More and more young women are getting breast cancer.
“Cancer is a disease of aging… But if you’re going to get a cancer in your 30s or 40s, if you’re a woman, it’s most likely to be breast cancer.”
According to the article,
“Between 2012 and 2021, the incidence rate of breast cancer overall increased by about 1 percent each year, while the incidence rate among women under age 50 increased by about 1.4 percent each year. Patients with ‘young-onset breast cancer; — which clinicians typically define as diagnosed before the age of 40 — are more likely than older patients to have aggressive forms of the disease, said Dr. Ann Partridge, interim chair of medical oncology at the Dana-Farber Cancer Institute in Boston” (Agrawal, 2025).
In light of younger women getting cancer, the U.S. Preventive Services Task Force lowered the recommended screening age for mammograms from 50 to 40 because in May of last year.
The article mentions that researchers and physicians are “not sure what is driving” increasing rates in young women, although they do concede that estrogen may be linked: “Over time, there have been several population-level shifts that affect women’s lifetime exposure to estrogen, potentially contributing to increasing rates of breast cancer across all ages.”
Many people claim that estrogen is not the cause of cancer because estrogen is higher in younger women, and breast cancer is more likely to occur in older women (although this is changing). I think this is a misinterpretation. Progesterone, which opposes all the actions of estrogen, is also much higher in younger women. This is actually what is protecting younger women from cancer.
Unfortunately, there is a lot of confusion in research. For example, the Women’s Health Initiative, one of the largest clinical trials to study the effects of hormones on women’s health became controversial when the results linked estrogen + progestin use to increased risks of breast cancer, heart disease, and stroke, leading to a sharp decline in hormone use. (Note: progestins are synthetic hormones and their actions more closely mimic estrogen/androgens on the cell. They are not the same as natural progesterone).
But researchers argued the risks were overstated and estrogen use was widely promoted again shortly after. Now, many claim estrogen does not cause cancer at all.
There are a lot of nuances, but the truth is, when doctors stopped prescribing estrogen and synthetic progestins following the initial findings of WHI, breast cancer incidences decreased 7% from 2002-2005.
It’s important to note that the authors of the study still maintain that estrogen and progestin use contribute to cancer and have not retracted their initial findings.
That being said, I think the most important thing to consider is the mechanism of how estrogen works on cells. We need to understand the direct biological effects of estrogen rather than just whether it statistically correlates with cancer. Studies can be misinterpreted, influenced by confounding variables, or limited by study design, but mechanisms tell us the actual biochemical interactions happening in the body.
There are several carcinogenic actions of estrogen that have been well-researched. Here are just a few:
- Estrogen stimulates uncontrolled cellular proliferation
- Estrogen metabolites can damage DNA
- Estrogen deprives tissues of oxygen
- Estrogen disrupts healthy metabolic processes and mitochondrial function (oxidative phosphorylation)
- Estrogen opposes progesterone & disrupts thyroid function
- Estrogen increases prostaglandins
- Estrogen increase inflammation and disrupts immune function
- Estrogen promotes fat storage which increases its own production
Many of the factors driving breast cancer are directly related to estrogen:
- Estrogen exposure itself:
- Puberty is starting younger because of estrogens in our environment increasing overall lifetime exposure to estrogen
- Xenoestrogens
- Hormonal contraceptives
- Chemicals in personal care products, pesticides, drinking water, etc.
- Low progesterone: Progesterone is a true “anti-estrogen.” It degrades estrogen receptors and opposes all of estrogen’s actions. While estrogen tells cells to proliferate, progesterone tells cells to differentiate. It reduces inflammation, protects DNA, and directly protects against cancer. Chronically high estrogen levels oppose progesterone.
- Obesity and excess body fat: Fat cells have the ability to make, store, and secrete their own estrogen, increasing the estrogenic burden on the body.
- Hypothyroidism / thyroid deficiency: High estrogen levels suppress thyroid function, disrupting cell function & metabolism and increase prolactin levels which synergizes with estrogen.
- Vitamin D deficiency: Healthy vitamin D levels are associated with lower estrogen levels because vitamin D regulates enzymes that produce estrogen, like aromatase, which converts testosterone into estradiol. Vitamin D also supports liver function, helping to clear excess estrogen from the body.
Many of the factors driving breast cancer are directly related to estrogen:
- Late pregnancy or no pregnancy: In pregnancy, progesterone levels can get up to 10 times the level in non-pregnant women. According to the NIH, pregnancy has a lifetime protective effect, decreasing the risk of breast cancer.
- Polyunsaturated fats (like those in seed oils). These fats:
- Act as weak estrogens / can bind to estrogen receptors
- Increase the concentration and sensitivity of estrogen receptors on cells
- Increase aromatase activity—the enzyme responsible for converting testosterone to estrogen
- Maternal intake is associated with abnormal mammary development and increased breast cancer risk in offspring (PMID: 10355854)
- Poor gut health / liver health: Estrogen is processed by the liver and excreted through the digestive tract, if your liver and gut aren’t properly functioning estrogen can recirculate.
- Chronic stress: Estrogen can be considered a stress hormone, increasing in response to cellular injury or physiological stress to promote repair and new cell growth. Without sufficient progesterone to balance it, these new cells fail to differentiate properly, leaving them in a highly excitable, proliferative state. This creates a self-perpetuating feedback loop, where estrogen-driven stimulation keeps the body in a prolonged state of stress and inflammation rather than resolving the damage.
Some things to consider:
Breast tissue is extremely sensitive to hormones and we know that at least 80 percent of cancers are driven by hormones.
Estrogen is classified as a carcinogen according to the World Health Organization.
We are exposed to significantly more estrogen than any previous generation.
When a woman is diagnosed with breast cancer, the usual first step in conventional care is to put a woman on an estrogen blocker like tamoxifen. If treatment involves blocking estrogen, it must be playing a role in cancer growth or development.
Estrogen can be stored in tissues, so it’s possible to have low levels on a blood test and still have high levels of estrogen. If a woman experiences fibroids, thickened uterus, irregular bleeding, dense breast tissue, etc. it is likely she has high tissue estrogen, regardless of levels in the blood. For this reason, basing treatment off of certain symptoms can be more beneficial than blood tests. Blood is tightly regulated and it’s only a singular snapshot of what is going on in the body.
Many researchers used to argue that high doses of estrogen were safe because once the estrogen receptors on cells were saturated, any additional estrogen had no effect. We know now that this isn’t true because estrogen can act independently on the cell regardless of the receptor. Because of this, it is highly likely that estrogen is driving even ER negative breast cancers too.
DES, a synthetic estrogen prescribed to pregnant women, directly contributed to cancer in millions of their daughters (cervical, breast, etc,), yet it is almost never discussed in the context of cancer and hormone therapy.
Women can produce estrogen into older age because it is stored and made by tissues like fat cells. However, older women do not produce progesterone because ovulation stops (after ovulation, progesterone is secreted). Because of this, older women can stay in a state of estrogen dominance even during menopause. Low progesterone is likely the cause of menopausal symptoms.
Low progesterone, along with early perimenopause and menopause onset, is becoming increasingly common in younger women.
I know it can be concerning to hear that a hormone our body naturally produces can contribute to cancer, but this is a complex, nuanced issue. Estrogen does influence our health, but its effects depend on balance, metabolism, and exposure levels. Unfortunately, our exposure to estrogen today is significantly higher than in the past due to environmental toxins, endocrine disruptors, pharmaceuticals, and dietary factors that were far less common in previous generations.
Hormones work together in an intricate dance, and it’s not just about having “enough” estrogen—it’s about having the right balance with other hormones like progesterone and thyroid hormones, which regulate estrogen’s effects. Anyone who claims estrogen can’t contribute to cancer is either missing the nuance of its mechanisms or unfamiliar with how cancer develops. It’s not about estrogen being “bad,” but about how it interacts in the body.