High Potassium Foods

High potassium foods, low potassium foods and associated potassium symptoms info

 

Salt Sensitivity Test And Hypertension

High potassium foods can help prevent hypertension. With a high potassium to sodium ratio in the diet a great deal of hypertension and the problems associated with hypertension can be prevented. One way to categorize hypertension is to divide it into salt sensitive and salt insensitive hypertension. People with salt sensitive hypertension have a larger elevation of their blood pressure than salt insensitive people when they take in salt. Even when their blood pressure is normal, the salt sensitive people will have increased mortality. And they will have an increase in the problems that are associated with hypertension, such as heart attacks and strokes. It has been estimated that 26% of people with normal blood pressure have salt sensitivity.

Test tubeA Simple Salt Sensitivity Test

It would be helpful to be able to determine who has salt sensitivity so that salt sensitive individuals could have strong advice concerning their salt intake. At the present time, there are a few tests that doctors can run to determine salt sensitivity. However they involve testing that is more complicated than taking a simple blood sample or a simple urine sample. Some researchers recently found a much simpler way to determine salt sensitivity (1). And in doing so, they found a linear relationship between a gene change and salt sensitivity.

The researchers found two different genes in kidney cells that they could test in cells that are shed into urine. These two genes are known to be responsible for a large percentage of sodium reabsorption by the kidney. The genes specifically make proteins that transport sodium in the kidney cell.

First the researchers tested subjects using the usual tests for salt sensitivity. Between one and five years later they checked for the two genes in kidney cells in the urine of these same subjects. They found a linear correlation between changes in these genes and salt sensitivity.

How The Test Helps

This provides a simple test that would allow doctors to advise their patients about salt intake. The standard tests used now are more complicated and involved, and only used for someone with hypertension. They would be hard to justify using for someone with normal blood pressure. And the test may provide the confirmation needed to motivate those salt sensitive patients who otherwise would not reduce their salt intake.

Almost everyone who is healthy would benefit from a high potassium sodium ratio in their diet. But there is some debate about whether increasing potassium, or lowering sodium, or simply improving the ratio is more important. A helpful study these researchers could do would be to study the potassium sodium ratio of the diet along with gene changes in test subjects. It could possibly help resolve the debate by correlating the potassium sodium ratio with blood pressure changes and gene changes.

This type of study would be especially helpful for those patients with so much kidney, heart, and blood pressure problems that they actually may be put at greater risk when put on a very low sodium diet. It may be that these patients would be helped more by increasing their potassium intake, while keeping their sodium intake at a higher level than necessary for healthy people.
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1. A linear relationship between the ex-vivo sodium mediated expression of two sodium regulatory pathways as a surrogate marker of salt sensitivity of blood pressure in exfoliated human renal proximal tubule cells: the virtual renal biopsy. Gildea JJ, Lahiff DT, Van Sciver RE, Weiss RS, Shah N, McGrath HE, Schoeffel CD, Jose PA, Carey RM, Felder RA. Clin Chim Acta. 2013 Jun 5;421:236-42. doi: 10.1016/j.cca.2013.02.021. Epub 2013 Feb 27.

A Potassium Channel Hypertension

Hypertension affects over 1 billion people. It contributes to 7 million deaths each year. Inheritance is felt to affect about 30 to 35% of blood pressure levels. The other 65 to 70% is under our control. The controllable aspect is influenced by physical activity, habits and the food we eat. There are two main components of our food that influence blood pressure levels. Sodium is one component. And potassium is the other. The ratio of these two components inside and outside our cells is what determines blood pressure. What we eat is what determines how much of each component is available.

Potassium Channel ProteinGenetics And Potassium

And genetics is what determines how the available potassium and sodium components are used. The interaction of these components with genetics is what determines the electrical charges within the cell.

You might say “What do I care about the genetics of blood pressure?” The reason you should care is because genetics is what determines how strong a potassium sodium ratio in your diet is needed to generate the proper electrical charges to prevent hypertension and to promote good health. Someone else with different genetics may lower their blood pressure with a diet that has no effect on your blood pressure.

The last post discussed genetic changes affecting how sodium is moved around in the cells (transporter proteins). Another previous post discussed an instance of genetic changes that influenced potassium’s effect on the manufacture of aldosterone (one hormone that raises blood pressure). There’s been a recent study (1) of changes in a potassium channel in our cells that affects aldosterone secretion.

This Study

In this recent study the researchers discovered a change in a potassium channel that is a major cause of secondary hypertension. Remember that normally an increase in aldosterone leads to an increase in sodium reabsorption in the kidney and a rise in blood pressure. Normally when there is an increase in potassium outside the cell, potassium will move into the cell.

In certain adrenal gland cells the resulting increase in membrane polarization (the difference in electrical charges across the membrane) leads to less aldosterone secretion. The lowering of aldosterone leads to less sodium reabsorption in the kidney and thus lower blood pressure. In some people blood pressure is high and does not come down, because they have a gene that prevents this normal sequence.

In this particular study, a gene variant was found that affected part of a potassium channel. The change meant that the channel no longer allowed only potassium to pass. The channel allowed sodium to pass through the potassium channel as well as potassium. This led to a decrease in the membrane polarization and an increase in aldosterone secretion. This increase in aldosterone meant that blood pressure increased.

The researchers found two variants, each of which let more sodium in. One variant was not as severe and let less sodium into the cell than the other variant did. This less severe variant led to an increased number of adrenal cells, resulting in overgrowth of the cells. However the more severe variant let in so much sodium that the cells died.

The change in blood pressure was not as bad in people with the more severe variant. The more severe variant resulted in fewer cells left alive to overproduce aldosterone. The less severe variant resulted in more and more cells, so there was more and more aldosterone.

To eliminate other possible explanations for the cell death, the researchers then grew the cells with the more severe variant in culture and did an experiment with the cells. The experiment showed that the cell death was indeed because of too much sodium getting inside the cells.

Although the involved cells died, the individuals with these cells did not die. The researchers felt that nearby immature adrenal cells replenished the dead cells. As the cells matured, they would overproduce aldosterone for a while and then they too would die. Some cells that overfunctioned may have stayed alive because other mechanisms in the cell compensated for the excess sodium inside the cell. Other studies indicated that this could occur if there were an increase in the sodium potassium pump removing sodium, or if there were a change in the activity of other potassium channels.

Two Concepts

So there are two important concepts that this particular study supports. It supports the importance of the balance of sodium and potassium inside the cell for proper function. And it supports that the variability in blood pressure is related to the function of the potassium channels, as well as the sodium channels and the sodium potassium pump.

The critical variable in each of these cases is the electrical charges across the membranes in the cell. These charges are determined by the potassium and sodium balance in the cell. The potassium and sodium in the cell are determined by the activities of the channels and pumps, and the proteins that transport potassium and sodium. When the membrane electrical charges change in the kidney, sodium reabsorption is affected, as discussed in the previous post. When the charge changes in the adrenal cells, aldosterone secretion is affected, as discussed in this present post.

When Genetics Meets Diet

Each of us have genes that vary from the genes in other people. Some of these gene variations help some of us to have better protection against hypertension than others have. But it is important for all of us to maintain an optimal potassium sodium ratio.

We can do nothing to change the differences in our genetic makeup. However if we do not have extreme genetic changes, such as the syndromes discussed in some recent posts, we can control how well our cells function. We can better control how well our cells function by controlling the potassium sodium ratio in our diet. Some of us will find good control with a ratio of 2 and some will need a ratio over 5. However, a satisfactory ratio can be found for the vast majority of us.
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1. Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Scholl UI, Nelson-Williams C, Yue P, Grekin R, Wyatt RJ, Dillon MJ, Couch R, Hammer LK, Harley FL, Farhi A, Wang WH, Lifton RP. Proc Natl Acad Sci U S A. 2012 Feb 14;109(7):2533-8. doi: 10.1073/pnas.1121407109. Epub 2012 Jan 30.

Salt Handling And Hypertension

There have been a large number of studies of genes associated with hypertension. It is been estimated that heritability contributes to about 30-35% of blood pressure levels. A high dietary sodium and low potassium intake interact with certain genes to determine blood pressure. Genome-Wide Association Studies (GWAS) have found a great number of genes associated with hypertension. Most of these genes involve sodium or potassium in one fashion or another. Many of the genes determine either channels that sodium or potassium pass through, transporter proteins for the ions, or ion pumps. A recent review (1) of several salt handling (sodium handling) genes in the kidney was done in 2014.

Salt Handling Gene ChartKidney Salt Handling

Each gene for salt handling in the cells of the kidney has rare variants. Although any individual gene variant is rare, there are a fair number of them in total. There are so many that these rare variants are probably what account for the wide variation in blood pressure, and the wide variation in blood pressure’s sensitivity to salt (2).

There are two well known inherited syndromes, known as Gitelman’s and Bartter’s syndromes, which have been proven to be caused by such variants. These salt handling genes affect sodium reabsorption and cause salt wasting by the kidneys.

And they show how there can be a variation in how such genes affect people. Bartter’s syndrome causes serious health problems very early. It often presents while the child is still in the womb, and almost always before age 6. Gitelman’s causes similar problems, but varies by being less severe. It usually does not present until adolescence or early adulthood. In some people it is so mild that it may go undetected.

Other Salt Handling Variants

There are only a few genes involved in these two syndromes. However there are many other gene variants that affect sodium movement in the cell, and sodium reabsorption in the kidney. And many more that affect potassium in the cell. These variants have more subtle effects, and would be expected to take longer to have a noticeable effect on health.

Since each individual gene variant is rare, only about 1% of the population is estimated to be a carrier of any particular variant. However because there are estimated to be a great number of variants, they are felt to commonly contribute to blood pressure variation. But the result would not be as extreme as occurs in these two known salt wasting syndromes.

Only a few of the gene variants associated with hypertension are felt to cause an increase in gene function. We discussed here one of the variants that increased the function of a potassium channel in certain adrenal gland cells. The original study (3) finding this increase in function stimulated a great deal of research.

The subsequent research resulted in an estimate that 90% of gene variants in channels reduce the function of the channel. This reduction in function is known to result in a reduction in the electrical charge within the involved cells.

Among effects of a reduced charge is slower passage of ions. In the case of kidney cells, the major salt handling variant is involved in the reabsorption of sodium. This slower passage of ions means less reabsorption of sodium by the kidney.

Effect Of Less Salt Reabsorption

When less sodium is reabsorbed a person is protected against a high intake of sodium. These people can eat more sodium and still not have a rise in blood pressure. And this protection against hypertension lasts throughout the person’s lifetime.

This particular study (1) reviewed 3 genes involved in the sodium reabsorption in the kidney. Each of these 3 genes had a large effect on blood pressure. Depending upon the exact type of effect there will be a variation in the amount of sodium resorbed, and thus in the susceptibility to high blood pressure. The chart shown above is adapted from (2). It shows the mean systolic blood pressure for those who do not carry one of the variants, and the lower systolic pressure for those who do carry one of the variants.

We discussed a similar gene in the post here about the Sardinian centenarians. Although through a slightly different mechanism, the result of the gene variation was less sodium reabsorption. This particular gene was present in 14% of the centenarians, which is much higher than the non-variant gene in the general population. In fact it is approximately 14 times as common as the 1% variation estimated for genes of this sort.

Because of this high multiple, it is likely that this gene contributes to the longer functional life found in the Sardinian centenarians. As will be discussed in a future post, the activity of these types of genes is more of a factor contributing to a longer life than is the effect from the pressure itself. The electrical charges within the cell are what matters. The electrical charges determine how your cells function, and thus how well your body functions.

Why Some People Have Less Effect From Salt

Thus we can see that the variability in blood pressure is related to the gene variants in the potassium channels, sodium channels, potassium transporters, and sodium transporters, as well as the sodium potassium pump. The interaction of these cellular structures determines the electrical charges within the cell. If the cells with gene variants are located in the heart, the result is a greater or lesser susceptibility to heart failure, as discussed in this post. If they are in the adrenal gland, they will affect blood pressure as discussed in this post. If they are in the kidney, they will affect sodium reabsorption and thus also affect blood pressure. And if they are located in all cells throughout the body, the results will be determined by the degree to which each cell’s function is affected.

If the estimate of 30-35% of blood pressure being genetic is broadly applicable to other functions of the body, then 65-70% of how well your body functions is not genetic. The choices you make in diet, physical activity, and habits (smoking, for example) are more important than genetics.

Too Early For Gene Profiles To Help You

Genetic studies are all in an early stage of application to human health. Although they are consistent with the importance of the potassium sodium ratio in the diet, they need further studies (the usual caveat of the scientist) to show the specifics of the genetic interaction with the dietary potassium sodium ratio. It is doubtful that there will ever be a population study that will show specifically that the potassium sodium ratio has a linear relationship with mortality for hypertension.

Higher Potassium Sodium Ratio Helps

However multiple epidemiology studies have shown the importance of potassium and the importance of sodium in determining blood pressure. There have also been multiple animal studies showing how different levels of potassium and sodium in the diet affect cells in the animals. These types of genetic studies show the variations in cells that can account for the effects in the animals. If more studies are done with pure genetic variants in animals, then the diet can be varied in the genetically variant animals to show a relationship of diet to cellular changes, such as was done in the series of heart failure studies discussed here.

Such studies will make it possible to know how high a potassium sodium ratio you need in your diet to avoid the problems of hypertension. Specific gene combinations can be assessed for the ratio that prevents the electrical charge changes leading to cellular dysfunction. You will be able to adjust your diet to your genetic profile.

It will be unusual that anyone will need more sodium than the present minimal recommendation from the Institute of Medicine. Salt wasting conditions, such as Gitelman’s and Bartter’s syndromes, would be such a situation, but are quite rare. And they are usually discovered at an early age. Other conditions requiring more sodium are unusual in the absence of disease.

Most people will need a higher potassium sodium ratio in their diet than they get in the typical American diet. But the ratio to protect against the health problems associated with hypertension will vary. Some will only need a slightly higher ratio, and others will need more. But the vast majority will be able to find a ratio in their diet that will protect against hypertension and its potentially devastating effects.
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1. Rare mutations in renal sodium and potassium transporter genes exhibit impaired transport function. Welling PA. Curr Opin Nephrol Hypertens. 2014 Jan;23(1):1-8. doi: 10.1097/01.mnh.0000437204.84826.99.

2. Rare independent mutations in renal salt handling genes contribute to blood pressure variation. Ji W, Foo JN, O’Roak BJ, Zhao H, Larson MG, Simon DB, Newton-Cheh C, State MW, Levy D, Lifton RP. Nat Genet. 2008 May;40(5):592-9. doi: 10.1038/ng.118. Epub 2008 Apr 6.

3. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Choi M1, Scholl UI, Yue P, Björklund P, Zhao B, Nelson-Williams C, Ji W, Cho Y, Patel A, Men CJ, Lolis E, Wisgerhof MV, Geller DS, Mane S, Hellman P, Westin G, Åkerström G, Wang W, Carling T, Lifton RP. Science. 2011 Feb 11;331(6018):768-72. doi: 10.1126/science.1198785.

Sodium Reabsorption Gene & Hypertension

Sardinia has a Blue Zone, made famous by Dan Buettner for its high percentage of centenarians. Due to its long-standing isolation, low immigration rate, and fairly uniform lifestyle, Sardinia is a great location to study genetic traits associated with longevity. There have been multiple studies of older Sardinians, including studies of the genetics of hypertension. Many genes affect hypertension. As discussed here, a Genome-Wide Association Study (GWAS) is a screening method to look for possible genes associated with a disease. It is especially helpful for diseases involving multiple genes, such as hypertension. However, it only shows an association. After screening, other methods are needed to determine if and how a gene affects a disease. A recent article (1) used some of these other methods to show that a particular sodium reabsorption gene (ATP1A1) that was not found by GWAS was involved in hypertension in older men in Sardinia.

Sodium reabsorption gene productSodium Reabsorption Gene

Primary hypertension is divided into 2 large categories – salt sensitive and non-salt-sensitive. In salt sensitive hypertension small increases in sodium in the body lead more easily to hypertension. The kidneys play a large role in hypertension because they reabsorb sodium. The reabsorption may lead to more sodium in the body.

In this recent study, researchers showed a major influence on blood pressure from a change in a gene (ATP1A1) that is involved in regulating the reabsorption of sodium by certain cells in the kidney. This sodium reabsorption gene is also involved in maintaining the sodium potassium balance in the cells that line blood vessels. When there is imbalance, the vessel lining cells become stiffer.

This particular gene is a gene that regulates the sodium potassium ATPase pump. The sodium potassium ATPase pump comes in several variations, but there is only one variation found in these particular kidney cells and in the blood vessel lining cells. Thus when this gene is affected, it has a major effect on how much sodium is reabsorbed by the kidneys and how stiff the blood vessels are. If the effect is to slow down the pump, less sodium is reabsorbed in the kidney, and the effect on blood pressure of excessive sodium in the diet will be less.

The Study

The researchers studied several hundred of the older men and women in Sardinia for two forms of this gene. They looked at 678 older (> 60 years old) Sardinians and determined the difference in blood pressure in those with the common form of the gene and those with a variant of the gene. In women the difference in the sodium reabsorption gene produced no difference in blood pressure. But in the men there was a large difference in blood pressure.

After finding that those men who had the variant had lower blood pressure (12mm Hg systolic and 6 mm Hg diastolic) than those with the usual gene, the researchers checked that the common gene and its variant both were functional. They used the two variations in cell lines grown in tissue culture and found that both gene variations were functional.

Then they raised mice with the altered gene and found a difference in blood pressure compared to those mice with the unaltered gene. Those with the altered gene produced 58% less protein from the gene and had much lower blood pressure (17 mm Hg lower systolic).

Although this gene is not the only cause of high blood pressure, this study shows that a change in this sodium reabsorption gene will cause a change in blood pressure in humans as well as mice. This is the kind of confirmational experiment that is needed when association studies are done on human populations.

Not Just Another Association Study

By testing a hypothesis with experiments, fewer misinterpretations of association studies will occur. In this case, the researchers saw an association of different blood pressure levels with two variations in a gene in humans. They tested the hypothesis that the two variations of the gene affected blood pressure differently. First they isolated the different variations of the gene and showed that both variations were functional. Then they showed that the uncommon variation slowed sodium reabsorption by certain kidney cells. Finally they showed that the two different variations of the gene had the same effect on blood pressure in mice as in humans.

So we have another piece of evidence showing the importance of the potassium sodium ratio in hypertension. The model proposed by Dr Guyton, discussed here, and now in medical textbooks has another piece supporting it.

In this particular case, the study shows the importance of the sodium potassium pump in the kidney to maintain a proper level of sodium and to prevent too much sodium from accumulating in the body. This study provides another piece of evidence that the accumulation of sodium in the body leads to hypertension, and that the potassium sodium ratio is important for blood pressure.

Food Tables

Links to food tables can be found by using the List Of Posts tab at the top of the page.
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1. A Functional 12T-Insertion Polymorphism in the ATP1A1 Promoter Confers Decreased Susceptibility to Hypertension in a Male Sardinian Population. Herrera VL, Pasion KA, Moran AM, Zaninello R, Ortu MF, Fresu G, Piras DA, Argiolas G, Troffa C, Glorioso V, Masala W, Glorioso N, Ruiz-Opazo N. PLoS One. 2015 Jan 23;10(1):e0116724. doi: 10.1371/journal.pone.0116724. eCollection 2015.

Aldosterone Secretion, Genes And Diet

A high potassium diet is the single most important factor to prevent hypertension. There is more extensive evidence for the role of the dietary potassium sodium ratio than for any of the other factors that may be involved in hypertension. There is evidence from epidemiological studies, population studies, basic physiological studies, and animal and tissue studies. Presently many studies are being done at the cellular and molecular levels to determine how processes at these levels cause hypertension.

We previously discussed, in this post, how a fully developed hypertensive heart failure model has shown the importance of a high potassium diet. The model is complete from the level of the heart organ to the level of molecules in the heart cells.

Aldosterone SynthaseAldosterone Secretion, Potassium And Hypertension

The model for aldosterone secretion by the adrenal gland is not as complete as the heart failure model. This is an important model because of the central role of aldosterone and the RAAS (renin-angiotensin-aldosterone system) in the development of hypertension. Potassium and the potassium sodium ratio play a central role here, just as they do in hypertensive heart failure.

By studying at the cellular level abnormal secretion of aldosterone by adrenal gland cells, such as occurs in primary aldosteronism, researchers can more fully understand how hypertension occurs. And they can possibly devise methods for how it can be prevented.

Primary aldosteronism is the main cause of secondary hypertension. Sometimes it runs in families. Sometimes it is caused by a tumor in the adrenal gland. It signifies that too much aldosterone is being produced by the adrenal gland(s) without outside stimulation. This is one of the same mechanisms that cause primary hypertension. And the end result is the same – high blood pressure.

Hypertension Genetics

By studying the cellular abnormalities in primary aldosteronism researchers can also learn a great deal about how primary hypertension occurs. In 2013 a European Journal of Endocrinology published its prize lecture (1) about the genetics of primary aldosteronism. The publication gave a nice summary of what was then known about primary aldosteronism at the cellular and genetic level. The publication reveals a great deal about how potassium can affect adrenal cells. The article also reveals at the cellular level how an increase or decrease in the blood level of potassium causes changes in aldosterone secretion, and thus in blood pressure.

The report discusses the multiple studies done on adrenal cells, many of which the author’s group did, especially in primary aldosteronism. The author discusses genetic studies on animals and human genomes. These studies have identified genes that are associated with increased aldosterone. Many of the abnormal genes were found to control the proteins in potassium channels, and the proteins involved in transporting potassium for the sodium potassium ATPase pump.

These abnormal proteins cause these channels and pumps to handle potassium so poorly that there is not enough potassium inside the cell to maintain the electrical charges needed for normal cell function. This is the same problem that occurs when not enough potassium (or too much sodium) is in the diet. The result is excessive secretion of aldosterone and a rise in blood pressure.

The Basics

Before discussing the article, let’s review the previously known basics. Many years ago researchers showed that an increase in extracellular potassium leads to an increase in aldosterone secretion into the blood stream. This initiates a series of reactions that lead to an increase in blood pressure. However the increase in blood pressure is just one of many effects previously discovered. An excessive aldosterone blood level, even without an increase in blood pressure, damages the cardiovascular system and the kidney.

Today’s Research

Much research today focuses on what happens inside cells. To study aldosterone secretion, molecular pathways inside the cell and the genes that affect the pathways are being studied. Much of the work is being done on mice with experimentally produced changes in their genes. They have what are called knockout genes, which are specific genes that no longer function.

Many of the genes leading to excessive aldosterone secretion are genes that affect the electrical charge of the cell membranes in the cells that secrete aldosterone. The electrical charge is determined by the function of potassium channels, sodium potassium pumps, and intracellular calcium. Calcium controls much of the signaling inside the cell, and is affected by channels and pumps itself.

One of the genes that was studied was the gene that makes the enzyme (pictured above) that makes aldosterone in the adrenal cells. Potassium outside the cell (and angiotensin II) regulates the gene that makes this enzyme. Very minor changes in the extracellular potassium concentration control a signaling cascade. The potassium causes a change in the calcium concentration inside the cell. The calcium change starts a cascade of signaling molecules. The final signaling molecule reaches the DNA in the nucleus to upregulate (or downregulate) the gene so more (or less) enzyme is made.

This cascade happens within minutes of the change in potassium concentration. And it continues to occur for days (even years) when there is chronic stimulation. There are a great many specific types of potassium channels in the cells that make aldosterone. Changes in any of these specific channels affect the electrical charge of membranes in the cell. This in turn affects molecular reactions in the cell. These reactions affect the production and secretion of aldosterone. An increase in aldosterone secretion occurs with these abnormal genes, even when renin (another molecule affecting blood pressure) stays low.

Circadian Rhythm And Hypertension

Interestingly, the researchers also discovered how our circadian rhythm was involved in aldosterone secretion. One of the genes that was knocked out in these mice was a gene that is a core gene for the circadian clock. This circadian clock gene was found to affect aldosterone secretion from the adrenal gland cells. The researchers found that high salt intake increased the secretion of aldosterone in these animals. Furthermore they found that a constant daily salt intake resulted in aldosterone-dependent weekly rhythms of sodium storage (along with water weight) in the body.

Genome Wide Association Studies (GWAS)

This method has been used to identify genes involved in many different diseases. For diseases related to aldosterone, DNA arrays from patients with adrenal tumors and familial adrenal syndromes are used to study a large quantity of genes. Variations in how frequently a gene occurs show an association that can be further investigated as possibly causing a change in aldosterone secretion.

These studies are the type of studies we discussed here. That post discussed a study that identified 130 hypertensive genes. The majority of the genes were associated with potassium, sodium and calcium activity.

Other Genetic Methods

The author’s group has used other genetic methods to identify genes that lead to excessive aldosterone secretion. These genes involve some specific potassium channels that allow calcium in the interior of the cell to start the cell signaling process for aldosterone secretion.

Another pair of genes they identified affects proteins carrying potassium to the sodium-potassium-ATPase pump. They found that the pump was slowed, resulting in a change in the electrical charge of cell membranes that led to more aldosterone secretion.

There have been more and more studies on how cells that secrete aldosterone increase their aldosterone secretion, and thus increase blood pressure. The electrical charge of the membranes in the cell is the key factor. This charge is determined by the potassium sodium ratio inside and outside the cell. When the charge cannot be maintained at an appropriate level, aldosterone secretion is affected.

Studies of the genes that cause increased aldosterone secretion are consistently showing how critical the potassium channels are. These channels are critical to maintaining the proper level of potassium inside cellular compartments. The proper level of potassium is critical to maintaining correct electrical charges throughout the cell. When potassium is genetically prevented from maintaining a proper level inside aldosterone secreting cells, hypertension results.

More common than this genetic prevention of potassium balance is dietary prevention of potassium balance. Too little potassium (or too much sodium) in the diet will mean that there will be too little potassium inside the cell. This will lead to improper electrical charges throughout the cell. No matter what causes these improper electrical charges, the result will be the same as occurs with the genetic changes. Aldosterone will be affected. Hypertension and organ damage will result.

Food Tables

To find links to tables of the amounts of potassium and sodium in various foods, click on the List Of Posts tab at the top of the page.
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1. Regulation of aldosterone secretion: from physiology to disease. Beuschlein F. Eur J Endocrinol. 2013 Apr 24;168(6):R85-93. doi: 10.1530/EJE-13-0263. Print 2013 Jun.

Bran to Prevent CHD And Hypertension

Many publications have shown that eating whole grain reduces the likelihood of diabetes, coronary heart disease, and hypertension. A recent article (1) analyzed 11 prospective studies about how whole-grain food prevents these diseases. It points to bran, and specifically a particular component of bran, as the most important preventive component of whole grain.

BranThe Results

In analyzing the studies, the authors determine that 40 gm of whole grain a day reduces these diseases. 40 gm per day (one bowl of cereal) of whole-grain reduces the incidence of hypertension about 20% and of diabetes about 50%. They then analyze the components of whole grain to find what aspect of whole grain is responsible for whole grain’s beneficial effects.

The FDA has defined a whole grain product as a product with at least 50% whole grain, and whole grain as having all three elements (bran, germ and endosperm) in the same proportions as an intact grain. It differs from an unbroken grain. Polished rice can be considered unbroken, but it does not have bran and germ.

The bran and germ are responsible for the beneficial effects of whole grain. Studies of refined grain (without bran and germ) have not shown the same reduction in diabetes, coronary heart disease and hypertension that whole grain has.

The authors feel that because whole grain has much more bran than germ, bran would contribute more to the beneficial effects of whole grain than the germ component would. They also cite several studies that determined that the beneficial effects of whole grain came from bran.

They then try to determine what it is about bran that confers the benefits. Fiber is the most often mentioned component in the medical literature. Other components the authors examined were vitamins, minerals, polyphenols, and the antioxidant ferulic acid (one of the polyphenols).

Fiber

The authors question today’s emphasis on indigestible fiber as the beneficial component of whole grain. Because Burkitt emphasized fiber in his classic study, indigestible fiber has been the subject of many of the studies about improved health from whole grain.

There are three separate benefits that can be attributed to fiber. The first is the stool bulking effect that speeds transit of the stool through the gut. The second is the formation of gels, which slows carbohydrate absorption. The third possible benefit is the formation of absorbable healthy fatty acids from fermentation of the fiber.

Bran And Aleurone

The authors place a greater emphasis on the nutritive aspects of bran. They find that the greatest concentration of these nutrients is in the aleurone. Aleurone is a major component of bran and is generally overlooked. It remains attached to bran during processing of whole grain. During processing, the production of bran results in approximately 50% live aleurone cells.

The remainder of bran is pericarp – the indigestible fiber. It is resistant to digestion and provides bulk to speed passage of stool. It resists our digestive enzymes and the enzymes secreted by bacteria in our gut. The main advantage it may provide is preventing prolonged exposure to possibly adverse toxic products that could affect us.

The bran aleurone, on the other hand, is nutrient rich with vitamins, minerals, and polyphenols (especially ferulic acid). Comparing whole wheat flour to wheat flour, for example, shows an 80 to 90% drop in thiamine, niacin and vitamin B6, and a 50 to 80% drop in minerals.

And bran has over 90% of the polyphenols in whole grains, while germ has only 1%. It also has 4 to 11 times as much vitamins and minerals as germ.

These minerals are found in the aleurone cells. The publication has some excellent photomicrographs showing the fluorescence from the minerals in the aleurone cells.

Phytates And Minerals

The minerals are chemically bound to phytates in the cells. Some other publications have raised concerns about the phytates in whole grain, as well as in legumes. Animal studies showed that consuming them led to a smaller proportion of minerals being absorbed. However, because food containing phytates has so much more mineral content, the actual amount of minerals absorbed is greater, even though the proportion is less.

Thus bran is a great source of minerals. The study emphasizes the role of magnesium in preventing hypertension and cardiovascular disease. It does not discuss the role of potassium, even though it admits that potassium is more abundant inside cell. The importance of magnesium in cardiovascular health is highly supported in the medical literature. But potassium and the potassium sodium ratio have even more extensive literature supporting their importance in preventing hypertension and cardiovascular disease.

Antioxidants

The authors also discuss the role of antioxidants. Antioxidants, especially ferulic acid, are abundant in bran. They are well aware of the findings that ORAC (the test tube antioxidant test) has no correlation with what happens in our bodies. They correctly points out that the use of antioxidant supplements as therapy reflects “a far too superficial view on how physiology manages and controls reactive oxygen and other reactive species.”

They point out how a host of enzymes are involved inside the cell to combat ROS (reactive oxygen species). Ferulic acid has been shown to activate some key antioxidant proteins. Thus they feel that the main antioxidant value in food is provided by stimulating the cells natural antioxidant mechanisms. And ferulic acid has been shown to do this.
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1. Whole grains, type 2 diabetes, coronary heart disease, and hypertension: links to the aleurone preferred over indigestible fiber. Lillioja S, Neal AL, Tapsell L, Jacobs DR Jr. Biofactors. 2013 May-Jun;39(3):242-58. doi: 10.1002/biof.1077. Epub 2013 Jan 28.

C Reactive Protein Reduced By Diet

Lately a great deal of medical research has been looking at inflammation as a possible cause of cardiovascular disease. Doctors and researchers use CRP (C reactive protein) to determine the amount of inflammation a person is experiencing. C reactive protein is a compound made in the liver and released into the blood stream in response to an inflammatory stimulus. The CRP test has been shown to correlate with inflammation and it is been found to correlate with the severity of coronary artery disease. A recent study (1) sought to determine if a diet could lower C reactive protein.

C reactive proteinEarly Research

This is still relatively early research since no studies have shown that reducing C reactive protein will reduce coronary artery disease. Also there were no studies prior to this one showing that cholesterol lowering diets, such as the NCEP (National Cholesterol Education Program), could reduce inflammation.

The NCEP diet is a low fat diet many doctors use to lower blood cholesterol. The researchers in this recent study wanted to find out if the NCEP diet could lower C reactive protein as much as a medication. A medication that has been shown to reduce C reactive protein is lovastatin.

In this particular study a variation of the NCEP diet was compared to lovastatin for its ability to reduce C reactive protein. The participants in the study were all on a low saturated fat diet for a month prior to the study.

They were then randomly chosen to be on the control diet only, or the control diet and lovastatin, or on the experimental diet. The control diet was the usual NCEP diet. The experimental diet was designed to provide more plant sterol, fiber, soy protein, and almonds.

The remainder of the experimental diet was fairly similar to the control diet. The experimental diet had the same amount of protein, slightly less carbohydrates, and slightly more fat and cholesterol than the control diet.

Differences In Diets

But the experimental diet probably differed in unintended ways as well as the intended ways. The intended ways the experimental diet differed was that it had 4 times the amount of vegetable protein and 40% more fiber.

Since it was not measured, the difference in the type of fiber in each diet was probably unintended. The experimental diet included oats and barley, whereas the control diet included whole wheat. Thus the experimental diet had more beta-glucan, a soluble fiber, and the control diet had more insoluble fiber. These types of fiber have different known effects in the body.

Another important difference not measured was the potassium and sodium in each diet. The potassium sodium ratio has been shown to affect the amount of inflammation in the heart in heart failure. A previous post discussed how inflammation can be reduced with a diet that has a high potassium to sodium ratio. This was shown directly in animals in the study cited in that post. Among other findings, the researchers directly saw the inflammation by looking at heart samples under the microscope.

These differences in the experimental diet rather than the designed differences may have been responsible for the results. Because of the increased amount of vegetables and nuts in the diet, it is highly likely that the people put on the experimental diet had a better potassium to sodium ratio. The blood pressure in the experimental group was also reduced more than in either the lovastatin or the control group. This is another indication of a better potassium to sodium ratio in the experimental group.

C Reactive Protein Lowered By Diet

So the researchers did find that the experimental diet reduced C reactive protein just as much as lovastatin did. And the increased intake of vegetables and nuts were likely the difference. But whether it was the vegetable protein, vegetable sterols and vegetable fiber (no matter what type) that made the difference is not clear.

The researchers did not measure the types of fiber and did not study potassium or sodium. The different types of fiber and the difference in potassium and sodium in the diets may have been the critical difference. Further studies that include these variables may help determine how much of the improvement in C reactive protein was due to potassium and sodium.

Food Tables

Links to tables of the potassium and sodium content of various foods can be found by clicking the List Of Posts tab at the top of the page.
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1. Direct comparison of dietary portfolio vs statin on C-reactive protein. Jenkins DJ, Kendall CW, Marchie A, Faulkner DA, Josse AR, Wong JM, de Souza R, Emam A, Parker TL, Li TJ, Josse RG, Leiter LA, Singer W, Connelly PW. Eur J Clin Nutr. 2005 Jul;59(7):851-60.

Whole Grain And Cardiovascular Disease

A follow-up study to the study in the last post was published just this past month. That previous study was one of the early reports on whole grain and cardiovascular disease. It showed that whole grain consumption lowers cardiovascular deaths. Along with some other early studies, it resulted in the FDA defining “whole grain” and allowing health claims for “whole grain” products.

The study in the last post has a link to the entire publication. The link to the recent study (1) is only to the abstract. However the basic findings were the same.

Whole WheatWhole Grain And Cardiovascular Disease

The original report was known as the Nurses’ Health Study and included over 75,000 participants. The present study included over 74,000 from the Nurses’ Health Study and over 43,000 from the Health Professionals Follow-up Study. This resulted in over 118,000 persons being studied for 2,727,006 person-years of follow-up.

Similar to the earlier study, the researchers divided the participants into 5 groups according to how much whole grain they ate. They then determined total mortality from all causes, cardiovascular mortality and cancer mortality for each group. As in the prior study a higher whole grain intake was associated with lower total and lower cardiovascular mortality.

They corrected the results for the same non-dietary factors that they had in the original study. Age, smoking, body mass index, physical activity, and a modified Alternate Healthy Eating Index were examined for the possibility of influencing the results. There was an improvement in mortality for those eating whole grain products compared to those who did not eat whole grain, even among those who had healthy habits in each of those categories.

They also looked for an association of eating whole grain with cancer mortality. Although their statistics showed a mild effect, it was not statistically significant. The researchers concluded that whole grain did not affect cancer deaths.

Importance Of Bran

Just like it did in the early study, bran appeared to have a very strong correlation with improved total mortality and improved cardiovascular mortality. It was the component of whole grain that had the strongest effect on mortality.

They also considered whether the germ in the grain had an effect. Germ had an improvement in mortality. But after the bran effect was corrected for, the improvement was not significant.

This study, like the prior study, used a food frequency questionnaire to determine the eating habits of the participants. So, as discussed in last week’s post, this study has the same strengths and weaknesses as the prior study concerning the data used.

The difference in fruit and vegetable consumption is another factor that may be influence cardiovascular mortality. Fruit and vegetable consumption is known to reduce the prevalence of cardiovascular disease. A large number of studies have shown this improvement.

Also a large number of studies have shown the improvement in heart and vascular health from a high potassium sodium ratio in the diet. Fruits, vegetables, and intact grains (and especially bran) all have high ratios. This high ratio seems to be the common thread in studies concerning diet and cardiovascular disease.
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1. Association Between Dietary Whole Grain Intake and Risk of Mortality: Two Large Prospective Studies in US Men and Women. Wu H, Flint AJ, Qi Q, van Dam RM, Sampson LA, Rimm EB, Holmes MD, Willett WC, Hu FB, Sun Q. JAMA Intern Med. 2015 Jan 5. doi: 10.1001/jamainternmed.2014.6283. [Epub ahead of print]

Early Whole Grains Study

Most people know that refined grain removes a great deal of the nutritional value of a grain. Whole grain is felt to be healthier because it has more nutritional value. A number of medical studies have been done that show a lower risk of heart disease for those people who eat more whole grain foods. One early whole grains study that is often discussed is from the Nurses’ Health Study (1).

Grain FieldThe Nurses’ Health Study

An early report was done on this prospective study of over 75,000 nurses during a 10 year period. In this particular whole grains study report (1) the nurses were divided into 5 groups. They were ranked according to how much whole grain they ate. The researchers compared the number of nonfatal and fatal heart attacks in the five groups. The percentage of people experiencing heart attacks decreased as the amount of whole grain eaten increased.

The study was started at a time when dietary fat was considered the main culprit in heart disease. Other components of food were only beginning to be considered. There was little emphasis on whole grain. This was one of the early studies of grain products.

The definition of whole grain by the FDA did not come until after this study had been started. The main sources of whole grain were dark bread and breakfast cereal. In this whole grains study, if only 25% of a cereal was whole grain or bran, it qualified as a whole grain cereal. Despite this difference, most subsequent studies using other whole grain definitions have confirmed their conclusions.

Most Americans eat very little whole-grain. The average American eats only 1/2 serving a day. In this particular study the group eating the least amount of whole grain ate 1/7 serving a day and those eating the most ate 2 1/2 servings a day.

Other food groups and food macronutrients were also considered as possible influences. In addition to studying grain, the researchers also followed the vegetable fruit and red meat intake. They also kept track of the fat and protein.

Most other food groups and macronutrients were consumed in approximately the same amount by the participants. There was no difference in the amount of red meat eaten by each group. And each group ate almost the same amount of fat and protein.

Other Possible Explanations For The Reduced Risk

One big difference was the amount of bran eaten by those eating more whole grain. Since whole grain contains bran, it would be expected that they ate more bran. What was unexpected was bran’s strong correlation with less cardiac risk. Among the whole grain factors examined, bran showed the strongest likelihood of being correctly correlated with less coronary heart disease.

Because bran has a very high potassium to sodium ratio this makes it likely that bran is a major, although not only, component in whole-grain that reduces cardiac risk. This study was before the contribution of low potassium intake to cardiac risk was well understood, so the potassium and sodium levels were not studied. Thus we do not know how much the potassium sodium ratio of bran contributed to the reduced risk.

The biggest difference in food group consumption among those eating more whole grain was that they also ate significantly more vegetables and fruit. Both vegetables and fruit are high potassium foods (as is bran and intact grain). So, like bran, they also provide a higher potassium sodium ratio. This may have been an additional contribution to the reduced cardiac risk in the higher whole grain groups. Other more recent studies that have measured potassium and sodium intake have shown the reduction of cardiac risk from a higher ratio.

Possible Non-food Explanations

One concern of the researchers was that the high grain eaters may have had the improved risk from leading a healthier lifestyle rather than from eating more whole grain. At the time of this whole grains study, other known confounders included smoking, alcohol drinking, and lack of physical exercise.

The researchers corrected for these factors, and then compared the lowest to the highest quintile of whole-grain intake.  They found that although these factors had an effect on cardiac risk, the effect did not erase the effect from whole-grain.

One example is that smoking may have explained the risk. If smokers and non-smokers were included, the risk was reduced by 33%. However if only non-smokers were looked at, the risk for nonfatal and fatal coronary heart disease was reduced by 50%. This indicated that smoking did not fully account for the risk reduction.

Some other problems studies face today are the same as they were at the time of the study. “Whole-grain” has a different meaning to different people. See this post to find out what can be labeled whole grain. This particular study was done with a food frequency questionnaire. Food frequency questionnaires are the most common way of estimating food intake. They ask the participants to estimate the amount of different types of food they have eaten. Memory is not always accurate.

Even with an accurate memory, there are labeling problems. There are so many food labeling problems for “whole-grain” that it is difficult to determine the true amount of whole-grain products that are eaten. This is true even if you record everything you eat while you are eating.

Up to 50% of the product can be other substances, such as the marshmallows found in cereal labeled “whole grain,” as discussed here. Some people may consider these types of cereal a whole-grain food when filling out the questionnaire. However such a cereal will be unlikely to reduce their cardiac risk.
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1. Whole-grain consumption and risk of coronary heart disease: results from the Nurses’ Health Study. Liu S, Stampfer MJ, Hu FB, Giovannucci E, Rimm E, Manson JE, Hennekens CH, Willett WC. Am J Clin Nutr. 1999 Sep;70(3):412-9.

LDL-Cholesterol And Dietary Fat

In the last century there was a lot of research into the connection of diet with coronary artery disease. Focus has changed over the years from one dietary factor to another. During the last half of the twentieth century the emphasis was on the effect of saturated fat in the diet on coronary artery disease. Because of the association of a high blood LDL-cholesterol with coronary artery disease, short term dietary studies have been done to find diets that can lower blood LDL-cholesterol.

Possible contributors to LDL-cholesterolThe Study

One of the diets showing modest effect was the NCEP diet. This diet has evolved over the years. It was based on the concept that less fat in the diet would lower cholesterol, known to be associated with atherosclerotic plaques and coronary artery disease. However a study done in 2003 (1) compared the LDL lowering ability of one version of the NCEP diet to a statin drug, lovastatin.

Statin drugs have been shown to reduce blood cholesterol and subsequent heart events in large randomized controlled studies. Early diets involving eating less fat showed modest improvements in blood cholesterol and cardiac events. This study tried to determine if a diet could do as well as a drug.

By delivering plant sterols, fiber, soy protein and nuts, this diet was able to reduce LDL-cholesterol as much as 20 mg of lovastatin. It also lowered the overall coronary heart disease risk score based on a well accepted risk equation.

No Change In Dietary Fat

The diet was able to do this without lowering the fat content of the diet. In fact, the total fat, saturated fat and cholesterol intakes were slightly more in the experimental diet than the control diet. This study showed that without lowering fat intake, a diet can be designed to lower the risk of coronary artery disease.

The researchers felt this diet reduced cholesterol absorption, and cholesterol formation in the liver. And it may have increased the loss of cholesterol from the body. Some prior basic science studies indicated these mechanisms as possible ways the components of the diet worked.

Sadly, the study did not determine the sodium and potassium content of the diet. Because of this we cannot know if a change in potassium and sodium intake contributed. But it does show that a low fat diet is not the only consideration for reducing the risk of heart disease.
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1. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. Jenkins DJ, Kendall CW, Marchie A, Faulkner DA, Wong JM, de Souza R, Emam A, Parker TL, Vidgen E, Lapsley KG, Trautwein EA, Josse RG, Leiter LA, Connelly PW. JAMA. 2003 Jul 23;290(4):502-10.

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Recommended

Two excellent books about high potassium foods and blood pressure reduction are available on Amazon. The first is a practical guide to changing your diet to a high potassium foods diet. It is helpful even if you do not have hypertension. The second is a scientific explanation of the diet. It discusses the changes to your body that occur with high potassium foods.

Practical Guide

Scientific Explanation

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