EP1858353A1

EP1858353A1 - Supplementary food composition

Info

Publication number: EP1858353A1
Application number: EP06743576A
Authority: EP
Inventors: Christian Leclerc
Original assignee: Larena SAS
Current assignee: Larena SAS
Priority date: 2005-03-15
Filing date: 2006-03-15
Publication date: 2007-11-28
Also published as: CA2601103A1; FR2883132B1; US20080206412A1; WO2006097629A1; FR2883132A1

Abstract

The invention concerns the domain of food. More particularly, it concerns a composition, preferably a supplementary food composition, comprising at least one organic mineral salt, said organic mineral salt contributing to the alkaline potency in an amount ranging from 2 to 200 milliequivalent, capable of buffering an acid load of 20 to 200 milliequivalent of hydrogen ions H+, that is 20 to 200 mmoles of H+, preferably from 40 to 100 milliequivalent. Said composition is useful for preparing a composition for preventing digestive and urinary mineral and ionic losses, for preventing and/or treating metabolic acidosis, hypertension, cerebral strokes, type 2 diabetes, osteoporosis, urinary lithiases and aging.

Description

Substitute food composition

The present invention relates to a suppletive food composition intended to be administered orally as a dietary supplement. This composition aims to improve the prevention of ionic and mineral disorders observed for example during aging, high protein and restrictive diets, low in minerals and in various pathologies such as metabolic acidosis, hypertension, cardiovascular diseases, type 2 diabetes, lithiasis,

Osteoporosis.

The contemporary diet can be at the origin of acid-base and mineral imbalances, as well as disorders of the ionic homeostasis which will lead to disturbances of the physiological functions even to potentiate various pathologies such as the hypertension, the cardiovascular diseases, 1 Osteoporosis, lithiasis and type 2 diabetes.

The current diet of Western populations is generally acidifying, resulting in increased mobilization of buffering powers of the body to maintain the pH of the body. This mobilization leads to ionic and mineral imbalances that result in increased renal acid excretion and urinary mineral and ionic loss. Acid renal excretion (NAE), a commonly used measure (NAE = titratable acidity + NH ₄ ⁺ - HCO ₃ ^" ) in acid-base metabolism studies, reflects not the acidic load of the meal, but the ability to an individual to manage this acid load The NAE correlates with the degree of metabolic acidosis Urinary mineral losses, especially calcium, are thus increased during a high NAE These mineral losses probably reflect ionic imbalances at the cellular level . In pathologies such as hypertension (HTA) and type 2 diabetes, elevation of free cytosolic calcium is observed while extracellular concentrations of ionized calcium are reduced. Such modifications are also encountered in the elderly. As a result, high cytosolic basal contents of free calcium and an alteration of calcium transport at the membrane level are found in the platelets, erythrocytes, lymphocytes and adipocytes of hypertensive subjects. Blood pressure correlates directly with intracellular calcium levels.

In type 2 diabetes, even in the absence of hypertension, intracellular calcium levels are also high. Calcium transport defects are found in all tissues in type 2 diabetics, including cardiac and skeletal muscles, arteries, kidney, liver, erythrocytes, osteoblasts, adipocytes and platelets.

Intracellular potassium is decreased in treated and non-hypertensive individuals, as well as in type 2 diabetics. In non-diabetic subjects, however, an inverse correlation was found between intracellular potassium and blood pressure level.

An inverse correlation is observed between intracellular levels of potassium and calcium in untreated normal and hypertensive individuals. In contrast, intracellular magnesium evolves concomitantly with potassium. Similarly, sodium chloride (NaCl) infusion increases intracellular sodium levels and decreases potassium levels.

All in all, a depletion of potassium and / or magnesium, and / or an excess of intracellular calcium could produce or predispose to vasoconstriction, HTA, but also contribute to insulin resistance, and abnormalities of glucido-insulin metabolism.

The ATP-dependent sodium / potassium pump (NaK-ATPase) is the main mechanism responsible for maintaining the low intracellular sodium concentration and the high intracellular potassium concentration. The pump

NaK-ATPase is responsible for maintaining the membrane potential. The activity and capacity of NaK-ATPase is under the control of hormones, contractile activity, exercise, nutrition and electrolyte status.

In animal models, potassium deficiency leads to a reduction in the concentration of NaK-ATPase in skeletal muscle. In humans, the potassium deficiency induced by diuretic treatments induces the same effects. A 53% reduction in muscle NaK-ATPase concentration results in a 88% reduction in the strength rate.

The physiological role of the sodium-calcium exchanger (Na / Ca) has not yet been clearly defined. In reperfused ischemic heart experiments, the increase in intracellular sodium slows calcium extrusion via the exchanger. This exchanger therefore plays an important role in ventricular arrhythmias by modifying the membrane potential.

Another sodium influx pathway in cardiac cells is the sodium / proton (NaVH ⁺ ) exchanger (NHE), which plays an important role in the regulation of intracellular pH and cell volume. NHE excretes a proton for an incoming sodium ion. The activity of NHE is very sensitive to intracellular pH. Proton extrusion via NHE is also inhibited by extracellular acidosis. Intracellular sodium can also regulate NHE, but is not the main regulator. Sodium exchanger / bicarbonate (Na ⁺ / HCO3 ^~) (NBC) plays a role in the extrusion of acid at the level of myocytes (via the influx of Na ⁺ and HCO3 ^"). The activity of the NBC is pH-dependent In physiological conditions, NBC and NHE play a similar role in sodium influx.

Sodium cotransport / potassium / 2 chlorides (Na ⁺ / K ⁺ / 2C1 ^~) (NKCC) plays an important role in maintaining the chlorine (Cl ^") intracellular. High concentrations of ^Cl" inhibit ion flow in both directions . Moreover, this transporter could be important in the regulation of cell volume.

The NaVMg ²⁺ exchanger is responsible in part for the extrusion of magnesium out of the cell. Although this antiport is not the main regulator of intracellular magnesium concentrations, it allows magnesium efflux proportionally to the extracellular sodium content.

NaCl loading is accompanied by increased cellular concentrations of sodium and calcium, but decreased magnesium levels. Conversely, a magnesium charge lowers intracellular sodium and increases intracellular magnesium levels. The decrease in intracellular sodium is accompanied by a drop in blood pressure. Supplementation with potassium and magnesium prevents the induction of NaK-ATPase inhibition. The effects of potassium and magnesium seem additive.

Potassium deficiency, including both hypokalemia and decreased intracellular potassium may be a consequence of magnesium deficiency. This magnesocurable and non-kaliocurable potassium depletion is related to membrane modifications and in particular to an inhibition of the magnesium-dependent NaK-ATPase activity, which is essential for the transport of potassium and sodium into the interior and exterior of the cell. cell. Magnesium also blocks the potassium currents exiting at the level of the potassium channels. On the other hand, magnesium is essential for the reabsorption of potassium in the loop of Henle and the magnesium deficit stimulates the secretion of renin and aldosterone, resulting in a kaliuria. Potassium deficiency contributes to the cardiovascular consequences of magnesium deficiency.

The mechanisms involved in the regulation of the intracellular levels of the different ions are not yet clearly defined. Sodium plays an important role in the activation of NaK-ATPase. Indeed, the sodium dietary sodium chloride provides induction of an inhibitor of NaK-ATPase activity, which contributes to the accumulation of sodium in the cell. On the other hand, if the sodium is introduced in a form other than chloride, it does not induce the synthesis of the NaK-ATPase inhibitor. Finally, NaCl facilitates the activity of the NaVH ⁺ exchanger. Conversely, potassium decreases the activity of this sodium-proton exchanger. In addition, potassium and magnesium inhibit synthesis of the NaK-ATPase inhibitor. Therefore, it appears that sodium chloride facilitates the cell's retention of sodium, while dietary potassium and magnesium facilitate the extrusion of sodium from the cell.

The cellular mechanisms described above and involved in ionic transport could be observed at the level of different organs such as, for example, the heart and the kidney. Regarding sodium, it seems confirmed that it is the combination of sodium and chlorine that has deleterious effects. The increase in vascular volume observed during a sodium chloride loading could be explained by the induction of an inhibitor of the NaK-ATPase pump. The effect of NaCl on vascular volume expansion is thought to be related to the role of Na / K / 2C1 cotransport in sodium retention at the renal level. This mechanism would be inoperative at low concentrations of chlorine in the tubular fluid.

As for calcium, it plays an important role at the cellular level. He intervenes in particular in the processes of muscular contraction, described in the problems of HTA. In spontaneously hypertensive rat SHR, a calcium-rich diet increases urinary sodium excretion, erythrocyte membrane Ca-ATPase activity reduces intracellular calcium concentration in platelets, and improves muscle cell relaxation. vascular smooth. This calcium effect appears to be related to an improvement in membrane hyperpolarization by opening calcium-activated potassium channels.

Several observational studies have clearly shown that in populations living on a diet low in NaCl, the level of blood pressure increases only very little or not at all with age. The most comprehensive study (Intersalt) showed that the higher the sodic intake, the greater the number of individuals in whom the systolic and diastolic pressures increase with age.

The hypothesis that magnesium deficiency promotes atherosclerosis is currently being considered.

In several experimental models, the magnesium deficiency promotes dyslipidemia, increases the peroxidation of lipoproteins and induces an inflammatory response.

Different studies have demonstrated a positive correlation between urinary excretion of calcium and metabolic acidosis. Thus, there is a buffer reaction involving the mineral reserves of the bone including calcium salts, bicarbonates, potassium. The phenomena can therefore cause bone loss, especially since the metabolic acidosis has an impact on the bone cells themselves, by inhibiting the osteoblastic function and by stimulating the resorption. Excess sodium also causes hypercalciuria. Insufficient sodium excretion causes an increase in blood volume, which causes an increase in urinary calcium.

Insufficient potassium intake increases sodium retention at the renal level, which increases hypercalciuria. In addition, hypokalemia stimulates bone resorption while potassium concentration decreases renal calcium excretion and rebalances serum calcium. A deficiency of magnesium causes hypocalcemia and inhibits the synthesis of active vitamin D: this deficiency is considered as an important risk factor for osteoporosis. In addition, the serum magnesium level is directly related to the in vitro proliferation of osteoblastic cells.

The incidence of lithiasis has increased steadily in recent decades. This is largely related to changes in eating habits: consumption of animal protein, NaCl, alcohol, intake of insufficient drink are all dietary factors aggravating the risk of urinary stones. Excessive intake of animal protein leads to a lowering of urine pH, while excretion of calcium, oxalate and uric acid is increased. Lithiases are also associated with acidification of the urine, linked in particular to the reduction of the excretion of citrates. In addition, urinary lithiasis is associated with significant mineral losses. Indeed, a high urinary sodium excretion is usually observed in people with stones.

Low consumption of magnesium, calcium and potassium as well as excessive concentration of NaCl may be risk factors for insulin resistance and diabetes. The epidemic data show a high prevalence (25%) of hypomagnesemia among diabetic subjects. Part of the depletion could be explained by a decrease in the net tubular reabsorption of magnesium in the different hyperinsulinemic states

(diabetes, obesity, hypertension ...) - In addition, a chronic magnesium deficiency could contribute to insulin resistance.

Depletion of intracellular free magnesium has also been found to be a feature of insulin resistance in hypertensive subjects.

Potassium depletion leads to changes in the expression of NaK-ATPase in skeletal muscle, heart and nerves, which may also play an important role in the pathophysiology of diabetes. In addition, the ionic hypothesis could explain the concomitant appearance of several pathologies during the polymetabolic syndrome. This is corroborated by the fact that insulin resistance and hyperinsulinemia are both associated with mineral imbalances.

The effect of potassium deficiency in the genesis of type 2 diabetes may also be related to a disturbance of magnesium homeostasis. Thus, low plasma concentrations of potassium could interfere with renal reabsorption of magnesium and therefore lead to hypomagnesemia.

A low-calcium diet leads to increased levels of parathyroid hormone (PTH) that can compromise the insulin sensitivity of fat cells, and probably many other cell types by inducing increased levels of intracellular calcium.

The effectiveness of calcium absorption decreases with age, frequently associated with inadequate dietary intake, vitamin D deficiency, and compensatory hyperparathyroidism. Aging is usually accompanied by renal changes including a decrease in glomerular filtration. The glomerular filtration rate decreases by about 1.05 ml / min per year in the elderly.

There is a gradual increase in blood acidity and a decrease in the bicarbonate content during aging. The blood changes reflect a growing metabolic acidosis during aging. In addition, age and diet are two independent factors in regulating the degree of acidosis, with aging increasing the acid load induced by the diet.

Age and glomerular filtration are two non-dissociable factors responsible for the control of blood acidity and plasma bicarbonates.

Metabolic acidosis promotes muscle protein catabolism. In addition, osteoporosis is characterized not only by a loss of bone calcium stock but also by an alteration of the protein matrix of the bone. It is easy to imagine that this type of synergy that can be established in case of prolonged metabolic acidosis can have very deleterious effects.

Sarcopenia is certainly a multifactorial phenomenon: slow erosion of muscle proteins, dysregulation of cytokines, degeneration of motor neurons, physical inactivity, decreased levels of hormones. But, another hypothesis is also advanced, in relation to the effects of metabolic acidosis. Indeed, the decline of renal function associated with an acidifying diet, in the elderly, could contribute to accentuate protein catabolism in these people.

The ability of fructo-oligosaccharides (FOS) to stimulate the proliferation of bifidobacteria helps to maintain intestinal flora. By this bifidogenic effect, the FOS prevent the appearance of diarrhea which can be at the origin of digestive losses mineral (Ca, Mg, K ...) and ionic (bicarbonates ...).

In addition to their effect on the intestinal flora and contrary to the effect of certain dietary fibers, the FOS facilitate the intestinal absorption of certain minerals. Thus, stimulation of the absorption of minerals such as Ca ²⁺ and Mg ²⁺ by inulin has been repeatedly confirmed in the rat. It appears that the use of different models (rats and hamsters) indicates an increase in absorption in the large intestine to result in an increase in bone density.

Kidney stones are the result of a complex between calcium and oxalate. An acidic charge is usually accompanied by an excess of oxalic acid contributing to the formation of these calcium crystals. Citrate plays an important role in the metabolism of calcium, and in particular in the inhibition of the formation of these calcium crystals. Thus, urinary citrate is an endogenous inhibitor of crystal formation by complexing with calcium. Low urinary citrate levels are associated with the development of kidney stones. In addition, the alkalizing drinks prevent the formation of calcium oxalate, uric acid and lithiasis. Thus, citric acid-rich fruit powders increase urinary pH and urinary excretion of citrate, reducing the risk of crystallization between calcium and oxalic acid.

In addition, citrate salts reduce the degree of metabolic acidosis, thereby limiting urinary mineral and ionic losses, while improving the bicarbonate status of the body. They help to reduce the NAE. Potassium plays a key role in maintaining ionic homeostasis at the cellular level. Indeed, potassium prevents the induction of the inhibitor of NaK-ATPase, and therefore contributes to the maintenance of the membrane potential. In addition, it reduces the risk of stroke. Finally, potassium intervenes at the urinary level by facilitating the excretion of citrate, thus preventing the formation of calcium crystals and thus lithiasis.

Calcium also prevents the development of lithiasis by preventing intestinal absorption of oxalates. Calcium also decreases the risk of developing diabetes.

In addition, calcium is essential in bone building. It is incorporated in the mineral fraction of the bone.

Adequate calcium intake appears to be essential for maintaining the skeleton, especially during metabolic acidosis induced by food.

Calcium is also involved in muscle contraction processes, described in HTA problems.

Magnesium, for its part, plays a role similar to that of potassium. Their effects are additive at the cellular level, in particular by their effect on NaK-ATPase. In fact, magnesium also prevents the induction of the inhibitor of this pump. In addition, at the cellular level, magnesium blocks outgoing potassium currents and facilitates the extrusion of sodium out of the cell.

Magnesium also acts as a cofactor for many enzymes. Its involvement in the functioning of NaK-ATPase makes it an important mineral in the maintenance of mineral balances at the cellular level.

Finally, magnesium has a number of effects on citrate metabolism and reduces saturation urinary calcium oxalate forming magnesium oxalate, more soluble than calcium oxalate.

In the digestive tract, magnesium can also form complexes with oxalates, thus reducing the intestinal absorption of oxalates.

We understand the importance of food intake in maintaining the ionic and mineral balance since most of the elements that participate in this maintenance are provided by food.

In the prior art, different compositions have been developed to try to remedy these problems of ionic imbalance. However, no composition described in the prior art give satisfactory results to overcome these problems of ionic imbalance and / or are difficult to administer for patients. In the case of the liquid compositions developed in the prior art, if they allow a simplified administration, they prove to be of a complex manufacture because of the poor solubility of some of their components.

The aim of the invention is to provide a food composition that enables micronutritional management with a view to preventing the occurrence of disorders related to mineral and ionic imbalances, as well as to increased mineral and ionic urinary excretions, such as metabolic acidosis. , hypertension, stroke, type 2 diabetes, osteoporosis, urinary lithiasis.

Thus, the present invention firstly relates to a composition, preferably a suppletive food composition, comprising at least one inorganic organic salt, which inorganic organic salt contributes to the alkaline power in an amount ranging from 20 to 200 mEq, capable of buffering a acid charge of 20 to 200 mEq of hydrogen ions H ⁺ , ie 20 to 200 mmol of H ⁺ , preferably 40 to 100 mEq.

Surprisingly, the inventors have found that the compounds used in the composition according to the invention have complementary modes of action, thus offering a synergy for a more effective action, and that the mixture of these in specific quantities makes it possible to obtain a composition in powder form dissolving without difficulty.

The inorganic organic salt may be selected from potassium salts, magnesium salts or calcium salts.

The composition according to the invention may comprise only one of these salts or any combination thereof. Preferably, the inorganic organic salt is a mixture of potassium, magnesium and calcium salts.

According to the invention, the inorganic organic salt may be chosen from citrate, malate, lactate or gluconate salts, preferably citrate salts. The composition according to the invention may comprise only one of these salts or any combination thereof.

Preferably, the inorganic organic salt may be chosen from potassium, magnesium or calcium citrates, most preferably potassium citrate and, particularly preferably, the inorganic organic salt is a mixture of potassium citrates, magnesium and calcium.

When a potassium salt is used, the potassium may be present in the composition according to the invention in an amount ranging from 2 mmol to 75 mmol, preferably from 10 mmol to 50 mmol. According to one particular form of the invention, the potassium may be present in the composition in the form of tri-potassium citrate. When a calcium salt is used, the calcium may be present in the composition according to the invention in an amount ranging from 1 mmol to 30 mmol, preferably from 5 mmol to 20 mmol. According to one particular form of the invention, the calcium may be present in the composition in the form of tri-calcium citrate.

When a magnesium salt is used, the magnesium may be present in the composition according to the invention in an amount ranging from 1 mmol to 20 mmol, preferentially from 4 mmol to 12 mmol. According to one particular form of the invention, the magnesium may be present in the composition in the form of tri-magnesium citrate.

The compositions according to the invention may be in the form of a powder for dilution, an oral solution, a powder for capsule, a tablet or even granules.

According to a preferred embodiment, the composition according to the invention is in the form of powder to be diluted.

According to another preferred embodiment, the composition according to is in the form of an oral solution.

Advantageously, said solution comprises a volume of

100 ml to 2 1 when the latter is intended for daily administration, preferably from 200 to 1000 ml and particularly preferably from 300 to 800 ml, in particular 500 ml.

According to a preferred embodiment, the composition according to the invention further comprises a prebiotic. By way of example, said prebiotic may be chosen from fructo-oligosaccharides of inulin or oligo-fructose type, galactooligosaccharides of transgalacto-oligosaccharide or galactotriose type, isomalto-oligosaccharides or even manno-oligosaccharides. Preferably according to the invention, the prebiotic may be chosen from fructo-oligosaccharides. Even more preferably, the prebiotic may be chosen from oligofructose fructo-oligosaccharides. The oligofructoses can be derived from chicory, onion, garlic, artichoke, leeks, salsify, asparagus, preferably chicory. The prebiotic may be present in the composition according to the invention in an amount ranging from 2 g to 15 g, preferably from 2 g to 6 g.

According to another preferred embodiment, the composition according to the invention further comprises fruit powder.

According to the invention, the fruit powder can be rich in organic salts, such as citrate salts and / or malate salts. The salts may be mineral citrate and / or mineral malate where the minerals may be potassium, calcium, magnesium, zinc, manganese, preferably potassium, calcium, magnesium, and most preferably potassium .

By way of example, said fruit powder may be chosen from lemon powder, orange powder, passion fruit powder, pomelo powder, red fruit powder such as gooseberry, blueberry or raspberry, or plum powder.

Preferentially, the fruit powder is lemon powder.

According to the invention, the fruit powder can contribute to the alkaline power in an amount ranging from 5 mEq to 30 mEq, capable of buffering an acidic charge of 5 to 30 mEq of H ⁺ hydrogen ions, ie 5 to 30 mmol of H ⁺ .

According to yet another preferred embodiment, the composition of the invention may further comprise vitamin D and / or glutamine.

Vitamin D may be present in the composition according to the invention in the form of cholecalciferol (vitamin D3), or ergocalciferol (vitamin D2). Preferably, vitamin D is present in the composition in the form of cholecalciferol (vitamin D3). Vitamin D may be present in the composition according to the invention in an amount ranging from 1 μg to 20 μg, preferably from 2.5 μg to 15 μg.

Glutamine may be present in the composition according to the invention in the form of free L-glutamine or proteins or protein extracts rich in glutamine. Preferentially, glutamine is present in the composition in the form of free L-glutamine.

Glutamine may be present in the composition according to the invention in an amount ranging from 100 mg to 10 g, preferably from 100 mg to 3 g. Those skilled in the art can adapt the amount of protein or protein extract containing glutamine to obtain the desired amount of glutamine in the composition according to the invention.

Said composition may further comprise any other

Active ingredient known for the treatment of disorders related to ionic and mineral imbalances, especially those known in diuretic treatments, antihypertensive treatments, treatments for type 2 diabetes, osteoporosis treatments, lithiasis treatments .

The compositions according to the invention may also, according to the formulation chosen, comprise any suitable excipient, such as an acidifier, an anti-caking agent, a dye, an aroma or a sweetener.

A preferred composition according to the invention comprises:

25.6 mmol of potassium as 2.78 g of tri-potassium citrate;

10 mmol of calcium in the form of 1.9 g of tri-calcium citrate; 6.25 moles of magnesium in the form of 1.43 g of tri-magnesic citrate.

Advantageously, said composition may also comprise:

5 g of fructo-oligosaccharide in the form of 5 g of chicory hydrolyzate;

from 1 to 10 πiEq alkaline in the form of 0.3 to 3 g of lemon powder.

These amounts correspond to a daily dose to be diluted in 500 ml or more of water.

The different amounts described above correspond to the quantities necessary for a daily administration. In the case where the administration of the composition according to the invention obey a different posology, the skilled person can adjust without difficulty these quantities to adjust to said new dosage. By way of example, a composition intended for a half-day administration will comprise the various components described above in an amount corresponding to half of the quantities described above.

Another subject of the invention is the use of the auxiliary composition according to the invention for the preparation of a composition intended to prevent the occurrence of disorders related to ionic and mineral imbalances.

In particular, the subject of the invention is the use of the composition according to the invention for the preparation of a composition intended to prevent and / or compensate mineral and ionic losses by urinary and / or digestive route, to prevent and / or to improve the ionic and mineral imbalances observed in metabolic acidosis, hypertension, stroke, type 2 diabetes, lithiasis, osteoporosis, aging and acidifying diets such as high protein and restrictive diets, low in minerals.

Advantageously, said composition according to the invention relates to the preparation of a composition intended to prevent and / or compensate for mineral and ionic losses through the urine.

In addition, the subject of the invention is the use of the composition according to the invention for the preparation of a composition rich in minerals for overcoming micronutrient deficiency.

Other features of the invention will appear in the following examples, without these constituting any limitation of the invention.

EXAMPLES

1; Preparation of a liquid composition

In a volume of water of 300 ml, the following different ingredients have been added:

- FOS (fructo-oligosaccharides) chicory: 5g

- Tripotassium citrate: 2.78 g (ie 1000 mg or 25.6 mmol of potassium)

Tricalcium citrate: 1.9g (ie 400 mg or 10 mmol of calcium)

Magnesium citrate: 1.43g (ie 150 mg or 6.25 mmol of magnesium)

- Fruit powder (lemon juice): 0,5g

- Aromas

Sweetener - Thickener

The different ingredients used correspond to an alkaline intake of about 65 mEg.

After stirring, the dissolution of the mixture is complete.

2) Urine dosage test;

A group of 60 people consumed in one day, 150 ml of the liquid composition described in 1). An urinary acid net excretion (NAE) assay was performed before and after said consumption according to the protocol written in the ENA-test kit designed by ABP.

The assay is performed on the urine collected during a period of 24 hours.

The value of NAE obtained correlates with the degree of metabolic acidosis.

The data collected were divided into percentiles (the ^50th percentile of the median value of urinary excretion for the group of 50 people). The results obtained are summarized in Table I.

Table I

The results show that the consumption of a half-dose of the composition described in 1) on a day makes it possible to lower the urinary acid net excretion, reflection the acid-base balance of the body. This effect is observed regardless of the severity of the metabolic acidosis.

In conclusion, the composition according to the invention makes it possible to reduce the degree of metabolic acidosis, and therefore the urinary excretion of minerals.

Claims

claims

1. A composition, preferably a suppletive food composition, comprising at least one inorganic organic salt, which inorganic organic salt contributes to the alkaline power in an amount ranging from 20 to 200 mEq, capable of buffering an acidic charge of 20 to 200 mEq d H ⁺ hydrogen ions, ie 20 to 200 mmol of H ⁺ , preferably 40 to 100 mEq.

2. The composition according to claim 1, characterized in that the inorganic organic salt is chosen from potassium salts, magnesium salts, calcium salts or a mixture of these, preferably the inorganic organic salt is a mixture of potassium, magnesium and calcium salts.

3. The composition according to claim 1, wherein the inorganic organic salt is chosen from citrate, malate, lactate or citrate salts.

4. The composition according to any one of claims 1 to 3, characterized in that said composition comprises potassium in an amount ranging from 2 mmol to 75 mmol, preferably from 10 mmol to 50 mmol.

5. The composition according to any one of claims 1 to 4, characterized in that said composition comprises calcium in an amount ranging from 1 mmol to 30 mmol, preferably from 5 mmol to 20 mmol.

6. The composition according to any one of claims 1 to 5, characterized in that said composition comprises magnesium in an amount ranging from 1 mmol 20 iranoles, preferably 4 iranoles to 12 mmoles.

7. The composition according to any one of claims 1 to 6, characterized in that it is in the form of a powder for dilution, oral solution, powder for capsule, tablet or granules, preferably under the form of powder to be diluted or an oral solution.

8. The composition according to any one of claims 1 to 7, characterized in that it further comprises a prebiotic.

9. The composition of claim 8, characterized in that the prebiotic is present in an amount ranging from 2g to 15 g, preferably from 2g to 6g.

10. The composition according to any one of claims 1 to 9, characterized in that it further comprises fruit powder.

11. The composition according to claim 10, characterized in that the fruit powder contributes to the alkaline power in an amount ranging from 5 mEq to 30 mEq, capable of buffering an acidic charge of 5 to 30 mEq of H ⁺ hydrogen ions. that is 5 to 30 mmol of H ⁺ .

12. The composition according to any one of claims 1 to 11, characterized in that it further comprises an acidifier, an anti-caking agent, a dye, a flavor and / or a sweetener.

13. A use of a composition according to any one of claims 1 to 12, for the preparation of a composition for preventing the occurrence of disorders related to ionic and mineral imbalances.

14. Use according to claim 13, characterized in that said composition is intended for to prevent and / or compensate mineral and ionic losses by the urinary and / or digestive system, to prevent and / or improve the ionic and mineral imbalances observed in metabolic acidosis, hypertension, cerebrovascular accidents, type 2 diabetes , lithiasis, osteoporosis, aging and acidifying diets such as high protein and restrictive diets, low in minerals.