Several population studies have clearly demonstrated the benefits derived from lowering salt intake in the diet1,2,3,4 irrespective of gender, ethnic group, presence or absence of hypertension. Lowering of blood pressure is associated with reduction of morbidity and cardiovascular complications with the caveat that the best blood pressure is the lowest at which one can function. Estimates are that worldwide the average intake of salt varies from 9 to 12 gm per day. Above studies show that a reduction to 5-6 gm of salt, i.e. 2gm of sodium (the amount of sodium is about 40% of total salt content) does have positive effect. However further sifting of the data reveals that responsiveness to salt follows an ethnic pattern, leading to the concept of salt-sensitive versus salt-insensitive groups. However, such distinction may be a misnomer because benefits are noticed overall. What is not debatable is that some ethnic groups tend to be very susceptible to salt intake and are subject to disproportionate complications. Hence modulation of dietary intake has become a widely recommended intervention. Dietary Approaches to Stop Hypertension, coined DASH4, is a cost-effective means to be proactive. The latest and most aggressive guideline as per WHO4,5 goes so far as to indicate that an intake of <1.5gm of sodium would be appropriate for populations at risk, namely blacks, people with insulin resistance, obese individuals or even those with high visceral fat in the absence of classic enlarged abdominal girth-this is seen especially in the Indian subcontinent6. Unlike the deleterious effects of sodium, in the absence of end-stage renal function, a diet high in potassium (as well as magnesium) is also beneficial to reduction of blood pressure. Fruits and nuts are the sources of potassium and magnesium respectively7.

With all of the above overwhelming data, it comes as a surprise that a trickle of studies have come up with results claiming that a low salt diet is associated with negative cardiovascular outcome8,9,10. The explanations offered vary from low salt causing a decrease in insulin sensitivity, an increase in aldosterone and catecholamines to  an increase in refined sugar intake causing damage due to  its toxic metabolites.

The question is what gives? How come we have such diametrically opposed data? The best answer against these studies can be found in large population studies from all over the world that keep showing the efficacy of a low salt diet approach. United Kingdom, Finland, Japan have all adopted similar recommendations and over the years have recorded noticeable reduction in cardiovascular complications11,12,13. The question still remains, how come? Studying people on low salt diet by definition implies looking at a skewed population. People on low salt diet usually are engaging in such a practice because of the advice of their physicians. As we stated above, the taste buds of the average citizen are such that the consumption of salt is far higher than necessary. Hence someone on low salt diet more than likely has hypertension, metabolic syndrome, endothelial dysfunction to begin with. Framing the data to show reduced insulin sensitivity is the equivalent of blaming the therapeutic intervention and ignoring the pathogenesis. Patients frequently use this as an excuse to refuse insulin by pointing out that people on insulin tend to lose their limbs. No study to date has documented patients with normal insulin sensitivity developing insulin resistance on a low salt diet. If this could be proven, then one would have a valid argument. However, knowing the state of the art on this matter, it’s hard to conceive that such intervention would result in the very pathology we are trying to prevent. As far as increase in aldosterone and catecholamines concentration, long term, this is not a complication of low salt intake4. The issue of carbs will be discussed later.

The one true iatrogenic complication that is encountered is the development of electrolytes disturbance when diuretic is used for treatment of hypertension. Hypokalemia and hypomagnesemia do carry arrhythmogenic properties. Not infrequently hypokalemia is paid attention to but not so much with hypomagnesemia, yet it can cause lethal arrhythmia14. A good rule of thumb is to look for and or treat empirically hypomagnesemia in the presence of diuretic-induced hypokalemia so long as patient has normal renal function. The correction of hypomagnesemia is crucial in the presence of persistent hypokalemia because the latter will not be corrected unless the former is, and it can also cause deterioration of CHF occasionally14.

The issue of cardiovascular complications of low salt diet is reviewed by Cogswell who did a meta-analysis and concluded that, “The application of Hill’s criteria to the putative association between low sodium intake and an increased risk of cardiovascular disease indicates that the association is not causal15…” This was a rigorous exercise of verifying and evaluating the reported results and not a mere opinionated assessment and as such, it gives her analysis scientific validity and heft. Fig 1 lists Hill’s criteria she used to probe the different studies and she found them wanting, not well designed and without robust proof.

Fig 1


  • What is the degree to which the exposure (low sodium intake) is associated with the outcome (cardiovascular disease)?
  • Has the association “been repeatedly observed by different persons, in different places, circumstances, and times”?
  • Is the observed association limited to the exposure and outcome?
  • “Does a particular diet lead to disease or do early stages of disease lead to those with peculiar dietetic habits?”
  • Is there a dose–response relationship between the exposure and outcome?
  • Is there a physiological basis for the observed association?
  • Does the “cause-and-effect interpretation” of the association “seriously conflict” with “generally known facts about the natural history and biology of the disease”?
  • “Is the frequency of associated events [outcomes]” affected by actions to prevent the exposure?
  • Does an exposure with a similar action (physiologically) cause the outcome?
  • *Adapted from Hill.16

Cogswell, M et al N Engl J Med 2016; 375:580-586

DiNicolantonio purports that low salt diet can induce more refined sugar intake as hypothesis without proof 8. This is his hypothetical explanation:

He references himself in a previous paper he wrote but it is a reprise of a hypothesis and there is no scientific proof provided17. I have yet to meet a patient consuming refined carbs, like soda, and eschewing potato chips or other salt-laden junk food. No one is disputing the havoc that refined carbs are creating and the obesity epidemic associated with this habit. However low salt consumption is not a culprit. The real problem that we clinicians face is patients not adhering to a low salt diet. It has been advocated that the best way to have patients accept this advice is a gradual decrease of the salt consumption. Overall, the evidence is robust that lowering salt intake is beneficial and there are decades of positive results to back the contention of a reduction of cardiovascular complications throughout the world for all ethnic groups.


  1. He Feng J, Li Jiafu, MacGregor Graham A. Effect of longer term modest salt reduction on blood pressure: Cochrane systematic review and meta-analysis of randomized trials. BMJ  2013; 346: f1325.
  2. Elliott Paul, Stamler Jeremiah, Nichols Rob, Dyer Alan, R, Stamler Rose, Kesteloot Hugo et al. Intersalt revisited: further analyses of 24 hour sodium excretion and blood pressure within and across populations BMJ  1996; 312 :1249.
  3. Borah PK, Kalita HC, Paine SK, et al. An information, education and communication module to reduce dietary salt intake and blood pressure among tea garden workers of Assam. Indian Heart J. 2018;70(2):252–258. doi: 10.1016/j.ihj.2017.08.008.
  4. Rust P., Ekmekcioglu C. (2016) Impact of Salt Intake on the Pathogenesis and Treatment of Hypertension. In: Islam M.S. (eds) Hypertension: from basic research to clinical practice. Advances in Experimental Medicine and Biology, vol 956. Springer, Cham.
  5. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med 2001; 344:3-10.
  6. Harpreet SB, et al. Comparison of Relative Waist Circumference between Asian Indian and US adults. Journal of Obesity. Volume 2014, Article ID 461956, 10 pages.
  7. Karppanen H. Minerals and blood pressure. Ann Med 1991 Aug:23(3):299-305.
  8. DiNicolantonio JJ, Lucan SC. The wrong white crystals: not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart 2014; 1: e000167.
  9. Oparil S. Low sodium intake — cardiovascular health benefit or risk? N Engl J Med 2014; 371:677-679.
  10. Graudal N, Jürgens G, Baslund B, Alderman MH. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens 2014; 27:1129-1137.
  11. He FJ, Pombo-Rodrigues S, Macgregor GA. Salt reduction in England from 2003 to 2011: its relationship to blood pressure, stroke and ischaemic heart disease mortality. BMJ Open 2014;4: e004549-e004549.
  12. Karppanen H, Mervaala E. Sodium intake and hypertension. Prog Cardiovasc Dis 2006; 49:59-75.
  13. Udagawa K, Miyoshi M, Yoshiike N. Mid-term evaluation of “Health Japan 21”: focus area for the nutrition and diet. Asia Pac J Clin Nutr 2008;17: Suppl 2:445-452.
  14. Ahmed F, Mohammed, A. Magnesium: The Forgotten Electrolyte-A Review on Hypo-magnesemia. Med Sci (Basel). 2019;7(4):56. Published 2019 Apr 4.
  15. Cogswell, ME, et al N Engl J Med 2016; 375:580-586.
  16. Hill AB. The environment and disease: association or causation? Proc R Soc Med 1965; 58:295-300.
  17. DiNicolantonio, JJ, Lucan, SC, O’Keefe, JH. An unsavory truth: sugar, more than salt, predisposes to hypertension and chronic disease. Am J Cardiol 2014; 114:1126–8.


Return to homepage