Some Thoughts on Sudden Cardiac Death – Part V

 Part IV of this series ended in the midst of my discussion of clinical conditions that are most associated with hypokalemia.  I will continue this discussion shortly.  However, after writing part IV, an interesting question was posed by a reader in response to the discussion on foods that are most likely, when consumed in excess, to induce potentially fatal hypokalemic states.  Of course, as you saw, those foods are almost always those that have a significant caffeine content.  The reader, though, quite understandably, noticed a glaring omission in this discussion – there was no mention of coffee.  Therefore, I would like to return to this discussion, focusing on a case report on coffee-induced hypokalemia.



In “Coffee-induced hypokalaemia” by Tajima (1) the author discusses a case report about the impact of hypokalemia induced by excess coffee intake.  Below you will see quotes that feature key points in this case presentation.  First please note the basics about the patient and the chief complaints:

“A 50-year-old female outpatient (height 150 cm, weight 44 kg) without significant past history was admitted in our hospital due to severe generalized muscle weakness and fatigue with high fever (38.7 oC).  She could not walk by herself, and both her grips were less than 10 kg.  Her blood pressure was normal (133/78 mmHg; pulse 70 beats/min, regular) and no other apparent abnormality was found on her physical examination.  She took no medications (including herbal medicines such as liquorice or laxatives) and no abnormality has been noted during her annual health checks: i.e. her renal and endocrinal functions were normal, and she was not diabetic.”

The history of onset of the symptoms are as follows:

“Her clinical onset was relatively rapid: i.e. she was quite normal around three days prior to presentation.  Firstly, she suffered progressive generalized muscle weakness and fatigue, and then her body temperature elevated.  At last, her muscle weakness became intolerable, and nausea with slight vomiting occurred (but no diarrhoea).”

Key laboratory findings were significant hypokalemia with elevated serum aldosterone, low blood urea nitrogen (BUN), increased C-reactive protein (CRP), increased white blood cell (WBC) count, and, in the urine, positive bacteria and WBC with low specific gravity.  In addition, her urine pH was 5.5.

The next quote discusses the patient’s history concerning coffee:

“She said that she usually takes >10 cups/day of strong coffee (without sugar) and haunts the lavatory day and night.  Using the analytical contents of coffee, her caffeine ingestion was estimated to be around >1200 mg/day, and her daily urine excretion volume was >3000 ml/day.  After the onset of her symptoms, she seemed to take coffee more than usual as a ‘remedy’ for her illness (but this made the matter rather worse).  Her blood caffeine concentration was 12.3 mg/l (around 10-12 hr after truncation of coffee ingestion), suggesting that she had surely overtaken coffee.  Since her aldosterone level was relatively high, it was possible that she had suffered a mild aldosteronism.”

Based on all of these findings, Tajima (1) concluded the following:

“From these findings, the author concluded that caffeine ingestion caused massive diuresis, the secondary aldosteronism and finally hypokalemia.”

Fortunately, potassium repletion induced a rapid improvement in symptoms:

“Since K+ replacement very quickly resolved her illness, hypokalaemia was very probably the main cause of her muscle weakness and fatigue…”

To give some perspective, the author next discusses blood levels of caffeine after two different usage scenarios:

“When caffeine is used therapeutically, the optimal blood concentration is suggested to be around 8-20 mg/l, and the maximal concentration in blood is <10 mg/l (typically 5-6 mg/l) after taking a single cup of coffee (containing  c.a. 100 mg caffeine) in healthy adults.  Our patient’s serum caffeine concentration of 12.3 mg/l indicates that she is certainly a heavy coffee drinker, but this level was still within a therapeutic rage (it had not reached a toxic level).”

However, given that the patient stopped drinking coffee 10-12 hours before being admitted for treatment, Tajima (1) estimates that her maximal plasma caffeine concentration was 20-40 mg/l.

Based on all of the above, the author concluded:

“In conclusion, it was considered that overdrinking coffee (caffeine) induced her hypokalaemia.  Probably, loss of potassium via the urine stream with secondary aldosteronism was the main cause of the hypokalaemia.”

So as to keep this study and the other studies I discussed on caffeine ingestion and ill-health related to caffeine-induced hypokalemia in perspective, several studies have noted that most individuals consuming caffeine-containing beverages will not demonstrate any negative effects.  However, given that we as clinicians do not deal with populations but individual patients, we must keep in mind the staggering percentage of the overall population that ingests caffeine-containing beverages of any type.  In the paper “Beverage caffeine intakes in the U.S.” by Mitchell et al (2) the authors point out that, in a nationally representative sample of 37,602 consumers aged 2 years or above, consumption rates were at their lowest at 43% of 2-5 year-olds and increased for every age demographic to the point where virtually 100% of those aged 65 years or older ingested caffeine-containing beverages.  Therefore, the fact that “most” consumers will experience no ill-effects means that even a few that do represents a very large population indeed.

I strongly feel that if we take a closer look at serum potassium levels (Recall that any level below 4.5 mmol/l is of potential concern even though the “official” low level is 3.5 mmol/l) and levels of caffeine intake from all sources, we will have a much better understanding of how to best address the needs of patients who have been told for years by both allopathic and alternative medicine practitioners that they have ailments that defy explanation and/or have no known cause.


Eating disorders

In previous newsletters in this series I have briefly noted that patients experiencing eating disorders are prone to hypokalemia and attendant cardiovascular risks.  The paper “Sudden death in eating disorders” by Jauregui-Garrido and Jauregui-Lobera (3) provides more detail on this patient population.  As the authors note, hypokalemia should always be ruled out with eating disorders that involve purging:

“…purging may increase the risk of hypokalemia and subsequent cardiac dysrhythmias, and self-induced vomiting increases the risk of additional complications.  In fact, QT prolongation and ventricular arrhythmia may develop in the setting of severe hypokalemia, exposing patients to high risk of sudden cardiac event.

It must be noted that risk of death is clearly linked to QT prolongation, mainly due to hypokalemia or to a starvation-derived remodeling of the heart.  The principal risk factors seem to be duration of illness (>10 years), chronic hypokalemia, plasmatic albumin chronically <3.6 g/100mL and absolute QT > 600 milliseconds.”

The authors go on to note that eating disorders that involve use of laxatives have also been associated with electrolyte imbalances:

“Medical problems associated with laxative abuse include electrolyte and acid/base changes that can involve the renal and cardiovascular systems and may become life threatening.  The same applies to the use/abuse of emetics.”

What is the clinical presentation of hypokalemia as the result of an eating disorder?  To answer this question I would like to review a particularly severe example in the case report “Recurrent aborted sudden cardiac death with seizures and rhabdomyolysis due to bulimia-induced hypokalemia.  Report of one case” by Finsterer and Stollberger (4).  The first quotes I would like to highlight discuss key points about the patient at the time she was admitted for evaluation and treatment.  Basic points are as follows:

“The patient is a 24 yo, Caucasian female, height 170 cm, weight 40 kg, who was admitted for aborted sudden cardiac death (SCD) due to ventricular fibrillation associated with a symptomatic, generalized tonic-clonic seizure.  She required cardio-pulmonary resuscitation (CPR) with defibrillation (3 times) and intubation.”

As noted in the following quote, the patient’s serum potassium was extremely low:

“Blood chemical investigations revealed hypokalemia of 1.9 mmol/L (normal, 3.5-5.1 mmol/L).”

The next few quotes discuss significant history:

“The individual history was positive for recurrent palpitations at age 9 and 10 y respectively.  Since age 15 y she suffered from an eating disorder associated with habitually induced vomiting, and, according to her relatives, chronic ingestion of furosemide and laxatives.”

In addition:

“At age 21 y (8/2009), she experienced aborted SCD due to ventricular fibrillation and hypokalemia of 1.7 mmol/l also requiring CPR.  Shortly after admission in 8/2009, she experienced another episode of ventricular fibrillation, which was self-limiting and did not require CPR.  Aborted SCD was complicated by heart failure, traumatic pneumothorax, pleural effusions requiring puncture, and pneumonia.  Cardiac MRI was normal.  One year prior to admission (age 23y), she experienced a non-triggered rhabdomyolysis resulting in acute renal failure.  She also reported rare migrainous attacks since puberty.”

The next few quotes highlight the authors thoughts on various aspects of the patient presentation.  First, what was the cause of the hypokalemia?

“The first point requiring discussion is the cause of the hypokalemia.  Generally, hypokalemia in the presented patient could have been induced by vomiting from bulimia, prerenal azotemia with fluid or potassium loss, rhabdomyolysis, intake of diuretics or laxatives, or hyperaldosteronism.  The most likely cause, however, is bulimia, since she admitted to induce recurrent vomiting since 10y.”

The hypokalemia, in turn, caused the ventricular fibrillation.  What is the most likely cause of the seizures?

“The most likely cause of the seizures was cerebral hypoxia during ventricular fibrillation.”

What about the rhabdomyolysis?  The authors state:

“Rhabdomyolysis at age 23y might be attributable to an unwitnessed seizure, severe hypokalemia, or subclinical, metabolic myopathy.”

Over exercise

Could over exercise deplete serum potassium and, under extreme circumstances no matter what the age, lead to catastrophic cardiac events?  Like you, I have been very disturbed by the occasional but still too frequent reports over the last 2-3 decades about top athletes in their teens and twenties suddenly dying of heart attacks while participating in an athletic event.  Of course, as I mentioned in part I of this series, the headlines invariably state that either the cause was unknown or there was a genetic defect in heart function or structure that led to the sudden and tragic demise.  However, as I also mentioned in part I, I have long wondered whether there is more to the story than what appears in the headlines.  For, if the sole issue was a genetic heart defect that has probably been present since birth, why didn’t the heart attack occur earlier, or later for that matter.  Why did it occur at the time it did?  In my mind there had to be an environmental trigger that, when combined with the genetic defect, led to the tragic death from a heart attack.

For years, as I mentioned, I have felt strongly that the environmental trigger was electrolyte imbalance, specifically relating to potassium, that, when combined with extreme exertion often in less than ideal temperatures, can lead to premature death.  However, for years I was unable to find published research that not only directly supported this contention but also provided the specific biochemistry and physiology underlying the ultimate failure in heart function.  Fortunately, in preparing for this newsletter series I came upon the paper “Hormonal and pharmacological modification of plasma potassium homeostasis” by Clausen (5).  As you will see, Clausen (5) not only makes a strong case for suboptimal potassium status as a major contributing factor but discusses exactly what happens concerning potassium metabolism.

Before presenting quotes from the paper that relate directly to over exercise and potassium, I would like to present some quotes that discuss key aspects of potassium metabolism that have not received the attention they deserve.  The first emphasizes that muscle plays an extremely important role in potassium homeostasis.  This, of course, is an extremely important issue when discussing potassium and athletes since pushing muscle physiology to its limits is something that many of the athletes who died prematurely of heart attack shared in common.

“…several tissues contribute to the acute short-term regulation of the K+ concentration in plasma and the extracellular space.  This review focuses on the skeletal muscles, which play a prominent role in the extrarenal K+homeostasis.  This is primarily because of the fact that the skeletal muscles contain the largest single pool of K+ in the body…this amounts to 2600 mmol, which is 46 times larger than the K+ content of the extracellular phase and 236 times larger than the K+ content of blood plasma.  Therefore, even modest relative changes in the release of K+ from the skeletal muscles cause marked changes in the concentration of K+ in plasma or in the extracellular phase.  Because of their high content of K+ channels, the skeletal muscles possess a large capacity for exchange of K+ with the extracellular space.”

Next, Clausen (5) discusses what happens to muscle potassium when environmental stressors such as over exercise occur:

Table III lists primary causes of hypokalemia that can be related to increased uptake of K+ into the muscles or inhibition of K+ release from the muscles.  Probably, the most common cause of acute hypokalemia is the rebound response seen after the hyperkalemia elicited by intense exercise.  Plasma Kdevelops an ‘undershoot’ to a level below that in the resting state, which may be related to increased activity of the Na+,K+ pumps.  This is because of the excitation-induced elevation of intracellular Na+ in the working muscle cells as well as the large increase in plasma catecholamines generally elicited by intense exercise.”

Most of the environmental factors mentioned by Clausen (5) that cause hypokalemia by altering muscle potassium physiology have already been discussed.  These include theophylline, caffeine, insulin, diuretics.  Another, which I will discuss in more detail later, is magnesium deficiency.  One other notable factor that I did not mention is sports doping.  Finally, a factor, which I will discuss shortly, is endotoxin increases in blood which can occur with leaky gut.

Below you will find what Clausen (5) has to say about the impact of theophylline and caffeine on potassium homeostasis:

“Acute theophylline intoxication was found to induce hypokalemia, which was inversely correlated with the plasma concentration of theophylline.  This affect was attributed to an intracellular shift of K+ into the muscles and related to the well-documented mobilization of endogenous catecholamines induced by theophylline.”

Concerning caffeine:

“Intoxication with caffeine was also shown to induce a massive release of endogenous catecholamines and a plasma K+ of 2.2. mM.  In a more recent case, a patient received an overdose of caffeine contained in a slimming agent.  At admission, plasma caffeine was 110 mg/L and plasma K+ 1.6 mM.  The half-life of the caffeine was 16 h.

“It should be noted that one of the degradation products of caffeine is theophylline, which might contribute to the mobilization of catecholamines and hypokalemia.”

The next quote discusses the impact on potassium homeostasis of endotoxin, which can increase in the bloodstream due to leaky gut.

“A recent study showed that endotoxin increases plasma adrenaline in healthy human subjects.  Concomitantly, plasma K+ was decreased, probably reflecting stimulation of Na+,K+-pump-mediated uptake of K+ in the muscles.”

What is the impact of trauma, a common occurrence in athletes, on serum potassium levels?  The findings are more than a bit sobering:

“A study on 500 patients with trauma showed that 46% had hypokalemia (<3.5 mM).  A prospective study reported in the same paper showed that trauma patients with hypokalemia had markedly higher plasma levels of adrenaline and noradrenaline, which were spontaneously restored within 36 h after admission.  Again, the hypokalemia was attributed to the elevated plasma levels of catecholamines.”

Still another cause of hypokalemia that has not received the attention it deserves is one that I will, as I mentioned, address in much more detail in a future newsletter – magnesium deficiency.  Clausen (5) states:

“Dietary deficiency of Mg and loss of Mg by diarrhea may also give rise to net loss of K+ and hypokalemia.”

Clausen (5) goes to point out that when magnesium deficiency is combined with the other causes of hypokalemia mentioned above, changes in cardiac function can occur:

“These types of longer-lasting hypokalemia when combined with the above-mentioned causes of acute hypokalemia will augment the risk of developing severe hypokalemia leading to arrhythmia.”

As I hope you can see from the information presented by Clausen (5) highlighted above, hypokalemia may be somewhat common in athletes.  Is there a relationship between hypokalemia and the tragic, highly publicized sudden deaths due to heart attack that have been occurring over the last 1-2 decades?  Clausen (5) begins to answer this question by presenting prevalence rates of cardiac related sudden death in athletes:

“A prospective study on 21,481 healthy male physicians showed 23 sudden deaths from cardiac causes associated with vigorous exercise.  The excess risk of sudden death during and after 30 min after vigorous exertion was one per 1.51 million episodes, similar to that reported in other populations.  The relative risk of sudden death was sevenfold higher among those who rarely engaged in vigorous exercise.”

Interestingly, incidence was much lower in women:

“A similar prospective study performed on 69,693 women, however, showed that the relative risk of sudden cardiac death during moderate to vigorous exercise was 19-fold lower than in the men, indicating that it is a very rare event in women.  Also, the risk may be reduced by regular exercise.”

What role does potassium metabolism play in cardiac related death with exercise?  Recall that after intense exercise serum potassium levels tend to rise and then drop.  With this in mind, consider the following:

“The exercise-induced sudden death may be related to the pronounced hyperkalemia caused by the rapid loss of K+ from the working muscles or to the subsequent rebound hypokalemia.  It should be noted that during intense exercise, plasma K+ may reach 8 mM, not only in the venous blood returning from the working leg muscles but also in the arterial blood.”

Recall that the general range for plasma potassium is 3.5 – 5.5 mM.  Therefore, after intense exercise, certain parts of the bloodstream will experience major elevations of potassium.  Clausen (5) continues:

“This implies that the heart is directly exposed to the hyperkalemia and the subsequent hypokalemia.  Such changes, in particular the hypokalemia, may cause arrhythmia.  An electrocardiographic study on 21 squash players showed that 2/3rds showed arrhythmia during or immediately after the play.  Indeed, in a study comprising 60 cases, squash playing was associated with sudden death.”

What physiologic mechanism does Clausen (5) propose to explain the above?

“Many studies have shown that training leads to upregulation of the content of Na+,K+ pumps in skeletal muscles.  This increase in Na+,K+ pump capacity is likely to favor the clearance of K+ from the plasma and thereby reduce exercise-induced hyperkalemia.  Indeed, this was documented in exercise studies.  Thus, training in general may provide protection against exercise-induced hyperkalemia, but more studies are needed to document this relationship.”

I’m sure I speak for everyone when I say how much it saddens me when I read about young athletes in the prime of life dying suddenly of a heart attack.  Of course, the irony of the news reports of the dead, as often noted in these reports, is that our society tends to regard these athletes as having been in “perfect health” right up until their “mysterious” deaths.  As I have long suspected, rightly so as suggested by Clausen (5), these athletes, even though their physical appearance suggests “perfect health,” may have significant vulnerabilities below the veneer that gives the appearance of perfection and invulnerability.  It is my hope that all of you who read this newsletter will do everything you can to educate young athletes that, even though it appears to them that training and performance are their only legitimate concerns at this stage of life, for a few ignoring diet and lifestyle may have tragic consequences.


As I hope I have demonstrated, low potassium levels are major risk factor for poor cardiac health.  Does it automatically follow that potassium supplementation optimally addresses this issue?  Several studies have suggested that the answer to this question is yes.  What follows is a review of just one study that supports this position.

The paper “Effects of a high salt intake and potassium supplementation on QT interval dispersion in normotensive healthy subjects” by He et al (6) addresses the cardiac health indicator discussed above in the section on eating disorders, QT interval dispersion.  Why is QT interval dispersion important?  The authors state:

“The degree of QT interval dispersion reflects regional differences in ventricular repolarization heterogeneity and electrical instability, which are important predictors of malignant arrhythmia and sudden cardiac death.  This parameter has been widely used in studies of hypertension, coronary heart disease, arrhythmia and other heart diseases as well as to evaluate drug efficacy.”

In this study, 64 normotensive men and women ranging from 28 to 60 years of age were evaluated.  Was supplementation of potassium valuable in terms of QT interval dispersion?

“…the significant increase in serum potassium level induced by oral potassium aspartate supplementation tends to reduce the degree of QT interval dispersion.”

Why, specifically, was the potassium supplementation so helpful?  He et al (6) state:

“One possible mechanism underlying these findings is elevation of the extracellular potassium ion concentration after oral potassium supplementation, which improves cardiac cell excitability and the action potential conduction velocity, increases the net myocardial repolarization current, shortens the action potential duration and narrows the action potential duration (APD) between Purkinje fibers and myocardial fibers, thereby improving myocardial repolarization heterogeneity.  Additionally, the fact that the degree of QT dispersion is shortened by oral potassium supplementation indicates that, in addition to antagonizing the pressor effect of sodium, supplementing potassium reduces the impact of a high salt intake on the QTd and QTdc values and lessens cardiac repolarization heterogeneity, which may have a preventive effect on arrhythmia.  Hence, in addition to salt restriction, increasing the potassium intake, thus improving the dietary potassium/sodium ratio, is an important strategy for the primary prevention of hypertension and cardiovascular disease.”


One of the most important clinical decisions we must make almost every day is one that is rarely addressed in published research.  What is the best form of a supplement for any given clinical situation?  In the case of potassium, potassium chloride is the predominant form found in the marketplace.  Is it the best for the needs of our particular patients?  The paper “Comparative effects of potassium chloride and bicarbonate on thiazide-induced reduction in urinary calcium excretion” by Frassetto et al (7) answers this question in relation to a common scenario seen in many of our patients – loss of calcium in the urine.

In this paper 31 healthy men and women aged 50 or greater were evaluated for four weeks.  The parameters of the study are as follows:

“After a baseline period of 10 days with three 24-hour urine and arterialized blood collections, subjects were randomized to receive either hydrochlorothiazide (HCTZ) 50 mg plus potassium (60 mmol daily) as either the chloride or bicarbonate salt.  Another 19 women received potassium bicarbonate (60 mmol) alone.  After two weeks, triplicate collections of 24-hour urines and arterialized bloods were repeated.”

(60 mmol of potassium equals 2400 mg)

Frassetto et al (7) begin their paper by highlighting the prevalence of acidosis in our society and how it affects bone health and the related increase in urinary calcium loss:

“Metabolic acidosis has been shown in in vitro and in vivo studies both to dissolve bone directly and to increase osteoclast activity, which increases bone resorption, releasing skeletal calcium for renal excretion.  Metabolic acidosis also promotes bone resorption and renal calcium excretion by directly inhibiting renal tubular calcium resorption.”

In our typical patient population the type of acidosis we tend to see is what Frassetto et al (7) call “chronic low-grade metabolic acidosis”:

“…otherwise healthy people can also have a chronic low-grade metabolic acidosis, expressed as a rise in steady state blood hydrogen ion levels and a fall in steady-state plasma bicarbonate levels, which results from eating the typically high net acid-producing American diets and from the decline in renal function that accompanies increasing age.”

They then point out that potassium bicarbonate can have a positive impact on acidosis plus calcium and bone loss:

“Neutralizing acidosis with potassium bicarbonate reduces bone resorption, presumably in part by direct effects on bone and in part by promoting renal retention of calcium.”

What were the results of the study?  As has been noted by several researchers, thiazide diuretics do reduce urinary calcium losses.  By adding potassium supplementation to the diuretic, though, the positive impact on urinary calcium was increased:

“Urinary calcium excretion decreased significantly in response to the administration of HCTZ in combination with either KHCO3 or KCl and in response to the administration of KHCO3 alone.  Previous studies have shown that in normal, healthy people, thiazides decrease urine calcium excretion and that potassium alkali salts also decrease urine calcium excretion.  Urine calcium excretion therefore decreased as expected in the KHCO3 group and in both HCTZ groups.  With respect to reducing urine calcium HCTZ + KHCO3 should have been at least as effective as KHCO3 treatment alone.  In fact, the effects of the two treatments were additive so that treatment with HCTZ and KHCO3 combined doubled the decrement in urinary calcium observed with either KHCO3 treatment alone or that observed during combined treatment with HCTZ and KCl.”

How did potassium bicarbonate and potassium chloride compare in terms of reducing urinary calcium?  As you will see in the concluding paragraph in the paper, potassium bicarbonate was clearly superior.  Furthermore, potassium bicarbonate was superior in terms of reduction of acidity:

“In summary, in the present study, KHCO3 was superior to KCl as an adjunct to HCTZ, not only inducing a twofold greater reduction in urine calcium excretion, but also completely neutralizing endogenous acid production and therefore correcting the pre-existing mild metabolic acidosis that normally accompanies ingestion of an acid-producing diet in older people.  Accordingly, for stone disease and osteoporosis treatment and prevention, the combination of HCTZ + KHCO3 may be preferable to that of HCTZ + KCl.”


As this series on potassium and CVD, with a focus on sudden cardiac death, nears its end, I would like to share a thought that has been occurring to me over the last several months as I have been reading and writing about the papers that form the basis for this series.  Based on what I see in both the mass media, the usual medical journals, and even what is presented at many nutrition and functional medicine seminars and symposia, it seems that we automatically assume and even joyfully anticipate that answers to issues such as chronic CVD and the horrors of sudden cardiac death that occur all too soon in beloved athletes, patients, friends and family must be ever more complex, expensive, and high tech.  While there is no question that this approach has certainly been successful in reducing cardiac mortality and morbidity (loss of quality of life), it still seems to me, based on my own experiences with patients, experiences reported by you, my customers, and what I have read in the newspapers about the latest unexpected and tragic death due to heart attack, we still have a ways to go.

Over the last 20 years or so I have taken it upon myself to go to the medical libraries and read the papers, such as those I have been describing in this series, that hardly anyone else reads.  What have I found?   In contrast to the prevailing pattern of increased complexity I described above that seems to be the norm today, I found increased knowledge and increased options for improving cardiac health through simplicity.  I found, at its essence, the heart is an electrical organ and therefore functions in a manner that adheres to the principles of fluid and electrolyte conductivity that apply to many other electrical systems, both animate and inanimate.  What is one of the most important principles when considering optimal flow of electricity?  Optimal balance of fluid and electrolytes.  In particular, when considering flow of electricity in living systems, my reading suggests that the three most important electrolytes are sodium, potassium, and magnesium.  Of course, we all understand the consequences of excess sodium.  Do we really understand the consequences of deficient potassium?  I think not.

Over the course of this series I have become more and more convinced that, very possibly, the best way to reduce even further the still too common tragedy of sudden cardiac death is to truly appreciate a somewhat disturbing reality.  What is this reality? Many individuals engage in sometimes dozens of activities a day, many of which they do not think twice about, that disturb potassium-related aspects of heart-based electrical activity to the point where a “death by a thousand cuts” scenario is created and tragic outcomes at virtually any age are a very real and frightening possibility.

Interestingly, even with all the ways I have discussed that people disturb their cardiac-related potassium metabolism, there is still one major way I have yet to discuss that in certain individuals will even further increase risk of adverse outcomes.  In the next and last installment of this series, I will discuss in detail a major contributing factor to suboptimal potassium physiology, magnesium deficiency and imbalances.

Moss Nutrition Report #264 – 08/01/2015 – PDF Version


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  2. Jauregui-Garrido B & Jauregui-Lobera ISudden death in eating disorders. Vascular Health and Risk Management. 2012;8:91-8.
  3. Mitchell DC et alBeverage caffeine intakes in the U.S. Food and Chemical Toxicology. 2014;63:136-42.
  4. Finsterer J & Stollberger CRecurrent aborted sudden cardiac death with seizures and rhabdomyolysis due to bulemia-induced hypokalemia.  Report of one one case. Rev Med Chile. 2014;142:799-802.
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  6. He M et alEffects of a high salt intake and potassium supplementation on QT interval dispersion in normotensive healthy subjects. Intern Med. 2015;54:295-301.
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