Not a year goes by that the nutrition sphere doesn’t have a “whipping boy” (or, in this case, nutrient).
In years past, it’s been sugar, high-fructose corn syrup, carbohydrates, fruit, and fat.
One nutrient that has been on and off the radar is salt.
Depending on which “expert” you listen to, you’ll hear a lot of conflicting information.
We’re here to set the record straight and tell you whether or not you need to be concerned about your daily salt intake.
Let’s first start by discussing the role of salt (sodium chloride) in the body.
What is Sodium and What Does It Do?
Sodium is an essential mineral and electrolyte involved with[1]:
- Muscle contraction
- Nerve function
- Blood volume
- Acid-base balance
Sodium balance in the body is closely linked to water balance in the body, and it is meticulously maintained by the kidneys.[1]
Does Sodium Cause Hypertension for Athletes?
The belief that sodium (salt) causes hypertension primarily stems from the fact that sodium regulates blood volume and extracellular fluid levels.
Additionally, a number of studies have found an association between higher levels of sodium intake and hypertension (high blood pressure).[2,3,4]
Other studies also suggest that higher salt intakes are significantly associated with a greater risk of stroke and other cardiovascular events.[4,5]
So, does this mean athletes need to be concerned with their sodium intake?
Let’s tap the brakes on that question for a second, and review some of the more recent research delving into the link between sodium and blood pressure.
A 2017 study in which researchers analyzed over 2,600 women and men over a period of 16 years to assess the long term effects of salt consumption on systolic and diastolic blood pressures noted that individuals with the lowest blood pressure levels had higher intakes of sodium and potassium while those with the highest blood pressure readings had lower intakes of both sodium and potassium.[6]
In fact, the lowest blood pressure among the subjects studied were those who consumed 4,000mg or more per day!
The authors concluded[6]:
“We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure. Our findings add to growing evidence that current recommendations for sodium intake may be misguided.”
Another massive study published in recent years followed 94,000 people from around the world for an average of eight years.[7]
Researchers only found evidence of an associated risk of cardiovascular disease and stroke when the average daily sodium intake exceeded FIVE grams (5,000mg) of sodium![7]
Now, it bears mentioning that some individuals are salt-sensitive, either due to genetics or lifestyle factors (sedentary, overweight, etc.).
For example, individuals with hypertension, diabetes and/or chronic kidney disease (CKD) tend to be more sensitive to the hypertensive effects of sodium. So, in these instances, sodium (salt) intake should be monitored.
Still, for individuals who maintain high levels of physical activity daily (like those who enter our transformation challenges), sodium intake likely isn’t a concern.
The reason for this is that intense exercise leads to greater nutrient requirements, including essential minerals like sodium and potassium.
Furthermore, if you train and/or work in a hot environment, your sodium needs go up considerably.
For instance, studies note that individuals working in hot environments for 10 hours can lose between 4,800-6,000 mg of sodium![8]
In case you weren’t aware, that’s roughly the equivalent of 12,000-15,000 mg of table salt a day!
Also worth mentioning is that some research indicates that low sodium diets are associated with increased insulin resistance, and insulin resistance is a key indicator for several chronic diseases, including type 2 diabetes and heart disease.[9,10]
Now, sedentary adults have substantially less need for sodium. In fact, the American Heart Association (AHA) lists the minimum physiological requirement for sodium as less than 500 mg a day.
But, based on the current body of evidence, it’s reductive to simply state that high sodium diets cause hypertension, when in fact there is considerable amounts of evidence to the contrary.
What may serve to be a point of greater emphasis is the total micronutrient intake during the day, not simply sodium.
More specifically, individuals should be concerned with their intake of sodium and potassium.
The Sodium-Potassium Link
As we mentioned at the beginning, sodium is the electrolyte responsible for regulating fluid balance outside the cell.
Potassium is the counterbalance to sodium, as it regulates fluid balance inside the cell.
In the body, the sodium-potassium pump facilitates the transportation of sodium and potassium ions across the cell membrane. To ensure this biological process works efficiently, sodium and potassium must be balanced within the body.
Furthermore, research indicates that individuals who are at the greatest risk of cardiovascular disease are those who consume too much sodium along with too little potassium -- basically what you get when eating a standard American diet that’s rich in overly processed foods and low in fruits and vegetables.
Processed, packaged foods are notorious for being high in sugar, salt, fat, and calories, while simultaneously being low in fiber, protein, and potassium (as well as other key micronutrients).
Therefore, to help ensure you’re hitting the recommended amounts of potassium each day, limit your intake of processed foods while focusing on consuming enough whole foods each day.
Some of our favorite potassium-rich foods, include:
- Avocado
- Potatoes
- Bananas
- Mushrooms
- Spinach
The Bottom Line on Consuming Too Much Salt Daily
Active, healthy individuals with no pre-existing conditions likely don’t need to worry about their salt intake. If anything, they may need to increase their salt intake, especially if they’ve followed the old dogma of limiting sodium intake.
Sedentary, overweight, and/or unhealthy individuals should monitor their sodium intake as they do not have as great of micronutrient requirements as active individuals.
At the end of the day, use common sense. Salt your food to taste, and don’t go overboard or overly restrict yourself.
References
- Strazzullo P, Leclercq C. Sodium. Adv Nutr. 2014;5(2):188-190. Published 2014 Mar 1. doi:10.3945/an.113.005215
- Stamler, J., Chan, Q., Daviglus, M. L., Dyer, A. R., Van Horn, L., Garside, D. B., Miura, K., Wu, Y., Ueshima, H., Zhao, L., & Elliott, P. (2018). Relation of dietary sodium (Salt) to blood pressure and its possible modulation by other dietary factors. Hypertension, 71(4), 631-637. https://doi.org/10.1161/hypertensionaha.117.09928
- Dietary sodium and blood pressure. (2004, May 1). Hypertension. https://www.ahajournals.org/doi/full/10.1161/01.hyp.0000126610.89002.c6
- Aburto NJ, Ziolkovska A, Hooper L, Elliott P, Cappuccio FP, Meerpohl JJ. Effect of lower sodium intake on health: systematic review and meta-analyses. BMJ. 2013;346:f1326.
- Strazzullo P, D’Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009;339:b4567.
- Moore, L. L., Singer, M. R., & Bradlee, M. L. (2017). Low Sodium Intakes are Not Associated with Lower Blood Pressure Levels among Framingham Offspring Study Adults. The FASEB Journal , 31(1 Supplement), 446.6-446.6. Retrieved from http://www.fasebj.org/content/31/1_Supplement/446.6.abstract
- Rust, P., & Ekmekcioglu, C. (2017). Impact of Salt Intake on the Pathogenesis and Treatment of Hypertension. Advances in Experimental Medicine and Biology, 956, 61–84. https://doi.org/10.1007/5584_2016_147
- Bates, Graham P, and Veronica S Miller. Sweat Rate and Sodium Loss during Work in the Heat. Journal of Occupational Medicine and Toxicology (London, England) 3 (2008): 4. PMC. Web. Jan. 2017.
- Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler GK. Low-salt diet increases insulin resistance in healthy subjects. Metabolism. 2011;60(7):965-968. doi:10.1016/j.metabol.2010.09.005
- Townsend RR, Kapoor S, McFadden CB. Salt intake and insulin sensitivity in healthy human volunteers. Clin Sci (Lond). 2007;113(3):141-148. doi:10.1042/CS20060361
