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What every perimenopausal and menopausal woman needs to understand about her own biology before making this decision

  • Writer: Dr. Lena Suhaila
    Dr. Lena Suhaila
  • May 9
  • 20 min read

By Dr. Lena Suhaila, ND, FABNO


A note before we begin. This article is for women navigating perimenopause or menopause and weighing whether HRT is right for them. If you have a history of ER-positive breast cancer or are currently in treatment, this isn’t your starting point. Most of my clinical work is with women in your situation, and that conversation looks different. Please start here instead.


Whether HRT is safe doesn't have a single answer, because it depends on your own biology, your risk profile, and your history far more than on any population average. For women without a hormone-sensitive cancer history, the research doesn't support either of the loud positions, that HRT is universally dangerous or universally fine. The evidence sits in between and is highly individual: the type of hormone, the route it's delivered, the timing relative to menopause, and your personal risk factors all change the calculation. For women with a history of ER-positive breast cancer or in active treatment, systemic HRT is a different and more cautious conversation, which is why this article separates the two from the start.


For everyone else, a quick acknowledgment first. Most of the research this article draws on was conducted on white European and American women. The evidence base has real gaps, and the population averages don’t always translate cleanly across all women. Your individual picture matters more than any average.


Why I’m writing this


Because most of my clinical work is with women who have cancer, systemic HRT has never been part of my prescribing practice. For my patients, who are navigating cancer or in survivorship, the answer was usually a clear no for systemic HRT, with clinical reasons specific to their situation. I’ve used vaginal estrogen when the evidence supports it and the picture calls for it, but systemic hormone replacement has always sat outside the conversation I was having with the women I work with.


What pushed me to dig in further was my different friend groups. Women I’d known for years started navigating perimenopause and menopause and coming to me with questions that didn’t come with a clean no attached. Different population, different risk profile, no obvious answer. They kept asking. I knew what I believed in the cancer context, but for them the question was genuinely open, and I wanted to be able to give them real answers rooted in the latest research. So I went back through the literature with fresh eyes and let it tell me what it was actually saying.


Once I started, I couldn’t stop. What I found wasn’t a clean answer in either direction. There are two very loud camps in this conversation. One says HRT is dangerous and should never be touched. The other advocates for it almost universally, as though the risks don’t exist. What struck me, the deeper I went, is that both camps are missing the most important part, which is that the answer depends entirely on who you are and what your individual biology looks like.


I’m going to share what I found.


What the WHI actually showed, and what it didn’t


The Women’s Health Initiative study is the reason so many women are still afraid of HRT two decades later, and honestly, the fear makes sense given how the results were reported. But what most women were told about that study and what the study actually showed are two very different things, and that gap is worth understanding.


The WHI used a specific type of hormone therapy: conjugated equine estrogen, which is estrogen derived from horse urine, combined with a synthetic progestogen called medroxyprogesterone acetate. It studied women with an average age of 63, most of whom were more than ten years past menopause. It wasn’t studying bioidentical hormones. It wasn’t studying the transdermal patches or gels most women use today. And it wasn’t studying women in early perimenopause, which is when hormonal support appears to have the most protective effects on the brain, the heart, and the bones.


The increased breast cancer risk that came out of that study was linked specifically to the synthetic progestogen arm, not to estrogen alone. Women who had hysterectomies and used estrogen only didn’t show the same increased risk. The synthetic progestogen drove the signal.


Research since the WHI has told a different story, and most women have never heard it.


A large UK study following over 43,000 women compared different types of hormone therapy directly against women who used no hormones at all. Bioidentical estrogen alone carried essentially no increased breast cancer risk compared to never-users. Micronized progesterone combined with estrogen showed an odds ratio of 0.99 compared to never-users, which is as close to identical risk as data can show. Meanwhile, synthetic progestins showed a clear 28 percent increased risk compared to women using no hormones at all [1].


The large French E3N cohort study, which followed over 54,000 postmenopausal women over nearly a decade, found the same pattern. Women using transdermal estradiol combined with micronized progesterone had essentially the same breast cancer risk as women who never used hormones at all. Women using synthetic progestins had a 40 to 60 percent higher risk depending on how long they used them [2].


So the picture looks like this: transdermal estradiol combined with bioidentical micronized progesterone, used for up to five years, appears to carry roughly the same breast cancer risk as not taking hormones at all. Beyond five years the data becomes less clear and calls for closer monitoring. The risk signal that scared a generation of women away from HRT was driven by a specific synthetic progestogen that most women in Europe and many women worldwide were never even prescribed.


Two decades of fear, traced back to one drug combination. Bioidentical estradiol and bioidentical progesterone are a different conversation entirely. That distinction alone changes the starting point for this decision [3,4].


Your body has to process estrogen the same way it processes everything else


Estrogen doesn’t just circulate, do its job, and disappear. Once it’s done its work, your body has to break it down and eliminate it. You already know this dynamic from food. You eat something, your body takes what it needs, breaks the rest down into smaller pieces, and clears the waste. If any part of that sequence runs slowly, you feel it. Bloating, sluggishness, the heaviness of something sitting too long where it shouldn’t be.


Estrogen runs through a similar sequence, mostly in your liver and your gut. How efficiently it moves through varies enormously from one woman to the next, based on genetics, diet, stress, and the overall health of those systems. The breakdown side is one half. Elimination is the other half, and elimination is where most of the action lives for the question of whether HRT is going to support you or strain you.


After estrogen has been broken down, what’s left can take one of two routes out of the body. One route is clean and efficient. The other produces reactive byproducts that need to be cleared quickly, before they cause damage. Which route your body favors, and how fast it moves things along, is exactly what you want to understand before deciding to significantly increase the amount of estrogen flowing in.


The two routes: clean exit versus reactive byproducts


The first route is called 2-hydroxylation. When estrogen goes this way, it gets converted into a relatively harmless metabolite called 2-hydroxyestrone. When that metabolite is then properly cleared from the body, it actually has some mild protective properties. This is the route you want estrogen taking.


The second route is called 4-hydroxylation. When estrogen goes this way, it gets converted into 4-hydroxyestrone, which can be further transformed into highly reactive compounds capable of damaging DNA and creating the kind of oxidative stress that contributes to cancer development. Human breast cancer tissue produces significantly higher levels of 4-hydroxyestrone than normal breast tissue. That’s not a coincidence.


Which direction estrogen takes depends largely on an enzyme called CYP1B1. An enzyme is simply a protein your body makes to drive a specific chemical reaction, like a biological switch. CYP1B1 lives primarily in hormone-sensitive tissues like breast tissue and the liver, and its job is to process estrogen into its downstream forms. Some women have a more active version of this enzyme that pushes more estrogen down the reactive 4-hydroxy route. Women on HRT who carry that more active CYP1B1 variant may have higher breast cancer risk than other HRT users, particularly with longer-duration use [5,6]. That’s a meaningful difference, and one of the central reasons knowing your own metabolic picture before starting HRT is so important.


The frequency of these enzyme variants differs across populations, and most of the data we have on how they interact with HRT comes from studies of women of European descent. The biology itself is the same. The population-level numbers may not translate cleanly across all women. This is part of why your individual picture matters more than any group average.


The clearance side: why elimination is where most of the action lives


Once estrogen has been broken down into its metabolites, whether the safe ones or the reactive ones, they still have to leave the body. That’s where a second enzyme comes in, called COMT, short for catechol-O-methyltransferase. COMT tags the reactive metabolites for elimination so the body can excrete them. Without that tag, they linger.


The process COMT uses to clear estrogen metabolites is called methylation, one of the most fundamental processes in the body, used for everything from DNA repair to neurotransmitter clearance to detoxification. It’s a labeling system that marks things as ready to go, so the liver and gut can finish the elimination work.


Some women have a genetic variation that makes their COMT enzyme three to four times slower than average. It’s called the Met/Met variant and it’s genuinely common, so if you have it, you’re far from alone. On its own, in everyday life, a slower COMT isn’t necessarily a problem. Picture what happens when you turn the tap up significantly, which is essentially what starting HRT does to the estrogen load in your system. The drain that was keeping up fine before is suddenly running behind. Reactive estrogen metabolites sitting in breast tissue longer than they should is exactly the scenario you want to understand before making this decision.


There’s one more layer that doesn’t get talked about enough. COMT doesn’t only clear estrogen metabolites. It also clears stress hormones, specifically adrenaline and noradrenaline, through the same pathway using the same enzyme capacity. A woman who’s chronically stressed is already using a significant share of her COMT capacity on her stress hormones, leaving less available for estrogen clearance. For most women in midlife, carrying enormous loads of responsibility, caregiving, work, the grief that comes with this stage of life and the world we’re navigating it in, and often a complete absence of the kind of communal support that would traditionally have distributed some of that weight, stress reduction is doing real biochemical work on hormone clearance. It belongs in the protocol, not next to it.


A note on alcohol


If you drink regularly, it’s worth knowing that alcohol affects this whole picture in three ways. It raises estrogen production by increasing aromatase activity. It competes with estrogen for liver clearance, so the reactive metabolites we just walked through sit longer than they should. And it depletes the exact nutrients COMT needs to function, including methylfolate, B6, and B12.


This is most of why even moderate daily drinking has been linked to increased breast cancer risk. If you’re considering HRT and you drink regularly, it’s worth looking at honestly before adding more estrogen to a system that’s already working harder than it should. I’ll go deeper on the alcohol and breast cancer story in a separate piece.


Why the standard hormone blood test doesn’t tell you what you actually need to know


One of the most common things I hear from women who’ve already seen their doctor about perimenopause or menopause is: my doctor checked my hormones and everything looked normal. Or: my estrogen was low so they gave me a dose and rechecked the blood level and it looked fine.


There’s a more basic problem with that approach. Estrogen doesn’t actually move through the body the way a standard blood test assumes.


Estrogen, like all steroid hormones, is a fat-soluble molecule. Think of it like oil. And just like oil and water don’t mix, estrogen doesn’t naturally float around freely in the watery part of your blood in large amounts. To travel through the bloodstream, it needs a carrier, something water-soluble that can transport it from one place to another.


That carrier is called sex hormone binding globulin, or SHBG. Picture SHBG as a shuttle bus. It picks up estrogen molecules, loads them on board, and carries them through the bloodstream to where they need to go, including to the liver for processing and eventual clearance. While estrogen is on the bus, it’s essentially inactive. It can’t enter your cells, can’t bind to receptors, and can’t do anything biologically useful until it’s released from the carrier.


Only the estrogen that isn’t riding the bus, the free unbound estrogen, is actually available to your cells and tissues. And that fraction is tiny, somewhere between one and three percent of the total estrogen in your blood at any given moment.


When a conventional lab measures your estradiol from a blood draw, what it’s measuring is the total amount in the serum, including everything sitting on those shuttle buses going nowhere biologically useful. You’re getting a number, but that number doesn’t tell you how much estrogen is actually free and active in your tissues, which is the only part that matters.


What makes this even more complicated is that SHBG levels vary enormously between women, and they’re influenced by a whole range of factors including genetics. Some women are simply wired to produce more SHBG than others. Thyroid function, insulin levels, liver health, body composition, and chronic stress all affect it too. A woman with a lot of shuttle buses running, meaning high SHBG, might have a high total estradiol on her blood test but actually very low biologically active estrogen, because most of it’s tied up in transport. A woman with fewer shuttle buses, meaning low SHBG, might have a seemingly low total estradiol but plenty of free active hormone. The blood test alone doesn’t tell you which situation you’re in.


This is why even the highly sensitive estradiol assays that some practitioners use, while better than standard tests for detecting very low levels, still don’t give you the complete picture. You’re looking at a snapshot of total serum concentration rather than understanding what’s actually being produced, how it’s being metabolized, which routes it’s taking, and how well it’s being cleared.


The DUTCH test measures hormones and their metabolites in urine, which reflects what your body has actually processed and excreted over time rather than a single moment in the bloodstream. It shows you not just levels but patterns: how estrogen is being broken down, which metabolic routes are dominant, and how well the clearance systems are functioning. It’s the difference between a single photograph and a full film of your entire hormonal processing system over time.


For the question women actually need answered when they’re considering HRT, what’s happening with your estrogen, how it’s being processed, and how well it’s being cleared, blood testing is the wrong tool. It shows you a single moment of total serum concentration, most of which is bound to a carrier and biologically inactive. It tells you nothing about which routes your estrogen is taking, how well it’s being cleared, or whether the system is favoring the safe pathway or the reactive one. The DUTCH test was designed for this question. Blood testing wasn’t.


Who needs the most careful assessment


The woman who needs the most careful pre-HRT workup is carrying a combination of factors: higher CYP1B1 activity sending more estrogen down the reactive route, slower COMT reducing her capacity to clear what’s produced, chronic stress competing for that same clearance system, regular alcohol intake pushing every variable in the wrong direction, and then adding a significant load of exogenous estrogen through HRT on top of all of it.


None of these individually are catastrophic. Together, without awareness and without the right preparation and monitoring, they create a picture worth understanding before starting anything.


And knowing your picture gives you the ability to change it. Several of these variables are highly responsive to targeted intervention, which is exactly what the preparation protocol below addresses.


What to check before you start


The DUTCH test. The DUTCH Complete or DUTCH Plus is what I consider the most important piece of pre-HRT assessment available. It’s a urine test that shows you not just your hormone levels but your actual estrogen metabolite ratios: how much is going down the safe 2-hydroxy route versus the reactive 4-hydroxy route, how well your COMT clearance is functioning, and whether your overall estrogen processing picture is balanced. It tells you not just what’s being produced but how well the whole system is running. Get it before you start HRT, and repeat it periodically if you proceed.


Your COMT and CYP1B1 genetics. If you’ve already done 23andMe, you can access this information by downloading your raw data file and uploading it to a third-party interpretation tool like Genetic Genie or Strategene. You’re looking for rs4680 for your COMT status and rs1056836 for your CYP1B1 status.


If you haven’t done 23andMe, I’d steer you away from it at this point. The company has sold its genetic database to pharmaceutical interests, and your DNA isn’t something you want circulating in corporate hands. Better options that are privacy-conscious and clinically useful are NutritionGenome (insert your affiliate link here) and 3X4 Genetics. Both are analyzed through a practitioner, both cover COMT and CYP1B1 alongside the other relevant genetics, and both provide interpretation that’s actually actionable rather than a raw data dump.


One important distinction: your genetics tell you your predisposition. The DUTCH tells you what’s actually happening in your body right now. A woman can have slow COMT genetically and still be clearing estrogen well if her nutrition, stress load, and gut health are favorable. You want both pictures if possible. If you can only do one, the DUTCH tells you the most about where you actually stand today.


BRCA status. If you have a known or suspected BRCA1 or BRCA2 mutation, the HRT conversation changes and requires specialist input. It isn’t an automatic disqualification, particularly in the context of surgical menopause where the benefits to the heart and bones are significant, but it calls for a more careful and individualized assessment.


The foundations: gut, liver, thyroid, and body composition. Before any hormonal support, it’s worth knowing that the systems responsible for processing and eliminating estrogen are actually working. Your liver handles the initial breakdown. Your gut handles the final elimination, and a disrupted gut microbiome can actually reactivate estrogen that was already on its way out of the body and send it back into circulation. Your thyroid governs the speed of liver detoxification, so unaddressed hypothyroidism quietly slows the whole system down. Body composition matters too. Fat tissue produces estrogen after menopause through a process called aromatization, which means supporting healthy body composition is part of the hormonal picture in a very direct and practical way.


Methylation support. COMT needs specific nutrients to function: B vitamins, particularly methylfolate and methylcobalamin rather than the inactive folic acid form, along with magnesium, zinc, and B6. A woman who also carries a variant in a related gene called MTHFR, which is extremely common, may have two layers of methylation slowdown happening simultaneously. Supporting these pathways nutritionally before starting HRT is one of the most impactful things you can do to prepare your system.


The preparation protocol


This foundational work changes your estrogen metabolism picture regardless of what you ultimately decide about HRT, and it’s appropriate for any woman navigating this transition.


Eat cruciferous vegetables regularly. Broccoli, cauliflower, kale, Brussels sprouts, and cabbage contain compounds called indole-3-carbinol and DIM that gently shift estrogen metabolism toward the safer 2-hydroxy route and dampen the activity of CYP1B1. Eating them raw or lightly steamed three to four times a week is the food-based approach. DIM as a targeted supplement is the more concentrated clinical option.


Support your methylation system. Methylfolate, methylcobalamin, B6, magnesium, and zinc all support the COMT enzyme and the broader methylation pathway. If you’ve been taking standard folic acid rather than methylfolate, it’s worth making the switch, particularly if you carry the MTHFR variant.


Support gut elimination. Your gut is your final estrogen exit route. Flaxseed supports both the fiber component and healthy estrogen clearance and has been specifically studied in the context of CYP1B1 and COMT genotypes. Calcium-D-glucarate helps prevent estrogen from being reabsorbed in the gut after it’s already been cleared.


Reduce inflammation. Both the reactive CYP1B1 pathway and impaired methylation clearance are worsened by systemic inflammation. An anti-inflammatory whole food diet, good sleep, omega-3 fatty acids, and genuine stress reduction all reduce the inflammatory load that pushes estrogen down the reactive pathway.


Keep insulin low. Chronically high insulin drives aromatase activity in fat tissue, which means your body produces more estrogen from your own androgens. It also slows clearance. Lower refined carbohydrates, adequate protein, daily movement, and quality sleep are the practical levers.


If you drink, look at it honestly. I covered the mechanism above. Even moderate drinking is working against the system you’re trying to support. If you drink regularly and you’re considering HRT, this is one of the more impactful changes you can make before adding hormonal support.


Food quality matters more than most people realize. Your estrogen metabolism system is built entirely from what you eat. The enzymes, the methylation cofactors, the gut bacteria that support healthy elimination, all of it depends on the quality, diversity, and nutrient density of your food. Organic where possible, whole foods over processed, adequate protein, good fats daily. You don’t have to do this perfectly. The goal is giving your system the raw materials it needs to do the work it’s already designed to do.


If you decide HRT is right for you: what form matters


If you’ve done this groundwork, your DUTCH picture looks reasonable, and you’re within the window where HRT appears most beneficial, the form you choose makes a significant difference.


Transdermal estradiol rather than oral estrogen. The skin route bypasses the liver entirely, which means none of the downstream effects on clotting factors, and delivers estradiol, the bioidentical form your body recognizes, rather than a mixture of equine estrogens.


Bioidentical micronized progesterone rather than synthetic progestins. The data on this is now consistent across multiple large studies. If a prescriber is offering you medroxyprogesterone acetate or any other synthetic progestin, it’s a completely reasonable and informed question to ask whether micronized progesterone is available instead.


The lowest dose that achieves the effect you’re looking for. There’s no benefit to using more than you need.


Monitor. A follow-up DUTCH test six to twelve months after starting gives you an objective picture of how your estrogen metabolism is responding. This is how you stay informed rather than just hoping for the best.


If HRT isn’t right for you: what actually works


Whether you’ve assessed your picture and decided against HRT, or it’s contraindicated for you, or you simply want to try the non-hormonal path first, there’s genuinely a lot available. Several of these interventions have evidence that rivals pharmaceutical options for specific symptoms.


For hot flashes and night sweats. Black cohosh has the strongest botanical evidence base for vasomotor symptoms. What makes it particularly relevant is that it doesn’t appear to work through estrogen receptor pathways, which means it’s appropriate even for women with hormone-sensitive histories. Research has shown it doesn’t stimulate growth of estrogen-sensitive breast cancer cells the way phytoestrogens can. A 2023 meta-analysis confirmed its efficacy [7]. The standard form is a standardized extract at 20 to 40 mg twice daily. Liver enzyme monitoring is prudent with long-term use as rare cases of liver sensitivity have been reported.


A whole food plant-rich diet incorporating soy has documented effects on hot flash frequency. A randomized controlled trial showed that a low-fat plant-based diet with soy reduced moderate to severe hot flashes dramatically in some participants [8]. The response varies because it depends partly on whether your gut microbiome produces a compound called equol from soy isoflavones, and not every woman’s does.


For sleep. Magnesium glycinate or magnesium threonate at 300 to 400 mg before bed is one of the most consistently useful interventions across the entire perimenopause and menopause picture. It supports the calming neurotransmitter GABA, reduces cortisol, and improves sleep architecture. Safe, well-tolerated, and essentially no downside.


Ashwagandha, specifically the KSM-66 standardized extract, works through the stress response system and has clinical data supporting improved sleep quality, reduced cortisol, and reduced anxiety, including in perimenopausal women. A 2024 meta-analysis of randomized controlled trials further confirmed significant reductions in perceived stress, anxiety, and serum cortisol [9]. 300 to 600 mg daily is the range used in most trials.


Phosphatidylserine is particularly useful for the woman who wakes at 3am with a racing mind. That pattern often reflects a cortisol rhythm that’s shifted out of its normal range, and phosphatidylserine supports healthy cortisol patterns in a targeted way.


For mood and cognitive symptoms. Everything in the first article in this series applies here. Exercise is the single most powerful non-hormonal intervention for both mood and cognitive function and belongs in the non-negotiable category. Serotonin support through food, morning sunlight, and gut health. Dopamine support through movement, challenge, and adequate protein. Citicoline for memory and focus. Magnesium for nervous system regulation and sleep.


Rhodiola rosea in combination with black cohosh has emerging evidence for broader menopausal symptom relief, with a randomized controlled trial showing the combination superior to black cohosh alone across hot flashes, mood, and cognitive symptoms [10].


For bone health. Weight-bearing and resistance exercise is the most evidence-supported non-hormonal intervention for bone density. Adequate calcium from food rather than high-dose supplements, vitamin D3 with K2 to direct calcium to bones rather than soft tissue, and magnesium all support bone health. If bone density is a significant clinical concern, it’s worth having a frank conversation with your provider about whether the bone-protective benefits of HRT warrant reconsidering even if you’d otherwise prefer to avoid it.


For estrogen metabolism regardless of what you decide. DIM, calcium-D-glucarate, flaxseed, methylation nutrients, and cruciferous vegetables support healthier estrogen metabolism patterns whether you’re on HRT or not. This is an ongoing protocol. It matters whether your estrogen is coming from your own ovaries, from fat tissue, or from exogenous supplementation.


What this all comes down to


Perimenopause and menopause aren’t problems to be fixed. They’re a transition your body is designed to move through, and the research is clear that how you move through it, in terms of metabolic health, inflammation, body composition, sleep, stress, movement, alcohol intake, and nutritional foundations, shapes what’s on the other side.


HRT, done thoughtfully with the right preparation and the right form, is a legitimate and often deeply beneficial option for many women. Understanding your own biology before you make that decision isn’t about adding more anxiety to an already complicated moment in your life. It’s about making sure that whatever you decide, you’re deciding with the most accurate picture of your own body available to you.


Every woman navigating this transition deserves that picture, and the more your individual biology differs from the populations most of this research was conducted in, the more your individualized assessment becomes the only honest starting point.


On the other side


Perimenopause and menopause get talked about as a slow leak of who you used to be. That framing doesn’t match what the body is actually doing. Your hormones are guiding you toward a different physiology, a different cognition, and for many women, a different sense of what they’re here to do.


How you prepare shapes how you move through it. The work is tending the soil. Supporting the body in the ways I’ve described throughout this piece, and making room for the part that isn’t medical at all. The grief, the recalibration, the slow loosening of who you used to be.


When the soil is tended well, what grows on the other side can be something genuinely beautiful. The energy returns differently. The priorities settle. The quiet, steady voice within becomes harder to ignore. There’s a clarity that wasn’t available before, and a ground to stand on that holds.


This is what I want for you, whatever you decide about HRT. The kind of transition where the version of yourself who comes out the other side is one you actually want to meet.


A note on supplements and dosing


The doses listed throughout this article are the ranges used in published clinical research. They are not personalized prescriptions. Supplements, even the ones that look benign, can interact with medications, affect liver enzymes, and behave differently in different bodies. Please don’t add anything to your routine based on this article alone, particularly if you are taking other medications, have a chronic condition, or have a personal or family history of cancer. Work with a qualified naturopathic, functional, or integrative medicine practitioner who can review your full picture before you start.


This article is for educational purposes and does not constitute individualized medical advice. Please work with a qualified naturopathic or integrative medicine provider to determine what is appropriate for your specific health history, genetics, and goals.


Affiliate disclosure: The link to Nutrition Genome above is an affiliate link, which means I may receive a small commission if you purchase through it at no additional cost to you. I only recommend tests and resources I use clinically.


References


1. Suissa S, Suissa K. Hormone replacement therapy and the risk of breast cancer. Obstetrics and Gynecology. 2022.

2. Fournier A, Berrino F, Clavel-Chapelon F. Unequal risks for breast cancer associated with different hormone replacement therapies: results from the E3N cohort study. Breast Cancer Research and Treatment. 2008;107(1):103-111.

3. Cagnacci A, Venier M. The controversial history of hormone replacement therapy. Medicina. 2019;55(9):602.

4. Stute P, Marsden J, Salih N, Cagnacci A. Reappraising 21 years of the WHI study: Putting the findings in context for clinical practice. Maturitas. 2023;174:8-13.

5. Reding KW, Weiss NS, Chen C, et al. Genetic polymorphisms in phase I and phase II enzymes and breast cancer risk associated with menopausal hormone therapy in postmenopausal women. Breast Cancer Research and Treatment. 2012;132(3):939-952.

6. Cerne JZ, Pohar-Perme M, Novakovic S, Frkovic-Grazio S, Stegel V, Gersak K. Combined effect of CYP1B1, COMT, GSTP1, and MnSOD genotypes and risk of postmenopausal breast cancer. Journal of Gynecologic Oncology. 2011;22(2):110-119.

7. Sadahiro R, Matsuoka LN, Zeng B-S, et al. Black cohosh extracts in women with menopausal symptoms: an updated pairwise meta-analysis. Menopause. 2023;30(7):766-773.

8. Barnard ND, Kahleova H, Holtz DN, et al. The Women’s Study for the Alleviation of Vasomotor Symptoms (WAVS): a randomized, controlled trial of a plant-based diet and whole soybeans for postmenopausal women. Menopause. 2021;28(10):1150-1156.

9. Arumugam V, Vijayakumar V, Balakrishnan A, Bhandari R, Boopalan D, Ponnurangam R, Sankaralingam Thirupathy V, Kuppusamy M. Effects of Ashwagandha (Withania somnifera) on stress and anxiety: A systematic review and meta-analysis. Explore (NY). 2024;20:103062.

10. Pkhaladze L, Davidova N, Khomasuridze A, Shengelia R, Panossian AG. Actaea racemosa L. is more effective in combination with Rhodiola rosea L. for relief of menopausal symptoms: a randomized, double-blind, placebo-controlled study. Pharmaceuticals (Basel). 2020;13(5):102.


Dr. Lena Suhaila is a naturopathic oncologist and the founder of Naturally Well Within. To learn more about her work, visit her About page.

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