supplements

I take 1200 mg of potassium chloride, and i was wondering how much magnesium I should be taking. I tried taurine, but it didn't seem to have any benefit. I wonder if most EPs even recommend supplements?
Thanks,
Barbara

Barbara
My EP doesn't "recommend" supplements but he doesn't give me a hard time about them either.
I am currently taking 1000-1200 mg of mag over 4 doses a day. But I started very slowly a year ago at 300 mg of mag over 3 doses and inched it up slowly to my bowel tolerance. In hindsight, I now believe I have been mag deficient for most of my adult life based on panic attacks, agitation and easily startled. All those symptoms have left since I have been diligent on supplementing.
I found taurine "agitating" until I had my ablation and now I feel it helps keep the pot and mag in the cells.
Cyndie

Barbara - Is your afib completely gone?

At the risk of repeating once again, taking a fairly large dose of potassium and not also taking optimal magnesium could be asking for trouble.

The rule is that you must have a very good base or optimal levels of intracellular magnesium before adding significant amounts of potassium. Otherwise, too much potassium w/o the optimal magnesium, can cause more afib.

A word of caution. Potassium chloride has the reputation for causing gastric distress, so if this happens, consider switching to another form of
potassium such as citrate, gluconate or glycinate.

Cynthia… The road to success: Optimizing intracellular magnesium is at the ‘heart’ of it all.

When I first joined the BB probably back in 2001, Patric Chambers, MD, (aka PC) was writing prolifically about the properties and function of both magnesium and potassium in heart cells… He contributed valuable input and some is preserved in the Conference Room. Every new reader here should take the time to read his contributions. [www.afibbers.org]


Following is an old post by PC and also a contribution By Herbert Mansmann, MD, with whom PC had many conversations on this topic.
It’s fairly technical, but you can get the gist of most of it and believe me, it is important information.

Since then, we have refined the recommendations on food sources of potassium and also minimal dosing requirements based mainly on individual success reports. It still remains highly individualized and each afibber needs to experiment by starting with low dosing and ramping up gradually.

Your heart depends on a good base of magnesium and then optimal potassium as well…(plus other nutrients).

Jackie

Author: PC (---.lsanca1.dsl-verizon.net)
Date: 01-02-03 18:19

Fellow fibbers,
"Effort only fully releases its reward after a person refuses to quit." - Napoleon Hill

I think these are words to live by in general but have special applicability for those of us struggling with LAF.

I've just returned from a week in the Big Apple and was frequently contemplating the riddle of LAF. The following is only my opinion and all the usual and customary disclaimers apply.

I FIRMLY believe that K+ (with or without Mg++ deficiency) is at the root of the problem probably for most and possibly for all LAFers. Although K+ is only part of the problem, it is the only part over which we have any real control. My reasons for thinking this are:

1) Abnormal K+ levels are highly arrhythmogenic, esp. for AF.

2) K+ supplementation diminishes the number of PACs for both myself and others.

3) Amongst the hyperthyroid, 10% have AF and 10% have hypokalemic periodic paralysis. Mg++ deficiency (and therefore hypokalemia) occurs commonly in hyperthyroidism.

4) Magnesium is required for K+ utilization (but not vice versa). WW has been extremely beneficial for me (neither AF nor leg cramps have completely disappeared however).

5) Dietary intake of Mg++, more than any other nutrient, has steadily decreased with the deteriorating American diet.

6) K+ supplementation appears to be almost uniformly discouraged by the traditional healthcare industry, esp. MDs.

7) This fear of K+ supplementation, frequently expressed on this BB, has in effect removed it from any rational supplementation regimen.

8) My intracellular Mg++ after two months of ww is at the very lower limit of normal. Phosphorus is also at the very lower limit of normal (P+ deficiency is commonly seen simultaneously with Mg++ and K+ deficiency). Ca++ was at the very upper limit of normal (parathormone mobilizes Ca++ and is increased when Mg++ is low). Despite aggressive K+ supplementation, this also is well below mid range.

9) Skeletal, smooth and cardiac muscle contraction is a biochemical event that involves four cations (Na+, K+, Mg++, Ca++). K+ and Mg++ would have to be the leading suspects in AF etiology. The other two have well recognized neurohormonal controls for low levels (parathormone for Ca++ and aldosterone for Na+). K+ and Mg++ do not.

10) In spite of the obvious complexity to the overall picture of LAF, this biochemical event has limited requirements, e.g., shortened refractory period, enhanced dispersion and increased PACs). Autonomic tone (vagal or sympathetic) can provide the first ingredient and hypokalemia (with or without Mg++ deficiency) can provide the last two.

11) K+ appears to be the common denominator for all my episodes - bedtime, postprandial, dehydration, hypoglycemia, GERD.

Mechanisms of hypokalemia:
1) GERD probably results in hypokalemia via the constant steady alkaline state (in plasma) that accompanies the slightly hyperacidic state (in the stomach). H+ and Cl- go into the gastric lumen and K+ and HCO3- go into the blood. This alkalosis results in increased urinary excretion of K+. This requires cardiac muscle cells to maintain its intracellular K+ concentration against a greater gradient.

2) Similarly for hypoglycemia and postprandial state where insulin and catecholamines cause intracellular (liver cells, fat cells, etc. but not heart cells) migration of K+ and decreased serum K+. Again the greater gradient promotes loss of intracellular cardiac myocyte K+.

3) Dehydration stimulates release of aldosterone to reabsorb Na+ and with it water at the expense of K+, which is excreted, thereby lowering serum K+.

These mechanisms for hypokalemia are all compounded in the face of Mg++ deficiency. Not only is GI absorption of K+ compromised but also renal K+ secretion/excretion is enhanced. The latter is mediated by ATP-inhibitable luminal potassium channels and decreased Mg++ means decreased ATP. Hypokalemia in this setting is relatively refractory to potassium supplementation and requires correction of the magnesium deficit.

A 10 inch banana contains 400 mg of K+. A pint of Tropicana OJ contains over 400 mg of K+. No one thinks twice about K+ when eating or drinking such things, but just mention K+ supplementation of any amount and the naysayers come out of the woodwork. With a few exceptions I think MDs are becoming contrarian indicators in the field of nutrition and supplementation.

Dr. Michael Lam (www.lammd.com) states that up to 15 grams per day is a healthy adult safe range. It seems to me that if your kidneys are not that healthy, you wouldn't be able to eliminate that much K+ in the first place and therefore wouldn't be having hypokalemic problems, i.e., LAF. Any reading for K+ below 4.0 is now considered low, according to the most recent sources. Previously normal range was 3.5-5.0. There isn't even an RDA for K+. The RDA for Vit C is still only 90 mg. Linus Pauling started taking 1500 mg in his mid 60s and died at the age of 94 in 1993 at which time he was taking 15 gms of Vit C per day.

LAF has been reported to be increased in those undergoing endoscopy, those hospitalized with an acute abdomen, those with irritable bowel syndrome or with GI dysmotility in general. Whether the AF is caused by the resulting vagal stimulation or these other maladies are just manifestations of similar muscular dysfunction is unknown.

It seems to me that anyone truly serious about curing their LAF has to look first at their intracellular Mg++ content. If low, then it has to be aggressively addressed first with ww and then IV infusion. I plan to try the ww a little longer before going the infusion route. However, in the meantime I believe that to have any real chance at avoiding further AF episodes K+ supplements are required.

I apologize in advance if this comes across as too technical, but much of this has been discussed in previous posts. Human physiology and biochemistry are not simple topics and it’s up to you to educate yourselves on much of this. www.google.com is a great place to start.
PC, MD v54

INTERACTION OF MAGNESIUM AND POTASSIUM
THE EVIDENCE OF POTASSIUM AND MAGNESIUM INTERACTION

The following references strongly support the need to correct Mg deficiency in order to correct potassium serum levels. While the type of MgD present in the following are serum Mg, and since normomagnesemia MgD has not been studied, it seems prudent to me that all types of MgD should be maximally treated if KD is present..

References:

Regardless of the cause, the ability to correct potassium deficiency is impaired when magnesium deficiency is present, particularly when the serum magnesium concentration is less than 0.5 mmol/L (1.2 mg/dL) Magnesium repletion improves the coexistent potassium deficit.(Gennari,NEJMed;1988,339:451-458).

“often the hypokalemia cannot be corrected without adequate Mg replacement” (Found under Bartter’s Syndrome in Wallach, J., 6th edition, 1996, p601).

Whang R, Whang DD Ryan MP.
Refractory potassium repletion. A consequence of magnesium deficiency. Arch Intern Med. 1992; 152:40-45.

Experimental and clinical observations support the view that uncorrected magnesium (Mg) deficiency impairs repletion of cellular potassium (K). This is consistent with the observed close association between K and Mg depletion. Concomitant Mg deficiency in K-depleted patients ranges from 38% to 42%. Refractory K repletion due to unrecognized concurrent Mg deficiency can be clinically perplexing. Refractory K repletion as a consequence of Mg deficiency may be operative in patients with congestive failure, digitalis toxicity, cisplatin therapy, and in patients receiving potent loop diuretics. Therefore, we recommend that: (1) serum Mg be routinely assessed in any patients in whom serum electrolytes are necessary for clinical management and (2) until serum Mg is routinely performed consideration should be given to treating hypokalemic patients with both Mg as well as K to avoid the problem of refractory K repletion due to coexisting Mg deficiency. [References: 74]

COMMENT: Whang also says, that in many of those with normal kidneys, the correction of the Mg deficiency will correct the sK level without additional potassium.

POTASSIUM FACTS AND SIGNS OF K DEFICIENCY

The daily intake of K in normal patients is 60 to 100 mEq and the amount eliminated is the same, 90% is execrated in the urine and 10% is in the stool.

The normal serum K is 3.5-5.5 mEq/L, and in children (Nelson Ped. on the Bartter’s web page) a value of < 2.5 mEq/L usually means Bartter’s.

Extracellular fluid is only 2-3 % of total body K.

Each 1 mEq/L decrease of serum K reflects a total body deficit of <200-400 mEq. A serum K of <2 mEq/L may reflect a total deficit >1000 mEq, (Wallach, J., 7th edition, 2000, p76).

24 hour urine K content is 40-120 mEq/day (Uptodate, 2002). In France the reference standard is said to be 35-80 mmol per day.

SYMPTOMS OF POTASSIUM DEFICIENCY

Any of the following symptoms should be discussed with your doctor, especially when you are asked how do you feel. This is very important when you have a disease where magnesium deficiency is likely or a disease where potassium deficiency is present.

It would be best if you kept a grading (1, best--10) of the extent of these in a daily diary. Future K dosing by your doctor, in part, is very likely to be decided on this type of information.

Chronic fatigue Irregular or rapid heart (palpitations)
Constipation Muscle weakness
Depression Nervousness
Headaches Respiratory distress
Insomnia Swollen feet and/or ankles (edema)

TREATMENT OF A LOW SERUM POTASSIUM

Most of this section depends on your doctor knowing how you are doing. You should not be self-managing this part of your treatment, unlike oral magnesium dose adjusting (a Mg over dose only causes diarrhea), except for an increase in your use of high potassium containing foods.

High content of K is found in the following foods:

K is highest in the following foods, > 25 mEq per 100 grams (about 3 ounces) are the following: dried figs, molasses and seaweed. Dried dates and prunes, nuts, avocados, bran cereals and wheat germ (both may bind Mg in bowels), lima beans: all of these in this group contain > 12.5 mEq per 100 grams. Many vegetables, fruits (including bananas), and most animal meats contain > 6.2 mEq per 100 grams. (Adapted from Gennari, F.J., NEJMed 1998, p. 339)

Several of these can be added to cooking foods if one also consumes the fluid component.

PHYSICIANS METHODS

The IV KCl dose is up to 10 mEq/ hour, need a cardiac monitor if go higher, and some use 20-40 mEq/hr. Each 1 gram of KCl contains 9.8 mEq of K..

The tablet of the product of K-DUR® 10 is an immediately dispersing extended release oral dosage form of potassium chloride containing 750 mg of microencapsulated potassium chloride (slowly released), a USP equivalent to 10 mEq of potassium in a tablet (PDR 2002). So some will need many pills, always in multiple dosing like every 4-8 hours.

If need 1,000 mEq, because sK is less than 2 mEq/L, this is an important reason for IV KCl, besides the cardiac danger of being to low.

7/30/02
Herbert C. Mansmann, Jr., MD Professor of Pediatrics
Associate Professor of Medicine
Jefferson Medical College
Thomas Jefferson University
Philadelphia, PA., 19107

Research taurine & L-arginine. I've had excellent results since using taurine. I plan on starting L-arginine when I receive the supplement. Also, there is some resent research on statins and reduction of a-fib. Check them out.