Diabetes

Diabetes, in the framework advanced by Ray Peat, is not a primary disease of sugar excess but a disorder of fatty acid oxidation that blocks the cellular use of glucose. 3 Peat argued that the medical concept of diabetes as a "sugar disease" has persisted for centuries despite evidence that restricting sugar often accelerated death in the original wasting form of the illness. 1 He maintained that the modern diagnosis of type 2 diabetes, which accounts for the vast majority of cases, is a medical invention to sell products and services, as it is defined simply by high blood sugar without investigating the underlying endocrine disruption. 2

The core mechanism, according to Peat, involves the Randle cycle, where elevated free fatty acids in the blood directly suppress mitochondrial respiration and block the ability of cells to oxidize glucose. 2 This creates a state where sugar accumulates in the bloodstream not because it was consumed in excess, but because it cannot be metabolized. Peat identified polyunsaturated fatty acids (PUFAs) from vegetable oils as the primary dietary driver of this process, noting that populations free of these oils are resistant to diabetes, and animals deficient in them cannot be experimentally poisoned into a diabetic state. 2 Georgi Dinkov has extended this by explaining that in type 2 diabetes, cells are already "clogged" with fat, so any ingested sugar simply circulates, raising blood glucose and spilling into urine. 8

Peat stressed that insulin is only a minor part of a complex regulatory system involving the pituitary, thyroid, and adrenal glands. 2 He argued that chronically high blood sugar is often driven by elevated cortisol, which itself is frequently a consequence of hypothyroidism. 2 A lack of thyroid hormone prevents the efficient oxidation of glucose, triggering a stress state that releases free fatty acids and further impairs sugar metabolism. 2 Therefore, Peat's therapeutic approach centered on identifying the hormonal cause of the high blood sugar, recommending tests for cortisol, free fatty acids, and lactic acid, and using interventions like thyroid optimization, aspirin, and vitamin D with calcium to restore mitochondrial respiration and lower stress. 3

The destruction of pancreatic beta cells, which defines type 1 diabetes, is also driven by oxidative damage from circulating PUFAs, while glucose actually supports the regeneration of these cells. 3 Peat illustrated this principle with the case of his father, who recovered from a severe wasting diabetic state by consuming only brewer's yeast for several weeks, a food rich in B vitamins and other factors that likely interfered with stress hormones. 5 He also noted that the apparent heritability of diabetes is often an epigenetic effect of the maternal intrauterine environment and nutrition, rather than a fixed genetic destiny, as the metabolic state of a starved or poorly nourished mother can program a "thrifty" phenotype in the fetus that persists for generations. 9