Policy options to reduce population salt intake
BMJ 2011; 343 doi: https://doi.org/10.1136/bmj.d4995 (Published 11 August 2011) Cite this as: BMJ 2011;343:d4995
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Sodium is an essential ion in the extracellular fluid. It is an essential cation in muscle contraction in all the muscle types viz. smooth muscle, heart muscle or skeletal muscle. Decreasing its quantity (reduced intake and increased excretion e.g. in diarrhoea and sweating in heat with exercise) will be detrimental to body's health. A recent study in McMaster university has the following results(1)(The urinary sodium excretion is taken as a surrogate indicator of its consumption):
The association between estimated urinary sodium excretion and CV events was J-shaped. Compared with baseline sodium excretion of 4 to 5.99 g per day, sodium excretion of greater than 7 g per day was associated with an increased risk of all CV events, and a sodium excretion of less than 3 g per day was associated with increased risk of CV mortality and hospitalization for CHF (1).
Reference:
1. O'Donnell MJ, Yusuf S, Mente A et al. Urinary Sodium and Potassium Excretion and Risk of Cardiovascular Events. JAMA. 2011;306(20):2229-2238. doi: 10.1001/jama.2011.1729
Competing interests: No competing interests
Dr Da Prato's premises are incorrect. The Asian populations he cites
actually have high stroke mortality rates [1] and high levels of blood
pressure [2]. Furthermore, he cites Dr Huang's paper in support. However,
the paper represents an anecdote from which a hypothesis is put forward.
The paper does not provide any experimental findings.
Dr Graudal's first statement is likewise incorrect. The TOHP Trial,
for instance, was carried out on a background of a contemporary American
diet with an average baseline daily sodium intake of 150-to-180 mmol.
Furthermore an average moderate reduction of 33-to-44 mmol/d caused a 52%
reduction in CVD outcomes and a 24% reduction in all-cause mortality at 18
months and a 21% and 17% reduction at 3-to-4 years, respectively. The
Belgian study did not achieve any difference in salt intake, hence,
unsurprisingly it produced no effect on measured outcomes. The example of
Finland is unique in the world. It is used not only to highlight the
substantial health benefits without adverse effects on cardiovascular
outcomes (as erroneously suggested by some) by a long term reduction in
salt intake, but it demonstrates how mandatory actions can be extremely
effective in the implementation of public health policies. His third point
has already been extensively dismissed in detailed scientific rebuttals in
response to the 2008 publication in the Cochrane library [3]. The lack of
acknowledgment in his correspondence is a regrettable omission that risks
misleading readers not conversant with the literature. The meta-analysis
by Strazzullo et al. did not include all-cause mortality because most of
the studies included did not report such results. We invite Dr Graudal to
reconsider the doubtful value of the recent published study he cites in
support of his views, given the overwhelming international criticisms
raised [4-6]. We are again surprised at these omissions.
Finally, blood
pressure is continuously distributed and there is no biological
justification for the definitions of 'normotension' or 'hypertension'.
Indeed, over the years, these definitions are constantly amended only to
guide the cost-effective use of drug therapy. Preventive medicine deals
with all people, not just the ill. In conclusion, further denial and
procrastination about dietary salt reduction will be costly in terms of
both avoidable illness and costs; it will also be ethically irresponsible.
Francesco P Cappuccio, Simon Capewell, Paul Lincoln, Klim McPherson
University of Warwick, WHO Collaborating Centre for Nutrition, Coventry;
University of Liverpool; National Heart Forum, London; University of
Oxford.
References
1. Liu M, Wu B, Wang W-Z, Lee LM, Zhang S-H, Kong L-Z. Stroke in
China: epidemiology, prevention, and management strategies. Lancet
Neurology 2007; 6: 456-64
2. He J, Gu D, Chen J, Wu X, Kelly TN, Huang JF, Chen JC, Chen CS,
Bazzano LA, Reynolds K, Whelton PK, Klag MJ. Premature deaths attributable
to blood pressure in China: a prospective cohort study. Lancet 2009; 374:
1765-72
3. Jurgens G, Graudal NA. Effects of low sodium diet versus high
sodium diet on blood pressure, renin, aldosterone, catecholamines,
cholesterols, and triglyceride. Cochrane Database of Systematic Reviews
2004, Issue 1. Art. No.: CD004022.
DOI: 10.1002/14651858.CD004022.pub2; pp.113-6
4. Campbell N, Cappuccio FP, Tobe SW. Unnecessary controversy
regarding dietary sodium: a lot about a little. Can J Cardiol 2011; 27:
404-6
5. He FJ, Appel LJ, Cappuccio FP, de Wardener HE, MacGregor GA. Does
reducing salt intake increase cardiovascular mortality? Kidney
International 2011; 80: 696-8
6. Aleksandrova K, Pischon T, Weickert C, Rebholz CM, He J, Bochud M,
Guessous I, Bovet P, Labarthe DR, Briss PA, Cook NR, Oliveira de Abreu-
Silva, Marcadenti A. Urinary sodium excretion and cardiovascular disease
mortality. JAMA 2011; 306: 1083-6
Competing interests: FPC is unpaid member of CASH, WASH, unpaid technical advisor to the WHO and the PAHO, Individual member of the National Heart Forum and Member of the Executive Committee and Trustee of the British Hypertension Society. SC is a Trustee of the Heart of Mersey. PL, KM & SC are Chief Executive, Chair and Trustee of the UK National Heart Forum. All the authors were member of the NICE CVD population prevention guideline development group. The publication does not necessarily represent the decisions or the stated policy of W.H.O. and the designations employed and the presentation of material do not imply the expression of any opinion on the part of WHO
It remains remarkable to me that the anti-salt medical faction
ignores or is intolerant of the obvious evidence that certain Asian
populations (Japanese, Chinese, and Koreans, for example) have a sodium
intake far in excess of the average Westerner, have normal/low blood
pressure, and live longer. Huang (1) noted that in her hometown in
northern China "hypertension is a rare disease and arteriosclerosis is a
virtually unknown condition" despite an average sodium chloride intake of
30 grams per day, perhaps three or more times that in England and America.
Her hypothesis is that we in the West may have a deficiency of sodium
since "all the hormones and ions involved in sodium conservation are
inducers of hypertension." One example provided is the known relationship
between aldosterone excess and magnesium and potassium wastage. The
evidence presented by the above rapid response that since 1960 salt intake
has increased by 50% while the incidence of hypertension has decreased by
50% in the West supports Huang's hypothesis of the toxic effect of a
sodium deficiency on blood pressure.
1) Huang, Yuhaun Wu. Sodium Chloride and hypertension. Medical
Hypotheses 1997; 49: 221-228.
Competing interests: No competing interests
Salt is one of the cornerstones on which the mammalian biochemical
structure is built. Total exclusion of salt from the diet leads to death.
Still, salt is considered by some to be toxic on a level comparable with
tobacco. In the analysis of "policy options to reduce salt intake"
Cappucio et al. (1) support this view and state that the question is not
whether to reduce salt intake, but how to do it. Considering the long-
lasting controversies in the science of sodium reduction (2-4), the
certainty of this statement is remarkable.
During the 20th century there has been a dramatic fall in blood
pressure (5) and the prevalence of hypertension (6) in USA, which probably
reflects the development in the Western World. This fall has happened
without an accompanying fall in salt intake (7). At present 85% of the US
population has a normal blood pressure (6). At least in the Western World
it is therefore essential to determine whether sodium reduction has a
significant effect on blood pressure in normotensives before advising
general sodium reduction. Large meta-analyses have shown this effect to be
about 1/0.2 mmHg (8,9). It is a question whether this effect is sufficient
to recommend general sodium reduction, especially comsidering the possible
side effects of sodium reduction (4,9,10).
Cappucio et al. state that RCTs have "consistently" shown dose-
response effects. This is not correct, as many studies have shown no
effect at all or inverse effects of sodium reduction on blood pressure
(9).
Cappucio et al. cite a lowering effect of sodium reduction on blood
pressure in two populationbased intervention studies from Portugal (11)
and Japan (12). The average salt intake in these two studies was 350 mmol
(11) and 250 mmol (12). Therefore these two studies cannot be used to
extrapolate to populations with a mean intake in the range of 120-210 mmol
which includes 95% of all communities (13). In another population based
intervention study, in which the sodium intake was about 180 mmol,
randomisation to low and high salt intake showed no effect of sodium
reduction on blood pressure (14).
Cappucio et al. claim that healthy physiological requirements of
salt are about 1 g per day. 1g is the minimal requirement, but there is no
scientific evidence to document that the minimal requirement is healthy.
Populations on minimal salt intake (for instance the Yanomamo Indians)
have extreme activation of the renin-aldosterone system (15). Severe
hyponatriaemia may develop in older people treated with diuretics and ACE
inhibitors, which could lead to serious side effects and even death (10).
This risk might increase if low-sodium intake was the rule in the whole
population. Furthermore many studies show that low salt intake is
associated with an increase in cholesterol, triglyceride, renin,
aldosteron and noradrenalin and possibly also in adrenalin (9). This is
not necessarily healthy, more likely the opposite.
Concerning evidence for effect of sodium reduction on morbidity and
mortality Cappucio et al. are referring to the meta-analysis by Strazzulo
et al (16). This analysis shows an increase in stroke with high sodium
intake of 21%. It also shows an increase in cardiovascular death, but this
is only significant because the stroke events are included in the
cardiovascular analysis. The fact is that only the stroke risk is
increased, not the cardial risk. If the Asian studies with extreme sodium
intakes of more than 200 mmol are excluded from the Strazzulo analysis,
there is no longer an increased stroke risk, which means that in the
Western populations with a mean sodium intake of about 150 mmol there is
no increased cardiovascular risk in people with normal salt intake
compared with low salt intake. On the contrary, the all-cause mortality
was lower in the normal sodium group than in low-sodium group. For unknown
reasons, Strazzulo et al. did not report such an analysis of the all-cause
mortality data.
Since 1970 all Western countries have experiencesd a fall in
cardiovascular disease and an increase in mean survival time With the
exception of Finland (17) there is no evidence to indicate that these
improvements were associated with reduced sodium intake, on the contrary.
Since 1960 salt intake increased by 50% (7) associated with a fall in
hypertension prevalence from 30% to 15% (6). Consequently there is no
reason to believe that the fall in blood pressure and increased survival
in Finland, as claimed by Cappucio et al., have anything to do with the
reduced sodium intake.
Cappucio et al. refer to large numbers of lives that could be saved
as a result of a general sodium reduction. These numbers are not based on
direct evidence, but on dubious assumptions from selected studies,
ignoring the many studies with contrasting results. This is emphasized by
the fact that several new population studies (18-20) and the older ones
included in the Strazzulo meta-analysis (16) show an increased all-cause
mortality risk in people on low sodium intake.
In our opinion there is no evidence to support that sodium reduction
has net beneficial effects on healthy normotensive persons. Lately, low
sodium intake has also been shown to be associated with increased
mortality in patients with diabetes (18,19) and heart failure (21). It is
therefore surprising that many countries uncritically have chosen to adopt
the sodium reduction principle, which probably is the largest delusion in
the history of preventive medicine. The question is not how to reduce
sodium intake, but whether to reduce sodium intake at all.
References
1) Cappucio F, Capewell S, Lincoln P, McPherson K. Policy options to
reduce population salt intake. BMJ 2011, 343: d4995.
2) Chapman CP, Gibbons TB. The diet and hypertension, a review.
Medicine 1949; 9:29-69.
3) Taubes G. The (political) science of salt. Science 1998; 281: 898-
907.
4) Graudal N, Galloe A. Should Dietary Salt Restriction Be a Basic
Component of Antihypertensive Therapy? Cardiovascular Drugs and Therapy
2000; 14: 381-386.
5) Goff DC, Howard G, Russel GB, Labarthe DR Birth cohort evidence of
population influences on blood pressure in the United States 1887-1994.
Ann Epidemiol 2001; 11: 271-279.
6) Gregg EW, Cheng YJ, Cadwell BL, Imperatore G, Williams DE, Flegal
KM, Narayan KM, Williamson DF. Secular trends in cardiovascular disease
risk factors according to body mass index in US adults. JAMA. 2005; 293:
1868-74.
7) Briefel RR, Johnson CL. Secular trends in dietary intake in the
United States. Annu Rev Nutr. 2004; 24: 401-31.
8) Midgley JP, Matthew AG, Greenwood CMT, Logan AG. Effect of reduced
dietary sodium on blood pressure. A metaanalysis of randomized controlled
trials. JAMA 1996; 275: 1590-1597.
9) Graudal NA, Galloe AG, Garred P. Effects of sodium restriction on
blood pressure, renin, aldosterone, catecholamines, cholesterols, and
triglyceride, A meta-analysis. JAMA 1998; 279: 1383-1391.
10) Bennett WM. Drug interactions and consequences of sodium
restriction.
Am J Clin Nutr 1997; 65(2 Suppl): 678S-681S.
11) Forte JG, Miguel JM, Miguel MJ, de P?dua F, Rose G. Salt and
blood pressure: a community trial. J Hum Hypertens 1989; 3: 179-84.
12) Takahashi Y, Sasaki S, Okubo S, Hayashi M, Tsugane S. Blood
pressure change in a free-living population based dietary modification
study in Japan. J Hypertens 2006; 24: 451-8.
13) McCarron DA, Geerling JC, Kazaks AG, Stern JS. Can dietary sodium
intake be modified by public policy? Clin J Am Soc Nephrol 2009; 4: 1878-
82.
14) Staessen J, Bulpitt CJ, Fagard R, Joossens JV, Lijnen P, Amery A.
Salt intake and blood pressure in the general population: a controlled
intervention trial in two towns. J Hypertens. 1988; 6: 965-73.
15) Oliver JW, Cohen EL, Neel JV. Blood pressure, sodium intake, and
sodium related hormones in the Yanomamo indians, a "no-salt" culture.
Circulation 1975; 52: 146-151.
16) Strazzullo P, D'Elia L, Kandala N-B, Cappuccio FP. Salt intake,
stroke, and cardiovascular disease: meta-analysis of prospective studies.
BMJ 2009; 339: b4567.
17) Karppanen H, Mervaala E. Sodium intake and hypertension. Prog
Cardiovasc Dis
2006; 49: 59-75.
18) Thomas MC, Moran J, Forsblom C, Harjutsalo V, Thorn L, Ahola A,
Wad?n J, Tolonen
N, Saraheimo M, Gordin D, Groop PH; FinnDiane Study Group. The association
between dietary sodium intake, ESRD, and all-cause mortality in patients
with type 1 diabetes. Diabetes Care 2011; 34: 861-6.
19) Ekinci EI, Clarke S, Thomas MC, Moran JL, Cheong K, MacIsaac RJ,
Jerums G. Dietary salt intake and mortality in patients with type 2
diabetes. Diabetes Care 2011; 34: 703-9.
20) Stolarz-Skrzypek K, Kuznetsova T, Thijs L, Tikhonoff V,
Seidlerov? J, Richart T, Jin Y, Olszanecka A, Malyutina S, Casiglia E,
Filipovsk? J, Kawecka-Jaszcz K, Nikitin Y, Staessen JA; European Project
on Genes in Hypertension (EPOGH) Investigators. Fatal and nonfatal
outcomes, incidence of hypertension, and blood pressure changes in
relation to urinary sodium excretion. JAMA 2011; 305: 1777-85.
21) Paterna S, Gaspare P, Fasullo S, Sarullo FM, Di Pasquale P.
Normal-sodium diet compared with low-sodium diet in compensated congestive
heart failure: is sodium an old enemy or a new friend? Clin Sci (Lond)
2008; 114: 221-230.
Competing interests: No competing interests
Cappuccio and colleagues provide an excellent review of the problems
with salt and strategies for reducing them. It is admirable for its
concision as well as its content.
But three constructive comments and supplements are appropriate, on
communication, regulation and taxation.
Communication: their principal policy recommendations are public
communications programmes and the reformulation of salt-bearing products.
Of these, messages to consumers will have much less impact.
"Public awareness" is of little use when consumers have little scope
for individual action. In developed countries, the vast majority of the
salt people eat comes already contained in manufactured products. And
identifying the healthier, reformulated versions of these is usually
arduous or impossible.
Worse, advice to consumers may be counterproductive. Health
advocates on salt often do not realise how their well-intentioned
injunctions alienate more than they attract. A dramatic reminder occurred
last month when the Daily Express devoted its whole front page to
reporting a Cochrane review that claimed to show little benefit from salt
reduction. The headline was: "Now salt is safe to eat: health fascists
proved wrong after lecturing us all for years".
Food manufacturers have long recognised this popular backlash. Which
is why so few of the many foods reformulated under the UK Food Standards
Agency's programme claim to be "reduced" or "low" in salt. Such claims
kill sales. So companies make reductions invisibly, incrementally,
imperceptibly.
The communications that count target companies. Outstanding
illustrations are CASH's regular surveys of the salt in competing products
in specific categories. They name-and-shame the high salt items, name-and
-praise those that have made significant cuts. Such assessments provide
actionable advice for consumers. More importantly, reputational damage to
brands hits lazy companies where it hurts, in sales, applying pressure to
reformulate.
Regulation: the authors claim that legal regulation is "necessary and
acceptable". They are wrong on both counts.
Their Table 2 lists 31 countries with initiatives on product
reformulation. Only two use a "mandatory" approach, and both are still in
the planning stage. The other 29 have organised cuts on a "voluntary"
basis. Regulation may be desirable, even superior, but it is not
necessary.
It is also improbable. In most developed countries, under
governments of both left and right, the long-term trend is in the opposite
direction, towards reducing the "burden" of regulation on companies.
The European Union abandoned the legal regulation of food composition
decades ago. The "1992 Programme" demolished hundreds of "recipe laws".
The chances of the EU reversing all this now to adopt a new regulation
limiting the salt in foods are nil. Public health advocates need to be
practical politicians too.
Taxation: one potential policy does not appear in the text at all,
but is noted in the final table - the taxation of salt. It merits more
attention.
Salt is cheap. Even in very high salt products, the cost of the
ingredient per portion is a tiny fraction of a penny. A tax of several
thousand percent (many multiples of the rate on tobacco or alcohol
anywhere in the world) could be applied without substantially affecting
retail prices. But it would stimulate cost-cutting reductions in bulk
purchases by manufacturers.
Unlike, say, taxes on soft drinks, public resistance would be weak.
A tax on salt would be hardly be noticed by consumers, who buy little of
it directly. In most developed countries, salt producers are not
politically influential players. For food manufacturers, it would an
extra cost to be managed, not fought over.
One reason for the oversight of this policy option is that the
authors work in an Anglo-Saxon economy, where these days raising taxes is
ideologically anathema. But theirs is an article for a global audience.
And other countries are more rational, more open to their persuasive cost-
benefit analysis. In such countries, an excise tax on salt could be
another instrument for applying pressure to reformulate manufactured
foods.
Prof J T Winkler
Director, Nutrition Policy Unit
London Metropolitan University (Retired)
28 St Paul Street
London N1 7AB
020-7226-1672
07880 752 788
Competing interests: No competing interests
1. Human males and human non pregnant females have no salt appetite,
as far as we know. Contrast appetite (= physiological need for salt, with
craving ( = habituation to salt intake, the taste bud theory). But human
pregnant females likely, and animal herbivores certainly, have salt
appetite. Would human herbivores (strict Vegans) have salt appetite as
their animal counterparts that seek salt licks? Probably so, if those
Vegans avoid most processed foods, as they would be expected to, from
their lifestyle choice.
2. Humans in environments that effect extreme obligatory water losses
- insensible water losses, sweating and GIT losses due typical tropical
diseases, have need for water and therefore salt retention. In fact this
observation was at the root of the discovery of the salt retaining hormone
Aldosterone by Conn in the Pacific. Would those in such environments
require a little bit more salt than their temperate dwelling hominid
counterparts?
3. African Americans with genetic propensity to salt sensitive
hypertension are now seen to be more responsive to both Diuretics (used in
salt sensitive hypertension) and Vasodilators (used in salt resistant
hypertension) - plus the lifestyle readjustments, than either alone.
Prudence in hypertensives minimising all predispositions, if they can, to
all types of hypertension regardless of cause.
4. Prescription of a global solution to a global health concern over
hypertension would be beneficial to some geographic, ethnic, racial groups
(talking genes and environment), but not to others.
Competing interests: No competing interests
The authors claim that we need only 1gm of salt per day.
I gather that sports drinks contain about 1gm of salt per litre of
fluid. It appears that, after matches, they are routinely distributed to
very valuable and highly paid footballers, following the advice of the
best nutritionists and sports scientists money can buy. Presumably this
reasoning applies to any one undertaking fairly strenuous manual work on a
hot day.
Is it not the case that the elderly are particularly at risk from
salt depletion in hot weather? Does lack of salt contribute to the very
high number of deaths among the elderly during heatwaves?
I am 54 years old with bp 119/73. What is the estimated increase in
my life expectancy were I to reduce my salt intake by 4gms a day which
then resulted in a blood pressure decrease of 2/1? I suggest that is what
is of interest to most people; their individual risk. Talk of "lives
saved" is nonsense. To begin with, lives are not saved: deaths are maybe
delayed and it is very important by how much. Secondly, by considering a
large population, for example that of our planet, impressive and, to the
man in the street, frightening statistics can be conjured up.
I'll refrain from making any general statements about Public Health,
as I don't wish to be banned from responding to future articles.
Competing interests: No competing interests
Re: Policy options to reduce population salt intake
This article, as well as the 12/20/2011 Lizzy Brewster article "High salt meals in staff canteens of salt policy," presume positive health outcomes from salt reduction that simply have never been well established.
A meta-analysis of 167 studies by Graudal and co-workers (1) confirmed and expanded upon previous reports that significant dietary sodium restriction from an average of above 150 mmol per day to a level of less than 120 mmol sodium per day resulted in limited but significant reductions in blood pressure. However, the meta-analysis went further to confirm and quantify the unfavorable impacts that sodium restriction had on several other risk factors for cardiovascular disease. These included significant increases in renin, aldosterone, adrenaline, noradrenalin, cholesterol and triglycerides. Renin and aldosterone were of particular concern as they have been repeatedly associated with increases in cardiovascular mortality in long-term follow-up studies (2).
In a recent study, published in the Journal of the American Medical Association (JAMA)(3), researchers found moderate salt intake to be associated with the lowest risk of cardiovascular events, whereas low intakes, equivalent to less than 3,000 mg sodium per day, were associated with an increased risk of cardiovascular death and hospitalization for congestive heart failure and higher intakes of greater than 7,000 mg sodium per day were associated with an increased risk of stroke, heart attack and other cardiovascular events. The familiar ‘J’-shaped curve, reminiscent of Bertrand’s Rule, appeared to describe the dose-response relationship.
The ongoing debate on salt and health does not result from a paucity of data, it results from an absence of dose-response data, and the Dietary Reference Intakes (DRIs) for sodium, the world’s supposed ‘bible’ on nutrients, admitted as much. The use of the surrogate blood pressure argument, in lieu of comprehensive dose-response evidence, has been a decades-long red herring, which only served to delay the acquisition this data so we may understand the relationship between salt and health.
Comparing the InterSalt study data on average salt consumption in around the world with life expectancies makes it clear that the more salt a population eats, the longer it will live. There is no question about this relationship whatsoever. While no cause and effect between sodium intake and lifespan is specifically implied, the data does demonstrate the compatibility between longevity and the associated levels of sodium intake.
It is of great interest that we consumed between 18-20 g salt per day from the early 1800s until the end of WWII, based on military archives for military rations around the world. During the War of 1812, despite its high cost, salt rations amounted to 18g per day (4). Declassified World War II documents regarding rations fed to American prisoners of war in Germany show a ration of 140g per week or 20g per day (5).
After World War II, when refrigeration began to replace salt as the main means of food preservation, salt consumption in the US, (and somewhat later in other countries, such as Finland) dropped dramatically to about half or 9 g/day and stayed at that level until now (6).
It is interesting that this drop took place without pressure from the Dietary Guidelines, the IOM, WHO or the FDA, and without the strident input of salt-reduction advocates. All it took was a natural shift to a cold-chain-based food supply and the wisdom of the body’s innate mechanism to maintain homeostasis.
It is time we start getting more evidence and fewer opinions. It is time for a RCT on the impact of salt reduction on an agreed range of accepted health outcomes.
References
(1) Graudal NA, Hubeck-Graudal T, Jürgens G. Effects of low-sodium diet vs. highsodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride (Cochrane Review). Am J Hypertens 2011; 25:1–15.
(2) Gonzalez MC, Cohen HW, Sealey JE, Laragh JH, Alderman MH. Enduring direct association of baseline plasma renin activity with all-cause and cardiovascular mortality in hypertensive patients. Am J Hypertens 2011; 24:1181–1186.
(3) O'Donnell MJ, Yusuf S, Mente A, Gao P, Mann JF, Teo K, McQueen M, Sleight P, Sharma AM, Dans A, Probstfield J, Schmieder RE. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA. 2011 Nov 23; 306(20):2229-38.
(4) Rations: The History of Rations, Conference Notes, Prepared by The Quartermaster School for the Quartermaster General, January 1949, accessed at http://www.qmfound.com/history_of_rations.htm on 12/20/2012.
(5) American Prisoners Of War In Germany, Prepared by Military Intelligence Service War Department, November 1945, Restricted Classification Removed - STALAG 17B (Air Force Non-Commissioned Officers) accessed at http://www.valerosos.com/AMERICANPRISONERSOFWAR.pdf on 12/20/2012.
(6) Bernstein AM, Willett WC, Trends in 24-h urinary sodium excretion in the United States, 1957-2003: a systematic review. Bernstein AM, Willett WC. Am J Clin Nutr. 2010;92(5):1172-1180. Epub 2010 Sep 8.
Competing interests: The author is employed by the Salt Institute and was formerly Director of the United Nations FAO Global Agro-Industries program and Scientific Secretary of the WHO/FAO International Consultative Group on Food Irradiation.