Acid-base balance is one of the most tightly regulated physiologic systems in the human body. In healthy individuals, chronic systemic acidification is highly unlikely because multiple compensatory mechanisms maintain arterial blood pH within a narrow range. Alkaline substances have established roles in medicine, but these are limited to clearly defined clinical contexts, such as chronic kidney disease (CKD) and selected forms of nephrolithiasis, rather than lifestyle modifications.

The “acidity myth” warrants a critical appraisal. Claims that acidic foods cause systemic acidity and diseases, such as cancer or osteoporosis, conflict with established biochemical and clinical evidence despite widespread commercial promotion.

Few biochemical concepts have been simplified to the same extent or marketed broadly in the supplement industry. Fatigue, impaired concentration, musculoskeletal pain, toxin accumulation, and accelerated aging are symptoms that are routinely attributed to alkaline wellness. For clinicians, the distinction is straightforward but essential: Evidence-based physiology of acid-base balance differs fundamentally from the popular construct driving these claims, which reflects persuasive marketing more than biochemical facts.

Physiologic Control

The body maintains arterial blood pH within a narrow range of approximately 7.35-7.45. Even small deviations are clinically meaningful because enzymes, ion channels, and cell membranes are extremely sensitive to changes in hydrogen ion concentration. Several coordinated systems stabilize acid-base homeostasis.

Immediate buffering occurs through chemical systems in the blood, primarily the bicarbonate-carbon dioxide (HCO₃-/CO₂) buffer. The lungs regulate volatile acid components within minutes by adjusting CO₂ exhalation. The kidneys provide long-term regulation through the excretion of nonvolatile acids and the reabsorption and generation of bicarbonate. When these mechanisms function normally, persistent pathologic alterations in systemic blood pH in otherwise healthy individuals are extremely unlikely.

Acid-Ash Hypothesis

Public interest in the acidity myth is often linked to the “acid-ash hypothesis.” In a simplified form, meat, cheese, grains, and coffee are classified as acid-forming foods, whereas fruits, vegetables, and potatoes are considered alkaline-forming foods. From this, the conclusion is drawn that the body can enter a chronically acidic state through an “acidifying diet,” which then causes ailments, a state that must be corrected with alkaline powders or alkaline diets.

Diet influences renal acid load. This effect can be estimated using models of potential renal acid load and endogenous non-carbonic acid production. Urinary pH reflects these dietary effects. However, equating acidic urine with an “acidic body” is misleading. Urinary pH represents renal excretory activity rather than arterial blood pH or clinically relevant metabolic acidosis (MA).

Sodium HCO₃ (NaHCO₃) is occasionally used as a home remedy for reflux. Although salt rapidly neutralizes gastric acid and may provide short-term symptom relief, its pharmacologic effects require caution.

The neutralization of hydrochloric acid generates CO₂, which can cause belching, gastric distention, and bloating. Increased intragastric pressure may promote the reflux of gastric contents into the esophagus, potentially worsening the reflux.

Repeated acid neutralization may also trigger acid rebound. An increase in intragastric pH can stimulate gastrin release and subsequent acid hypersecretion. Although this effect is best documented with calcium-containing antacids, similar mechanisms may occur with other neutralizing agents, such as potassium citrate.

Some individuals report transient relief followed by symptom recurrence, leading to repeated dosing, a pattern that can perpetuate rather than resolve the symptoms.

Kidney Diseases

However, the problematic lifestyle concept of “acidosis” has clear clinical relevance in CKD. Declining renal function reduces the capacity to excrete nonvolatile acids, resulting in MA, which is characterized by reduced serum bicarbonate concentrations. In patients with CKD, MA is associated with adverse effects on muscle and bone metabolism and may contribute to disease progression.

Oral NaHCO₃ is used to normalize serum bicarbonate levels. Large trials, such as BiCARB, have not demonstrated substantial improvements in clinical endpoints; however, the intervention remains pathophysiologically sound and widely used.

Some meta-analyses have reported improvements in renal function parameters. Increased sodium load is a clinically relevant consideration, particularly in individuals with hypertension.

In urologic practice, evidence supporting urinary alkalinization is stronger. Citrate supplementation increases urinary pH and citrate concentration, inhibiting calcium oxalate crystallization. Randomized trials have demonstrated that citrates reduce the recurrence of stone formation. Long-term observational data have shown sustained reduction in stone formation rates. Targeted urinary alkalinization is therapeutically relevant for uric acid stones because these stones partially dissolve at increased pH.

In sports medicine, NaHCO₃ has been studied for its ability to increase extracellular buffering capacity during high-intensity physical activity. Measurable effects on performance have been documented in selected settings. Importantly, this research is hardly relevant for healthy individuals with low levels of physical activity because it deals with an extremely short-term metabolic situation, not with chronic, everyday acidosis.

Bone Health

The debate surrounding the effects of an allegedly “alkalinizing” diet on bone health has persisted for years. It has long been argued that an acid-forming diet leads to bone loss because calcium is mobilized from the bone to buffer excess acid, thereby promoting osteoporosis. Although biologically plausible, systematic reviews and meta-analyses have not provided reliable evidence that alkaline diets or supplements prevent osteoporosis or produce clinically meaningful improvements in bone mineral density. However, the proposed association remains controversial.

Limited Indications

Despite limited medical indications, the “acidity myth” has achieved commercial success because it offers a simple explanation for complex and multifactorial ailments. Urinary pH testing provides objective confirmation, and the proposed intervention using alkaline powders or tablets appears straightforward.

In clinical practice, clear indications for alkali treatment are limited primarily to MA in CKD and the treatment or prevention of certain kidney stones. In otherwise healthy individuals with nonspecific symptoms, robust evidence supporting alkaline wellness claims is lacking. Any perceived improvement is attributable to nonspecific or placebo effects.

This story was translated from Medscape’s German edition.