Oxidative stress
208 sourcesRay Peat's understanding of oxidative stress differs from the mainstream antioxidant narrative. While he acknowledged that oxidative damage is a major driver of aging and disease, he argued that the primary source of damaging oxidation is not insufficient antioxidant intake but excessive polyunsaturated fat in tissues. PUFAs undergo lipid peroxidation, producing a chain reaction of free radicals and toxic aldehydes (MDA, HNE, acrolein) that damage DNA, proteins, and mitochondria.
Rather than megadosing antioxidant supplements, Peat recommended reducing the source of oxidative stress: eliminating PUFAs from the diet and waiting for tissue stores to deplete (a process taking 4+ years). Meanwhile, vitamin E, selenium, and aspirin provide protection against ongoing PUFA peroxidation. He noted that efficient mitochondrial respiration actually produces minimal harmful reactive oxygen species — it's when respiration is compromised that damaging oxidation increases.
Key Positions
- The primary source of oxidative stress is lipid peroxidation of stored polyunsaturated fats
- PUFA peroxidation produces toxic aldehydes (MDA, HNE) that damage DNA, proteins, and mitochondria
- Lipofuscin (age pigment) is the visible accumulation of lipid peroxidation damage
- Reducing dietary PUFAs is more effective than antioxidant supplementation
- Vitamin E is the primary defense against fat-soluble peroxidation
- Iron catalyzes lipid peroxidation — excess iron accelerates oxidative damage
- Efficient mitochondrial respiration produces minimal reactive oxygen species
Sources
208 items-
Unsaturated fatty acids: Nutritionally essential, or toxic?
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Using Sunlight to Sustain Life
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VV Fitness Blog - Vahdaneh Vahid
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Vashinvetala (formerly Pranarupa)
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Vegetables, etc. - Who Defines Food?
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Vitamin E: Estrogen antagonist, energy promoter, and anti-inflammatory
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Water: swelling, tension, pain, fatigue, aging
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When energy fails: Edema, heart failure, hypertension, sarcopenia, etc.