Acidosis

Acidosis is not a simple state of excess acid in the body, but a complex metabolic disturbance centered on the failure of oxidative energy production, with the accumulation of lactic acid being a primary consequence rather than the root cause. 2 Ray Peat argued that the popular conception of acidosis as a systemic acidic condition is fundamentally flawed, because a healthy, respiring cell actively maintains a mildly acidic internal state (around pH 6.8-6.9) through the production of carbon dioxide, while the blood is kept slightly alkaline. 2 When a cell is stressed and cannot produce adequate CO2, it shifts internally to an alkaline state and begins inefficiently producing lactic acid, which acidifies the cell's external environment. 3 This distinction is critical: the internal alkalinity of the stressed cell, not an acidic interior, is the pathological shift, while the measurable acidity in tissues and blood is a sign of this underlying respiratory defect. 3

The central mechanism driving pathological acidosis is the Randle Cycle, a metabolic competition where increased oxidation of free fatty acids (FFA) directly inhibits the oxidation of glucose. 1 Georgi Dinkov has synthesized this with Otto Warburg's observations, describing a vicious feedback loop: the lactic acidosis of the Warburg "Effect" blocks glucose oxidation, which in turn increases both fatty acid oxidation and synthesis, further suppressing glucose metabolism and generating more lactic acid. 1 This cycle is a necessary and sufficient condition to trigger cancerization of healthy tissue, a process that can be initiated by drugs like metformin that promote acidosis and can be reversed by blocking systemic acidosis with agents like baking soda. 2 Peat similarly emphasized that estrogen, stress, and unsaturated oils promote this pathology by increasing free fatty acids and inhibiting thyroid function and glucose metabolism. 8

From a chemical perspective, Peat rejected the simple Brønsted-Lowry acid-base model for physiological regulation, instead pointing to the Lewis acid theory where an acid is an electron acceptor. 4 In this framework, the carbon atom in carbon dioxide acts as a powerful, instantaneous electron acceptor, making it the primary physiological acidifying agent without needing to form carbonic acid. 4 This aligns with the historical view that the oxidation of sugar in tissues is a controlling factor in regulating blood alkali, where the administration of glucose alone is often sufficient to correct the symptoms of clinical acidosis by restoring the cell's ability to produce CO2. 2 The condition is therefore not a matter of neutralizing the body's alkali with acids, but of restoring oxidative glucose metabolism to break the cycle of lactic acid production and fatty acid dominance. 2

The clinical definition of acidosis as a mere reduction in the blood's "alkaline reserve" of bicarbonate has been recognized as inadequate for over a century. 9 Yandell Henderson noted that healthy individuals at high altitude could have blood alkali levels indicating marked acidosis yet feel extremely well, proving that a low bicarbonate level alone is not the critical feature of the disease state. 9 The true danger is the metabolic acidosis seen in critical illness, such as COVID-19, where lactic acid rises to lethal levels as carbon dioxide falls. 10 Dinkov notes that the primary therapy for this condition should be carbon dioxide, which can oxidize lactic acid back to pyruvate, rather than merely buffering the acid with bicarbonate infusions. 10 Peat advised that preventively, one should avoid foods containing bacterial lactic acid, like yogurt and sauerkraut, and prioritize light and thyroid-supportive nutrition to maintain a high background of CO2 production that prevents the shift to anaerobic glycolysis. 8