ALKALINE DIET
The existence of an “alkaline diet” capable of improving bone health is a controversial topic (Frasseto et al., 2018). In a person with normal renal and respiratory function, diet does not significantly alter blood pH, although it can influence the net production of endogenous acid and the amount of acid the kidneys must eliminate. An acidifying diet can be defined as one whose metabolism generates a greater net production of non-volatile acids that must be neutralized and eliminated, primarily by the kidneys. This acid load arises mainly from three processes: the net release of protons from organic phosphate compounds, the oxidation of sulfur-containing amino acids to sulfates, and the endogenous formation of incompletely metabolized organic acids. Conversely, a more alkaline diet, rich in fruits and vegetables, for example, provides organic anions such as citrate and malate, which, once metabolized, generate bicarbonate and reduce the net acid load. This primarily alters renal acid excretion, which can lead to variations in urinary pH. However, blood pH remains tightly regulated.
ACID-BASE BALANCE AND pH Acid-base balance is essential for the proper functioning of the body. This is why blood pH always lies within a very narrow range, between approximately 7.35 and 7.45. The body produces acids, particularly during the metabolism of proteins, sulfur-containing amino acids, and other normal cellular processes. The kidneys are responsible for eliminating this acid load and regenerating bicarbonates, thus contributing to the maintenance of physiological blood pH. In cases of renal failure and the development of metabolic acidosis, H+ ions are neutralized by the mobilization of carbonates, phosphates, and calcium from bone minerals. This acidosis can promote protein catabolism, loss of muscle and bone mass, inflammation, and general metabolic deterioration. It is assumed that an acidic diet, rich in protein, phosphates, and other acidic nutrients, typical of the Western diet, would negatively impact bone health, while another diet, rich in alkaline components from vegetables, would mitigate this effect. However, these mechanisms associated with a state of metabolic acidosis do not correspond to the small variations induced by a typical diet in a healthy individual, given that the pH is maintained within a very narrow range.
ACIDITY AND CALCIUM LOSS
Furthermore, the existence of acute calcium losses in urine, associated with the consumption of foods high in protein or phosphorus, a higher acid load, or other dietary changes, has been considered evidence. However, these acute calcium losses do not necessarily imply a loss of bone calcium. Calciuria also depends on intestinal absorption, acute changes in renal filtration and reabsorption, and acute changes in the levels of hormones such as PTH, vitamin D, sodium, and other minerals. Therefore, increased urinary calcium excretion and subsequent calcium retention can occur without necessarily resulting in a negative body calcium balance. Indeed, diets rich in protein or phosphorus can increase calciuria while simultaneously enhancing intestinal calcium absorption, and from an epidemiological perspective, they may even be associated with higher bone density than diets lacking these elements, which do not cause such acute calcium losses. Protein, phosphorus, and sodium can increase certain components of acid load or calciuria, but this does not automatically lead to bone loss: protein provides amino acids to the extracellular matrix and muscles, increases IGF-1 levels, and can promote calcium absorption. Phosphorus, meanwhile, is essential for hydroxyapatite formation, and the sodium-induced increase in calciuria can activate compensatory mechanisms of calcium metabolism, including, in some studies, an increase in PTH, 1,25(OH)₂D, and intestinal calcium absorption. However, the extent and relevance of this compensation depend on the context, particularly calcium intake. The final effect therefore depends on the mineral and energy context, and more specifically on the availability of sufficient calcium. In cases of low calcium intake, a high sodium or protein load can make maintaining calcium balance more difficult, whereas with sufficient calcium intake, this same exposure may be neutral or even lead to improved bone mineral density. Consequently, acute changes in urinary pH, calciuria, or resorption markers should not be interpreted in isolation as bone deterioration, as the body adjusts intestinal absorption, PTH, vitamin D, renal function, and bone remodeling through various mechanisms.
ACIDITY AND ACID CHARGE OF FOOD
Other points can be confusing. The pH of a food does not determine its metabolic acid load. A lemon is acidic in the mouth and stomach, but its organic anions can be metabolized to produce bicarbonate. This is why fruits and vegetables often contribute to a lower renal acid load. Conversely, other foods can generate acid after they are metabolized, particularly through the metabolism of sulfur-containing amino acids and certain phosphorus compounds. Acid load refers to the amount of non-volatile acids the body produces through metabolism. Foods high in animal protein, some grains, and certain Western diets tend to generate a higher net acid load, while fruits and vegetables provide alkaline precursors. Animal proteins, especially due to their sulfur-containing amino acid content such as methionine and cysteine, tend to increase net acid production. Some grains also contribute to the acid load. On the other hand, fruits and vegetables contain organic anions such as citrate and malate which, once metabolized, can produce bicarbonate or alkaline equivalents.
DOES SUBCLINICAL ACIDOSIS EXIST?
Having outlined the main weaknesses of the model, subclinical acidosis could be more significant with age, which tends to acidify the blood to some extent, or in cases of even mild renal insufficiency, when the capacity to eliminate the acid load decreases without overt acidosis. With age, there is a slight tendency toward an increase in systemic acid load, with a rise in H+ ion concentration and a decrease in plasma bicarbonate. This has been interpreted as a very low-grade chronic metabolic acidosis, probably partly related to the decreased renal capacity to excrete acid (Frassetto, L., & Sebastian, A. 1996). Furthermore, studies in individuals with stage 1 to 3 chronic renal failure show that H+ ion retention tends to increase progressively with a decrease in glomerular filtration rate, before the onset of overt metabolic acidosis. Serum bicarbonate could therefore be a relatively late and imperfect marker of the entire phenomenon. Another question arises: can subclinical acidosis exist even in the presence of a healthy kidney? Furthermore, relatively low bicarbonate concentrations, even close to normal, have been associated with a decrease in bone mineral density.
BONE AS A BUFFER
Bone also contains significant amounts of carbonate. In response to proton overload, the dissolution of minerals, releasing bases and minerals, can contribute to the buffering effect. If this process, although small, continues over several years, its importance could be cumulative. Osteoclasts are specifically designed to function in an acidic environment: they themselves generate H⁺ ions to dissolve hydroxyapatite. Osteoclasts showed an approximately 6.7-fold increase in bone resorption activity when the pH decreased from 7.4 to 7.0, with rapid changes in their morphology and gene expression (Davies et al., 2025). This demonstrates that pH is a regulatory signal for osteoclasts, although this experimental pH represents a much larger variation than that observed in cases of subclinical acid retention. Nevertheless, osteoblasts and osteoclasts possess mechanisms capable of detecting H⁺ ions as a biological signal. Theoretically, it is therefore plausible that a diet could increase net endogenous acid production and enhance resorption activity without inducing clinical acidosis. For example, in a metabolic test, modifying the acid-base load through diet resulted in a change in urinary pH of approximately 1 unit, while blood pH changed by only 0.014 (Buclin et al., 2001). This demonstrates that small changes in bicarbonate or pH can occur without causing systemic acidosis, given the renal acid excretion system in urine and the activation of organic buffer systems.
ACIDIFICATION OF THE LOCAL TISSUE MICROENVIRONMENT
Furthermore, blood pH can be perfectly normal while some extracellular microenvironments exhibit a lower pH. Tissues continuously produce CO2, lactate, and protons. In bone, this phenomenon is particularly important because osteoclasts, through their physiological activity, create an extremely acidic microenvironment beneath their rough surface to dissolve hydroxyapatite. Blood pH does not accurately reflect the interstitial pH of each tissue. Few dietary studies provide consistent evidence of this type of acidification, even locally. Some controlled studies with a protein intake of 2 g/kg/day do not show systemic acidosis, and other studies with increased protein intake have not demonstrated a decrease in musculoskeletal pH through muscle microdialysis (Boschmann et al., 2020). In fact, in human muscle, the interstitial pH variations measured during exercise are far greater than the simultaneous variations in venous pH. Physical exercise and the acidification it induces are linked to good overall health, even in people who engage in intense physical activity throughout their lives. A diet rich in protein and with a high renal acid potential can increase urinary acidity and calciuria without necessarily increasing bone resorption. Furthermore, no consistent epidemiological link has been established between protein consumption and poorer bone health. In addition, protein increases the intestinal absorption of calcium and IGF-1.
EPIDEMIOLOGY AND INTERVENTION STUDIES: Epidemiologically, systematic reviews of observational studies tend to show an increased risk of fracture with a high dietary acid load, although this risk is generally low (Mirzababaei et al., 2025). However, vegan populations tend to have lower bone density and a higher fracture prevalence despite lower protein intake and consumption of less acidifying foods (Ogilvie et al., 2022). Another interesting piece of evidence comes from studies that have directly attempted to increase alkalinity through supplementation. For example, some studies on potassium bicarbonate show a reduction in urinary calcium excretion and some resorption markers in older adults, although the evidence regarding clinical endpoints is insufficient to demonstrate that this intervention results in a definitive reduction in fractures. Other relevant clinical trials, conducted over a longer period, have not demonstrated a clear benefit. A relevant controlled clinical trial, conducted with 276 women over two years, revealed no difference in CTX, P1NP, or lumbar or hip bone density (Macdonald et al., 2008). A meta-analysis from 2026 showed no significant effect on resorption markers or other relevant endpoints (AlSejari et al., 2026).
SUBCLINICAL ACIDIFICATION AS A PHYSIOPATHOLOGICAL PROCESS
Furthermore, subclinical acidification can also occur in the context of inflammatory catabolism due to insufficient energy and protein intake and metabolic disorders associated with more fragile health. In other words, diet can contribute to the overall acid load, but the development of subclinical acidosis also depends on the body’s ability to manage it. Thus, age, metabolism, and kidney health could represent a greater “acid load” than diet alone. With age, renal acid excretion, available bicarbonates, and the functional reserve of tissues such as muscles and bones may decrease, while chronic diseases, inflammation, and metabolic disorders can increase endogenous acid production or reduce its compensation. Moreover, low protein intake in older adults poses a greater problem for general health, muscle mass, function, and the risk of falls and fractures than the role that subclinical acidification might play.
FINAL COMMENTS
In summary, the hypothesis of an “alkaline diet,” strictly understood as a significant change in blood pH, is difficult to support in individuals with normal acid-base balance. However, dietary acid load can indeed alter kidney function, acid excretion, and certain parameters of mineral metabolism. This effect could be amplified when the body’s physiological capacity for compensation decreases, as occurs with age or in cases of kidney disease. A diet rich in plant-based foods is advisable for several reasons, including a lower acid load, without sacrificing sufficient protein, energy, or mineral intake, which could pose a greater risk to bone health than simply attempting to alkalize the diet.
