Free radicals

Free radicals are reactive molecular fragments that occur even in healthy cells, and can damage the cell. 1 Ray Peat's perspective on free radicals is deeply rooted in the early 20th-century work of Moses Gomberg, who first demonstrated their physical existence, and W.F. Koch, a chemistry professor who immediately applied this discovery to biology, postulating that quinones in the mitochondria handle energy via free radical reactions. 2 This view was initially rejected by mainstream science, which held that free radicals were purely toxic and incompatible with life, a stance that led to the government twice attempting to jail Koch. 2 Peat argued that the official view only began to shift in 1954 when Barry Commoner's group measured free radicals in living tissues, around the same time Denham Harman formulated his mitochondrial free radical theory of aging. 5

Peat distinguished sharply between productive and destructive free radical activity. He explained that when thyroid and oxygen are working properly, the electron transport chain involves lots of free radical activity, but it is all productive and protective; the faster oxygen is run through the mitochondria under the influence of thyroid, the less free radical damage occurs to the cell's structure. 3 He likened this to a laboratory with negative pressure, where a rapid flow of electrons keeps the system tightly ordered, preventing them from "wandering off" and causing damage. 9 In contrast, slowing metabolism or removing oxygen creates a state where electrons have no place to go, generating toxic free radical damage. 9 This framework directly opposes the old "rate of living" theory, which posited that slowing oxygen consumption would slow aging. 9

The primary source of destructive free radical cascades in the body, according to Peat, is the ingestion of polyunsaturated fats (PUFAs). He demonstrated that even at room temperature, oils like safflower oil spontaneously oxidize, sucking up oxygen and forming toxic liquid peroxides, a process greatly accelerated at body temperature and catalyzed by iron and heavy metals. 2 Peat stated that PUFAs are the main material that causes an "explosion" of free radicals once the process is started by factors like endotoxin and nitric oxide. 2 He cited a century of studies, including a 1927 experiment, showing that a fat-free diet extends lifespan and prevents cancer, and noted that animals deficient in PUFAs have a metabolic rate about 50% higher and can survive extreme physical trauma that kills normally fed animals. 2

Peat also warned that substances typically considered pure antioxidants, such as synthetic ascorbic acid, can become potent free radical generators in the presence of catalytic heavy metals like iron. He recounted a chemist's finding that pure vitamin C in distilled water produced a concentration of free radicals equivalent to a killing dose of X-rays, and noted that even a few milligrams of the synthetic form triggered allergic reactions he did not experience from high-vitamin C foods. 2 He extended this pro-oxidant potential to plant polyphenols and flavonoids, explaining that in a reduced cellular state, vitamin C and similar substances can react with ferrous iron to produce the highly toxic hydroxyl radical. 7 The most important source of hydroxyl radicals during stress is the ferrous ion released when heme oxygenase degrades heme, a process exacerbated by carbon monoxide or hypoxia which keeps iron in its reduced, radical-producing state. 7 Peat maintained that the main protective action of substances like aspirin and bioflavonoids is not merely scavenging radicals, but improving the oxidative state of the cell to minimize their production. 2