I receive a fair number of emails asking me to post about hormone replacement therapy (HRT) for women. Frankly, I’ve been avoiding it, for two reasons. First, I don’t see many patients for this issue. While some Endocrinologists do, I find that most peri- or postmenopausal women in my region discuss HRT with their Gynecologist, primary care provider, or naturopath. While I do follow the medical literature regarding HRT, opportunities for me to prescribe it come few and far between.
Second, I tend to write about things that have not been beat to death elsewhere on the internet – at least not beat in exactly the same way that I would cover it. There is already plenty of excellent debunkery to counteract the quackery about HRT.
So why am I writing about HRT now, and – more importantly – why should you give credence to anything I say, given my lack of clinical experience in this arena? I decided to write this post because, despite all the good information out there, you either: aren’t finding it, aren’t sure whom to believe, or you simply want my opinion because I’m the “most trusted endocrinologic source on the internetTM.”*
I also figure that, if Alternative Medicine can publish the copious nonsense that ruins the signal-to-noise ratio on the internet, then it’s probably okay for me to point out fallacies and offer better advice when I think I have it. But, because I value the trust you have placed in me, I did go one step further. I discussed every aspect of this post with one of my closest friends, who is a well-respected Obstetrician/Gynecologist of nearly 20 years. As good as I may be at dissecting medical literature, that should be used as an adjunct to clinical experience – not a substitute.
In the interest of full disclosure, which I know you don’t get at most Alt Med sites, you should take this post with a grain of salt. This post is based on my interpretation of the medical literature and my relationship with one OB/GYN specialist. I am using this trusted friend as a proxy for how most mainstream Gynecologists practice. She has won just about every type of award out there over the years – best teacher at a medical school, top doctor among her peers, top doctor among patients, etc. So I think she knows what she’s talking about, but that’s an assumption.
In order to keep this focused and manageable, the scope of this post will be fairly narrow. I will explore what Estrogen Dominance means, why peri- and postmenopausal women should not spin their wheels trying to test for it, and a sensible philosophy for treating symptomatic women at this stage of life. The following topics will be outside the scope of this post, but may be covered in future posts: the risks of and indications for HRT, testing for and use of bio-identical HRT, PCOS (polycystic ovarian syndrome), and other “reproductive stage of life” hormone issues. Nonetheless, some of the content in this post will be applicable to the issues I’m not covering today.
What is Estrogen Dominance and Why Should You (not) Care About it?
The main problem with the theory of Estrogen Dominance is that, depending on who you ask, it means different things to different people. Most medical doctors don’t use the term but might think it refers to a reproductive-age woman with anovulatory cycles (no egg is released during the menstrual cycle). Alternative Medicine might use it to refer to any premenopausal woman with a constellation of nonspecific symptoms (fatigue, bloating, mood changes, poor sleep, etc) that are often what we call “symptoms of a busy life.” Extreme Alties use it to refer to people who have been “poisoned” by endocrine disrupting chemicals with estrogenic effects, from their food supply or plastics they use. Or, Estrogen Dominance could refer to a perimenopausal woman with hot flashes and other menopausal symptoms.
When evaluating any medical theory you encounter on the internet, you should ask yourself two questions: is it coherent, and does it generate meaningful search results on PubMed?
Estrogen Dominance certainly fails the coherence test. If one tries to boil the theory down to something sensible, the best one can do is say that ED (Estrogen Dominance, not Erectile Dysfunction!) describes a state in which there is more estrogen than progesterone. This, of course, describes normal ovarian physiology for most of a woman’s reproductive life:
Attribution: Chris 73 / Wikimedia Commons [GFDL 1.3 (www.gnu.org/licenses/fdl-1.3.html) or CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0)]
As you can see, estradiol starts rising significantly in the late follicular phase, with progesterone levels still fairly flat until they finally start rising during the luteal phase. Advocates of finding pathology in this normal process seem to believe that, when estradiol is high and progesterone is low, hysteria ensues and hormones need balancing – whatever that means. Another way of looking at this is – please scroll back up to the diagram for a second – if Estrogen Dominance is bad, then the menstrual cycle should have evolved to simply be one long luteal phase, with no follicular phase. That would ensure a proper “natural balance” of estrogen and progesterone, right? There’s only one problem: every female on the planet would have only one egg that could be fertilized over the course of her life, leading to a contraction of the world population and eventual extinction of humans. That is not happening.
The ED theory seems to abound in the treatment of symptomatic peri- and postmenopausal women, so that’s where I’d like to focus.
Claim: Classic medical teaching says that estrogen levels fall as a woman enters menopause, until the ovary loses the ability to make much at all. Mainstream medicine attributes hot flashes to these low estrogen levels. But, there is evidence that estrogen levels are high, not low, in perimenopause. This proves that high estrogen levels, in combination with low progesterone levels (Estrogen Dominance), are responsible for a woman’s symptoms. Obviously, the correct treatment is to give progesterone to help antagonize the excessive estrogen levels, alleviating symptoms.
HD: Partly True. Surprised? Expecting “Mostly False?” It is true that we used to think estrogen levels fell from the onset of menopause through the transition until the ovary was barely capable of making any. One of the most elegant studies demonstrating that estrogen levels are actually high in perimenopause was published in JCEM by Santoro et al in 1996. While the authors found that estrogen was high and progesterone low in the study population, they could only postulate that dysfunctional uterine bleeding and other gynecologic symptoms might be related to this hormonal milieu.
In fact, nobody has been able to figure out the precise pathophysiology for many menopausal symptoms, particularly hot flushes. Nonetheless, the claim that mainstream medicine believes that hot flushes are due to low estrogen levels is false. If we believed that, then all women between their 50s through death should be walking around in a constant state of flushing. They aren’t. We don’t. We believe that hot flushes are due, at least in part, to the rollercoastering estrogen levels seen during the menopausal transition. This theory that wild swings of estrogen in perimenopause cause symptoms is consistent with the data presented by Dr. Santoro and her colleagues.
Claim: It is inappropriate to give estrogen + progesterone (E+P), the mainstream standard of care, because estrogen levels are already high.
HD: False. As stated earlier, we believe that menopausal symptoms are due to wide swings in estrogen levels. Giving estrogen alone or E+P will provide a steady state level of estrogen, reducing the wide swings. Proponents of the ED theory claim that supplemental estrogen or E+P will not suppress the body’s own production of estradiol, because the hypothalamus/pituitary are too “dysregulated” at this time of life. Basically, they’re saying that the pituitary gland’s stimulation of the ovary to make estradiol will not respond to the negative feedback of E or E+P medication. To the best of my knowledge, there is no data to support this assertion. When we give steady doses of these hormones, that should result in suppression of pituitary gonadotropins (the hormones that stimulate the ovaries).
Claim: Progesterone-only medication is the most appropriate treatment for perimenopausal symptoms.
HD: Mostly False. There is no medical evidence to support this claim. However, if standard E or E+P therapy doesn’t work as desired, or if the woman prefers P alone, that’s fine. There’s nothing wrong with trying oral, natural micronized progesterone, which can be given cyclically in a higher dose or continuously in a lower dose.
Claim: You should test your estradiol and progesterone levels, to see if you suffer from Estrogen Dominance.
HD: False. You’ve seen the graphic above. If you are cycling regularly, you know that your hormone levels will depend entirely on when within the cycle they are drawn. The only thing those numbers can tell you is that you are cycling (not talking about fertility/ovulation issues today), which you kind of already knew! If you are perimenopausal and starting to have some irregular cycles plus other symptoms, you know there’s a good chance that your estradiol levels will be swinging widely, which should not affect your choice of treatment. If you are postmenopausal, then it’s ludicrous to test anything, because estrogen and progesterone levels will be low, by definition.
Remember when I recommended asking yourself two questions when evaluating a medical theory you find on the internet? I’ve already addressed ED’s lack of coherence. The second question is, what do you find when you plug the search term into PubMed? In the case of Estrogen Dominance, you find nothing of value, which should be a giant red flag. Do yourself a favor: forget about the theory, certainly don’t try to test for it, and work with your doctor to find a hormonal regimen that adequately addresses your menopausal symptoms.
Come back soon for my next post, Are Bioidentical Hormones Safe?
*Lest I cause the U.S. Patent and Trademark Office’s knickers to become twisted, I should make it clear that I have not trademarked this ridiculous phrase.
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Image Credit: Photo by Chris Sabor on Unsplash
49 Replies to “Why You Shouldn’t Care About Estrogen Dominance”
Good article thank you. There are coaches that use the concept of estrogen dominance when working with clients (fat loss). The idea is that you can´t lose weight when you suffer from estrogen dominance. So after a test (saliva) you perhaps show normal estrogen levels but low progesterone (should be >99 pg in the luteal phase). They argue that this may be the reason you dont lose weight. Do you think a saliva test is a valid tool to test estrogen and progesterone? Do you think this concept is a good one? Thank you.
Good question. I believe those salivary tests are absolutely worthless. To the best of my knowledge, there is no evidence suggesting that one can infer anything about weight management from checking estrogen and progesterone levels.
Thank you. The company that uses salivary testing for estrogen is called cerascreen. I don´t know how strong the evidence is for saliva hormones but I think it all comes down to free vs. bound hormones. The question is whether this estrogen test is a good surrogate marker. Some use it for cortisol/testo, ok. Would you mind to explain why you do think that salivary tests are absolutely worthless? Or do you have any adress where I can ask for more information (Endocrine Society, etc.).
Just found this http://clinchem.aaccjnls.org/content/clinchem/early/2008/08/29/clinchem.2008.108910.full.pdf and this https://www.endocrine.org/~/media/endosociety/Files/Publications/Scientific%20Statements/jc-2009-2509v2.pdf
The first link is to a paper about applicable uses for salivary testing. There are definitely uses for it, but not for guiding postmenopausal HRT or trying to help people lose weight by testing estrogen.
The second link is to a guideline paper for HRT.
The issue comes down to clinical data. While there are many tests that have a “reference range” given by a lab, there may not be any clinical data showing how those tests can actually be interpreted in a meaningful way.
One exception in endocrinology would be the use of a bedtime salivary cortisol to screen for Cushing’s. That test has been validated as a clinically useful way to screen for that condition.
But most salivary tests have little to no data in that regard and are worthless. Especially when trying to use estrogen and progesterone levels in almost any way other than by a fertility specialist.
I find a lot of Dr Prior’s work interesting, and thought I would share this particular post in re: effectiveness of progesterone only for the treatment of perimenopausal symptoms (hot flashes/ hot flushes in particular):
Yes, I’ve read several of her posts/articles. She appears to be quite passionate about the topic.
Great article! And yes, the alt/complimentary claims estrogen dominance is the source of about 30 ailments. Looking forward to future articles on this subject, maybe more on their claims that progesterone is the cure all for all gyn disorders, and its usually the OTC transdermal natural progesterone they recommend, not oral micronized progesterone. Thank you for sharing your knowledge!
What about the alt/complimentary camp saying only use bio identical hormones not synthetic because synthetic turns off any body hormones and bio identical does not.
I’ve not heard that claim, but if that’s what they’re saying, it is false.
What about the alt/comp camp claiming that the bodies own progesterone acts as a 5 alpha reductase inhibitor therefore when the levels drops in perimenopause this is the cause of female pattern hairloss therefore supplement with progesterone, they claim this is more effective and safer than the drugs on the market to block androgens, like Propecia. You know the endrocine system, hoping you can clarify. To me if progesterone were the answer, then everyone would be using this and not the drugs with some known side effects. Most MD’s will not give females propecia and for men it comes with side effects. I wonder where they get their “science” and their claims. Thanks for all you do
I’m not quite sure where they get these claims, but this is a nice, concise review paper on FPHL (female pattern hair loss): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5419033/#!po=32.9268
As you will see, estrogen/progesterone therapy is an option for treatment of FPHL, though it doesn’t have the most robust body of evidence. There are other treatments with better evidence, as described in the paper. Also, side effects with drugs like spironolactone or finasteride/dutasteride are generally minimal and not serious, while hormone therapy has some rare but potentially serious side effects.
Doctor, in regards to the body’s progesterone acting as an androgen blocker protecting hair, or at least the claims made by alt/complimentary saying so, what are they twisting with the endocrine system to get such a statement? My dermatologist and gynecologist have not heard this claim before. They both say lowering estrogen levels can change hair and if supplementing with estrogen to help this issue one also needs progesterone if an intact uterus. They also say estrogen dominance causes about 30 medical/gyn issues, there needs to be more truth and facts and science on the web because when one google searches theses issues, every response is based on alt/compl view.
You’ve hit on one of the main points of this site: whenever there is a paucity of data about something, Alt Med is happy to step in and provide all the answers you could ever want to hear. As for using progesterone-only for hair loss, I suspect they get this idea by extrapolating the data for cyproterone acetate, a potent antiandrogen/weak progestin. Cyproterone is used in Europe and I believe Canada, but it is not available in the US. It has many potentially serious side effects.
I don’t know if that’s why Alt Med thinks they can throw any old progestin at hair loss to make it better, but that’s my guess. The other guess would be that estradiol/progesterone combination therapy is often used for hair loss when the hair loss is thought to be due to elevated androgen levels. To the best of my knowledge, there are no data looking at P only for treating hair loss.
I’m eagerly awaiting your next post. I don’t want to rush you, but I am imminently embarking on HRT, and so am in Full-Internet-Research-Mode (TM). Hoping I can bug you with a couple questions here. I skimmed the “guideline” paper linked to in a comment above, and there seems to be consensus on the benefits of HRT, and probably also that estrogen should be delivered transdermally. I ran across a possible argument for preferring an estrogen cream to a patch (besides more precision in dosing, possibly): estrogen cycles on a daily basis, with the level dropping at night, to allow for hgh to be produced. (And so estrogen cream should be applied earlier in the day.) Is there anything to that? The other question is: do you have an objection to delivering estrogen and progesterone cyclically, a la Wiley Protocol? I’m not in the “more is better” crowd, nor into trying to use hormones as a feel-good drug. But trying to stimulate the hormone receptors, as well as provide for regular shedding of the lining you’re creating by HRT, are both things that make sense to me in what I’ve read so far. I even ran across a site/paper that recommended using something like the Wiley Protocol in transgender females, FWIW.
I’m going to cover some of this in the next post. I can’t say that an FDA-approved cream is or isn’t going to be better than a patch with respect to increased precision of dosing. If we’re talking about a compounded cream, however, it’s a good bet that it won’t be consistent with respect to the dose, due to the known problems compounding pharmacies have with quality control (more to come in the next post). As for the cycling, HGH, etc…I am not familiar enough with this argument to comment.
No doubt I’ll have to tweak whatever I end up doing after I read your next post. But it’s nice to know that I shouldn’t worry about Estrogen dominance as I wade into this.
I found an actual paper that talks about the diurnal cycling of Estradiol:
If I read it correctly, and integrate it with another paper that says peak Estradiol in the system occurs 6 hours after the application of a creme…
…that means we should all wake up at midnight (or thereabouts) to apply our estrogen creme! Oh, joy. I want my own hormones back…
The problem with this logic is that you are assuming that symptom relief will correlate with blood/salivary levels of the hormones, time to peak level, etc. Neither blood nor salivary levels are useful, as you cannot say that a particular level or time to peak will correlate more or less with symptoms. Ironically, alt med wrongly preaches treating people based on symptoms for the thyroid/adrenals/etc. They also wrongly try to quantify menopausal HRT and treat based on levels, when all they need to do is treat based on symptoms. More to come in next post.
Ok, that helps, thanks. I’ll wait to hear you present your full argument for why the two should be treated differently–i.e., what the proper standard of “need” is. Perhaps as a woman with symptoms, I’m a little biased about the precision I’d like to bring to this HRT endeavor? It’s quite possible!
It is attractive to think that your levels can be titrated to some optimal number. I get it. But that is not the way HRT works. It is a symptoms-based therapy.
Well, and disease-prevention, yes? So that’s where optimal levels could be relevant? (I was going to wait to bring that point in until your next post to see what you said first.)
Nope. Not for disease prevention either. No optimal level is known.
If I am well-informed, postmenopausal hormone replacement therapies are becoming recently less popular. It seems that their effect on the risk of developing breast cancer and cardiovascular diseases outweights their protecting ability (against osteoporosis and, well, cardiovascular diseases).
Not my field of expertise, therefore take my word with a pinch of (iodidized) salt:-)
Sorry for the typo, iodinized.
It’s true that we don’t usually start HRT with the intent to protect against OP or CV disease; rather, we initiate it if hot flashes or other menopausal symptoms are severe enough to warrant it. But, the risks that were publicized with the WHI trials were overstated. Over the last 15+ years, the data has been parsed with greater nuance, and it’s clear that the risks are not as bad as once thought.
Thank you for the answer.
I am a layperson who stumbled upon this post while looking for another, and the headline grabbed me. As a sample of one, I can tell you that reading a (different) blog post about estrogen dominance probably saved my life. I am in my 2-3 year of perimenopause and uncharacteristically developed intense, dark mood swings that had me normalizing suicide if not actually planning it. When given birth control pills, the crying was almost uncontrollable. So I hid and suffered for another year, pulling off the side of the road to battle the bleakness and beg for a way to replace myself so my children would not suffer (then a few days would go by and Id say, “huh, that was weird”). Happened like clockwork each month, with other symptoms I don’t care to detail that are consistent with a boatload of estrogen.
Finally, finally, finally some random blogger in Canada used the phrase “estrogen dominance” and described the hormonal shifts in a way that made it make sense (she wasn’t selling anything). I was able to beg my gynecologist (yes, you have to beg for these things, doctors are so tightfisted with therapies anymore) into trying progesterone only. I was a changed woman almost immediately. I don’t know about “balance” and what the levels look like on a line-graph (reminds me of biorhythms in the 1970s) but I can tell you from my perspective that getting my hormones back to a symphony vs. a free-form jazz band has potentially saved my marriage, job, and life.
Not being in the medical field I cannot tell exactly what your objection is, the term, the trend, the tests, but please know that there are very real, intense dynamics going on with some women.
Of course, I understand that these types of symptoms are scary and awful. And I’m pleased that progesterone worked for you. The point of my post is that we should not be attempting to quantify a phenomenon that – because of the physiology I explained – defies quantification. If someone wants to use progesterone-only because it works better for them than E+P, have at it. No problem. But it has nothing to do with estrogen dominance.
Can taking Prometrium alone, in a smaller continuous dose, suppress ovulation during perimenopause?
It is not intended for that purpose; its main target is the uterine lining. One should assume that ovulation could still occur while taking it during perimenopause.
Ah, I see how my question was interpreted, which makes sense given how I worded it. I am going to try and back up and reframe.
I will try to keep my background high level, as I am NOT looking for advice on how to manage my specific symptoms, only to provide a bit of context. My primary goals are to manage my symptoms and to promote ovulation at the same time. However, when I searched PubMed, there was not a lot of information on dosing P only in a perimenopausal woman, so I am trying to gather information in order to make the most informed decision I can.
My GYN has me dosing P only to attempt to manage my sometimes debilitating perimenopausal symptoms. We are avoiding E for now, as I have endometriosis and heavy bleeding. *To note: I know that P is not a treatment for endometriosis. I recently had laparoscopic wide excision surgery with an endometriosis specialist, so am attempting to manage my perimenopausal symptoms post surgery without ovarian suppression.*
In your post, you mentioned:
“There’s nothing wrong with trying oral, natural micronized progesterone, which can be given cyclically in a higher dose or continuously in a lower dose.”
So, my question is: What is the impact on ovulation if taking Prometrium continuously in a lower dose? I am guessing it is mostly dependent on the individual? And also, can you define higher and lower dose?
I really appreciate and enjoy your posts, and the peek behind the curtain, so to speak. I don’t have thyroid issues, I just enjoy reading the well thought out, backed by references, content that you generate. I actually found your website when trying to research estrogen and progesterone…there is a lot of quackery out there, and since I am in a gray area, I’m trying to avoid it to the best of my ability. Thank you!
Thanks for your question and feedback, Leah. I would define low-dose as 100mg daily and high-dose as 200mg daily (though the higher dose is usually only used for part of the month, not all 30 days). As for a negative impact on ovulation, I would think it would be fairly minimal, but I don’t know if it would actually promote ovulation. I am aware that fertility experts (I am NOT one) sometimes use progesterone to try to prevent miscarriage in high-risk women, after conception has occurred, but I don’t know if they use progesterone in a “pro-ovulatory” fashion.
The fertility world is one with which I don’t have much familiarity or expertise, unfortunately.
Thank you, HD! We are finished building our family, so I am not wanting to promote ovulation for fertility (and, promote wasn’t the correct word choice either. I suppose “not impair” would have been a better descriptor. I am just a super communicator today). Rather, my goal is to reap the brain/breast/mood/heart benefits of my own estrogen/progesterone, yet manage my perimenopausal symptoms at the same time…all while trying not to flare endometriosis. It seems that many women in my situation either go on birth control or elect to have a hysterectomy + bilateral oophorectomy + HRT, so I’m just wading in a grey area here. Not looking for any more information, just thought I’d put my questions out there in case there are other women like me looking for information 🙂
Abstract below is straight from PUBMED on Estrogen dominance
Estrogen is a pivotal enzyme for survival and health in both genders, though their quantum, tropism, tissue-specific distribution, and receptor affinity varies with different phases of life. Converted from androgen via aromatase enzyme, this hormone is indispensable to glucose homeostasis, immune robustness, bone health, cardiovascular health, fertility, and neural functions. However, estrogen is at the center of almost all human pathologies as well-infectious, autoimmune, metabolic to degenerative. Both hypo and hyper level of estrogen has been linked to chronic and acute diseases. While normal aging is supposed to lower its level, leading to tissue degeneration (bone, muscle, neural etc.), and metabolite imbalance (glucose, lipid etc.), the increment in inflammatory agents in day-to-day life are enhancing the estrogen (or estrogen mimic) level, fueling ‘estrogen dominance’. The resultant excess estrogen is inducing an overexpression of estrogen receptors (ERα and ERβ), harming tissues, leading to autoimmune diseases, and neoplasms. The unprecedented escalation in the polycystic ovary syndrome, infertility, breast cancer, ovary cancer, and gynecomastia cases are indicating that this sensitive hormone is getting exacerbated. This critical review is an effort to analyze the dual, and opposing facets of estrogen, via understanding its crosstalk with other hormones, enzymes, metabolites, and drugs. Why estrogen level correction is no trivial task, and how it can be restored to normalcy by a disciplined lifestyle with wise dietary and selective chemical usage choices has been discussed. Overall, our current state of knowledge does not disclose the full picture of estrogen’s pleiotropic importance. Hence, this review should be a resource for general public as well as researchers to work in that direction.
Please cite the source (journal/title), thanks.
I would love to read this article but didn’t want to purchase it. At a brief glance, it seems to stick out among other articles related to estrogen simply because of the title-all the other articles are very specific research etc-this one seems to have a sweeping claim with the words “how to tame it,” as if estrogens are bad need to be manipulated in order to be healthy. Love this blog!
You refer to estrogen levels in peri- and post-menopausal women, but what are your thoughts on estrogen dominance in women who have not yet reached this? And to add in personal facts, ones who have had a unilateral oopherectomy, and fibrocystic breasts with a lumpectomy (non-cancerous).
I’m not sure I understand the question, Amanda.
Do you believe that too much estrogen can cause an issue? Is too much estrogen a thing? Especially in women of younger age. I have very specific symptoms and an estrogen level that measures 2.5x the top end of normal. My endocrinologist seemed very bothered by the level and we are running another battery of tests, but I just wondered what your thoughts were.
If you mean, do young women overproduce estrogen and need to do something about it, the usual answer to that would be no. But I suppose there may be some caveats to that which are beyond the scope of this post.
I have almost double the amount of estrogen and my hair is falling out to the point where I have a bald spot but I guess there’s no reason to worry about it.
I’m in my 20s and I took a quiz from this website https://hormonesbalance.com/ and I took it 4 times. The first two said that I was highly estrogenic, the 3rd said that I was low in estrogen and the last one said I was somewhat estrogenic. I am dealing with depression and anxiety and I have also been diagnosed with ADHD and autism. I am dealing with heavy periods (first 3days). So is it real? Is what I am dealing with a symptom of estrogen dominance?
I realize this is quite old, but I figured I’d comment. My parents are into functional medicine and took me to those sorts of doctors growing up, and my mom has talked about estrogen dominance. I think your definition may be missing some of what is claimed by at least some CAM practitioners. If I remember correctly, the idea is that the ratio of estrogen to progesterone is too high by some specific amount (not that estrogen is simply higher) at a particular point in the cycle (maybe early luteal phase? – this is when some of them have you take a saliva test). I’m not advocating for the idea of estrogen dominance here, but the criticism related to levels changing throughout the cycle loses some of its teeth if they test at a specific time. Just commenting because I wouldn’t want someone who is into CAM to read this and think, “Well, that’s not how my doctor does it, so I can write this blog off.”
Thanks for this thoughtful comment, Via. Assuming that a woman is cycling regularly and that one could accurately determine that one is testing her at the same time every month, the question would be: what testing should be used?
The salivary testing is worthless due to a lack of standardization and data to actually know what is normal and abnormal.
Blood testing is likely to show pretty wide variations in E and P numbers, even if done at the same time every month. But even if you could get consistent blood results, I don’t believe there are data to suggest what the optimal ratio of E:P is.
So even if a functional doctor says the E and P are “out of balance,” I think the retort to that should be, where is the evidence backing up what defines “optimal balance?”
I know this is an old post but I wanted to comment anyways because some of the concepts promoted by alt medicine have stressed me out thinking something is now wrong with me. Specifically the ratio of estrogen to progesterone during the peak of the luteal phase where the “optimal ratio” is supposed to be between 100-500 for Progesterone:E2 (converting progesterone to pg/ml and dividing by E2)
I’ve been under some bad stress so my period is off but I’ve always been regular/had one every month and never have any bad pms symptoms/heavy bleeding, etc. But I’ve tested my ratio during this phase and it’s not super low but it’s under 100 so that’s got me worried because of all the metabolic health effects that they say can happen if your ratio is bad. I just can’t find any data on why 100-500 is optimal. It seems like to be anywhere toward the the mid to top of that range your progesterone would have to be sky high and estrogen would be towards the lower end which would almost seem like a hormonal imbalance within itself.
You just seem like a very reasonable person within the field and I wanted to get your take on this.
Olivia, I apologize, but my site policy prevents me from giving individualized advice. I can say, however, that I’ve never heard of these “optimal” ratios. It could be because I am ill-informed, but it could also be because there are no data to support the claim.