Antioxidants

Antioxidants are more accurately described as chain breakers that halt harmful free-radical chain reactions, but they do not inhibit normal cellular oxidation. 1 Peat argued that the public understanding of antioxidants has been fundamentally skewed by denying the protective role of carbon dioxide and oxidation, noting that the stronger the oxidation in the normal respiratory route, the safer the organism. 5 The healthy, active cell maintains a highly oxidized state, with roughly 500 times more oxidized NAD than reduced NADH. 10 In contrast, cancer cells possess a very powerful intrinsic antioxidant system, and restoring health requires overcoming that antioxidant state. 8

The body's innate antioxidant network includes glutathione, superoxide dismutase, catalase, and circulating uric acid, which is considered quantitatively the main antioxidant defense inside cells. 4 However, Peat cautioned that an excess of antioxidant enzymes can be pathological; the genetic overdose of superoxide dismutase in Down's syndrome creates accelerated aging, and adding the extra gene to animals replicates this effect. 8 The crucial distinction lies in the cell's redox balance. When a cell is irritated or stressed, it shifts into a reduced state where molecules like ascorbic acid and Vitamin E become reduced to sop up toxic fragments, but the system can become stuck in this over-reduced, over-electrified form, preventing a return to normal oxidative function. 10

The danger of the reduced state is amplified by the presence of polyunsaturated fats (PUFA) and iron. When oxygen is insufficient, electrons that cannot be taken up by oxygen locate on iron atoms, activating the iron to attack PUFAs and initiate an oxygen-wasting free-radical cascade. 3 This process creates lipofuscin, or age pigment, which functions as a powerful oxygen sink that starves mitochondria. 3 In this context, reduced vitamin C becomes a reductant that reacts with iron to produce the highly toxic hydroxyl radical. 2 Peat emphasized that lactate should be seen as the polar opposite of carbon dioxide, with higher lactate levels indicating a shift away from the oxidative state and closer to death. 5

Many plant-derived "antioxidants" are polyphenolic compounds that overlap almost completely with estrogenic substances. 6 Peat noted that these same chemicals were historically classed as tannins and identified as effective carcinogens in the 1970s after topical burn treatments led to skin cancer. 6 In contrast, Vitamin E and Vitamin C are electrically tuned to specific roles within the cell's tightly organized system. 7 When functioning properly, dehydroascorbic acid—the oxidized form of vitamin C—is eight times more concentrated inside the cell than outside and acts as an oxidant that maintains cell structure. 2 Peat argued that Vitamin E was originally understood as an anti-estrogen regulator of sex hormones before being reclassified as an antioxidant, a shift that obscured its primary anti-inflammatory identity. 9

The fundamental therapeutic goal is not to indiscriminately supply reducing agents but to restore efficient mitochondrial oxidation of glucose, which minimizes radical production at its source. 2 As oxidative metabolism is revved up—for example, by adding thyroid hormone—fewer electrons escape to cause dangerous free radicals. 7 Substances like aspirin and bioflavonoids protect against lipid peroxidation not primarily by direct radical scavenging, but by improving the oxidative state of the cell and increasing mitochondrial respiration. 2 The so-called "super" antioxidants marketed as many times more powerful than Vitamin E are tested in vitro and act like dynamite, failing to integrate into the cellular system and potentially causing harm. 7