With roots tracing back to the eugenics and population control movements, birth control pills do much more than prevent ovulation. They can also destroy women's health. Ditto for hormone replacement therapy. Study after study shows the deleterious effects of both estrogen and Big Pharma's synthetic analogues.
The Disturbing Truth About Oral Contraceptives
One of the properties of estrogens is their ability to increase the cells’ ability to hold water, which is why women with estrogen dominance are prone to edema (water retention). Cellular swelling is both a characteristic of the cellular stress response and a signal for cellular proliferation. Cellular swelling and proliferation are also hallmarks of cancer
Estrogen has been shown to replicate the shock phase of the stress reaction in animals
Progesterone, a progestational molecule, nourishes the embryo and is essential to prevent miscarriage. It’s also an antistress molecule and anti-estrogenic
Synthetic progestins, while having some of the activity of progesterone, do not have the same physiological effects as endogenous progesterone. In fact, in some cases, they can have the opposite effect
The 1965 to 1985 Coronary Drug Project found that Premarin, a weak estrogen, increased cancer, heart disease and mortality rates. The Nurses’ Health Study, which began in 1976, found that hormone replacement therapy (HRT) increased the risk of ischemic stroke and cancer, and the Framingham Heart Study showed an increased risk of heart disease for estrogen users
The Women’s Health Initiative, which began in 1991, found women who used either Premarin alone or in combination with Provera, the synthetic progestin used in birth control shots, had elevated rates of vascular diseases, cognitive decline, cancers and more
The video above reviews the shady backstory of the birth control pill, the roots of which can be traced back to the eugenics and population control movements. As noted in this video, birth control pills do not "just prevent ovulation by mimicking hormones." They do a whole lot more. They also destroy women’s health.
Estrogen and Progesterone
Chapter 1 of the video reviews the biological roles of estrogen and progesterone, the two sex hormones associated with contraception. While estrogen is routinely referred to as "the female hormone," this is misleading, as it’s not exclusive to women. Moreover, there’s not just one estrogen but several.
Estrogens do play a role in female sexuality and reproduction. The word originates from "estrus," which signifies an animal’s receptivity to being mounted by a male.
In the early 1900s, the use of animal tissues and substances to correct deficiencies in humans started taking off. For example, we discovered we could use insulin from dogs and thyroid hormones derived from porcine tissue to treat diabetes and hypothyroidism.
Estrogen and progesterone were also initially isolated from animal tissue, but it was difficult, time-consuming and costly. One ton of animal organs were required to obtain a single gram of progesterone, forcing researchers to start looking for alternatives, as a therapeutic daily dose of progesterone is typically 30 mg. As explained in the video:
"In the coming decades, the pursuit to create synthetic analogues of these hormones was driven by the pharmaceutical industry’s idea that they would have many beneficial effects for women: restoring their youth and fertility and, of course contraception, just to name a few. However, various esteemed academics warned about the potential of estrogens to cause cancer and other health issues, heavily cautioning its use even at low doses.
It was already shown in the 1930s that the very estrogen that was set to be marketed as a method to prevent miscarriages, known as DES [diethylstilbestrol, a synthetic estrogenic compound], was capable of inducing miscarriage or abortion in animals even at small doses ... It was also known to cause a host of other problems, including cancer, in animals as well."
The Physiological Role of Estrogen
One of the properties of estrogens is their ability to increase the cells’ ability to hold water, which is why women with estrogen dominance are prone to edema (water retention). Cellular swelling is both a characteristic of the cellular stress response and a signal for cellular proliferation.
During the follicular phase of the menstrual cycle, estrogen stimulates the uterine lining and follicles to swell and multiply in preparation for the fertilization of an egg. Similarly, during and after pregnancy, breast tissue swells and grows larger to facilitate milk production.
But cellular swelling and proliferation is also a hallmark of cancer. Indeed, the word oncology comes from the Greek word "oncos," which simply means swelling.
In his 1997 book, "From PMS to Menopause: Female Hormones in Context,"1 biologist Ray Peat2 stated that estrogen had been shown to replicate the shock phase of the stress reaction in animals. According to Peat, the physiological purpose of estrogens is to stimulate cell division by triggering water uptake by the cell.
Peat also suspected that estrogen was a metabolic inhibitor that slows down energy production in the cell. Otto Warburg, after whom the Warburg Effect was named, stated that "the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar."
In simpler terms, this is when your body has more than enough oxygen to burn (oxidize) glucose in your mitochondria but instead shuttles glucose outside the mitochondria into the cytoplasm to oxidize or burn in glycolysis and produce lactate. This is the classic form of energy production in cancer cells.
It is not that cancer burns sugar for fuel; it is that cancer burns glucose inefficiently in glycolysis and not mitochondria, despite having enough oxygen present. This is typically due to mitochondrial metabolic dysfunction.
Essentially, this means anything that limits or prevents your cells’ ability to efficiently burn glucose in your mitochondria is capable of causing cancer, and according to Peat, estrogen may be doing just that. As noted in the video:
"These properties of estrogen are often overlooked, as research narrowly tends to focus on the actions of cell receptors. However, it’s been shown that cancers that do not contain receptors for estrogen still grow when exposed to estrogen, and subside when estrogen is lowered, so the actions of receptors cannot explain everything."
The Physiological Role of Progesterone
Progesterone and estrogen are antagonists, meaning progesterone is anti-estrogen and estrogen is antiprogesterone. Progesterone, a progestational molecule, nourishes the embryo and is essential to prevent miscarriage. However, because it signals that your body is already pregnant, which prevents ovulation, it also acts as a contraceptive. This makes perfect sense if you think about it.
Once you’re pregnant, you cannot ovulate and get pregnant again until after the pregnancy is completed. It’s not the absolute amount of progesterone that counts, though. Rather, it’s the ratio of progesterone to estrogen that determines their effects.
The Estrogen Explosion
Menopause used to be viewed as a natural part of a woman’s life cycle. Sometime after the age of 50 or so, women stop menstruating and are no longer fertile. Rarely, if ever, was this considered a condition that needed treatment.
That started to change in the early 1940s with the advent of DES, the first estrogenic compound used to protect against miscarriages in women with a history of fetal loss and to "revitalize" women who were past their prime. As explained in the video:
"The first estrogen to be used as a drug, DES, was not patented. Due to this, there was no incentive for the companies to compete against one another to sell it.
By instead colluding together, these companies were able to successfully lobby the FDA, and in 1941 DES was approved for therapy of menopause, now under the elegant name of menopausal hormone replacement therapy or HRT, a landmark moment in history that essentially birthed ‘Big Pharma’ as we know and hate today ...
Women were now told they could restore their youth: increasing their energy for chores, their attractiveness and their sex drive. This was true to an extent. Estrogen had been recognized to be a powerful stimulant and brain excitant, again characteristic of stress and shock."
Since then, many synthetic compounds, especially plasticizing compounds, have been developed that have estrogenic properties. Today, we know them as endocrine disruptors or xenoestrogens. DES, the first endocrine-disrupting chemical, is strikingly similar in composition to bisphenol-A (BPA), which the FDA banned for use in baby bottles and sippy cups in 2012.3
Many pesticides, preservatives, organic pollutants, drugs and even textiles also have estrogenic activity. Polyester, for example, mimics estrogen, and in one study, eight female dogs dressed in polyester dog clothing became unable to reproduce, due to insufficient progesterone levels.
Plants can also have estrogenic activity and are known as phytoestrogens. Interestingly, it’s been proposed that one of the roles of phytoestrogens is to discourage herbivores from eating them by inhibiting their reproduction. Clover, for example, can cause permanent infertility in sheep, and this has been known since the 1930s.
How Estrogen Works in Contraceptives
In his Ph.D. thesis, "Age-Related Oxidative Changes in the Hamster Uterus,"4 Peat detailed the effects of estrogen on aging, menopause, stress and fertility. He found that older animals had insufficient amounts of oxygen in the uterus to keep the embryo alive long enough for successful implantation, and younger animals given estrogen experienced the same problem.
As a result, Peat argued that estrogen prevents implantation of the embryo by reducing oxygen in the uterus. What’s more, a sufficiently large dose can kill the embryo or fetus at any stage of the pregnancy. On the flip side, he found that older animals that would normally be infertile due to age remained fertile when given a supplement of vitamin E and progesterone. As noted in the video:
"Mifepristone, also known as the abortion pill, actually works by blocking the effects of progesterone, which means it effectively enhances the effect of estrogens. Of course, now mifepristone is making national headlines for its highly questionable safety, which seems to be in line with relative estrogenic excess and progesterone deficiency.
It’s likely that we are now seeing history repeat itself, as childbirth is becoming medicalized, and women are being experimented on with estrogenic pharmaceuticals for greater agendas."
Synthetic Progestins — A Timeline
In 1943, chemist Russell Marker started extracting progesterone from wild Mexican yams. However, progesterone is poorly absorbed when taken orally, so women had to take inconveniently large doses.
In 1951, Syntex S.A (later acquired by Roche) developed norethindrone, the first synthetic progestin (progesterone analogue). A year later, G. D. Searle (now a Pfizer subsidiary), came up with its own synthetic progestin, called norethynodrel. Both norethindrone and norethynodrel are derivatives of testosterone, the primary androgenic hormone.
Progestins tend to lower and can completely shut down endogenous progesterone production, leaving estrogen unopposed.