The high ratio diet, consisting of low sodium intake and high potassium foods, has more scientific support than any other diet. And this scientific support is growing. Studies of indigenous groups gave the first clues. The Yanomami have a low sodium, high potassium, alkaline diet and have no hypertension. How can this occur? Such a diet has been shown to increase aldosterone, which is associated with hypertension. The effect on blood pressure of a high ratio diet was predicted many years ago by doctors Guyton, Young and Hall. A recent study (1) explains how this effect occurs at the molecular level.
The last post discussed that a low sodium, high potassium, alkaline diet results in very high levels of aldosterone in the blood. The Yanomami, who have no hypertension, have up to 10 times the level of aldosterone found in normotensive Westerners. Aldosterone is at the end of a renin-angiotensin-aldosterone system stimulation. And an elevated blood level of aldosterone is associated with hypertension in Westerners. How can it be elevated in Yanomami and not result in hypertension?
Best Known Mechanism
The best known way that the kidney handles potassium is to exchange it with sodium in the principal cells of the connecting tubule in the kidney. Sodium is reabsorbed at the ENaC and potassium is excreted at the ROMK of the principal cell. However, as discussed in the last post, the best ratio of potassium excretion to sodium reabsorption that this method can handle is a ratio of 0.67.
That study (2) explained how the kidney can excrete a much higher ratio of potassium to sodium than 0.67 in animals on a low sodium, high potassium, alkaline diet. But it did not explain the role of aldosterone, since the high blood level of aldosterone did not result in hypertension like it does in Westerners.
Previously
The present study (1) was built on prior studies of this same group. As discussed in the last post, this group of researchers previously found that in the intercalated cells (IC) there is an increase of BKa/b4 channels from a low sodium, high potassium, alkaline diet. These channels can excrete a much bigger load of potassium, creating a much higher ratio of potassium to sodium in the urine.
In the Yanomami, the ratio can exceed 150 to 1. This is accomplished by recycling sodium and chloride in the kidney when the diet is alkaline. With recycling, no sodium needs to be exchanged directly for potassium, because the increase in BKa/b4 channels lets more potassium flow according to potassium's electrochemical gradient.
However, the researchers found that this type of diet was associated with a high blood aldosterone level. These high blood aldosterone levels are normally associated with an increase in blood pressure. But with this type of diet there is no increase in blood pressure. The researchers found that the aldosterone level on this diet was as much as 10 times the amount on a control diet.
The researchers had found the elevated blood aldosterone level was associated with increased potassium excretion and increased sodium reabsorption. They sought to control the aldosterone level to see if aldosterone was necessary and sufficient for the increase in BKa/b4 channels and the increase in potassium excretion. In other words, they sought to see if aldosterone was responsible, or if something else the animals produced could be the cause of increased BKa/b4 channels and increased potassium excretion.
What The Researchers Did
The researchers put mice on a low sodium, high potassium, alkaline (LNaHK) diet. Then they removed the adrenal glands so that no aldosterone would be produced. In some of the mice they did not replace the aldosterone at all. In other mice they partially replaced the aldosterone. And in a third group, they replaced aldosterone fully, so that the blood level of aldosterone reached the level they had found in normal mice that had been on the LNaHK diet.
What The Researchers Found
What they found was that those mice that had no replacement of aldosterone died quickly. These mice collected an excessive buildup of potassium in the blood.
The mice with a low replacement of aldosterone also had a buildup of potassium in the blood. But the buildup was slower. These mice did not die until several days later than the mice with no replacement.
In the third group, the researchers replaced aldosterone to the same blood level as found in normal mice after a low sodium, high potassium, alkaline diet. None of these mice died. These mice did well with normal blood pressure and no buildup of potassium.
When the researchers looked at the kidneys, they found that there was an increase in the BKa/b4 channels in the ICs proportional to the amount of aldosterone replaced. This confirmed the researchers' previous finding of increased BKa/b4 channels in normal animals on a low sodium, high potassium, alkaline diet.
And they found that the amount of potassium excreted in the urine was proportional to the BK channels. They also found the fluid volume of urine increased proportionally to the amount of potassium excreted. This resulted in a lower blood volume in the animals.
It has been long known that a high level of potassium in the blood stimulates the adrenal gland to secrete aldosterone. And it was known that aldosterone stimulates the kidney to excrete more potassium. With this study it is now known at the molecular level what the effect of aldosterone is on the kidney to accomplish this. And it is known how the diet affects this process.
Conclusion
The researchers concluded that aldosterone is necessary to generate the increase in BKa/b4 channels so that potassium can be excreted at a high ratio to sodium. The potassium that is excreted carries fluid with it to reduce blood volume. The researchers speculated that a potassium induced osmotic diuresis may be responsible for the reduction in blood pressure and cardiovascular disease that is found in those humans who are on this low sodium, high potassium, alkaline diet.
So just as there is a very good model for the high ratio diet and hypertensive heart disease (discussed here), there is now a good model for how the high ratio diet interacts with the kidney to reduce hypertension, and heart disease. The strong epidemiological evidence that resulted in clinical studies showing a large advantage for this diet has progressed beyond the physiological studies of Guyton, Young and Hall to showing how, at the cellular and molecular level, the effects are achieved.
To take advantage of the latest scientific evidence for the most important aspect of your diet, start your high ratio diet today.
______________________
1. Low Na, high K diet and the role of aldosterone in BK-mediated K excretion. Cornelius RJ, Wen D, Li H, Yuan Y, Wang-France J, Warner PC, Sansom SC. PLoS One. 2015 Jan 21;10(1):e0115515. doi: 10.1371/journal.pone.0115515. eCollection 2015.
2. Relation between BK-a/ß4-mediated potassium secretion and ENaC-mediated sodium reabsorption. Wen D, Cornelius RJ, Rivero-Hernandez D, Yuan Y, Li H, Weinstein AM, Sansom SC. Kidney Int. 2014 Jul;86(1):139-45. doi: 10.1038/ki.2014.14. Epub 2014 Feb 26.
