Effect of High Dietary Sodium Intake in Patients With Postural Tachycardia Syndrome
Open accessAbstract
Background: 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. Objectives: We tested whether a high sodium (HS) diet reduces orthostatic tachycardia (ΔHR) and upright heart rate (HR) compared with low sodium (LS) diet in POTS patients, and secondarily its effect on plasma volume (PV) and plasma norepinephrine. Methods: We enrolled 14 POTS patients and 13 healthy controls (HC), 23–49 years old, in a crossover study with six days of LS (10 mEq sodium/day) or HS (300 mEq sodium/day) diet. We measured supine and standing HR, blood pressure, serum aldosterone, plasma renin activity, blood volume, and plasma norepinephrine and epinephrine. Results: In POTS, HS diet reduced upright HR and ΔHR compared with LS diet. Total blood volume and PV increased, and standing norepinephrine decreased with HS compared with LS diet However, upright HR, ΔHR and upright norepinephrine remained higher in POTS than in HC on HS diet [117 (98–121) beats per minute (bpm), 46 (32–55) bpm, and 753 (498–919) pg/mL in POTS vs. 85 (77–95) bpm, 19 (11–32) bpm, and 387 (312–433) pg/mL in HC], despite no difference in the measured PV. Conclusions: In POTS patients, high dietary sodium intake compared with low dietary sodium intake increases plasma volume, lowers standing plasma norepinephrine, and decreases…
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- Findingown data
On low sodium diet, POTS patients had higher standing plasma norepinephrine than healthy controls.
“Both supine [248 (162–332) vs. 135 (104–225) pg/mL, P=0.030] and standing [959 (736–1161) vs. 520 (391–693) pg/mL, P<0.001] plasma norepinephrine, and orthostatic changes in plasma epinephrine and norepinephrine were greater in POTS than in HC on LS diet.”
Quote in the paperSubstantial claim - Findingown data
During low sodium diet, POTS patients had lower red blood cell volume than expected volumes estimated from sex, height, and weight.
“During the LS diet phase, TBV, PV and RBV in patients with POTS were all significantly less than the expected volumes estimated from the individual’s sex, height and weight.”
Quote in the paperSubstantial claim - Findingown data
On high sodium diet, measured red blood cell volume was significantly lower in POTS patients than healthy controls.
“Measured TBV and RBV, but not PV, were significantly lower in POTS patients than HC during HS diet.”
Quote in the paperNot a substantial claim - Findingown data
On low sodium diet, POTS patients had higher standing plasma epinephrine than healthy controls.
“Standing plasma epinephrine was higher in POTS patients than HC on a LS diet [59 (33–86) vs. 30 (24–46) pg/mL, P=0.030]”
Quote in the paperNot a substantial claim - Findingown data
In healthy controls, high sodium diet decreased supine and standing serum aldosterone compared with low sodium diet.
“Serum aldosterone was also lower on the HS diet than LS diet in HC in both supine and standing postures.”
Quote in the paperNot a substantial claim
- Findingown data
In POTS patients, a high sodium diet did not change supine, upright, or orthostatic change in systolic or diastolic blood pressure compared with a low sodium diet.
“Neither supine, upright, nor orthostatic change in systolic or diastolic BP differed between patients on HS vs. LS diets.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, high sodium diet decreased supine heart rate compared with low sodium diet.
“patients with POTS experienced decreases in ΔHR, supine and upright HR, and standing plasma norepinephrine following a short-term period of dietary sodium intake of 300 mEq/day compared with a period of 10 mEq sodium/day.”
Quote in the paperSubstantial claim - Findingown data
In healthy controls, high sodium diet did not change red blood cell volume deviation compared with low sodium diet.
“with no change in the RBV deviation between diets.”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, there was a non-significant trend for a lower symptom burden score on high sodium diet than low sodium diet.
“There was a non-significant trend for a lower symptom burden score in POTS on HS diet than LS diet [16 (10–27) vs. 33 (24–41) au, P=0.109].”
Quote in the paperNot a substantial claim - Findingown data
On low sodium diet, measured total blood volume was significantly lower in POTS patients than healthy controls.
“Measured TBV and PV were significantly lower in POTS patients than HC during LS diet, while differences in measured RBV did not reach significance (P=0.060).”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet (300 mEq/day for six days) reduced orthostatic tachycardia (ΔHR) compared with a low sodium diet (10 mEq/day).
“Compared with LS diet in POTS patients, HS diet was associated with a smaller ΔHR [46 (32–55) bpm on HS vs. 60 (55–64) bpm on LS, P=0.001; Figure 2].”
- Also stated in: § Results: · plain
“In POTS, HS diet reduced upright HR and ΔHR compared with LS diet.”
- Also stated in: § Conclusions · plain
“patients with POTS experienced decreases in ΔHR, supine and upright HR, and standing plasma norepinephrine following a short-term period of dietary sodium intake of 300 mEq/day compared with a period of 10 mEq sodium/day.”
Quote in the paperSubstantial claim - Also stated in: § Results: · plain
- Findingown data
In POTS patients, high sodium diet did not change red blood cell volume deviation compared with low sodium diet.
“as the RBV deviation remained similar during both diets.”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet reduced upright heart rate compared with a low sodium diet.
“These patients also had lower upright HRs on HS diets than on LS diets.”
- Also stated in: § Results: · plain
“In POTS, HS diet reduced upright HR and ΔHR compared with LS diet.”
- Also stated in: § Conclusions · plain
“patients with POTS experienced decreases in ΔHR, supine and upright HR, and standing plasma norepinephrine following a short-term period of dietary sodium intake of 300 mEq/day compared with a period of 10 mEq sodium/day.”
Quote in the paperSubstantial claim - Also stated in: § Results: · plain
- Findingown data
On high sodium diet, POTS patients were more symptomatic than healthy controls.
“Patients with POTS were more symptomatic during the HS diet compared to HC.”
Quote in the paperSubstantial claim - Findingown data
In healthy controls, high sodium diet did not change supine, upright, or orthostatic change in systolic and diastolic blood pressure compared with low sodium diet.
“Nor did supine, upright or Δsystolic and diastolic BPs differ between LS and HS diets for the control population.”
Quote in the paperNot a substantial claim - Findingown data
During low sodium diet, POTS patients had lower plasma volume than expected volumes estimated from sex, height, and weight.
“During the LS diet phase, TBV, PV and RBV in patients with POTS were all significantly less than the expected volumes estimated from the individual’s sex, height and weight.”
Quote in the paperSubstantial claim - Findingown data
In healthy controls, high sodium diet decreased supine plasma renin activity compared with low sodium diet.
“Supine PRA in HC was lower with a HS diet than a LS diet [0.3 (0.1–1.5) vs. 2.7 (1.5–5.0) ng/mL/hr, P=0.029]”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet decreased standing plasma renin activity compared with a low sodium diet.
“as was standing PRA [2.9 (1.5–5.0) vs. 25 (11–28) ng/mL/hr, P=0.002]”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, POTS patients had lower upright and Δ diastolic blood pressure than healthy controls.
“On a LS diet, POTS patients had a greater ΔHR and upright HR and lower upright and Δdiastolic BP than HC.”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet increased total blood volume compared with a low sodium diet.
“Total blood volume and PV increased, and standing norepinephrine decreased with HS compared with LS diet”
- Also stated in: § Comparison between HS and LS diets response in POTS · plain
“The deficit in TBV was reduced with HS.”
Quote in the paperSubstantial claim - Also stated in: § Comparison between HS and LS diets response in POTS · plain
- Findingown data
In healthy controls, there was a non-significant trend for an increase in total blood volume deviation with high sodium diet compared with low sodium diet.
“There was a non-significant trend for an increase in TBV deviation with HS diet compared with LS diet [8.3 (−1.3–29) vs. 3.7 (−6.6–11)%, P=0.064].”
Quote in the paperNot a substantial claim - Findingown data
In healthy controls, high sodium diet attenuated the orthostatic increase in aldosterone compared with low sodium diet.
“The orthostatic increase in aldosterone was significantly attenuated by HS vs. LS diet”
Quote in the paperNot a substantial claim - Findingown data
On high sodium diet, POTS patients had greater orthostatic tachycardia (ΔHR) than healthy controls.
“On a HS diet, POTS patients had a greater upright HR and ΔHR than HC, but other HR and BP parameters were not different between groups.”
Quote in the paperSubstantial claim - Findingown data
In healthy controls, the rise in plasma renin activity with standing did not differ between high and low sodium diets.
“but PRA’s rise was not different between diets.”
Quote in the paperNot a substantial claim - Findingown data
On low sodium diet, differences in measured red blood cell volume between POTS patients and healthy controls did not reach significance.
“Measured TBV and PV were significantly lower in POTS patients than HC during LS diet, while differences in measured RBV did not reach significance (P=0.060).”
Quote in the paperNot a substantial claim - Findingown data
In healthy controls, high sodium diet increased plasma volume deviation compared with low sodium diet.
“This was based almost entirely on an increase in PV deviation with the HS diet [15(1.8–38) vs. 5.6 (−2.0–14.9)% P=0.002]”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet reduced the change in plasma norepinephrine with standing (Δnorepinephrine) compared with a low sodium diet.
“and Δnorepinephrine during HS was less than during LS.”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, percent deviations in total blood volume, plasma volume, and red blood cell volume were greater in POTS patients than healthy controls.
“Percent deviations in TBV, PV and RBV were greater in patients with POTS than HC.”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, POTS patients had greater orthostatic changes in plasma epinephrine and norepinephrine than healthy controls.
“Both supine [248 (162–332) vs. 135 (104–225) pg/mL, P=0.030] and standing [959 (736–1161) vs. 520 (391–693) pg/mL, P<0.001] plasma norepinephrine, and orthostatic changes in plasma epinephrine and norepinephrine were greater in POTS than in HC on LS diet.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet decreased standing serum aldosterone compared with a low sodium diet.
“Serum aldosterone was also lower on the HS diet than LS diet in POTS patients in both supine and standing postures and increased less with standing during the HS diet.”
Quote in the paperSubstantial claim - Findingown data
In healthy controls, high sodium diet decreased standing plasma renin activity compared with low sodium diet.
“as was standing PRA [1.0 (0.8–1.9) vs. 7.3 (3.3–9.3) ng/mL/hr, P=0.008].”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, individual symptom scores for mental confusion, palpitations, lightheadedness, and headache trended toward lower on high sodium diet than low sodium diet.
“those for mental confusion [2 (0–3) vs. 5 (0–7) au, P=0.062], palpitations [2 (1–5) vs. 6 (3–8) au, P=0.125], lightheadedness [3 (0–5) vs. 6 (3–7) au, P=0.125] and headache [0 (0–2) vs. 4 (0–6) au, P=0.125] trended toward a lower score on HS diet”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, measured plasma volume was significantly lower in POTS patients than healthy controls.
“Measured TBV and PV were significantly lower in POTS patients than HC during LS diet, while differences in measured RBV did not reach significance (P=0.060).”
Quote in the paperSubstantial claim - Findingown data
In POTS patients on high sodium diet for five full days, orthostatic tachycardia (ΔHR) still met the POTS criterion of ≥30 bpm.
“However, patients on HS for five full days still met the criteria for POTS of ΔHR≥ 30 bpm”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet decreased supine plasma epinephrine compared with a low sodium diet.
“Supine plasma epinephrine was lower with HS diet than LS diet [11 (5.7–2.0) vs. 21 (12–31) pg/mL, P=0.009]”
Quote in the paperNot a substantial claim - Findingown data
On high sodium diet, measured total blood volume was significantly lower in POTS patients than healthy controls.
“Measured TBV and RBV, but not PV, were significantly lower in POTS patients than HC during HS diet.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet decreased supine serum aldosterone compared with a low sodium diet.
“Serum aldosterone was also lower on the HS diet than LS diet in POTS patients in both supine and standing postures and increased less with standing during the HS diet.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet reduced the increase in serum aldosterone with standing compared with a low sodium diet.
“Serum aldosterone was also lower on the HS diet than LS diet in POTS patients in both supine and standing postures and increased less with standing during the HS diet.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet decreased standing plasma norepinephrine compared with a low sodium diet.
“standing plasma norepinephrine was lower on HS than on LS diet [753 (498–919) vs. 959 (736–1161) pg/mL, P=0.017; Figure 3]”
- Also stated in: § Results: · plain
“Total blood volume and PV increased, and standing norepinephrine decreased with HS compared with LS diet”
- Also stated in: § Conclusions · plain
“patients with POTS experienced decreases in ΔHR, supine and upright HR, and standing plasma norepinephrine following a short-term period of dietary sodium intake of 300 mEq/day compared with a period of 10 mEq sodium/day.”
Quote in the paperSubstantial claim - Also stated in: § Results: · plain
- Findingown data
In POTS patients, a high sodium diet reduced the increase in plasma renin activity with standing compared with a low sodium diet.
“as was standing PRA [2.9 (1.5–5.0) vs. 25 (11–28) ng/mL/hr, P=0.002] and the increase in PRA with standing.”
Quote in the paperSubstantial claim - Findingown data
On high sodium diet, POTS patients had greater upright heart rate than healthy controls.
“On a HS diet, POTS patients had a greater upright HR and ΔHR than HC, but other HR and BP parameters were not different between groups.”
Quote in the paperSubstantial claim - Findingown data
In POTS patients, a high sodium diet did not change supine plasma norepinephrine compared with a low sodium diet.
“Although supine plasma norepinephrine in POTS patients did not differ between HS and LS diets”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet decreased supine plasma renin activity compared with a low sodium diet.
“Supine PRA was lower with HS diet than LS diet in POTS patients [0.7 (0.2–1.6) vs. 4.1 (0.9–4.7) ng/mL/hr, P=0.039]”
Quote in the paperSubstantial claim - Findingown data
On high sodium diet, other catecholamine parameters did not differ between POTS patients and healthy controls.
“During the HS phase of the study, standing plasma norepinephrine and Δnorepinephrine were significantly higher for POTS patients than HC, but other cateholamine parameters were not different between POTS and HC.”
Quote in the paperNot a substantial claim - Findingown data
On high sodium diet, measured plasma volume was not significantly lower in POTS patients than healthy controls.
“Measured TBV and RBV, but not PV, were significantly lower in POTS patients than HC during HS diet.”
Quote in the paperNot a substantial claim - Findingown data
On high sodium diet, Δnorepinephrine was significantly higher in POTS patients than healthy controls.
“During the HS phase of the study, standing plasma norepinephrine and Δnorepinephrine were significantly higher for POTS patients than HC, but other cateholamine parameters were not different between POTS and HC.”
Quote in the paperNot a substantial claim - Findingown data
On high sodium diet, other heart rate and blood pressure parameters did not differ between POTS patients and healthy controls.
“On a HS diet, POTS patients had a greater upright HR and ΔHR than HC, but other HR and BP parameters were not different between groups.”
Quote in the paperNot a substantial claim - Findingown data
During low sodium diet, POTS patients had lower total blood volume than expected volumes estimated from sex, height, and weight.
“During the LS diet phase, TBV, PV and RBV in patients with POTS were all significantly less than the expected volumes estimated from the individual’s sex, height and weight.”
Quote in the paperSubstantial claim - Findingown data
On high sodium diet, standing plasma norepinephrine was significantly higher in POTS patients than healthy controls.
“During the HS phase of the study, standing plasma norepinephrine and Δnorepinephrine were significantly higher for POTS patients than HC, but other cateholamine parameters were not different between POTS and HC.”
Quote in the paperNot a substantial claim - Findingown data
In healthy controls, high sodium diet decreased supine, standing, and Δ plasma norepinephrine compared with low sodium diet.
“Supine, standing, and Δplasma norepinephrine levels were lower for HC on the HS diet compared with the LS diet (Figure 3).”
Quote in the paperNot a substantial claim - Findingown data
In POTS patients, a high sodium diet increased plasma volume compared with a low sodium diet.
“Total blood volume and PV increased, and standing norepinephrine decreased with HS compared with LS diet”
- Also stated in: § Comparison between HS and LS diets response in POTS · plain
“This was based almost entirely on an increase in PV and a reduction in the PV deficit with the HS diet compared to LS diet [−.63 (−9.7–8.4) vs. – 11 (−17—2.6) %, P=0.001]”
- Also stated in: § Sodium Loading in POTS · plain
“the ~11% PV deficit in patients with POTS on LS diet was reduced to <1% on HS diet.”
Quote in the paperSubstantial claim - Also stated in: § Comparison between HS and LS diets response in POTS · plain
- Findingown data
On low sodium diet, POTS patients were more symptomatic than healthy controls.
“Patients with POTS were more symptomatic during the LS diet compared to HC.”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, POTS patients had greater orthostatic tachycardia (ΔHR) than healthy controls.
“On a LS diet, POTS patients had a greater ΔHR and upright HR and lower upright and Δdiastolic BP than HC.”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, POTS patients had greater upright heart rate than healthy controls.
“On a LS diet, POTS patients had a greater ΔHR and upright HR and lower upright and Δdiastolic BP than HC.”
Quote in the paperSubstantial claim - Findingown data
On low sodium diet, POTS patients had higher supine plasma norepinephrine than healthy controls.
“Both supine [248 (162–332) vs. 135 (104–225) pg/mL, P=0.030] and standing [959 (736–1161) vs. 520 (391–693) pg/mL, P<0.001] plasma norepinephrine, and orthostatic changes in plasma epinephrine and norepinephrine were greater in POTS than in HC on LS diet.”
Quote in the paperNot a substantial claim - Interpretationreasoning
The restoration of plasma volume contributed to improvement, although not normalization, in POTS.
“suggesting that the restoration of PV contributed to improvement, although not normalization, in POTS.”
Quote in the paperSubstantial claim - Premisecitation
Many POTS patients have decreased plasma volume.
“Many POTS patients have a decreased plasma volume (6–8) and high standing plasma norepinephrine (9).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [6] Raj, 2005, Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome, Circulation source
Not checked in the free run.
- cites [7] Raj, 2007, Blood volume perturbations in the postural tachycardia syndrome, Am J Med Sci source
Not checked in the free run.
- cites [8] Mustafa, 2011, Abnormalities of angiotensin regulation in postural tachycardia syndrome, Heart Rhythm source
Not checked in the free run.
- Interpretationreasoning
The reduced plasma volume could underlie the higher upright heart rate and orthostatic tachycardia in patients with POTS.
“The reduced PV could underlie the higher upright HR and ΔHR in patients with POTS.”
Quote in the paperSubstantial claim - Interpretationown data
Under the conditions of this study, disturbed sodium retention (salt wasting) did not prevent restoration of circulating blood volume.
“Under the conditions of this study, therefore, disturbed sodium retention (“salt wasting”) did not prevent restoration of circulating blood volume”
Quote in the paperSubstantial claim - Interpretationreasoning
High sodium diet led to improvement, although not normalization, of orthostatic tachycardia in POTS.
“and HS diet led to improvement, although not normalization, of orthostatic tachycardia.”
Quote in the paperSubstantial claim - Premisecitation
Many POTS patients have high standing plasma norepinephrine.
“Many POTS patients have a decreased plasma volume (6–8) and high standing plasma norepinephrine (9).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [9] Garland, 2007, The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome, Neurology source
Not checked in the free run.
- Premisecitation
Studies that reported a plasma volume deficit in POTS patients despite a normal- to high-sodium diet suggest that patients may not effectively respond to dietary sodium with plasma volume expansion.
“Studies that reported a plasma volume deficit in POTS patients despite a normal- to high-sodium diet (≥150 mEq sodium/day) (6, 14, 15), suggest that patients may not effectively respond to dietary sodium with plasma volume expansion.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [6] Raj, 2005, Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome, Circulation source
Not checked in the free run.
- cites [14] Jacob, 1997, Hypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system, Am J Med source
Not checked in the free run.
- cites [15] Fu, 2010, Cardiac origins of the postural orthostatic tachycardia syndrome, J Am Coll Cardiol source
Not checked in the free run.
- Interpretationown data
Volume depletion cannot totally explain POTS.
“Volume depletion, therefore, cannot totally explain POTS.”
Quote in the paperSubstantial claim - Premisecitation
Acute sodium and volume expansion with intravenous saline can reduce orthostatic tachycardia (ΔHR) in adults.
“acute sodium and volume expansion with intravenous saline can reduce the orthostatic tachycardia (ΔHR) in adults (12).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [12] Jacob, 1997, Effects of volume loading and pressor agents in idiopathic orthostatic tachycardia, Circulation source
Not checked in the free run.
- May combine two claims. 15
- Classified as probably not a substantial claim. 19
May combine two claims.
Findingown dataOn high sodium diet, for total blood volume and plasma volume, small deficits compared to expected volumes in POTS patients contrasted with a surplus in healthy controls.
“For TBV and PV, the small deficits compared to expected volumes in POTS contrasted with a surplus in HC.”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn healthy controls, high sodium diet did not change supine heart rate, upright heart rate, or orthostatic tachycardia (ΔHR) compared with low sodium diet.
“There were no differences in supine HR [HS:62 (53–75) bpm; LS: 70 (57–73) bpm, P=0.133], upright HR [HS:85 (77–95) bpm; LS:96 (88–101) bpm, P=0.091] or ΔHR [HS: 19 (11–32) bpm; LS: 23 (19–36) bpm, P= 0.266)] with HS diet compared to LS diet in HC (Figure 2).”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataIn POTS patients on high sodium diet, upright symptom scores exceeded those of healthy controls despite a plasma volume deficit of <1% from expected.
“and the upright symptom scores exceeded those for our HC, despite a deficit of <1% from the expected PV.”
Quote in the paperSubstantial claimMay combine two claims.
Findingown dataIn POTS patients, a high sodium diet did not change standing or Δ plasma epinephrine compared with a low sodium diet.
“but there were no differences in standing or Δ plasma epinephrine between diets.”
Quote in the paperNot a substantial claimMay combine two claims.
InterpretationreasoningThe low plasma volume in POTS might exaggerate postural central hypovolemia, prevent adequate compensation for the drop in venous return, and amplify orthostatic tachycardia.
“The low PV in POTS might exaggerate the postural central hypovolemia, prevent adequate compensation for the drop in venous return and amplify ΔHR.”
Quote in the paperSubstantial claimMay combine two claims.
Interpretationown dataTreatment with a high sodium diet, although helpful, is not sufficient to normalize patients with POTS.
“Treatment with a HS diet, although helpful, is not sufficient to “normalize” patients with POTS”
Quote in the paperSubstantial claimMay combine two claims.
PremisecitationA high sodium diet and increased water intake are often prescribed to expand plasma volume in patients with POTS.
“A high sodium diet (10–12 g NaCl/day equivalent to 170–205 mEq or mmoles sodium/day) and increased water intake (2–3L/day) are often prescribed to expand plasma volume in patients (3, 4, 10).”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [3] Raj, 2020, Canadian Cardiovascular Society position statement on postural orthostatic tachycardia syndrome (POTS) and related disorders of chronic orthostatic intolerance, Can J Cardiol
Not checked in the free run.
- cites [4] Sheldon, 2015, 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope, Heart Rhythm source
Not checked in the free run.
- cites [10] Garland, 2015, Postural tachycardia syndrome: beyond orthostatic intolerance, Curr Neurol Neurosci Rep source
Not checked in the free run.
May combine two claims.
Interpretationown dataBlood volume expansion by salt loading could load the baroreceptor and effect a decrease in nerve activity, with less subsequent release of synaptic norepinephrine, and the return of supine plasma norepinephrine to healthy control values.
“Blood volume expansion by salt loading could load the baroreceptor and effect a decrease in nerve activity, with less subsequent release of synaptic norepinephrine, and the return of supine plasma norepinephrine to healthy control values, as demonstrated in our patients.”
Quote in the paperNot a substantial claimMay combine two claims.
Interpretationown dataHigh sodium diet reduced upright plasma norepinephrine in POTS even though high plasma norepinephrine levels suggest these patients were hyperadrenergic.
“Importantly, HS reduced upright plasma norepinephrine in POTS, even though the high plasma norepinephrine levels suggest that these patients with POTS were “hyperadrenergic”.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationElevations in plasma norepinephrine suggest an increase in sympathoneural tone.
“Elevations in plasma norepinephrine suggest an increase in sympathoneural tone (10).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [10] Garland, 2015, Postural tachycardia syndrome: beyond orthostatic intolerance, Curr Neurol Neurosci Rep source
Not checked in the free run.
Classified as probably not a substantial claim.
Interpretationown dataThis study provides solid data to support recommendations for increased dietary sodium intake in POTS.
“This study provides solid data to support the recommendations for increased dietary sodium intake in POTS (3, 4).”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [3] Raj, 2020, Canadian Cardiovascular Society position statement on postural orthostatic tachycardia syndrome (POTS) and related disorders of chronic orthostatic intolerance, Can J Cardiol
Not checked in the free run.
- cites [4] Sheldon, 2015, 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope, Heart Rhythm source
Not checked in the free run.
Classified as probably not a substantial claim. May combine two claims.
PremisecitationA plasma volume deficit should stimulate the renin-angiotensin-aldosterone system to promote sodium retention, but this regulatory link might be defective in POTS.
“Although a plasma volume deficit should stimulate the renin–angiotensin–aldosterone system to promote sodium retention, this regulatory link might be defective in POTS (6).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [6] Raj, 2005, Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome, Circulation source
Not checked in the free run.
Classified as probably not a substantial claim.
PremisecitationSymptoms improve in children with POTS following supplementation with sodium chloride capsules.
“Symptoms improve in children with POTS following supplementation with sodium chloride capsules (11)”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [11] Zhang, 2012, Twenty-four-hour urinary sodium excretion and postural orthostatic tachycardia syndrome, J Pediatr source
Not checked in the free run.
Probably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductreasoningParticipants ate a low-monoamine caffeine-free diet containing 150 mEq sodium on study Day 1 to mitigate effects of any dietary extremes prior to study.
“Participants ate a low-monoamine caffeine-free diet containing 150 mEq sodium on study Day 1 to mitigate effects of any dietary extremes prior to study.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductown dataThe study used a randomized 2-arm crossover design.
“A randomized 2-arm crossover study compared the upright HR and ΔHR during a low sodium (10 mEq sodium/day, LS) or high sodium (300 mEq sodium/day, HS) diet in patients with POTS (Figure 1).”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenThe study was approved by the Vanderbilt Institutional Review Board and registered on ClinicalTrials.gov (NCT01547117).
“The Vanderbilt Institutional Review Board approved this study, and it was registered on ClinicalTrials.gov (NCT01547117).”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
InterpretationreasoningThe ability of a high sodium diet to improve heart rate, plasma volume, and norepinephrine abnormalities in POTS might not be maintained over the long term.
“The ability of a HS diet to improve the HR, PV and norepinephrine abnormalities in POTS might not be maintained over the long term.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Study design and conductown dataThe primary outcomes were ΔHR and upright HR in POTS patients on high sodium diet compared with low sodium diet.
“The primary outcomes for this study were ΔHR and upright HR in POTS patients while on HS diet compared to ΔHR and upright HR in these patients on LS diet.”
Quote in the paperSubstantial claimClassified as probably not a substantial claim.
Study design and conductcitationPlasma volume was determined by the indicator tracer-dilution technique using the DAXOR BVA-100 Blood Volume Analyzer system.
“Plasma volume (PV) was determined by the indicator tracer-dilution technique, using the DAXOR BVA-100 Blood Volume Analyzer system (6) (DAXOR Corporation), on Day 7.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [6] Raj, 2005, Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome, Circulation source
Not checked in the free run.
Classified as probably not a substantial claim.
Study design and conductcitationExpected plasma volume and total blood volume were determined for each individual based on height, weight, and gender.
“Expected PV and TBV were determined for each individual based on their height, weight, and gender (21).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [21] Feldschuh, 1977, Prediction of the normal blood volume. Relation of blood volume to body habitus, Circulation source
Not checked in the free run.
May combine two claims.
Study design and conductown dataThe study did not obtain baseline measurements during a normal sodium diet, so it cannot comment on changes from usual heart rate, plasma norepinephrine, or blood volume as a result of sodium manipulation.
“We did not obtain baseline measurements during “normal sodium diet” so we are unable to comment on changes from usual HR, plasma norepinephrine or blood volume as a result of sodium manipulation.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataThe study did not evaluate the sodium sensitivity of participants.
“We did not evaluate the “sodium sensitivity” of our participants, as this is not usually done in clinical practice either.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataThe Vanderbilt Orthostatic Symptoms Scale (VOSS) was used to measure standing symptom burden.
“Patients were asked to report their standing symptom burden at the end of the Stand portion of the posture study, using the Vanderbilt Orthostatic Symptoms Scale (VOSS) (16).”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [16] Coffin, 2012, Desmopressin acutely decreases tachycardia and improves symptoms in the postural tachycardia syndrome, Heart Rhythm source
Not checked in the free run.
Classified as probably not a substantial claim.
Study design and conductnone givenA P<0.025 threshold was used for statistical significance for the two primary outcomes.
“P<0.05 was considered statistically significant, except for the 2 primary outcomes where a P<0.025 threshold was used for statistical significance.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductnone givenThe findings are limited by the relatively short-term design of the protocol.
“The findings are limited by the relatively short-term design of our protocol.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenThe two diet phases were scheduled at least one month apart and for the same phase of the menstrual cycle.
“The two diet phases were scheduled at least one month apart and for the same phase of the menstrual cycle.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Study design and conductown dataAll participants provided written informed consent.
“All participants provided written informed consent prior to starting study-related activities.”
Quote in the paperNot a substantial claimMay combine two claims.
Study design and conductown dataThe findings were limited because VOSS scores were lacking for some participants and there was significant inter-patient variability due to the subjectivity of the VOSS tool.
“Our findings were limited because we lacked VOSS scores for some participants (see Supplemental Table 1) and there was significant inter-patient variability in responses due to the subjectivity of the VOSS tool.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
Study design and conductnone givenUrinary sodium measurements confirmed diet compliance.
“Urinary sodium measurements confirmed diet compliance.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
Study design and conductnone givenAlthough participants were not told whether they were consuming low or high sodium diet, the diet assignment was apparent.
“Although participants were not told whether they were consuming LS or HS diet, we acknowledge that it was apparent.”
Quote in the paperNot a substantial claim
The paper relies on this without support.
There are no published data about the value of a high sodium diet in POTS.
“There are no published data about the value of this simple dietary strategy.”
The paper relies on this without support.
Many POTS patients have adapted a high sodium diet despite the prior paucity of evidence.
“Given that many POTS patients have adapted a HS diet (despite the prior paucity of evidence), a “normal sodium diet” would have been hard to define.”
The paper relies on this without support.
A normal sodium diet would have been hard to define.
“Given that many POTS patients have adapted a HS diet (despite the prior paucity of evidence), a “normal sodium diet” would have been hard to define.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Plasma NE >600 pg/ml has been documented in healthy subjects with volume depletion, in patients with diabetic neuropathy, and in patients with neuropathic orthostatic hypotension.
“Indeed, plasma NE >600 pg/ml has been documented in healthy subjects with volume depletion,13 in patients with diabetic neuropathy,25 and even in patients with neuropathic orthostatic hypotension.26”
From Hyperadrenergic Postural Tachycardia Syndrome: Clinical Biomarkers and Response to Guanfacine (2024) · cites this paper as [13]
The Results (Comparison of Low Salt Diet Response between POTS and Healthy Controls; page unavailable) report standing plasma norepinephrine of 520 (391–693) pg/mL in healthy controls on a low-salt diet, documenting values above 600 pg/mL. But the Results (Comparison between HS and LS diets response in healthy controls; page unavailable) say their blood volumes on that diet were not significantly different from expected volumes, so the paper does not establish that those controls were volume-depleted. The other patient groups have separate citations in the citing sentence and are not attributed to this source. (LLM, conf=0.84)
Experimental — accuracy not yet measuredHigh sodium intake leads to expanded plasma volume, and reduced upright norepinephrine levels and heart rate in patients with POTS.
“A small 2021 case–control crossover study found that high sodium intake leads to expanded plasma volume, and reduced upright norepinephrine levels and heart rate in patients with POTS,41”
From Diagnosis and management of postural orthostatic tachycardia syndrome (2022) · cites this paper as [41]
There was a non-significant trend for lower symptom burden scores after upright posture in POTS on the high salt diet compared to the low salt diet, particularly for mental confusion, palpitations, light-headedness and headache.
“There was a non-significant trend for lower symptom burden scores after upright posture in POTS on the high salt diet compared to the low salt diet, particularly for mental confusion, palpitations, light-headedness and headache (Garland et al., 2021”
From Self-reported symptom burden in postural orthostatic tachycardia syndrome (POTS): A narrative review of observational and interventional studies (2023) · cites this paper as Garland et al., 2021
Multiple reports suggest triggering of autoimmunity in the post-acute phase of COVID-19 infection.
“Finally, the patients should be investigated for the presence of traditional autoimmune and inflammatory plasma biomarkers, as multiple reports suggest triggering of autoimmunity in the post-acute phase of COVID-19 infection169.”
From Sinus Tachycardia: a Multidisciplinary Expert Focused Review (2022) · cites this paper as [169]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Supine epinephrine median falls outside its stated interquartile range
MinorThe paper says clinical and biochemical results are reported as medians with interquartile ranges, but the reported high-sodium median of 11 pg/mL exceeds its stated upper quartile of 2.0 pg/mL.
“Supine plasma epinephrine was lower with HS diet than LS diet [11 (5.7–2.0) vs. 21 (12–31) pg/mL, P=0.009]”
“Continuous data are presented as mean ± SD for demographics and median (interquartile range) for clinical and biochemical data.”
Cites
Freeman, R., Wieling, W., Axelrod, F. B., Benditt, D. G., Benarroch, E., Biaggioni, I., Cheshire, W. P., Chelimsky, T., Cortelli, P., Gibbons, C. H., et al. (2011) · Autonomic Neuroscience · doi:10.1016/j.autneu.2011.02.004 · Cited by 1,243 · see citing works
Self-citationSheldon, R. S., Grubb, B. P., Olshansky, B., Shen, W.-K., Calkins, H., Brignole, M., Raj, S. R., Krahn, A. D., Morillo, C. A., Stewart, J. M., et al. (2015) · Heart Rhythm · doi:10.1016/j.hrthm.2015.03.029 · Cited by 1,013 · see citing works
Self-citationCardiac origins of the postural orthostatic tachycardia syndrome
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Prediction of the normal blood volume. Relation of blood volume to body habitus.
Feldschuh, J., & Enson, Y. (1977) · Circulation · doi:10.1161/01.cir.56.4.605 · Cited by 315 · see citing works
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Self-citationRaj, S. R., Black, B. K., Biaggioni, I., Paranjape, S. Y., Ramirez, M., Dupont, W. D., & Robertson, D. (2009) · Circulation · doi:10.1161/circulationaha.108.846501 · Cited by 225 · see citing works
Self-citationRaj, S. R., Guzman, J. C., Harvey, P., Richer, L., Schondorf, R., Seifer, C., Thibodeau-Jarry, N., & Sheldon, R. S. (2020) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2019.12.024 · Cited by 223 · see citing works
Self-citationEffects of volume loading and pressor agents in idiopathic orthostatic tachycardia
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Self-citationPostural tachycardia syndrome – Diagnosis, physiology, and prognosis
Arnold, A. C., Ng, J., & Raj, S. R. (2018) · Autonomic Neuroscience · doi:10.1016/j.autneu.2018.02.005 · Cited by 186 · see citing works
Self-citationAcetylcholinesterase inhibition improves tachycardia in postural tachycardia syndrome
Raj, S. R., Black, B. K., Biaggioni, I., Harris, P. A., & Robertson, D. (2005) · Circulation · doi:10.1161/circulationaha.104.497594 · Cited by 171 · see citing works
Self-citationHypovolemia in syncope and orthostatic intolerance role of the renin-angiotensin system
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Self-citationPostural tachycardia syndrome: beyond orthostatic intolerance
Garland, E. M., Celedonio, J. E., & Raj, S. R. (2015) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-015-0583-8 · Cited by 160 · see citing works
Self-citationThe hemodynamic and neurohumoral phenotype of postural tachycardia syndrome
Garland, E. M., Raj, S. R., Black, B. K., Harris, P. A., & Robertson, D. (2007) · Neurology · doi:10.1212/01.wnl.0000267663.05398.40 · Cited by 159 · see citing works
Self-citationStreeten, D. H. P., Thomas, D. F., & Bell, D. S. (2000) · The American Journal of the Medical Sciences · doi:10.1016/s0002-9629(15)40790-6 · Cited by 138 · see citing works
Postural orthostatic tachycardia syndrome: mechanisms and new therapies
Mar, P. L., & Raj, S. R. (2020) · Annual Review of Medicine · doi:10.1146/annurev-med-041818-011630 · Cited by 122 · see citing works
Self-citationCoffin, S. T., Black, B. K., Biaggioni, I., Paranjape, S. Y., Orozco, C., Black, P. W., Dupont, W. D., Robertson, D., & Raj, S. R. (2012) · Heart Rhythm · doi:10.1016/j.hrthm.2012.05.002 · Cited by 88 · see citing works
Self-citationBlood Volume Perturbations in the Postural Tachycardia Syndrome
Raj, S. R., & Robertson, D. (2007) · The American Journal of the Medical Sciences · doi:10.1097/maj.0b013e318063c6c0 · Cited by 80 · see citing works
Self-citationStewart, J. M., Glover, J. L., & Medow, M. S. (2006) · Clinical Science · doi:10.1042/cs20050254 · Cited by 77 · see citing works
Streeten, D. H. P., Thomas, D., & Bell, D. S. (2000) · The American Journal of the Medical Sciences · doi:10.1097/00000441-200007000-00001 · Cited by 75 · see citing works
Twenty-four-hour urinary sodium excretion and postural orthostatic tachycardia syndrome
Zhang, Q., Liao, Y., Tang, C., Du, J., & Jin, H. (2012) · The Journal of Pediatrics · doi:10.1016/j.jpeds.2012.01.054 · Cited by 66 · see citing works
Effects of Norepinephrine Reuptake Inhibition on Postural Tachycardia Syndrome
Green, E. A., Raj, V., Shibao, C. A., Biaggioni, I., Black, B. K., Dupont, W. D., Robertson, D., & Raj, S. R. (2013) · Journal of the American Heart Association · doi:10.1161/jaha.113.000395 · Cited by 64 · see citing works
Self-citationAbnormalities of angiotensin regulation in postural tachycardia syndrome
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Self-citationNeuronal and hormonal perturbations in postural tachycardia syndrome
Mar, P. L., & Raj, S. R. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00220 · Cited by 52 · see citing works
Self-citationMelatonin reduces tachycardia in postural tachycardia syndrome: a randomized, crossover trial
Green, E. A., Black, B. K., Biaggioni, I., Paranjape, S. Y., Bagai, K., Shibao, C., Okoye, M. C., Dupont, W. D., Robertson, D., & Raj, S. R. (2014) · Cardiovascular Therapeutics · doi:10.1111/1755-5922.12067 · Cited by 33 · see citing works
Self-citationMar, P. L., Raj, V., Black, B. K., Biaggioni, I., Shibao, C. A., Paranjape, S. Y., Dupont, W. D., Robertson, D., & Raj, S. R. (2014) · Journal of Psychopharmacology · doi:10.1177/0269881113512911 · Cited by 24 · see citing works
Self-citationTakeda, R., Stickford, A. S. L., Best, S. A., Yoo, J., & Fu, Q. (2020) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00197.2020 · Cited by 11 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Diagnosis and management of postural orthostatic tachycardia syndrome
Raj, S. R., Fedorowski, A., & Sheldon, R. S. (2022) · Canadian Medical Association Journal · doi:10.1503/cmaj.211373 · Cited by 95 · see citing works
Self-citationMathias, C. J., Owens, A., Iodice, V., & Hakim, A. (2021) · American Journal of Medical Genetics Part C: Seminars in Medical Genetics · doi:10.1002/ajmg.c.31951 · Cited by 65 · see citing works
Sinus Tachycardia: a Multidisciplinary Expert Focused Review
Mayuga, K. A., Fedorowski, A., Ricci, F., Gopinathannair, R., Dukes, J. W., Gibbons, C., Hanna, P., Sorajja, D., Chung, M., Benditt, D., et al. (2022) · Circulation: Arrhythmia and Electrophysiology · doi:10.1161/circep.121.007960 · Cited by 59 · see citing works
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“…(0-7) (0-7) Bourne et al., 2021 ++++++++ + +++++ +++++ ++ Proof-of-concept trial Coffin et al., 2012 ++++++++ + +++++++ ++++ +++ Proof-of-concept trial Garland et al., 2021 +++++++++ + +++++++ +++++ +++ Proof-of-concept trial, no placebo Green et al., 2014 ++++++++ + +++++++ ++++ +++…”
Hyperadrenergic Postural Tachycardia Syndrome: Clinical Biomarkers and Response to Guanfacine
Okamoto, L. E., Urechie, V., Rigo, S., Abner, J. J., Giesecke, M., Muldowney, J. A. S., Furlan, R., Shibao, C. A., Shirey-Rice, J. K., Pulley, J. M., et al. (2024) · Hypertension · doi:10.1161/hypertensionaha.124.23035 · Cited by 13 · see citing works
“The ROC analysis using PGIC also showed that a conservative cutoff of ∆ DBP VM2 >17 mm Hg identified a response to guanfacine with 77% specificity and 72% sensitivity (area under the curve, 0.774 [95% CI, 0.627–0.920]; P =0.006).”
InfluentialSelf-citation
- Authors
- Garland, E. M., Gamboa, A., Nwazue, V. C., Celedonio, J. E., Paranjape, S. Y., Black, B. K., Okamoto, L. E., Shibao, C. A., Biaggioni, I., Robertson, D., Diedrich, A., Dupont, W. D., & Raj, S. R.
- Affiliations
- Vanderbilt University Medical Center (US)
- Vanderbilt University (US)
- University of Calgary (CA)
- Corresponding author
- Raj, Satish R.
- ORCID
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2021-05
- Volume
- 77
- Issue
- 17
- Pages
- 2174-2184
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC8103825
- OpenAlex
- W3159564827
- Semantic Scholar
- 69817a7caf1fa65b46c09734247205ab5efa8a6e
- Cited by
- 65
- References
- 26
- Citations by year
- 2026: 17 · 2025: 10 · 2024: 10 · 2023: 7 · 2022: 13 · 2021: 8
- FWCI
- 8.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Surgery › Cardiovascular Syncope and Autonomic Disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Electrolyte and hormonal disorders
- Keywords
- postural orthostatic tachycardia syndrome, sodium restriction, orthostatic tachycardia, plasma norepinephrine, plasma volume, blood volume, hypovolemia, plasma renin activity, aldosterone, epinephrine, heart rate, blood pressure, orthostatic intolerance, crossover trial, young adults, women
- MeSH terms
- Adult, Blood Pressure, Female, Heart Rate, Humans, Male, Middle Aged, Norepinephrine, Posture, Sodium, Dietary, Biomarkers, Cross-Over Studies, Postural Orthostatic Tachycardia Syndrome, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-11.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-11.
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