461 lines
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461 lines
34 KiB
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<html>
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<head><title>Estriol, DES, DDT, etc.</title></head>
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<body>
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<h1>
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Estriol, DES, DDT, etc.
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</h1>
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<article class="posted">
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<p>
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A review of the use of estrogens reported in J.A.M.A. (only up to 1987) found nearly 200 different
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"indications" for its use. (Palmlund, 1996.) Using the conservative language of that journal, such use
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could be said to constitute wildly irresponsible "empirical" medical practice. More appropriate language
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could be used.
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</p>
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<p>
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Pollution of the environment and food supply by estrogenic chemicals is getting increased attention.
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Early in the study of estrogens, it was noticed that soot, containing polycyclic aromatic hydrocarbons,
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was both estrogenic and carcinogenic. Since then, it has been found that phenolics and chlorinated
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hydrocarbons are significantly estrogenic, and that many estrogenic herbicides, pesticides, and
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industrial by-products persist in the environment, causing infertility, deformed reproductive organs,
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tumors, and other biological defects, including immunodeficiency. In the Columbia River, a recent study
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found that about 25% of the otters and muskrats were anatomically deformed.
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</p>
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<p>
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Estrogenic pollution kills birds, panthers, alligators, old men, young women, fish, seals, babies, and
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ecosystems. Some of these chemicals are sprayed on forests by the US Department of Agriculture, where
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they enter lakes, underwater aquifers, rivers, and oceans. Private businesses spray them on farms and
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orchards, or put them into the air as smoke or vapors, or dump them directly into rivers. Homeowners put
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them on their lawns and gardens.
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</p>
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<p>
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Natural estrogens, from human urine, enter the rivers from sewage. Many tons of synthetic and
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pharmaceutical estrogens, administered to menopausal women in quantities much larger than their bodies
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ever produced metabolically, are being added to the rivers.
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</p>
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<p>
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In the same way that weak estrogens in the environment may become hundreds of times more estrogenic by
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synergistic interactions (J. A. McLachlan, et al., <em>Science,</em> June 7, 1996), combinations of
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natural, medical, dietary, and environmental estrogens are almost certain to have unexpected results.
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The concept of a "protective estrogen" is very similar to the idea of "protective mutagens" or
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"protective carcinogens," though <em>in the case of estrogens, their promoters don't even know what the
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normal, natural functions of estrogen are.
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</em>
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</p>
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<p>
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In November, 1995, an international conference was held to study the problem of "Environmental
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endocrine-disrupting chemicals," and to devise strategies for increasing public awareness of the
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seriousness of the problem. Their "Statement from the work session" says "New evidence is especially
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worrisome because it underscores the exquisite sensitivity of the developing nervous system to chemical
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perturbations that result in functional abnormalities." "This work session was convened because of the
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growing concern that failure to confront the problem could have major economic and societal
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implications." <strong>"We are certain of the following: Endocrine-disrupting chemicals can undermine
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neurological and behavioral development and subsequent potential of individuals...."</strong>
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"Because the endocrine system is sensitive to perturbation, it is a likely target for disturbance."
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"Man-made endocrine-disrupting chemicals range across all continents and oceans. They are found in
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native populations from the Arctic to the tropics, and, because of their persistence in the body, can be
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passed from generation to generation." <strong>"...many endocrine-disrupting contaminants, even if less
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potent than the natural products, are present in living tissue at concentrations millions of times
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higher than the natural hormones."</strong> "The developing brain exhibits specific and often narrow
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windows during which exposure to endocrine disruptors can produce permanent changes in its structure and
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function."
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</p>
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<p>
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In spite of this increased exposure to estrogens, there is a new wave of advertising of estrogenic
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substances, based on the idea that weak estrogens will provide protection against strong estrogens. The
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environmental background of estrogenic pollution already provides a continuous estrogenic exposure. In
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the 1940s, Alexander Lipshuts demonstrated that a continuous, weak estrogenic stimulus was immensely
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effective in producing, first fibromas, then cancer, in one organ after another, and the effect was not
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limited to the reproductive system. How is it possible that the idea of "protection" from a weak
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estrogen seems convincing to so many? Isn't this the same process that we saw when the nuclear industry
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promoted Luckey's doctrine of "radiation hormesis," literally the claim that "a little radiation is
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positively good for us"?
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</p>
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<p>
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DES (diethyl stilbestrol) is one of the most notorious estrogens, because studies in humans revealed
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that its use during pregnancy not only caused cancer, miscarriages, blood clots, etc., in the women who
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used it, but also caused cancer, infertility, and deformities in their children, and even in their
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grandchildren. (But those transgenerational effects are not unique to it.)
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</p>
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<p>
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Besides the absurd use of DES to prevent miscarriages, around 1950 it was also used to treat
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vulvovaginitis in little girls, for menstrual irregularity at puberty, to treat sterility, dysfunctional
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bleeding, endometriosis, amenorrhea, oligomenorrhea, dysmenorrhea, migraine headaches, nausea and
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vomiting, and painful breast engorgement or severe bleeding after childbirth.
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</p>
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<p>
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DES is a "weak" estrogen, in the sense that it doesn't compete with natural estrogens for the "estrogen
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receptors." (Estriol binds more strongly to receptors than DES does: "Cytosolic and nuclear estrogen
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receptors in the genital tract of the rhesus monkey," J. Steroid Bioch. 8(2), 151-155, 1977.) Pills
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formerly contained from 5 to 250 mg. of DES. The 1984 <em>PDR</em> lists doses for hypogonadism and
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ovarian failure as 0.2 to 0.5 mg. daily. In general, dosage of estrogens decreased by a factor of 100
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after the 1960s.
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</p>
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<p>
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An aggressively stupid editorial by Alvin H. Follingstad, from the Jan. 2, 1978, issue of JAMA, pages
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29-30, "Estriol, the forgotten estrogen?" is being circulated to promote the use of estriol, or the
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phytoestrogens. It argues that women who secrete larger amounts of estriol are resistant to cancer.
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</p>
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<p>By some tests, estriol is a "weak estrogen," by others it is a powerful estrogen.</p>
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<p>
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When estriol was placed in the uterus of a rabbit, only 1.25 mcg. was sufficient to prevent implantation
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and destroy the blastocyst. (Dmowski, et al., 1977.) Since the effect was local, the body weight of the
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animal doesn't make much difference, when thinking about the probable effect of a similar local
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contentration of the hormone on human tissues. The anti-progestational activity of estriol and estradiol
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are approximately the same. (Tamotsu and Pincus, 1958.)
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</p>
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<p>
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When 5 mg. of estriol was given to women intravaginally, this very large dose suppressed LH within 2
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hours, and suppressed FSH in 5 hours. Given orally, 8 mg. had similar effects on LH and FSH after 30
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days, and also had an estrogenic effect on the vaginal epithelium.. These quick systemic effects of a
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"weak estrogen" are essentially those of a strong estrogen, except for the size of the dose. (Schiff, et
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al., 1978.)
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</p>
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<p>When administered subcutaneously, estriol induced abortions and stillbirths (Velardo, et al.)</p>
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<p>
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Another indication of the strength of an estrogen is its ability to cause the uterus to enlarge. Estriol
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is slightly weaker, in terms of milligrams required to cause a certain rate of uterine enlargement, than
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estradiol. (Clark, et al., 1979.) But isn't the important question whether or not the weak estrogen
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imitates all of the effects of estradiol, including carcinogenesis and blood clotting, in addition to
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any special harmful effects it might have?
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</p>
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<p>
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When added to long-term culture of human breast cancer cells, estriol stimulated their growth, and
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overcame the antiestrogenic effects of tamoxifen, even at concentrations hundreds of times lower than
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that of tamoxifen. "The data do not support an antiestrogenic role for estriol in human breast cancer."
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(Lippman, et al., 1977.)
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</p>
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<p>
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Studies of the urinary output of estriol/estradiol in women with or without breast cancer do not
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reliably show the claimed association between low estriol/estradiol and cancer, and the stimulating
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effect of estriol on the growth of cancer cells suggests that any alteration of the estrogen ratio is
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likely to be a <em>consequence</em> of the disease, rather than a cause. The conversion of estradiol to
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other estrogens occurs mainly in the liver, in the non-pregnant woman, as does the further metabolism of
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the estrogens into glucuronides and sulfates. The hormonal conditions leading to and associated with
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breast cancer all affect the liver and its metabolic systems. The hydroxylating enzymes are also
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affected by toxins. Hypothyroidism (low T3), low progesterone, pregnenolone, DHEA, etiocholanolone, and
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high prolactin, growth hormone, and cortisol are associated with the chronic high estrogen and breast
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cancer physiologies, and modify the liver's regulatory ability.
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</p>
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<p>
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The decreased output of hormones when the fetal-placental system is dying is a natural consequence,
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since the placenta produces hormones, and during pregnancy converts estradiol to estriol. Since
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estradiol in excess kills the fetus, its conversion by the placenta to estriol is in accord with the
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evidence showing that estriol is the more quickly excreted form. (G. S. Rao, 1973.) The conversion of
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16-hydroxy androstenedione and 16-hydroxy-DHEA into estriol by the placenta (Vega Ramos, 1973) would
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also cause fetal exhaustion or death to result in lower estriol production. But a recent observation
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that a surge of estriol production precedes the onset of labor, and that its premature occurrence can
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identify women at risk of premature delivery (McGregor, et al., 1995) suggests that the estriol surge
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might reflect the mother's increased production of adrenal androgens during stress. (This would be
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analogous to the situation in the polycystic ovary syndrome, in which excessive estradiol drives the
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adrenals to produce androgens.)
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</p>
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<p>
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Estetrol, which has one more hydroxyl group than estriol, is a "more sensitive and reliable indicator of
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fetal morbidity than estriol during toxemic pregnancies," because it starts to decrease earlier, or
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decreases more, than estriol. (Kundu, et al., 1978.) This seems to make it even clearer that the decline
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of estriol is a consequence, not a cause, of fetal sickness or death.
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</p>
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<p>
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A 1994 publication (B. Zumoff, "Hormonal profiles in women with breast cancer," <em>Obstet. Gynecol.
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Clin. North. Am. (U.S.) 21(4),</em> 751-772) reported that there are four hormonal features in women
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with breast cancer<strong>:</strong> diminished androgen production, luteal inadequacy, increased
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16-hydroxylation of estradiol, and increased prolactin. The 16-hydroxylation converts estradiol into
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estriol.
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</p>
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<p>
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A new technique for radiographically locating a hormone-dependent breast cancer is based on the fact
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that estriol-sulfate is a major metabolite of estradiol. The technique showed the tumor to have about a
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six times higher concentration of estriol-sulfate than liver or muscle. (N. Shimura, et al., "Specific
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imaging of hormone-dependent mammary carcinoma in nude mice with [131I]-anti-estriol 3-sulfate
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antibody," <em>Nucl. Med. Biol. (England) 22(5),</em> 547-553, 1995.)
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</p>
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<p>
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Another association of elevated conversion of estradiol to estriol with disease was found to occur in
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men who had a myocardial infarction, compared to controls who hadn't. (W. S. Bauld, et al., 1957.)
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</p>
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<p>
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The estrogens in clover have been known for several decades to have a contraceptive action in sheep, and
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other phytoestrogens are known to cause deformities in the genitals, feminization of men, and anatomical
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changes in the brain as well as functional masculinization of the female brain. (Register, et al., 1995;
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Levy, et al, 1995; Clarkson, et al., 1995; Gavaler, et al., 1995.) The effects of the phytoestrogens are
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very complex, because they modify the sensitivity of cells to natural estrogens, and also modify the
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metabolism of estrogens, with the result that the effects on a given tissue can be either pro-estrogenic
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and anti-estrogenic. For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an
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antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased
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bioavailability of both estrone and estradiol. (W. Schubert, et al., "Inhibition of 17-beta-estradiol
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metabolism by grapefruit juice in ovariectomized women," <em>Maturitas (Ireland) 30(2-3),</em> 155-163,
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1994.)
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</p>
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<p>
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Why do plants make phytoestrogens? There is some information indicating that these compounds evolved to
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regulate the plants' interactions with other organisms--to attract bacteria, or to repel insects, for
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example, rather than just as pigment-forming materials. (Baker, 1995.) The fact that some of them bind
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to our "estrogen receptors" is probably misleading, because of their many other effects, including
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inhibiting enzyme functions involved in the regulation of steroids and prostaglandins. Their
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biochemistry in animals is much more complicated than that of natural estrogens, which is itself so
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complicated that we can only guess what the consequences might be when we change the concentration and
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the ratio of substances in that complex system. (See quotation from Velardo, et al., page 6)
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</p>
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<p>
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These "natural" effects in sheep were forerunners of the observed estrogenic effects in wild animals,
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caused by pollutants. Twenty-five years ago I reviewed many of the issues of estrogen's toxicity, and
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the ubiquity of estrogenic substances, and since then have regularly spoken about it, but I haven't
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concentrated much attention on the phytoestrogens, because we can usually just choose foods that are
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relatively free of them. They are so often associated with other food toxins--antithyroid factors,
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inhibitors of digestive enzymes, immunosuppressants, etc.--that the avoidance of certain foods is
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desirable. Recently an advocate of soybeans said "if they inhibit the thyroid, why isn't there an
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epidemic of hypothyroidism in Asia?" I happened to hear this right after seeing newspaper articles about
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China's problem with 100,000,000 cretins<strong>;</strong> yes, Asia has endemic hypothyroidism, and
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beans are widely associated with hypothyroidism.
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</p>
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<p>
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When I first heard about clover-induced miscarriages in sheep, I began reading about the subject,
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because it was relevant to the work I was doing at that time on reproductive aging. Sheep which are
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adapted to living at high altitude, where all animals have reduced fertility, have an adaptive type of
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hemoglobin, with a greater affinity for oxygen. Fetal hemoglobin, in animals at sea-level, has a great
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affinity for oxygen, making it possible for the fetus to get enough oxygen, despite its insulation from
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the mother's direct blood supply. The high-altitude-tolerant sheep have hemoglobin which is able to
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deliver sufficient oxygen to the uterus to meet the needs of the embryo/fetus, even during relative
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oxygen-deprivation. These sheep are able to sustain pregnancy while grazing on clover. It seemed evident
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that estrogen and high altitude had something in common, namely, oxygen deprivation, and it also seemed
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evident that these sheep provided the explanation for estrogen's abortifacient effects.
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</p>
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<p>
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Estrogen's effects, ranging from shock to cancer, all seem to relate to an interference with the use of
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oxygen. Different estrogens have different affinities for various tissues, and a given substance is
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likely to have effects other than estrogenicity, and the presence of other substances will modify the
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way a tissue responds, but the stressful shift away from oxidative production of energy is the factor
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that all estrogens have in common. Otherwise, how could suffocation and x-irradiation have estrogenic
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effects?
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</p>
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<p>
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Pharmaceutical misrepresentations regarding the estrogens rank, in terms of human consequences, with the
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radiation damage from fall-out from bomb tests and reactor-leaks, with industrial pollution, with
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degradation of the food supply--with genocide, in fact.
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</p>
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<p>
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Advertising gets a bad name when it can't be distinguished from mass murder. At a certain point, we
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can't afford to waste our time making subtle distinctions between ignorance and malevolence. If we begin
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pointing out the lethal consequences of "stupid" or quasi-stupid commer- cial/governmental policies, the
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offenders will have the burden of proving that their actions are the result of irresponsible ignorance,
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rather than criminal duplicity. From the tobacco senators to the chemical/pharmaceutical/food/energy
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industries and their agents in the governmental agencies, those who do great harm must be held
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responsible.
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</p>
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<p>
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The idea of corporate welfare, in which public funds are given in massive subsidies to rich
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corporations, is now generally recognized. Next, we have to increase our consciousness of corporate
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responsibility, and that ordinary criminal law, especially RICO, can be directly applied to
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corporations. It remains to be seen whether a government can be made to stop giving public funds to
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corporations, and instead, to begin enforcing the law against them--and against those in the agencies
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who participated in their crimes.
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</p>
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<p>
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In the U.S., the death penalty is sometimes reserved for "aggravated homicide." If those who kill
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hundreds of thousands for the sake of billions of dollars in profits are not committing aggravated
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homicide, then it must be that no law written in the English language can be objectively interpreted,
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and the legal system is an Alice in Wonderland convenience for the corporate state.
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</p>
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<p>Copyright: Raymond Peat, PhD 1997</p>
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<p>PO Box 5764 Eugene, OR 97405</p>
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<p> </p>
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<p><strong><h3>REFERENCES</h3></strong></p>
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<p>
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Dr. Bernard Weiss, Dept. of Environmental Medicine, University of Rochester School of Medicine,
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Rochester, NY. and 17 others, work session on environmental endocrine-disrupting chemicals, Nov. 5-10,
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1995.
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</p>
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<p>
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Isaac Schiff, et al., "Effects of estriol administration on the hypogonadal woman," Fertil. Steril.
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30(3), 278-282, 1978.
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</p>
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<p>
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N. P. J. Kundu, et al., "Sequential determination of serum human placental lactogen, estriol, and
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estetrol for assessment of fetal morbidity," Obstet. Gynecol. 52(5), 513-520, 1978.
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</p>
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<p>
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M. E. Lieberman, et al., "Estrogen control of prolactin synthesis in vitro," P.N.A.S. (USA) 75(12),
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5946-5949, 1978.
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</p>
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<p>
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Marc Lippman, et al., "Effects of estrone, estradiol and estriol on hormone-responsive human breast
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cancer in long term tissue culture," Cancer Res. 37(6), 1901-1907, 1977.
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</p>
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<p>
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W. P. Dmowski, et al., "Effect of intrauterine estriol on reproductive function in the rabbit," Fertil.
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Steril. 28(3), 262-8, 1977.
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</p>
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<p>
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W. S. Bauld, et al, "Abnormality of estrogen metabolism in human subjects with myocardial infarction,"
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<em>Canadian Jour. Biochem. and Physiol. 35(12),</em> 1277-1288, 1957. (The conversion of estradiol to
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estriol was higher in men with previous myocardial infarction than in controls.)
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</p>
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<p>
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R. A. Edgren and D. W. Calhoun, "Interaction of estrogens on the vaginal smear of spayed rats," <em>Am.
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J. Physiol. 189(2),</em> 355-357, 1957. "Employing the vaginal smear as an index of effect,
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combinations of various estrogenic substances were tested for interaction. Studies were concentrated at
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the approximate 50% response level." "These data are interpreted as indicating simple additive
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relationships among the compounds tested." "Curiously then, estrogens that showed inhibitory
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interrelationships when tested on uterine growth had <strong>simple additive interactions when tested on
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the vaginal smears." "...it seems reasonable to postulate that a given hormone combination may evoke
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differing levels of response in different target organs, and particularly, that increase of one
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component may increase response at one site while decreasing it at another. Many steroids...are
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present in the mammalian circulation during various phases of the sex cycle and are known to modify
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the effects of any given estrogen. This hormonal multiplicity apparently constitutes an
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estrogen-buffering system and supports the hypothesis that sexual responses depend '...upon a rather
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precise hormonal homeostasis.'"</strong>
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</p>
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<p>
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R. C. Merrill, "Estriol: A review," <em>Physiol. Revs. 38(3),</em> 463-480, 1958. <strong>"...estriol
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itself is a potent estrogen, contrary to the usual conception of its being just a metabolite of the
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more potent estrone and estradiol.</strong> Although ordinarily less effective than estrone and
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estradiol in promoting vaginal cornification, estriol, under optimum conditions, approaches their
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effectiveness for this purpose. Estriol is more potent than estrone or estradiol in causing
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establishment and opening of the vaginal orifice, in promoting imbibition of uterine fluid, in
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increasing lactic dehydrogenase activity in the uterus, and in stimulating mitotic activity in the
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epidermis of the mouse ear. The activity of estriol is of the same order of magnitude as that of estrone
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and estradiol in other estrogenic actions, such as to promote uterine growth at low concentrations
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(although less effective at high doses), to increase beta-glucuronidase and reduced diphosphopyridine
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nucleotide oxidase activity in the uterus, to reduce motility of the uterus in vivo, and to stimulate
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ovarian growth, body weight, phagocytosis of carbon by reticuloendothelial cells, ciliary movements of
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the buccopharyngeal mucose of the frog, and new bone formation. The fibromatogenic activity of estriol
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in the guinea pig is much less than that of estrone or estradiol. Recent experiments suggest and partly
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verify the hypothesis that estriol stimulates the cervix, vagina and vulva more effectively than estrone
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or estradiol, whereas the latter are much more effective on the corpus uteri."
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</p>
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<p>
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T. Miyake and G. Pincus, "Anti-progestational activity of estrogens in rabbit endometrium," <em>Proc.
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Soc. Exptl. Biol. and Med. 99(2)</em> 478-482, 1958. "The anti-progestational activity of 4
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estrogens--estrone, estradiol, estriol, and stilbestrol--administered subcutaneously with progesterone
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into Clauberg rabbits has been demonstrated...." <strong>"The anti-progestational activities of these
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estrogens are approximately the same."</strong> "...estrogen may depress reactivity of the
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endometrium to progesterone rather than neutralize or inactivate progesterone in the body."
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</p>
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<p>
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J. T. Velardo, et al., "Effect of various steroids on gestation and litter size in rats," <em>Fertility
|
|
and Sterility 7(4),</em> 301-311, 1956. "...certain metabolites of estrogenic and progestative
|
|
substances that were previously considered to be 'weak' or inert may well play a role in the
|
|
reproductive process." <strong>"We have been impressed with the probability that any endocrine
|
|
receptor-organ response is not accomplished by the independent action of one hormone alone. It
|
|
appears more likely that such response is the physiological expression of the sum total of the
|
|
biologic hormones and their metabolites in concert on the receptor organs."</strong> "The effect of
|
|
estriol on the birth rate of these rats was more dramatic." "...when estriol was used before mating, it
|
|
reduced the litter size to 66 per cent of the controls." "However, when the same dose was employed from
|
|
the day of mating and daily thereafter beyond the time of usual implantation, 6 days later, a reduction
|
|
of live births to 33 per cent of the controls was produced. In this experiment the medication was
|
|
withheld until after ovulation had presumably occurred. The presence of placental scars and an increased
|
|
incidence of abortions and stillbirths argues against the possibility that the fertile ova have been
|
|
'locked' by the estrogen in the tubes." "...the incidence of placental scars, abortions, and stillbirths
|
|
further bears witness to the possibility that the steroids employed interfered with the optimum
|
|
differentiation of progestational endometrial changes, rather than affecting any suppression of
|
|
ovulatory mechanisms."
|
|
</p>
|
|
<p>
|
|
B. Register, et al., "Effect of neonatal exposure to diethylstilbestrol, coumestrol, and beta-sitosterol
|
|
on pituitary responsiveness and sexually dimorphic nucleus volume," <em>P.S.E.B.M. 208,</em> 72, 1995.
|
|
</p>
|
|
<p>
|
|
J. R. Levy, et al., "Effect of prenatal exposure to the phytoestrogen genistein on sexual
|
|
differentiation in rats," <em>P.S.E.B.M. 208,</em> 60, 1995.
|
|
</p>
|
|
<p>
|
|
B.D. Lyn-Cook, et al., "Methylation profile and amplification of proto-oncogenes in rat pancreas induced
|
|
with phytoestrogens," <em>PSEBM 208, </em>116, 1995.
|
|
</p>
|
|
<p>
|
|
J. S. Gavaler, et al., "Phytoestrogen congeners of alcoholic beverages: Current status,: <em>PSEBM
|
|
208,</em> 98, 1995.
|
|
</p>
|
|
<p>
|
|
A. I. Nwannenna, et al., "Clinical changes in ovariectomized ewes exposed to phytoestrogens and
|
|
17beta-estradiol implants," <em>PSEBM 208,</em> 92, 1995.
|
|
</p>
|
|
<p>
|
|
P. L. Whitten, et al., "Influence of phytoestrogen diets on estradiol action in the rat uterus,"
|
|
Steroids 59, 443-449, 1994. <strong>"Coumestrol did not antagonize the uterotrophic action of estradiol
|
|
when administered either prior to, or jointly with, E2 treatment, or when administered orally or
|
|
parenterally." "These findings contradict the assumption that all phytoestrogens are necessarily
|
|
antiproliferative agents...."</strong>
|
|
</p>
|
|
<p>
|
|
M. E. Baker, "Endocrine activity of plant-derived compounds: An evolutionary perspective,"<em>
|
|
PSEBM 208,</em> 131, 1995.
|
|
</p>
|
|
<p>
|
|
I. Palmlund, "To cell from environment," Chapter 19 in <em>Cellular and Molecular Mechanisms of Hormonal
|
|
Carcinogenesis,</em> published by Wiley-Liss.
|
|
</p>
|
|
<p>
|
|
J. H. Clark, et al., "Nuclear binding of the estrogen receptor: Heterogeneity of sites and uterotropic
|
|
response," <em>Steroid Hormone Receptor Systems,</em> page 17, 1979.
|
|
</p>
|
|
<p>
|
|
P. Vega Ramos, et al., "Formation of oestriol from C19, 16-oxygenated steroids by microsomal
|
|
preparations of human placenta," <em>Res. on Steroids, vol. V,</em> page 79, Proc. of the Fifth Meeting
|
|
of the International Study Group for Steroid Hormones, edited by M. Finkelstein, et al., 1973.
|
|
</p>
|
|
<p>G. S. Rao, "Enzymes in steroid metabolism," <em>Res. on Steroids, vol. V, </em>page 175, 1973.</p>
|
|
<p>
|
|
L. H. Carter and C. B. Harrington, <em>Administrative Law and Politics</em> HarperCollins, 1991.
|
|
"Capture occurs when agencies informally promote the very interests they are officially responsible for
|
|
regulating." In 1925, Coolidge's appointment of "anti-public" W. E. Humphrey to the FTC led some of its
|
|
former supporters to call for the abolition of the FTC.
|
|
</p>
|
|
<p>
|
|
<strong>
|
|
"If nearly a century of regulatory history tells us anything, it is that the rules-making agencies
|
|
of government are almost invariably captured by the industries which they are established to
|
|
control."</strong> Robert Heilbroner, In the Name of Profit, 1972, p. 239. "Federal economic
|
|
regulation was generally designed by the regulated interest to meet its own end, and not those of the
|
|
public or the commonweal." Gabriel Kolko, <em>The Triumph of Conservatism: A Reinterpretation of
|
|
American History, 1900-1916,</em> 1963.
|
|
</p>
|
|
<p>
|
|
"It is a given in the modern doctrine of most tort laws that the existence of potential liability if
|
|
anything encourages citizens to use greater thoughtfulness and care in their daily actions, and no
|
|
obvious reasons suggest the same dynamic should not affect public officials." Adm. Law. & Pols., p.
|
|
404. "That Congress decided, after the passage of the Fourteenth Amendment, to enact legislation
|
|
specifically requiring state officials to respond in federal court for their failures to observe the
|
|
constitutional limitations on their powers is hardly a reason for excusing their federal counterparts
|
|
for the identical constitutional transgressions." <strong>"In situations of abuse, an action for damages
|
|
against the responsible official can be an important means of vindicating constitutional
|
|
guarantees...." Justice White, Butz v. Economou, p. 409, Adm. Law & Pols.
|
|
</strong>
|
|
</p>
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