While estrogen replacement is generally regarded as beneficial, if not crucial, for women entering into menopause, a closer look reveals it can cause severe problems and you do not, in fact, want high levels of estrogen.

Originally called adipin, estrogen got its name from its association with weight gain, as in adipose (fat) tissue. In the mid-‘50s, when the drug industry started pushing synthetic estrogens, this knowledge faded from memory.

One of the most infamous early synthetic estrogens prescribed was diethylstilbestrol (DES), which caused fetal malformations and deaths, and cancers in the mothers who took it. DES was eventually withdrawn and banned for use in humans.

DES is not estrogen itself but rather a chemical that mimics estrogen’s actions by activating estrogen receptors. In fact, DES can potentially activate these receptors even more strongly than natural estrogen. This alone is a strong indication that estrogen excess is of serious concern. Studies looking at the effects of estrogen and estrogenic chemicals only add to the certainty.

Estrogen Is Carcinogenic

The National Institutes of Health added steroidal estrogens used in estrogen replacement therapy and oral contraceptives to its list of KNOWN human carcinogens all the way back in December 2002.¹ In my mind, estrogen and excess linoleic acid are the two primary reasons for most cancers.

Likewise, the Women’s Health Initiative (WHI) studies, which began in 1991,² showed estrogen replacement therapy in menopausal women significantly increased the risk of heart attacks, strokes, dementia, Parkinson’s disease and cancer, not just in the breast but all female reproductive organs.

In October 2023, I interviewed bioenergetic researcher Georgi Dinkov about the hazards of estrogen. I’ve included that interview above for your convenience.

As noted by Dinkov in a recent blog post,³ that interview apparently “struck a nerve” with a doctor who “went through the trouble of writing an extensive blog post trying to debunk the already established fact that estrogen is a carcinogen, by claiming that most of that data stems from the WHI studies, and that those are now considered flawed, ergo estrogen cannot be considered a carcinogen.”

In response, Dinkov sent the doctor a long, yet not exhaustive, list of academic articles and studies demonstrating that estrogen is indeed a mutagenic carcinogen — and that any chemical with estrogenic properties poses a serious threat to health.

Hundreds of Everyday Chemicals Linked to Increased Breast Cancer Risk

As just one example, a January 2024 paper⁴ in Environmental Health Perspectives identified 279 estrogenic compounds commonly found in consumer products that induce mammary tumors in animals, and another 642 chemicals that could potentially increase the risk of breast cancer by stimulating estrogen or progesterone signaling. As reported by Environmental Health News:⁵

“… More than 900 chemicals commonly found in consumer products and the environment have been linked to breast cancer risk in a new study. The study … identified 921 chemicals that could potentially increase the risk of breast cancer and found that 90% are ubiquitous in consumer products, food and drinks, pesticides, medications and workplaces.

The list includes chemicals like parabens and phthalates, which are commonly found in makeup, skin and hair care products; and numerous pesticide ingredients, including malathion, atrazine and triclopyr, which are used on food and in household pest control products in the U.S.

Breast cancer among young women has increased in recent years.⁶ Between 2010 and 2019, diagnoses among people 30 to 39 years old increased 19.4%, and among those ages 20 to 29, rates increased 5.3%. This change is too fast to be explained by genetics, so researchers have begun looking more closely at potential environmental causes for the disease.

A 2020 study⁷ found that women who used chemical hair straighteners more than six times a year had about a 30% higher risk of breast cancer than those who didn’t use chemical straighteners. Those products typically contain one or more of the chemicals identified in the new study as increasing the chances of getting breast cancer.”

Everyday Items May Expose You to Hazardous Levels of Estrogen

In modern times, many synthetic compounds, especially plasticizing compounds, have been developed that have estrogenic properties. Other terms for such compounds are endocrine disruptors and xenoestrogens.

DES is strikingly similar in composition to bisphenol-A (BPA), which the U.S. Food and Drug Administration banned for use in baby bottles and sippy cups in 2012.⁸ Many pesticides, preservatives, organic pollutants, drugs and even textiles also have estrogenic activity. Polyester and spandex, for example, contain high levels of estrogen-mimicking BPA.⁹ As noted by Dinkov:¹⁰

“… it looks like we are bathing 24×7 in a toxic sea of almost 1,000 chemicals with such properties (aka xenoestrogens), and given their ubiquity in food, drugs, industry, household, hospitals, and even nature it is little surprise the population of Western countries is sicker than ever.

Considering the sheer number of chemicals involved and the near impossibility of avoiding them, keeping the metabolic rate high (helps with excretion of xenoestrogens) and usage of anti-estrogenic chemicals (eg. vitamin E, progesterone, pregnenolone, aspirin, DHT, antihistamines, etc) becomes that much more important.”

The Physiological Role of Estrogen

Estrogen’s carcinogenic properties can in part be explained by its ability to increase cells’ ability to hold water. This 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,”¹¹ biologist Ray Peat¹² 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.

This is one of the greatest books in health I have ever read. Currently it is out of print and being sold by resellers for $350. I hope to connect with Ray’s widow later this year and get permission to republish his book with a new publishing company I am starting called Joy House and hope we can republish it later this year.

Peat believed that estrogen is 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 cells are sick and unable to effectively burns glucose in their mitochondria so they must shift to inefficiently burn glucose in glycolysis in the cytoplasm, 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, this is precisely what estrogen is doing.

Obesity, Especially in Women, Is Estrogen-Driven

Estrogen can also promote the accumulation of fat around the thighs, hips and buttocks through several mechanisms. For starters, it influences where fat is stored in the body. Women tend to store fat in these areas due to having higher estrogen levels than men. This pattern is often referred to as the “pear-shaped” body type.

Estrogen also promotes the differentiation and proliferation of fat cells (adipocytes) in the subcutaneous fat layer, which is particularly prevalent in the thighs, hips and buttocks and therefore leads to increased fat storage in these areas.

As mentioned, estrogen also plays a role in regulating metabolism, including glucose and lipid metabolism. Higher estrogen levels can promote the uptake and storage of fatty acids in adipose tissue, contributing to fat accumulation in the lower body.

Hormonal interactions and cellular signaling also play a role. Estrogen interacts with other hormones involved in fat metabolism, such as insulin and cortisol, and these interactions can influence fat deposition and distribution in the body, favoring storage in the lower body regions.

Bioidentical estrogens are every bit as dangerous as synthetic ones and are dangerous, in any amounts, unless they are balanced by an abundance of the natural forms of thyroid, progesterone, and DHEA.  Estrogen is a cumulative toxin, because it causes changes in every system of your body, even when present in normal amounts. These cumulative changes appear to accelerate aging in all tissues.

Estrogens are one of the primary factors contributing to increasing your cancer risk, along with the plastic burden contributing their xenoestrogens, as both decrease mitochondrial function. Progesterone is the antidote because it is not only anti-estrogen but is a potent cortisol blocker and will improve mitochondria production of cellular energy by blocking estrogen and cortisol.

Progesterone is the main female hormone, and is a protective hormone during pregnancy, but it is also important in men since it is a general brain-regulating and protective hormone. Lastly, adipose tissue contains estrogen receptors, and estrogen signaling can directly affect the function and activity of fat cells. It promotes the expression of genes involved in fat storage and inhibits genes associated with fat breakdown.

Fasting Isn’t the Answer

Contrary to popular belief, extended fasting isn’t the answer if you’re trying to reshape a pear-shaped body type.¹³ The reason for this is because chronic fasting often ends up burning more muscle than fat. As reported in the Times of India seven years ago:¹⁴

“Dr. Purwa Duggal says stubborn fat in areas such as abdomen, thighs, hips, butt, etc are linked to high estrogen. Prolonged starvation does not necessarily mean burning fat. It may initially cause muscle wasting or utilization of glycogen stores.

Catecholamines, which are fight or flight hormones produced in the body in response to stress, are required to burn fat. ‘Blood flow to stubborn fat areas is usually very poor, as a result, the catecholamines are unable to reach the area to mobilize the fat. Even if the fat is mobilized, while it continues to be in the blood stream, it may get re-deposited in the original areas,’ she adds.”

How to Lower Your Estrogen Load

One of the most important strategies aside from avoiding estrogen and xenoestrogens is to take natural progesterone. Most formulations are not effective as they are oral or transdermal. Ideally it should be dissolved in a high-quality vitamin E with MCT oil and rubbed on mucous membranes like your cheeks or gums. Typical doses are 25 to 50 mg once or twice a day.

Considering the health risks associated with estrogen excess, here are some commonsense strategies that can help you limit your exposure and lower your estrogen load: