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