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<h1>Menopause and its causes</h1>
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<a href="/"><img class="epic" src="/icons/chads/chad.png"></a>
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<p class="nav"><span class="nav-left">Listed under <a href="/ray-peat.html">Ray Peat</a>.</span><span class="nav-right"><a href="/theme.html">Theme</a></span></p>
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<p>From the <a href="https://raypeat.com/articles/articles/menopause.shtml" target="_blank">original article</a> in 2006. Author: <a href="https://raypeat.com/" target="_blank">Ray Peat</a>.</p>
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<p>When
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I was in graduate school at the University of Oregon, everyone in our
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lab was working on the problem of reproductive aging. Previously,
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people in the lab had established that the ovaries didn't "run
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out of eggs." There was never really any basis for that ridiculous
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belief. Many people just said it, the way they said "old
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eggs" (but never old sperms) were responsible for birth defects,
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or that "estrogen is the female hormone," a deficiency of
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which is the cause of menopausal infertility. (Old sperms have
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been implicated in some birth defects<strong>. </strong>
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People who are newly married, for example, were found to have children
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with fewer birth defects than people of the same age who had been married
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a long time, suggesting that more frequent intercourse involves fresher
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sperms.) When ovaries have been treated with x-rays to destroy
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their ability to ovulate, they have been found to produce more estrogen
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than before. Ovulation is one thing, and the production of hormones
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is another thing. You can't determine whether ovulation has occurred
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by measuring the hormones.</p>
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<p>Knowing
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the large amount of work that has gone into our understanding of the
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age-related decline in fertility, it is disturbing to see people on
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television and in popular health books saying that menopause occurs
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when the "ovaries run out of eggs."</p>
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<p>Around
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1970, many people were saying that aging was caused by the loss of brain
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cells. There is a glimmer of truth in that silly idea, just as
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there would be in saying that "aging is caused by the death of
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skin cells," making the skin thinner and drier and less elastic.
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Both the brain and the skin are sources of steroid hormones, and it
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is possible that the death of skin cells and neurons is one factor in
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the age-related decline in the "sex steroids." An organism
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would be an easier thing to understand if cells just did their job for
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a certain period of time, and then died. A man named Hayflick
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has given people some publications to cite, when they want to simplify
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things by saying that aging occurs when cells have used up their quota
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of 50 divisions, but there are many more studies that clearly show that
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Hayflick's limit is nothing but a product of the cells' environment.
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The cell's environment, the signals and substances and energy it receives,
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is complex, but real progress is being made in understanding the things
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involved in the aging process. Luckily, the infinite complexity
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of the environment is channeled into an understandable array of processes
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by the cell's systematic ways of responding.</p>
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<p>I
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knew, from talking with L. C. Strong,1 that early reproductive maturity
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was associated with early death; in his strains of cancer-prone mice,
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he showed that high estrogen was the cause of early puberty, a high
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cancer incidence, and a relatively short life. D. A. Snowdon,
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et al., showed that the occurrence of menopause at an early age in women
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is associated with a greater risk of death from all causes, including
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strokes and coronary heart disease.2 (They saw ovarian aging as
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an indicator of general aging.) P. W. F. Wilson, et al., reported
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that postmenopausal estrogen use was associated with an increased incidence
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of heart disease and stroke.3 P. M. Wise showed that estrogen
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accelerates aging of the central nervous system, destroying the nerves
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which regulate the pituitary gonadotropins, and causing ovarian failure
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and infertility.4 Many other studies of particular tissues show
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that estrogen accelerates the rate of aging. </p>
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<p>In
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my work with hamsters, I found that the infertility that developed at
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middle age was caused by a high rate of oxygen consumption in the uterus,
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causing the oxygen needed by the developing embryo to be consumed by
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uterine tissues, and causing suffocation of the embryo. This is
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the central mechanism by which the estrogen-containing contraceptives
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work<strong>:</strong> at any stage of pregnancy, a sufficient dose of estrogen
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kills the embryo.</p>
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<p>Polvani
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and Nencioni,5 among others, found that in women, the onset of menopause
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(the first missed period, suddenly increased bone loss, nervous symptoms
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such as depression, insomnia, and flushing) corresponds to the failure
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to produce progesterone, while estrogen is produced at normal levels.
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This results in a great functional excess of estrogen, because it is
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no longer opposed by progesterone. Typically, it takes about four
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years for the monthly estrogen excess to disappear. They suggested
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that the bone loss sets in immediately when progesterone fails because
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cortisol then is able to dominate, causing bone catabolism; progesterone
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normally protects against cortisol. Other researchers have pointed
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out that estrogen dominance promotes mitosis of the prolactin-secreting
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cells of the pituitary, and that prolactin causes osteoporosis; by age
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50, most people have some degree of tumefaction of the prolactin-secreting
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part of the pituitary. But estrogen dominance (or progesterone
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deficiency) also clearly obstructs thyroid secretion, and thyroid governs
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the rate of bone metabolism and repair. Correcting the thyroid
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and progesterone should take care of the cortisol/prolactin/osteo- porosis
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problem.</p>
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<p>P.
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M. Wise4 has demonstrated that the "menopausal" pituitary
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hormones, high levels of LH and FSH, are produced because the regulatory
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nerves in the hypothalamus have lost their sensitivity to estrogen,
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not because estrogen is deficient. In fact, he showed that the
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nerves are desensitized precisely by their cumulative exposure to estrogen.
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If an animal's ovaries are removed when it is young, the regulatory
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nerves do not atrophy, and if ovaries are transplanted into these animals
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at the normally infertile age, they are fertile. But if animals
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are given larger doses of estrogen during youth, those nerves atrophy
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prematurely, and they become prematurely infertile.</p>
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<p>The
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mechanism by which estrogen desensitizes and kills brain cells is now
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recognized as the "excitotoxic" process, in which the excitatory
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transmitter glutamic acid is allowed to exhaust the nerve cells.
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(This explains the older observations that glutamic acid, or aspartic
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acid, or aspartame, can cause brain damage and reproductive failure.)
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Cortisol also activates the excitotoxic system, in other brain cells,
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causing stress-induced atrophy of those cells.6 Progesterone and
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pregnenolone are recognized as inhibitors of this excitotoxic process. </p>
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<p>Besides
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estrogen's promotion of excitotoxic cell death, leading to the failure
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of the gonadotropin regulatory system, estrogen's stress-mimicking action
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probably tends to increase the secretion of LH, in ways that can be
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corrected by supplementing progesterone and thyroid. Since Selye's
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work, it has been known that estrogen creates the same conditions as
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occur in the shock phase of the stress reaction. (And shock, in
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a potential vicious circle, can increase the level of estrogen.7)
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It has recently been demonstrated that estrogen stimulates the adrenal
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glands, independently of the pituitary's ACTH. This can increase
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the production of adrenal androgens, leading to hirsutism, and other
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male traits, including anabolic effects.8</p>
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<p>It
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was established in the 1950s that estrogen "erases" memories
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in well trained animals. I suppose that acute effect is related
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to the chronic toxicity that leads to cell death. (In the 1940s,
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DES was sold to prevent miscarriages, though it was already known that
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it caused them<strong>;</strong> then there was the argument that it slowed aging
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of the skin, despite the Revlon studies at the University of Pennsylvania
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showing that it accelerates all aspects of skin aging<strong>;</strong> lately
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there has been talk of promoting estrogen to improve memory<strong>.</strong>)</p>
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<p>Estrogen's
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nerve-exciting action is known to lower seizure thresholds<strong>;</strong> premenstrual
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epilepsy is probably another acute sign of the neurotoxicity of estrogen.</p>
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<p>When
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fatigue and lethargy are associated with aging, the brain stimulating
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action of estrogen can make a woman feel that she has more energy<strong>.</strong>
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(Large doses given to rats will make them run compulsively<strong>;</strong> running
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wheels with odometers have shown that they will run over 30 miles a
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day from the influence of estrogen.) Estrogen inhibits one of
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the enzymic routes for inactivating brain amines, and so it has more
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general effects on the brain than just the glutamate system. This
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generalized effect on brain amines is more like the effects of cocaine
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or amphetamine. If that is a woman's basis for wanting to use
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estrogen, a monoamine oxidase inhibitor would be safer.</p>
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<p>The
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reason for the menopausal progesterone deficiency is a complex of stress-related
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causes. Free-radicals (for example, from iron in the corpus luteum)
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interfere with progesterone synthesis, as do prolactin, ACTH, estrogen,
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cortisol, carotene, and an imbalance of gonadotropins. A deficiency
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of thyroid, vitamin A, and LDL-cholesterol can also prevent the synthesis
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of progesterone. Several of the things which cause early puberty
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and high estrogen, also tend to work against progesterone synthesis.
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The effect of an intra-uterine irritant is to signal the ovary to suppress
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progesterone production, to prevent pregnancy while there is a problem
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in the uterus. The logic by which ACTH suppresses progesterone
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synthesis is similar, to prevent pregnancy during stress. Since progesterone
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and pregnenolone protect brain cells against the excitotoxins, anything
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that chronically lowers the body's progesterone level tends to accelerate
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the estrogen-induced excitotoxic death of brain cells. </p>
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<p>Since progesterone
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and pregnenolone protect brain cells against the excitotoxins, anything
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that chronically lowers the body's progesterone level tends to accelerate
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the estrogen-induced excitotoxic death of brain cells. </p>
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<p>Chronic constipation,
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and anxiety which decreases blood circulation in the intestine, can
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increase the liver's exposure to endotoxin. Endotoxin (like intense
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physical activity) causes the estrogen concentration of the blood to
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rise. Diets that speed intestinal peristalsis might be expected
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to postpone menopause. Penicillin treatment, probably by lowering
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endotoxin production, is known to decrease estrogen and cortisone, while
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increasing progesterone. The same effect can be achieved by eating
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raw carrots (especially with coconut oil/olive oil dressing) every day,
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to reduce the amount of bacterial toxins absorbed, and to help in the
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excretion of estrogen. Finally, long hours of daylight are known to increase
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progesterone production, and long hours of darkness are stressful.
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Annually, our total hours of day and night are the same regardless of
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latitude, but different ways of living, levels of artificial illumination,
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etc., have a strong influence on our hormones. In some animal
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experiments, prolonged exposure to light has delayed some aspects of
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aging.</p>
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<p>General
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aging contributes to the specific changes that lead to menopause, but
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the animal experiments show that fertility can be prolonged to a much
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greater age by preventing excitotoxic exhaustion of the hypothalamic
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nerves. The question that still needs to be more clearly answered
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is, to what extent can general aging be prevented or delayed by protecting
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against the excitotoxins? Minimizing estrogen (and cortisone)
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with optimal thyroid activity, and maximizing pregnenolone and
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progesterone to prevent excitotoxic cell fatigue, can be done easily.
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A diet low in iron and unsaturated fats protects the respiratory apparatus
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from the damaging effects of excessive excitation, and--since pregnenolone
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is formed in the mitochondrion--also helps to prevent the loss of these
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hormones. </p>
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<h2>References</h2>
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<small>
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<p>1. L. C.
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Strong, Biological Aspects of Cancer and Aging, Pergamon Press, 1968.</p>
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<p>2. D. A.
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Snowdon, et al., "Is early natural menopause a biologic marker
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of health and aging? Am. J. Public Health 79, 709-714, 1989.
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</p>
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<p>3. P. W.
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F. Wilson, et al. [The Framingham Study], N. E. J. M. 313(17), 1038-1043,
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1985 </p>
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<p>4. P. M.
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Wise, "Influence of estrogen on aging of the central nervous system:
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Its role in declining female reproductive function," in Menopause:
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Evaluation, Treatment, and Health Concerns, pages 53-70, 1989.
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</p>
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<p>5. Nencioni, T.,
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and F. Polvani, Calcitonin, p. 297-305, A. Pecile, editor, Elsevier,
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N.Y., 1985.</p>
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<p> </p>
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<p>6. T. I. Belova,
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"Structural damage to the mesencephalic reticular formation induced
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by immobilization stress," Bull. Exp. Biol. & Med. 108(7),
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126030, 1989. </p>
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<p>7. F. Fourrier,
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et al., "Sex steroid hormones in circulatory shock, sepsis syndrome,
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and septic shock," Circ. Shock 43(4), 171-178, 1994.
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</p>
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<p>8. E. C. Ditkoff,
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et al., "The impact of estrogen on adrenal androgen sensitivity
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and secretion in polycystic ovary syndrome," J. Clin. Endocrinol.
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Metab. 80(2), 603-607, 1995. </p>
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<p>9. C. Bain,
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et al., "Use of postmenopausal hormones and risk of myocardial
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infarction," Circulation 64, 42-46, 1981. </p>
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<p>10. T. L.
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Bush, et al., "Estrogen use and all-cause mortality: Preliminary
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results from the Lipid Research Clinics Program follow-up study,"
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JAMA 249, 903-906, 1983.</p>
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<p>11. M.
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S. Hunter and K. L. M. Liao, "Intentions to use hormone replacement
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therapy in a community sample of 45-year-old women," Maturitas
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20(1), 13-23, 1994. (Women who expressed an intention to use hormone
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replacement therapy at menopause reported significantly lower self-esteem,
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more depressed mood, anxiety, and negative attitudes toward menopause.
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The also expressed stronger beliefs in their doctors' ability--as opposed
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to their own--to control their menopause experience.)</p>
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<p>12. L.
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Dennerstein, et al., "Psychological well-being, mid-life and the
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menopause," Maturitas 20(1), 1-11, 1994. </p>
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