Library:Natural Estrogens
A Ray Peat newsletter, 2008-03-16.
Read the original on raypeat.com →
The fact that an extremely large number of naturally occurring compounds, and an unlimited number of synthetic compounds, have an estrogen-like activity has been exploited by the drug companies to produce patented proprietary drugs, especially the contraceptives.
The promotion of “natural estrogens” is a new marketing strategy that capitalizes on the immense promotional investment of the drug companies in the concept of estrogen replacement as “therapy.”
Estrogen marketing has entered a new phase, based on the idea of “specific estrogen-receptor modulators,” the idea that a molecule can be designed which has estrogen's “good qualities without its bad qualities.” This specific molecule will be “good for the bones, the heart, and the brain,” without causing cancer of the breast and uterus, according to the estrogen industry. Meanwhile, soybeans are said to contain estrogens that meet that goal, and it is often said that “natural estrogens” are better than “synthetic estrogens” because they are “balanced.”
Estrogen's effects on cells are immediate and profound, independent of the “estrogen receptors.”
Japanese women's relative freedom from breast cancer is independent of soy products: traditional soy foods aren't the same as those so widely used in the U.S., for example, soy sauce doesn't contain the so-called soy estrogens, and tea is used much more commonly in Japan than in the U.S., and contains health protective ingredients. The “estrogenic” and “antioxidant” polyphenolic compounds of tea are not the protective agents (they raise the level of estrogen), but tea's caffeine is a very powerful and general anti-cancer protectant. The influential article in Lancet[16, 9] used a method known to produce false results, namely, comparing the phytoestrogens (found in large amounts in soybeans) in the urine of women with or without breast cancer. For over fifty years, it has been known that the liver excretes estrogens and other toxins from the body, and that when (because of liver inertia) estrogen isn't excreted by the liver and kidneys, it is retained in the body. This process was observed in both animals and humans decades ago, and it is also well established that estrogen itself suppresses the detoxifying systems, causing fewer carcinogens to be excreted in the urine. Ingram's evidence logically would suggest that the women who have cancer are failing to eliminate estrogens, including phytoestrogens, at a normal rate, and so are retaining a higher percentage of the chemicals consumed in their diets. Flavonoids and polyphenols, like our own estrogens, suppress the detoxifying systems of the body.
Our bodies produce estrogen in a great variety of tissues, not just in the ovaries. Fat cells are a major source of it. The tendency to gain weight after puberty is one of the reasons that women's estrogen levels rise with aging throughout the reproductive years, though this isn't the basic reason for estrogen's lifelong growing influence, even in men.
Our diets provide very significant, if not always dangerous, amounts of estrogen. “Weak estrogens” generally have the full range of harmful estrogenic effects, and often have additional toxic effects. American women who eat soy products undergo changes that appear to predispose them to cancer, making their tissues even more unlike those of the relatively breast-cancer resistant Japanese than they were before eating the soy foods.
People under stress, or who have a thyroid deficiency, or who don't eat enough protein, typically have elevated estrogen levels. The accumulation of the “essential fatty acids,” the polyunsaturated oils, in the tissues promotes the action of estrogen in a variety of ways, and this effect of diet tends to be cumulative, and to be self-accelerating.
Science is a method that helps us to avoid believing things that are wrong, but there is a distinct herd instinct among people who “work in science,” which makes it easy to believe whatever sounds plausible, if a lot of other people are saying it is true. This is just as evident in physics as it is in medicine. Sometimes powerful economic interests help people to change their beliefs, for example as the insurance industry helped to convince the public of the dangers of smoking. Two of the biggest industries in the world, the estrogen industry and the soy bean industry, spend vast amounts of money helping people to believe certain plausible-sounding things that help them sell their products. Sometimes they can achieve great things just by naming the substance.
Estrogenicity can be defined most simply as “acting the way estrogen does,” (originally, the term “estrogen” meant “producing estrus,” the female readiness to mate) and since our natural estrogen does many things, the definition is often, for practicality, based on the rapid changes produced in certain female organs by estradiol, specifically, the enlargement of the uterus by first taking up a large amount of water, and secondarily by the multiplication of cells and the production of specific proteins. A similar process occurring in the breast is also recognized as an important feature of the estrogen reaction, but as we try to define just what “estrogenicity” is, we see that there is something deeply wrong with this method of defining a hormone, because we are constantly learning more about the actions of estrogen, or of a specific form of the molecule. Calling it “the female hormone” distracted attention from its many functions in the male, and led to great confusion about its antifertility actions and its other toxicities. Many biologists called it “folliculin,” because of the ovarian follicle's significant role in its production, but the pharmaceutical industry succeeded in naming it in relation to one of its functions, and then in extending that idea of it as “the producer of female receptivity” to the even more misleading idea that it is “the female hormone.” But when people speak about the “estrogenicity” of a substance, they mean that it has properties that parallel those of “folliculin,” the particular group of ovarian hormones that includes estradiol, estrone, and estriol.
Over the last 100 years, thousands of publications about estrogen's toxicity have created a slight resistance to the consumption of the major estrogen products. One ploy to overcoming this resistance is to call certain products “natural estrogen,” as distinguished from “synthetic estrogens.” The three main estrogens in our bodies are estradiol, estrone, and estriol, though there are many other minor variants on the basic molecule. These three estrogens, singly or in combinations, are being sold as natural estrogens, with their virtues explained in various ways. Implicit in many of these explanations, is the idea that these are safer than synthetics. They are sometimes contrasted to the “horse estrogen” in Premarin, as if they are better because they are like the estrogens that people produce. But it was exactly the normal human estrogens, produced by the ovaries, that led to the basic discoveries about the toxicity of estrogen, its ability to produce cancer in any organ, to cause seizures, blood clots, birth defects, accelerated aging, etc.
Although I would suppose that a hormone from a horse might be “more natural” for a person's body than a hormone from a plant, the word “natural” as used in the phrases “natural food store,” or “natural medicine,” has come to be associated strongly with things derived from plants. The health food industry, now largely taken over by giant corporations to sell products that weren't producing as much revenue when sold in supermarkets and drugstores, has helped to create a culture in which botanical products are thought to be especially good and safe. Naturally grown free-range chickens used to be favored, because they could eat anything they wanted, but now eggs laid by factory chickens, eating an industrial corn-and-soy diet, are from “vegetarian chickens,” because the marketers know the public will favor eggs that have the vegetarian mystique.
Biologically active molecules have both general and specific properties. Estrogenicity is a general property, but all molecules which have that property also have some other specific properties. Estriol is a little more water soluble than estrone, so it interacts with every body system in a slightly different way, entering oily environments with slightly less ease, etc.
The estrogen which occurs in yeasts, estradiol, is identical to the major human estrogen, and it is thought to have a reproductive function in yeasts, though this isn't really understood. A feature of this molecule, and of all other molecules that “act like estrogen,” is the phenolic function, an oxygen and hydrogen group attached to a resonant benzene ring. Phenol itself is estrogenic, and the phenolic group is so extremely common in nature that the number of existing estrogenic substances is great, and the number of potential molecules with estrogen-function is practically infinite.
The phenolic group has many biological functions. For example, it commonly functions as an “antioxidant,” though something which functions as an antioxidant in one situation is often a pro-oxidant in another situation. The molecule can have catalytic, germicidal, aromatic, neurotropic, and other functions. But it also always has, to some degree, the “estrogenic” function. This overlap of functions probably accounts for why so many plants have significant estrogenic activity. (Natural estrogens, like other phenolics, including the flavonoids, are also mutagenic.)
The estrogenic properties of legumes were studied when sheep farmers found that their sheep miscarried when they ate clover. (I think it's interesting how this terribly toxic effect has been neglected in recent decades.) All legumes have this property, and all parts of the plant seem to contain some of the active chemicals. In beans, several substances have been found to contribute to the effect. The estrogenic effects of the seed oils and the isoflavones have been studied the most, but the well-known antithyroid actions (again, involving the oils, the isoflavones, and other molecules found in legumes) have an indirect estrogen-promoting action, since hypothyroidism leads to hyperestrogenism. (Estrogens are known to be thyroid suppressors, so the problem tends to be self-accelerating.)
The various specific actions of the many estrogenic substances in beans and other legumes haven't been thoroughly studied, but there is evidence that they are also—like estrogen itself—both mutagenic and carcinogenic.
The estrogen-promoting actions of soy oil apply to all of the commonly used polyunsaturated fatty acids. The same fatty acids that suppress thyroid function, have estrogenic effects.
The isoflavones (many of which are now being promoted as “antioxidants” and “cancer preventives”) are toxic to many organs, but they have clear estrogenic effects, and are active not only immediately in the mature individual, but when they are present prenatally, they cause feminization of the male genitalia and behavior, and early maturation of the female offspring, with the tissue changes that are known to be associated with increased incidence of cancer.
There are interesting associations between vegetable “fiber” and estrogens. Because of my own experience in finding that eating a raw carrot daily prevented my migraines, I began to suspect that the carrot fiber was having both a bowel-protective and an antiestrogen effect. Several women who suffered from premenstrual symptoms, including migraine, had their serum estrogen measured before and after the “carrot diet,” and they found that the carrot lowered their estrogen within a few days, as it relieved their symptoms.
Undigestible fiber, if it isn't broken down by bowel bacteria, increases fecal bulk, and tends to speed the transit of material through the intestine, just as laxatives do. But some of these “fiber” materials, e.g., lignin, are themselves estrogenic, and other fibers, by promoting bacterial growth, can promote the conversion of harmless substances into toxins and carcinogens. When there is a clear “antiestrogen” effect from dietary fiber, it seems to be the result of accelerated transit through the intestine, speeding elimination and preventing reabsorption of the estrogen which has been excreted in the bile. Laxatives have this same effect on the excretion of estradiol.
Some of the isoflavones, lignins, and other phytoestrogens are said to prevent bowel cancer, but some of them, e.g., lignin, appear to sometimes increase its likelihood.
The phytoestrogens appear to pose a risk to organs besides the breast and uterus, for example the liver, colon, and pancreas, which isn't surprising, since estrogen is known to be carcinogenic for every tissue. And carcinogenesis, like precancerous changes, mutations, and reduced repair of DNA, is probably just an incidental process in the more general toxic effect of acceleration of aging.
References
[edit]- Arts C. J. M.; van Berg H. D.; Thussen J. H. H. Effects of Dietary Fiber on N-Nitrosomethylurea-Induced Mammary Tumors and on Plasma Estrogen Levels in Rats. JNCI Journal of the National Cancer Institute 83(18), 1347–1348. DOI: 10.1093/jnci/83.18.1347
- B R. L. [Estrogens of Vegetable Origin]. Ginecologia y obstetricia de Mexico 66, 111–8, 1998. URL: https://pubmed.ncbi.nlm.nih.gov/9608188
- Baird D. D. Dietary Intervention Study to Assess Estrogenicity of Dietary Soy among Postmenopausal Women. Journal of Clinical Endocrinology Metabolism 80(5), 1685–1690. DOI: 10.1210/jc.80.5.1685
- Benassayag C.; Vallette G.; Hassid J.; Raymond P.; Nunez E. A. Potentiation of Estradiol Binding to Human Tissue Proteins by Unsaturated Nonesterified Fatty Acids. Endocrinology 118(1), 1–7, 1986. DOI: 10.1210/endo-118-1-1
- Birt D. F.; Markin R. S.; Blackwood D.; Harvell D. M.; Shull J. D.; Pennington K. L. Dietary Lignin, an Insoluble Fiber, Enhanced Uterine Cancer but Did not Influence Mammary Cancer Induced ByN-Methyl-N-Nitrosourea in Rats. Nutrition and Cancer 31(1), 24–30, 1998. DOI: 10.1080/01635589809514674
- Boeryd B.; Hallgren B. The Influence of the Lipid Composition of the Feed Given to Mice on the Immunocompetence and Tumour Resistance of the Progeny. International Journal of Cancer 26(2), 241–246. DOI: 10.1002/ijc.2910260217
- Brown J. P.; Dietrich P. S.; Brown R. J. Frameshift Mutagenicity of Certain Naturally Occurring Phenolic Compounds in the 'Salmonella/Microsome' Test: Activation of Anthraquinone and Flavonol Glycosides by Gut Bacterial Enzymes. Biochemical Society Transactions 5(5), 1489–1492. DOI: 10.1042/bst0051489
- Bruning P. F.; Bonfrer J. M. G. Possible Relevance of Steroid Availability and Breast Cancer. Annals of the New York Academy of Sciences 538(1), 257–268, 1988. DOI: 10.1111/j.1749-6632.1988.tb48870.x
- Nhmrc National Breast Cancer Centre. Phytoestrogens and Their Role in Breast Cancer. 1997.
- Clapp N. K.; Henke M. A.; London J. F.; Shock T. L. Enhancement of 1,2-Dimethylhydrazine-Induced Large Bowel Tumorigenesis in Balb/C Mice by Corn, Soybean, and Wheat Brans. Nutrition and Cancer 6(2), 77–85, 1985. DOI: 10.1080/01635588509513810
- Dees C.; Foster J. S.; Ahamed S.; Wimalasena J. Dietary Estrogens Stimulate Human Breast Cells to Enter the Cell Cycle. Environmental Health Perspectives 105(Suppl 3), 633, 1997. DOI: 10.2307/3433382
- Deodutta Roy M. P. C. Biochemical and Molecular Changes at the Cellular Level in Response to Exposure to Environmental Estrogen-Like Chemicals. Journal of Toxicology and Environmental Health 50(1), 1–30, 1997. DOI: 10.1080/009841097160573
- Dugrillon A. Iodolactones and Iodoaldehydes- Mediators of Iodine in Thyroid Autoregulation. Experimental and Clinical Endocrinology Diabetes 104(S 04), 41–45. DOI: 10.1055/s-0029-1211700
- Grubeck-Loebenstein B.; Kletter K.; Kiss A.; Vierhapper H.; Waldhäusl W. [Endemic Goiter in Austria. Is Iodine Deficiency the Primary Cause of Goiter?]. Schweizerische medizinische Wochenschrift 112(44), 1526–30, 1982. URL: https://pubmed.ncbi.nlm.nih.gov/7156942
- Hilakivi-Clarke L.; Cho E.; Clarke R. Maternal Genistein Exposure Mimics the Effects of Estrogen on Mammary Gland Development in Female Mouse Offspring. Oncology Reports 5(3), 609–16. DOI: 10.3892/or.5.3.609
- Ingram D.; Sanders K.; Kolybaba M.; Lopez D. Case-Control Study of Phyto-Oestrogens and Breast Cancer. The Lancet 350(9083), 990–994, 1997. DOI: 10.1016/s0140-6736(97)01339-101339-1)
- Ishizuki Y.; Hirooka Y.; Murata Y.; Togashi K. The Effects on the Thyroid Gland of Soybeans Administered Experimentally in Healthy Subjects. Folia Endocrinologica Japonica 67(5), 622–629, 1991. DOI: 10.1507/endocrine1927.67.5_622
- Lewis S. J.; Oakey R. E.; Heaton K. W. Intestinal Absorption of Oestrogen. European Journal of Gastroenterology Hepatology 10(1), 33–40, 1998. DOI: 10.1097/00042737-199801000-00007
- Lewis S. J.; Heaton K. W.; Oakey R.; McGarrigle H. H. G. Lower Serum Oestrogen Concentrations Associated with Faster Intestinal Transit. British Journal of Cancer 76(3), 395–400, 1997. DOI: 10.1038/bjc.1997.397
- Lhoste E. F.; Roebuck B. D.; Stern J. E.; Longnecker D. S. Effect of Orchiectomy and Testosterone on the Early Stages of Azaserine-Induced Pancreatic Carcinogenesis in the Rat. Pancreas 2(1), 38–43, 1987. DOI: 10.1097/00006676-198701000-00006
- Martin M. E.; Vranckx R.; Benassayag C.; Nunez E. A. Modifications of the Properties of Human Sex Steroid-Binding Protein by Nonesterified Fatty Acids. Journal of Biological Chemistry 261(6), 2954–2959, 1986. DOI: 10.1016/s0021-9258(17)35879-935879-9)
- McPherson-Kay R. Fiber, Stool Bulk, and Bile Acid Output: Implications for Colon Cancer Risk. Preventive Medicine 16(4), 540–544, 1987. DOI: 10.1016/0091-7435(87)90069-790069-7)
- Musey V. C.; Collins D. C.; Musey P. I.; Martino-Saltzman D.; Preedy J. R. Age-Related Changes in the Female Hormonal Environment during Reproductive Life. American Journal of Obstetrics and Gynecology 157(2), 312–317, 1987. DOI: 10.1016/s0002-9378(87)80159-x80159-x)
- Obermeyer W. R.; Musser S. M.; Betz J. M.; Casey R. E.; Pohland A. E.; Page S. W. Chemical Studies of Phytoestrogens and Related Compounds in Dietary Supplements: Flax and Chaparral. Experimental Biology and Medicine 208(1), 6–12. DOI: 10.3181/00379727-208-43824
- Petrakis N. L.; Barnes S. L.; King E. B.; Lowenstein J.; Wiencke J. K.; Lee M. M.; Miike R.; Kirk M.; Coward L. Stimulatory Influence of Soy Protein Isolate on Breast Secretion in Pre- and Postmenopausal Women. Cancer epidemiology, biomarkers prevention: a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 5(10), 785–94, 1996. URL: https://pubmed.ncbi.nlm.nih.gov/8896889
- Reed M.; Beranek P.; Cheng R.; James V. Free Fatty Acids: A Possible Regulator of the Available Oestradiol Fractions in Plasma. Journal of Steroid Biochemistry 24(2), 657–659, 1986. DOI: 10.1016/0022-4731(86)90134-290134-2)
- Rodriguez P.; Fernández-Galaz C.; Tejero A. Controlled Neonatal Exposure to Estrogens: A Suitable Tool for Reproductive Aging Studies in the Female Rat. Biology of Reproduction 49(2), 387–392. DOI: 10.1095/biolreprod49.2.387
- Roy D. Is Exposure to Environmental or Industrial Endocrine Disrupting Estrogen-Like Chemicals Able to Cause Genomic Instability. Frontiers in Bioscience 3(4), d913–921, 1998. DOI: 10.2741/a332
- Schipper H. M.; Desjardins G. C.; Beaudet A.; Brawer J. R. The 21-Aminosteroid Antioxidant, U74389F, Prevents Estradiol-Induced Depletion of Hypothalamic β-Endorphin in Adult Female Rats. Brain Research 652(1), 161–163, 1994. DOI: 10.1016/0006-8993(94)90332-890332-8)
- Silva I.; Rodrigues A.; Gaspar J.; Maia R.; Laires A.; Rueff J. Involvement of Rat Cytochrome 1A1 in the Biotransformation of Kaempferol to Quercetin: Relevance to the Genotoxicity of Kaempferol. Mutagenesis 12(5), 383–390, 1997. DOI: 10.1093/mutage/12.5.383
- Sloan D. A.; Fleiszer D. M.; Richards G. K.; Murray D.; Brown R. A. The Effect of the Fiber Components Cellulose and Lignin on Experimental Colon Neoplasia. Journal of Surgical Oncology 52(2), 77–82, 1993. DOI: 10.1002/jso.2930520204
- Smith D. A.; Walker B. E. Evidence of Hypothalamic Involvement in the Mechanism of Transplacental Carinogenesis by Diethylstilbestrol. Cancer Letters 67(1), 55–59, 1992. DOI: 10.1016/0304-3835(92)90008-j90008-j)
- Sun B.; Fukuhara M. Effects of Co-Administration of Butylated Hydroxytoluene, Butylated Hydroxyanisole and Flavonoids on the Activation of Mutagens and Drug-Metabolizing Enzymes in Mice. Toxicology 122(1-2), 61–72, 1997. DOI: 10.1016/s0300-483x(97)00078-400078-4)
- Suzuki Y.; Nanno M.; Gemma R.; Yoshimi T. Plasma Free Fatty Acids, Inhibitor of Extrathyroidal Conversion of T4 to T3 and Thyroid Hormone Binding Inhibitor in Patients with Various Nonthyroidal Illnesses. Endocrinologia Japonica 39(5), 445–453, 1992. DOI: 10.1507/endocrj1954.39.445
- Vallette G.; Christeff N.; Bogard C.; Benassayag C.; Nunez E. Dynamic Pattern of Estradiol Binding to Uterine Receptors of the Rat. Inhibition and Stimulation by Unsaturated Fatty Acids. Journal of Biological Chemistry 263(8), 3639–3645, 1988. DOI: 10.1016/s0021-9258(18)68972-068972-0)
- Whitten P. L.; Lewis C.; Russell E.; Naftolin F. Potential Adverse Effects of Phytoestrogens. The Journal of Nutrition 125(3 Suppl), 771S-776S, 1995. DOI: 10.1093/jn/125.suppl_3.771s
- Zhu B. T.; Taneja N.; Loder D. P.; Balentine D. A.; Conney A. H. Effects of Tea Polyphenols and Flavonoids on Liver Microsomal Glucuronidation of Estradiol and Estrone. The Journal of Steroid Biochemistry and Molecular Biology 64(3-4), 207–215, 1998. DOI: 10.1016/s0960-0760(97)00163-500163-5)
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