The sodium-potassium balance (Pt. 2)

The exchange pumps

The outward sodium current generated by the sodium-potassium pump must move back into the cell to complete a closed circuit. Sodium must do this through what is known as the ‘exchange pumps’. These pumps are also located on the cell membrane and their job is to regulate other functions of the cell: the ‘sodium-acid exchange acid pump (Na+/H+)’ controls the levels of acid inside the cell, and the ‘sodium-calcium exchange calcium pump’ (Na+/Ca2+) controls the amount of calcium inside the cellThis means that every cell in the body takes advantage of the sodium current generated by the sodium potassium pump in order to perform other functions. Like we said before, a slowing down of the sodium-potassium pump will have tremendous consequences on overall health, including these two pumps.

The sodium acid (Na+/H+) exchange acid pump

As we saw in previous blogs, cell detoxification is an essential part of health. We explained that as a normal part of a cell’s life, cells produce acid that needs to be removed on a regular basis; failure to do so would result in the shutting down of the energy machinery and the death of the cell. If there was no mechanism to pump acid out of the cell, since the inside is negative, compared to the outside, this would pull so much acid inside the cell that the pH inside the cell would go down to about 6.0, far too low to be compatible with healthy function. The ‘acid pump’, therefore, has the important job of removing excess acid (H+) out of the cell.

The acid pump gets its energy not from ATP but from the electrical current generated by the sodium-potassium pump (via sodium ions). It works by exchanging sodium for acid across the cell membrane, this means that sodium moves into the cell and an acid is taken out. Its main role is to keep acid from piling up in the cell, but it also has the important function of influencing the pH of the inside of the cell which in turn affects directly how enzymes inside the cell function. In turn, this regulates many cellular functions, one very important example is the hormone insulin.

Dr. Richard D. Moore, together with other doctors, obtained evidence that insulin increases the pH inside the cell via the sodium-acid exchange pump by moving acid outside of the cell and therefore increasing the pH inside the cell. They theorized that through this mechanism insulin stimulates glycolysis, the first step in the metabolism of glucose, as it enters the cell. Dr. Moore discovered that when there is no sodium outside the cell, the sodium-acid exchange pump runs backwards, pumping acid into the cell. Low potassium can also cause sodium to stay inside the cell. This shows once again how an imbalance between sodium and potassium inside and outside the cell can have catastrophic consequences for health.

Other aspects of health that are affected by this imbalance are:

  1. Protein synthesis
  2. Cell growth
  3. The manufacture of new DNA and subsequent cell division

This also explains how diet is crucial in this aspect, eating too many acidic foods can cause electrolyte imbalances, changing pH levels to a state of acidosis (3). A diet high in alkalizing minerals like kelp, garlic, found in the ‘Heart and Body Extract’, and green leafy vegetables can bring our bodies back to the balance it needs to function properly. What is important to remember here is that the pH inside the cell depends on the balance between sodium and potassium.

The sodium-calcium exchange calcium pump (Na+/Ca2+)

Another pump that uses the electrical current produced by the sodium potassium pump is the ‘sodium-calcium exchange calcium pump’ (Na+/Ca2+). This pump removes excess calcium from the inside the cell, by exchanging one calcium ion (Ca2+) for three sodium ions. This means it moves three sodium ions in and takes one calcium out. Since this pump is powered by the sodium-potassium pump, anything that slows this pump will slow the sodium-calcium pump, with tremendous implications for our health. How? Keeping the level of calcium inside the cell low is critical, because small variations in this low level of calcium influence cell function greatly. For example, a small increase in the level of calcium inside muscle cells causes them to contract more than needed, leading to hypertension.

The increase in calcium inside cells results in other imbalances like:

  1. Decreased effectiveness of insulin (inability of insulin to remove glucose from the blood, leading to diabetes)
  2. Disturbance of fat and cholesterol metabolism
  3. Narrowing of the smallest arteries leading to high blood pressure
  4. Increased growth and division of cells

All of this creates an increase in the pH inside cells through the body, possibly leading to the development of cancer.

Sodium-potassium imbalances, excess calcium and hypertension

Low potassium slows the sodium-potassium pump increasing sodium inside the cells and decreasing membrane potential across the cell surface. Dr. Moore warns about the ‘deadly’ consequences of a dietary imbalance between sodium and potassium, consequences that have only begun to be understood. This imbalance is seen mostly in people with hypertension, therefore high blood pressure is an indicator of low potassium (hypokalemia).

The level of sodium inside cells of hypertensive lab rats was found to be a 40% higher and the voltage of their membranes was decreased by 3%, compared to rats with normal blood pressure. Thus, high blood pressure can be used as an indicator of low potassium and high sodium inside the cells.

This imbalance also has consequences in the other pumps we looked at. The sodium-calcium exchange pump is very sensitive to increased sodium inside the cells. An increase of 5% sodium translates into at least 15-20% increase in the level of calcium, which could cause as much as 50% increase in resting tension of the small resistance arteries. For hypertensive rats this was observed to be much higher, up to 100-200% higher. In kidney cells this meant a 64% increase.

What does this elevated calcium translate into? First of all, in muscle cells this increase means the muscles contract more. In the smaller arteries this increased tone, narrows the artery, increases peripheral resistance and raises blood pressure. An increase in the calcium levels inside sympathetic nerves that regulate blood vessel contraction would also increase the release of transmitting hormones such as epinephrine (adrenaline). This causes further contraction of the smooth muscle cells of the small resistance arteries.

High calcium inside cells also means:

  1. Increase in growth and division of cells
  2. Increase in the production of collagen
  3. Alterations in protein synthesis
  4. Alterations on the rate at which proteins are made and the way they are assembled together into larger structures

We are out of balance

Since it is the balance of sodium and potassium that counts, our high sodium and low potassium diets put us at risk. Our bodies are not designed to withstand such an extreme dietary imbalance, especially when it is maintained through the years.

In practical terms, increasing the sodium-potassium ratio should be done always slowly according to Dr. Moore, because a body deficient in potassium takes more time to adapt to increased dietary potassium. The presence of hypertension, diabetes, kidney disease and some drugs can slow the body’s adaptation to increased dietary potassium. In these cases, changes in the potassium to sodium balance may require the advice of a physician.

Because the body has so many complex and interrelated regulatory mechanisms, once they are adapted to a situation they require some time to adapt to another. We should not make changes to the body too quickly, because it may not be able to adapt. Since sodium and potassium are interconnected with so many regulatory systems, changing the dietary level of these two minerals too suddenly, especially if they are changed at the same time, could be dangerous.

What is more, since the kidneys excrete excess potassium, an excessive elevation of potassium could result in kidney disease serious enough to involve an inability to excrete potassium. Therefore, Dr. Moore advises to consult with a doctor to rule out kidney problems before increasing the sodium-potassium ratio.

People with hypertension, on diuretics, with magnesium deficiency or hypokalemia, diabetes, kidney insufficiency, and metabolic acidosis all can have an inability to regulate potassium. This is also the case of users of certain drugs like beta blockers, potassium sparing diuretics, ACE inhibitors, etc. A good idea is to start by slowly reducing the intake of sodium through a period of one week, once it has been decreased significantly, one can start increasing potassium with an alkaline diet.

How out of balance are we?

Our dietary intake of potassium should be at least 4-5 times higher than that of sodium. Our ancestors used to have this ratio, even higher on potassium (16:1 ratio). However, our current dietary sodium is about ten times what it should be, around 4,000 mg/day. To make matters worse the average American diet gets about half the daily potassium necessary. This translates into a ratio of 0.6, much worse than 1:1.

How much sodium and potassium do we need?

Surprisingly, a lot less sodium than we think. Some health care professionals estimate we need from 50 mg to 230 mg per day. This points to a minimum required amount of sodium of not more than 100 mg-300 mg. The ‘National Academy of Sciences’ recommends a minimum daily intake of 500 mg. The FDA recommendation is of 2,500 mg a day. Other health care professionals using ‘hair tissue mineral analysis’ (HTMA) like Dr. Robert Selig, explain that ratios are very personal and should only be recommended based on a study of the person’s mineral ratios on a regular basis (twice a year). This is due to the fact that there are many factors influencing mineral ratios in the body like stress, environmental conditions, etc. For this, a hair sample of the patient is taken in order to study the present levels of minerals inside and outside the cell. Blood tests are not considered reliable according to HTMA practitioners because the blood is only a transport system, therefore it does not show how much is actually being used by the cells.

When it comes to potassium, Dr. Young estimates that healthy adults should consume as much as 10,000 mg/day. According Dr. Eric Berg, a minimum of 4,700 mg is needed, that is 7 to 10 cups of vegetables a day. This recommendation goes along the alkaline diet we discussed in previous blogs.

A simple solution

Decreasing the risk of hypertension, stroke, osteoporosis, and other salt linked health problems can be as simple as decreasing salt intake while at the same time increasing the amount of potassium rich foods. This can be done with a personalized hair tissue mineral analysis to better evaluate mineral levels in the person’s body.

An alkaline diet, together with a good nutritional supplement like the ‘Heart and Body Extract’ can support the body’s own regulatory mechanisms toward a balanced sodium-potassium ratio.

In conclusion

Electrolytes are electrically charged minerals that are significant for providing the infinitesimally small units of life called ‘cells’ with the electrical energy they need to do their work. They exist within cells as well as in the fluid that surrounds our cells, and they create an electrical flow when they are in the right balance. Potassium is a specially important mineral for a healthy heart that is usually missing in our diet. In today’s blog we learned that it is the right balance between sodium and potassium that is key for proper heart function. An alkaline diet and the ‘Heart and Body Extract’ can help you bring your body back to balance.

Thank you for reading.



(2)  Boynton, Herb, et al. The Salt Solution. Avery, 2001.




The sodium-potassium balance (Pt. 1)

The health of the cell is of utmost importance for the heart. A balance of electrical minerals (electrolytes) both inside and outside the cell provides a flow of energy that allows the heart to beat with the proper rhythm (1). Due to the constant pumping action of the heart, a steady and constant flow of this electrical energy is key for proper heart function. This is made possible by the presence of pumps on the cell membrane that turn each of our cells into a small battery, capable of releasing and storing energy and maintaining an electrical charge.

We saw how an alkaline diet, together with a good nutritional protocol, like the ‘Heart and Body Extract’, are the best sources of these electrolytes, namely, sodium, potassium, calcium and magnesium. We also saw how potassium has a critical role for heart health as pointed out by the ‘National Council on Potassium in Clinical Practice’. Such research represents a new focus in the field of cardiology, and one that is receiving much interest from many health care professionals. One of these health care professionals is Richard D. Moore, M.D., Ph. D., who in his book ‘The salt solution’ (2), goes into deep detail about the importance of balancing sodium and potassium for heart health. He has worked with other doctors and published his research on how the sodium potassium pump influences insulin in the body.

In today’s blog, we will focus on his work. Specifically, we will look at how the sodium-potassium pump works to keep our heart healthy, and how it is needed to keep other important pumps working in the cell, the ‘sodium-acid exchange acid pump’, and the ‘sodium-calcium exchange calcium pump’.

Basics of cell biology 

90% of the potassium in the body is found within cells.This compartmentalization depends on its active transport through the cell membrane by the sodium-potassium pump. Before we look deep into this mechanism, we need to understand something basic in cell biology: all cells consist of a surface membrane called ‘plasma membrane’. Across this plasma membrane there is a voltage difference, with the inside of the cell being negative with respect to the outside. This voltage difference is made possible by the presence of the sodium-potassium pump, which acts as a microscopic electric generator of current carried by positive sodium ions.

The main job of this pump is to move sodium out of the cell and move potassium in. The purpose of this distribution is to generate a voltage between the inside and the outside of the cell: With each cycle, the sodium-potassium pump moves more sodium ions out than potassium ions in. The sodium pumped out is positively charged while the inside of the cell is negatively charged.This movement of electric current out of the cell leaves the inside more negative. In this manner, the sodium-potassium pump generates an electrical current, creating a powerful electric field across the cell membrane. The negative charge, and the lower concentration of sodium inside the cell, create a very strong ‘tug’ which makes sodium ‘want’ to leak back into the cell. This acts like a ‘sodium battery’ that is capable of performing work in a manner similar to a car battery.

The energy this battery creates is so crucial, that life could not be possible without it. This is proven by the astonishing number of pumps the body has: each of our 100 trillion cells have between 800,000 and 30 million of these pumps on the cell membrane (4). This great amount of electricity the human body is capable of generating also means that just a slight slowing down of these pumps can mean a tremendous decline in overall health.

It was originally thought that only nerve, muscle and kidney cells made use of the sodium-potassium pump. The reason for this might have been the fact that nerve and muscle cells have the largest potential (70 and 90 Volts respectively). However, it is now known that all cells in the body use the sodium-potassium pump. A nerve impulse, for example, consists of a 1 millisecond switching of the membrane potential from a negative value to a positive value and then back to the negative. This is accomplished by sodium ions rushing into the cell: as sodium rushes into the cell, the positive charge it carries makes the inside more positive. As the inside becomes positive potassium rushes outside the cell. All this process provides the signal for muscles and nerves to contract. When this happens several times, it is the equivalent of ‘running down’ of a battery, which is thought to be responsible for the fatigue we experience when we exercise. The sodium-potassium pump has the key job of restoring the cell’s energy by pushing the extra sodium back out and pulling the missing potassium back into the cell.

The obligatory link between sodium and potassium

Too much focus has been put on just limiting sodium for improving heart health, however, the sodium-potassium pump proves that it is not possible to isolate either sodium or potassium. It is the right ratio of the two that brings cells back into a healthy balance. This is because in the body sodium and potassium oppose one another, when one goes up the other goes down. Increasing potassium causes sodium to be excreted through the kidneys and vice versa. According to Dr. Moore, it makes no sense to talk about one without mentioning the other. He explains that there is a reciprocal relation between the levels of sodium and potassium inside the cell: anything that decreases sodium will increase potassium and vice versa, because the sodium-potassium pump moves sodium and potassium in different directions. In practical terms, without enough potassium, excess sodium cannot be lowered within the cells, in other words, to lower sodium in the cell, it must be replaced by potassium. This is one of the reasons why low salt diets don’t work for people with high blood pressure.

The teeter-totter rule

Dr. Moore refers to this as the ‘teeter-totter rule’. He explains that in the body it is not possible to affect sodium without affecting potassium. Not getting enough potassium and lowering salt intake cannot possibly restore the normal level of potassium and sodium within the cells. This is because sodium and potassium work together: When potassium goes into the cell, sodium must come out and vice versa, because the pressure inside the cells and the pressure outside must remain constant. An indicator of a healthy sodium-potassium pump is a ratio of around 14 to 1 of potassium to sodium inside the cell, and outside the cell the fluid should contain 30 times more sodium than potassium.

We could therefore say that heart health is not a matter of how much sodium or potassium one gets from the diet, but a matter of balance between the two. However, our present diet contains much more salt than our ancestors used to consume, and this has brought an imbalance to the body. Too much salt, without potassium to balance it out, can damage the heart, blood vessels and even bones. Only the right sodium-potassium ratio can reverse this damage.

More roles of the sodium-potassium pump

As we mentioned earlier, the sodium-potassium pump is present in all the cells of the body. Therefore, it has many different and important functions. So far we have explained that the job the sodium-potassium pump has is to move sodium out of the cell while moving potassium in for cells to be able to conduct electricity. But the sodium-potassium pump could do this without generating electricity, and since the body always works to conserve energy, there must be a very important reason for this. What is the purpose for generating electricity?

First of all, this pump helps maintain order in the body, by keeping sodium on one side of the cell and potassium on another side.

Secondly, the strength of this electric field also influences the structure and function of many proteins in the cell, and these proteins, in turn, play an important role in:

  1. Transporting substances into and out of the cell
  2. Transmitting hormonal signals, and
  3. Carrying out a host of enzymatic reactions

Thirdly, the sodium-potassium pump affects a number of functions which in turn influence:

  1. Cholesterol levels
  2. How well the heart pumps
  3. It influences fat metabolism
  4. It allows nerves and muscles to conduct electrical signals
  5. It allows sodium to be reabsorbed into the kidneys
  6. It provides the power for regulation of levels of acid, calcium, and sugar inside the cell (sugar metabolism)
  7. It governs cell growth and division, which makes it significant for cancer prevention
  8. It regulates the response to hormones, including insulin

A minor slowing of the sodium potassium pump can affect all of these aspects of health.

Implications for heart energy

Nowhere in the body is the sodium-potassium pump best exemplified than in the heart. Not only because of the number of sodium-potassium pumps heart cells contain, but because the heart is a pump. A pump can be defined as a device that uses energy to move something in a direction opposite to the direction the substance would naturally move if left alone. For any pump to work, energy is required. Both the sodium-potassium pump and the heart use ATP as a source of energy (for more information on ATP please refer to previous blogs). This is the equivalent of a quarter of the energy our body obtains from the food we eat. In this manner, the heart uses energy to move blood against the potential energy force of blood pressure. In the case of the sodium-potassium pump, it also takes energy to move sodium out of the cell, generating an electric current also requires energy. A malfunction of the sodium-potassium pump can mean high blood pressure, stroke, but also osteoporosis, peptic ulcer, stomach cancer, and asthma.

The importance of potassium in heart health (Pt. 2)

Consensus guidelines for the use of potassium replacement in clinical practice

Low serum potassium concentration is perhaps the most common electrolyte abnormality encountered in clinical practice. According to the ‘National Council on Potassium in Clinical Practice’, in order to maintain normal levels of potassium several factors must be take into account such as:

  1. Baseline potassium values
  2. The presence of underlying medical conditions (such as CHF)
  3. The use of medications that alter potassium levels (eg, non–potassium-sparing diuretics) or that lead to arrhythmias in the presence of hypokalemia (eg, cardiac glycosides)
  4. Patient variables such as diet and salt intake, and
  5. The ability to adhere to a therapeutic regimen

Because of the multiple factors involved, guidelines should be directed toward patients with specific disease states, such as those with cardiovascular conditions, and toward the general patient population. The following list encompasses the guidelines developed at the 1998 meeting of the National Council on Potassium in Clinical Practice. This council has also called for the continued research on potassium to determine specific recommendations.

General Guidelines

  1. Dietary consumption of potassium-rich foods should be supplemented with potassium replacement therapy.
  2. Potassium replacement is recommended for individuals who are sensitive to sodium or who are unable or unwilling to reduce salt intake; it is especially effective in reducing blood pressure in such individuals. A high-sodium diet often results in excessive urinary potassium loss.
  3. Potassium replacement is recommended for individuals who experience nausea, vomiting, diarrhea, bulimia, or diuretic/laxative abuse. Potassium chloride has been shown to be the most effective means of replacing acute potassium loss.

Patients with hypertension

  1. Patients with drug-related hypokalemia (therapy with a non–potassium-sparing diuretic) should receive potassium supplementation.
  2. In patients with asymptomatic hypertension, an effort should be made to achieve and maintain serum potassium levels of at least 4.0 mmol/L. This can be achieved with a diet high in potassium-rich foods as well as potassium supplementation.

Patients with CHF

Potassium replacement should be routinely considered in patients with CHF, even if the initial potassium levels appear to be normal (eg, 4.0 mmol/L).The majority of patients with CHF have an increased risk of hypokalemia. In patients with CHF or myocardial ischemia, mild-to-moderate hypokalemia can increase the risk of cardiac arrhythmia. In addition, diuretic-induced hypokalemia can increase the risk of life-threatening arrhythmias.

The risk of hyperkalemia secondary to drug therapy with ACE inhibitors or angiotensin II receptor blockers, makes the regular monitoring of serum potassium level a life saving strategy for these patients. Stress is something also to be considered in these patients as it can trigger the secretion of aldosterone, and therefore a loss of potassium levels.

Patients with cardiac arrhythmias

Maintenance of optimal potassium levels (at least 4.0 mmol/L) is critical in these patients and routine potassium monitoring should be mandatory. Patients with heart disease are often susceptible to life-threatening ventricular arrhythmias. In particular, such arrhythmias are associated with heart failure, left ventricular hypertrophy, myocardial ischemia, and myocardial infarction. Magnesium supplementation should be considered too in order to facilitate the cellular uptake of potassium.

Patients prone to stroke

In patients at high risk for stroke, including those with a history of atherosclerotic or hemorrhagic cerebral vascular accidents, achieving optimal levels of potassium should be a priority. Although the effectiveness of potassium supplementation in reducing the incidence of stroke in humans has not been demonstrated in randomized controlled trials, prospective studies suggest that the incidence of fatal and nonfatal stroke

correlates inversely with dietary potassium intake. In addition, the association of stroke with hypertension is well known.

Patients with diabetes

Patients with diabetes show a marked decline in the levels of potassium, accompanied by a high incidence of cardiovascular and renal complications. Potassium levels should be closely monitored in patients with diabetes and potassium replacement therapy should be administered when appropriate.

Patients with renal impairment

Data suggest a link between potassium levels and lesions of the kidneys in patients with renal disease or diabetes. Animal studies have demonstrated that potassium may offer a protective effect on the renal arterioles. The clinical implications of these findings are not yet clear.

In conclusion

Electrolytes are electrically charged minerals that are significant for providing the infinitesimally small units of life called cells with the electrical energy they need to do their work. Electrolytes exist within cells as well as in the fluid that surround our cells, and can create an electrical flow when they are in the right balance. One of these electrolytes is potassium, which has been shown to have a great positive effect in heart health. A diet rich in potassium, paired with the many benefits of supplemental potassium, like the ‘Heart and Body Extract’ will ensure your heart is well taken care of. Get your bottle today!

Thanks for reading.




(3) Wilson, Lawrence D. “Nutritional Balancing and Hair Mineral Analysis.” Nutritional Balancing and Hair Mineral Analysis, Center for Development, Inc., 2010, pp. 316–317.


The importance of potassium in heart health (Pt. 1)

When it comes to the health of the cell, we have seen that the right balance of electrolytes inside and outside of the cell is key to allow energy into the cell. For heart health this is important because the proper flow of electrolytes into and out of the heart cells is required to keep the heart from filling up with water (cardiac edema) and to keep the electrolytes present that allow the heart to beat properly. This is made possible by the presence of pumps on the cell membrane, called ‘sodium-potassium pumps’, that turn each of our cells into a little battery capable of releasing and storing energy and maintaining an electrical charge.

We also saw how the ‘Heart and Body Extract’, and an alkaline diet are the best sources of these electrolytes, namely, sodium, potassium, calcium and magnesium. In today’s blog, we will focus on the role of potassium in heart health, as observed by the ‘National Council on Potassium in Clinical Practice’. According to this council, low potassium is the most common electrolyte abnormality encountered in clinical practice, a condition known as ‘hypokalemia’ (1).

The ‘National Council on Potassium in Clinical Practice’ 1998 meeting

The critical role potassium has for heart health was studied in depth at a 1998 meeting of the ‘National Council on Potassium in Clinical Practice’. The Council was a multidisciplinary group comprising specialists in cardiology, hypertension, epidemiology, pharmacy, and compliance.

The main focus of this meeting was to study how maintaining normal levels of potassium in the body could help reverse challenging heart conditions. The evidence accumulated confirmed the crucial role potassium has for reducing the risk of life-threatening cardiac arrhythmias, high blood pressure and stroke. As a result of this meeting and its findings, new guidelines for potassium replacement therapy in clinical practice were established.

This initiative represented a new approach to the field of cardiology as, so far, potassium had not been the focus of treatment in any cardiological conditions. Quite the contrary, the many health challenges caused by hypertension and heart failure, had mandated the introduction of drugs that, according to the authors, disrupt electrolyte homeostasis, a fact that emphasizes the serious role of potassium.

The sodium-potassium pump

In their research, the authors were able to prove that, in healthy circumstances, potassium is one of the most abundant electrolytes in the body. Of the total body potassium content (about 3500 mmol), 90% is sequestered within cells, where it does all its work. This compartmentalization depends on its active transport through the cell membrane by the sodium-potassium pump, which maintains an intracellular positively charged ion ratio of 1:10. The smallest percentage of potassium can be found in the blood, as the blood is the main carrier for potassium to the cells. The loss of just 1% (35 mmol) of total body potassium content would seriously disturb the delicate balance between intracellular and extracellular potassium and would result in profound physiologic changes.

Clinical implications of potassium depletion

Potassium depletion, hypokalemia, is one of the most common electrolyte abnormalities encountered in clinical practice. More than 20% of hospitalized patients have this deficiency, and up to 40% of patients treated with thiazide diuretics.

The kidneys, being the major regulators of potassium levels, account for approximately 80% of potassium transit from the body; this is reason why kidney dysfunction can result in low levels of potassium.

But potassium homeostasis also depends to a large extent on the acid-alkaline balance in the body. Acidosis causes the cells to lose potassium. What is more, increases in insulin or glucose, and type 2 diabetes can affect potassium homeostasis as well.

Drugs like decongestants and bronchodilators can temporarily reduce potassium and increase sodium. Other potential causes include diuretic therapy, inadequate dietary potassium intake, high dietary sodium intake, and low magnesium. In most cases, hypokalemia is secondary to drug treatment, particularly diuretic therapy. Diuretics inhibit sodium reabsorption in the kidneys, creating a favorable electrochemical change toward potassium loss.

Hypokalemia occurs less frequently in patients with uncomplicated hypertension who take a diuretic but is more common in patients with congestive heart failure (CHF), nephrotic syndrome, or cirrhosis of the liver, who take an equivalent dose of a diuretic and consume approximately the same amount of potassium from food.

Aside from potassium-wasting drugs, hypokalemia is most commonly caused either by abnormal loss through the kidney due to metabolic alkalosis or by loss in the stool secondary to diarrhea.

According to other healthcare professionals, potassium deficiency is caused by the ‘improper processing of food over the last 100 years, complicated by the fact that the food industry has used super phosphate fertilizers’ (2).

Because potassium is a major intracellular positively charged ion, the tissues most severely affected by potassium imbalance are muscle and kidney cells. Manifestations of hypokalemia include generalized muscle weakness, paralytic ileus, and cardiac arrhythmias. Severe untreated hypokalemia, may progress to acute renal failure.

Protective effect of potassium

Data gathered from animal experiments and epidemiologic studies suggest that high potassium may reduce the risk of stroke. Part of the protective effect of potassium may be due to the fact that potassium lowers blood pressure. Other protective mechanisms include:

  1. Reduction of free radical formation, and oxidative stress
  2. May reduce macrophage adherence to the vascular wall, an important factor in the development of arterial lesions

In 1987, the results of a 12-year prospective population study showed that the relative risk of stroke-associated mortality was significantly lower with higher potassium intake. In fact, the study demonstrated that just a 10-mmol higher level of daily potassium intake was associated with a 40% reduction in the relative risk of stroke mortality. This apparent protective effect of potassium was independent of other nutritional variables, including caloric intake, dietary levels of fat, protein, and fiber, intake of calcium, magnesium, and alcohol. The authors also noted that the effect of potassium was greater than that which would have been predicted from its ability to lower blood pressure.

Similarly, an 8-year investigation of the association between dietary potassium intake and subsequent risk of stroke in 43,738 US men, aged 40 to 75 years, without previously diagnosed cardiovascular disease or diabetes was conducted. During the study follow-up, only 328 strokes were documented. The association between low potassium intake and subsequent stroke was more marked in hypertensive men.

Other investigators also found that the use of potassium supplements was inversely related to the risk of stroke, particularly among hypertensive men. They speculated that this relationship might be due, at least in part, to a reduction in the risk for hypokalemia.

Clinical implications in hypertension

Studies have shown a strong relation between potassium depletion and essential hypertension. Increasing the intake of potassium appears to have an antihypertensive effect that is evident in effects like vasodilation, and lower cardiovascular reactivity to norepinephrine or angiotensin II.

Similarly, correction of diuretic or laxative abuse can also raise potassium level and lower blood pressure.

The large-scale Nurses’ Health Study found that dietary potassium intake was inversely associated with blood pressure. Specifically, intake of potassium-rich fruits and vegetables was inversely related to systolic and diastolic pressure.

Similarly, 24-hour urinary potassium excretion, and the ratio of urinary sodium to potassium were found to be independently related to blood pressure in the ‘Intersalt’ study, a 52-center international study of electrolytes and blood pressure.

Additional information was provided by the ‘Rotterdam Study’, which evaluated the relationship between dietary electrolyte intake and blood pressure in 3,239 older people (age ≥55 years).

Another recent meta-analysis evaluating the effects of oral potassium supplementation on blood pressure, included 33 clinical trials involving 2,609 participants. The results demonstrated that potassium supplementation was associated with a significant reduction in systolic and diastolic blood pressure. The greatest effects were observed in participants who had a high sodium intake. This analysis suggests that low potassium intake may play an important role in the genesis of high blood pressure.

Clinical Implications in ‘Congestive Heart Failure’ (CHF)

Potassium depletion is commonly seen in patients with CHF, a condition that is characterized by electrolyte disturbances. CHF is linked to renal dysfunction and neurohormonal activation, both of which stimulate aldosterone, sympathetic nervous tone, and hypersecretion of adrenaline.

The researchers have observed a common misperception regarding angiotensin-converting enzyme (ACE) inhibitor therapy is that these drugs enhance potassium retention, thereby eliminating the need to add potassium or potassium-sparing diuretics to ACE inhibitor therapy. What they observed is that, in many cases, the prescribed dosages of ACE inhibitors in patients with CHF are insufficient to protect against potassium loss. Their recommendation is that potassium levels must be closely monitored in all patients with CHF, even those taking ACE inhibitors, to minimize the life-threatening risk of hypokalemia.

Clinical implications in patients with arrhythmias

Mild-to-moderate hypokalemia can increase the likelihood of cardiac arrhythmias in patients who have cardiac ischemia, heart failure, or left ventricular hypertrophy. This is not surprising taking into account the important role that potassium plays in the electrophysiologic properties of the heart. The resting membrane potential (RMP) (the difference in electrical charge inside and outside the cell) is determined by the ratio of intracellular to extracellular potassium. Changes in potassium levels modifies the amount of electricity able to pass the cell membrane and can have profound effects on impulse generation and conduction throughout the heart. Changes in this ratio, such as those induced by diuretic therapy, can alter cardiac conduction greatly.

Something significant observed during this research is that patients with hypertension who were prescribed non–potassium-sparing diuretics had approximately twice the risk of sudden cardiac death compared with users of potassium-sparing therapy.

To prove the link between hypokalemia and clinical heart arrhythmia and to determine the relationship of diuretic-induced hypokalemia, 17 hypertensive men receiving diuretics were studied. These patients had increased frequency and complexity of ventricular ectopic activity during diuretic therapy. However, oral potassium supplements or potassium-sparing agents reduced the complexity and frequency of arrhythmias by 85%, even after discontinuation of diuretic therapy.

There is also evidence that hypokalemia can trigger sustained ventricular tachycardia or ventricular fibrillation, particularly in the case of acute myocardial infarction.

Potassium supplementation strategies

All this evidence has led the authors to suggest that increasing potassium is necessary in the case of cardiac arrhythmias, such as heart failure, myocardial infarction or ischemic heart disease.

Repletion strategies should include eating foods high in potassium, potassium salts substitutes, and supplements. Potassium salts include potassium chloride, potassium phosphate, and potassium bicarbonate. Potassium phosphate is found primarily in food, and potassium bicarbonate is typically recommended in the case of metabolic acidosis (pH <7.4).

In our blog covering the alkaline diet we saw how fresh fruits and vegetables are a great source of alkalizing minerals, especially potassium. This includes kelp and garlic (3) found in the ‘Heart and Body Extract’; but also food sources like avocados, peas, beans, nuts, cocoa, seafood, and dark green vegetables.

According to Dr. David Jockers, “Kelp is extraordinarily rich in alkaline buffering nutrients such as sodium, potassium, magnesium and calcium. It is also a phenomenal source of chlorophyll to boost blood cell formation and purify the blood” (4).

The role of magnesium in potassium repletion

Magnesium is an important cofactor in potassium absorption and necessary for the maintenance of intracellular potassium levels. Research has demonstrated that long term magnesium deficiency could lead to the inability to replete potassium. It has been observed that many patients with potassium depletion most frequently also have magnesium deficiency. This is especially the case of patients on diuretics, which cause a substantial loss of intracellular potassium and magnesium. Some diuretics accelerate the excretion of magnesium by reducing its reabsorption in the kidneys.

It is thereby recommended considering the repletion of both magnesium and potassium for patients with hypokalemia.