Salt in food

[Guest guest]

Hi All,

Salt may be too much in foods, according to:

Feng J He and Graham A MacGregor

Salt in food

The Lancet 365, Iss 9462, Mar 5-11 2005 844-845

Correspondence

Sharp, in his Comment on labelling salt in food (Dec 11, p

2079),1 seems to support a reduction in salt intake, and call for

clearer labelling of salt content in food. However, in the second

paragraph, he seems to pour cold water on this and cast doubt on the

link between salt intake and cardiovascular disease.

Although the effect of salt reduction on cardiovascular deaths is

extrapolated from blood pressure data,2 prospective epidemiological

studies have shown that a lower salt intake is related to a lower

risk of stroke,3 coronary heart disease,4 and heart failure.

Sharp fails to put into perspective the comparison of reducing

salt intake with other dietary or lifestyle interventions. No outcome

trials show a reduction in mortality on stopping smoking, reducing

fat intake alone without fish oil supplements, losing weight,

increasing fruit and vegetable consumption, or increasing exercise.

Indeed, for most of these factors, no attempt has been made to do

long-term trials owing to the innate difficulty of conducting and

funding such trials, and to the ethics of randomly putting a group of

people on, for example, a high salt diet for the rest of their lives.

The totality of evidence for reducing salt, including

epidemiological, migration, intervention, treatment, animal, and

genetic studies, is stronger than for any other lifestyle

interventions.

Sharp also claims that not everyone will benefit from blood-

pressure lowering. However, he fails to mention the meta-analysis of

1 million individuals that showed a continuous relation between blood

pressure and cardiovascular risk down to 115 mm Hg systolic or 75 mm

Hg diastolic,5 and that most of the adult population (83% in England)

have a blood pressure above this level and will benefit from blood-

pressure lowering. At the same time, Sharp does not point out that

reducing salt intake lowers blood pressure significantly in

normotensive and hypertensive individuals.2

From a public-health perspective, reducing salt intake is one of

the easiest strategies to carry out, in that around 80% of salt

consumed is hidden in processed, canteen, restaurant, and fast food.

Therefore, a strategy of small reductions (10–20%), which are not

detected by the human salt taste receptors and cause no problems in

food technology, could easily be made across all foods to which salt

has been added. If such reductions were repeated every 1–2 years,

within 5 years salt intake in the UK would be reduced by about 6 g

per day. This reduction would not necessarily involve consumers

changing their dietary habits, unlike other lifestyle interventions.

This gradual reduction is the current policy of the UK government and

the Food Standards Agency, who for once are leading the world in

public health.

The benefits will be large. For instance, in the UK, a

conservative estimate suggests that 35 000 deaths—and therefore about

70 000 events— from stroke and coronary heart disease would be

prevented per year if salt intake was reduced by 6 g per day.2 It is

our view that other countries need to look at the example being set

by the UK and start taking action now to prevent large numbers of

unnecessary strokes and heart attacks occurring.

References

1 D Sharp, Labelling salt in food: if yes, how?, Lancet 364 (2004),

pp. 2079–2081.

2 FJ He and GA MacGregor, How far should salt intake be reduced?,

Hypertension 42 (2003), pp. 1093–1099.

3 C Nagata, N Takatsuka, N Shimizu and H Shimizu, Sodium intake and

risk of death from stroke in Japanese men and women, Stroke 35

(2004), pp. 1543–1547.

4 J Tuomilehto, P Jousilahti, D Rastenyte, V Moltchanov, A Tanskanen

and P Pietinen, Urinary sodium excretion and cardiovascular mortality

in Finland: a prospective study, Lancet 357 (2001), pp. 848–851.

5 Prospective Studies Collaboration , Age-specific relevance of usual

blood pressure to vascular mortality: a meta-analysis of individual

data for one million adults in 61 prospective studies, Lancet 360

(2002), pp. 1903–1913.

Salt in food

A Hoption Cann

The Lancet 365, Iss 9462 , Mar 5-11 2005, 845-846

Correspondence

Sharp1 discusses the controversy that surrounds salt

restriction in individuals with hypertension and in the general

population. However, all salt is not created equal—at least not at

the point of manufacture. While the debate on sodium restriction

continues, no mention is made of the fact that much of the world's

salt supply is now iodised. In some countries, such as the USA and

Canada, iodine is only added to table salt, whereas in others such as

Germany, it is used in the food industry as well.2

Even in countries with long-established iodisation programmes, an

increasing prevalence of iodine deficiency has been seen. In the USA,

for example, the First National Health and Nutrition Examination

Survey (NHANES I) found moderate to severe iodine deficiency (<50

ìg/L in urine) in one in 40 individuals in the early 1970s, and 20

years later, in one in nine individuals (NHANES III).3 This reduction

in iodine intake has paralleled the general decline in sodium intake—

primarily from iodised salt.3 A similar reduction in iodine status

has occurred in a number of developed countries where salt is

iodised. Inducements to reduce salt intake have been implicated in

the decreasing iodine status in Australia and New Zealand.4 In

Austria, the recent decline in urinary iodine concentrations may be

due to lower salt intake, but it could also result from the

availability of non-iodised salt in Austria after the country joined

the European Union.2

Although sodium restriction has been associated with a reduction

in blood pressure, how a simultaneous reduction in iodine intake

might affect cardiovascular disease risk over the long term is

unknown. In studies of animals fed iodine-reduced diets,3

concentrations of thyroid-stimulating hormone were found to increase,

whereas concentrations of thyroid hormone (ie, triiodothyronine) in

plasma remained unchanged; however, for cardiac tissue in particular,

a reduction in thyroid hormone concentrations was seen. Therefore,

even for individuals with normal concentrations of thyroid hormone in

serum, as in subclinical hypothyroidism, there may be insufficient

concentrations of thyroid hormones in tissue when iodine intake is

limited. Correspondingly, Fruhwald and colleagues5 investigated the

prevalence of thyroid disorders in 61 patients with idiopathic

dilated cardiomyopathy. Only two patients (3%) showed completely

normal thyroid morphology and function. Moreover, the duration of

cardiomyopathy was significantly correlated with thyroid gland

volume, suggesting that iodine deficiency (the most common cause of

goitre) secondary to sodium restriction was the underlying cause.

Thus, there is evidence to suggest a potential negative effect of

salt restriction in regions where salt is iodised.

The Japanese have a diet that is remarkably high in sodium and

iodine, yet rates of coronary heart disease are low. It would be

interesting to determine whether iodine has a role in this reduced

risk of heart disease. Prospective epidemiological studies examining

the underlying influence of iodine intake on cardiovascular disease

risk or its consequences in individuals with a history of

cardiovascular disease are warranted.

References

1 D Sharp, Labelling salt in food: if yes, how?, Lancet 364 (2004),

pp. 2079–2081.

2 Iodine deficiency disorders (IDD) Prevalence and Control Program

Data (http://www.people.virginia.edu/~jtd/iccidd/mi/idd.htm)

(accessed Dec 14, 2004).

3 SA Hoption Cann, JP van Netten and C van Netten, Iodized salt and

hypertension, Arch Intern Med 162 (2002), pp. 104–105.

4 CD Thomson, Selenium and iodine intakes and status in New Zealand

and Australia, Br J Nutr 91 (2004), pp. 661–672.

5 FM Fruhwald, S Ramschak-Schwarzer and B Pichler et al., Subclinical

thyroid disorders in patients with dilated cardiomyopathy, Cardiology

88 (1997), pp. 156–159.

Cheers, Al Pater.