The bread of the 21^st century

Trevor C Beard

Senior Research Fellow, Menzies Centre for Population Health, Hobart

Introduction

I first met Jo Rogers at a meeting of the Food Standards Committee of the National Health and Medical Research Council. I was so impressed with her contribution that I often consulted her afterwards, especially when I discovered that we had a mutual interest in salt. Her death has been a personal loss to me and to everyone who knew her.

I learnt by accident at a committee meeting of the Australian Nutrition Foundation (ANF) in the 1980s that Jo Rogers had served sandwiches made from 'salt free' (no added salt) bread. The filling is more noticeable than the bread in a sandwich, and I think no-one else realised that we shared with Jo Rogers what I hope will be the bread of the 21st century. At present the maximum of eight servings of cereal foods sometimes recommended (1) would provide 56 mmol of sodium with standard bread slices or 74 mmol with toast thickness. As the recommended dietary intake (RDI) is 40 to 100 mmol per day (2,3), you can follow either the cereal guideline or the RDI for sodium, but not both if your cereal is ordinary bread.

How important is the RDI for sodium?

A commercial newsletter recently alleged that the influence of salt on blood pressure 'is probably trivial' and any reduction possibly 'hazardous' (4). If true, this would have been 'some turnaround', as Cherry Ripe called it in The Australian. However, the original source was a Belgian report which stated that the public would only accept trivial changes, which of course would have trivial effects (5). The alleged health hazards have not been substantiated. It is reassuring to note that, according to a report in The Hobart Mercury, the publisher of the commercial newsletter may develop functional foods for hypertension (Commins P. Healthy profits in food design. The Hobart Mercury, Thursday 28 November 1996) which of course will depend heavily on the effectiveness and safety of low salt diets.

It is remarkable that high blood pressure (BP) falls so often with a lower salt intake. Hypertensive patients who have eaten excess salt for 50 years may start to recover within four to six weeks. At a perfectly normal BP of 100/60 mm Hg there is little, if any, change but people who have had some rise of BP with age, for example to 120/80 mm Hg, can usually expect a small fall (6). Most people with hypertension (³ 140/90 mmHg) also have a partial recovery (6). Even malignant hypertension with a BP in excess of 250/140 mm Hg shows a partial reduction in BP in 70% of cases whose sodium intake is reduced below 10 mmol per day with a diet of fruit and cereal (7). This is the only non-pharmacological measure known to reverse malignant hypertension.

Cases completely refractory to dietary change are a minority, and the dietary guideline, 'Choose low salt foods' often permits anti-hypertensive drug doses to be reduced or even discontinued (8). Low salt foods are defined in the Food Standards Code (9) as foods with a sodium content £ 120 mg/100 g (£ 52 mmol/kg). Any high salt food of course can compromise the result, especially a staple such as bread, which exceeds the definition by 400 to 500%.

The international consensus

Some of the adverse effects of salt on human health (10,11) are shown in Table 1. Salt in preservative concentration is associated with chronic gastritis (12), and its role as a co- carcinogen in cancer of the stomach (12) has been confirmed experimentally in rats (13). Cancer societies warn the public against salt-cured foods (14).

An intake of sodium in excess of the RDI causes an obligatory loss of calcium in the urine, with special relevance to kidney and bladder stones (15) and osteoporosis (15). It increases total body water by about two litres (17), and this fluid retention is a factor in oedematous states such as idiopathic oedema (18), premenstrual syndrome (19), carpal tunnel syndrome (20) and Meniere's syndrome (24). Young women referred to me with Meniere's syndrome generally lose their premenstrual syndrome (PMS) as well as the vertigo after choosing low salt foods exclusively, including bread.

Table 1. Some conditions caused or aggravated by a high salt intake (10,11)

Among the many other effects, hypertension is especially important because it is so common. National Heart Foundation survey data show that over half of urban Australian women have hypertension before their 70th birthday (22). The even higher male prevalence falls after the age of 60 years with a higher mortality from heart disease and stroke, sequelae of hypertension (23). The need for lifelong medication for such a common condition makes hypertension one of our most expensive diseases, and few discoveries in public health could be more important than the clear evidence that it is preventable.

Essential hypertension is a multifactorial disease. The international consensus attributes it to an interaction between genetic predisposition and avoidable environmental factors: overweight, lack of physical exercise, excess alcohol consumption, excess dietary sodium, inadequate dietary potassium and psychological factors (24). The relative importance of sodium tends to be underestimated. One of several reasons for this is that thin people and teetotallers make it easy to demonstrate the association with overweight and alcohol, just as the better health of non-smokers strongly highlights the link between lung cancer and cigarettes. If everyone smoked 40 cigarettes a day, lung cancer would be quite common but would have no demonstrable link with cigarettes. Similarly, the demonstrable association between salt and hypertension is weakened by the absence of salt teetotallers'. Everyone eats high salt bread and much the same range of salted groceries, the source of 75% of their salt intake (25).

Salt teetotallers do exist, however, in small numbers. They live in about 20 'salt free' (no added salt) societies (26). The Intersalt study examined random samples stratified by age and sex from three of these populations and found mean blood pressures of 96/61, 100/62 and 108/63 mm Hg, with less than 1% prevalence of hypertension and little, if any, rise of BP with age (27). People who leave these societies tend to develop hypertension, revealing the same genetic predisposition that we have (28). Sceptics point out correctly that the migrants may also gain weight, take less exercise, drink alcohol and eat less fruit and vegetables (less potassium). They may also find acculturation stressful.

The crucial experiment therefore would be to introduce salt to a salt free tribe with no other intervention except to measure their blood pressure at intervals. No ethics committee would ever allow this. However, chimpanzees in zoos get hypertension on a diet of Purina Monkey Chow which contains added salt, and the crucial experiment has been done with salt free chimpanzees in West Africa. Chimpanzees are our closest animal relative, with over 98% of the human DNA sequences. A randomised controlled trial-meeting the gold standard of evidence-based practice-demonstrated hypertension in chimpanzees within two years after adding salt to their usual diet of fruit and vegetables while all other factors were held constant, including the social and emotional stability of the group (28).

Six levels of dietary intake of salt

A stepwise increase in the perception of salt taste depends on a logarithmic increase in concentration (29), and the analogy with drug dosage, where stepwise responses commonly involve doubling or halving, would suggest a log scale for the other effects of salt. The Yanomama Indians have the lowest sodium excretion rate found in any free-living human society, and their intake (as distinct from their excretion rate) has been estimated at a little over 6 mmol per day (30). Multiplied repeatedly by 2.5 this reaches 1600 mmol in six steps (Figure 1).

Figure 1. Different levels of salt intake according to habitat and diet, and behaviour at one animal dietary level (0) and six human levels of sodium intakes (1-6)

A sodium intake of 6 to 16 mmol per day is found in salt free societies with a largely vegetarian diet, and 40 mmol per day is about as far as it can be extended with meat and fish (30). These were obviously normal intakes during human evolution. Where they still exist today high blood pressure is virtually absent (27).

An intake of 40 to 100 mmol per day is the Australian RDI for sodium (2,3). It is a compromise between the optimum and the feasible, and based on the hope that a little added salt may be relatively harmless (3). Hypertension is an important public health problem with sodium intakes of 100 to 250 mmol per day, the usual range in an industrial society (27). Stroke was the most common cause of death with sodium intakes of 250 to 650 mmol per day in Akita in northern Japan (31) and parts of rural Portugal (32), before salt intake was reduced there by educational campaigns. The top level of 650 to 1600 mmol per day is an experimental diet. In one study every volunteer (n = 14) whose sodium intake reached or exceeded 1200 mmol per day had a rise of blood pressure within three days (33).

Why do we like salt?

A love of salt is often considered natural 'because animals love it too', but salt-seeking as a group behaviour has not been reported in humans. It is confined to herbivores on continental grasslands remote from the coast (30). At such a low sodium intake we too might have marginal sodium deficiency and display salt hunger, but even the most salt free human group-the Yanomama Indians-detest salt when they first taste it (34). The Yanomama (n = 195) who joined the Intersalt study had a mean sodium excretion rate of 0.9 mmol per day and a median of 0.2 mmol per day (27). In our society sodium excretion is roughly 90% of intake, but very low intakes such as the estimated 6 to 8 mmol per day of the Yanomama (30) are largely recycled and not excreted.

Even the Yanomama can rapidly acquire a liking (hedonic preference) for salt (34). It comes as easily as the taste for beer and tobacco, and I regard hedonic preference in the absence of physiological need as evidence of an acquired taste. Further up the scale, an intake as high as the RDI implies complete familiarity with the taste of salt, together with the expected hedonic preference. The fact that clients who adopt moderately low salt diets (the level of the RDI) can no longer tolerate a pizza implies that the two levels above the RDI (levels 4 and 5 in Figure 1) are associated with further adaptation-an exaggerated preference.

Much of the salt in food goes undetected

From this point I will use units of mass for foods because the regulations and the commercial labels have not yet adopted international (SI) units for electrolytes. Salted peanuts taste far more salty than any brand of cornflakes, yet their sodium content is 340 mg/100 g (148 mmol/kg) while cornflakes are almost three times more salty, with one brand having a sodium content of 1020 mg/100 g (443 mmol/kg). This would be understandable if cornflakes contained a lot of other sodium compounds, but most of the sodium is added salt. Peanuts have all the salt on the surface where it is tasted, while a great deal of the salt inside the cornflakes is not tasted.

This principle underlies an experiment by Beauchamp and colleagues (35). People who habitually salted their food used far more discretionary salt when given a low salt diet (as expected), but surprisingly their total sodium excretion remained well below 100 mmol per day. Despite explicit pressure to add as much salt as they liked, they used only a fraction of the amount needed to restore the total sodium content of ordinary (high salt) meals. Surface salt added at the table is nearly all tasted. This highlights the value of the dietary guideline, 'Choose low salt foods and use salt sparingly'. Low salt foods make the difference even when table salt is added liberally (35).

Belgium versus the UK

A Belgian trial in the review cited earlier (5) achieved only a small reduction in sodium intake, men reaching 170 mmol per day, and women 132 mmol per day. Yet at about the same time no less than 22% of a random sample of the British population excreted less than 100 mmol per day in their urine. About 15% of men (n = 681) and 29% of women (n = 712) apparently observed the RDI for sodium on at least one day. A single 24-hour urine collection is a poor index of habitual consumption, nevertheless the association with hypertension was strong enough to reveal a clear trend in Figure 2. The figure shows that hypertension is more common at higher sodium excretion rates. Apparently while a Belgian town would only accept trivial changes with trivial effects, over 20% of a random sample of the British population were adopting (by their own choice) a sodium excretion rate low enough to be associated with a lower blood pressure and a lower prevalence of hypertension (28,36).

Figure 2. Distribution of normotensive (n=1425) and hypertensive (n=263) respondents by urinary sodium excretion rate in the Dietary and Nutrition Survey of British Adults, 1986-7 (36)

The key to avoiding salt

Added salt greatly extends the range of sodium content of common foods (Figure 3). Compare the sodium content of breast milk of 14mg/100g (6 mmol/kg) with the hypertonic concentration of >320 mg/100g, or >0.85% salt (140 mmol/kg) in common processed foods. Concentrations of >1000 mg/100 g, or >2.5% sodium chloride (434 mmol/kg) are associated with cancer of the stomach. These concentrations are not confined to olives and anchovies. They occur in such staple foods as cheese, corned beef and best-selling breakfast cereals. Many are saltier than seawater, which contains 1068 mg/100g (464 mmol/kg) (39).

Figure 3. Sodium content of some foods ^(a)

(a) SR, salt-reduced. Figures in brackets: 120 mg/100g (52 mmol/kg) is the upper limit for low salt foods; 345 mg/100g (150 mmol/kg) is the approximate upper limit for reduced salt bread as sold (the Food Standards Code defines it by dry weight).

A booklet in which Jo Rogers joined me as co- author (38) points out that the key to avoiding salt is to follow the guideline 'Choose low salt foods' as defined in the Food Standards Code (<120 mg of sodium per 100 g). People have to be taught the meaning of the nutrition information panel on food labels because it is not self- evident. I was very impressed with a proposal by Kellogg Aust. Pty Ltd (39) to provide a low salt box on food labels which might or might not contain a tick. Corn Flakes would carry no tick (Figure 4A). However, this was disallowed in the 1995 Code of Practice on Nutrient Claims as it was considered ambiguous to some consumers. Kellogg Aust. Pty Ltd must now omit the box when there is no tick (Figure 4B).

The guideline to choose low salt foods is lost on consumers who cannot identify them (taste is no guide). Shoppers need help with the other guidelines as well, and I offer Figure 4C as a first draft. Labels with colour printing would fill the square, circle and triangle with green, yellow and red respectively.

Figure 4. Three ways of providing simple nutrition information at the point of sale.   A food company used a panel depending on the presence or absence of ticks (A), but new regulations have precluded any mention of salt on a cornflakes packet, even without a tick (B). Each nutrient in the dietary guidelines could be represented by one of the three symbols (C). The example shown would have a high total fat content, a moderate saturated fat and sugar content and a low salt content.

The 'good food, bad food' controversy

In 1994 the National Food Authority (as it then was) issued a Discussion Paper on Functional Foods (40) containing the following statement on page 27:

Contemporary food and nutrition policy and nutrition education initiatives in Australia have adopted the adage that: 'there are no good or bad foods, only good or bad diets'. This view has been affirmed in the National Food and Nutrition Policy, the dietary guidelines for Australians and nutrition statements from the National Health and Medical Research Council. It is a view that has been accepted and promulgated with almost unique consensus by dietitians, scientists and the food industry alike.

However, I will remind this audience that the Council of Australian Food Technology Associations (CAFTA, as it then was) used this very phrase in 1988 to argue that corporate sponsors should automatically be entitled to use the logo of 'Nutrition '88' on all their products. As CAFTA was adamant, the ANF reluctantly withdrew from 'Nutrition '88'. Other withdrawals included the Dietitians Association of Australia, the Home Economics Association and the National Heart Foundation. As President of the ANF Jo Rogers wrote in her letter to CAFTA:

To say that all foods are good foods may be true as far as the law is concerned, but certainly not with respect to nutrition education. Whilst I never talk about junk food I would also never refer to certain foods as 'good' foods. Indeed there are many foods on the market that would never be missed in a healthier society.

Hearing dietitians proclaim that there are no bad foods would be reassuring - and grossly misleading - to a cardiac patient who had bought a food consisting of little else but saturated fat. Instead of being manipulated by this parrot phrase, Jo Rogers repudiated it on our behalf, and I think the ANF should continue to repudiate it for the reasons that she gave.

The ANF pyramid

Jo Rogers discriminated even among the foods that we do endorse. In the ANF healthy eating pyramid she put cereals, fruit and vegetables at the bottom (eat most) and relegated other good foods to narrower sections. Other food selection guides, such as those promoted by CSIRO, the US Department of Health and Kellogg Aust. Pty Ltd, put cereals alone at the bottom.

Cultivation of cereals is a recent human artefact and other primates such as chimpanzees still depend on fruit and vegetables. All their staple foods give them hypertension if salt is added (28). Monkey Chow has a salt content of about 6 g/kg or about 100 mmollkg (28)-a sodium content of about 240 or 230 mg/100 g in units of mass. The ten top selling Australian breakfast cereals all contain more salt than this, and eight contain it in hypertonic concentration (Table 2). Should the bottom (eat most) of the healthy eating pyramid include foods that are too salty for chimpanzees? And why do they use so much salt, when the best selling cereal of all (Weet-Bix) has the lowest sodium content? After excluding one heavily advertised outlier (Kellogg's Corn Flakes), you will find that in Table 2 the market share is almost inversely proportional to the sodium content, with a P-value of 0.06 in a sample of nine (Blizzard L, Menzies Centre for Population Health Research, Hobart, 1997, personal communication). Sales of Weet-Bix survived a reduction from its original sodium content of 440 to 280 mg/100 g (191 to 122 mmol/kg) in 1983, and since 1990 it has had a steady turnover without salt (as Lite-Bix) with a sodium content of 20 mg/100 g (9 mmol/kg).

Table 2. The ten top selling breakfast cereals ranked by market share and (inversely) by sodium content, Australia, 1997 (a)

Source: Market share, Retail World Marketing Guide, 1997; sodium content, product labels, April 1997.

Salt free cereals are highly palatable with fruit for breakfast, and fruit can be served with salt free cereal at the evening meal too, with a low fat custard or low fat yoghurt. I can see no place for salt in a sweet dish. All the large manufacturers include salt free breakfast cereals in their range, many of which have held their market niche for decades with little, if any, promotion from dietitians. Paying only lip service to the guideline to avoid high salt foods, we are apparently blind to the fact that they are especially out of place at the bottom of the ANF Pyramid (eat most).

The National Heart Foundation 'Pick the Tick' program

Even the National Heart Foundation's 'Pick the Tick' program endorses high salt foods at the bottom of the pyramid. Their liberal endorsement of breakfast cereals with a hypertonic salt content (sodium up to 400 mg/100 g) seems especially pointless when Weet-Bix can lead the market with 280 mg/100g. I have always applauded the National Heart Foundation for doing something constructive when no one else was taking any initiative, and I have watched the tick program with interest. I do not think anyone could have foreseen its present predicament with bread.

The initial criterion for sodium content of 345mg/100g (150mmol/kg) seemed an appropriate starting point for bread, with room for further reduction. But even at 345 mg/100 g the industry objected that consumers could tell the difference and would not buy it. This is a fatal objection because the 'tick' has to pay for itself, and products that carry it must have a bigger market to meet the administrative and other costs of the program. Raising the criterion to 450 mg/ 100g brought it within the range for standard bread and bread rolls of 400 to 725 mg/100 g (173-315 mmollkg). If the standard range is mandatory even for bread with a tick, the National Heart Foundation will permanently endorse the status quo. As we saw earlier, trivial changes have trivial effects (5).

The tick experiment was worthwhile but bread has shown that the obligation to increase profits right from the start is a fundamental flaw that sets some products up for failure. Standard bread with the tick damages the credibility of the rest of the program.

Does the salt in bread really matter?

The salt content of fresh bread (about 1.4%) would be unpleasant in soup, where it can all be tasted. It is high enough to give a jam sandwich no less than two-thirds of the salt content of a Vegemite sandwich. The Working Party on Sodium in the Australian Diet noted that when bread supplies most of the energy needed for manual labour - as it should - it supplies over half the total daily sodium intake (Hosking M, Royal Prince Alfred Hospital, Sydney, 1984, personal communication). With a food like that at the bottom of the pyramid (eat most), what is the relevance of a salt shaker at the top with a line through it?

A gradual reduction in sodium intake may not be the best approach. It may be better to advise people to cut out salt - an approach that is similar to advising smokers that to stop smoking is not only better than cutting down, it is also easier. The palate adapts very rapidly to a change of flavour such as taking tea without sugar to avoid 'empty kilojoules'. If some people need tea without sugar, about two million Australians need bread without salt. It is for many people the key to a lower blood pressure without medication (or with a lower anti-hypertensive dose), and it is the key to abolishing the fluid retention of PMS and Meniere's syndrome. I have seen people's lives transformed by including bread in the simple dietary guideline to choose low salt foods. As salt cannot be tasted in low salt bread there is a preference for salt free (no added salt) bread, which provides even greater latitude with the rest of the diet. The 1995 Code of Practice on Nutrient Claims reserves the term 'salt free' for foods with a sodium content of no more than 5 mg/ 100 g. An amendment raising this to 23 mg/ 100 g would be more practical for bread.

Salt free bread, as defined in this Oration (no added salt), is on sale in every Australian capital city including Darwin, and we have a professional responsibility to introduce it to the people who need it. Tourists in village accommodation in Tuscany can buy only salt free bread. Though unfamiliar at first, the taste is easily acquired, and they discover that bread has been salt free in Tuscany for about 300 years (originally to avoid the salt tax). I have met people who realised for the first time that bread contained salt when they read the instruction book for their new bread machine. While still eating ham and bacon, some have started making their own bread without salt and found it excellent. In southern Tasmania Woolworths supermarkets (trading As 'Purity') sell no less than six different varieties of salt free bread.

The 21st century has to resolve a fundamental conflict between two dietary guidelines (eat more bread and cereals and choose low salt foods). We have full support from the food industry - low salt and no added salt breakfast cereals and bread are already on the market. The problem is public ignorance - a challenge for nutrition education, which is supposed to be our job. Jo Rogers set the example. Jo Rogers was no eccentric, she was one of Australia's most notable dietitians, and a woman ahead of her time. Jo Rogers served salt free bread at ANF meetings over a decade ago.

References

1. Cashel K, Jeffreson S. The core food groups. Canberra: NHMRC, 4995:34.
2. Bullock JR. Sodium, In: Truswell AS, Dreosti IE, English RM, Rutishauser INE, Palmer N, editors. Recommended nutrient intakes: Australian papers. Sydney: Australian Professional Publications, 1990:176-81.
3. Beard TC. Sodium update. In: Truswell AS, Dreosti IE, English RM, Rutishauser THE, Palmer N, editors. Recommended nutrient intakes: Australian papers. Sydney: Australian Professional Publications, 1990:182-90.
4. Kellogg's 'Update' and media release. Issue 2.97 (April 1997), page 1.
5. Staessen JA, Lijnen P, Thijs L, Fagard R. Salt and blood pressure in community-based intervention trials. Am J Clin Nutr 1997;65(suppl):66IS-670S.
6. Law MR, Frost CD, Wald NJ. By how much does dietary salt reduction lower blood pressure? III-analysis of data from trials of salt reduction. BMJ 1991;302:819-24.
7. Medical Research Council. The rice diet in the treatment of hypertension. Lancet 1950;2:509-13.
8. Beard TC, Cooke HM, Gray WR, Barge R. Randomised controlled trial of a no-added-sodium diet for mild hypertension. Lancet 1982;2:455-8.
9. Australia New Zealand Food Authority. Food Standards Code, Section R8. Low sodium and low salt content foods. Canberra: Australian Government Publishing Service, 1997.
10. Antonios TFF, MacGregor GA. Deleterious effects of salt intake other than effects on blood pressure. Clin Exper Pharm Physiot 1995;22:180-4.
11. Antonios TFF, MacGregor GA. Salt-more adverse effects. Lancet 1996;348:250-1.
12. Joossens JV. Stroke, stomach cancer and salt. In: Kesteloot H, Joossens JV, editors. Epidemiology of arterial blood pressure. The Hague: Martinus Nijhoff, 1980:489-508.
13. Takahashi M, Nishikawa A, Furukawa F, Enami T, Hasegawa T, Hayashi Y. Dose-dependent promoting effects of sodium chloride (NACI) on rat glandular stomach carcinogenesis initiated with N- methyl-M-nitro-N-nitrosoguanidine. Carcinogen 1994;15:1429-32.
14. American Institute for Cancer Research. Diet, nutrition and cancers of the colon and rectum. Washington DC: AICR Information Series, undated.
15. Muldowney FP, Freaney R, Moloney MF. Importance of dietary sodium in the hypercalciuric syndrome. Kidney Int 1982;22:292-6.
16. Goulding A. Osteoporosis: why consuming less sodium chloride helps to conserve bone. NZ Med J 1990; 103:120-2.
17. Freis ED. Salt, volume and the prevention of hypertension. Circula- tion 1976;53:589-95.
18. MacGregor GA, Markandu ND, Roulston JE, Jones IC, de Wardener HE. Is idiopathic oedema idiopathic? Lancet 1979;1:397-460.
19. Birnbaum S. Fluid and electrolyte metabolism in the gynecologic patient. Clin Obstet Gynecol 1975;7:178-83.
20. Beard TC. Salt in medical practice. Hobart: Menzies Centre for Population Health Research, 1991:60.
21. Nelson JR. Vertigo. In: Beeson PB, McDermott W, editors. Textbook of Medicine, 12th edn. Philadelphia: WB Saunders, 1967:1479-80.
22. National Heart Foundation of Australia. Risk factor prevalence study: survey no. 3-1989. Canberra: NHF, 1990:44.
23. Kirkendall WM. Essential hypertension. In: Genest J, Kuchel 0, Hamet P, Cantin M, editors. Hypertension: physiopathology and treatment, 2nd ed. New York: McGraw Hill, 1983:732-53.
24. WHO/ISH Guidelines Committee. Third WHO/ISH meeting on prevention of hypertension and cardiovascular disease. Puerto Cervo, Italy: June 15-17, 1995.
25. James WPT,,Ralph A, Sanchez-Castillo CP. The dominance of salt in manufactured food in the sodium intake of affluent societies. Lancet 1987;1:426-9.
26. Tobian L. The relationship of salt to hypertension. Am J Clin Nutr 1979;32(suppl):2739-48.
27. Intersalt Cooperative Research Group. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Br Med J 1988;297:319-28.
28. Denton D, Weisinger R, Mundy Ni, Wickings EJ, Dixson A, Moisson P, et al. The effect of increased salt intake on blood pressure of chimpanzees. Nature Medicine 1995; 1: 1009-16.
29. Meiselman HL. Adaptation and cross-adaptation of the four gustatory qualities. Percept Psychophys 1968;4:368-72.
30. Denton D. The hunger for salt. Berlin: Springer-Verlag, 1984.
31. Sasaki N. High blood pressure and the salt intake of the Japanese. Jpn Heart J 1962;3:313-24.
32. Forte JG, Pereira Miguel JM, Pereira Miguel MJ, de Pddua F, Rose G. Salt and blood pressure: a community trial. J Human Hypertens 1989;3:179-84.
33. Luft FC, Rankin LI, Bloch R, Weyman AE, Willis LR, Murray RH, et al. Cardiovascular and humoral responses to extremes of sodium intake in normal black and white men. Circulation 1979;60:697-706.
34. Chagnon NA. Yanomamo: the fierce people, 3rd ed. New York: Holt Rinehart Winston, 1983:63.
35. Beauchamp GK, Bertino M, Engelman K. Failure to compensate decreased dietary sodium with increased table salt usage. JAMA 1987;258:3275-8.
36. Beard TC, Blizzard L, O'Brien DJ, Dwyer T. Association between blood pressure and dietary factors in the dietary and nutritional survey of British adults. Arch Intern Med 1997; 157:234-8.
37. Seawater. Britannica CD, version '97. Encyclopaedia Britannica, Inc, 1997.
38. Beard TC, Rogers J. The key to avoiding salt. Hobart: Salt Skip Incorporated, 1990.
39. Irwin T. Kellogg's adopts new on-package approach to nutrition education. Nutrition News (newsletter of National Heart Foundation of Australia). Issue No. 13, March 1995:7.
40. National Food Authority. Functional foods: policy discussion paper. Canberra: National Food Authority, 1994:27.

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