optimal levels. Excess tissue magnesium has a sedative and hypotensive effect and supplementation must be used with caution in renal disease. B-complex vitamins, especially B-6 appear to enhance magnesium transport. Kidney function is the major excretory pathway for magnesium. In kidney disease excess retention of magnesium can cause impairment of kidney and CNS function. High intravenous doses of magnesium have been used ineclampsia, asthmatic attacks and to convert intractable cardiac arrhythmias. Patients with cardiac failure and renal disease may retain magnesium in the tissues. ACE inhibitors also cause magnesium retention.
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CALCIUM -
DESIRABLE INTRACELLULAR REFERENCE RANGE:
3.2-5.0 mEq/l

Calcium is involved in secretory functions of tissues at the cellular level.
Neurotransmission and neuromuscular transmission require regulated calciummovements. Structure of the supportive tissues, bone and cartilage, involves normal calcium metabolism. Serum calcium is narrowly regulated by endocrine secretions. Intracellular calcium may vary much more than serum levels and tissue imbalances can cause a variety of syndromes affecting bone/tooth formation, blood clotting, heart rhythm, and permeability of cell membranes.
RDA for CALCIUM is 800-1,200 mg

LOW CALCIUM
Deficiency of cellular calcium may be expressed with symptoms of peripheral numbness, brittle fingernails, fragile bones, cardiac palpitations, hypertension, insomnia, CNS irritability leg and muscle cramps, osteomalacia, osteoporosis, and periodontal disease. There is evidence that low tissue calcium contributes to PMS, and muscle flaccidity. Cardiomyopathic heart tissue appears to have diminished concentrations of calcium. True decrease in the physiologically active Ca++ occurs in many situations, including hypoparathyroidism, vitamin D deficiency, chronic renal failure, magnesium deficiency, prolonged anticonvulsant therapy, acute pancreatitis, massive transfusion, and alcoholism.

HIGH CALCIUM
Elevated tissue calcium may be a sign of mobilization of bone calcium into soft tissues signaling early signs of developing osteoporosis. High intracellular calcium interferes with ATP formation, muscle contraction, relaxation, enzyme activity, and neuromuscular transmission. Increased cellular calcium predisposes to spasm of peripheral arterioles leading to increased blood pressure. Calcium may also be a factor in plaque formation,
angina, hypertension and athero-arteriosclerosis. Calcium channel blockers as well as magnesium affects movement of calcium into the soft tissues and heart muscle. Parathyroid hormone, which regulates calcium, is increased when magnesium is low. PTH is lowered when magnesium stores are high. Hypomagnesia occurs commonly in hyperthyroidism. Hypercalcemia is seen in malignant neoplasms (with or without bone involvement), primary and tertiary hyperparathyroidism, sarcoidosis, vitamin D intoxication, Paget's disease of bone, thyrotoxicosis, acromegaly, and the diuretic phase of renal acute tubular necrosis.
In summary: Elevated intracellular calcium might indicate loss of calcium from skeletal tissues and might possibly indicate that the adequate intake of daily calcium be maintained or increased, depending on the judgment and diagnosis of the physician.
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POTASSIUM -
DESIRABLE INTRACELLULAR REFERENCE RANGE:
80.0-240.0 mEq/l

Potassium is essential for normal nerve and muscle function and has a profound effect on maintaining normal cardiac function. The extent of potassium loss in tissue cannot be accurately assessed by serum measurements alone. Adequate measurements of TISSUE and serum potassium are essential in determining cellular fluid balance. Maintenance of cardiac skeletal and smooth muscle and nerve function depends on adequate potassium gradients between intra and extracellular spaces. All neuromuscular activity is dependent on both sodium and potassium for maintaining the electro-potential in both nerves and muscle. The major means of regulation of potassium is though the kidneys, as well as the
gastrointestinal tract and skin. Serum potassium may not reflect the tissue levels when potassium is given. EXA testing provides information before a crisis of potassium loss or excess is identified in serum. Lack of magnesium is a major factor in loss of potassium.
RDA for POTASSIUM is 1875-5625 mg.

LOW POTASSIUM
Low magnesium leads to low tissue potassium since magnesium is absolutely needed for potassium transport into tissue. Risk for cardiac irritability, irregularity and hypertension have related to loss of cellular potassium Depletion occurs when potassium output exceeds intake. Loss may be seen in adrenal insufficiency, excess sweating, diuretic use, steroid use, alcoholism, dietary loss, diarrhea, vomiting, renal disease, alkalosis, and malabsorption. High protein weight loss programs or diabetic keto acidosis can cause lose of K as well as Mg due to excretion of ketones during the sudden mobilization of fats.

HIGH POTASSIUM
Tissue potassium may be elevated despite normal serum levels. The EXA test reveals the tissue levels in the face of either excess or low potassium in the serum. Excess potassium can cause profound changes in membrane potentials and altered EKG readings. Elevated tissue potassium may be due to intravenous administration, hormonal therapy (excess insulin), acidosis, or dietary intake. Cellular electrolyte levels and resting membrane potentials are affected by tissue potassium, sodium and calcium concentrations. Potassium in tissues is about 30-40 times greater than serum
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SODIUM -
DESIRABLE INTRACELLULAR REFERENCE RANGE:
3.8-5.5 mEq/l

Sodium balance is a reflection of Na intake and output. ATP driven sodium and potassium pumps are vital in maintaining the gradients of potassium and sodium inside and outside the cell. These pumps are highly dependent on magnesium to energize the enzymes of the active transport process.
Cellular charge, function and integrity are a combination of sodium and potassium pumps, which maintain electrolyte and mineral balance in cellular events.
RDA for SODIUM is 1100-3300 mg

LOW SODIUM
Sodium is the principal cation of the serum. Changes in Na levels tend to affect other ionic compartments. Sodium loss may be due to vomiting, diarrhea lack of intake, excessive sweating fever, hot environment, exercise, as well as adrenal insufficiency, hypoaldosterism, diuretic use and renal disease. Burn patients may also lose sodium. Lack of sodium chloride might cause muscle cramps, dizziness, and possible convulsions. Some individuals respond to low sodium intake with hypotension. Renal sodium excretion can be affected by cardiac output, multiple endocrine factors, and diuretics. Diuretic treated patients may be subjects for both potassium
and magnesium support.

HIGH SODIUM
Diets high in sodium might increase of sodium in the body causing swelling or edema. Water retention elevates the blood pressure, puts a strain of the heart and kidneys and results in congestive heart failure. In liver disease, venous obstruction causes fluid to leak into the abdominal space (ascites) which lowers the effective blood volume which in turn causes salt and water retention as seen in heart failure. Hypertension can result from sodium and water retention. Renal disease will also result in salt and fluid retention Excess sodium can upset the delicate potassium/sodium balance which influences all neuromuscular activity including cardiac function.

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CHLORIDE –
DESIRABLE INTRACELLULAR REFEERENCE RANGE:
3.4-6.0 mEq/l

The amount of chloride ions in the body is a reflection between intake and output and parallels that of sodium ingestion. Chloride is present in higher concentrations in the serum than inside the cells. Chloride ions tend to diffuse into the cells to a negatively charged cytoplasm and are pushed out along an electrical gradient until balance is achieved. If sodium/potassium ATP driven pumps are not working, (possible Mg depletion), chloride tends to enter the cell causing them to swell. Cell integrity is a result of ion movements to maintain homeostasis along with sodium and potassium.
RDA for CHLORIDE is 1100-3300 mg.

LOW CHLORIDE
Dehydration caused by infectious diseases and diarrhea or severe vomiting with fever, can cause deficits in body chlorides. Excessive sweating, exercise, hot environment, and conditions similar to sodium depletion are factors. Renal disease and adrenal insufficiency (hypoaldosteronism) may cause low body chloride. Restriction of salt intake tends to lower chloride intake as does extensive renal loss and some diuretics. Low sodium diets can lower the chloride levels. Osmotic diuresis as seen in diabetes mellitus may deplete chloride. When cellular potassium is low, chloride levels are also lower, since chloride is transported with sodium and potassium.

HIGH CHLORIDE
Excessive cellular chloride has been reported to contribute to hypertension. The negative chloride ions tend to diffuse into tissues along with potassium and sodium. Potassium internal cell concentration is 30 times greater than outside the cells. Thus, high chloride results when positive sodium and potassium ions move into the tissues. High levels may be caused by sodium retention or high salt intake as well as kidney malfunction, or side effects of corticosteroids. Changes in cellular chloride are seen in dehydration, renal tubular acidosis, acute renal failure, diabetes insipidus, prolonged diarrhea, salicylate toxicity, respiratory alkalosis, hypothalamic lesions, and adrenocortical hyperfunction.
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PHOSPHOROUS -
DESIRABLE INTRACELLULAR REFERENCE RANGE:
14.2-17.0 mEq/l

Phosphorus is needed for the formation of cell membranes, DNA and RNA
structure, and the formation of high-energy compounds such as ATP. Phosphorous is among the most abundant constituents of all tissues. The Calcium-Phosphorous balance is essential for bone formation, soft tissue structure and energy transduction within all muscles and nerves.
RDA for PHOSPHOROUS is 800-1200 mg

LOW PHOSPHOROUS
Low levels of cellular phosphorous my be caused by low dietary intake,
malabsorption, and hypoparathyroidism, The malnutrition effects seen in alcoholics may occur following 2-4 day of hospitalization due to decreased levels of ATP in red cells, causing less oxygen to the vital tissues. Diarrhea, vomiting magnesium deficiency or use of aluminum-containing antacids may deplete phosphorous. Anorexia, dizziness, bone pain, muscle weakness and waddling gait along with rises in serum creatinine kinase might indicate muscle injury along with myopathy. Hypophosphatemia can also be seen in a variety of biochemical derangements, including, sepsis, hypokalemia, malabsorption syndromes, and hyperinsulinism.

HIGH PHOSPHOROUS
Excessive cellular phosphorus may block magnesium entry and combine with calcium within cells. During a myocardial infarction phosphorous and calcium may crystallize into destructive intracellular materials, which damage heart muscle. High cellular calcium and phosphorus compounds prevent exit of calcium in tissues. When more phosphorus than calcium is ingested, PTH tends to favor bone demineralization and accumulation of Ca in soft tissues thus affecting multiple normal enzyme actions. Diets of soft drinks, red meat and wine, cheeses, and dairy products have high phosphorus along with some water supplies Hyperphosphatemia may occur in myeloma, Paget's disease of bone, osseous metastases, Addison's disease, leukemia, sarcoidosis, vitamin D excess, healing fractures, renal failure, hyperparathyroidism, diabetic ketoacidosis, and acromegaly.

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INTRACELLULAR ELECTROLYTE RATIOS

Ratios indicate physiological relationships between vital cellular elements. If all individual elements are within the reference ranges it is possible to have a ratio out of the range. If elements being ratioed read in the high or low end of the range, their altered physiologiclal balance may be of importance in cell homeostasis. The significance of the ratio is to maintain opitmal balance between all electrolytes for determining risk factors associated with either an excess or deficiency of intracellular ions. If the
indiviual elements are within reference ranges, a borderline Magnesium and high Potassium could produce a pardoxical ratio. Therefore, Individual element concentrations should be evaluated for their effects on ratios.

MAGNESIUM/CALCIUM
Range: (6.1-12.2)
As this ratio lowers, cardiac risk factors increase and ATP production decreases. Serious pathology such as calcinosis, atherosclerosis, vascular occlusion, acute myocardial vasospasm or infarction with related arrhythmias are believed to be related to such imbalances.

PHOSPHORUS/CALCIUM
Range: (3.5-6.0)
If both phosphorus and calcium are high, the relationship in the ratio may be in the desirable range. However, Tendon, ligament and bone structures are related to ratios of phosphorus and calcium. Increased indvidual levels of calcium or phosphate in soft tissues can adversely affect enzyme systems, reducing transport and synthesis of high energy compounds.

MAGNESIUM/PHOSPHORUS
Range: (1.8-3.0)
Depression of Mg/P in tissue tends to block entry of magnesium into cells which may result in lowered intracellular enzyme activity. Excessive dietary
phosphorus can cause physiological cellular changes particularly when the Mg/Ca ratio is also low.

POTASSIUM/CALCIUM
Range (19.1-38.0)
Both calcium and potassium might be elevated but the ratios could be in range. Potassium lowers the tendency towards increased peripheral arterial
resistance, and spasm in renal and coronary circulation. High cellular calcium has been shown to increase intracellular potassium concentration.

POTASSIUM/MAGNESIUM
Range: (2.4-4.8)
Magnesium has a potassium sparing effect and is the rate limiting ion for potassium transport. In most cases, when magnesium is low..potassium is low. If magnesium is borderline (low), and intracellular potassium is out of range (high), a high paradoxical ratio may result. It would be best to look at the individual element concentrations.

POTASSIUM/SODIUM
Range: (19 .4-38.9)
Active transport of K and Na produces major energy processes, normal cell volume, and is vital to ion transport, as well as producing the membrane potentials for all secretory functions, neurotransmission, and neuromuscular activity. Serum potassium levels are not good indicators of tissue levels. This ratio is vital to establishment of homeostasis for normal function of intracellular biochemical events.

Thank you, Erling. When Hans puts Jackie's Observational Report in some place easy to access, maybe he can put this one there too.
PeggyM

Great information.

Thank you

Valli

I agree with Peggy this valuable summary should be readily and permanently available.

Josiah

Nice job, Erling. Keep it coming. Can't get too much of this type of information.

Lois

Erling,

Excellent summary. As Peggy suggested I'll put it into a .pdf file and add it to my resource section (work in progress :~)). I wonder if it would be worthwhile to include part of the following information:

"Afibbers are magnesium-deficient
HARTFORD, CONNECTICUT. Magnesium (Mg) is an enormously important mineral being a cofactor in over 300 enzymatic reactions continuously taking place in the body. Magnesium is also a vital component of the skeletal structure and about 65% of the body’s magnesium stores are found in bone, another 34% is found in transcellular fluids, and the remaining 1% is found in extracellular fluids such as blood. It is thus clear that measuring magnesium in blood serum is not likely to be a very accurate measure of the body’s overall magnesium status.

There is increasing evidence that magnesium plays a crucial role in preventing and terminating cardiac arrhythmias. A group of cardiologists and pharmacologists at the Hartford Hospital reasoned that a pre-procedure infusion of magnesium might help prevent the acute development of atrial fibrillation following a radiofrequency ablation for this disorder. As a first step in proving or disproving this hypothesis, they decided to do a trial in which half the participants would have saline solution (0.9% sodium chloride) with 4 grams of magnesium sulfate (800 mg elemental magnesium) infused over a 15-minute period just prior to accessing the left atrium in a standard PVI procedure, while the other half would just have a saline solution infusion.

The trial involved 22 patients with paroxysmal or persistent afib. Samples of venous blood (for determination of extracellular Mg concentration) and buccal scrapings (scrapings from inside the cheek) were collected before the start of the procedure, 15 minutes after the completion of the infusion, at the end of the ablation procedure, and at 6 hours after the infusion. The blood samples (serum) were analyzed for extracellular magnesium concentration and the buccal scrapings were analyzed (using the EXAtest) for intracellular magnesium concentration as well as for concentrations of calcium, potassium, sodium, chloride, and phosphate. At least one study has shown that there is an excellent correlation between the magnesium (intracellular) content of buccal scrapings and that of myocytes (heart cells). The major findings are as follows:

• None of the study participants were deficient in Mg at baseline when considering blood serum values only. The average serum Mg concentration was 2.08 mg/dL versus the normal lower limit of 1.6 mg/dL.

• The majority (89%) of participants were magnesium-deficient at baseline when considering intracellular (EXAtest) values only. The average intracellular Mg concentration was 32.2 mEq/IU versus a normal lower limit of 33.9 mEq/IU. NOTE: The unit is defined as x-ray intensity (peak divided by background) divided by unit cell volume.

• There was no correlation whatsoever between serum magnesium and intracellular magnesium concentrations.

• Serum levels of Mg rose rapidly in the magnesium infusion group 15 minutes post-infusion and, although declining over the 6-hour observation period, remained considerably higher than the level in the placebo group (saline infusion only).

• Intracellular level of Mg increased rapidly in the magnesium infusion group 15 minutes post infusion and continued to rise throughout the 6-hour observation period. Somewhat surprisingly, the intracellular Mg level also increased somewhat (over baseline) in the placebo group over the 6-hour period. The Hartford researchers speculate that the ablation procedure itself, most likely the anaesthesia, facilitates the transfer of magnesium from serum to intracellular space.

• The intracellular calcium concentration increased significantly in the Mg infusion group post infusion, but gradually reverted to baseline over the 6-hour period.

• The intracellular potassium concentration increased by about 50% from baseline to the end of the PVI procedure and then began to drop off at the 6-hour mark.

The authors of the report conclude that future studies are needed to evaluate the electrophysiologic benefits of magnesium repletion and the effects of routine procedures and anaesthesia on intracellular electrolytes.
Shah, SA, et al. The impact of magnesium sulfate on serum magnesium concentrations and intracellular electrolyte concentrations among patients undergoing radio frequency catheter ablation. Connecticut Medicine, Vol. 72, May 2008, pp. 261-65

Editor’s comment: A 2006 LAF Survey (LAFS-11) found that, among a small sample of 7 afibbers who had EXAtest results, all 7 were either below or very close to the lower normal limit. The Hartford report provides important additional evidence to support the conclusion that afibbers are likely low in intracellular magnesium even though their blood serum levels may be normal. It is also of interest that replenishing magnesium via an infusion not only increases intracellular Mg concentration, but also increases intracellular potassium levels. This is all good support for our long-held conviction that lone afibbers with normal kidney function are likely to benefit from supplementing with magnesium, potassium, and taurine (facilitates the uptake of Mg and K)."

I think it is particularly important that everyone realizes that the results of the regular blood test for magnesium are useless.

Hans

Peggy,

Yes indeed! I will add it to my new Resources section on the web site.

Hans

Erling, George, Jackie, Hans an anyone else with an opinion on this subject

Do all of you subscribe to the theory that all of us should be trying to "cram" in (George that was your term) as much magnesium as possible (bowel tolerance considered, assuming healthy kidneys), in our water, glycinate, sublingual chloride, intramuscular shots etc, etc ? I found that things have gotten much better as I have continued to push my levels higher. I am ready for a swim in the Sea of Japan, even though it is a very rough sea.

Steve

Thanks for this Erling.

What concerns me most from my last Exa was my IC Mg/Ca ratio at 3.7 (range 6.1 - 12.2). (I read that most folks with low IV mag have highish IC Ca.)

My K/Na was pretty good towards top of range.

I do mag chloride foot-soaks most nights, take 600mg mag glyc/day divided doses, and am currently having a course of IM injections (1g elemental mag each) in a concerted effort to up my IC mag levels from the paltry 30.7 it was this Feb gone. I do wonder whether or not excessive chloride might become an issue with the foot-soaks - maybe George has a view one way or the other if he reads this.

I am going to go out and get me some soda water and MoM today and add the famous WW to my daily Mag hit!

Once the Mag IMs as per above have been concluded in a few weeks, I'll get another Exa done (if they'll DO another one for ME!?!)

Regards,

Mike

Steve - in a word, Yes. Optimizing magnesium is the key and the initial focus of The Strategy. Without Mg you aren't going anywhere. Now, as mentioned in the report, many things interfere with reaching optimal levels or even remaining optimal so it's a constant vigil. A key indicator, of course, would be diminished AF or totally absent AF. If symptoms return, then the IC Mg levels may have been reduced from what is 'optimal' in your body. Just be aware that the pushing upwards to optimal, needs to be done very slowly, or you'll get the bowel tolerance issue in the form of diarrhea. The two soft bowel movements a day is a signal you've reached tissue saturation. So..proceed slowly and over an extended period of time.
There is no rushing this process. Jackie

Hi Mike,

It seems reasonable that your low Mg/Ca ratio is secondary to your low Mg, even beyond the obvious reason. It would be helpful if your full exatest results were here too, in the original format. You're gonna get there, Mike - I can feel it in my (mag rich) bones!
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Hi Steve,

I'm taking the liberty of posting your exatest results, in what I think is the original format so that it matches that of the interpretation guide, as I suppose was intended by Exatest. I think it should help to have the numbers on the same thread as the guide.

I'm also posting my results from last year, which could be meaningful for readers to ponder because of having been free of AF for many years. Let's see how it works.

Erling
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Steve's exatest results

Intracellular levels, mEq/L (range in parentheses):

MAGNESIUM: 30.7 (33.9 - 41.9)
CALCIUM: 7.0 (3.2 -5.0)
POTASSIUM: 160.8 (80.0 -240.0)
SODIUM: 3.6 (3.8 - 5.8)
CHLORIDE: 4.6 (3.4 - 6.0)
PHOSPHOROUS: 19.0 (14.2 - 17.0)

Intracellular elemental ratios:

PHOSPHOROUS / CALCIUM: 3.3 (3.5 - 4.3)
MAGNESIUM / CALCIUM: 3.7 (6.1 - 12.2)
MAGNESIUM / PHOSPHOROUS: 1.6 (1.8 - 3.0)
POTASSIUM / CALCIUM 16.1 (19.1 - 38.0)
POTASSIUM / MAGNESIUM: 4.5 (2.4 - 4.8)
POTASSIUM / SODIUM: 33.5 (19.4 - 38.9)
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Erling's exatest results

Intracellular levels, mEq/L (range in parentheses):

MAGNESIUM: 41.5 (33.9 - 41.9)
CALCIUM: 4.6 (3.2 - 5.0)
POTASSIUM: 85.5 (80 - 240) (very low)
SODIUM: 4.6 (3.8 - 5.8)
CHLORIDE: 3.9 (3.4 - 6.0)
PHOSPHORUS: 16.8 (14.2 - 17.0)

Intracellular elemental ratios:

PHOSPHORUS / CALCIUM: 3.7 (3.5 - 4.3)
MAGNESIUM / CALCIUM: 9.0 (6.1 - 12.2)
MAGNESIUM / PHOSPHORUS: 2.5 (1.8 - 3.0)
POTASSIUM / CALCIUM: 18.6 low (19.1 - 38.0)
POTASSIUM / MAGNESIUM: 2.1 low (2.4 - 4.8)
POTASSIUM / SODIUM: 18.6 low (19.4 - 38.9)

Mike - take note of the comment in the latest Taurine deficiency post....

specifically the statements:

Urinary magnesium wasting can result from taurine insufficiency.

Deficient taurine may result in increased cellular calcium and sodium and reduced magnesium.

Jackie

Erling,

Thanks for the vote of confidence (-:

BTW; those Exa results in your last post above (i.e. the set before your own figures) aren't Steve's; they're mine! Although I gotta say that I wish they weren't /-: Here's hoping that the next set look a lot better and rather more like yours!

Kind regards,

Mike

Jackie,

Thanks for that. I have for some time now been taking 2-3000mg/day of Taurine.

Your posting made reference to how low Taurine could result in higher IC Ca and Na, whilst my IC Ca was high, my IC Na was actually a little below range.

Kind regards,

Mike

Okay, Mike - you may want to increase the taurine. Since your Na is already low, then the Ca becomes the important focus... extra taurine could help retain more IC magnesium and in so doing, the Ca will be automatically shut out. Jackie

Hey Mike,

Sorry about that! Frustrating, confusing time spent searching past posts for results, and thought I had it right. On 7-20 Steve wrote: "Today I am going to do the Exatest, the gold standard." I thought I remembered him posting results, and thinking that was a really fast turnaround! - too fast, probably his results aren't back yet! But my blunder works out well: it was your results i wanted to see here anyway. Simply scrolling up and down allows easy comparison with the interpretation guide.

Erling

Mike,

Yea, you can like my results for the high Mg - I do too! - but notice that all 3 K ratios were low, the probable reason for the really weird heart-rate changes I had been experiencing at the time, specifically the low K/Na ratio (Jackie, 'The Strategy'. p.1: Moore, all pages). See "My Exatest and its lesson" [www.afibbers.org]

Erling

Hey Steve, you there? - read my goofy screw-ups? Now this takes the cake: I just found your results! Right there in plain sight! You had posted them on 7-22, just 2 days after the 7-20 test, and that really was a very fast turn-around. If you don't live in Walla Walla WA, maybe its Medford OR? Anyway, now I finally am taking the liberty of posting your results, w/post. My only comment is what you already know: the numbers look great, and you're already doing everything right to further improve your IC magnesium. I applaud you!

Erling
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Author: Steve (---.hsd1.ma.comcast.net)
Date: 07-22-10 15:24

Hi Erling et al.,

Here are my complete results. I would greatly appreciate your comments.

Mag 34.3 (33.9-41.9)
Cal 4.3 (3.2-5.0)
K 204.9 (80.0-240.0)
Na 4.1 (3.8-5.8)
Chloride 4.2 (3.4-6.0)
Phosphorous 16.1 (14.2-17.0)

Phos/Cal 4.4 (3.5-6.0)
Mag/Cal 6.7 (6.1-12.2)
Mag/Phos 2.1 (1.8-3.0)
K/Cal 33.1 (19.1-38.0)
K/Mag 5.1 (2.4-4.8)
K/Na 37.8 (19.4-38.9)

Thanks again,
Steve
================

Earling & Jackie....per your request to bring my results to the board.....

Intracellular levels, mEq/L (range in parentheses):

MAGNESIUM: 34.4 (34.0 - 42.0)
CALCIUM: 3.4 ( 3.2 - 5.0)
POTASSIUM: 108.5 (80.0 - 240.0)
SODIUM: 4.0 ( 3.8 - 5.8)
CHLORIDE: 3.9 ( 3.4 - 6.0)
PHOSPHORUS: 15.2 (14.2 - 17.0)

Interacellular elemental ratios:

PHOSPHORUS/CALCIUM: 5.4 ( 3.5 - 6.0)
MAGNESIUM/CALCIUM: 8.6 ( 6.1 - 12.2)
MAGNESIUM/PHOSPHORUS: 2.3 ( 1.8 - 3.0)
POTASSIUM/CALCIUM: 22.3 ( 19.1 - 38.0)
POTASSIUM/MAGNESIUM: 2.7 ( 2.4 - 4.8)
POTASSIUM/SODIUM: 21.2 (19.4 - 38.9)

Any comments would be appreciated.