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• The dangers of mandating policy in the absence of clear evidence
  Morton Satin
  Published on: 23 November 2010

• Published on: 23 November 2010

  The dangers of mandating policy in the absence of clear evidence

  • Morton Satin, Vice President

  It is quite incredible how far the notion of a population-wide benefit accruing from salt reduction has gone in view of the contradictory clinical evidence. In the first instance we know that the population response to salt reduction is rather limited (2-6 mm Hg) and heterogeneous, with 30% experiencing a small drop in BP, about 20% experiencing an increase in BP and the residual 50% o the population undergoing no impac...

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  It is quite incredible how far the notion of a population-wide benefit accruing from salt reduction has gone in view of the contradictory clinical evidence. In the first instance we know that the population response to salt reduction is rather limited (2-6 mm Hg) and heterogeneous, with 30% experiencing a small drop in BP, about 20% experiencing an increase in BP and the residual 50% o the population undergoing no impact at all (1) .

  Indeed, the most recent evidence seems to indicate that so-called salt sensitivity on either side of the response is due to a genetically- based imbalance of aldosterone production. Those with abnormally high production of aldosterone show a slight reduction in BP with decreased salt intake (2) while abnormally low aldosterone levels may be responsible for the demonstrated increase in BP with reduced salt intakes (3). In both cases, since abnormal aldosterone levels carry a range of risks aside from hypertension, the strategy should be to manage aldosterone, not salt.

  In the second instance, the Geoffrey Rose reduced-salt approach to slightly reduce blood pressure across the entire population in hopes of achieving meaningful reductions in the incidence of cardiovascular disease (CVD) will only possibly work in the absence of negative consequences. Using this approach, a population-wide reduction in salt intake will inevitably result in a population-wide increase in renin-angiotensin- aldosterone system (RAAS) activity - also considered to be a risk factor for CVD, thus shifting the curve towards a higher risk. Without incorporating the normal increase in RAAS activity expected with salt reduction, the concept behind the approach is fundamentally flawed

  This year (2010) has shown a number of models projecting savings in lives and treasure based upon the flawed speculation in Rose's population approach. No new clinical evidence has been presented - only an extrapolation of old controversial evidence - the equivalent of lipstick on a pig. This latest paper falls into this genre of using assumptions that are based upon a highly biased view of the available evidence. There have been more meta-reviews questioning the benefits of population-wide sodium reduction (4)(5)(6), than supporting it (7).

  More recently, Harvard researchers Adam Bernstein and Walter Willett (8) found that the amount of sodium consumed by Americans over the past four decades has remained unchanged, while the rates of hypertension have increased significantly. This data reveals a total disconnect between rising rates of hypertension/obesity and salt consumption. Yet, the purported connection between rising hypertension and salt consumption was the myth behind the recommended figures we all use.

  Because an adequate dietary recommended intake for sodium "could not be established because of inadequate data from dose-response studies" (9), the figure was subjectively and arbitrarily set at 1,500 mg/day. Somehow this figure morphed into an international standard as if it was based upon real evidence - but it wasn't. The same for the upper limit of 2,300 mg Na/day, precisely 100 mmoles - as if we were all cast in Avogadro's image.

  The idea of mandatory sodium reduction referred to in the paper by Cobiac et al, in view of so much contradictory evidence seem to throw caution to the wind. Surely, before mandatory measures are considered that will limit the intakes of a nutrient to a level lower than previously experienced in recorded human history and considerably less than that of any other modern society in the world, some pause should be taken to carry out a full dispassionate review of all the available evidence. As an employee of the salt industry, I would certainly recuse myself from such a review and would hope that all other committed activists and advocates on all sides of the issue do likewise, so that it can proceed in a fully objective manner. Consumers deserve no less.

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  (1) Miller, J.Z., Weinberger, M.H., Daugherty, S.A., et al. "Heterogeneity of blood pressure responses to dietary sodium restriction in normotensive adults," J Chronic Dis, 40, 245-250, (1987).

  (2) Kammerer, C.M. et al, "Linkage of Plasma Aldosterone Concentration to Chromosome 5 in Families of African Ancestry," American Heart Association High Blood Pressure Research - 2010 Scientific Sessions, Washington, DC, Oct., 14, (2010).

  (3) Makhanova, N., Sequeira-Lopez, M.L.S., Gomez, R.A, Hyung-Suk Kim, and Smithies. O., "Disturbed Homeostasis in Sodium-Restricted Mice Heterozygous and Homozygous for Aldosterone Synthase Gene Disruption," Hypertension, 48, 1151-1159, (2006).

  (4) Hooper L, Bartlett C, Davey SG, Ebrahim S. Advice to reduce dietary salt for prevention of cardiovascular disease. Cochrane Database Syst Rev. 2004;(1):CD003656.

  (5) Institute for Quality and Efficiency in Health Care. Executive summary of report A05- 21B, Benefit assessment of non-drug treatment strategies in patients with essential hypertension: reduction in salt intake (Nutzenbewertung nichtmedikament?ser Behandlungsstrategien bei Patienten mit essenzieller Hypertonie: Kochsalzreduktion). Cologne, Germany, June 18, 2009. Executive summary in English can be accessed at: http://www.iqwig.de/download/A05-21B_Executive_Summary_Nondrug_ treatment_strategies_for_hypertension-reduction_in_salt_intake.pdf

  (6) Jurgens G, Graudal NA. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglycerides. Cochrane Database Syst Rev. 2004;(1):CD004022

  (7) He FJ, MacGregor GA. Effect of longer-term modest salt reduction on blood pressure. Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD004937.

  (8) Bernstein, AM and Willett, WC, Trends in 24-h urinary sodium excretion in the United States, 1957-2003: a systematic review. Am J Clin Nutr doi: 10.3945/ajcn.2010.29367.

  (9) Institute of Medicine, "Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate," (National Academy Press, Washington, DC, 2005).

  Conflict of Interest:

  The author is employed by the Salt Institute

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  Conflict of Interest:
  None declared.

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