Introduction
Sodium’s gotten a lot of flack over the years. For fifty years or more, we’ve been told to reduce sodium intake for lower blood pressure and lower cardiovascular risk factors overall. However, the world of nutrition is a little more nuanced than that and these types of blanket recommendations almost never pan out for everyone.
Sodium is an integral electrolyte that’s 100% necessary for a lot of different functions in the body; from nerve impulses and muscle function to controlling fluid volume in your bloodstream. Although salt-sensitive hypertension does exist and does have a genetic component, in most cases it’s an artifact of other health conditions present. For the majority of healthy individuals, sodium restriction may actually cause more harm than good. Let’s dive in.
Layout:
- Where did the current sodium guidelines come from? Where did the “fact” that increased sodium leads to high blood pressure come from?
- What does the weight of the data about sodium and blood pressure say?
- What could make someone susceptible to salt-sensitive hypertension?
- The dangers of restricting sodium intake
- How to figure out how much sodium to actually take in.
Since this is a lengthier post, I’ll provide a summary first.
Summary:
- The salt and blood pressure connection is based on a hypothesis of scientific principles as well as correlational and circumstantial data that didn’t hold up as well as the science has evolved.
- Salt sensitive hypertension does exist – It can be caused by cases of insulin resistance, very low potassium intakes, and certain genetic polymorphisms.
- The dangers of salt restriction in healthy individuals include high insulin levels (possibly leading to insulin resistance), higher heart rate, stress on the kidneys and adrenals, decreased exercise performance, and increases in triglycerides and cholesterol.
- A healthy, insulin sensitive individual with everything average – activity levels, average split macros, etc, should be fine taking in between 3500 and 6000mg of sodium per day. However, this figure is relative, read on if you want specific recommendations for specific circumstances.
The Origin of the Salt-Hypertension Hypothesis
One of the main things nearly everyone thinks about when they think about salt and possible negative effects is blood pressure. Where did the salt-blood pressure connection come from? Surprisingly, not from strong data on outcomes with salt and blood pressure. In other words, not actually from testing if salt raised blood pressure in randomized, clinically controlled trials.
There were some weak observational studies at the time, but it mainly came from a hypothesis based on foundational scientific principles. Mechanistic thinking based on principles can be quite helpful in some cases, but it can occasionally be misleading, or not actually pan out that way in real life circumstances, which is what’s going on here.
Let’s look at the original salt-blood pressure hypothesis. When we eat salt, so the theory goes, we also get thirsty, so we drink more water. In the salt-high blood pressure hypothesis, that excess salt then causes the body to hold on to that increased water, in order to dilute the saltiness of the blood. Then, the resulting increased blood volume would automatically lead to higher blood pressure.
Nothing in that statement is inherently wrong, except for the last sentence. Sodium does cause increased water retention, but a healthy person will go back to homeostasis quite quickly.
Like I mentioned in brief earlier, there was some circumstantial evidence around that time to support the hypothesis. Data was gathered on salt intakes in various populations, and in some cases correlations of higher sodium intake and blood pressure were seen.
However, correlation doesn’t equal causation. Way too many of our nutritional faux pas these days are because we try to draw causation from correlation and then base entire nutritional guidelines on that.
Salt and Blood Pressure – What the Newer Data Says
What we actually see in most healthy individuals is that increased salt intake causes a fleeting, transient, inconsequential rise in blood pressure that goes away quite quickly.
For a few stats, evidence in the medical literature suggests that approximately 80% of people with normal blood pressure (less than or equal to 120/80 mmHg) are not sensitive to the blood pressure-raising effects of salt at all.
Among those with prehypertension, roughly 75% are not sensitive to salt, and even among those with full-blown hypertension, about 55% are totally immune to salt’s effects on blood pressure. Even in those that do have all out hypertension, over half aren’t even sensitive to salt.
Causes of Sodium-Sensitive Hypertension
Basically, they blamed it on the wrong white crystal; the real culprit here is cocaine. Totally kidding, but obviously cocaine is going to raise your blood pressure (plus its illegal), so don’t do that. I’m talking about sugar!
Insulin Resistance
For most, in moderation, it’s fine, but what I’m referring to here is the chronic overconsumption of it leading to insulin resistance. This is probably the most common factor.
Your body has very complex mechanisms of regulating your sodium balance in the body. The kidney is directed to either reabsorb sodium back into circulation or excrete it via urine based on different hormonal factors.
In a healthy individual, an appropriate amount of salt is reabsorbed and an appropriate amount is excreted, leading to neutral effects on blood pressure
However, in cases of insulin resistance, we have a few factors causing the kidneys to reabsorb significantly more salt than it should. High insulin signals the kidneys to reabsorb sodium. Aldosterone also tends to be elevated in cases of insulin resistance, and this hormone also causes the kidneys to reabsorb sodium and excrete potassium.
When we have this excess sodium in the blood without the ability to excrete it, then the salt-blood pressure hypothesis rings true. The chronic increased fluid volume within the bloodstream will raise blood pressure.
Low Potassium Intakes Coupled with High Sodium Intakes
Blood pressure regulation is very much based on the balance of sodium and potassium within the body. If potassium is quite low but sodium is quite high, this can indeed lead to an increase in blood pressure. We see this happening as one of the mechanisms of insulin-resistant salt-sensitive hypertension; aldosterone causes the kidneys to excrete more potassium and retain more sodium, effectively leading to the same result as lower intakes of potassium and higher intakes of sodium.
This mainly occurs in cases of people eating the standard american diet. Most processed foods are very rich in sodium but devoid of potassium. If one makes foods like that even 50% of their diet, there is a risk there.
However, if someone is eating mostly whole foods, potassium intake naturally rises. Potassium is rich in a lot of different whole foods, and you’re most likely getting enough if you just eat a varied whole foods diet. Combine that with the fact that there’s minimal extra sodium in whole foods, you can salt your food to taste and be getting a good balance.
Genetic Basis
The genetic basis involves one of the factors we talked about earlier: Aldosterone. The release of aldosterone is one of final products of a system known as the renin-angiotensin-aldosterone system, or the RAAS system.
Simplified, this system is in place in order to modulate and raise blood pressure in cases of low blood pressure, such as dehydration, blood loss, or electrolyte imbalances. However, research has identified that a specific polymorphism in the ACE gene causes more aldosterone release in general, which may contribute to salt-sensitive hypertension.
Those are some of the main factors that could cause someone to be salt-sensitive hypertensive, and two of them are totally lifestyle-based, and the other is on the more rare side.
Dangers of a Low Sodium Diet
For everyone else, let’s now dive into the potential dangers of restricting salt intake too much.
Increased Heart Rate
One of the larger dangers of restricting salt intake; when you restrict salt intake, your blood fluid volume goes down. When this happens, the RAAS system we talked about earlier activates, and this causes increases in aldosterone to maintain blood pressure, but it also causes increases in the catecholamines, epinephrine and norepinephrine. These are the primary hormones of the sympathetic nervous system, which in turn increases heart rate.
In some cases, heart rate can raise as much as 25% with salt restriction, and this increase in heart rate, if let go on over time, will increase risk of CVD and cardiac events.
Raises Insulin Levels
When you restrict sodium intake, the body has compensation mechanisms to ensure that you still have adequate sodium within the body, and one of these mechanisms is a rise in insulin levels.
As we talked about earlier when we talked about salt-sensitive hypertension, insulin acts at the kidneys to help retain salt, so, in effect, this restriction of sodium causes the body to elevate basal insulin levels in order to help retain more salt at the levels of the kidneys.
However, higher basal insulin levels have knock-on effects on a lot of other things and is one reason why, when some people restrict salt, they begin to have a lot of sugar cravings. Higher insulin floating through the bloodstream is directly damaging to the endothelial lining and promotes atherosclerosis. If let gone on long enough, this could lead to insulin resistance and raise risk for metabolic syndrome and Type 2 Diabetes.
Kidney and Adrenal Stress
The kidneys, at a simplified level, are a fantastic filter. The human body has on average, 1 to 1.5 gallons of blood and the kidneys filter this entire volume of blood around 40 times per day, which results in around 3.2 to 3.6 pounds of salt filtered per day.
The real kidney stress occurs when the kidneys have to significantly ramp up their salt reabsorption. This process is taxing and requires ATP to do so, so if you’re consistently eating a low sodium diet, this can stress the kidneys over time.
As far as the adrenals, as we talked about earlier, a low salt diet is going to increase the levels of epinephrine and norepinephrine in the blood, and if sodium levels are quite low, this will also increase cortisol. Therefore, on a long-term salt-restricted diet, this could potentially cause more adrenal stress than we want.
Triglycerides and Cholesterol
Rises in triglycerides and LDL cholesterol are consistently seen in RCTs (gold standard of studies) that restrict salt. Even as far back as the original DASH trial that spawned the DASH diet (for those unaware, one of the first sodium restricted diet protocols). In that trial, only modest reductions in blood pressure were seen in already hypertensive individuals from restricting salt intake, but triglycerides and LDL increased significantly.
Just for another example, in a 2012 RCT comparing different salt intakes, the arm with the lowest sodium intake only had a 1% decrease in blood pressure in hypertensives (no decrease in individuals with normal blood pressure), but there was a consistent 7% increase in triglycerides.
Triglycerides are one of the more important markers on a lipid panel, and elevated levels can indicate insulin resistance. Insulin levels play highly into triglyceride levels, so this makes sense if the diet was also raising the insulin levels.
This all may sound a little bit scary, but I wouldn’t go in the exact opposite direction and start taking salt shots every few hours or anything like that. This is really only seen in salt-restricted states, which just so happens to fall around the current american guidelines for salt intake which are 2300mg/day. Yes, alot of those above effects have occurred at sodium intakes between 1500 – 2300 mg/day, which has spurred a lot of controversy in the scientific world with a lot of prominent experts pushing to increase the sodium guidelines.
How to Figure out Your Sodium Needs
Most things in nutrition are individualized and sodium intake is no different, so how do you know how much sodium you should take in every day? This depends on a lot of factors, so let’s go through a few.
The average healthy individual (good insulin sensitivity, etc) with average activity levels, eating moderate macros all the way around would be totally fine on 4000 to 6000mg/day – 5000mg might be a good sweet spot.
However, there are other factors that may increase your need for salt:
Remember one of the things that causes sodium retention at the kidneys: Insulin. We then have to think about when insulin levels would be very low; one of those situations would be a ketogenic diet.
Ketogenic Diet
Indeed, if someone is very low carb or ketogenic, that sodium figure would increase to around 7000 to 8000 mg baseline, and even more if they’re highly active since the kidneys waste a lot of sodium in these states.
This figure should be especially paid attention to once someone transitions into a VLC or keto diet strategy from a mixed diet. During the transition period, the kidneys waste even more sodium since the kidneys haven’t adapted to the new state yet. After about a month, the kidneys start conserving a bit more sodium, but needs are still increased compared to a mixed diet.
Chronically Low Calorie
The reason behind this one is much the same as the last one; low insulin. If someone has been underfeeding themselves compared to their energy expenditure, and is very lean, insulin is going to also be at a rock bottom state.
Obviously, the best move here is to increase calories and reverse diet, but if its a situation where that’s not available yet; such as someone is dieting hard for a photoshoot, then sodium needs will be increased. Probably not to the same level as a ketogenic diet, but close.
Untreated Hypothyroidism or Adrenal Insufficiency
Untreated hypothyroidism causes a decrease in cardiac output, and with that, anti-diuretic hormone (ADH) levels increase. ADH is another fluid balance hormone; when elevated, we retain water, and when low, we let go of water.
Connecting that to sodium, as ADH levels increase, this decreases the ability to excrete free water and regulate sodium levels in the blood correctly. In addition to that, it’s been observed that some hypothyroid patients have higher urinary excretion of sodium as well. This can be mitigated by treating the hypothyroidism; either the underlying issue causing it or with medication (preferably the former).
In adrenal insufficiency, we see the exact same mechanism. If someone is cortisol deficient, ADH rises in order to compensate, and then we have the whole process we just explained happening again.
Higher Levels of Exercise
The level of increased sodium you may need depends on the length of exercise and how much you’re sweating. I do have a podcast on hydration out there, where we dive deep into this. In that episode, I talk about how everyone has a different level of salt that they sweat out during exercise.
Some people excrete a significant amount and some less. If you get done exercising and you have this visible white residue on your clothes after they dry, you’re probably someone that excretes a little bit more than average.
With any exercise that causes you to sweat excessively, such as longer endurance exercise like running/swimming/rowing, Crossfit, and some high volume resistance training workouts, its safe to go with the recommendations I made in the hydration podcast – 1100-1200 mg of sodium (½ tsp) per liter of water per hour.
Meaning, take a half tsp of sodium, mix it in a liter of water, and consume one of these sodium-infused liters per hour of intense exercise. These days, supplements like LMNT can help you do this in a tasty way. If you’re just doing regular strength training and not sweating a lot, this probably isn’t necessary, but then again it also probably wouldn’t hurt to do this.
As we come to a close, there are certain signs you should look for to see if you’re low on sodium or need more sodium intake:
- Cold extremities
- Dark urine
- Decreased skin turgor (the skin remains “tented” when it is pinched)
- Decreased urine output
- Dry axilla (armpit or underarm) and tongue
- Poor capillary refill (takes longer than 2 seconds for the nail bed to return from white to pink after being pinched)
- Postural tachycardia/dizziness/hypotension (occurs after rising from a seated or
- reclined position)
- Salt cravings
- Syncope (loss of consciousness from low blood pressure)
- Thirst
Conclusion
I’m hoping this has provided you with a little more clarity on that beautiful, food-enhancing crystal we call salt. If you’re a healthy, active individual, then you shouldn’t shy away from it – It has performance enhancing effects in exercise, keeps your heart rate normal, takes stress off the adrenals and kidneys, and is one factor keeping insulin levels normal.
References
Andrew Mente et al. Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies. The Lancet. ARTICLES| VOLUME 388, ISSUE 10043, P465-475, JULY 30, 2016. DOI:https://doi.org/10.1016/S0140-6736(16)30467-6
Graudal NA, Hubeck‐Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database of Systematic Reviews 2017, Issue 4. Art. No.: CD004022. DOI: 10.1002/14651858.CD004022.pub4. Accessed 09 February 2022.
Niels Graudal et al. Conflicting Evidence on Health Effects Associated with Salt Reduction Calls for a Redesign of the Salt Dietary Guidelines. Progress in Cardiovascular Diseases. Volume 61, Issue 1, May–June 2018, Pages 20-26. https://doi.org/10.1016/j.pcad.2018.04.008
Andrew Mente et al. Sodium Intake and Health: What Should We Recommend Based on the Current Evidence? Nutrients 2021, 13(9), 3232; https://doi.org/10.3390/nu13093232
Esteban Poch et al. Molecular Basis of Salt Sensitivity in Human Hypertension. 1 Nov 2001 https://doi.org/10.1161/hy1101.099479. Hypertension. 2001;38:1204–1209.
Graudal NA, Hubeck-Graudal T, Jürgens G. Reduced Dietary Sodium Intake Increases Heart Rate. A Meta-Analysis of 63 Randomized Controlled Trials Including 72 Study Populations. Front Physiol. 2016 Mar 24;7:111. doi: 10.3389/fphys.2016.00111. PMID: 27047393; PMCID: PMC4805644.
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Jessani N, Jehangir W, Behman D, Yousif A, Spiler IJ. Secondary adrenal insufficiency: an overlooked cause of hyponatremia. J Clin Med Res. 2015 Apr;7(4):286-8. doi: 10.14740/jocmr2041w. Epub 2015 Feb 9. PMID: 25699130; PMCID: PMC4330026.
James DiNicolantonio. The Salt Fix : Why the Experts Got it all Wrong–and How Eating More Might Save Your Life. New York : Harmony Books, [2017].
