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INTRODUCTION
Electrolytes are minerals in the blood and other body fluids that carry a positive or negative electrical charge. Electrolytes affect body functions in many ways, including: 1. the maintenance of water balance in the body, 2. blood acidity (pH), 3. acid-base balance and pH levels, 4. the transport of nutrients into cells, and 5. the contribution to the proper functioning of the nerves, heart, muscles and brain. Mainly extracellular electrolytes are sodium (Na+), chlorine (Cl-) and bicarbonate (HCO-3), while mainly intracellular are potassium (K+), calcium (Ca++), phosphorus (P) and magnesium (Mg++).
SODIUM
Distribution of Na+ in body fluid compartments
The total amount of Na+ in the body is 4150 mEq and about 40% of this amount is found in the bones, while the rest is found mainly in the extracellular fluid. The type of sodium that needs special attention is that which is "rapidly exchanged". This means that across the cell membrane, this particular sodium has the ability to quickly diffuse and exchange with other ions, such as K+. The total amount of rapidly exchangeable Na+ in the body is 2900 mEq, while the extracellular fluid has 138 to 145 mEq/l of plasma [1].
Sodium homeostasis
Na+ is the main electrolyte of the body's extracellular fluid, which underlines its importance for the human body, as changes in its concentrations lead to osmotic changes in cells and tissues. Chlorine and bicarbonate radicals primarily bind sodium. These three are the most basic ions of the extracellular space [1]. The role of the kidney is important for the homeostasis of water and electrolytes, a process necessary to maintain the balance between the organism and the environment. Its main function is the filtration of plasma and the removal of waste substances, always in relation to the components taken in from food and the derivatives of metabolism. The ureters reabsorb a greater amount of water and Na from the filtrate, preventing their loss in the urine. In the distal convoluted tubule and collecting tubules, 10-15% of the water and electrolytes of the filtrate are reabsorbed. Acid-base balance is achieved by reabsorption of the appropriate amount determined by osmolarity, hormonal and physical factors [1].
Dietary sodium intake
Na+, contained in dietary salt, is essential for human homeostasis. For millions of years, our ancestors ate less than 0.25g of salt per day, while today's average daily intake is close to 10g in most countries [2]. Excessive intake of Na+ is considered to have negative effects on blood pressure (BP) and the cardiovascular system, negatively affecting the health of the body. Researchers from the UK Biobank who collected information on urinary electrolytes and blood pressure measurements from over 450,000 adults found a direct relationship between the amount of sodium excreted in urine and blood pressure [3]. The DASH (Dietary Approaches to Stop Hypertension) diet is a low Na+ dietary model (rich in fruits and vegetables and low in saturated fat and cholesterol) and has a favorable BP effect. In addition to lowering blood pressure, adopting the DASH dietary model offers protection against osteoporosis, cancer, cardiovascular disease, stroke, and diabetes. In the DASH-Sodium study, 412 people with slightly high blood pressure or mild hypertension who were not on blood pressure medication were randomly assigned to follow either a DASH diet or a control diet with varying amounts of daily sodium intake (50, 100, and 150 mmol/day). The study showed that in all three cases blood pressure levels decreased, however the most significant difference was observed in the groups with the lowest Na+ intake showing the greatest reduction in blood pressure [4]. A review of 36 studies with 6,736 adults found that consuming less Na+ was linked to a drop of 3.39 mmHg in systolic BP and 1.54 mmHg in diastolic BP, and it did not harm kidney function or metabolic and hormonal profiles [5].
However, Na+ restriction does not have the same BP-lowering effect in all subjects. People who are sensitive to salt (salt-sensitive) benefit more from limiting their consumption compared to salt-tolerant people, i.e. people who show resistance to salt consumption/ Na+ [6]. Regarding cardiovascular risk, many studies based on multiple 24-h urine collections reported a direct positive linear relationship between Na+ intake and cardiovascular disease. A recent observational study showed that 24-h estimates of Na+ consumption based on urine dipsticks overestimated sodium consumption at lower levels and underestimated sodium consumption at higher levels compared with direct measurement of 24-h urinary Na+ excretion [7]. Despite a global awareness campaign to reduce Na+ intake in our diet, little progress has been made. A prospective study in Australia, involving 904 individuals with diabetes, revealed this. After 24-h urine collection, it appeared that only 7% and 5% of participants met guideline criteria for dietary Na+ and K+, respectively [8]. Data from a study published in 2023 revealed that adding Na+ to the diet resulted in an increased incidence of type II diabetes, primarily through risk factors such as increased body weight, adipose tissue deposition, and high levels of inflammation [9]. A systematic review of the literature associated increased Na+ consumption with the development of Nonalcoholic Fatty Liver Disease (NFLD) mainly through the disruption of appetite-regulating hormones. This process results in increased caloric intake, weight gain, and the development of insulin resistance, prompting the liver to absorb more free fatty acids and synthesize fat, culminating in steatosis [10]. Furthermore, excessive dietary Na+ intake has been linked to many other adverse medical conditions, such as urolithiasis through a high urinary Na/K ratio and subsequent increased urinary Ca++ excretion, inhibiting renal tubular reabsorption of Ca++ [11].
Additionally, Wu et al reported that Na+ consumption may be an independent risk factor for gastric cancer. Multiple mechanisms of the effect of Na+ on the gastric mucosa have been studied, such as direct damage from the high sodium concentration and appearance of epithelial hyperplasia, increasing the possibility of endogenous mutations, accelerating the process of intestinal metaplasia, increasing the colonization of H. Pylori in the stomach, etc. leading to chronic inflammation, such as atrophic gastritis and gastric ulcer which are considered precancerous conditions [12]. Dietary Na+ was thought to increase the risk of asthma in preschool children, as reported in a recent study by Qu et al. [13] Children are at greater risk for developing asthma because age is an important factor in determining Na+ sensitivity. On the other hand, literature data correlates the effect of reduced dietary Na+ intake (< 2g per day) with the risk of osteoporosis. A low-sodium diet is known to activate the renin-angiotensin-aldosterone system (RAAS), and components of the RAAS are found in bone tissue. When RAAS is activated, it stimulates osteoclast formation and inhibits osteoblast activity to cause osteoporosis. In addition, insufficient Na+ intake leads to a lack of other important nutrients. A dietary plan low in Na+ increases the risk of osteoporosis by consuming fewer calories and increasing bone resorption indices [14]. A significant percentage of Na+, in addition to being added to food to increase flavor, is used in food processing for both palatability and preservation [15].
The most commonly known sodium-related food additives are the following:
- Monosodium L- glutamate (MSG) due to its taste-improving effect is now intentionally added in small proportions to various foods, either in the form of the monosodium salt (food additive: E621), or as a protein hydrolyzate component [15].
- Sodium nitrite is widely used in the meat products industry as a preservative, with the number E250. It contributes to the stabilization of the color of meat products, while simultaneously inhibiting the growth of various types of bacteria, including Clostridium botulinum, which is responsible for the occurrence of botulism in humans [15].
- Sodium bicarbonate is the substance most used as a rising agent and at the same time acidity regulator with code E500 [15].
- Sodium chloride (salt) has the property of preventing the growth of microorganisms, which is why it is used for food preservation (defatting) [15].
- Sodium salts of citric acid are mainly used as acidity regulators as well as flavoring ingredients. It increases the stability of the structure in jams and reduces the spoilage of fruits due to enzymatic actions [15].
- Sodium benzoate (E211) enters the individual cells and increases their overall acidity, thus creating conditions hostile to the growth of fungi or bacteria [16].
- Sodium salt of propionic acid, a natural acid found in small amounts in many foods, such as types of Swiss cheese. Propionic acid and its salts are used as preservatives, mainly against fungi [17].
POTASSIUM
Distribution of K+ in the various compartments of body fluids-homeostasis
K+ is the body's main intracellular cation (98%) and plays an important role in normal cellular function, with an intracellular concentration of 140-150 mEq/L. Its concentration in the extracellular compartment varies between 3.5-5.5 mEq/L [1]. The highest concentration of K+ in the intracellular space is maintained by the active function of the protein pump Na+-K+-ATPase, which is located in the cell membrane and promotes the exit of Na+ from the cells and the entry of K+ into them. Potassium performs very basic physiological functions. In particular, it enters the metabolism of the cell, taking part in the regulation of biological functions, such as the synthesis of nucleic acids, proteins and glycogen [1]. Furthermore, the ratio of K+ concentrations in the intracellular and extracellular spaces is the most determining factor in creating and maintaining the membrane potential (Em) across the cell membrane. In addition, it is related to cellular activity (cell proliferation, cell growth) and plays a role in the excitability of skeletal muscle, heart, brain (and nerves) and smooth muscle fibers [1]. The regulation of K+ distribution in intracellular and extracellular fluid is influenced by many physiological and pathological factors. This regulation should be highly efficient, since movement of even a small percentage, of the order of 1.5 - 2%, of intracellular K+ into the extracellular fluid can lead to an increase in plasma K+ concentration of up to 8 mEq/L [1]. The main factors influencing potassium homeostasis in the body, apart from the Na+ - K+ - ATPase pump, are catecholamines, insulin, blood potassium concentration, physical exercise, extracellular pH, hyperosmolality, cell lysis and aldosterone [1].
Dietary intake of potassium
In the Salt Substitute and Stroke Study (SSaSS), a significant reduction in cardiovascular events and mortality was reported when replacing normal salt (100% NaCl) with a K+-enriched salt substitute (75% NaCl and 25% KCl) leading to a relative a 57% increase in K+ intake and a relative decrease in Na+ consumption by 8.1% [18]. World Health Organization (WHO) guidelines recommend a K+ intake of > 3.5 g/day, while reducing Na+ intake to < 2 g/day, which is based on clinical studies to lower blood pressure (BP). This amount of intake helps maintain lower blood pressure levels, reducing the risk of developing kidney stones and possibly reducing osteoporosis [19]. A systematic literature review and Bayesian meta-analysis of 104 studies from 52 countries found that global K+ intake (2.25 g/day) remains below WHO guidelines, and only 14% of the world's population managed to achieve an average intake K+ according to the recommendation target. There was, in fact, considerable variation in the geographical distribution of the findings, with the lowest average potassium intake reported in Asia and the highest intake in Eastern and Western Europe [20]. High-quality data show that increased K+ intake lowers blood pressure in hypertensive subjects without adverse effects on blood lipid concentrations, catecholamine concentrations, or renal function in adults. Higher K+ intake was associated with a 24% lower risk of stroke (moderate quality data). These results suggest that increased K+ intake is potentially beneficial for most people without impaired renal potassium metabolism in the prevention and control of elevated blood pressure and stroke [21].
Patients with chronic kidney disease (CKD) are usually placed on a low K+ diet. It is reported, however, that this particular dietary pattern may be associated with folic acid deficiency. Serum folic acid levels should be investigated before initiation of potassium restriction in patients with grades 3 and 4 CKD to identify individuals with folic acid deficiency or borderline serum levels who should receive folic acid replacement therapy. This intervention is essential as folic acid deficiency is one of the etiological factors of anemia that patients with CKD experience22. In particular, in patients with end-stage CKD undergoing hemodialysis sessions, a dietary pattern of balanced K + intake is necessary, because higher dietary K + intake is associated with an increased risk of death in this population [23]. Evidence indicates that a diet that includes foods rich in K+ has multiple health benefits, which may also be attributed to the content of other elements, such as vitamins, minerals and fiber. Benefits include lowering BP and reduced risk for cardiovascular disease and stroke. Foods high in potassium may also prevent the progression of CKD and reduce the risk of mortality [24]. But with the risk of developing unwanted complications such as hyperkalemia and acidosis, CKD patients need to follow dietary patterns of limited K+ intake, nullifying the benefits of a diet rich in fruits and vegetables. Recent data indicate that adjunctive therapy with the newer K+ sequestrants may allow the liberation of dietary choices and the optimization of therapy with inhibitors of the Renin Angiotensin Aldosterone System (RAAS) in patients with CKD and a history of hyperkalemia [24]. In contrast to Na+ additives in foods consumed daily, the use of additives (e.g. in uncooked meat and poultry products) that increase K+ and P content by three and twofold, respectively, has been underestimated. Frequently, this modification may not be visible by inspecting the food label. This fact is particularly dangerous in hemodialysis patients, as it increases the risk of hyperkalemia [25].
BICARBONATE
In inorganic chemistry, bicarbonate (HCO⁻3) is a step in the process of removing a hydrogen ion from carbonic acid (H2CO3). Normally, cells produce and excrete large amounts of carbon dioxide (CO2) during the aerobic metabolism of carbohydrates and fats, which in turn reacts with water (H2O) in the presence of the enzyme carbonic anhydrase and is converted into carbonic acid (H2CO3) [26]. This breaks down into bicarbonate (HCO⁻3) and hydrogen ions (H⁺), with which it is in equilibrium:
[CO2] + [H2O] ⇄ [H2CO3] ⇄ [HCO⁻3] + [ Η⁺]
The HCO3/H2CO3 system is the most basic buffering system in the extracellular fluid that contributes to maintaining the acid-base balance. Changes in the intracellular concentration of acids [H⁺], and by extension the pH, cause changes in the shape and function of the body's proteins and enzymes, leading to potentially life-threatening conditions [27].
Buffers are compounds that can bind or release H⁺, depending on the initial change of the latter, in order to maintain pH at normal levels and prevent changes in cell function. Thus, HCO⁻3 has the ability to function both as weak acids and as bases, minimizing the changes of H⁺ [28]. The kidneys and lungs are the two main body systems that affect the concentration of HCO⁻3. Regarding the kidneys, they have the main role in the elimination and excretion of HCO⁻3. HCO⁻3 is filtered daily from the glomeruli in the precaudal, in a percentage that corresponds to the degree of glomerular filtration of the organism but also according to their concentration in the blood [26]. There, they react with the H⁺ secreted by the urinary tubules to form CO2, which diffuses into the interior of the cell and is converted to HCO⁻3, which in turn returns to the plasma. Thus, under normal conditions, all filtered HCO⁻3 is reabsorbed in the tubular part of the kidney, with the main point of regulation of excretion being the proximal convoluted tubule, as 85% [27] is reabsorbed there. In order for the change in H⁺ concentration to be the minimum, the action of the respiratory center is also modified and the concentration and, by extension, the partial pressure of carbon dioxide, through respiration [26]. The Henderson and Hasselbalch equation [28] are the basis for calculating the pH of a buffer solution. Using the components of the bicarbonate buffer the following form of the equation is obtained, which clearly shows the relationship between pH, HCO⁻3 and CO2 (Figure 1).
CO2 is a substrate for the synthesis of HCO⁻3 and any change in its concentration affects the reabsorption of HCO⁻3 from the urinary tubules and by extension their concentration in the extracellular space [26]. Normal values of HCO⁻3 in the extracellular fluid are 24 (22-26) mEq/L [26].
DIETARY INTAKE OF BICARBONATE
Although the main source of HCO⁻3 is through endogenous production, the consumption of certain foods containing their precursor molecules indirectly contributes to a small increase in their concentration in the blood [29]. Such foods are considered:
- Fruits and Vegetables: Natural sources of HCO⁻3 for the body are primarily fruits and vegetables. Green leafy vegetables, cruciferous and root vegetables, citrus fruits and other products such as bananas, apples and melons are the main representatives of this category. A special mention deserves citrus fruits and in general products containing citric acid as it is absorbed by the intestine and almost completely metabolized into HCO⁻3 [29].
- Mineral Water: HCO⁻3 is a natural component of mineral water. Some of them contain HCO⁻3 salts in increased concentrations [29].
- Sodium Bicarbonate (NaHCO⁻3): Available in various forms such as oral capsules or tablets or even intravenous solutions. It is also popularly known as baking soda. When NaHCO⁻3 is mixed with an acidic ingredient such as vinegar, CO2 gas is produced and thus the dough rises [29].
- HCO⁻3 supplements in various forms such as potassium bicarbonate or magnesium [29].
Unlike the Mediterranean diet which is more focused on fruits and vegetables and products such as fish and poultry, the "Western" diet is focused on eating proteins that tend to produce more acids. For several years, there has been research interest in the "base-producing diet", i.e. the diet that is based on eating foods that contain "bases" and limiting those that increase the concentration of acids in the body, as it is considered that it can influence the acid-base balance and additionally help in the treatment of certain diseases [30]. Part of this diet, in addition to fruits and vegetables, are also products that include HCO⁻3 as an additional supplement.
CONSUMPTION OF HCO⁻3 AND THE EFFECTS ON THE BODY
Gastrointestinal System (GI)
The role of these products, and especially mineral waters containing HCO⁻3, has been studied in particular in people suffering from disorders of the gastrointestinal tract such as indigestion, heartburn or gastroesophageal reflux. Specifically, the HCO⁻3 included in these waters reacts with the hydrogen ions of the gastric fluid and neutralizes them, making the environment of the stomach less acidic [30]. In fact, it is considered that they achieve a greater regulatory capacity than the corresponding antacid treatment. These changes also affect the action of local hormones such as gastrin, which at pH>3 acquires a longer duration of action, contributing to the digestion and absorption of food [31]. STOMACH STILL is a recently published study, the first randomized, double-blind, placebo-controlled study to demonstrate the superiority of drinking mineral water rich in HCO⁻3 in the treatment of heartburn in adult patients with recurrent episodes. It was also associated with an improvement in quality of life but also with a reduction in the use of on-demand medication [32]. Furthermore, considering that delayed gastric emptying is a key pathophysiological mechanism of functional dyspepsia, it has been shown that consumption of HCO⁻3 solutions accelerated this rate, as recorded using scintigraphic techniques after ingestion of radionuclide-labeled meals, improving symptoms that occur after taking the meal. Thus, it appears that this influence on gastric motility brings about a weakening of the dyspeptic symptoms that appear during the postprandial period [33]. Other literature data add that the consumption of mineral waters with an increased concentration of HCO⁻3 in combination with a diet rich in plant fibers brings greater benefits in the treatment of constipation [34].
Skeletal System
As early as 1968, Wachman and Bernstein [34] suggested that bone loss may result, at least in part, from the continuous mobilization of skeletal calcium salts, which act as labile bases, to balance the endogenous acid produced by the diet. In the same context, they emphasized that the reduction of the intracellular pH and the concentration of HCO⁻3 in the plasma are independent factors of inhibition of osteogenesis and stimulation of bone resorption [35]. Since then, there has been research interest regarding the degree of influence of HCO⁻3 consumption in delaying the onset of bone metabolic disorders. Apart of the Framingham study [36], which generally focused on researching risk factors for osteoporosis, also looked at the effect of consumption of specific ingredients and dietary patterns on bone density [36]. It confirmed the theory that an alkaline diet reduces bone wear and the likelihood of fractures by analyzing, in addition to fruit and vegetable consumption, the positive benefits of supplemental potassium and magnesium bicarbonate as they were associated with significantly less loss of bone density over four years, especially in the male population of research [36]. In general, the protective role of potassium bicarbonate in the skeleton has been demonstrated since the last century, as it was shown to improve the balance of calcium in the body, increasing the concentrations of osteocalcin and reducing the excretion of hydroxyproline in the urine, mitigating or even reversing bone loss arising in the long term in postmenopausal women [37].
The consumption of HCO⁻3 through mineral waters brings the same positive benefits, even in premenopausal women with normal blood calcium concentrations. HCO⁻3-rich mineral waters reduced bone resorption indices and, by extension, age-related bone loss [38]. Despite the positive results of the studies mentioned, there are also clinical studies that showed that the intake of potassium bicarbonate as a supplement does not protect against bone loss [38]. The data, therefore, are not clear. Thus, more emphasis is placed on increased intake of potassium and HCO⁻3 precursor molecules through the adoption of a diet rich in fruits and vegetables.
Urinary System
As already mentioned, the kidneys have the most basic role in the management of HCO⁻3 in the body and thus any change in their function directly affects their concentration in the plasma [26]. In cases of acute renal failure and hyperkalemia, the administration of NaHCO⁻3 aims to reduce its extracellular concentration as it can cause potentially life-threatening arrhythmias. Thus, when HCO-3 is added to the body, H⁺ ions leave the cells to neutralize it, exchanging with K⁺ ions, resulting in a decrease in the concentration of K⁺ in the extracellular fluid [26]. People with advanced chronic kidney disease (CKD), especially with GFR < 30 ml/min, often experience metabolic acidosis, due to the inability of the kidneys to eliminate the daily acid load, leading to an increase in H⁺ and a decrease in HCO⁻3. This is a situation that the body cannot deal with alone, when there is a severe impairment of renal function, and thus modern guidelines suggest additional treatment in patients with CKD and HCO⁻3 < 22 mEq/L [39].
A randomized controlled trial by Brito Ashurst et al. [39] showed that oral supplemental NaHCO⁻3 slowed the rate of decline in renal function in subjects with CKD and metabolic acidosis, but did not affect proteinuria or blood pressure. In other words, it appeared that HCO⁻3 has an independent role in the control of kidney function. Furthermore, considering that metabolic acidosis, as a condition, is associated with increased protein catabolism and therefore malnutrition and chronic inflammation, the study indicated that its additional administration improved the nutritional status of these patients, increasing the concentration of proteins such as albumin, the low values of which are associated with mortality in patients with CKD [39]. Recently published studies, such as that of Rasheed et al. who dealt with the effect of oral administration of NaHCO⁻3 in patients undergoing hemodialysis, confirmed the above findings [40]. In addition, metabolic acidosis aggravates the vascular disorders of these patients, through the production of molecules such as angiotensin II, aldosterone and endothelin, stimulating the deposition of calcium in the vessels. This condition is associated with increased mortality in patients with CKD. Correction of acidosis by administration of HCO⁻3 appears to prevent deposition and improve vascular function. However, the effects of NaHCO⁻3 on long-term cardiovascular function have not yet been clearly elucidated, and there are data to support that their persistent and marked plasma concentration (> 26 mmol/L) increases cardiovascular risk. Therefore, there is a reservation regarding their role in the cardiovascular system [41].
Therefore, the administration of HCO⁻3 to people with CKD has a place mainly when metabolic acidosis coexists, in order to avoid the negative effects that this entails. Metabolic acidosis is associated with increased mortality and morbidity as it affects a variety of metabolic pathways and accelerates bone resorption, disrupts glucose metabolism, increases protein catabolism, stimulates inflammation and leads to malnutrition and sarcopenia [42]. The next question that preoccupied the scientific community is whether this treatment can be achieved with the normal diet or requires supplementary administration of HCO⁻3, in the context of enhancing the alkaline diet. Thus, studies in patients with CKD due to arterial hypertension, stage 3 and 4, compared the effects of daily fruit and vegetable consumption with those of daily oral NaHCO⁻3. It appeared that in the first year, both strategies were able to improve the rate of kidney damage and metabolic acidosis, without statistically significant differences between them, confirming that a diet rich in bases derived from fruits and vegetables is an effective alternative for these people [43].
Muscular System
During intensive exercise, i.e. when a quick and large expenditure of energy is necessary, the organism is fueled by anaerobic metabolism, i.e. that which does not require the presence of oxygen. Thus, with anaerobic glycolysis, glycogen, stored in the muscles and liver, is rapidly broken down into glucose, producing energy (ATP). The end product of this process is lactic acid, a strong acid that breaks down into lactate and H⁺. The body's ability to produce glucose in this way is limited as acidity increases and hydrogen cations accumulate within the muscles. A decrease in intramuscular pH results in inhibition of glycolytic enzymes and has been associated with a decrease in strength and power output and, by extension, with the appearance of muscle fatigue [44]. The body's normal HCO⁻3 is the first line of defense against acidity. When they reach their maximum buffering capacity, lactate and H⁺ exit the cell. Thus, it is argued that by increasing the concentration of HCO⁻3 in the extracellular fluid, H⁺ will leave the muscles faster (due to a transmembrane difference in concentration) and thus their accumulation will be delayed and therefore the appearance of muscle fatigue [45]. Since 2018, the International Olympic Committee ranked NaHCO⁻3 in the top five nutritional supplements that improve the performance of athletes [46]. Studies focusing on bicarbonate supplementation have documented significant improvements in the performance of athletes in various sports, reinforcing the theory of an ergogenic effect of HCO⁻3. Muscle biopsies during exercise and after NaHCO⁻3 ingestion confirmed that improving intramuscular pH results in a faster rate of glycolysis and ATP resynthesis [47].
CONCLUSION
Increased sodium intake has been associated with increased BP and increased risk of cardiovascular disease, particularly stroke and coronary heart disease. Even in the absence of an increase in BP, excess dietary Na+ can adversely affect multiple target organs and tissues, including the blood vessels, heart, kidneys, and brain regions (stem nuclei) that control BP. On the other hand, low dietary K+ intake appears to lead to increased blood pressure, while increased K+ intake reduces salt sensitivity and favorably affects BP and has a stronger effect on CVD risk than sodium alone. or potassium. The Na/K ratio may be an independent predictor of cardiovascular events in the adult population and has a stronger effect on cardiovascular disease risk than sodium or potassium alone. A balanced Na/K ratio should be considered to prevent secondary diet-induced hypertension as a risk factor for cardiovascular disease.
Dietary intake of HCO⁻3 either through natural sources or supplements can significantly affect health. They are an essential component of the body and actively participate in its homeostasis through the HCO3/H2CO3 regulatory system, so any excess or insufficient intake can disturb the body's acid-base balance. It is important to note that although incorporating HCO⁻3-rich foods or supplements into the diet can provide health benefits, especially for people with specific conditions, the effects of taking them can be complex and vary depending on the individual organism, age, gender or general condition. Their excessive consumption has been associated with electrolyte disturbances and possible adverse effects. In addition, adopting a balanced diet that includes all food groups in appropriate concentrations is the basis for achieving and maintaining optimal health.
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