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Conditions

Menopause

perimenopause, post-menopause

Menopause is not a state of estrogen deficiency caused by the ovaries running out of eggs, but rather a systemic condition driven by progesterone deficiency and unopposed estrogen action. Peat argued that the pharmaceutical industry created and promoted the false definition of…

11 passages
2 authors
1997–2021
Most-cited: Ray Peat

Menopause is not a state of estrogen deficiency caused by the ovaries running out of eggs, but rather a systemic condition driven by progesterone deficiency and unopposed estrogen action. Peat argued that the pharmaceutical industry created and promoted the false definition of menopause as an estrogen deficiency to expand the market for estrogen replacement therapies. In reality, the repeating cycles of ovulation expose the hypothalamus and pituitary gland to cumulative estrogen, which desensitizes and "ages" these regulatory tissues, disrupting normal gonadotropin cycles. The failure to produce progesterone, while estrogen production continues at normal or even elevated levels, results in a great functional excess of estrogen because it is no longer opposed.

The central mechanism of menopause involves the aromatase enzyme, which is present in fat cells, fibroblasts, smooth muscle cells, and virtually all other tissues, and continues to produce estrogen locally throughout the body even after ovarian function ceases. This local production means that while serum estrogen may appear low, the tissue-bound estrogen is actually elevated because, in the absence of progesterone, the enzymes that normally inactivate estrogen for excretion are impaired. Progesterone activates the enzymes that attach a sugar or sulfuric acid molecule to estrogen, making it water-soluble and allowing it to leave the cell for excretion; without this, the active, oil-soluble estrogen accumulates inside cells. Stress, cortisol, and prolactin all increase aromatase activity, while thyroid and progesterone inhibit it, creating a vicious cycle where declining thyroid function and rising stress amplify local estrogen production.

The symptoms and degenerative changes of menopause are driven by this estrogen dominance and the loss of progesterone's protective effects. Progesterone normally protects against cortisol, prolactin, and adrenal androgenic hormones, and its decline leads to increased inflammatory processes, lower body temperature, and a sudden increase in degenerative diseases. The drop in body temperature at menopause occurs because progesterone is thermogenic, and estrogen independently causes vasodilation and increased heat loss. Peat demonstrated that if young ovaries are transplanted into estrogen-exposed old animals, they fail to function, but if ovaries are removed in youth and transplanted into old animals that were spared cumulative estrogen exposure, they function normally, proving that the brain and pituitary, not the ovaries, are the primary site of menopausal change.

Perimenopause is characterized by decreasing progesterone production at a time when estrogen may be at a lifetime high, leading to symptoms such as migraines, weight gain, and premenstrual headaches. The sluggish intestine resulting from declining thyroid function increases endotoxin absorption, which further poisons the ability to burn calories and suppress estrogen. Postmenopausally, the cycling pituitary continues to affect the adrenal glands and other organs, and progesterone remains an important regulator of pituitary and brain function, with protective effects against osteoporosis, hypertension, and hirsutism. Dinkov has emphasized that the postmenopausal state is specifically a deficiency of progesterone with an excess of estrone sulfate, which can easily convert into all other estrogens, and that studies giving postmenopausal women progesterone have shown a reversal of osteoporosis, while estrogen studies have not even stopped bone loss.

The practical approach to menopause involves restoring the balance between estrogen and progesterone by supporting thyroid function, ensuring adequate dietary protein and cholesterol, and using cyclic or continuous progesterone supplementation. Progesterone supplementation, typically 10 to 15 milligrams daily during the second half of the cycle for perimenopausal women, or continuously for postmenopausal women, helps restore normal thyroid function and opposes the unopposed actions of estrogen, cortisol, and prolactin. Even after ovarian removal, the adrenal glands and brain continue to produce progesterone, and maintaining adequate cholesterol levels is essential because cholesterol is the precursor for both progesterone and testosterone. The goal is to prevent the local production of estrogen from getting out of control, as stress activates the aromatase enzyme inside every cell of the body, producing estrogen that will not be measured in the bloodstream but will drive tissue degeneration.

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