NAD+
NAD+ and NADH are redox cofactors. NAD+ accepts electrons; NADH donates them into the respiratory chain.
Peat's view
[edit]Thyroid-driven oxygen consumption keeps NAD+ concentration hundreds of times higher than NADH, preventing lactic acid production and toxic redox cycling.[1] Elsewhere Peat put a specific figure on this ratio in a healthy oxidized cell, about 200 to 1.[2] Niacinamide and dietary B3 support NAD pools. Fashionable NAD-IV and precursor marketing outruns solid lifestyle basics: sleep, food, thyroid, low PUFA. Measure function (temperature, pulse, labs) over boutique assays alone.
NAD/NADH ratio and pyruvate dehydrogenase
[edit]Pyruvate dehydrogenase (PDH) activity, the rate-limiting gate from glycolysis into the Krebs cycle, depends on a favorable NAD/NADH ratio plus thiamine and magnesium as cofactors. When PDH is downregulated, as in hypothyroidism and cancer metabolism, pyruvate and NADH accumulate; the body then oxidizes that excess NADH back to NAD+ using pyruvate itself as the oxidant (via LDH), generating lactate even when oxygen is present.[3] Raising niacinamide intake expands the total NAD+NADH pool and can restore PDH activity through the NAD/NADH ratio; quinone-type oxidants such as vitamin K2, emodin, and methylene blue achieve the same effect by directly re-oxidizing NADH to NAD+ without adding to the pool, letting PDH resume even under cancer-like excess-glycolysis conditions.[3] Biotin offers a parallel route: it activates pyruvate decarboxylase, an alternative enzyme that shares PDH's thiamine/magnesium cofactor requirement and lets accumulated pyruvate reach the Krebs cycle when PDH itself is impaired.[3] Methylene blue additionally lets electrons bypass a blocked complex I-III and can activate complex IV (cytochrome c oxidase) directly, alongside thyroid (T3) and progesterone as the most effective pro-metabolic agents in this scheme, with DHEA, niacinamide, pregnenolone, and magnesium next.[3]
See also
[edit]References
[edit]- ↑ Ray Peat, "Fatigue, Aging, and Recuperation." "Thyroid stimulation of oxygen consumption tends to prevent lactic acid production, because it keeps the cytoplasm in a state of relative oxidation, i.e., it keeps the concentration of NAD+ hundreds of times higher than that of NADH. NADH is required for the conversion of pyruvate to lactate. It is also the source of reducing potential in many kinds of toxic redox cycling, that generate lipid peroxides."
- ↑ Ray Peat, "Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer." "...keeping the cell highly oxidized, with a ratio of NAD+/NADH of about 200."
- ↑ 3.0 3.1 3.2 3.3 Georgi Dinkov (haidut), post in "NAD/NADH Ratio - The One Metabolic Cause To Rule Them All," Ray Peat Forum thread, 2017.