Fibroids in Perimenopause: Why They Grow and What Drives Yours

You were told you have fibroids, and then you were told what usually follows: they’re common, they’re benign, we’ll keep an eye on them. Maybe you were offered the pill for the bleeding, or surgery if they grow. What you weren’t told is why they’re there, or why yours might be growing faster than someone else’s.

Fibroids grow under oestrogen, and early perimenopause is when oestrogen is least held in check. The phase itself sets up the conditions.

The perimenopause backdrop: oestrogen running unopposed

Fibroids are oestrogen-dependent — benign growths in the uterine muscle, dense with oestrogen receptors, that feed on oestrogen. Early perimenopause hands them the ideal conditions.

Here’s why. Your ovaries start skipping ovulation — anovulatory cycles, months where no egg is released. No ovulation means no corpus luteum, and no corpus luteum means little or no progesterone. Progesterone is what balances and opposes oestrogen, so as it crashes, oestrogen runs unopposed — and in this phase it also swings to high, erratic peaks. This is the Progesterone Shift: oestrogen dominance, oestrogen high and unchecked relative to progesterone. [More on early perimenopause and the Progesterone Shift →]

Oestrogen is measurably higher in perimenopausal women, not lower — one of the most misunderstood facts of this transition. That’s the environment fibroids grow in.

Why fibroids actually form: oestrogen plus oxidative stress

Oestrogen is the fuel, but the spark is oxidative stress. Nearly 70% of fibroids carry a mutation in the MED12 gene, and that mutation is set off by high oxidative stress in the uterus — the mutated cells then overproduce collagen, the stiff fibrous mass that defines a fibroid.

This is the unifying idea, and it makes the long risk-factor lists make sense: almost every fibroid risk factor works by doing one of two things — raising oestrogen, or raising oxidative stress. Often both. Read a detailed analysis here.

COMT and fibroids: a two-phase story

The COMT enzyme (catechol-O-methyltransferase) is one of the main routes your body uses to clear used oestrogen — and its genetic speed is tied to fibroids in a way that looks contradictory until you separate starting a fibroid from growing one. The research points to two different genotypes driving two different phases.

Fast COMT — initiation. Oestrogen is broken down into intermediate catechol oestrogens (2-hydroxy and 4-hydroxy). A fast enzyme pumps these intermediates out rapidly — and if they aren’t methylated and neutralised quickly enough, they oxidise into reactive quinones that bind DNA and mutate the muscle stem cells of the uterine wall. That genotoxic hit is what sparks new fibroid clones, which is why the high-activity Val/Val (fast) genotype is linked to developing fibroids in the first place, and to developing several of them.

Slow COMT — growth. Once a fibroid clone exists, its growth runs on oestrogen. A slow enzyme leaves active oestrogen circulating in the blood and uterine tissue far longer, so the local environment stays oestrogen-dominant — continuous fuel that stimulates smooth-muscle proliferation and matrix deposition, ballooning a small fibroid into a large, symptomatic mass. This is the slow-clearance route, and it’s amplified by perimenopause’s unopposed oestrogen (the Progesterone Shift) and by two other clearance systems: the gut estrobolome, where beta-glucuronidase reactivates oestrogen the liver had packaged for disposal, and the liver itself, slowed by alcohol, a heavy processed-food load, and nutrient gaps.

So it’s not one variant or the other — Fast tends to initiate, Slow tends to grow. That distinction matters, because it’s exactly what determines which support approach fits you (below). Slow COMT also clears adrenaline slowly, so it tends to travel with unprovoked anxiety — if your fibroids arrive alongside that nervous-system overwhelm, the slow-clearance picture is likely part of yours. [More on the COMT gene in perimenopause →]

Early warning signs

Fibroid symptoms overlap with a lot else — ovulatory dysfunction, endometriosis, endometrial polyps — so many women never connect them to fibroids and go undiagnosed for a long time. Others have fibroids with no symptoms at all. Small ones often stay silent and don’t affect daily life. Larger ones tend to announce themselves:

• Heavy bleeding — heavy periods, large clots, and bleeding between cycles are the most common sign, and a frequent cause of iron deficiency and anaemia, with the ongoing tiredness and weakness that follow.
• Pelvic pressure, pain, or low back pain — often an early sign; the pain can be sharp, or like menstrual cramps but worse.
• A full, heavy abdomen — as fibroids grow and take up space in the uterus and pelvis, you can feel full, as though after a large meal.
• Needing to urinate more often — a fibroid large enough to press on the bladder. Rarely, one obstructs the ureter, which needs treatment if it progresses.
• Pain during sex — from the same abdominal fullness. Not everyone feels it, but pain with intercourse is worth getting evaluated.
• Bowel symptoms — constipation or a recurrent urge to empty the bowels.
• Sudden, severe pelvic pain — rare, but urgent: it can mean a fibroid has outgrown its blood supply and started to break down. Seek medical care straight away for sharp pelvic pain that comes on fast, or severe vaginal bleeding.

Fibroids can also affect fertility and pregnancy, so if you’re trying to conceive, they’re worth evaluating even without symptoms.

What raises your fibroid risk

These are the drivers that matter most in perimenopause — each works by raising oestrogen, oxidative stress, or both:

• The oestrogen dominance of perimenopause itself — the backdrop above
• Sugar and insulin resistance — insulin drives aromatase, the enzyme that makes oestrogen; fibroids express roughly three times the aromatase of surrounding tissue
• Excess body fat, especially visceral — fat tissue produces oestrone (a strong oestrogen) and inflammatory signals, and lowers the SHBG that would otherwise bind circulating oestrogen
• Alcohol — raises oestrogen; consistent drinkers carry a notably higher fibroid risk
• Gut dysbiosis — recirculates oestrogen through the estrobolome
• Slow COMT and MTHFR gene variants — slow oestrogen clearance and reduce the antioxidant capacity that would otherwise limit oxidative stress
• Low vitamin D — see below
• Some HRT combinations — certain oestrogen–progestin combinations can drive fibroid growth; one to monitor with your clinician

Devices, infections, and everyday exposures

Some drivers sit outside diet and hormones, but matter enough to name.

The copper coil. Copper IUDs raise copper while lowering zinc and iron — and low zinc is linked to the heavy bleeding, and then the anaemia, common among coil users. They also set off local inflammation (IL-1, IL-6, TNF-α) of the kind tied to fibroid growth, and copper builds up in the body over time. Because oestrogen increases copper absorption, and copper excess is itself linked to oestrogen dominance, heavy and painful periods, and anxiety, a copper coil can feed the exact loop that drives fibroids. One review suggested limiting copper IUD use to two years to reduce oxidative damage. (A conversation for you and your clinician — not a directive to remove anything.)

Pelvic infection. Fibroids are associated with chlamydia and pelvic inflammatory disease, and the risk rises around fivefold when infection occurs alongside a copper coil.

The vaginal and cervical microbiome. Women with fibroids show raised Firmicutes bacteria in the cervical and vaginal microbiome — the same shift associated with obesity.

Phthalates and plastics. Phthalates — in food packaging, cosmetics, and hundreds of household products — are linked to fibroids. DEHP, the phthalate that makes plastics flexible, directly enhances MED12 and drives fibroid growth. The exposure can even cross generations: endocrine-disrupting chemicals encountered in the womb raise a daughter’s later fibroid risk. This is a reducible exposure — glass over plastic, fragrance-free where you can, fewer processed-and-packaged foods.

This is a summary. The full, referenced risk map — including prolactin, hypertension, and iodine — is on the complete clinical reference →.

Why Black women are hit harder

Black women are diagnosed with fibroids roughly three times as often as white women, develop them earlier, and tend to have larger, more numerous fibroids with more severe symptoms.

Some of this is genetic, and it maps onto the two-phase model. The fast (Val/Val) COMT genotype — the one linked to fibroid initiation, through the genotoxic metabolites that spark new clones — is markedly more common in Black women: in Al-Hendy’s work it was present in around 47%, compared with 30% of Hispanic and 19% of white women. A genotype tilted toward initiation, in a population also facing the exposures below, is a plausible part of why fibroids start earlier and in greater number.

Part of it is biology meeting geography. Melanin is a natural sunscreen — protective against the sun, but it also blocks the UVB your skin needs to make vitamin D. Around 80% of Black American women are vitamin D deficient, and vitamin D acts directly on fibroid tissue (below). It’s a preventable risk factor.

The rest is structural, and it isn’t the woman’s doing either: higher chronic-stress load, greater environmental-contaminant exposure, chemical hair relaxers linked to increased risk, and a healthcare system more likely to dismiss symptoms, delay diagnosis, and delay referral. The disparity sits in genetics, exposures, and access — not in the women.

Vitamin D: the standout lever

Vitamin D is the clearest single intervention here. Every study in one systematic review found vitamin D deficiency in women with fibroids; deficiency raises fibroid risk by around a third, and supplementation has been shown to slow fibroid growth — partly by reducing COMT activity and partly by restoring the DNA-repair systems that keep oxidative damage in check.

Test your 25(OH)D rather than guessing, then correct a deficiency into a healthy range under guidance. This is the one lever that acts on the growth itself, and it’s the same nutrient that addresses much of the disparity above.

Tests that show what’s driving it

• DUTCH urine test — shows not just your oestrogen level but how you metabolise it (the Phase 1 and Phase 2 pathways), so clearance problems become visible
• Vitamin D (25(OH)D) — the lever above
• Ferritin and iron — heavy bleeding depletes iron, and low iron worsens the bleeding
• Luteal progesterone / progesterone-to-oestradiol ratio — confirms the oestrogen dominance driving growth

The full testing panel is on the complete clinical reference →.

The approach: match the support to the phase

Because Fast COMT tends to initiate fibroids and Slow COMT tends to grow them, the most useful support isn’t one-size-fits-all — it follows your phase. Some foundations serve everyone; the rest splits by variant.

Shared foundations (whatever your COMT):

• A hormone-balancing diet — lower-glycaemic and lower-inflammatory: steady blood sugar, reduce alcohol, and test for gluten sensitivity if oestrogen is high (gluten can slow a key oestrogen-clearing enzyme)
• Correct vitamin D — the one lever that acts on fibroid tissue directly, anti-fibrotic and anti-inflammatory
• Reduce xenoestrogens — the phthalates, plastics, and synthetic fragrances that add to the total oestrogen load

If you run Fast COMT — the goal is to block initiation

The risk here is genotoxic quinones sparking new fibroid clones, so the work is to neutralise them and stop proliferation:

• N-acetylcysteine (NAC) — an antioxidant that reduces reactive catechol-oestrogen quinones back to safe forms, shielding the uterine stem cells from the mutation that starts a fibroid
• EGCG (green tea extract) — for Fast COMT this one is useful. In a placebo-controlled trial, concentrated green tea extract reduced fibroid volume by around a third and eased symptoms, and the effect is mediated through COMT: EGCG slows the hyper-reactive enzyme and downregulates the growth factors fibroid cells use to multiply
• Vitamin D — as above, halting the collagen matrix that gives a fibroid its structure

If you run Slow COMT — the goal is to speed clearance

Here oestrogen lingers and feeds existing fibroids, so the work is to move it out faster — without stalling an already-slow enzyme:

• Magnesium — the cofactor COMT depends on; low magnesium drops its speed further
• DIM, I3C, or sulforaphane (from cruciferous vegetables) — shift liver detoxification down the safer 2-hydroxy pathway rather than the proliferative 4-hydroxy one
• Calcium-D-glucarate — blocks the gut enzyme beta-glucuronidase, so oestrogen the liver has packaged for disposal isn’t reactivated and reabsorbed
• Vitex (chasteberry) — to support the progesterone-to-oestrogen ratio
• A caution on green tea: high-dose EGCG inhibits COMT — helpful for a fast enzyme, but for Slow COMT it stalls an already-sluggish system, worsening the backlog of oestrogen and stress hormones (more anxiety, worse dominance). This is the piece that makes generic “drink green tea for fibroids” advice wrong for exactly the slow-clearance women it’s often aimed at. A cup or two of brewed tea is a gentler matter than concentrated extract; extract also carries its own cautions (tannins block iron absorption, which matters if you’re bleeding heavily). [More on the COMT gene in perimenopause →]

In practice I I do a three-month trial, then reassess symptoms and fibroid size, and continue in three-month blocks while monitoring. If symptoms recur or fibroids grow, more direct medical measures come back onto the table.

Work with me

If you have fibroids and want to understand what’s driving yours — the oestrogen picture, your clearance pathways, your vitamin D — that’s exactly what I map with women in perimenopause. The discovery call is free, 30 minutes, no obligation. Let’s have that conversation.

Book a discovery call →

References

1. Al-Hendy A, Salama SA. Catechol-O-methyltransferase polymorphism is associated with increased uterine leiomyoma risk in different ethnic groups. J Soc Gynecol Investig. 2006;13(2):136–144. DOI — the high-activity Val/Val (fast) genotype carried 2.5× the fibroid risk; Val/Val cells showed enhanced oestrogen-driven proliferation, and COMT inhibitors induced apoptosis. (Fast → initiation.)
2. Dzhemlikhanova L, et al. Catechol-O-methyltransferase Val158Met polymorphism is associated with increased risk of multiple uterine leiomyomas. J Clin Pathol. 2016;70(3):233–236. DOI — Val/Val (fast) linked to multiple fibroids. (Fast → number.)
3. de Oliveira E, et al. The catechol-O-methyltransferase (COMT) gene polymorphism and prevalence of uterine fibroids. Maturitas. 2008;60(3–4):235–238. DOI — the low-activity (Met/slow) allele was associated with large fibroids. (Slow → growth.)
4. Shen Y, et al. Role of single nucleotide polymorphisms in estrogen-metabolizing enzymes and susceptibility to uterine leiomyoma in Han Chinese. J Obstet Gynaecol Res. 2014;40(4):1077–1084. DOI — COMT Val158Met a risk factor for fibroids.
5. Zhang D, Rajaratnam V, Al-Hendy O, Halder S, Al-Hendy A. Green tea extract inhibition of human leiomyoma cell proliferation is mediated via catechol-O-methyltransferase. Gynecol Obstet Invest. 2014;78(2):109–118. — EGCG’s anti-fibroid effect acts through COMT.
6. Roshdy E, et al. (Al-Hendy A). Treatment of symptomatic uterine fibroids with green tea extract: a pilot randomized controlled clinical study. Int J Womens Health. 2013;5:477–486. DOI — concentrated green tea extract reduced fibroid volume by roughly a third and eased symptoms.