Cortisol

Cortisol is a glucocorticoid hormone whose central function, as Ray Peat described it, is to turn protein to sugar under stress, a catabolic process that breaks down muscle, skin, and thymus tissue to provide glucose via gluconeogenesis. 2 Peat argued that while this emergency adaptation is protective in acute crises, its chronic elevation is inseparable from low metabolic rate and a deficiency of the protective steroids pregnenolone, progesterone, and DHEA, which are the main opponents of cortisol. 2 When thyroid function is efficient, cholesterol is converted massively into these stabilizing steroids; without them, the body resorts to cortisol as its next best adaptive procedure, spending the organism rapidly to survive. 2

Peat situated cortisol within Hans Selye's framework, where each steroid has a curve of overlapping functions, and he emphasized that cortisol's anti-inflammatory reputation is merely a side effect of its broader catabolic, anti-anabolic nature. 4 It directly opposes the anabolic and protective effects of androgens like testosterone, which concentrates intensely in the heart and brain to shield vital organs. 2 A large dose of cortisol slumps protective progesterone and testosterone, causing tissues that are not well-protected to shrink rapidly; skin thins, blood vessels weaken, and easy bruising occurs, a process that over years leads to strokes, osteoporosis, and typical aging conditions. 2 Peat noted that cortisol also blocks the liver enzymes that convert thyroxine into the active T3 hormone, further suppressing metabolism. 6

Danny Roddy has summarized that cortisol is released from the adrenal glands to break down protein into amino acids for glucose, and that the liberated amino acids tryptophan, methionine, and cysteine can themselves suppress the metabolic rate. 5 He noted that excess cortisol initially feels good due to its anti-inflammatory and euphoric properties, but overtime causes muscle wasting, immunity depression from thymus destruction, and sexual and mood problems. 5 Georgi Dinkov has extended this by detailing a glucocorticoid rebound effect, where cortisol simultaneously inhibits inflammatory enzymes like cyclooxygenase while up-regulating their genetic expression, so that upon cessation, inflammatory prostaglandin and serotonin production overshoots baseline, making the organism worse than before treatment. 8 Dinkov also highlighted that serotonin is the most potent central controller of cortisol production via the 5-HT2C receptor, meaning that elevated serotonin directly stimulates cortisol synthesis and release. 9

Peat identified that practically everything harmful—including estrogen, which he called a shock hormone—increases both estrogen and cortisol, while the first barrier to harm is the group of steroids: pregnenolone, progesterone, DHEA, and testosterone. 1 He recommended supporting oxidative metabolism and thyroid function so that cholesterol can be converted into these protective hormones, along with adequate protein, Vitamin A, and Vitamin D to block and reverse cortisol's effects. 3 Dinkov has warned that stressing the organism to lose weight through fasting or excessive exercise up-regulates cortisol synthesis peripherally, creating a machinery that produces even more cortisol, which is itself obesogenic, blocking the insulin receptor and increasing fatty acid synthase activity. 7 Roddy notes that simple interventions like eating enough carbohydrate and salt can help get a hold of cortisol. 10