Biotin

Biotin (vitamin B7) is a B vitamin that functions as a critical cofactor for mitochondrial oxidative metabolism, specifically by enabling an alternative entry point into the Krebs cycle when the primary pathway is blocked. 2 Peat expressed caution about high-dose supplementation, noting that animal studies from 50 years ago showed moderate overdoses could cause liver cancer, and he recommended sticking to around 1 milligram per day. 1 Dinkov has extensively investigated pharmacological doses of biotin, finding that it acts as a cofactor for the enzyme pyruvate carboxylase, which converts pyruvate into oxaloacetate, thereby bypassing a blocked pyruvate dehydrogenase complex and sustaining the Krebs cycle. 3

The therapeutic potential of high-dose biotin became apparent in a landmark human trial for primary progressive multiple sclerosis, a disease with no known remissions. 3 In that study, 300 milligrams of biotin daily led to a striking amelioration of symptoms, with researchers concluding that biotin dramatically improved the energetic status of the organism by increasing carbon dioxide production, lowering lactate, and reducing free fatty acids and triglycerides in the blood. 3 Dinkov has cited this trial and other in vitro work showing that pharmacological biotin concentrations tripled cellular carbon dioxide production, confirming its role as a mitochondrial nutrient that shifts metabolism away from fatty acid oxidation and toward glucose oxidation. 3

In Dinkov's own cancer experiments, biotin was the decisive addition that converted tumor growth arrest into regression. 2 While vitamin B1 (thiamine) alone flattened the tumor growth curve and the combination of B1 and B3 (niacinamide) stopped growth temporarily, adding biotin at a human-equivalent dose of 150–200 milligrams daily caused the tumor to start declining. 3 The mechanism involves biotin's role in providing a bypass for pyruvate when the main gateway enzyme, pyruvate dehydrogenase, is completely blocked by excessive fatty acid oxidation, a state characterized by a low NAD+/NADH ratio. 3 This combination of B1, B3, and B7 ultimately stopped tumor growth completely, achieving what Dinkov termed a dormant remission. 2

Beyond cancer and multiple sclerosis, intracellular biotin deficiency has been implicated in other degenerative conditions. 4 Dinkov has noted that normal blood levels of biotin do not reflect intracellular status, and autopsy studies of Huntington's disease patients confirmed a brain-specific deficiency of both thiamine and biotin, with pharmacological supplementation ameliorating symptoms by improving oxidative metabolism and increasing ATP and CO2 synthesis. 4 He has also pointed out that a biotin deficiency leads to a buildup of unused electrons from food, which can be shunted into lactate production, fat synthesis, or uncontrolled tissue growth. 6 Dietary sources like egg yolks and liver provide adequate biotin for healthy individuals, but the raw egg white protein avidin binds biotin and can induce a deficiency, adding to the reasons Dinkov advises against consuming egg whites without the yolks. 7