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Hormones

Estrogen

If we named hormones according to their place of origin, as Selye suggested, we could call estrogen folliculin (as Selye did because it is produced abundantly in the ovarian follicle), or adipin, because it is sometimes produced in fat cells. But it can be produced by many…

12 passages
3 authors
1997–2021
Most-cited: Ray Peat

Estrogen is a hormone whose central biological action, according to Ray Peat, is the interference with oxidative metabolism, reducing cellular energy to turn on a primitive type of growth. Peat argued that estrogen's effect mimics the shock phase of the stress reaction, acting to decrease tissue oxygenation and shift cells toward a more primitive, water-logged state conducive to division. He emphasized that estrogen is not simply "the female hormone," as it is produced in both sexes, can be synthesized in fat cells and the testicles, and its excess can even produce hirsutism and other masculine traits by overstimulating the adrenal glands. Georgi Dinkov has extended this view, describing estrogen as a signal of environmental distress—starvation, stress, or cold—that turns on metabolic switches associated with disease, including the inhibition of glucose oxidation and the stimulation of fat synthesis.

The hormone's mechanism is rooted in a profound disruption of cellular energetics and structure. Peat proposed that estrogen's biological effects result from its direct action on cell water, causing it to become more like bulk, high-dielectric water, a state associated with fatigue and aging. This hydration shift is linked to the uptake of water and loss of potassium, which Peat considered the simplest reaction a cell is capable of, underlying the coherent activation of processes from chromosomes to the cytoskeleton. Estrogen steals oxygen from mitochondria, promoting lactic acid formation and a shift toward inefficient glycolysis, while also stimulating the synthesis of porphyrins and the enzyme heme oxygenase, which generates carbon monoxide. This metabolic pattern, characterized by increased lactate and ammonia, is analogous to tumor metabolism and is opposed by thyroid hormone, which promotes oxygen delivery and cellular energy.

Peat consistently framed estrogen as a central mediator of degeneration and disease, directly contradicting claims of its protective effects. He noted that estrogen structurally weakens joint tissues, aggravating osteoarthritis, and that it retards bone growth rather than preventing osteoporosis, with young women having thinner bones than men due to estrogen's early inhibition of bone formation. In the cardiovascular system, estrogen increases the tendency for blood clot formation and vascular spasms, and the famous Framingham study found its use increased heart attacks by 50% and strokes by 100%. Peat argued that the belief in estrogen's heart protection is based on the isolated, out-of-context observation that it raises the HDL/LDL ratio, a change also associated with a higher incidence of cancer. He further identified estrogen as deeply involved in carcinogenesis, not primarily through direct DNA damage, but by disrupting the mitotic apparatus and causing defective cell division, while simultaneously protecting aberrant cells through the antioxidant functions of carbon dioxide and biliverdin.

The activity and toxicity of estrogen are amplified by dietary context and opposed by a network of protective substances. Peat highlighted that the accumulation of polyunsaturated fatty acids in tissues promotes estrogen's action in a cumulative, self-accelerating manner. The body possesses multiple antiestrogenic systems, including thyroid, progesterone, testosterone, and various detoxification pathways like sulfation and glucuronidation. Danny Roddy has synthesized this by noting that progesterone supports oxidative energy and opposes all of estrogen's effects, while estrogen has an inverse relationship with this "real" feminizing hormone, and is itself increased by stress, low thyroid, and inflammation. Peat maintained that the varied, specific outcomes of estrogenic stimulation—whether feminization or masculinization, growth or tumefaction—are determined not by estrogen itself, but by the organism's resources and the effectiveness of these defensive, neutralizing systems.

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