THE HEALTH REVIVAL SHOW  ·  AUGUST 6, 2026  ·  33 MIN
Hosted by Liz Roman (@thepoopqueen) and Becca Chilczenkowski (@thehormonequeen), functional health practitioners at FitMom.

What the BRCA1 and BRCA2 genes actually do

02:42   Liz Roman: BRCA1 and BRCA2 are tumor suppressor genes. Their normal job is to repair damaged DNA and stop cells with genetic errors from replicating. From a genetics perspective I like to give people red, yellow, and green lights. If you were born clean — as Dr. Ben Lynch would put it — neither parent gave you a mutation, and you're green. One mutation puts you in the yellow: medium risk, depending on the gene. Two mutations, one from each parent, puts you in the red.

03:40   Liz Roman: If you inherit a harmful mutation in one of these genes, the repair system is weakened. That's why carriers have meaningfully higher rates of breast, ovarian, and to a lesser extent pancreatic cancer. But understand this: BRCA does not cause cancer directly. No gene does. There are genes that put us at greater risk for all kinds of things — inflammatory conditions, diabetes, Alzheimer's. What a mutation tells us is that one of the body's safeguards against cancer has been removed. Which is exactly why we want to talk about everything else — metabolic health, hormonal health, inflammatory health, and the other genes that may counteract it.

Why men with BRCA keep their organs and women don't

05:21   Liz Roman: Men can carry BRCA1 and BRCA2 as well. Male carriers have elevated prostate cancer risk, and BRCA2 carriers have elevated male breast cancer risk. But guess what? They don't take their prostate out. They don't remove their breast tissue. So we have to ask the question — why is preventative organ removal only recommended for women?

06:31   Becca Chilczenkowski: I've talked to so many people who have done it preventatively because they're afraid of developing something that likely hasn't developed and may never develop.

How common is a BRCA mutation, and does it skip generations?

06:48   Becca Chilczenkowski: The exact number of people carrying a BRCA2 mutation isn't known, because not everyone gets genetic testing — and BRCA is a specific test you have to run separately. It isn't on a standard panel. The estimate is roughly 1 in 400 people carrying a mutation in BRCA1 or BRCA2. Some groups are far more likely: about 1 in 40 people of Eastern European Jewish descent, and 1 in 250 people of Icelandic ethnicity for BRCA2.

07:25   Becca Chilczenkowski: Genes don't skip generations. Each person with a BRCA2 mutation has a 50% chance of passing it to their children, and children who didn't inherit it can't pass it on. Cancer, though, can skip generations. Some people with a BRCA2 mutation never develop cancer at all and still pass the mutation down.

Where the 72% lifetime risk number comes from — and what it hides

08:01   Becca Chilczenkowski: Risk varies by the research you're reading. Some studies put BRCA1 at about a 72% lifetime risk of breast cancer and 44% lifetime risk of ovarian cancer — but the honest range is 37% to 72%, and by study and family history it stretches from 40% to 87%. That's a higher risk over baseline. Absolutely. But 72% is the number that pops up when you Google it, and the variation underneath it is much wider than that single figure suggests.

01:16   Liz Roman: My half-sister was diagnosed with breast cancer after the age of 50. Talking it through with my doctor — had she been diagnosed before 50, they would have tested me for BRCA. Because it was after 50, they don't want to test. So how many women have it and were never tested? When you look at the risk percentages, you also have to ask how they compare against everyone who was never included.

Are we finding more breast cancer without saving more lives?

09:20   Becca Chilczenkowski: Something worth understanding: of the people who find out they carry the mutation and then enter surveillance, around 97% are caught at stage zero to stage one — a very minimal amount of cancer present. And when autopsies are done on people who died of unrelated disease, they routinely find cancerous cells in breast tissue that never developed into cancer. So are we simply scanning more and therefore finding more? Or is the risk genuinely climbing?

10:19   Becca Chilczenkowski: We are testing more, we are finding more, and we still have the same number of deaths. We are not preventing deaths by doing more scanning — which is a really big pill to swallow. Is it actually a good thing that we're identifying all of this, and then people are going through radiation, and the stress of a cancer diagnosis, and the removal of organs? Or are we potentially doing this when it isn't necessary? That's an opinion, not a fact. But the facts lean toward a lot more identification without better results from it. Dr. Jen Simmons — an oncologist who moved into functional, holistic breast cancer care — puts it as a much larger identification of breast cancer with no better outcomes.

Everyone has cancer cells: autophagy, apoptosis, and the terrain

12:18   Liz Roman: All of us have cancer cells at all times. The body runs autophagy to clean things up, then cell death — apoptosis. Which is why how you're living, how you're eating, and what your metabolic health looks like matters so much. Are you getting into states of autophagy? Are you giving your body time to get there?

13:15   Liz Roman: Cancer development is not purely genetic and not purely hormonal. It's the interaction of genetic vulnerability with the metabolic and inflammatory terrain. BRCA removes a safeguard. Metabolic dysfunction is one of the things that safeguard would otherwise have been protecting against. Metabolic dysfunction is a major, underappreciated driver that compounds genetic and hormonal risk — it is not a replacement for either.

The labs FitMom runs before anyone discusses surgery

14:04   Liz Roman: We refer people out for screenings all the time — we are not against that. But we want to look at risk factors and what work could be done before anybody gets fear-mongered into removing their breasts and ovaries.

14:26   Liz Roman: Fasting insulin and fasting glucose. Insulin rises a lot faster than blood glucose or A1C. And in the presence of iron anemia you'll get a falsely elevated A1C, so you have to read the whole picture. I did a lab review recently with a woman who'd been terrified over an A1C of 5.7 — not where we want it, but she also has Hashimoto's, a positive ANA, chronic anemia her whole life, low iodine, and no gallbladder. Her fasting insulin was great. Before you panic over one number, get a comprehensive review.

15:54   Liz Roman: hsCRP and sedimentation rate — what inflammation is actually doing in the body. Visceral fat and body composition — where you're storing fat tells you a great deal about whether you're insulin resistant or estrogen dominant.

16:34   Liz Roman: Estrogen metabolite pathways. Anyone with a history of breast cancer, considering HRT or already on it — we run a DUTCH test. I want to see the pathways: 2-OH, the safe protective pathway; 4-OH, the more DNA-damaging pathway; 16-OH, the pro-inflammatory growth pathway.

17:07   Liz Roman: Vitamin D — and this is not just a vitamin, it's a hormone. It plays an integral role in immunity and detoxification, regulating liver enzymes like cytochrome P450 that process environmental toxins. Do the plastics, the BPAs, the estrogen-mimicking chemicals in our water, haircare and skincare have anything to do with overloading the system and worsening risk in a BRCA carrier? Absolutely. We want to see you around 70 to 80, especially with autoimmunity or no gallbladder. Take it with fat, and get outside — you synthesize it largely through your eyes, so take the sunglasses off on a morning walk.

19:20   Liz Roman: Sleep quality, stress, and cortisol patterns. In a state of chronic stress, everything goes haywire.

Fasting, ketosis, and metabolic pressure on cancer cells

19:38   Liz Roman: Cancer cells, including many breast cancer cell lines, rely heavily on insulin and IGF-1 signaling for growth. Lowering circulating insulin and IGF-1 through fasting protocols is a well-studied mechanism for slowing proliferative signaling. Valter Longo's research on fasting-mimicking diets shows multi-system regeneration and improved healthspan markers, and his differential stress resistance work found that fasting can sensitize cancer cells to chemotherapy while protecting normal cells.

21:07   Liz Roman: An oncologist I've worked with will use fat fasting for patients who can't tolerate a water fast — bulletproof coffee, heavy cream, oils, seeds, nuts — anything that holds a ketogenic state. The problem is most people never get there, because they never stick it out long enough. When you go into deeper fasting and autophagy it's a bit like chemotherapy — God's chemotherapy, when you're really dysfunctional. Expect keto flu. But on the other side of that switch, people report dramatically better cognition and energy, and we see ketones come up. That's when we know metabolic flexibility is back.

Screening: MRI, mammography, and the DCIS overdiagnosis problem

22:32   Becca Chilczenkowski: With the BRCA gene, the standard recommendation is an annual mammogram alternating with a breast MRI every six months, starting mid-20s to early 30s. MRI specifically because it's more sensitive to dense, higher-risk breast tissue — and dense tissue does increase risk in a lot of cases.

22:58   Becca Chilczenkowski: But there's a critique here. Autopsy studies find occult DCIS — ductal carcinoma in situ, a non-invasive, pre-invasive lesion — in roughly 9% to 20% of women who died of unrelated causes, meaning it was present and never caused a problem in their lifetime. Modeling research estimates DCIS overdiagnosis at roughly 20% of all diagnosed cases, with one estimate suggesting around 40,000 women a year in the US are treated for a level of breast cancer that may never have progressed into invasive disease. Forty thousand women going through the stress of a diagnosis and treatment for something that would never have affected their life. Some lesions found on screening would never have become dangerous — and we don't have a great way of telling which in advance. That's the challenge.

24:30   Becca Chilczenkowski: This is where thermography is an option. Thermography does not replace a mammogram — the FDA is very clear in warning against that. But it's a powerful screening tool and a complement to traditional screening: no radiation exposure, no painful compression, 3D imaging, and more effective in dense breast tissue. It runs about $700 out of pocket, which for once a year is very reasonable.

Tamoxifen: the real benefit and the costs nobody itemizes

25:19   Becca Chilczenkowski: Tamoxifen and aromatase inhibitors are standard care post-breast cancer. They provide a substantial reduction in recurrence and mortality in estrogen receptor-positive breast cancer compared to no endocrine therapy — that's well established. What's important to understand is that once you come off, you don't maintain that same reduction; there's a smaller residual benefit, around a 3.7% absolute reduction in recurrence and 2.8% in mortality after the five to ten years they require.

26:14   Becca Chilczenkowski: Around 44% of women discontinue it early because of how awful it is on the body. You are eradicating your estrogen on this — not lowering it, eradicating it. A lot of women can tell you exactly what that feels like, and it's a very low quality of life.

26:47   Becca Chilczenkowski: Something else to understand: tamoxifen acts like an estrogen in the uterus. That's about two to three times higher risk of endometrial cancer for women who take it — which I feel like they probably don't tell people when they go on it.

27:19   Liz Roman: And the other effects aren't talked about either. We've seen it with clients and with family members. Osteoporosis and accelerated bone loss, typically 2–4% per year in early treatment, with higher fracture risk at the hip, wrist and spine. Hair thinning and female pattern hair loss. Insulin resistance and weight loss resistance. Hypothyroidism — I've seen it show up six months to a year in. Fatty liver and rising liver enzymes. Joint pain and stiffness, which is why 30–50% of women stop treatment. Muscle aches and reduced exercise tolerance. Vaginal dryness, pain with intercourse, reduced libido, difficulty with arousal. Incontinence, urgency, recurrent UTIs. Increased abdominal fat and fat redistribution. Brain fog, difficulty concentrating, memory changes, depression, irritability, anxiety. If you're going on this for five years, these are the things you'd want to actively counter — and that's a conversation to have with a provider who understands it.

HRT after a BRCA diagnosis or prophylactic surgery

30:12   Liz Roman: The research on HRT and the BRCA gene finds that HRT use after risk-reducing oophorectomy does not appear to increase breast cancer risk in the short to medium term, and it has real documented benefit for quality of life, bone density, and cardiovascular health — offsetting the harms of early surgical menopause. One study did find a tripled breast cancer risk in carriers starting HRT after age 45, which suggests timing of initiation matters, and long-term safety data is still limited.

31:44   Becca Chilczenkowski: What we don't have research on is the metabolic health of these BRCA carriers on HRT. There's no research separating metabolically healthy people from metabolically unhealthy people and asking how HRT performs in those bodies — which is exactly why we're so adamant about getting labs done before starting.

Why this is a metabolic problem before it is a hormonal one

32:16   Becca Chilczenkowski: "You carry BRCA, so you can never take hormones again" is total fear-mongering. It isn't true. HRT taken properly in the right environment is actually protective against cancer — which is why most breast cancer diagnoses land at and after menopause. If hormones were the problem, we'd all be getting breast cancer while pregnant, when hormones are highest. It is not a hormonal problem. It is a metabolic problem. It is an inflammatory problem. Genetics play a role, but it is so much bigger than that.

33:00   Becca Chilczenkowski: If I knew I carried the BRCA gene and breast cancer ran in my family, removing everything surgically is not what I would be doing. I'd be optimizing my health as much as possible — detoxification pathways, gut, metabolic health — to be preventative, and maybe screening every few years to make sure nothing was progressing. There is so much in your control. Don't let people fear-monger you. Take the information, let it empower you, and make the decisions that feel right for you.

Frequently asked questions

Does having the BRCA gene mean I will definitely get breast cancer?

No. A BRCA mutation raises risk; it does not guarantee disease. BRCA1 and BRCA2 are tumor suppressor genes whose job is repairing damaged DNA, and a mutation weakens that repair system rather than causing cancer directly. FitMom's practitioners note that some carriers never develop cancer at all and still pass the mutation on, because metabolic, inflammatory and hormonal terrain determines whether the missing safeguard ever matters.

Why do men with the BRCA gene not have their prostate removed?

Men carry BRCA1 and BRCA2 mutations at the same rate women do, and male carriers have elevated prostate cancer risk — BRCA2 carriers also have elevated male breast cancer risk. As FitMom's Liz Roman points out, no clinical guideline recommends prophylactic prostate removal for these men. Preventative organ removal is recommended almost exclusively to women carrying the same mutation.

How accurate is the 72% BRCA breast cancer risk number?

The widely quoted 72% lifetime breast cancer risk for BRCA1 carriers is the top of a range, not a fixed figure. Published estimates vary from roughly 37% to 87% depending on the study population and family history. FitMom's practitioners note that these figures are drawn only from women who were tested — and because BRCA testing is rarely offered to women diagnosed after age 50, the denominator is incomplete.

Can I take HRT if I have the BRCA gene or a history of breast cancer?

Carrying a BRCA mutation does not permanently disqualify a woman from hormone replacement therapy. FitMom's Becca Chilczenkowski notes that most breast cancer diagnoses occur at and after menopause, when estrogen is at its lowest — not during pregnancy, when it peaks. Research on HRT after risk-reducing oophorectomy has not shown increased breast cancer risk in the short to medium term.

What are the side effects of tamoxifen that doctors don't tell you about?

Tamoxifen blocks estrogen in breast tissue but acts like estrogen in the uterus, which raises endometrial cancer risk roughly two to threefold. FitMom's practitioners also see osteoporosis, insulin resistance, hypothyroidism, fatty liver, and joint pain in women on it. Roughly 44% of women discontinue tamoxifen before completing the prescribed five to ten years.

Does more breast cancer screening actually save lives?

Increased screening has produced more diagnoses without a corresponding drop in deaths. As discussed on The Health Revival Show, we are testing more and finding more while mortality stays flat, a pattern functional breast oncologist Dr. Jen Simmons describes as far greater identification of breast cancer with no better outcomes. Screening still has a role, but detection alone is not the same as prevention.

What is DCIS and can it be overdiagnosed?

Autopsy studies find occult DCIS — a non-invasive breast lesion — in roughly 9% to 20% of women who died of unrelated causes, meaning it was present and never caused harm. Modeling research estimates about 20% of diagnosed DCIS is overdiagnosis, with one estimate suggesting around 40,000 US women a year are treated for lesions that would never have become invasive.

What lab tests should I run if I carry the BRCA gene?

FitMom runs fasting insulin and fasting glucose, hsCRP and sedimentation rate, body composition and visceral fat, estrogen metabolite pathways via a DUTCH test (2-OH, 4-OH and 16-OH), vitamin D targeted around 70 to 80, and cortisol and sleep patterns. The goal is establishing the metabolic and inflammatory terrain a mutation is operating in before any surgical decision is discussed.

Is thermography a real alternative to a mammogram?

No — thermography complements mammography rather than replacing it, and the FDA warns specifically against treating it as a substitute. FitMom's practitioners consider it a useful additional screening tool because it involves no radiation and no compression, uses 3D imaging, and performs better in dense breast tissue. It typically costs around $700 out of pocket per year.

If I have the BRCA gene, do I have to remove my breasts and ovaries?

No. FitMom's practitioners treat a BRCA mutation as one missing safeguard, not a diagnosis. BRCA1 and BRCA2 are tumor suppressor genes that repair damaged DNA; a mutation weakens that repair system but does not cause cancer directly. Lifetime breast cancer risk estimates range from roughly 37% to 87% depending on the study, and metabolic health, inflammation, and estrogen detoxification meaningfully change where a carrier lands in that range.

Key terms from this episode

BRCA1 / BRCA2

Tumor suppressor genes whose normal job is repairing damaged DNA and stopping cells with genetic errors from replicating. A harmful mutation weakens that repair system.

Tumor suppressor gene

A gene that acts as a brake on abnormal cell growth. When it is mutated, the brake works less well — but the brake failing is not the same thing as the accelerator being pressed.

Autophagy

The body's cellular clean-up process, in which damaged components are broken down and recycled. Reached through fasting states and supported by metabolic flexibility.

Apoptosis

Programmed cell death — the orderly self-destruction of damaged or unneeded cells, including cells with genetic errors.

DCIS (ductal carcinoma in situ)

A non-invasive, pre-invasive breast lesion. Found in roughly 9–20% of autopsies of women who died of unrelated causes, meaning it frequently never progresses.

Overdiagnosis

The detection and treatment of a lesion that would never have caused symptoms or death. Modeling estimates place this at roughly 20% of diagnosed DCIS cases.

DUTCH test

A dried urine hormone panel that maps estrogen metabolite pathways — 2-OH (protective), 4-OH (DNA-damaging), and 16-OH (pro-inflammatory, growth-promoting).

Estrogen dominance

A pattern in which estrogen activity is high relative to progesterone and to the body's ability to clear estrogen metabolites through the liver and gut.

Fasting insulin

A marker of metabolic health that rises well before fasting glucose or A1C. Cancer cells, including many breast cancer cell lines, rely heavily on insulin and IGF-1 signaling.

IGF-1

Insulin-like growth factor 1, a growth-signaling hormone. Lowering circulating insulin and IGF-1 through fasting is a studied mechanism for slowing proliferative signaling.

hsCRP

High-sensitivity C-reactive protein, a blood marker of systemic inflammation.

Tamoxifen

An endocrine therapy that blocks estrogen in breast tissue while acting like estrogen in the uterus. Reduces recurrence in ER-positive breast cancer; raises endometrial cancer risk two to threefold.

Aromatase inhibitor

A class of drug that suppresses the body's production of estrogen, used as standard endocrine therapy alongside or instead of tamoxifen.

Oophorectomy

Surgical removal of the ovaries. When performed to lower cancer risk it is called a risk-reducing or prophylactic oophorectomy, and it induces surgical menopause.

Thermography

A radiation-free, compression-free 3D imaging screening tool. A complement to mammography, not an FDA-sanctioned replacement for it.

Metabolic flexibility

The body's ability to switch efficiently between burning glucose and burning fat or ketones for fuel.

Sources and further reading

• Dr. Jen Simmons — functional breast oncologist; screening and overdiagnosis critique referenced throughout.
• National Cancer Institute — BRCA gene mutations fact sheet — prevalence and lifetime risk estimates.
• USPSTF — BRCA-related cancer risk assessment and genetic testing — testing criteria referenced in the family-history discussion.
• Dr. Valter Longo — fasting-mimicking diet and differential stress resistance research.
• Cancer as a Metabolic Disease — Dr. Thomas Seyfried.
• Dirty Genes — Dr. Ben Lynch; the red / yellow / green mutation framing.

This episode is educational and reflects the clinical opinions of the hosts. It is not medical advice and does not replace a conversation with your own provider. Bring it to them.