Too early to attach blanket health warnings to all drugs containing sodium, irrespective of conjugate anionBMJ 2014; 348 doi: https://doi.org/10.1136/bmj.g1404 (Published 12 February 2014) Cite this as: BMJ 2014;348:g1404
- Ossie Ferdinand Uzoigwe, medical writer1
George and colleagues postulate that increased oral sodium load raises blood pressure, thus precipitating the adverse cardiovascular outcomes observed.1 This explanation is intuitive, cogent, and attractive but more complex processes may be at work. Not all sodium salts have a hypertensive effect. It has been well established since the 1980s that the pressor effect associated with sodium salts is restricted to sodium chloride and other halides. It does not occur with non-halide sodium salts.2 3 4 5 6 7 It has been consistently shown that increased oral intake of non-halide sodium salts such as citrate, bicarbonate, and phosphate does not increase blood pressure or cause hypertension.2 3 4 5 6 7 It seems to have been forgotten that the pressor is the combination of sodium and chloride. This is important, because effervescent, dispersible, and soluble tablets generally do not contain sodium chloride, as verified by examining the active ingredients and excipients of the drugs listed by George and colleagues. The predominant ions in solution are sodium citrate, sodium carbonate, or sodium hydrogen carbonate.8
The reported effect may manifest itself by alternative mechanisms. Many sodium containing tablets are analgesics. Acute and chronic pain have consistently been linked to hypertension.9 Imperfect matching between the sodium tablet and non-sodium tablet cohorts with regard to this class of drug may make a demonstrable difference. Interestingly, the findings of a similar population study that explored the effect of proton pump inhibitors (PPI) on cardiovascular outcomes, with extensive adjustment for confounders, were similar to those of the current study.10 PPI usage was most strongly linked to an increase in stroke but was also associated with myocardial infarction. These effects were independent of co-medication with clopidogrel. The authors suggested that it may be due to imperfect adjustment for confounders and the existence of latent risk factors for which insufficient correction was performed. They could not exclude the possibility of PPIs altering the gastric milieu and thus affecting the absorption of agents with cardiovascular tropisms. A similar mechanism cannot be discounted here. It is premature to attach blanket health warnings to all preparations containing sodium, irrespective of conjugate anion. The causative agent and mechanism for the adverse effects must be precisely determined. It cannot be assumed to be the sodium content in isolation.
Cite this as: BMJ 2014;348:g1404
Competing interests: None declared.
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