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Magnes Res 1989 Sep;2(3):195-203

Recommended dietary amounts of magnesium: Mg RDA

J. Durlach

CHU Cochin--Port Royal, 27 Rue du Fg St. Jacques, F-75674 Paris Cédex 14, France

Preliminary data on this subject were presented at the International Workshop "Recommended Dietary Amounts of Minerals" organized by the International Life Sciences Institute, European Branch, at Limelette Castle near Brussels, May 5-6, 1989.

Summary: In developed countries, the recommended dietary amounts of magnesium have been set at 6 mg/kg day. The magnesium requirements for optimal health in the adult population depend on mesological and constitutional conditioning factors. They may intervene at every stage of magnesium metabolism: absorption, circulation, storage and excretion. The influence of other nutrients is more significant on magnesium absorption than on urinary excretion. Among the multiple interactions it is important to emphasize the maintenance of a Ca/Mg ratio close to 2 in the intake. Magnesium deficit and stress reinforce each other in a pathogenic vicious circle. The Bw35 allele of HLA typing and behavioural type A discriminate two constitutional factors increasing magnesium requirements. The effective passive regulatory mechanism for magnesium overload, the lability of the active regulatory mechanisms for magnesium deficit and the considerable need for exchangeable magnesium are factors which attribute special importance to balance studies in determining the magnesium intake which prevents negative magnesium balance and magnesium deficiency.

Marginal primary magnesium deficit affects a large proportion of the population (15 to 20%), in keeping with a daily mean magnesium intake slightly over 4 mg/kg day versus the Mg RDA of 6 mg/kg day. A physiological oral magnesium load test, evaluated through non-specific and specific clinical and paraclinical items, constitutes the best proof that the clinical pattern depends on an insufficient magnesium intake, confirmed after one month of supplementation. Further research appears necessary. It would be advisable to carry out long-term magnesium balance studies in European countries on the self-selected diets of adults, together with comparisons of direct evaluation of magnesium in the diet with data obtained from tables of food composition. Magnesium intervention trials should be planned to determine whether magnesium supplements decrease the pathogenic consequences of magnesium deficit and particularly to evaluate the efficiency of magnesium supplements in latent tetany (hyperventilation syndrome, "idiopathic" Barlow's disease). Supplementation should consist of a high magnesium density nutrient such as magnesium in water, which has better bioavailability than magnesium-fortified foods.

Key words: Balance, deficit, excess intake, load, magnesium, marginality, needs, recommended allowances, requirements, supplementation, turnover.


Magnesium is an essential metal. The magnesium requirement should not be determined in terms of an absolute amount. The requirement is relative since it is strictly correlated with various mesological and constitutional conditioning factors. Therefore recommended dietary amounts of magnesium (Mg RDA) must agree with the data from balance studies in healthy adults and with prevention of the clinical manifestations of marginal primary magnesium deficit.

The aim of this paper is (1) To analyse the conditioning factors of magnesium requirements; (2) To define Mg RDA in developed countries according to balance studies; (3) To show the consistency between Mg RDA and prevalence of marginal primary magnesium deficit in human beings; and (4) To suggest further research.

Conditioning factors of Mg requirements

I shall successively consider magnesium essentiality and the related physiological oral magnesium load test, the concepts of absolute and relative requirements and the nature of the conditioning factors.

Mg essentiality and physiological oral Mg load test

In 1926, Jehan Leroy proved the essential character of magnesium for mice. Subsequently, in the thirties the groups of E. MacCollum and D.M. Greenberg revealed many of the physiological properties of magnesium, examining in the rat the multiple effects of a lack of magnesium in the diet on development, reproduction, neuromuscular apparatus and humoral balance. They then studied the specific reversibility of such deficits using a physiological oral load of magnesium. These studies provided the first experimental basis in animals for a diagnostic test of magnesium deficiency by oral loading with physiological doses of magnesium, and while high intakes of magnesium have non-specific pharmacological effects, oral physiological doses are devoid of any such activity. Their effectiveness in a clinical context constitutes the best tool to diagnose magnesium deficiency1.

Absolute and relative requirements

"Absolute magnesium requirement" is an erroneous concept for magnesium--as well as for all the minerals. In experimental deficiency, it is possible to study the effects of the lack of a single nutrient in the same environmental conditions and in a homogeneous strain. Such an approach does not mirror the multiplicity of interacting factors that affect nutritional requirements. The magnesium requirement is thus relative, according to individual differences which may be either genetic or environmental1,2.

Conditioning factors of Mg requirements

Conditioning factors may intervene at every stage of magnesium metabolism: absorption, circulation, storage and excretion. Intestinal absorption is the sum of simple passive diffusion (one third) and of active process of facilitated diffusion (two thirds). The latter may play a role in regulating processes. Magnesaemia is remarkably stable in healthy subjects. On the average less than 30% of the Mg intake is absorbed. Total body Mg is 1000 mmol, i.e. 24 g. The maintenance of the gradient between intra- and extra-cellular Mg is active: efflux by active diffusion and influx by facilitated diffusion, which are both energy-dependent processes.

Excretion is essentially renal. It is very important to note that reabsorption functions very close to saturation1. Intestinal excretion and sweat are generally of secondary importance.

Mesological conditioning factors

The main mesological conditioning factors which concern Mg requirements are other constituents of the diet and stress among the environmental factors.

Other nutrients and Mg requirement

All the macronutrients and micronutrients interfere with Mg requirements. Slightly acid diets rich in protein (especially animal protein), unsaturated fatty acids, medium chain triglycerides and volatile fatty acids, sodium, vitamin B, lactose and vitamin D favour Mg absorption. The absorption of magnesium is also linked to that of water, which modifies the physicochemical nature of magnesium1-3. Lastly, diets which enhance the secretion of insulin, PTH, 1,25(OH2)D and perhaps certain polypeptide digestive hormones (i.e. VIP, CEP) improve Mg absorption and thus may also intervene in Mg storage. Conversely some vegetable proteins, ammonia compounds, saturated fats, dietary fibres, phytic acid, an excess of phosphorus, calcium or alcohol, and slight alkalinity tend to inhibit Mg absorption1.

Expansion of extracellular fluid (especially in cases of sodium sensitivity), any agent causing hypercalcaemia (calcium, vitamin D, lactose), proteins, all sugars metabolized in the kidney (such as glucose), alcohol, acidifiers, diets which enhance ADH, and aldosterone all increase magnesuria.

Conversely phosphorus and the D vitamins (in moderate doses) and diets which enhance secretion of calcitonin, PTH, the insulin, or glucagon reduce magnesuria.

The influence of other nutrients on Mg requirement has a more significant effect on Mg absorption than on urinary Mg excretion4. Among the multiple interactions between various nutrients and magnesium, it is particularly important to stress the maintenance of a Ca/Mg ratio close to 2 in the intake5.

Stress and Mg requirement

Stress is capable of inducing magnesium deficit through two main types of neurohormonal mechanisms. Stress makes three major regulatory systems of Mg homeostasis ineffective: it replaces hypersecretion of physiological doses of adrenaline by large amounts of catecholamines, it reduces secretion of insulin, and it increases urinary loss of taurine. Stress induces three types of hypersecretion (ADH, thyroid hormones and corticoids) which increase magnesium urinary leakage. These different elements combine to induce a state of magnesium depletion that is due mainly to hypermagnesuria (Fig. 1, Stress induction of magnesium deficit).

Figure 1.

Conversely magnesium deficit creates a state of hypersusceptibility to stress, even in cases of chronic marginal deficit1,6. Thus magnesium deficit and stress reinforce each other in a pathogenic vicious circle (Fig. 2, The pathogenic "vicious circle": magnesium deficit-stress.)

Figure 2.

Constitutional conditioning factors

Constitutional conditioning factors may intervene in individual differences in Mg requirements at several stages. In the cell the efficiency of the enzyme activities may be variable, requiring different levels of magnesium as cofactors. Neurohormonal factors which either regulate or disturb magnesium metabolism may be constitutionally more or less labile. Two markers of these constitutional differences are currently available. In people carrying the Bw35 allele, erythrocyte magnesium--and to a lesser extent plasma magnesium--are lower than in all the other HLA groups7. The interindividual HLA typing differences in magnesium metabolism reflect genetic differences in the activity of the quinidine-sensitive Na2+/Mg2+ exchange8. Secondly, using a synchromatic Jenkins test to determine behavioural type A or B, it has been shown that classification as type A indicates predisposition to magnesium deficit, probably because of an increased stress susceptibility and a trend to high alcohol ingestion1.

Balance studies

I shall now discuss the evaluation of Mg RDA in developed countries in relation to balance studies in healthy adults and the respective values of other evaluations of magnesium requirements.

Data from Mg balance studies

As early as 1964 9 and subsequently in updated papers2,10-12, M.S. Seelig, analysing a large review of balance studies in developed countries, concluded that the minimum Mg intake required to maintain metabolic balance in equilibrium was about 6 mg/kg body weight per day, that is to say 330 mg for a 55 kg woman and 420 mg for a 70 kg man. As early as 1968, our initial personal data13 and subsequent updated reviews1,14 have been in good agreement with this level of Mg intake to ensure zero or positive Mg balance (Fig. 3, A comparative study in men and women of magnesium balance...). It is appropriate to note that it is customary when determining Mg balances to ignore not only the small dermoskeletal and menstrual losses but also magnesium in sweat, which can be a real accessory mechanism of deficit. Thus one often obtains an exaggeratedly optimistic estimate of Mg balance1,10.

Figure 3.

Significance of balance studies

It appears perfectly logical that an intake of a nutrient less than the sum of the daily losses must at some time result in deficiency and that such an intake must therefore be considered inadequate. Nevertheless this assumption may be erroneous in determining human requirements for minerals if considerable adaptation of the pool size to the habitual intake is possible (with concomitant conservation of good health, independently evaluated)15. This is not usually the case with magnesium.

Efficiency of the regulatory mechanism for Mg overload

Regulation of Mg metabolism against an overload is very efficient. The renal reabsorptive mechanisms of Mg function at or very near saturation. In healthy persons, compensating hypermagnesuria represents an effective passive regulatory mechanism for Mg overload. Positive Mg balance in healthy subjects does not induce toxicity1 and negative Mg balance does not arise from a compensatory mechanism of a Mg overload1.

Lability of regulatory mechanisms for Mg deficit

The complex mechanisms which tend to compensate for an insufficient magnesium intake are most often labile active mechanisms. Their failures are well known, and in keeping with narrow limits of adaptation to negative balances for an ion of which the needs are high1. Positive balances, after an insufficient intake of magnesium, indicate retention of the ion to satisfy a thirst for magnesium created by Mg deficiency, the consequences of which will therefore progressively be alleviated1.

Importance of Mg turnover

Daily turnover of magnesium is particularly high. The ratio of the Mg pool to total body Mg is about 8.1%, a ratio more than 15 times that of the corresponding selenium ratio, 30 times that of calcium and 400 times that of iron. This very high turnover is not really compatible with a compensatory decrease in the pool size when the habitual intake is reduced. Conversely the high need for exchangeable Mg for normal health induces a substantial increase in the pool size during severe Mg deficit, which might be a defence reaction1,16.

Thus the effective passive regulatory mechanism for Mg overload, the lability of the active regulatory mechanisms for Mg deficit, and the large need for exchangeable Mg are factors which attribute special importance to Mg balance studies in determining Mg intake sufficient to prevent negative magnesium balance and magnesium deficiency.

Other evaluations of Mg RDA

In animal husbandry and in experimental nutrition--in vitro or in vivo--a minimal intake to prevent partial aspects of a mineral deficiency (growth, reproduction, lactation) may be studied. But in human nutrition such studies of functional requirement are not permissible for evident ethical reasons. Nevertheless the evaluation of Mg RDA in terms of the amount required to prevent hypomagnagnesaemia appears analogous to these laboratory-based studies, and there is now much experimental and clinical data showing that severe magnesium deficit may exist without a decrease in magnesaemia1,2,5,16. In the human being, Mg RDA must be optimal for health, obviously insuring a normal degree of storage and preventing the development of marginal primary magnesium deficit.

Marginal primary Mg deficit

Overt and marginal deficiency and Mg requirements

Firstly, and most to blame for physicians' reluctance to accept the possibility that Mg deficiency might be contributory to medical problems, is the classical concept that the daily requirement of a nutrient is the amount that prevents overt signs and symptoms of deficiency. Acute and subacute experimental and clinical data on Mg deficit have contributed greatly to knowledge of the physiological and pathological importance of Mg1,11,17. But it is the experimental clinical form of marginal primary Mg deficit which is linked with marginal intakes1,2,5,18.

Marginal primary Mg deficit in human beings

Neuromuscular hyperexicitability due to marginal primary magnesium deficit accounts for its nonspecific symptomatology. Latent tetany, with or without mitral valve prolapse, allergy or pseudoallergy represent by far the most frequent expressions of marginal magnesium deficiency.


Latent tetany due to primary magnesium deficit affects a large proportion of the population (15 to 20%)1,18,24. This large prevalence--established in Europe--is not surprising because of the marginal nature of the magnesium intake. The magnesium concept of the so-called "idiopathic mitral valve prolapse" has important epidemiological implications: the high prevalence of this disorder (5% of the population in the USA) implies a three- to four-fold higher incidence of latent tetany due to primary magnesium deficit since "idiopathic mitral vale prolapse" occurs in only one third or one quarter of the cases. Therefore, both in the USA and in Europe, latent tetany due to primary magnesium deficit should affect a large part of the population; such a similar prevalence would not be surprising since the marginal nature of the magnesium intake is much the same in the two continents23,24. Furthermore this prevalence of marginal primary magnesium deficit seems consistent with the estimation of nutrient deficiency using probability analysis25,26 in populations where the mean Mg daily intake is slightly above 4mg/kg day1-3,13,14,27-38 versus Mg RDA set at 6mg/kg day1-3.

Physiological oral Mg load test

Since the principal form of expression of marginal dietary intake remains latent tetany due to magnesium deficit, it is essential to seek out its manifestations and in general the diagnosis relies on the magnesium oral loading test conducted with physiological doses17-24. The dose of magnesium to be administered is 5mg/kg day of a well absorbed salt for at least one month, because of the high Mg turnover. At this physiological dose level oral magnesium is totally devoid of the pharmacodynamic effects of parenteral magnesium. Correction of symptoms (clinical or paraclinical [tracings or biochemical data], non-specific [other ions, enzymes] or specific [Mg concentrations, usually in plasma, erythrocytes and daily urine, and in lymphocytes when possible]) constitute the best proof that the clinical pattern is due to an insufficient magnesium intake. These variables should be checked after one month of physiological oral magnesium supplementation. In forms of magnesium deficit where depletion is due to dysregulation of the factors which control magnesium metabolism, the response remains partial after the one month physiological loading test; in these cases the test should be followed by the best possible investigation of the magnesium dysregulating factors1,18-24.


Two types of further research appear necessary: long-term studies of magnesium balance in adults consuming self-selected diets in European countries, and magnesium intervention trials.

New Mg balance studies in Europe

The importance of balance studies in determining RDA requires new projects to be started in European countries. Food habits and environmental factors may intervene in the estimation of the RDA. The results of long-term studies of magnesium balance in adults consuming self-selected diets are more significant than those carried out in metabolic units, which may be biased by the particular psychological profiles of volunteers and by the different types of foods chosen, i.e. foods with different phosphorus levels39,40. Self-selected diets usually reveal negative magnesium balances4,27-40. In order to update food composition tables it might be interesting to compare the magnesium levels in raw, processed and cooked samples of the diet with the data obtained from diet histories41. These studies should involve various socioeconomic groups and be followed by supplementation studies.

Mg intervention trials

Intervention studies should be planned to determine whether magnesium supplements given to at risk population groups will reduce the incidence of the risk. The well-defined populations should be those presenting with neuromuscular hyperexcitability due to primary magnesium deficiency with or without "idopathic" mitral valve prolapse, allergy or pseudoallergy. Therefore these studies should deal mainly with the efficiency of magnesium supplementation in latent tetany (or hyperventilation syndrome) and in Barlow's disease. The same type of studies in populations with cardiovascular disease or urolithiasis seems more hazardous because of the multiplicity of their causes.

When choosing a magnesium supplement the energy intake should be taken into consideration. Supplementation should be achieved using a high magnesium density nutrient3,26,34,42,43 with the best possible bioavailability1,3. This requirement is met by magnesium in water whether in its natural form--from the tap or bottled--or in an artificial form by addition of a soluble Mg salt to ordinary water1,3,44. Supplementation of bread with magnesium has been considered45, as well as specially formulated table salts46,47. However these new salts have a triple purpose since they increase both the Mg and K intake while decreasing the Na intake, and they thus correspond to a more complex intervention.


1. Durlach, J. (1988): Magnesium in clinical practice, pp. 386. London, Paris: John Libbey.

2. Seelig, M.S. (1986): Nutritional status and requirements of magnesium with consideration of individual differences and prevention of cardiovascular disease. Magnesium-Bull. 8, 171-185.

3. Durlach, J., Bara, M. & Guiet-Bara, A. (1989): Magnesium level in drinking water: its importance in cardiovascular risk. In Magnesium in health and disease, ed Y. Itokawa & J. Durlach pp. 173-182. London, Paris: John Libbey.

4. Lakshmanan, F.L., Rao, R.B., Kim, W.W. & Kelsay, J.L., (1984): Magnesium intakes, balances and blood levels of adult consuming self-selected diets. Am. J. Clin. Nutr. 40, 1380-1389.

5. Drueke, T., Gairard, A., Guegen, L., Hercberg, S. & Mareschi, J.P. (1986): Minéraux en alimentation humaine. Apports nutritionnels recomandés pour divers groupes d'individus bien portants. Actualisation du calcium, du fer, du phosphore et du magnésium. Cah. Nutr. Diet. 21, 339-356.

6. Heroux, O., Peter, D. & Heggtveit, A. (1977): Long term effect of suboptimal dietary Mg on Mg and Ca contents of organs on cold tolerance and lifespan, and its pathological consequences in rats. J. Nutr. 107, 1640-1652.

7. Henrotte, J.G. (1989): Recent advances on genetic factors regulating blood and tissue magnesium concentrations. Relationships with stress and immunity. In Magnesium in health and disease, ed Y. Itokawa & J. Durlach. London, Paris: John Libbey.

8. Feray, J.C., Franck, G., Garay, R. & Henrotte, J.G. (1989): Inter-individual differences in red cell Mg2+ contents are related to the activity of a Na2+-Mg2+ exchanger. Possible relationship with HLA-associated genetic factors (abstract). Magnesium Res. 2, 124.

9. Seelig, M.S. (1964): The requirement of magnesium by the normal adult. Summary and analysis of published data. Am. J. Clin. Nutr. 14, 342-390.

10. Seelig, M.S. (1971): Human requirement of magnesium: factors that increase needs. In 1st International Symposium on Mg Deficit in Human Pathology,, Vol. 1, ed J. Durlach, pp. 11-38. Vittel: SGEMV publ.

11. Seelig, M.S. (1980): Magnesium deficiency in the pathogenesis of disease: early roots of cardiovascular, skeletal and renal abnormalities, p. 488. New York: Plenum Press.

12. Seelig, M.S. (1981): Magnesium requirements in human nutrition. Magnesium-Bull. 3, 26-47.

13. Amiot, D., Hioco, D. & Durlach, J. (1969): Fréquence du déficit magnésique chez le sujet normal et dans diverses ostéopathies. J. Med. Bescançon 5., 371-378.

14. Durlach, J., Rayssiguier, Y. & Laguitton, A. (1980): Le besoin en magnésium et son apport dans la ration. Méd. Nutr. 16, 15-21.

15. Mertz, W. (1987): Use and misuse of balance studies. J. Nutr. 117, 1811-1813.

16. Rousselet, F. & Durlach, J. (1971): Techniques analytiques et explorations pratiques du métabolisme magnésique en clinique humaine. In 1st International Symposium on Mg Deficit in Human Pathology, Vol. 1, ed J. Durlach, pp. 65-90. Vittel: SGEMV publ.

17. Shils, M.E. (1969): Experimental production of Mg deficiency in man. In The pathogenesis and clinical significance of Mg deficiency, ed E.B. Flink & J.E. Jones, pp. 847-855. Ann. N.Y. Acad. Sci. 162.

18. Durlach, J. (1989): Magnesium: clinical forms of primary magnesium deficit. Workshop on "Modern life styles, lower energy intake and micronutrient status". Palma de Mallorca, 2-4 March 1989. ILSI Europe (in press).

19. Durlach, J. (1969): Spasmophilia and magnesium deficit (Spasmophilie et déficit magnesique), pp 142. Paris: Masson.

20. Durlach, J. (1976): Neurological manifestations of magnesium imbalance. In Handbook of clinical neurology ed P. Vinken & G.W. Bruyn, pp. 545-579. Amsterdam, N.Y., Oxford: North Holland.

21. Durlach, J. (1980): Clinical aspects of chronic magnesium deficit. In Magnesium in health and disease, ed M. Cantin & M.S. Seelig, pp. 883-909. New York, London: Spectrum Press.

22. Durlach, J. (1985): Neurological disturbances due to magnesium imbalance. In Metal ions in neurology and psychiatry, ed S. Gabay, J. Harris & B.T. Ho, pp. 121-128. New York: A.R. Liss publ.

23. Durlach, J. & Durlach, V. (1986): Idiopathic mitral valve prolapse and magnesium. State of the art. Magnesium-Bull. 8, 156-159.

24. Durlach, J. (1988): Les rapports entre le magnésium et le prolapsus de la valve mitrale. Revue Med. Fonctionnelle 20: 121-172.

25. Anderson, G.H., Peterson, R.D. & Beaton, G.H. (1982): Estimating nutrient deficiencies in a population from dietary records: the use of probability analysis. Nutr. Res. 2, 409-416.

26. Harper, H.E. (1987): Evolution of Recommended Dietary Allowances. New Directions? Annu. Rev. Nutr. 7, 509-537.

27. Greger, J.L., Gruner, S.M., Ethyre, G.M., Abernathy, R.P. & Sickles, V. (1979): Dietary intake and nutritional status in regard to magnesium of adolescent females. Nutr. Rep. Int. 20, 235-244.

28. Huber, H.G., Disney, G.W. & Mason, R.L. (1981): Urinary excretion and dietary intake of magnesium in girls. Nutr. Rep. Int. 23, 127-134.

29. Tallas, P.G. (1981): Dietary intake of female college students. Proc. Alaska Sci. Conf. 32, 14.

30. Marier, J.R. (1982): Quantitative factors regarding magnesium status in the modern-day world. Magnesium 1, 3-15.

31. Morgan, K.J., Stampley, G.L., Zabik, M.E. & Fisher, D.R. (1985): Magnesium and calcium dietary intakes of the US population. J. Am. Coll. Nutr. 4, 195-206.

32. Morgan, K.J., & Stampley, G.L. (1985): Low magnesium to calcium ratios in American self-selected diets. J. Am. Coll. Nutr. 4, 344.

33. Chorazy, W. & Bliwert, K. (1985): Evaluation of magnesium consumption in chosen population in Poland as a measure of its proper concentration in a body. Magnesium-Bull. 7, 161.

34. Rouaud, C. (1985): Le magnésium. Information Diététique Part 3 22-30.

35. Rouaud, C. (1986): Consommation alimentaire d'étudiantes de la région parisienne: étude particulière du magnesium. Méd. Nutr. 22, 295-300.

36. Guilland, J.C., Moreau, D., Boggio, V., Durlach, J. & Klepping, J. (1986): Evaluation of dietary magnesium intake in France. Magnesium-Bull. 8, 269.

37. Hill, A.D., Morris, E.R., Ellis, R., Moy, T. & Moser, P.B. (1986): Mineral balance of adult men consuming self-selected diets. Fed. Proc. 45, 375.

38. Desenclos, J.C., Rouaud, S., Soustre, Y., Berthier, A.M., Hercberg, S. & Dupin, H. (1988): Magnésium hyperexcitabilité neuromusculaire et pression artérelle: Etude dans une population de femmes salariées de la region parisienne. Med. Nutr. 24, 279-284.

39. Suzuki, K., Uehara, M., Endo, Y. & Goto, S. (1988): The effects of dietary magnesium levels on excess phosphate diet. J. Japn. Soc. Magnesium Res. 7, 117-122.

40. Franz, K.B. (1989): Influence of phosphorus on intestinal absorption of calcium and magnesium. In Magnesium in health and disease. ed Y. Itokawa & J. Durlach. London, Paris: John Libbey.

41. Riche, D. & Desenclos, J.C. (1985): Apports en magnésium. Etude comparative de quelques tables de composition. Med. Nutr. 21, 351-356.

42. Astier-Dumas, M., Gargominy, N. & Hoint, F. (1984): Densité nutritionelle en magnésium: à propos de quelques produits prêts à être consommés. Méd. Nutr. 20, 397-399.

43. Riché, D. (1986): La couverture des besoins en magnésium: un problème de densité nutritionelle. Information Diététique, Oart 4, 23-27.

44. Hese, A., Weber, A. & Miersch, W.D. (1988): Magnesium-Substitution durch Minerali-vasser. Therapie-Woche 38, 2510-2513.

45. Ranothra, G.S., Lee, C. & Gelroth, J.A. (1980): Expanded cereal fortification: bioavailability and functionality (flavor) of Mg in bread. J. Food Sci. 45, 915-917.

46. Pitkanen, H. (1982): Industrial possibilities to interfere with the salt problem: dietary Na(K + Mg) ratio. Magnesium 1, 298-303.

47. Angeli, G., Moretti, G.B., Bertone, V. & Amaglio, A. (1988) Dieta iposodica e ipertensione arteriosa: effeto favorevole sul colesterolo HDL di una nuova associazione polisalina iposodica. Clin. Ter. 125, 417-424.

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