Prolactin

Prolactin is a pituitary hormone that Ray Peat identified as a fundamental stress hormone, rising not only during pregnancy and lactation but also in response to aging, estrogen, serotonin, and endotoxin. 3 Peat argued that prolactin is a potent metabolic inhibitor, suppressing mitochondrial function, decreasing oxidative metabolism, and interfering with thyroid hormone action while promoting glycolysis and lactate production. 2 He traced its pathological effects across multiple tissues, noting that it mobilizes calcium from bones, inhibits progesterone formation, and acts on secretory membranes in the kidney, gut, and skin. 2 Dinkov has extended this by emphasizing that prolactin serves as the best blood surrogate for tissue estrogenic activity and serotonin, with a correlation coefficient over 0.9, making it a far more reliable marker of stress than direct steroid measurements. 11

The relationship between prolactin and thyroid function is central to Peat's framework. Prolactin and TSH tend to increase together, and Peat observed that prolactin directly decreases thyroid gland activity. 2 He considered mild hypothyroidism the likely underlying cause of elevated prolactin, recommending thyroid supplementation, salt, and even small amounts of vitamin B6 (around 10 mg daily) to lower it. 2 This bioenergetic perspective reframes prolactin not as an isolated reproductive hormone but as an indicator of systemic energy failure. Dinkov has noted that prolactin is chronically elevated in virtually all chronic diseases and that levels considered "normal" by contemporary lab ranges—recently raised to an upper limit of 22 ng/mL for males—are far above the historical healthy mean of around 5 ng/mL. 3

Peat documented a direct causal chain linking estrogen to prolactin-driven tissue destruction. He highlighted the epidemic of pituitary tumors requiring surgery that followed the introduction of the birth control pill, a 300-fold increase in prolactin surgeries driven by estrogen's stimulatory effect on prolactin secretion. 5 He also criticized the widespread use of estrogen to prevent osteoporosis, pointing out that estrogen increases prolactin, which in turn mobilizes calcium from bone and contributes to the very bone loss it was meant to treat. 2 The same pathway explains why SSRI antidepressants, which increase serotonin and consequently prolactin, were found to cause osteoporosis with prolonged use. 3 Serotonin produced in the intestine was later discovered to be a basic cause of bone loss, connecting intestinal health directly to prolactin-mediated pathology. 3

In the context of hair loss, Peat rejected the dihydrotestosterone (DHT) hypothesis as biologically absurd, noting that young males with the highest androgen levels have the lowest rates of baldness. 7 He instead framed balding as a bioenergetic problem driven by prolactin, which he described as a "molting" hormone in insects analogous to hair shedding in humans. 7 Roddy has elaborated that prolactin terminates the anagen (growth) phase of the hair follicle, shifting it into catagen and telogen, and that it activates the enzyme liberating arachidonic acid for inflammatory prostaglandin production. 2 Dinkov has pointed to the development of prolactin receptor antagonists like ABS-201, which completely reversed balding and even graying in macaques, as direct validation of Peat's view. 7 Roddy characterizes the balding individual as perpetually experiencing a winter metabolism marked by higher prolactin, cortisol, estrogen, and histamine, with thyroid hormone serving as the master regulator that, through carbon dioxide production, inhibits excess prolactin and parathyroid hormone. 9