Wil - K supplementation

Hi Wil,

In this post, < [www.afibbers.org];, you said,” I got up, took about 2 gms of potassium…”

I was just wondering if you have any data supporting your choice of 2 grams K or if it is just “enough?” I say this as I routinely take 1.5 grams K morning & evening (well now it is usually a “bunch of pills” as I take K citrate pills & don’t like to count). I often wonder if I’m really wasting a lot of K that gets immediately excreted in my urine.

The only data I have is that my fasting serum K (12 hours after supplement intake) is ~4.2 mmol/l and 4 hours after supplements and eating, my serum K is ~4.8 mmol/l. As my target is to keep the serum K > 4.0 mmol/l, it obviously works. However I could be overdoing it, at no harm except to my pocketbook.

I recall that you had a formulation of K in water that you drank more or less continually to achieve similar results of serum K in the “sufficient range.”

Any comments?

George

You are way ahead of me. You have done some gathering of blood plasma K concentration data. My potassium level was measured soon after a-fib appeared, but I don't have a record of the concentration other than remembering it was "normal".

Five years ago (and the exact amounts are fuzzy) I took about a liter of fresh squeezed grapefruit juice, to which I added some amount of potassium chloride. I think it ended up being 2 or 3 grams of K which I sipped throughout the day.

Since then I have been inconsistent about potassium, going from none for long periods to several grams per day for long periods. For the last year I've probably averaged a gram per day, but for many weeks it was more, and many weeks I didn't supplement at all. I haven't seen any indications that it matters, in my case.

Anytime noticeable heart misbehavior appears I immediately increase K supplementation and the misbehavior usually goes away. But, I can't argue that the K helped, because the misbehavior might have gone away without the K. If it seems I've become undisciplined (or even chaotic) about K supplementation I would have to plead guilty.

I have no doubt that low potassium and low magnesium intake probably helped promote the development of a-fib. Prior to a-fib I always faded out in hot weather and exhibited other lifelong symptoms associated with low magnesium (migraines and constipation). Water and sodium didn't help in hot weather, and possibly made matters worse. Since a-fib, there are indications that I have gradually saturated my body with magnesium, and the fading out in hot weather has disappeared (and the migraines have moderated and the constipation disappeared). This leads to speculation that the bigger problem pre-a-fib was a magnesium deficit.

An increase in magnesium stores may have allowed my body to better utilize and store potassium, and to maintain a normal potassium level, but that is speculation too. Data supporting a long term potassium deficiency is much weaker than the data supporting a long term Mg deficiency.

I'm afraid this doesn't help you much with your dilemma.

Hi Wil,

Thanks for filling me in. I always viewed the half life of K in my system as being pretty short. My first (known) day of afib, my serum K was 3.2 mmol/l. They gave me ~700 mg in pill form in the ER. Four or five days later, it was 4.1 in the doctor's office. Several months later, it was 4.1, while I was in persistent afib. This is all before I started regular suplementation.

Several months prior to starting afib, I had an annual test with 3.4 or 3.5 mmol/l. I surmised that I had intermittent episodes of hypokalemia which could initiate afib. So I set about making sure that this didn't happen again. Therefore, my guess is that most days I'm sending a lot of K down the drain in my urine. It is cheap insurance.

I also put pure KCl powder in a salt shaker and use it to season my food.

For me Mg and taurine are also key players. I don't think I've ever gotten to Mg saturation even after 3 years of supplementation.

As I recently posted in the current CR, last week I spoke to a friend whom three years ago, had two very symptomatic afib episodes. At that time, I suggested magnesium, potassium and taurine. He experimented over time. I talked to him and he is still in NSR, settling on 1,500 mg of magnesium glycinate a day. 500 mg at each meal. He says it, "keeps me regular, but nothing more." Obviously magnesium is his issue. He says he can "feel" his heart settle down when he takes the Mg.

Cheers,

George

Again, my memory of what level of Mg supplementation I started with if fuzzy, but it was just under 1000 mg per day. The maximum tolerable level has declined with time, and now seems to be around 100 mg per day.

You could argue that the decrease argues more for inadequate intake in years past (and a much more stressful life) rather than an inherently inadequate system. It will be interesting to see if you and your friend also find that the maxiumum tolerable dose goes down in time.

I talked to him and he is still in NSR, settling on 1,500 mg of magnesium glycinate a day. 500 mg at each meal. He says it, "keeps me regular, but nothing more." Obviously magnesium is his issue. He says he can "feel" his heart settle down when he takes the Mg.

George thanks for posting this because it serves as an excellent example of biochemical individuality. It's obvious he is a huge user of magnesium and the fact that he can feel his heart settle down is confirmation. I know of another person who is not an afibber, but who suffers from heart palps at night but with a nightly dose of only 200 mg. his heart becomes peaceful.

I have some publications on Hypokalemia....not found online and I'll excerpt for you on the potassium homeostasis issue... (later as I have to type it) not found online. But here's an abstract of another report:

Am J Med. 1984 Nov 5;77(5A):3-10.
Potassium homeostasis and clinical implications.
Brown RS.

The clinical estimation of potassium balance generally depends on the level of serum potassium. Since the extracellular fluid contains only 2 percent of the total body potassium, it must be recognized that potassium deficits are usually large before significant hypokalemia occurs, whereas smaller surfeits of potassium will cause hyperkalemia.

The total body potassium is regulated by the kidney in which distal nephron secretion of potassium into the urine is enhanced by aldosterone, alkalosis, adaptation to a high potassium diet, and delivery of increased sodium and tubular fluid to the distal tubule.

However, the distribution of potassium between the intracellular and extracellular fluids can markedly affect the serum potassium level without a change in total body potassium. Cellular uptake of potassium is regulated by insulin, acid-base status, aldosterone, and adrenergic activity.

Hypokalemia, therefore, may be caused by redistribution of potassium into cells due to factors that increase cellular potassium uptake, in addition to total body depletion of potassium due to renal, gastrointestinal, or sweat losses. Similarly hyperkalemia may be caused by redistribution of potassium from the intracellular to the extracellular fluid due to factors that impair cellular uptake of potassium, in addition to retention of potassium due to decreased renal excretion.

An understanding of the drugs that affect potassium homeostasis, either by altering the renal excretion of potassium or by modifying its distribution, is essential to the proper assessment of many clinical potassium abnormalities.

Both hypokalemia and hyperkalemia may cause asymptomatic electrocardiographic changes, serious arrhythmias, muscle weakness, and death. Hypokalemia has also been associated with several other consequences, including postural hypotension, potentiation of digitalis toxicity, confusional states, glucose intolerance, polyuria, metabolic alkalosis, sodium retention, rhabdomyolysis, intestinal ileus, and decreased gastric motility and acid secretion.

PMID: 6388326 [PubMed - indexed for MEDLINE]

Check this one as well:
[www.ionchannels.org]

Additionally, back on 8/27/04, Hans wrote for the Conference Room
The Importance of Potassium.... worth reviewing and then in CR #37, PC goes into the fluctuations of potassium levels... I know you know this, but I'm just flagging it for new readers.

I'll be back with the excerpts from the Hypokalemia publication.

Jackie

Thanks Jackie.

From CR37 [www.afibbers.org], PC references this paper:
[www.medscape.com]
(requires free registration)

This excerpt may be of interest:

Potassium and Magnesium Interrelationship
As is the case for K+, Mg++ is one of the principal intracellular cations, and pathologic conditions causing an imbalance in one of these cations typically have some effect on the other. In the congestive heart failure patient, for example, the neurohormonal activation characteristic of congestive heart failure as well as aggressive diuretic therapy, which serves to further stimulate the renin-angiotensin-aldosterone system (RAAS), could cause deficiencies in these two important cations.

The clinical problems of hypokalemia and hypomagnesemia largely parallel one another.[9,10] Findings from a survey in nearly 1000 patients showed hypokalemia to be present in up to 42% of patients with hypomagnesemia. Isolated perturbations in K+ do not significantly influence Mg++ homeostasis, but abnormalities in Mg++ balance can be accompanied by secondary K+ depletion. When hypomagnesemia and hypokalemia coexist, Mg++ repletion is not uncommonly required before K+ status can be corrected.[10]

Mg++ and/or K+ depletion can play a pivotal role in the genesis of cardiac arrhythmias, particularly in patients with underlying ischemic heart disease.[10] Mg++ has important electrophysiologic effects; it plays a critical role in the regulation of energy sources and in the control of ion pumps, and it has a direct membrane stabilizing effect on excitable myocardial membranes without adversely affecting repolarization time.

George