Various health authorities tell us that consuming too much salt is bad for the heart. More specifically, experts are concerned about the intake of sodium compared with potassium. The World Health Organization advises adults to consume less than 5 grams of salt, less than 2 grams of sodium, and more than 3.5 grams of potassium each day.
The concern is largely based on observations that a high sodium intake, or a low potassium intake relative to sodium, can increase blood pressure. The American Heart Association has even stricter guidance and recommends an intake of no more than 1.5 grams of sodium per day. This guidance is based on studies that have suggested that sodium intake below this level is associated with lower blood pressure. The mechanisms by which sodium intake influences blood pressure are not yet fully understood, but they are thought to be related primarily to the intimate relationship between sodium and water.
When sodium is absorbed through the gastrointestinal tract, it brings water with it, keeping the body hydrated. The major liquids of the body are sustained because of sodium. Without sodium the liquid component of blood and the liquids that surround the body’s cells would lose their water, leading to dehydration and death.
The body uses various systems to try to keep the correct balance of sodium and water. Information is sent from the blood vessels and the brain that tells the kidneys to retain sodium or excrete sodium in the urine. Sodium intake also causes changes in thirst as a means of regulating water relative to sodium.
If too much sodium is consumed, sodium’s affinity with water is believed to cause an increase in the liquid volume and an increase in the pressure within the blood vessels. Potassium does not have the same affinity with water. In fact, potassium and sodium are antagonistic to each other; potassium counters the effects of sodium, and vice versa.
The intracellular space (inside the body’s cells) contains a lot more potassium than the extracellular space (the liquid surrounding the body’s cells) and the reverse is true for sodium. Therefore, the body clearly requires an appropriate balance of sodium and potassium, but the current recommendations for sodium intake might not be serving us well.
Studies on salt intake are somewhat problematic. Comparing data between various studies is difficult because two different methods are used for measuring salt intake: measuring urinary sodium excretion and estimating dietary intake. Twenty-four-hour urinary sodium excretion might be the most accurate method, since 90–95 percent of sodium intake is excreted in the urine. However, it is not practical to collect twenty-four-hour’s worth of urine, particularly during an extended study period, so researchers have suggested that fasting morning urine is a reliable substitute. Urinary sodium excretion does not account for sodium loss due to sweat.
Dietary intake is measured with the aid of food diaries and questionnaires. However, there is considerable room for inaccuracies if the study participant does not recall all of the foods they consumed. Further inaccuracies can arise because of differences in the sodium content of common foods and if table salt is not included in the analysis. In addition, portion size needs to be accurately accounted for.
Dietary recommendations for salt intake are largely based on clinical studies that use urinary analysis. But population surveys have used dietary recall for the analysis, and there is no existing method for comparing these two different measurements.
The analysis is made more complicated by differences in how each person consumes sodium. One person might have a higher sodium intake because of consuming processed foods such as ready- made meals, whereas another person might be getting their sodium from a more balanced diet that also includes more fresh fruit and vegetables. Therefore, some diets might be high in sodium but also high in potassium. Some people’s diets could also be high in other cardio-protective nutrients that could be offsetting the otherwise negative impact of the sodium.
Notwithstanding these difficulties in interpreting the data, studies have generally, on balance, shown a connection between lower sodium intake and lower blood pressure, although the reduction in blood pressure associated with lower sodium intake is often quite small. For example, an analysis completed by the Cochrane Hypertension Group found that a modest reduction in sodium intake resulted in an average reduction of 5 mmHg in systolic blood pressure and a reduction of 2.7 mmHg in diastolic blood pressure for people with high blood pressure. People with normal blood pressure had smaller reductions (2.3 mmHg for systolic and 1 mmHg for diastolic). Mathematically, if a 2 mmHg reduction in diastolic blood pressure is applied across a very large population (such as nationwide), this would result in an overall 6 percent reduction in heart disease risk. But how relevant these small reductions in blood pressure are for individual people is debatable.
Since blood pressure fluctuates as a result of a wide range of different conditions, it is important to look for a connection between lower sodium intake and an actual reduction in cardiovascular problems, rather than looking at changes in blood pressure alone. Such studies have had mixed results; some have confirmed an increased risk of cardiovascular disease in connection with a high sodium intake, while others have not. In fact, overall, researchers have suggested that the relationship between sodium intake and cardiovascular disease follows a J-shaped curve whereby both a low and high sodium intake could involve an increased risk.
Statistically, the lowest cardiovascular risks have been seen with a sodium intake of 3–5 grams per day, with an increased risk associated with both higher levels (above 5 grams per day) and lower levels (below 3 grams per day). This is important because although the data does confirm some kind of connection with sodium intake, the current recommendations are set too low and are associated with an increased risk. As mentioned above, health authorities currently recommend a sodium intake of 1.5–2 grams per day. Overall, this level of intake is associated with an increase in cardiovascular problems.
Health authorities could have become blinded by the blood pressure–lowering effect of a very low-sodium diet, and they could have failed to consider the other effects of such a diet. A very low-sodium diet has been shown to alter levels of some hormones and cytokines that are involved in cell-to-cell communication. A moderate, rather than low, sodium intake has even been shown to improve outcomes for some heart failure patients.
As mentioned, we should also consider potassium intake, not just sodium intake, as there is some evidence that potassium might exhibit a similar relationship. A study that analyzed the data from approximately 39,000 patients in the United States who had already suffered a heart attack found a U-shaped curve. Similar to sodium, both low and high levels of potassium were associated with an increased cardiovascular risk, with the lowest risk associated with moderate potassium levels.
The J-shaped and U-shaped curves for sodium and potassium respectively might be a further indication that the levels relative to each other are what is most important. Indeed, there is some data suggesting that a higher sodium-to-potassium excretion ratio is more strongly associated with increased cardiovascular risk than that of sodium or potassium alone.
Sodium/Potassium Balance after Heart Attack
The importance of the correct balance of sodium and potassium is further illustrated by the observation of heart muscle tissue after a heart attack. In an acute heart attack, tissue damage can be seen in three zones of heart muscle tissue. The core area consists of necrotic tissue and dead cells due to the absence of oxygen. Next to this there is an area of severe injury that is composed of cells that will die if the metabolic derangement cannot be corrected. Last, surrounding this area is a less ischemic zone, where cellular function is impaired but is reversible. In short, there is a gradient of extent of damage and metabolic derangement, with the extent of damage gradually reducing with increasing distance away from the necrotic core.
The damage gradient correlates with the amount of sodium inside the cell. As mentioned, there is a lot more sodium outside the cell (the extracellular space) than inside the cell. Under healthy conditions, there is a powerful mechanism for constantly pumping excess sodium out of the cell, the sodium-potassium pump; however, after a heart attack the membrane of the cell is damaged and additional sodium enters the cell. The excess sodium increases the liquid volume of the cell, causing it to swell, and cellular function and the ability to pump the excess sodium out of the cell is impaired.
The outer area of tissue damage typically corresponds with a 50 percent increase in the amount of sodium in the cell. The intermediate zone corresponds with a 200 percent increase in sodium, and the inner necrotic core has a 300 percent increase in sodium.
At the same time a similar, but reverse, situation is observed with potassium. Normally there is much more potassium inside the cell than outside, but after a heart attack there is a decrease in the potassium content inside the cell that again corresponds with the degree of tissue damage within the three affected zones.
These observations led Dr. Demetrio Sodi Pallares of Mexico City to develop a polarizing solution to help correct the sodium-potassium deregulation after an acute heart attack. The solution was based on earlier work done by Henry Laborit, a French researcher, and consisted of glucose, insulin, and potassium. The insulin helps the glucose and potassium into the cell.
Dr. Pallares had quite dramatic positive results using the polarizing solution in the 1960s, and a number of prominent cardiologists around the world also started administering it. At that time, and in a number of studies completed since, the polarizing solution reduced the number of deaths, the amount of tissue damage, and complications such as arrhythmias after a heart attack.
In fact, the potential benefits of the polarizing solution also extend into other areas of medicine that are beyond the scope of this topic and involve the electrical potential across the cell membrane and the additional use of electromagnetic fields. A more detailed discussion is available in the excellent book Bioelectromagnetic and Subtle Energy Medicine.
[This article is an extract from my book Statin Nation: The Ill-Founded War on Cholesterol, What Really Causes Heart Disease, and the Truth About the Most Overprescribed Drugs in the World]