Fasting

Fasting is a stress state that accelerates tissue catabolism, and Ray Peat consistently argued against its practice as a health intervention. Peat explained that after glycogen stores are depleted—typically within 24 hours in a healthy person—the body begins breaking down its own tissues to produce glucose, with cortisol rising to mobilize amino acids from muscle and skin. 1 He cited research showing that on a complete water fast, 80% or more of weight loss came from the destruction of muscle and skin, whereas a very low-calorie diet with adequate minerals shifted loss almost entirely to fat. 1 Peat emphasized that the liver’s detoxification capacity is shut down by fasting, as the sulfation and glucuronidation systems are suppressed, causing estrogen to rise. 1

The nightly fast during sleep already imposes a degenerative stress, which Peat viewed as a model for understanding longer fasts. As blood sugar falls overnight, free fatty acids are mobilized, a process that is inefficient, requires more oxygen, and damages mitochondria. 6 Peat noted that bone loss in women occurs primarily at night, with calcium appearing in morning urine, because the body runs out of glycogen and relies on inefficient fat oxidation. 6 He contrasted this with the therapeutic use of sugar in the late 19th century, where feeding diabetics large amounts of sucrose interrupted the destructive process of fat oxidation and supported the regeneration of insulin-producing beta cells, which are killed by free fatty acids. 6

Georgi Dinkov has extended this critique by documenting that intermittent fasting leads to a 2:1 ratio of muscle loss to fat loss, an outcome even prominent fasting advocates have acknowledged as unacceptable. 2 Dinkov also highlighted human studies showing that a 24–48 hour fast inhibits the enzyme 17,21-lyase, decreasing androgen synthesis while increasing aldosterone and showing trends toward elevated cortisol and aromatase activity. 7 He has further argued that the lipolysis triggered by fasting floods cells with free fatty acids that are directly toxic, damaging organs like the kidneys and liver and inhibiting hair follicle growth. 5

Peat acknowledged that the apparent benefits of caloric restriction in animal studies were confounded by the reduction of specific harmful dietary components. He stated that restricting PUFA, cysteine, methionine, tryptophan, and iron—rather than calories themselves—was responsible for increased metabolic rate and decreased oxidative damage. 9 He pointed to later research where animals allowed to eat unlimited fat, protein, and carbohydrate, but with heavy metals kept low, lived longer. 2 Dinkov has proposed that aspirin may function as a caloric restriction mimetic, replicating the anti-inflammatory and autophagy-related benefits of fasting without the risks of muscle catabolism or elevated stress hormones. 8

For those recovering from calorie-restricted or intermittent fasting protocols, Peat advised monitoring temperature and pulse rate as indicators of metabolic recovery, aiming for 37°C and a pulse of 80–85 beats per minute after breakfast. 3 He recommended using small, physiological doses of T3—such as 1–4 micrograms per hour or 10 micrograms with a meal—to rapidly relieve symptoms of metabolic suppression. 3 Peat also noted that providing even small amounts of glucose and minerals like sodium, calcium, magnesium, and potassium during low-calorie periods could greatly reduce tissue loss compared to complete fasting. 1