Two papers carry most of the weight in this debate. The 2021 JACC crossover study by Garland, Raj and colleagues compared 10 mEq and 300 mEq of sodium per day for six days each in 14 women with POTS and 13 healthy controls, and reported that the high sodium diet increased total blood volume and plasma volume, lowered standing plasma norepinephrine, and reduced upright heart rate and the rise in heart rate on standing. The same paper reported that upright heart rate, the heart rate rise and upright norepinephrine all remained higher in the POTS group than in the healthy controls even on the high sodium diet, so it describes improvement rather than normalisation. The 2022 Autonomic Neuroscience review by Stock and colleagues then reported that while short term benefit has support, "randomized studies assessing the efficacy and long-term side effects of these recommendations are lacking", and its authors suggested that modest rather than robust increases in salt intake may be enough.
Short term, in a small crossover trial, the measurements moved. Long term, the evidence has not been generated. What that means for you is a conversation with the clinician who manages your care.
If you are looking for the primer on what POTS is, that lives on our page about electrolytes for POTS. This article is only about what the research says.
Why these two papers keep coming up
Search for evidence on sodium and POTS and you will find the same two citations behind almost everything, usually paraphrased into something more confident than either paper actually says. One is a controlled feeding study. The other is a review that looked for long term trials and reported what it did not find. They answer different questions, and reading them together is what makes the picture honest.
Everything below describes what the papers reported. It is not guidance, and it is not a recommendation from us.
Study one: the 2021 JACC crossover trial
Citation: Garland EM, Raj SR, et al. "Effect of High Dietary Sodium Intake in Patients with Postural Tachycardia Syndrome." Journal of the American College of Cardiology, vol. 77, no. 17, 4 May 2021, pp. 2174 to 2184. doi:10.1016/j.jacc.2021.03.005. PMID 33926653.
Why it was done. The paper is unusually blunt about the gap it was filling. Its own background section states that high sodium intake "is recommended for the treatment of postural tachycardia syndrome (POTS) to counteract the hypovolemia and elevated plasma norepinephrine that contribute to excessive orthostatic tachycardia, but evidence of its efficacy is not available." In other words, the advice was already standard practice before anyone had run this trial.
Who was in it. The authors enrolled 14 women with POTS and 13 healthy controls, aged 23 to 49. Fourteen is a small number, and that matters for how far the result generalises.
How it was designed. It was a crossover study, meaning every participant did both diets and acted as their own comparison. Each person spent six days on a low sodium diet of 10 mEq of sodium per day and six days on a high sodium diet of 300 mEq of sodium per day, as stated in the paper by Garland, Raj and colleagues. Participants started with a run-in day: the paper notes they "ate a low-monoamine caffeine-free diet containing 150 mEq sodium on study Day 1." These were controlled research diets, not a plan for anyone to copy, and any change to your own sodium intake belongs with your doctor.
What was measured. Supine and standing heart rate, blood pressure, serum aldosterone, plasma renin activity, blood volume, and plasma norepinephrine and epinephrine.
What it reported
On the high sodium diet compared with the low sodium diet, in the POTS group, the paper reported:
- Reduced upright heart rate and reduced delta heart rate, the rise in heart rate from lying to standing.
- Increased total blood volume and increased plasma volume.
- Decreased standing plasma norepinephrine.
The conclusion as printed reads: "In POTS patients, high dietary sodium intake compared with low dietary sodium intake increases plasma volume, lowers standing plasma norepinephrine, and decreases delta-HR."
What it did not report
This is the part that gets dropped in summaries. Even on the high sodium diet, the POTS group did not look like the healthy controls. The paper reports upright heart rate of 117 beats per minute in POTS versus 85 beats per minute in healthy controls, a delta heart rate of 46 bpm versus 19 bpm, and upright norepinephrine of 753 pg/mL versus 387 pg/mL, all measured on the high sodium diet. The authors describe these as remaining higher in POTS than in the controls despite no difference in measured plasma volume between the groups.
So the fair reading is that the high sodium diet moved the numbers in the direction the authors were testing for, and the POTS group was still measurably different from the control group at the end of it. Improvement, not normalisation.
The limits worth naming
Anyone quoting this study should also be willing to say the following out loud:
- 14 patients is a small sample.
- Six days per arm is a short exposure. It says nothing about a year, or a decade.
- The comparator was 10 mEq of sodium per day, which is a research floor rather than a normal diet, so the contrast between the arms is wide by design.
- The outcomes were physiological measurements. This was not a trial of how people felt or functioned over time.
None of that makes the study weak. It makes it what it is, which is a careful short term mechanistic experiment, and it is a lot better than the nothing that preceded it.
A note on units: mEq, mmol and mg
Research papers on sodium usually work in milliequivalents (mEq) or millimoles (mmol), while food labels work in milligrams. The JACC paper supplies the key itself: "For sodium, potassium and chloride, 1 mEq = 1 mmole." Converting millimoles of sodium into milligrams is then simple arithmetic on sodium's atomic weight, roughly 23 mg per mmol. On that arithmetic, the study's 300 mEq arm works out at about 6,900 mg of sodium per day and the 10 mEq arm at about 230 mg per day. Those milligram figures are our conversion for readability, not numbers the paper prints, and both describe supervised research diets rather than a target for anyone at home. What any intake figure means for you is a question for the clinician who manages your care.
One more unit trap sits on top of that one. Salt and sodium are not the same measure. Salt is roughly 40 percent sodium by weight, so the mass of salt is about two and a half times the mass of the sodium inside it, which is why a source that states an amount of salt reads far higher than a source stating sodium. A great deal of confusion in POTS discussions comes from treating the two as interchangeable, and it gets worse when a source uses the words salt and sodium as if they were synonyms. Our salt to sodium converter handles that conversion if you need it.
Study two: the 2022 Autonomic Neuroscience review
Citation: Stock JM, Chelimsky G, Edwards DG, Farquhar WB. "Dietary sodium and health: how much is too much for those with orthostatic disorders?" Autonomic Neuroscience, vol. 238, 2022, article 102947. doi:10.1016/j.autneu.2022.102947. PMID 35131651.
This one is a review, not a trial. Its job was to look across the literature and ask what is actually known about raising sodium intake in people with orthostatic disorders, including the long term.
What it reported
The central finding is a gap. The authors write: "While there is evidence to support the short-term benefits of increasing NaCl intake in these patients, there are few studies assessing the benefits and side effects of long-term high dietary NaCl." Elsewhere they describe "a paucity of research on the long-term effects of this practice" and state plainly that "randomized studies assessing the efficacy and long-term side effects of these recommendations are lacking."
They also flag a specific unanswered question: "To the best of our knowledge, to date there have not been any published studies that have investigated the effect of sodium supplementation on BPV in patients with orthostatic disorders." BPV there is blood pressure variability.
The review is cautionary in tone rather than promotional. It notes that "high dietary salt can adversely impact multiple target organs, often independent of changes in BP."
The authors' own bottom line
This is the sentence to carry with you, because it is the authors' conclusion rather than anyone's paraphrase of it: "Modest, rather than robust, increases in NaCl intake may be sufficient to alleviate symptoms but also minimize any long-term negative effects."
That paper should not be cited as support for pushing intake as high as possible. Its authors did not say that. Whether a modest increase, a large one, or none at all is right for you is a clinical judgement, and it depends on things a review article cannot know about you.
Why expert consensus is not the same as trial evidence
Most of the numbers circulating about POTS and sodium come from consensus documents, and consensus documents grade their own confidence. It is worth learning to read those grades, because they are printed right next to the advice and almost never quoted alongside it.
- The 2015 Heart Rhythm Society expert consensus statement (Sheldon RS, Grubb BP 2nd, Olshansky B, et al., Heart Rhythm 2015;12(6):e41 to e63) attaches its salt and fluid advice for POTS to a Class IIb, Level of Evidence E rating. Class IIb is the "may be considered" tier, and Level E means expert opinion. The wording in the document is permissive rather than directive, and it is conditioned on tolerance.
- The 2020 Canadian Cardiovascular Society position statement (Raj SR, Guzman JC, Harvey P, et al., Canadian Journal of Cardiology 2020;36(3):357 to 372) grades its salt and water recommendation as a Strong Recommendation based on Low-Quality Evidence. Those two halves are not a contradiction. A guideline group can be confident about what to advise while being clear that the underlying trial base is thin.
Nothing about this means the advice is wrong. Expert consensus is how medicine operates when the trials do not exist yet, and clinicians who treat a lot of POTS patients have real information that no trial has captured. It does mean that anyone telling you high sodium is "proven" for POTS is overstating the published record, and anyone telling you it is baseless is ignoring both the guideline consensus and the 2021 crossover data.
The published figures themselves vary widely between sources and are stated in different units, which is a subject of its own. If you want them laid out with their units and evidence grades intact, read how much sodium doctors recommend for POTS. Raising sodium is also not right for everyone and that decision belongs with a clinician, which is covered in when more sodium is not right for you.
What you can accurately say at an appointment
If you want to bring this into a consultation, these statements are all defensible from the papers above:
- "There is a 2021 JACC crossover trial by Garland and Raj comparing high and low sodium diets in POTS, and it reported increased plasma volume, lower standing norepinephrine and reduced orthostatic tachycardia on the high sodium arm."
- "That same trial reported the POTS group still had higher upright heart rate and norepinephrine than healthy controls on the high sodium diet, so it showed improvement rather than normalisation."
- "It was 14 patients over six days per arm, so it is short term and small."
- "The 2022 Stock review in Autonomic Neuroscience reported that randomised long term evidence on high sodium intake in orthostatic disorders is lacking, and its authors suggested modest rather than robust increases."
- "The guideline figures are graded as expert opinion or low quality evidence by the guideline bodies themselves."
What you should not say, because no published paper supports it, is that high sodium intake is proven to treat POTS, or that it has been shown safe over years.
If your clinician wants the sources rather than the summary, send them to our POTS source list for clinicians, which carries the Garland 2021, Sheldon 2015 and Raj 2020 citations in full. Our broader approach to reading and citing hydration research is set out on the science page.
The honest summary
The mechanism has short term experimental support in a small controlled trial. The long term question has not been answered, and the review authors who looked hardest for that answer recommended restraint rather than maximalism. Both of those things are true at the same time, and holding both is more useful than picking whichever one suits the argument.
You are the person who has to live inside the result. The papers are worth reading in the original, the citations above are complete enough to find them, and the decision about your own intake sits with you and the clinician who knows your history.
Sources
- Garland EM, Raj SR, et al. "Effect of High Dietary Sodium Intake in Patients with Postural Tachycardia Syndrome." Journal of the American College of Cardiology, vol. 77, no. 17, 4 May 2021, pp. 2174 to 2184. doi:10.1016/j.jacc.2021.03.005. PMID 33926653.
- Stock JM, Chelimsky G, Edwards DG, Farquhar WB. "Dietary sodium and health: how much is too much for those with orthostatic disorders?" Autonomic Neuroscience, vol. 238, 2022, article 102947. doi:10.1016/j.autneu.2022.102947. PMID 35131651.
- Sheldon RS, Grubb BP 2nd, Olshansky B, et al. "2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope." Heart Rhythm, vol. 12, no. 6, 2015, pp. e41 to e63. doi:10.1016/j.hrthm.2015.03.029. PMID 25980576.
- Raj SR, Guzman JC, Harvey P, et al. "Canadian Cardiovascular Society Position Statement on Postural Orthostatic Tachycardia Syndrome (POTS) and Related Disorders of Chronic Orthostatic Intolerance." Canadian Journal of Cardiology, vol. 36, no. 3, March 2020, pp. 357 to 372.
- National Institute of Neurological Disorders and Stroke. "Postural Tachycardia Syndrome (POTS)," last reviewed 13 March 2026.
This article describes published research. It is not medical advice, and it is not a recommendation to change your sodium or fluid intake. Talk to the clinician who manages your care before you change anything.
