Some Thoughts on Sudden Cardiac Death – Part VI

Part V of this series ended with a promise that I would be discussing research on the important and intimate relationship between potassium and magnesium metabolism.  In particular, because magnesium plays a major role in the transport of potassium into the intracellular compartment, magnesium deficiency can largely negate the potentially positive effects of any dietary or supplemental potassium protocol.  Therefore, evaluation of magnesium status should be a top priority whenever need for potassium is being considered.

However, after writing that newsletter, a major paper on electrolyte disturbances associated with diabetes mellitus appeared in The New England Journal of Medicine.  Included in this paper was some clinically relevant information on potassium status in diabetics that was not included in my review of the literature on potassium and diabetes mellitus that appeared in part IV of this series.  Therefore, I would now like to provide a brief review of that section on potassium from this paper, after which I will proceed with the promised review of the literature on the relationship between potassium and magnesium.


In part IV of this series, I discussed the relationship between potassium and diabetes in terms of hypokalemia that can be caused by a combination of whole body depletion of potassium and administration of insulin that can take the little remaining potassium and shift it in a massive way into the intracellular compartment.  In contrast, in “Electrolyte and acid-base disturbances in patients with diabetes mellitus” by Palmer and Clegg (1) the authors discuss the equally important concerns about hyperkalemia that can occur with insulin deficiency.

Of course, our conventional intuitive thinking would lead us to assume that, when whole body amounts of potassium are depleted, a deficiency of insulin will lead to low serum potassium.  Interestingly, just the opposite is true.  Why?  As you will see in the following quote from the Palmer and Clegg (1) paper, insulin deficiency leads to a movement of intracellular potassium to extracellular compartment, leading to hyperkalemia:

“Insulin deficiency, which is more common in type I diabetes than in type 2 diabetes, is an important factor in the net efflux of potassium from the cell.  In patients with type 2 diabetes, the insulin-mediated uptake of glucose is impaired, but the cellular uptake of potassium remains normal, a situation that is consistent with the divergence of intracellular pathways that follows activation of the insulin receptor.”

As you will see in the next quote, the fact that, with insulin deficiency, potassium can get into the cell but glucose cannot, osmotic imbalances in the balance between intracellular and extracellular water occur.  This causes potassium to leave the cell and accumulate in the extracellular compartment:

“Hyperkalemia can be caused by an increase in plasma tonicity that results from the redistribution of potassium from the intracellular space to the extracellular space.  The efflux of potassium from the cell is due to intracellular dehydration, which results from the osmotically induced, transcellular movement of water.  This movement creates a favorable gradient for the efflux of potassium.”

Of course, with the above in mind, you would expect an association between hyperkalemia and diabetic ketoacidosis.  Palmer and Clegg (1) state:

“Hyperkalemia is frequently present on admission in patients with diabetic ketoacidosis, even though total-body potassium is reduced.”

Before continuing, please note again the relationship emphasized in the above quote.  For virtually every nutrient, we have been taught over the years that low total body levels will always lead to low serum levels.  In the case of potassium with diabetics, the opposite is true.  Low body stores will lead to elevated serum levels.

Is the hyperkalemia seen with diabetic ketoacidosis a manifestation of an acidotic state?  After all, as we know, hypokalemia is often a manifestation of low-grade chronic metabolic acidosis.  Interestingly, the answer is no:

“In these circumstances, the hyperkalemia is caused by a redistribution of potassium that results from hypertonicity and insulin deficiency – not by metabolic acidosis.”

Another potassium-related scenario that can be clinically significant in the case of diabetics is the fact that so many diabetic patients are being prescribed beta-blocker drugs.  Palmer and Clegg (1) point out:

“…potassium shifts that are the result of hypertonicity and insulin deficiency are counterbalanced by marked increases in sympathetic-nerve activity; this increased activity moves potassium into cells by stimulating β2-adrenergic receptors.  In patients receiving nonselective beta-blockers, increased adrenergic activity may worsen hyperkalemia because unopposed stimulation of α-adrenergic receptors favors the cellular efflux of potassium.”

Diabetes-related hyperkalemia and sudden cardiac death

The primary theme of this whole series has been that low serum potassium is a major potential factor contributing to sometimes catastrophic cardiac events.  Could hyperkalemia as seen with diabetics pose the same risk?  As you may recall from part IV of this series, the hyperkalemia seen with excessive exercise and the hypokalemia that follows has certainly been associated with abnormalities in cardiac function.  As pointed out in the paper “Management of hyperkalemia: An update for the internist” by Kovesdy (2), hyperkalemia, as with hypokalemia, can pose a threat to cardiac health whether the cause is diabetes or any other health issue.  The author states:

“Hyperkalemia is one of the most clinically important electrolyte abnormalities due to the cardiac arrhythmias it can cause, which can result in increased mortality.  Usually, hyperkalemia is caused by excess dietary potassium, disordered cellular redistribution, abnormalities in potassium excretion, or a combination of these.  The most common risk factor for hyperkalemia is chronic kidney disease, together with one or more ancillary conditions that cluster with it, such as acute kidney injury, cardiovascular disease, or diabetes mellitus, along with the medications used to treat these conditions.”

Specifically, what alterations occur with heart function as a result of hyperkalemia?  Kovesdy (2) states:

“Extracellular hyperkalemia results in a lesser negative resting potential, with a decreased conduction velocity and an increased repolarization rate, leading to fascicular and atrioventricular nodal blocks.  Clinically, these manifest in electrocardiogram changes characterized by peaked T-waves, PR-interval prolongation, and QRS widening, and in more severe cases, bradyarrhythmias, ventricular fibrillation, or asystole.  There is no single threshold above which hyperkalemia is considered imminently dangerous.  Adverse events have been described with levels >5 mEq/L, but the risk increases substantially with higher concentrations of serum potassium.”

Concerning diabetes in particular, the author states:

“Diabetic patients suffering from insulin deficiency and hypertonicity may have difficulty redistributing acute potassium loads into the intracellular space, and also, they can suffer from hyporeninemic hypoaldosteronism and diminished tubular potassium secretion.”

As I mentioned earlier in this series, it is ideally important in terms of optimizing cardiac health to make sure that serum potassium levels are at 4.5 mEq/L or slightly above.  It also appears equally important in terms of optimizing cardiac health that serum potassium levels are no higher than 5.0 mEq/L or slightly above.


Based on all the information presented thus far in this series, it certainly could be expected that some would conclude that, in terms of electrolyte status, optimization of both serum and intracellular potassium levels is all that is needed to reduce the odds of sudden cardiac death.  However, there is more to this story, as I have suggested several times in past newsletters.  In fact, as you will see, without optimal magnesium status, it is highly likely that efforts to optimize potassium levels will not yield the outcomes we may have expected in relation to cardiac health.

Of course, I realize that, for the vast majority of you, the fact that magnesium is vitally important for cardiac health is nothing new.  However, what may be less understood is the fact that both magnesium and potassium rely heavily upon each other to do their respective jobs.  Furthermore, this reliance is so interwoven that, despite all the attention magnesium has received over the years and continues to receive, it is highly likely that the clinical results from magnesium supplementation will inevitably fail to live up to the “hype” if potassium status is less than optimal.

With this reality in mind, I would now like to review several papers on magnesium with emphasis not only on basic functions of magnesium and its role in cardiac health but on the specific ways that magnesium and potassium rely upon each other in various cellular functions.  To begin this discussion, first consider as a review some basic facts about magnesium as noted in the paper “Magnesium metabolism in health and disease” by Musso (3):

“Magnesium is the main intracellular divalent cation, 99% of it being in the intracellular space.

The recommended Mg dietary content for adults is approximately 420 mg/day in men and 320 mg/day in women.  However, the usual dietary Mg intake falls below this recommendation in a large proportion of the population.”

Under basal conditions the small intestine absorbs 30-50% of Mg intake, although this percentage diminishes with increasing amount of magnesium intake, senescence, and chronic renal disease.  Magnesium absorptive process is, in part, under the influence of active vitamin D.”

Before continuing please notice again the role of vitamin D in magnesium absorption.  Certainly one of the biggest complaints we receive about magnesium supplementation, no matter what the form, is the side effect of gas and diarrhea which is primarily an outcome caused by poor absorption.  Therefore, for those patients who report GI-related side effects when ingesting optimal doses of a quality magnesium supplement, check and see if vitamin D status is suboptimal.

Musso (3) continues:

“Normal serum Mg ranges between 1.7-2.2 mg/dl, or 0.75-0.95 mmol/l, or 1.5-1.9 mEq/l at any age (1 mmol = 2 mEq = 24 mg Mg), and approximately 20% of this cation is bound to albumin in the intravascular compartment.  Serum Mg concentration correlates poorly with its body content, because patients with Mg deficiency may have normal serum Mg levels.”

In what scenarios might magnesium deficiency be more prevalent?  The author states:

“Three physiopathologic mechanisms can induce Mg deficiency: reduced Mg absorption (e.g. malabsorption), increased urinary Mg losses (e.g. diuretics), or intracellular shift of Mg (e.g. hungry bone syndrome).

Even though, during nutritional deficiency states, the intestine is able to increase its absorptive capability by as much as 40% compared with normal, malnutrition can lead to Mg deficit, especially in the setting of chronic alcoholism.  Enteric diseases which induce malabsorption (e.g. inflammatory bowel disease) may also cause Mg deficiency related to the digestive tract.”

The next quotes I would like to feature from this paper highlight the relationship between magnesium and some common clinical entities:

Kidney stones

“Magnesium also has an important role as a nephrolithiasis inhibitor, acting more effectively in combination with citrate.  Magnesium citrate slows brushite crystal growth rate, nucleation rate, and supersaturation of urine.  In addition, because Mg competes with calcium in binding oxalates, in both the gut and urine, the ratio of Mg/Ca in the urine is used as an estimate of stone risk.”

Bone disease

As we all know, bone is more than just an issue of calcium.  Musso (3) points out:

“Epidemiologic studies have demonstrated a positive correlation between dietary Mg intake and bone density and/or an increased rate of bone loss with dietary Mg reduction.”

In addition:

“In most species, including humans, Mg deficiency results in impaired parathyroid hormone (PTH) secretion and/or PTH end organ resistance.  Serum 1,25 (OH)2D levels are also low in Mg-deficient humans and rats.”

Heart and vascular disease

Then, of course, there is the well-known connection between magnesium and cardiovascular health.  Musso (3) states:

Hypomagnesemia is an essential feature of heart failure associated with complex ventricular arrhythmias which, consequently, can be alleviated/abolished by magnesium supplementation, because of enhanced automaticity or triggered activity.  Factors known to contribute to magnesium depletion in this population include reduced dietary intake (anorexia), exaggerated urinary excretion generated by diuretics, and/or activation of the neurohormonal and renin-angiotensin-aldosterone system that leads to stimulation of aldosterone and antidiuretic hormone secretion, which inhibits tubular magnesium reabsorption and thus exaggerates urinary magnesium loss.”

The next quote discusses magnesium in terms of one of the allostatic load principles I have discussed repeatedly over the years – in addition to the impact directly seen with a deficiency of a key nutrient there will be an additional impact by virtue of the fact that being deficient is stressful:

“Magnesium depletion contributes to an increase in catecholamine secretion.  In patients suffering from arterial hypertension, catecholamines have been demonstrated to regulate intracellular magnesium loss in lymphocytes, thus creating a loop in which magnesium deficiency induces catecholamine secretion while elevated catecholamines stimulate further magnesium loss.  Both mechanisms contribute to vasoconstriction and further hypertension.  Magnesium has been demonstrated to inhibit catecholamine release by a mechanism involving blockade of voltage-gated calcium channels, thus breaking the deleterious loop and lowering systemic blood pressure.  Another potential cardiovascular protective action of magnesium was attributed to LDL-cholesterol oxidation and oxidative stress reduction.”

Still more research on the relationship between magnesium and CVD

Does more research exist that supports the claim made by Musso (3) above that disturbances in magnesium metabolism can lead to not just chronic heart dysfunction but acute cardiac crises?  The answer is certainly yes.  First, consider the paper “Plasma and dietary magnesium and risk of sudden cardiac death in women” by Chiuve et al (4).  The authors begin by reiterating the continued disturbing statistics on sudden death related to CVD:

“Sudden death from cardiac causes accounts for >50% of all coronary artery disease (CAD) deaths, with estimates ranging from 184,000 to 462,000 annually.  Most patients who suffer sudden cardiac death (SCD) are not at high risk on the basis of established criteria, and up to 55% of men and 68% of women have no clinically recognized heart disease before sudden death.”

Before continuing, please notice again the statement above that, based on established criteria, over half of the people who experience sudden death due to cardiac dysfunction had no clinically recognized heart disease.  To me, this suggests a critical need to reevaluate our criteria for determining heart disease so that we begin to start considering criteria that are not so “established.” As I hope I have convinced you by now, an in depth knowledge of potassium and magnesium metabolism for any particular patient would certainly qualify in this regard.

What were the findings of the Chiuve et al (4) study?

“In this large prospective cohort of women, magnesium measured in diet and plasma was associated with a lower risk of sudden cardiac death.  Women in the highest compared with the lowest quartile of dietary and plasma magnesium had a 34% and 77% lower sudden cardiac death risk, respectively.”

What is the metabolic and physiologic reason for this relationship?  The authors state the following that primarily but not exclusively relates to the role of magnesium in heart rhythm.  In this quote please notice the statement about potassium homeostasis which I will discuss in much more detail shortly:

“…several lines of evidence support a specific antiarrhythmic action of magnesium.  Extracellular magnesium influences cardiac ion channel properties and regulates potassium homeostasis through activation of sodium potassium ATPase.  Magnesium administration suppresses early after depolarizations and dispersion of repolarization, whereas magnesium deficiency results in polymorphic ventricular tachycardia and sudden cardiac death in animal models.  In clinical studies, magnesium therapy is efficacious in the treatment of arrhythmias secondary to acquired torsades de pointes or hypomagnesemia.  Apart from antiarrhythmic actions, magnesium may also influence sudden cardiac risk though other pathways, including improvements in vascular tone, lipid metabolism, endothelial function, inflammation, blood pressure, diabetes, and inhibition of platelet function.”

Why is it that we are not paying more attention to magnesium need in our patients who might be at risk for sudden cardiac death?  One reason is that the most common lab test for magnesium status, plasma magnesium, is a very poor indicator:

“As in previous studies, plasma and dietary magnesium are not strongly correlated in this population.  Plasma magnesium concentrations are under tight homeostatic regulation by a variety of mechanisms, most notably by renal excretion; therefore, plasma magnesium is a poor surrogate for magnesium intake.”

However, despite this poor correlation between plasma status and dietary intake, other research has documented a relationship between specific serum levels and sudden cardiac death.  In the paper “Suboptimal magnesium status in the United States: are the health consequences underestimated?” by Rosanoff et al (5), the following is stated:

“Occurrence of sudden cardiac death was reportedly reduced by almost 40% in subjects with serum magnesium levels of ≥1.75 mEq/L compared with subjects having serum magnesium levels of ≤1.5 mEq/L in 14232 adults aged 45-64 years who were followed up in for 12 years”

However, despite these findings, it is still important that we keep in mind, as noted above, that an individual with what appears to be an optimal serum magnesium could still be at considerable risk for sudden cardiac death.

In line with the idea suggested in the previous quote that serum magnesium levels are useful in predicting sudden cardiac death is the study “Serum magnesium and risk of sudden cardiac death in the atherosclerosis risk in communities (ARIC) study” by Peacock et al (6).  This paper begins with the similar sobering statistics about sudden cardiac death incidence that were discussed above:

“Sudden cardiac death (SCD) is a major public health problem comprising more than half of all cardiovascular disease (CVD) deaths in the USA.  Even with estimates of coronary heart disease (CHD) mortality declining by more than 50% from 1950 to 1999, the relative proportion of SCD of all CVD deaths in the USA simultaneously increased during this time.”

What were the results of the study?  While no precise serum magnesium numbers were provided in terms of SCD risk, the following was stated:

“The main finding from this analysis was a significantly reduced risk of SCD in the highest quartile compared to the lowest quartile of serum Mg in a prospective cohort with over 173,000 person years of follow-up.”

What about magnesium in relation to blood pressure and stroke?

As you probably know, dietary magnesium intake has a significant relationship with incidence of high blood pressure and stroke, as stated by Bain et al (7) in the study “The relationship between dietary magnesium intake, stroke and its major risk factors, blood pressure and cholesterol, in the EPIC-Norfolk cohort”:

“Lower dietary magnesium intake was associated with higher BP and stroke risk, which may have implications for primary prevention.”

What is the reason for this effect?  The authors state:

“Magnesium has a number of metabolic roles in the body and may influence BP and blood lipids through different mechanisms.  Magnesium may serve as a natural calcium channel blocker, exhibit beneficial effects on platelet coagulation, have a potential role in vasodilation and has been associated with reduced coronary artery calcification.  Other proposed mechanisms include increased peroxidation of lipoproteins with subsequent acceleration of atherosclerotic plaque formation and low magnesium may facilitate an increase in inflammation which is associated with negative changes in lipid profile.  Higher magnesium intake has been associated with lower risk of Type II diabetes, metabolic syndrome and cardiovascular disease (CVD).”


As I have demonstrated above, there is no question that magnesium status has a massive impact as in independent risk factor in terms of sudden cardiac death and CVD in general.  However, I feel the massive impact of magnesium on these issues can only be truly understood when the intimate relationship between magnesium and potassium is fully appreciated.  Therefore, I would now like to highlight several papers that specifically discuss how magnesium and potassium work together to create health when optimally balanced and how they create ill-health when out of balance.

First, consider this quote from the Musso (3) paper discussed above:

“Hypomagnesemia can, by itself, induce hypokalemia (often refractory to potassium repletion until Mg deficit is corrected)…”

Next, consider this quote from “Protective role of magnesium in cardiovascular diseases: A review” by Chakraborti et al (8) that provides more detail on this relationship:

“The arrhythmogenic effect of Mg2+ deficiency may be related to its effect in maintaining intracellular K+.  Mg2+ is necessary for Na+/K+ATPase which is responsible for active transport of K+ intracellularly during the action potential duration.  Mg2+ is also involved in regulating K+ influx through different K+ channels.  A deficiency of myocardial Mg2+ can lead to a decrease in intracellular K+ due to a less efficient Na+/K+ ATPase system and also by the loss of inward rectification.  As the resting membrane potential is determined in part by the intracellular K+concentration, a decrease in intracellular K+ results in a less negative resting membrane potential.  This results in prolongation of the QT interval and enhanced vulnerability of ventricular arrhythmias.”

What you are now about to read are some highlights from a book chapter entitled “Extra- and intracellular potassium and magnesium, diuretics, and arrhythmias” by Dyckner and Wester (9).  The first quote provides more detail on the impact of magnesium on arrhythmias mentioned above:

“Magnesium may influence the incidence of cardiac arrhythmias in different ways, e.g., through a direct effect, through an effect on potassium metabolism, or through an effect on calcium metabolism as a calcium blocking agent.  The influence of potassium metabolism is thought to be mediated through the sodium potassium pump.  Magnesium is known to be a necessary activator of Na-K-ATPase, which supplies the energy for the sodium-potassium pump.  Thus, lack of magnesium will lead to impaired pumping of sodium out from the cell and of potassium into the cell.”

Before continuing, please note again the last sentence in the above quote.  As I have mentioned repeatedly, optimal balance between intra- and extracellular potassium in the cardiac cell is crucial for proper rhythmic activity.  Without optimal magnesium status, which is influenced not only by dietary intake plus a host of other factors such as chronic inflammation and insulin resistance, both of which are often as common, if not more so, as poor dietary intake, it will be very difficult if not impossible to maintain optimal intracellular potassium levels.

As a demonstration of the important role magnesium plays in optimizing potassium levels in cardiac muscle, Dyckner and Wester (9) discussed a clinical study.  In this study, potassium and magnesium in serum and muscle were considered in 54 hypokalemic patients before and after correction of hypokalemia.  The quote below describes the specifics of the study:

“In this group, 26 had congestive heart failure, 17 had arterial hypertension, 9 had liver diseases, and 2 had other diagnoses.  Of the patients 43% were on diuretic treatment.  One to 2 days after the hypokalemia was observed, a 3-hour ECG was registered on tape-recorder and a skeletal muscle biopsy was performed.  The hypokalemia was then corrected during 3 days to 3 weeks, until persistently normal serum potassium levels were obtained and the patients were judged to be in steady state.  The potassium supplementation was given either i.v. or per os.  After correction of the hypokalemia, ECG was again recorded for 3 hours and a new muscle biopsy was performed.”

What impact did this very aggressive approach to potassium supplementation have on muscle potassium?  Virtually none:

“Despite a significant increase in serum potassium levels, there was no increase in muscle potassium.  The ECG recordings showed no change in the incidence of ventricular ectopic beats.”

Again, please note that not only did the potassium supplementation have no effect on muscle potassium levels, there was no improvement in abnormal heart function.  Could this be due to poor magnesium status?  The authors state:

“Of the 54 patients six had a normal muscle magnesium content in combination with a low muscle potassium content.  These patients showed a highly significant increase in muscle potassium after potassium supplementation.  These results also imply the importance of magnesium as a necessary activator of Na-K-ATPase.”

Before continuing, please note again that only those patients with normal muscle magnesium demonstrated increased muscle potassium after aggressive potassium supplementation.  These results led Dyckner and Wester (9) to conclude:

“The supplied potassium was able to enter the cell only in the patients with a normal muscle magnesium content.”

In another study performed by the authors, both supplemental magnesium and potassium were evaluated on 34 hypokalemic patients, 20 of whom had congestive heart failure and 13 had arterial hypertension.  All were taking diuretic medications.  Finally, one patient was an alcoholic.  The patients were divided into three groups.  One group was given only i.v. magnesium sulfate.  The second group received i.v. magnesium sulfate followed by i.v. potassium chloride.  The third group received both i.v. supplements but in reverse order.

The results for groups two and three were assessed via muscle biopsy and frequency of ventricular ectopic heartbeats.  In group two, magnesium sulfate, which was given first, significantly increased muscle potassium.  No further increase was seen with potassium supplementation which was given second.  In group three, which received potassium chloride first, no significant change in muscle potassium was seen after this initial supplementation.  However, after the follow-up magnesium supplementation muscle potassium increased significantly.  Concerning ventricular ectopic heartbeats, no change was seen after potassium infusion.  However, magnesium infusion led to significant decreases in the frequency of ventricular ectopic heartbeats.  These findings led Dyckner and Wester (9) to conclude:

“Again, the results fit very well with the theory that magnesium has an effect on potassium metabolism through an influence on Na-K-ATPase.”

Therefore, as I hope you can see, despite the well- known claims that both potassium and magnesium are important for optimal heart health, the fact of the matter is that neither will have a significant impact on heart muscle function without optimal levels of the other.  Furthermore, even though this has been a newsletter series that emphasizes the importance of optimal potassium levels on heart health, efforts to optimize potassium levels will have a minimal clinical impact unless magnesium status is also seriously evaluated.


I close my eyes and I’m back to April of 1985.  This was an exciting time for me, having just sold my dental practice in Michigan and moved east to Massachusetts to start my career in the supplement industry.  I was very confident that, armed with my protocols, my multis, my digestive aids, and all the other goods and services I was offering to my practitioner customers, I was going to make great inroads in patient care.  Ultimately, do I feel I made a difference?  Yes, I believe so.  However, around the year 2000 I got the feeling that I had fallen short of my patient care goals using what I thought was more than enough when I started in 1985.  What did I feel I needed to add to make my presence in the world of health care more effective?  Several important concepts came to mind that I have been pursuing now for the last 15 years, such as functional medicine, stress and allostatic load physiology, neurophysiology, immunology, etc.  However, as I mentioned in the beginning of this series, it was my father’s death of ventricular tachycardia in 2002 that made me realize there was one area of human physiology about which I needed much more expertise than I had previously: fluid and electrolyte metabolism.  Of course, my studying and the courses I had taken during my first 15 years in the industry had given me a certain level of proficiency in this area.  Nevertheless, I also knew that, despite all my reading and studying on minerals up to that time, I was woefully ignorant about how a certain group of minerals, electrolytes specifically, interacted with each other and water to affect human health, and cardiac function in particular.  Interestingly, I took some comfort in knowing that I was not alone in my ignorance.  For, it became quickly apparent upon talking with experts on fluid and electrolytes and reading their papers that this may be the most complicated and difficult aspects of human physiology to understand.  Nevertheless, driven by my father’s death, I persisted in my passion and drive to learn more.

As I continued to learn more, I came to fully realize that we needed to go beyond what we, as clinical nutritionists, tend to discuss the most when considering electrolytes – the fact that most people tend to ingest too much sodium and too little magnesium.  For, there was another electrolyte that, even though it was part of all the basic nutrition classes we all took, received vastly less attention clinically.  As I read more and more about potassium, I came to realize that this vastly under-appreciated electrolyte is an essential cog in the wheel that allows sodium and magnesium to perform their respective physiologic and biochemical roles effectively.  This is certainly one major reason why K Alkaline, which is a potassium bicarbonate product, was the first product in the Moss Nutrition Professional Line.

There is, though, one other reason why I have been focusing so heavily on potassium over the years.  It has to do with the way people die in this country.  Ideally, most people die due to a general failure of most, if not all, physiologic systems, mainly due to old age.  Of course, whenever a loved one dies, no matter what the age, or cause, we mourn.  However, what often lessens the pain is the fact that the death was not entirely unexpected or premature.

In contrast, though, we are seeing more and more, and at increasingly younger ages, unexpected, premature and tragic deaths where one key organ fails in a person where the rest of the body is in reasonably good shape.  Of course, in the preceding sentence “unexpected” is the key word.  For the more we have the ability to monitor organ health before complete organ failure we have more power to prevent “premature” and “tragic” from occurring.  Interestingly, our ability to monitor increasing levels of organ dysfunction before outright failure as health care professionals has improved tremendously with key organs such as the lungs, kidneys, and pancreas.  Why is the heart such a notable exception?  When we see a heart fail suddenly, is this a function of our inability to monitor subtle declines in function or is the fact that, unlike the other organs mentioned, apparently well-functioning hearts really can suddenly fail?

In my opinion, for many, if not most people who, with no obvious signs or symptoms in advance, experience sudden cardiac death, it is probably a combination of the two.  Because the heart, for obvious reasons, is so resilient and adaptable, a significant loss of optimal tissue function and integrity can occur with no measureable or obvious signs or symptoms.  However, it is also my opinion that, because the heart is so uniquely reliant on electrical conductively, which is a function of fluid and electrolyte metabolism, a catastrophic “straw that breaks the camel’s back” can occur for various reasons at almost any age under circumstances that can be anticipated with better understanding and appreciation.

While there is certainly much that is still misunderstood and under-appreciated about the heart, I strongly feel that the research presented in this series makes abundantly clear one reason for sudden cardiac death – sudden and dramatic changes in intracellular and/or extracellular potassium levels or major disturbances in the intraceullar:extracellular potassium ratio.  Furthermore, I feel the research also makes it abundantly clear that what we are most ignorant of in terms of potassium, the heart, and  sudden cardiac failure is how many of the everyday occurrences in virtually everyone’s life, which are generally benign and/or mildly disruptive from a metabolic standpoint, can, for certain individuals with certain genetic propensities and a lifetime of stressors that have created suboptimal but clinically invisible disturbances in potassium metabolism, create suddenly and, to use a bad pun, “in a heartbeat,” a catastrophic cardiac crisis.  In particular, based on what I have presented, these everyday occurrences that might create a cardiac crisis for some are the following, particularly when occurring in combination with each other:

  • Significant daily intake of any caffeine containing beverage, food, or pharmaceutical.
  • Use of high blood pressure medication.
  • Skipping meals and then ingesting any meal which will create a significant hyperinsulinemic spike.  Generally, these meals have a high carbohydrate:protein ratio.  This has been classically described as the refeeding syndrome.
  • Excessive exercise (Is carbohydrate loading followed by intense exercise, a popular practice for many athletes, a major contributor to suboptimal potassium metabolism in the heart for certain individuals?  I wonder.)
  • Dietary magnesium deficiency or loss of magnesium due to insulin resistance, elevated cortisol levels, low-grade chronic metabolic acidosis.

Unfortunately, because suboptimal potassium metabolism often does not become clinically apparent until a crisis occurs, it can be difficult to identify in advance those individuals most susceptible to metabolic and lifestyle-related potassium-induced cardiac crises.  However, as I pointed out earlier in this series, I feel there is one important, readily available sign that we often ignore because it is assumed to be insignificant.  What is this sign?  Serum potassium below 4.5 mEq/L.  As I pointed out, credible research shows that, from a cardiac standpoint, for individuals with genetic propensity and/or a lifestyle lending itself to disturbances in potassium metabolism (Some combination of the everyday occurrences mentioned above), the optimal serum potassium range is what would typically be considered as on the high side – 4.5-5.0 mEq/L.  Furthermore, the research I presented makes it exquisitely clear that the heart is extraordinarily sensitive to sometimes minute increases or decreases in potassium content.  Therefore, contrary to conventional thinking, again in certain susceptible individuals, even slight decreases from the optimal serum potassium levels mentioned above, 4.5-5.0 mEq/L, to 4.2-4.4 mEq/L for example, can increase the risk for a cardiac event significantly. Recall the quote from MacDonald et al (10) from part I of this series:

“In class I to III heart failure, a lower serum potassium concentration (4.1 mmol/l vs 4.4 mmol/l is an independent predictor of sudden death.”

As I mentioned in part I of this series, in the blood chemistry performed six months before his death from ventricular tachycardia in February of 2002, my father, someone who had been engaging in activities for years that are well known to adversely affect potassium and cardiac metabolism, demonstrated serum potassium that was 4.4 mEq/L – close to optimal but, obviously, based on the quote above and his death due to ventricular tachycardia, not close enough.

In closing, I want to make it clear that it was not my intention to convince you that we can now discard everything we have learned about optimizing heart health over the years and just focus on potassium.  Rather, given the very high rate of sudden cardiac death that continues to persist in spite of all we have learned and implemented with our patients and the public at large, I hope I have made it clear that we need to add to this body of knowledge because we have been missing something big.  However, unlike many key health care discoveries over the last few decades, I feel we have not been missing this big thing because it is complicated, subtle and hard to identify.  Instead, I feel we have been missing this big thing mainly because it is so basic, so obvious, and our daily lives are so ingrained with activities that adversely affect it, we simply cannot or will not see it for what it truly is.  Let’s start seeing potassium for what it truly is and change the conversation so that sodium and magnesium are not the only electrolytes we talk about.

Moss Nutrition Report #265 – 10/01/2015 – PDF Version


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  2. Kovesdy CPManagement of hyperkalemia: An update for the internist. Am J Med. 2015;Published online ahead of print.
  3. Musso CGMagnesium metabolism in health  and disease. Int Urol Nephrol. 2009;41:357-62.
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