Sodium is an essential mineral that is responsible for various functions in the body such as fluid, electrolyte, blood volume & pressure, acid-base balance, and the creation of action potential of neurons and muscles. Sodium can be found in great quantities in extracellular fluid and when partnered with other ions, can create an action potential, or electrical impulse, within a cell.
These electrical impulses travel along neurons in our nervous system. They create an excitable action to encourage a response to an external stimulus. Sodium is an integral component of our nervous system and our ability to generate movement!
But how? Sodium-potassium pumps!
Sodium-potassium “pumps” exist within the membrane of our individual body cells and are responsible for creating the action potential and electrical nerve impulses that our neurons carry to stimulate muscle movement through the constant facilitation of sodium and potassium concentrations inside and outside our cells.
For visual reference, here is a really great GIF of Drake acting like a sodium-potassium pump:
The sodium-potassium pump itself, otherwise known as the Na+/K+ ATPase, is an integral, transmembrane protein that facilitates this process. A transmembrane protein is a pathway that completely bisects the cell membrane and act as an entryway for molecules to enter and exit the cell.
3 Na+ ions in the cytosol (fluid on the inside of a cell) bind to the transmembrane protein. This also causes ATP (adenosine triphosphate) to bind to the protein, which is then broken down into ADP (adenosine diphosphate) when a phosphate is released. This energy transfer causes the transmembrane protein to change shape, pumping the 3 Na+ out into the extracellular fluid (fluid on the outside of a cell), and allowing 2 K+ ions to enter the transmembrane protein gateway. The 2 K+ is pumped into the cell and the protein returns to its original shape as it prepares to continue the cycle.
In this process, both Na+ and K+ are moving against their electrochemical gradient. The electrical gradient outside of a cell is more positive than the gradient within the cell. This negative charge difference indicates the polarization of the cell and is also considered a cell’s resting membrane potential. Consequently, the rush of Na+ and K+ ions in and out of a cell membrane triggers the depolarization and repolarization, or change in electrical gradient, of a cell. This process creates action potential and thus stimulates electrical nerve impulses from axon to axon. Without sodium, this electrical stimulus would not occur, muscle movement would be impaired, and our body as we know it would not function as we need it to sustain life.
Overconsumption & Health Implications
Despite the importance of the existence of sodium within our body for neurological function alone, the overconsumption of dietary sodium is linked to high blood pressure and has been the focus of health studies for decades. High blood pressure, or hypertension, is also linked to increased risk of cardiovascular disease, stroke, and early death, and is responsible for over approximately 400,000 deaths every year in the United States [1, 2]. Although the CDC recommends containing sodium intake to 2,300mg or less per day, 90% of Americans over the age of 2 years old are consuming at least 3,400mg of sodium daily [2]. However, the hypertension epidemic is not unique to the United States – this is an issue that spans across the globe. It is estimated the 2.5 million lives could be spared every year if sodium intake levels were reduced to the RDA [3].
There is evidence that dietary sodium intake in relation to potassium intake may also be a determinant in the control and prevention of hypertension. Increased blood sodium levels and risk of high blood pressure may be correlated to low potassium intake, and that increasing potassium in relation to sodium intake may lower the risk of hypertension by balancing excess sodium [4]. Chmielewski et al. (2017) created a study in which sodium, potassium, and systolic blood pressure levels were observed in 4,716 individuals aged 12-14 years of age. They found that adolescents who showed the greatest disparity between sodium levels and potassium levels were of greatest risk of high systolic blood pressure [4].
Individuals who reported sodium levels that were greater than or equal to 7500 mg/d did not simultaneously report that their potassium levels were less than 700 mg/d. However, there was a correlation between high systolic blood pressure and individuals who received less than 700 mg/d of potassium. They did find a linear correlation between the highest reports of systolic blood pressure and variances in sodium/potassium (Na+/K+) ratios greater than or equal to 2.5mg/mg [4].
Although increasing potassium intake in relation to sodium levels may protect against the negative effects of excess sodium and may even promote the reduction of blood pressure, the mechanisms and relationship between potassium and hypertension is still unknown. In general population adult studies, increasing dietary potassium to lower blood pressure has not yielded consistent successful results but should be part of the conversation regarding lowering the risk of high blood pressure and hypertension [5].
Nutritionally, it can be easy to retrieve potassium dietarily, assuming that bioavailability is favorable and that nutrient uptake within the body is optimal. The United States Department of Health has a great table that ranks nutritional sources of potassium by the amount of available nutrient based off 100g servings which can be viewed here.
Considering these recent studies and meta-analyses, it is still clear that we continue to need quality, methodological studies that seek to discover the reduction of risk of hypertension and risk of CVD. It still ominously remains that the overconsumption of sodium as we age is a leading cause of cardiovascular disease and stroke [6].
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