12 Jan 2018 Are You Still Restricting Salt?
I was planning on writing about the current salt and sodium recommendations and the lack of solid research supporting them, but I realized that there are already enough comprehensive articles written about that (like this one). Instead, I’ll quickly summarize the absurdity of the current sodium recommendations and focus on the problems caused by restricting salt.
Some Ridiculous Guidelines
The current Dietary Guidelines for Americans recommend that we consume less than 2,300 mg sodium per day and less than 1,500 mg sodium for individuals with high blood pressure (1), the World Health Organization recommends that we consume less than 2,000 mg sodium per day (2), and the American Heart Association recommends an ideal limit of no more than 1,500 mg sodium per day for most adults (3).
These recommendations are aimed at reducing hypertension and cardiovascular disease. However, they’re at odds with much of the research, which shows that the current sodium recommendations are between 2 and 4 times lower than what is ideal for cardiovascular health and health in general.
Sodium intakes of 4,000-6,000 mg per day are associated with the lowest risk of cardiovascular death and hospitalization for congestive heart failure (4) while consuming under 2,300 mg sodium per day is associated with increased cardiovascular disease mortality and all-cause mortality (5). And, even consuming less than 3,600 mg per day is associated with greater cardiovascular disease mortality (6).
Sodium, the (Almost) Perfect Scapegoat
Ridiculous recommendations aside, sodium is an extraordinarily important mineral that has been wrongly blamed for causing hypertension and cardiovascular disease. This blame comes primarily from sodium’s ability to attract water.
When we consume sodium, the amount of sodium in our blood increases, which increases our blood volume because sodium attracts water.
Our blood pressure is a function of the volume of blood in circulation and the constriction or relaxation of our blood vessels. When our blood volume increases or blood vessels constrict, our blood pressure increases, and vice versa.
So, it’s assumed that increasing sodium consumption increases blood pressure by increasing the blood volume. It’s then assumed that this high blood pressure leads to cardiovascular disease. By the same line of thinking, sodium is blamed for increasing swelling, bloating, and water retention due to its attraction for water.
But, like the “calories-in versus calories-out” model of fat loss, these ideas are based on oversimplified models of the human body that ignore that we adapt to our environments.
When the blood volume is increased from increased salt consumption, our bodies adapt by increasing the amount of sodium they excrete and relaxing our blood vessels. This allows us to maintain a relatively steady blood pressure, while also allowing for optimal blood flow, mineral balance, and energy production. This is easier to explain by describing what happens when we don’t consume enough sodium.
What Happens When We Don’t Consume Enough Salt?
Contrary to the mainstream ideas, a low salt intake actually contributes to poor cardiovascular health and swelling and bloating.
When we reduce our salt intake, the amount of sodium in the blood is reduced, which causes an immediate reduction in blood volume and blood pressure. This is why reducing salt intake is suggested for reducing high blood pressure.
But it doesn’t end there.
Maintaining adequate blood pressure is extremely important for transporting nutrients and waste throughout our bodies. So, when our blood pressure is acutely reduced, our stress systems are activated in response (7).
Our stress systems constrict our blood vessels and release the stress hormone aldosterone, which reduces the amount of sodium that we excrete in our kidneys, allowing us to maintain higher sodium (and water) levels in our blood (8). This keeps our blood volume and blood pressure at the levels needed to transport nutrients and waste throughout the body.
But, while this balancing act allows us to maintain blood volume and blood pressure in the short term, it comes at a cost: the sodium we would normally excrete in our kidneys is replaced with potassium and magnesium (9). This means that when we reduce our salt consumption, we lose greater amounts of potassium and magnesium.
Like other adaptive processes, this isn’t a problem in acute situations. But when continued chronically, losing potassium and magnesium can contribute to high blood pressure and inhibit our bodies’ ability to produce energy.
Sodium, Swelling, and Energy Production
Potassium and magnesium are balanced with sodium in the cellular environment. Potassium and magnesium are housed within our cells, while sodium remains outside of the cell. This also keeps water outside of the cells (with sodium), which is an important feature of a healthy cell.
When we lose potassium and magnesium due to a low sodium intake, there is less potassium and magnesium in our cells. This then allows more sodium to enter the cell, bringing water with it, which causes the cell to swell (10). The increase in aldosterone due to a low sodium intake also contributes to this cell swelling (11, 12, 13).
This swelling is a real problem – a swollen cell can’t properly produce or use energy (14). Not only is this disastrous for our metabolism, which lies at the foundation of our health, but it can also contribute to cardiovascular problems!
When the cells in our blood vessels swell due to their lack of potassium and magnesium, it inhibits their ability to relax and causes our blood vessels to constrict (like a swollen muscle after working out) (15, 16, 17). This helps to make up for the reduced blood volume from less salt consumption, but also restricts blood flow throughout our bodies and can cause other cardiovascular problems.
In other words, when we eat less salt, our blood pressure is maintained via our stress systems. But, when this occurs over time, we lose potassium and magnesium, leading to cell swelling that inhibits energy production and can cause cardiovascular problems.
How Much Salt Should We Eat?
On the other hand, consuming enough salt allows for optimal energy production, adequate blood volume, reduced swelling and bloating, and sparing of potassium and magnesium. This allows for proper metabolic function, cardiovascular function, and really all other functions.
So, should we eat salt to our heart’s content?
Pretty much! Our sense of taste has been designed to dictate our nutrient intake. When we don’t have enough sodium, we have a stronger desire to eat salty foods, and vice versa (20). So, we can just listen to what our bodies need and allow that to dictate how much salt we consume.
In other words, salt to taste!
If you’re worried about your blood pressure, then make sure you’re getting enough potassium and magnesium. Reducing sodium intake may drop your blood pressure a few points, but it doesn’t translate to better cardiovascular health.
- Ahmad, Faraz, and Holly H McPeak. “Using the 2015-2020 Dietary Guidelines for Americans to Help Improve the Diet of Older Individuals.” gov, Office of Disease Prevention and Health Promotion, 27 May 2016, www.health.gov/news/blog/2016/05/using-the-2015-2020-dietary-guidelines-for-americans-to-help-improve-the-diet-of-older-individuals/.
- “WHO Issues New Guidance on Dietary Salt and Potassium.” WHO, World Health Organization, 13 Jan. 2013, who.int/mediacentre/news/notes/2013/salt_potassium_20130131/en/.
- “Shaking the Salt Habit to Lower High Blood Pressure.” American Heart Association, 13 Nov. 2017, heart.org/HEARTORG/Conditions/HighBloodPressure/MakeChangesThatMatter/Shaking-the-Salt-Habit-to-Lower-High-Blood-Pressure_UCM_303241_Article.jsp#.WlgTuKinE2w.
- O’Donnell, Martin J, et al. “Urinary Sodium and Potassium Excretion and Risk of Cardiovascular Events.” JAMA, Nov. 2011, doi:10.1001/jama.2011.1729.
- Cohen, HW, et al. “Sodium Intake and Mortality in the NHANES II Follow-up Study.” The American Journal of Medicine, vol. 119, no. 3, Mar. 2006, pp. e7–e14., doi:10.1016/j.amjmed.2005.10.042.
- Stolarz-Skrzypek, K., et al. “Fatal And Nonfatal Outcomes, Incidence Of Hypertension, And Blood Pressure Changes In Relation To Urinary Sodium Excretion.” JAMA, vol. 305, no. 17, May 2011, pp. 1777–1785., doi:10.1001/jama.2011.574.
- Graudal, Niels A., et al. “Effects of Sodium Restriction on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterols, and Triglyceride: A Meta-Analysis.” JAMA, vol. 279, no. 17, 6 May 1998, pp. 1383–1391., doi:10.1001/jama.279.17.1383.
- Arai, Keiko, and Chrousos, George P. “Aldosterone Deficiency and Resistance.” Updated 11 May 2016. In Endotext: De Groot LJ, Chrousos G, Dungan K, et al., editors. South Dartmouth (MA): MDText.com, Inc. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279079/.
- Horton, Richard, and Edward G. Biglieri. “Effect of Aldosterone on the Metabolism of Magnesium.” The Journal of Clinical Endocrinology & Metabolism, vol. 22, no. 12, Dec. 1962, pp. 1187–1192., doi:10.1210/jcem-22-12-1187.
- Bilbrey, G. L., et al. “Skeletal muscle resting membrane potential in potassium deficiency.” The Journal of clinical investigation, 52, no. 12, 1973, pp. 3011–18. doi:10.1172/JCI107499.
- Peat, Ray. Water: Swelling, Tension, Pain, Fatigue, Aging. Retrieved from raypeat.com/articles/articles/water.shtml.
- Dyckner, T., and P. O. Wester. “Effect of magnesium on blood pressure.” BMJ, 286, no. 6381, 1983, pp. 1847–49. doi:10.1136/bmj.286.6381.1847.
- Haddy, F. J. “Potassium effects on contraction in arterial smooth muscle mediated by Na+, K+-ATPase.” Federation proceedings, 42, no. 2, 1983, pp. 239–45.
- Leaf, A. “Cell Swelling: A Factor in Ischemic Tissue Injury.” Circulation, 48, no. 3, 1973, pp. 455–58. doi:10.1161/01.CIR.48.3.455.
- Mihailidou, Anastasia S., and John W. Funder. “Nongenomic effects of mineralocorticoid receptor activation in the cardiovascular system.” Steroids, 70, 5-7, 2005, pp. 347–51. doi:10.1016/j.steroids.2005.02.004.
- Krishna, G G. “Effect of Potassium Intake on Blood Pressure.” Journal of the American Society of Nephrology, vol. 1, no. 1, July 1990, pp. 43–52.
- Oberleithner, H., et al. “Endothelial cell swelling by aldosterone.” The Journal of membrane biology, 196, no. 3, 2003, pp. 163–72. doi:10.1007/s00239-003-0635-6.
- Peat, Ray. Salt, Energy, Metabolic Rate, and Longevity. Retrieved from raypeat.com/articles/articles/salt.shtml.
- Coelho, Michella, et al. “High- or Low-Salt Diet from Weaning to Adulthood: Effect on Body Weight, Food Intake and Energy Balance in Rats.” Nutrition, Metabolism and Cardiovascular Diseases, vol. 16, no. 2, Mar. 2006, pp. 148–155., doi:10.1016/j.numecd.2005.09.001.
- Lindemann, Bernd. “Sodium Taste.” Current Opinion in Nephrology and Hypertension, vol. 6, no. 5, Sept. 1997, pp. 425–429., doi:10.1097/00041552-199709000-00003.