Endometriosis

Endometriosis is fundamentally a condition driven by unopposed estrogen acting on tissues that have shifted into a primitive, inflammatory metabolic state. 2 Ray Peat argued that the disease is not merely a matter of excess circulating estrogen, but of local estrogen production within the lesions themselves. The abnormal endometrial cells express the enzyme aromatase, which manufactures estrogen, creating a self-perpetuating cycle where the estrogen then activates cyclooxygenase to turn polyunsaturated fatty acids into inflammatory prostaglandins, which in turn stimulate more aromatase activity. 1 This vicious cycle is normally prevented by the surge of progesterone after ovulation, which should cause the cells to stop producing estrogen, but in endometriosis this protective interruption fails. 2

The metabolic underpinning of this process is a shift away from oxidative metabolism toward a reductive, glycolytic state characterized by the production of lactic acid. 2 Peat cited research showing that unopposed estrogen causes lactate to appear in the uterine lining, and that this dedifferentiated, stem-like cellular environment, stabilized by a reducing redox balance, is essential for the abnormal cell division and inflammation seen in the disease. 2 The structural proteins that form the mitotic apparatus are stabilized by this reducing environment, and the activated cells transmit their regressed metabolic state to neighboring cells via lactate secretion. 2 This connects the local hormonal disruption directly to a failure of cellular respiration, where pyruvic acid is reduced to lactic acid instead of being oxidized by oxygen. 2

Peat identified hypothyroidism as the basic systemic problem enabling this process, describing a vicious circle where low thyroid function permits estrogen to rise, and the elevated estrogen then further blocks thyroid action, particularly by interfering with the liver's conversion of T4 to the active T3 hormone. 3 He reported that correcting hypothyroidism with proper thyroid supplementation could turn off endometriosis symptoms immediately, sometimes within two to three days. 2 The liver's role is also compromised, as the estrogen-thyroid disruption and constant growth hormone stimulation effectively feminize the liver, impairing its ability to detoxify estrogen. 2 Peat noted that simply reducing estrogen exposure can alleviate symptoms, and that a diet providing adequate protein, sugar, trace minerals, and vitamins supports the physiological resolution of the cycle. 1

Therapeutic intervention, in Peat's framework, centers on breaking the estrogen-prostaglandin-aromatase loop. He recommended aspirin or other prostaglandin blockers to reduce the formation of estrogen and inflammation, noting that aspirin alone can greatly reduce symptoms. 1 Because polyunsaturated fats are the essential substrate for the cyclooxygenase enzyme that produces inflammatory prostaglandins, eliminating them from the diet is central to treatment; even stored polyunsaturated fats released from tissues under stress can feed the cycle. 2 Peat advised that sugar and niacinamide can limit the release of these fatty acids into the bloodstream, backing up the function of aspirin. 7 Georgi Dinkov has extended this understanding by noting that a compromised gut barrier and translocating bacteria, leading to endotoxin-driven chronic inflammation, may be an additional contributing factor, as the body forms fibrotic tissue to encapsulate the bacteria, a pattern also observed in rheumatoid arthritis and lupus. 2