I’ve always been skeptical of the argument that sodium (from salt) is bad for you because it raises your blood pressure and increases your risk of cardiovascular disease.
I was a competitive cyclist for a number of years when I was younger, and more recently I’ve gotten into playing competitive squash. Both are sweaty endurance sports.
Guess what happened when I didn’t consume adequate amounts of salt after long, hard training sessions in which I lost plenty of fluid?
I’d feel weak, irritable, and fatigued with the added symptoms of headaches, low blood pressure, and cramps.
When I did consume plenty of salt, these problems went away, and my recovery and performance improved. My food also tasted a lot better…
So it seemed clear to me that sodium was vital for someone like myself that was active and training a lot.
But what about people who weren’t training as much or losing as much fluid? Did they need to be consuming a reasonable amount of salt also?
I didn’t think about this question much for several years. And then I started learning about low carb diets.
I started following a mostly (i.e. 80% of the time) ketogenic diet a couple of years ago to treat ongoing autoimmune issues (mainly joint inflammation and mild skin conditions like psoriasis), suboptimal cognitive function (lack of focus and mental clarity) and mental health issues (mild depression). I fell down a rabbit-hole of learning about metabolism, energy systems, mitochondrial health, and the impact of sugars (including alcohol and fructose) on human health. I read books and watched conference presentations by people like Paul Saladino, Jason Fung, Shawn Baker, Paul Mason, Robert Lustig, Rick Johnson, Tim Noakes, Jeff Volek, and Stephen Phinney. YouTube videos from Low Carb Down Under (a great YouTube channel with talks that explore these ideas) were regularly playing in the background while I worked from home.
In short, going low-carb helped tremendously. All of the above health issues I had been dealing with (for as long as I can remember) went away. I was no longer dealing with chronic joint pain and stiffness. I felt happy, calm, and my mind was clear. My diet mostly consisted of steak, eggs, full-fat yogurt, and butter, which are foods I loved eating. I didn’t ‘bonk’ during exercise and could pretty much train for as long as I wanted. It was like a dream come true!
But from time to time, I’d experience issues. Those familiar symptoms of low sodium and electrolyte imbalances would come back - something that is known as the ‘keto flu’, and I didn’t need to be training hard for these symptoms to reappear. I started to learn that consuming plenty of sodium was vital in this context too (of someone following a low-carb diet), and once I began to supplement it, along with plenty of magnesium, I’d feel great again.
Interestingly, throughout this whole process, I experienced the opposite of what the traditional ‘salt is bad for you’ perspective was telling me - that increased salt intake would lead to high blood pressure and cardiovascular problems. My blood pressure was more normal than it had ever been. My resting heart rate and heart rate variability were consistently good, even when I was training a lot, and I’d recover from hard training sessions easily without having sore joints. All of my blood markers for inflammation, metabolic health and lipids were normal.
So, what was going on? Was I an exception to the rule, or did the ‘salt is bad for you’ argument have a lot more contextual nuance to it? Why did many studies correlate increased salt intake in the diet with poor cardiovascular and other health outcomes, when I had been experiencing the opposite?
After pondering those questions, it was time to dive into the research.
This article contains some of what I learned. In this article, we will explore the role of sodium in the human body and the benefits of sodium. We’ll then explore the history of how recommendations to lower salt intake came into being, and we’ll go through the research that supports the (potentially misleading) idea that sodium causes high blood pressure. Finally, we’ll discuss why a low sodium diet may cause more harm than good (for most people).
Let’s dive in.
The Role of Sodium
Salt is composed of two essential minerals: sodium and chloride.
Sodium helps with conducting electrical impulses (important for muscle contraction, cognitive function, and nerve impulse transmission) as well as the movement of amino acids, vitamins, neurotransmitters, and other compounds in and out of cells (by establishing osmotic gradients between the intracellular and extracellular fluid).
Chloride is important for the maintenance of stomach acidity so we can properly digest food, for immune cell function, and for a healthy inflammatory response during infection.
We’ve written before about the essential role of sodium in the human body:
Sodium isn’t an optional mineral. You need it to function properly, and if you don’t have enough of it, your body will do all sorts of things to conserve the precious sodium and other minerals that you do have. It does this by upregulating certain hormones that make you pee out less sodium in your urine. Consuming too much salt will do the opposite. It turns out that the ability of our bodies to regulate blood sodium concentrations is quite advanced…
Sodium deficiency (known has hyponatremia) presents with a bunch of symptoms that basically makes you feel like you want to crawl up into a ball in the fetal position and lie down on the floor. Symptoms include fatigue, headaches and migraines, brain fog, and impaired sympathetic cardiovascular adjustments to stress.
We have also explained here how the need to obtain sodium is hardwired into our psychobiology. Basically, animals experiencing a sodium deficiency will experience their pleasure and reward systems being altered such that they seek out sodium and consume it in excess in an attempt to ‘future-proof’ against further possible depletions. Unresolved sodium appetite can also induce behavioral characteristics that are “qualitatively similar to psychological depression as well as induce plasticity in brain regions implicated in motivation, reward, and drug sensitization and withdrawal”.
Our bodies have quite an advanced system of maintaining sodium homeostasis, primarily through the hormones aldosterone and vasopressin (also known as antidiuretic-hormone). These systems allow healthy people to generally be able to maintain normal blood pressure in response to extremes of sodium intake (i.e. both very high and very low).
Benefits of Sodium
About 50-70% of our bodies are made up of water, and about a third of that water comprises the extracellular fluid between our cells. The main electrolyte in this fluid is sodium. Moreover, the amount of extracellular fluid you have is proportional to the amount of sodium in your body. This means that when your sodium gets too low, your extracellular fluid volume will drop along with it.
A fall in extracellular fluid volume can cause a bunch of problems, especially for athletes trying to perform. Your body will find it much more difficult to thermoregulate, as it is harder for your heart to pump blood to your skin to cool you down. It also becomes more difficult to pump blood to your muscles, which can lead to symptoms of fatigue, reduced explosiveness and work capacity, and cramps.
Consuming water alone is not sufficient to maintain your extracellular fluid volume under conditions of fluid loss (i.e. profuse sweating, like exercising in the heat), as it will cause your blood sodium concentration to drop. This leads to a condition called hyponatremia, which leads to a very significant decrease in performance and wellbeing, and has even been fatal in certain endurance events (like triathlons). Tim Noakes’ book Waterlogged is instructive on this subject (of preventing hyponatremia in endurance athletes).
An Example of Sodium in Practice
One interesting example of the role of sodium in maintaining hydration and performance came from research done by NASA at the end of the 20th century.
During spaceflight, astronauts are subject to a prolonged state of microgravity which induces a variety of physiological adaptations including bone loss, muscle atrophy, fluid shifts, and decreased plasma volume. NASA astronauts were experiencing as much as a 3-4% deficit in total body fluid levels during typical missions, causing symptoms such as lightheadedness, fatigue, and even blackouts.
In response, NASA conducted a study testing hydration drinks containing different carbohydrate and electrolyte mixtures. They found that fluid formulation containing sodium compounds near isotonic concentrations (i.e. the same as blood plasma) was more effective than dilute mixtures at restoring and increasing plasma volume. Note that an isotonic saline solution will contain about 9g of salt (equal to 3.5g of sodium) in 1L of water (which is quite a lot of salt).
To combat this, NASA tested lots of drinks containing different carbohydrates and electrolyte mixtures and found that the more sodium you put in a drink, the more effective the drink would retain in the body and bloodstream, thus correcting dehydration.
Pre-loading Sodium
It turns out that not only can we consume sodium to restore blood plasma to normal, we can also ‘pre-load’ with concentrated sodium solutions before engaging in physical activity to get the benefits of an elevated level of blood plasma.
Typical sports drinks, which contain ~200-500mg of sodium per litre, are useless for this. They are far too dilute to make any difference. If anything, they will make the problem worse, because they will likely dilute your blood sodium concentration.
On the other hand, consuming a 0.9% saline solution (i.e. 3.5g of sodium in 1L of water) can be distasteful because of how salty it is, and it can also cause digestive distress in some people.
Dr. James Dinicolantonio, in his book ‘Win: Achieving Peak Athletic Performance…’, explains that, based on the current literature, at least ~1900mg of sodium per litre is necessary to increase blood volume, which higher amounts of 3700-4300mg per litre are optimal to consume prior to vigorous exercise or competition. These solutions have been shown to be able to boost blood volume by as much as 8-10%, while vigorous exercise can cause a drop in blood volume of around 8-10% in just 5-15 minutes. Drinking these high-salt solutions prior to competition can eliminate or reduce the plasma volume drop that occurs with exercise, which can improve athletic performance.
Our recommendations for sodium pre-loading are as follows:
- Drink a mixture of ~1500mg of sodium in 500ml of water the night before training/competition.
- Make a mixture of 3500mg of sodium in 1L of water; drink at least 500ml about 90 minutes before competition, and aim to finish drinking at least 45 minutes before the start of competition, so your body can adjust in the interim.
- Whatever you do, do not drink water in excess prior to competition, as this will dilute your blood sodium levels, and possibly lead to decreased performance.
We’ll go into further detail around sodium pre-loading strategies, and how much sodium you should be consuming under different conditions, in a further article.
Now that we’ve covered the benefits of sodium, let’s look at the research behind the recommendations for us to lower our salt intake.
Recommendations for Lower Sodium
The history of research between sodium intake and hypertension is controversial. The earliest study was from as far back as 1904, and was refuted three years after publication.
This ambiguity continued for several decades, until a physician named Wallace Kempner more successfully established a link between sodium and blood pressure by treating hypertensive patients with a low-salt diet.
One of the more impactful pieces of research following this period, which was able to influence modern recommendations around salt intake, came from Lewis Dahl in the 1960s and 70s.
Dahl bred two strains of rats (now known as ‘Dahl rats’) that differed in their susceptibility to developing salt-induced hypertension, proving that high blood pressure from a high-salt diet is somewhat influenced by genetics.
Dahl also performed population studies in which he observed that hypertension was common in societies with higher-than-average salt intakes.
These findings were used to establish the US Dietary Guidelines in 1980 to “avoid too much sodium”.
Today, several health organisations recommend to lower sodium intake to a level below 2.3g/day on the premise that lowering of sodium intake will lower blood pressure and, in turn, will result in a lower incidence of cardiovascular disease. This level of salt intake has not been achieved by any modern population in the world, as most people in developed societies consume around 3-5g of dietary sodium per day. Policy recommendations from the American Heart Association are even more aggressive by advocating for less than 1.5g/day, a level that is not substantiated by strong evidence and that can cause potential harm.
Note that (as quoted in this paper), “these guidelines were developed without effective interventions to achieve long term sodium intakes at low levels in free-living individuals and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with average levels of intake)”.
Other research contends that a range of 3-5g, which is what people actually consume, is actually optimal. It also argues that sodium intake is more of a J-curve, where values too high or too low can cause increased risk of adverse health outcomes:
Conceptual diagram of health risk by sodium intake levels based on the current evidence. The lowest risk range (i.e., “sweet spot”) for sodium intake is at ~3 to 5 g/day. Image credit: Sodium Intake and Health: What Should We Recommend Based on the Current Evidence? - PMC (nih.gov)
Moreover, there’s a reason that this level may be optimal. Our bodies tightly regulate our salt intake through neural and hormonal mechanisms.
Research by David McCarron from UC Davis has shown that sodium intake of 2.6-4.8g per day is predictable, constant for more than 50 years and across at least 45 countries. This consistency is defined by the body’s physiology and biological need for sodium, not by government policies or the food supply.
McCarron is critical of sodium recommendations in the US:
"Fortunately, human physiology is not easily deluded. Whether our policy leaders can accept that reality or whether they choose to continue defending this fallacy, it is apparent that sodium intake in free-living individuals will not be modified by any attempt of the government. That has been the case for at least the past 50 years and will likely be well into the future."
There is also the fact that, internationally, the countries with the highest average life expectancy are many of those with the highest average sodium intake.
So it seems clear that there is some controversy between what the research shows and policy recommendations for sodium intake.
But is the research on sodium and adverse health outcomes all that insightful, anyway? In the next section, we’ll explore some of the factors that complicate our ability to draw conclusions from the data.
Challenges in Sodium Research
The first issue is that over time, the amount of salt within foods has been increasing as a result of the higher proportion of processed foods (which are higher in sodium) being consumed. As a result, higher sodium intake may become confounded with higher processed food intake. This means that correlations between sodium and adverse health outcomes may really just be correlations between processed food intake and poor health.
The second issue in identifying the optimal sodium intake is the lack of a valid and reliable method to objectively quantify sodium intake in a large number of people.
The first option is to use surveys or questionnaires. These are simple and easy to administer, but unreliable and inaccurate.
The second option is to use urine samples. The gold standard of assessing dietary sodium intake is to use multiple 24-h urine collections. While very accurate, this approach is time intensive, expensive and relies on participants to comply with collection requests. Studies have shown that most of the time they don’t. For example, in a study by the U.S. Centers for Disease Control in 2018, 30% of individuals didn’t provide even a single complete collection of urine.
Other studies have attempted to correct for this issue by instead using single fasting urine samples and then using this data in a formula to estimate mean sodium intake. The three main methods are known as the Kawasaki, INTERSALT, and Tanaka methods. They aren’t appropriate for use in clinical settings but in large population studies they work reasonably well (although they aren’t perfect). We won’t get into the nitty gritty methodological details, but it’s worth being aware of them.
Note that most sodium studies are interested in looking at the relationship between sodium intake and cardiovascular related events. The issue is that these events are quite rare in healthy populations (about 1% annually). This means that you need a very large sample size (several tens or even hundreds of thousands of individuals), and they need to be enrolled and followed for a decade or more to detect differences in risk for clinical events (e.g., a stroke or heart attack).
These issues are not unique to sodium - they affect all nutrition studies. Lastly, research like this can only really be done as observational studies, which are much lower in quality (i.e. prone to bias, spurious correlations, placebo effects, etc.) than randomized control trials (which are the gold standard of research methodologies). Some consider RCTs to be the only valid design to evaluate therapeutic efficacy.
We’ll write more about the pros and cons of different research methods in nutrition science in another article. Now that we are aware of the challenges of observational research, let’s look at the evidence on sodium intake and health outcomes, starting with blood pressure.
Sodium and Blood Pressure:
The consensus in the scientific literature is that there is reasonable and convincing epidemiological evidence of a positive relationship between sodium intake and blood pressure.
Physiologically, this makes sense: a large increase in sodium will increase your blood plasma, which can increase your blood pressure.
However, when you get into the weeds of the research, you find that the evidence isn’t all that convincing, and there certainly isn’t enough evidence to be telling people to lower their salt intake below 2.3g per day.
The research can be split into randomized control trials (RCTs) and observational studies.
Most of the RCTs are short term (95% have less than 6 months duration) with relatively few participants. Where they are able to show that sodium intake supposedly increases blood pressure, the strength of the relationship deteriorates with longer follow-up durations. This is because it’s nearly impossible to achieve and sustain a low sodium intake (<2.3 g/day), even with intense dietary counseling.
While some of the RCTs have been somewhat influential on recommendations to lower sodium intake (such as the DASH-Sodium Trial), the observational research is arguably more relevant and impactful, so we’ll focus our attention there.
The INTERSALT Study (1997)
The first study to talk about is the INTERSALT study.
Published in 1988, this was the first large international study on sodium and blood pressure. It included just over 10,000 people aged 20-50 from 52 collection centres in 39 countries and measured sodium using 24-hr urine collection.
They found that:
- Body mass index and heavy alcohol intake had strong, significant independent relations with blood pressure in individual subjects
- After adjusting for body mass index, alcohol consumption, and potassium excretion, they found a weak positive association between sodium intake and blood pressure in 33 of 53 centres (which was statistically significant in eight). There were negative correlations in 19 centres.
Basically, the evidence of the study was not very convincing when you look at results from individual centres. But if you were to pool all the centres together and look at cross-centre results, they were able to establish statistically significant positive correlations between sodium intake and blood pressure.
The problem is that these results weren’t robust. They didn’t hold up once outliers and other factors were accounted for.
Firstly, four specific centres had very low sodium intake and correspondingly low median blood pressure. When these were removed as outliers, the pooled statistical significance of the study decreased materially. The significance of results also decreased once alcohol intake and body mass intake were controlled for.
You can see this in the series of charts below, taken directly from the study. Notice the change in the slope of the line of best fit through the data:
Secondly, the authors admitted that certain factors might affect blood pressure across populations (e.g. physical activity, climate, cultural factors), but these wouldn’t be relevant when looking at individual centres.
As an example, one of the very low sodium groups were the Yanomamo (native to Brazil). They had a “low body mass index and the almost nonexistence of obesity, no alcohol ingestion, low ingestion of saturated fat, high ingestion of fibers, relatively high physical activity, and the several cultural consequences of living in an isolated community without the psychosocial stress of civilization and without a monetary system or dependence on a job”.
Basically, there are a lot of other factors relevant to them having low blood pressure than sodium intake!
What’s more, while this group have a very low incidence of cardiovascular disease, they are described as having small stature and a low life expectancy ranging between 29 and 46 years.
Another large study (with just over 7000 participants) in Scotland published around the same time in 1988 also found no association between sodium intake and BP.
Take a look at this quote from the abstract:
“...the most likely explanation of these results is that the relation between sodium and blood pressure in the population is weak and that potassium and alcohol are of greater importance.”
The PURE Study (2014)
The second piece of research to talk about is the PURE study from 2014.
Compared to INTERSALT the study:
- Was much larger (included more than 102,000 adults from 18 countries);
- Included persons over 59 years of age; and
- Had a substantially larger group of participants from China (42% vs. 6% in INTERSALT) where the average estimated sodium excretion was higher than other countries.
The PURE study did find a positive relationship between sodium intake and blood pressure, but this relationship was only strong at high levels of intake above 5g a day and when the older age cohort was included in the analysis. Removing these factors led to a weak relationship (similar to INTERSALT).
There are some other issues with this study. First, the authors noted that it was the combination of high sodium and low potassium intake that had a strong relationship with high blood pressure.
Basically, if you consume a lot of sodium with very little potassium (which a standard diet full of processed food will give you), this can lead to high blood pressure.
We’ll write a lot more about the research on potassium in future articles.
Secondly, the method for measuring sodium excretion wasn’t exact. The authors actually noted that there was a 10% overestimation of 24-hour sodium excretion with the method they used (i.e. taking a fasting morning urine sample and using a formula to estimate 24-hour urinary excretion).
The Framington Study (2017):
Lastly, there is the Framington Study from 2017, which looked at blood pressure in low and high salt groups.
The study accounted for the confounding factors of age, sex, education, height, physical activity, cigarette smoking, and alcohol intake in their regression analysis. The authors mention that while they expected dietary sodium intake to be positively associated with high blood pressure, the opposite was found, with the high salt group having the lowest blood pressure. Low potassium intake correlated significantly with high blood pressure, as did low calcium and low magnesium.
As a result, they concluded that their data “provides no support for lowering sodium intakes among healthy adults to below 2.3 g/day as recommended”, and that low intake of other relevant minerals is just as important as high sodium intake when it comes to blood pressure.
Sodium and Cardiovascular Health
Now let’s briefly look at the research on sodium intake and cardiovascular events.
A meta-analysis of the totality of data in 2014 showed that both extremes of sodium consumption (both above 5 g/day and below 2.7 g/day) were associated with an increased risk of adverse events.
This confirms what we were talking about before - that the sweet spot is something like 3-5g of sodium per day (depending on your activity level and fluid intake), and significantly more or significantly less than this is not optimal. The PURE Study mentioned above also found that the lowest risk of events were between 3 and 5 g per day.
The consensus of the literature was put simply in this literature review from 2021:
“Collectively, there is no robust evidence that lowering sodium below an intake of 3 g/day is likely to lead to a lowering of cardiovascular disease or death compared to a sodium intake of 3 to 5 g/day. There are, however, concerns that sodium intake below 3 g/day may be associated with a higher risk of death compared to intakes between 3 and 5 g/day.”
Is Salt Bad for You? Key Takeaways
Putting all this together, we think that the evidence in support of the idea that sodium is bad for you is not convincing.
The research is not consistent, the evidence is limited, and there are way too many extraneous factors that can bias results (which are difficult to control for in observational studies).
We also don’t think that following a low sodium diet is a good idea based on our own experience (being athletes ourselves and talking to customers), especially if you are physically active. Otherwise, you’re setting yourself up for hyponatremia and the range of unpleasant symptoms that come with it (like cramps, fatigue, headaches, and poor cognition).
If you do have high blood pressure, we don’t recommend you cut the sodium out of your diet, but that you increase your intake of the other electrolytes (magnesium, potassium, and calcium), which have been shown to lower blood pressure (see the Framington Study above), and to reduce your intake of sugar, which is inflammatory.
The other important thing to keep in mind is that nutrition is personal.
If I’m following a low carb diet, and you’re not, the fact is that I’m going to need more salt and other minerals, and my blood pressure is going to respond differently to yours. Or if I were a triathlete training in the hot sun for hours everyday, I’d need to dramatically up my electrolyte intake to replace electrolytes lost in sweat and tolerate the training load.
So even if the data were convincing, it wouldn’t be all that relevant!
So if you’re following a low carb diet, an athlete, or someone who does intermittent fasting (for a while I was doing all three…), we recommend you consider supplementing with additional electrolytes.
The point of this article was to show you that yes, sodium is good for you and no, you don’t need to be worried about the impact of that extra salt on your blood pressure.
I noticed a huge difference in my energy, fatigue, cognition, and recovery when I upped my electrolyte intake. I stopped feeling dizzy, getting a raspy voice, and having headaches. Individual needs will vary but I’d aim to get something like 4-6g of sodium a day, and adjust from there.
You can make your own electrolyte mix at home (we’ve written about this here). A glass of water with half a teaspoon of salt and lime juice also does the trick, but make sure that you’re getting plenty of the other electrolytes from your diet (like calcium, potassium, and magnesium) if you go down this route.
Or, if you prefer the added convenience of a formulated hydration mix, you can check out our products.
Thanks for reading!