Besides Endocrine Therapy, What Are My Options? Start With Why the Cancer Grew in the First Place

Published: October 29, 2026


Every week, the same question shows up in my comments, emails and my DMs. It comes in a hundred different versions, but it always lands in the same place.

“What do I do if I don’t want to take endocrine therapy?”

Many of them have already started the medication, felt their joints lock up, and their brain go foggy, and are wondering if this is really what the next five to ten years have to look like. And almost all of them have been told some version of the same thing: if you stop, the cancer will come back.

I want to address that question honestly. But I can’t answer it without first changing the question. Because I think the way we’ve been taught to think about breast cancer is far too small.

What Most Women Have Been Told

Here’s the story most women hear after a diagnosis of estrogen receptor-positive breast cancer:

“Your cancer is fed by estrogen.” “We need to take away the estrogen.” “There’s nothing you did, and nothing you can do, except finish treatment.” “Once you have cancer, the body can’t fix it. We have to cut it out, burn it, or block it from returning”

Cancer was never a one-hormone disease. When we shrink it down to “estrogen is the fuel,” we lose sight of everything else that went wrong, and everything else we could be doing.

Cancer Is a Checks-and-Balances Problem

Your body has an extraordinary security system built into every cell. And it doesn’t rely on one lock. It has layers.

  • Repair crews. Genes like BRCA1 and BRCA2 work with estrogen to fix damaged DNA every single day.

  • Checkpoints. Cells have “stop and check” moments before they divide. If something looks wrong, the cell pauses to repair it or dies.

  • A self-destruct button. Damaged cells are supposed to retire themselves through a process called apoptosis (programmed cell death).

  • Patrol officers. Your immune system, including natural killer cells and T cells, looks for cells that don’t belong and removes them.

  • The neighborhood. The tissue around a cell, its blood supply, oxygen, fuel, inflammation level, and hormone signals all shape what that cell does next.

Cancer researchers describe cancer as a group of abilities a cell gains, one by one, that let it slip past these safeguards: ignoring stop signals, avoiding death, hiding from the immune system, and rewiring how it uses fuel [1]. It is not one switch flipped. It is many layers failing over time.

Think of your house with a smoke detector, a sprinkler system, a fire extinguisher in the kitchen, and a fire station two blocks away. A spark doesn’t burn your house down. A spark burns your house down when the detector battery is dead, the sprinklers are clogged, and the fire truck is stuck in traffic, all at the same time.

That’s what a cancer diagnosis tells me. Not “you have too much estrogen.” It tells me that several safety layers were not keeping up.

We All Carry Abnormal Cells

This part really stuck with me when I first dug into it.

When researchers looked at autopsy studies of women who were never diagnosed with breast cancer in their lifetime, the median rate of DCIS (an early, non-invasive breast cancer) was 8.9%. That’s about 9 out of every 100 women walking around with cancer-type cells in the breast, never knowing it [2]. In normal, healthy-looking skin, scientists have found that roughly 1 in 5 to 1 in 3 cells already carry a known cancer-driver mutation [3].

So why don’t all of those turn into cancer? Because the checks and balances are working.

Immunologists describe three phases.

  • First, the immune system eliminates abnormal cells.

  • Second, when it can’t fully clear them, it holds them in a long standoff called equilibrium.

  • Third, only if the cells find a way to hide or the defenses weaken do they escape and grow [4].

In a Japanese study that followed more than 3,600 adults for 11 years, people whose natural killer cells were more active at the start had about 40% lower cancer risk than people with low activity [5].

That tells me something important. The body is not a passive bystander that cancer simply “happens to.” It is actively managing abnormal cells all the time.

The Body Can Do More Than We’ve Been Told

One of the biggest ideas I want to challenge is that once cancer starts, the body has no say in what happens next. That idea runs deep in Western medicine. And I think it’s wrong.

Researchers have documented that cancer cells can sit quietly for years in a dormant state, held in check by the immune system and the tissue around them [6]. That’s the body doing its job, even after cancer is present.

And here’s a study that doesn’t get talked about nearly enough. Norwegian researchers compared women who had three rounds of mammograms over six years with a similar group who had only one mammogram at the end. If every invasive cancer kept growing, both groups should have ended up with the same number of cancers. They didn’t. The screened group had 1,909 cancers per 100,000 women, versus 1,564 per 100,000 in the comparison group [7]. The researchers raised the possibility that some screen-detected invasive cancers naturally regress and disappear on their own [7]. That interpretation is still debated, and it does not tell any one woman that her tumor will go away. But it cracks the idea that cancer only ever moves in one direction.

There are also many people who have lived long, full lives after choosing paths their oncologist didn’t recommend. Their stories are not proof that any one approach works for everyone. They are proof that “nothing you do matters” was never the whole truth.

Estrogen Is a Regulator

This is where I struggle most with how breast cancer is treated.

Estrogen is not simply a growth signal. It’s a master regulatory hormone. It talks to your bones, brain, blood vessels, muscles, metabolism, and immune cells. And it talks to the DNA repair system itself. Estrogen receptors interact with the DNA damage response, including BRCA1-related repair pathways, in complex ways that depend on the cell and its situation [8].

Dr. Zsuzsanna Suba, a researcher whose work I follow closely, has gone further. She proposes that strong estrogen signaling helps keep DNA stable, and that weak or blocked estrogen signaling may be part of how cells lose their footing in the first place [9]. If that model is accurate, and I believe that it is, then it begs the question: what if blocking a regulator (estrogen) also blocks some of the protection it provides?

There’s even a twist from mainstream oncology itself. In women whose metastatic breast cancer had stopped responding to aromatase inhibitors, about 3 in 10 had their cancer shrink or stay stable when they were given estradiol, a form of estrogen [10]. If estrogen were only fuel, that would make no sense. It makes perfect sense if estrogen is a regulator whose effects depend on context.

Here’s the picture that I can’t shake. Blocking estrogen is like standing at the bottom of a waterfall with a bucket. You are working very hard at the very last step. Block, block, block, forever. But no one is walking upstream to ask why the riverbank gave way.

Cancer Cells Don’t Use Just One Road

Even when we completely block estrogen, cancer cells respond to other signals.

Breast cancer cells also respond to insulin, IGF-1 (insulin-like growth factor 1), and other growth factors. These signals run through internal pathways with names like PI3K/AKT/mTOR and MAPK. The pathways cross-talk constantly. When one road pathway is blocked, cancer cells can learn to rely more heavily on another one. This is one of the main ways conventional medicine explains cancer resistance to endocrine therapy [11]. (Dr. Suba has a different interpretation).

Insulin deserves special attention. In a study of 512 women with early breast cancer, those in the highest quarter of fasting insulin levels had about twice the risk of distant recurrence, and about three times the risk of death, compared with women in the lowest quarter [12].

So when we put all of our attention on one hormone, we can miss the signals that may matter just as much.

The Honest Numbers on Endocrine Therapy

I want to be fair here, because women deserve real numbers, not fear and not hype.

Endocrine therapy does lower recurrence risk at the population level. In the large pooled analysis of tamoxifen trials, about 33 out of 100 women taking tamoxifen for five years had a recurrence over 15 years, compared with about 46 out of 100 women who didn’t take it [13]. For aromatase inhibitors compared with tamoxifen, breast cancer deaths at 10 years were 12.1 out of 100 versus 14.2 out of 100 [14]. That’s about 2 fewer deaths per 100 women.

Now look at what those numbers also say. Most women in both groups did not recur. Many women recurred despite taking the drug. And the benefit is averaged across thousands of women, so it can’t tell you whether you are one of the women it helps.

Then there’s the cost. In one survey of 200 women taking an aromatase inhibitor, 47% reported new or worsening joint pain [15]. Blocking estrogen affects every cell and system in the body, not just the joints. In a study of 8,769 women, only 49% took their endocrine therapy for the full duration on schedule [16]. Women are not quitting because they’re careless. They’re quitting because they feel terrible. That should tell us something important about estrogen's importance.

You know my position. I have serious doubts about long-term estrogen blockade. I think we are asking women to give up a hormone that protects nearly every system in their body, for years, often without an honest conversation about the size of the benefit or what it costs them to live that way.

“But I Did Everything Right”

I hear this one all the time. And I believe you. You ate the salads, you went to the gym, you did “all the things” to stay healthy.

But I want to offer a gentle, bigger lens. This is not about blame. It’s about looking at your whole life as a story your body has been writing since before you were born.

  • Before birth. Women whose mothers took DES, a synthetic estrogen prescribed in pregnancy decades ago, had a higher breast cancer risk after age 40: 3.9 out of 100 versus 2.2 out of 100 in women who weren’t exposed [17]. None of those women made a “bad choice.”

  • Childhood and puberty. Nutrition, infections, stress, and chemical exposures during the years when breast tissue is forming.

  • Your reproductive years. Synthetic hormones, pregnancies or no pregnancies, breastfeeding, years of disrupted sleep.

  • Midlife. Falling hormones, rising insulin resistance, losing muscle, chronic stress, alcohol, poor sleep, and an immune system that has been working overtime for decades.

  • Random hits. Some DNA mistakes simply happen when cells copy themselves. Researchers estimate that about two-thirds of the mutations in cancers come from these random copying errors [18].

Researchers also estimate that about 42% of cancer cases in U.S. adults are linked to risk factors that can be changed [19]. So it’s both. Some hits were out of your control. Some things are in your control now.

If most of us stood back and walked through our whole life, we could all find something. A decade of terrible sleep. Years of grief or caregiving. A job that ran on cortisol and caffeine. Blood sugar that had been creeping up. That is a map. And a map is where your care begins.

If You Say No to Endocrine Therapy, You Are Saying Yes to Something Bigger

This is the part I feel most strongly about.

If you decide not to take endocrine therapy, you are not choosing to do nothing. You are choosing a different route. And that route has to be serious.

I believe that if you get diagnosed with cancer and you don’t want cancer again, you need to drastically change your life. Something went wrong with your body's checks and balances, and it's telling you. Small tweaks are not the answer. A whole-body rebuild is.

Here’s what I’d want that rebuild to include.

Muscle and movement. Muscle is an endocrine organ. When it contracts, it releases signaling proteins called myokines. In breast cancer survivors, a single session of strength training or interval training raised several of these myokines, and blood drawn right after exercise slowed breast cancer cell growth in the lab by 19% to 29% [20]. After 12 weeks of training, resting blood still slowed cancer cell growth by 22% to 25% [21]. Those are lab results, not proof of fewer recurrences. But the population data point the same way. In a study on nurses with breast cancer, walking about 3 to 5 hours per week was linked to roughly half the risk of dying from breast cancer [22]. And in a randomized trial in colon cancer, a 3-year structured exercise program lowered recurrence, new cancer, or death. At 8 years, 90 out of 100 people in the exercise group were alive, compared with 83 out of 100 in the health-education group [23].

Metabolic health. Get your fasting insulin, glucose, A1c, and body composition checked. Work on insulin sensitivity through protein, fiber, fewer refined carbs, strength training, and sleep [12]. The goal isn’t zero insulin. The goal is balance.

Food as information. Real food, enough protein to protect muscle, healthy fats, and less alcohol. Your cells are rebuilt from what you give them.

Sleep and circadian rhythm. Your repair crews do a huge part of their work at night. Darkness, consistent sleep times, and morning light all matter.

Your nervous system. Chronic stress changes immune function and blood sugar. Grief, fear, and burnout deserve real care.

Your environment. Look at what you breathe, drink, and put on your skin. Not out of fear, but out of respect for a body that’s already working hard.

Hidden infections and inflammation. Ongoing infections or inflammation deserve a real medical workup.

Hormone optimization. For many women, this is the conversation no one will have with them. Your hormones are part of your checks and balances, and deserve a clinician who will look at the full picture with you, including the risks of going without them.

A real team and real monitoring. Choosing a different route doesn’t mean going it alone. Find clinicians, including integrative and functional clinicians, who will track your labs, your imaging, and how you feel. Decide in advance what you’ll do if something changes.

What I Want Us to Start Asking

I’m not asking anyone to ignore their cancer. I’m asking us to stop ignoring the woman it grew in.

For decades, the main question has been, “How do we stop this cancer?” I want to add a second question that deserves just as much time and money: “How do we restore the checks and balances that were supposed to protect her in the first place?”

What if we spent as much effort supporting healthy cell regulation, immune surveillance, DNA repair, metabolic health, and hormone balance as we spend figuring out how to block the last step?

Women deserve that conversation. They deserve real numbers. And they deserve to be treated as a whole person, not a receptor status.

Your body is not your enemy. It has been protecting you your whole life, and it’s still trying. Partner with it. Find providers who will partner with you. And remember that you get to decide which route you take.

Want to Learn More?

References

1. Hanahan, D. (2022). Hallmarks of cancer: New dimensions. https://doi.org/10.1158/2159-8290.CD-21-1059

2. Welch, H.G., et al. (1997). Using autopsy series to estimate the disease “reservoir” for ductal carcinoma in situ of the breast: How much more breast cancer can we find? https://doi.org/10.7326/0003-4819-127-11-199712010-00014

3. Martincorena, I., et al. (2015). High burden and pervasive positive selection of somatic mutations in normal human skin. https://doi.org/10.1126/science.aaa6806

4. Dunn, G.P., et al. (2002). Cancer immunoediting: From immunosurveillance to tumor escape. https://doi.org/10.1038/ni1102-991

5. Imai, K., et al. (2000). Natural cytotoxic activity of peripheral-blood lymphocytes and cancer incidence: An 11-year follow-up study of a general population. https://doi.org/10.1016/S0140-6736(00)03231-1

6. Aguirre-Ghiso, J.A. (2007). Models, mechanisms and clinical evidence for cancer dormancy. https://doi.org/10.1038/nrc2256

7. Zahl, P.H., et al. (2008). The natural history of invasive breast cancers detected by screening mammography. https://doi.org/10.1001/archinte.168.21.2311

8. Suba Z. (2024). Estrogen Regulated Genes Compel Apoptosis in Breast Cancer Cells, Whilst Stimulate Antitumor Activity in Peritumoral Immune Cells in a Janus-Faced Manner. Current oncology (Toronto, Ont.), 31(9), 4885–4907. https://doi.org/10.3390/curroncol31090362

9. Suba, Z. (2015). DNA stabilization by the upregulation of estrogen signaling in BRCA gene mutation carriers. https://doi.org/10.2147/DDDT.S84437

10.  Ellis, M.J., et al. (2009). Lower-dose vs high-dose oral estradiol therapy of hormone receptor-positive, aromatase inhibitor-resistant advanced breast cancer: A phase 2 randomized study. https://doi.org/10.1001/jama.2009.1204

11. Osborne, C.K., et al. (2011). Mechanisms of endocrine resistance in breast cancer. https://doi.org/10.1146/annurev-med-070909-182917

12. Goodwin, P.J., et al. (2002). Fasting insulin and outcome in early-stage breast cancer: Results of a prospective cohort study. https://doi.org/10.1200/JCO.2002.20.1.42

13.  Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). (2011). Relevance of breast cancer hormone receptors and other factors to the efficacy of adjuvant tamoxifen: Patient-level meta-analysis of randomised trials. https://doi.org/10.1016/S0140-6736(11)60993-8

14.  Early Breast Cancer Trialists’ Collaborative Group (EBCTCG). (2015). Aromatase inhibitors versus tamoxifen in early breast cancer: Patient-level meta-analysis of the randomised trials. https://doi.org/10.1016/S0140-6736(15)61074-1

15. Crew, K.D., et al. (2007). Prevalence of joint symptoms in postmenopausal women taking aromatase inhibitors for early-stage breast cancer. https://doi.org/10.1200/JCO.2007.10.7573

16. Hershman, D.L., et al. (2010). Early discontinuation and nonadherence to adjuvant hormonal therapy in a cohort of 8,769 early-stage breast cancer patients. https://doi.org/10.1200/JCO.2009.25.9655

17. Hoover, R.N., et al. (2011). Adverse health outcomes in women exposed in utero to diethylstilbestrol. https://doi.org/10.1056/NEJMoa1013961

18. Tomasetti, C., et al. (2017). Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention. https://doi.org/10.1126/science.aaf9011

19. Islami, F., et al. (2018). Proportion and number of cancer cases and deaths attributable to potentially modifiable risk factors in the United States. https://doi.org/10.3322/caac.21440

20. Bettariga, F., et al. (2025). A single bout of resistance or high-intensity interval training increases anti-cancer myokines and suppresses cancer cell growth in vitro in survivors of breast cancer. https://doi.org/10.1007/s10549-025-07772-w

21. Bettariga, F., et al. (2026). Effects of resistance versus high-intensity interval training on myokines and cancer cell suppression in breast cancer survivors: A randomized trial. https://doi.org/10.1249/MSS.0000000000003848

22. Holmes, M.D., et al. (2005). Physical activity and survival after breast cancer diagnosis. https://doi.org/10.1001/jama.293.20.2479

23. Courneya, K.S., et al. (2025). Structured exercise after adjuvant chemotherapy for colon cancer. https://doi.org/10.1056/NEJMoa2502760

Disclaimer: This article is for educational and informational purposes only and is not intended to replace personalized medical advice or individualized care. It is meant to help you understand your physiology, explore evidence-based options, and make informed choices about your health and wellness. Healthcare should be a partnership, not a permission slip, and proactive care is just as essential as treatment. Use this information to engage in open, collaborative discussions with your provider or to make empowered decisions that align with your own values, goals, and comfort level. You are the ultimate authority on your body.


 
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Could There Be Another Explanation? Rethinking Estrogen, Endocrine Therapy, and Breast Cancer