The redemption of HRT

Ding dong! The witch is dead! Or, at least, the witch-hunt over hrts.

The beginning lay, catastrophically, with the cancellation of the Women's Health Initiative Study in 2002. There was a huge worldwide panic in the press, with the end message that using HRTs caused breast cancer. An immediate response followed, in which roughly 50% of the women in the US stopped taking HRT. Over time, attempts were made to suggest other ways of interpreting the data and stances softened, but the basic message persisted: HRT was too dangerous to use.

Whilst HRT supporters continued to explore how hormonal support in menopause, especially surgical menopause, could still be safely used, the costs began to accrue. Studies have suggested that nearly 50,000 women in the US, who were in surgical menopause and quit HRTs because of the study-related panic, died due to that decision.

Further, there were significant fiscal costs both to women and to the general economy from the morbidity due to hot flashes and other untreated menopausal issues. Between 1999 and 2011, says one study:

Women with hot flashes used more healthcare services, particularly outpatient services, than women without symptoms, the researchers found. The extra services added up to $1,336 more per person per year compared to women without symptoms, and the indirect economic loss due to missed work was an extra $770 per woman per year.

Additionally, the authors of that study attributed about $300 million in losses per year to untreated hot flashes, and for the full population of the US, expand that loss estimate to $billions. In Europe, a similar study/estimate suggests a loss of more than €100 million per year just in the Netherlands alone.

But misery isn't measured in currency or even deaths alone. The vast number of women untreated and told to swallow their symptoms because they were "just depressed" or otherwise had failed at talking themselves out of anything more than "a few warm spells" (the classic medical description of menopause presented by many doctors) cannot be counted. But we felt it and we saw it in the discussions online amongst the menopause community, as women struggled to make sense of their symptoms in a climate that forbade them treatment and turned the blame back on themselves. At best, we hoped that with time the more sensible interpretations of the study outcome would take hold and those stances would soften in the decades ahead.

A shocking statement

And that's how things continued until March of 2017. That's when a startling review article was published in Climacteric, the journal of the International Menopause Society, by R.D. Langer, whose background is cited as:

The author was the Principal Investigator for the WHI Vanguard Clinical Center at the University of California, San Diego for the entire primary study period from 1993 through 2005, Chairman of the WHI Principal Investigators Committee from 1994 to 1995, a member of the WHI National Steering Committee from 1994 to 2005, and Chairman of the WHI Observational Study Scientific Advisory Committee from 1996 to 2005. 

Here's the full citation:

R. D. Langer (2017): The evidence base for HRT: what can we believe?,
Climacteric, DOI: 10.1080/13697137.2017.1280251 (alternate link)

Basically, the author asserts that many of the research team were shut out of the decision to publish the initial WHI results (which resulted in the study cancellation) paper and were given neither time to review the release nor comment upon it. Further, the timing worked out such that the press release came out before anyone capable of reading the results could have access to them. And, finally, the press release itself was manipulated to emphasize the breast cancer risks...even though they did not exist when the data was correctly analyzed. The author summarizes in terminology rare in the medical press:

The unmistakable and deliberate focus of the small group of self-appointed authors was to trumpet a finding of harm from breast cancer – the science and statistics notwithstanding. This was deeply embedded in the paper and emblazoned in the press release.

The author concludes:

The WHI trials were soundly designed to address the questions the program was intended to answer, with planned procedures duly noted in the protocol. That good science became distorted and ultimately caused substantial and ongoing harm to women for whom appropriate and beneficial treatment was either stopped or never started. Key faults have included: failure to properly identify the study goals and population characteristics in presenting and interpreting the results; inappropriately generalizing the findings to a key sub-group – newly menopausal women – that was not adequately represented; inappropriately generalizing the findings from specific medications to an entire class; failure to put the findings in the context of existing knowledge (taking the position that the prior studies were simply wrong); favoring publicity, fear and sensationalism over science; and departing from protocol – focusing on unadjusted results, while avoiding planned analyses with proper adjustments and better statistical power.

That's pretty powerful stuff, isn't it? Basically, the WHI-mediated panic was an historical blip. But although we saw a followup editorial or two, it certainly escaped notice in the popular press.

Where could we expect to go from there? At the time, in presenting it to our discussion group, we suggested:

As women, we can work to correct the misunderstandings of women and we can bring this review of Langer's to the attention of our doctors when they insist upon the dangers of hrt. It took mere moments for this disaster to unfold upon us women in menopause; it will likely take decades before the damage is undone, especially amongst the doctors who may resist any updating of their opinions. 

But then!

Well, as it turns out, we were wrong and we couldn't be happier about that.

Although they released the news on a major US holiday weekend, the North American Menopause Society, one of the most conservative of guideline-publishers and one of the ones to jump most thoroughly on the take-hrt-and-die post-WHI bandwagon, published a new set of menopause treatment guidelines that totally revised their stance on HRT use, even in women with the BRCA mutations and even on use by older women.

Here's an article summarizing the new statement:
Don't Be Nervous About Hormone Therapy for Menopause, Says NAMS (free signup required to read)

And here's The 2017 hormone therapy position statement of The North American Menopause Society in its journal abstract and in full.

What it says

First of all, the position paper states its applicability:

Key to initiating or continuing HT in an individual woman is an understanding of the benefits and risks of age at initiation or time since menopause, specific formulations or types of HT, the duration of therapy, the need for monitoring during therapy, potential risks of continuation, and the need for shared decision making.

The use of HT is considered for different cultural or minority populations of women, including those with surgical menopause, early menopause, or primary ovarian insufficiency (POI) and for women aged older than 65 years.

The paper also cites the scientific foundation for its conclusions:

based on material related to methodology, a review of key studies and evidence-based literature, and presentation and synthesis of evidence. It was written after this extensive review of the pertinent literature and includes key points identified during the review process. 

And they provide another whole document of the actual scientific background, should anyone want to consider the basis for their points. This may not mean a lot to you, but it's part of establishing how and why doctors can take faith in this as "evidence-based medicine." In other words, they've got the evidence in spades...or at least 58 pages worth of it.

The statement as a whole is fairly clearly composed and not difficult to read and we encourage women to read it for themselves. There are key points identified and clearly listed out after each section, and we for the most part agree with all of them. Perhaps startlingly, there's very little in there that's actually new or different from our own understanding, carefully sifted from research and consideration and spelled out here on the site.

Amongst the things that did catch our eye, however, was the reference (p6, vasomotor symptoms) to a 300 mg dose of progesterone:

Micronized progesterone 300 mg nightly significantly decreases VMS (hot flashes and night sweats) compared with placebo and improves sleep. Synthetic progestins have also shown benefit in studies. No long-term study results are available.

We're a little wary of that one because of the risk of depression and vertigo with doses like that, not to mention the risk profile suggested in research about breast and cancer risk. For a lot of women, this wouldn't just "improve" sleep; it would be akin to general anesthesia! So we look at the "no long-term study results" as an important flag on this one, not to mention years of women's attempts to follow Dr. John Lee's advice that the more progesterone a woman can take, the better she'll be (spoiler: we have found many women's experiences to disagree strongly with this). In fact, elsewhere in the statement is the concession that high doses of progestins may be associated with depression.

We're pleased to see that in general, NAMS is distinguishing between the effects of oral as opposed to transdermally-delivered HRTs. This is big, not the least of which is because for years Premarin was taken as being synonymous with all HRTs and thus tarred all HRTs with any effect of either its specific formulation or its delivery route.

We're also pleased that this paper recognizes that women who have a hysterectomy with retained ovaries often experience subsequent early menopause:

For women whose ovaries are retained at the time of hysterectomy, there is a two-fold increased risk of ovarian failure, and 20% or more of these women may develop symptoms of diminished ovarian reserve within 1 year 

Many women have been denied HRT following a hysterectomy because they nominally still have ovaries. Documenting that those ovaries may experience reduced output can make a great difference for these women. We've known about this statistic for years, but judging by the number of women complaining about this situation, not as many doctors as we might hope do.

And for those who have had an oophorectomy, there is no longer a "wait and see if you need it" (which we've always felt rather meant "demonstrate enough suffering to show you deserve it") aspect. The guidance is clear:

Unless contraindications are present, ET is indicated for women who have had a bilateral oophorectomy and are hypoestrogenic to reduce the risk for VVA and dyspareunia and osteoporosis, with observational data suggesting benefit on atherosclerosis and CVD, and cognitive decline and dementia.

The paper notes that estrogen has been demonstrated to reduce joint pains and stiffness. That's something that women have been told for years was not and could not possibly be related to menopause, leading to lengthy diagnostic journeys through the autoimmune disease realm. Once more, women's experiences are validated here, and that should vastly improve our ability to be successful in advocating for and obtaining appropriate treatment.

Finally, there is a demonstrated improvement in quality of life with HRT that may make the risks of HRT acceptable. What a notion! Women want to feel well and they're willing to accept some risks to do so. Again, this is quite in keeping with what we have seen women pleading for during the whole WHI brownout on HRT.

In the area of osteoporosis, there are no surprises other than the endorsement of HRT for preserving bone density. Of interest, however, is the statement that "Bone protection dissipates rapidly after HT discontinuation, but no rebound in fracture risk has been found." This suggests that when women finally do decide to quit HRT, they aren't going to immediately shatter. That doesn't negate the need for good bone maintenance practices throughout menopause, but it gives some hope that relinquishing HRT doesn't automatically mean going onto a bisphosphonate.

One important area this position paper identifies and begins to clarify is what women with hormone-related cancers should do.

For women with breast cancer, low-dose vaginal estrogen should be considered and prescribed in consultation with their oncologists.

Note that this doesn't default to an OB-GYN or family doctor. This is specialty territory, and so this is where we need to turn to an oncologist. If you've been forbidden HRT because of a vague "family history" of cancer, you deserve a full and detailed workup of your history and actual genetic risks rather than depending upon something Aunt Martha said once. And if you have been treated or are now being treated for breast cancer and are in pain from GSM (formerly known as vaginal atrophy), this holds out considerable hope that you might be able to use this most effective treatment if nonhormonal measures have been unavailing.

With respect to genetic risk for cancer,

Limited observational evidence suggests that HT use does not further increase risk of breast cancer in women with a family history of breast cancer or in women after oophorectomy for BRCA 1 or 2 gene mutation.

But for women who have or who have had breast cancer, the outlook remains unfavorable:

Systemic HT is not recommended for survivors of breast cancer, although selected cases with compelling reasons may be discussed in conjunction with an oncologist after nonhormone options have been unsuccessful.

More detailed analysis of risks involved with lung, colon, and ovarian cancer are in the statement, but women concerned about those areas definitely need to read the statement itself.

And this is the summary given of their overall evaluation and advice:

Hormone therapy formulation, dosing, regimen, route of administration, and the timing of initiation of therapy likely produce different effects, although these have yet to be evaluated in head-to-head RCTs, and there is a significant difference in the benefits and risk of estrogen alone compared with estrogen combined with different progestogens, at least as studied in the WHI. The concept of ‘‘lowest dose for the shortest period of time’’ may be inadequate or even harmful for some women. A more fitting concept is ‘‘appropriate dose, duration, regimen, and route of administration.’’ Given the more favorable safety profile of estrogen alone, longer durations may be more appropriate. Risk stratification by age and time since menopause is recommended. Transdermal or lower doses of HT may decrease risk of VTE and stroke.

We want to underscore this notion of ‘‘appropriate dose, duration, regimen, and route of administration.’’ This pretty much adopts an individualized evaluation of a woman's situation and goals as the standard, rather than an arbitrary "best" HRT or dose or age guideline. This is big. This is great. This is going to take some work within the fundamentally patriarchal field of medicine, but oh, what a wonderful goal.

And who agrees with it?

The new NAMS statement includes a lengthy list of endorsements quoted at the end, and we are copying this out just to demonstrate how widespread this revision of the "party" line now is:

This NAMS position statement has been endorsed by Academy of Women’s Health, American Association of Clinical Endocrinologists, American Association of Nurse Practitioners, American Medical Women’s Association, American Society for Reproductive Medicine, Asociacio´n Mexicana para el Estudio del Climaterio, Association of Reproductive Health Professionals, Australasian Menopause Society, Chinese Menopause Society, Colegio Mexicano de Especialistas en Ginecologia y Obstetricia, Czech Menopause and Andropause Society, Dominican Menopause Society, European Menopause and Andropause Society, German Menopause Society, Groupe d’e´tudes de la me´nopause et du vieillissement Hormonal, HealthyWomen, Indian Menopause Society, International Menopause Society, International Osteoporosis Foundation, International Society for the Study of Women’s Sexual Health, Israeli Menopause Society, Japan Society of Menopause and Women’s Health, Korean Society of Menopause, Menopause Research Society of Singapore, National Association of Nurse Practitioners in Women’s Health, SOBRAC and FEBRASGO, SIGMA Canadian Menopause Society, Societa` Italiana della Menopausa, Society of Obstetricians and Gynaecologists of Canada, South African Menopause Society, Taiwanese Menopause Society, and the Thai Menopause Society. The American College of Obstetricians and Gynecologists supports the value of this clinical document as an educational tool, June 2017. The British Menopause Society supports this Position Statement.

How will this affect me?

If you're already taking HRT, relax. We still have data that suggests that our lowest effective dose still relates to least risks, especially with regard to combined HRT (estrogen + progestogen). But we also know that "lowest" really means the one that makes us feel the way we define "well" in menopause to be. With the new statement, though, we no longer have to fight off our doctor's insistence that we stop HRT after five years of use (a disastrously simplistic reading of the original WHI study cancellation report) or, really, at any particular age milestone. That cap is lifted and it's now supported that we can continue to reap benefits from ongoing HRT use. We'll still argue that we need to reappraise our level of need for supplementation as we age , but that's just housekeeping.

If you quit HRT and are now thinking about going back on it to regain its benefits, sorry. It's still felt that the evidence is strong enough, even for transdermal HRTs, that they raise clotting risk enough that if we have been off of them for any substantial time (something like a matter of months), our risks upon resuming are not adequately offset by benefits. This may be negotiated according to amount of time and the quality and quantity of our symptoms, though, so it's not yet an absolute ban. We may see this thinking revisited in time and we'll let you know if we see anything that changes that position, but for now, "no" seems to be the authoritative word. But even if we've stopped systemic HRT, don't forget that we can continue using vaginal HRT to support those local tissues and functionality without that concern.

If you want to take HRT and your doctor says no, it's too dangerous and gives you cancer, this statement provides your best argument, hot from the medical press and international approval. But remember, our doctors are busy and even if they have time to read journals, this may still be beyond their usual subscription list. So feel free to share the link to the position statement and call attention to the fact that so many international agencies have endorsed it. 

And for the sake of all women in menopause, we can bring this up in conversation. While women often conspire in a general silence about menopause (no, we don't know why and it makes no sense, really), so much of the WHI-related anti-HRT panic was passed along woman-to-woman. So now we can reverse this trend by talking with our fellow women when the topic arises and make sure that if they are not comfortable in their menopause, they know about this latest information on HRT and recommendations for its use. We focused so long on its dangers, and that totally caused everyone to lose sight of its benefits. We finally have solid, science-based ground that we can use to help turn that conversation around.

Surgical menopause, hrts, and headaches

Headaches aren't special to menopause or even the surgical variety, but for those prone to them, hrt can involve some special concerns.

Headaches due to low estrogen

This may be one of the earliest symptoms to hit us after we have a hysterectomy—once the headache from not being able to have coffee before surgery wears off! Some folks develop a lingering, grinding headache that they just can't shake until their hrt is properly adjusted to their needs. For them, headaches become a tuning symptom, something we know has a specific meaning for our own body.

If we've not immediately gone onto hrt after surgery, doctors are sometimes worried that a headache during the recovery period means we're having or are at high risk for a stroke and shouldn't have hrt. While there is validity to ruling stroke out, especially when we've just had surgery, and while there is a slightly higher risk of stroke in the first year of using an oral hrt, some women are left with their doctors' refusal to prescribe just because they are still afraid of that risk. That says something rather sad about their faith in their own diagnostic capabilities and it says something terrible about a woman being able to get the care she needs. Shopping for a new doctor can, sadly, be about the only way out of this trap.

Generally speaking, headaches due to low estrogen tend to abate pretty well once our estrogen levels are meeting our needs.

Headaches from high estrogen

Yes, this happens too.

Decreasing the dose is the right answer for risk and for this kind of headache. How can we tell which is which, high vs low? By the other symptoms that appear with the headaches, just as with any other aspect of hrt tuning.

In general, the tactic of adding a diuretic (water pill) to hrt with the goal of reducing fluid retention from excessive estrogen is not an effective strategy for dealing with this kind of headache, let alone the risks posed by excessive estrogen exposure. It's a common medical response, however, to see each new symptom of imbalance as a separate disease that requires separate medication. We need to be alert to the state of our hrt balance and, if our doctor wants to prescribe diuretics when we think we're in hormone overload, we should be prepared to advocate for our own preferences. Suggesting a trial of dose reduction before adding a new drug is not an inappropriate proposal and a doctor willing to work with us should prove amenable to this kind of trial.

If going down in dose of an hrt doesn't cover our overall hormone needs but that previous dose being the next increment up presents excess, then we can understand that to mean that this isn't the best hrt for our bodies and that we could make more progress by moving along to a new hrt. While we always advocate adjusting dose before giving up on an hrt that appears to be delivering, there's only so far we can adjust things. If we're bracketing our needs without being able to find an acceptable middle ground, we're there. Moving along is likely to be more satisfying sooner.

Headaches upon taking an HRT dose

Some of us don't consider ourselves prone to headaches but then when we begin taking hrt, BLAM. These are often those who had semi-regular headaches during their former menstrual cycle, and if so, that's a great clue we can use in tuning our hrt.

In the situation of menstrual cycle headaches or right-after-taking-hrt headaches, the culprit often seems to be the rapid rise of estrogen levels; once a woman is a few hours or days into a dose, it abates. Because every dose of hrt takes us from a lower level to a higher one, especially early in our adjustment period, we're simply recreating the hormonal setting of those earlier cyclical headaches.

For these women, the key seems to be getting onto a stable level of hormonal support and a dependable delivery, so that they're not swinging up and down with each dose. While there will always be an uptake curve at one end of an hrt dose and a wash-out curve at the other end, once we stack several days' doses on top of each other, we reach a background level of hormonal supply that keeps us supported between doses. Some women, alas, take this sort of situation to mean they need to overlap their hrt doses or take them in tiny increments under the impression that a perfectly even and continuous delivery is necessary. In fact, however, this is something our bodies can sort out for themselves if those doses are adequate to permit us that background leveling between doses. While it's still the case that some hrts will be more comfortable than others for a woman sensitive to this dynamic, there's no single answer as to which those hrts will be.

Headaches with HRT

This is a bit different from the above situation in that a person on a poorly-fitting hrt may have frequent headaches as part of a picture of poor coverage: jangly nerves, anxiety, poor sleep, mood instability, and a general sense that they're walking a knife edge of disaster, not at ease in their skin. This situation tends to persist through dose adjustments up and down and even with a change of hrts. Often, these folks come to our forums summarizing their experience as "I can't tolerate hrt."

But frequently that's not the full story. Often these users, even when they've explored dose adjustments, have pretty much stuck to the estradiol hrts. And that's understandable because most of the hrts on the market today are estradiol hrts. We tend to divide the hrt market into human-identical estradiol and Premarin, and Premarin's reputation is a difficult one for many women to embrace. Routinely, more doctors seem to be offering estradiol than Premarin (or the other conjugated estrogens), and people are choosing estradiol hrts on their own.

But estradiol is the active form of estrogen and it seems that some of us don't want that much activity dumped into our system at once. These users seem to do better whwith an hrt that is comprised of some or all estrone rather than 100% estradiol. Estrone is a much less active form of estrogen, even a storage form, and it can be much gentler in its impact.

It feels, watching what the surgical menopause community is discussing, as though this problem is showing up more today than it did, say, a decade or two ago. But that was when we more freely used progesterone to take the edge off of a poorly-fitting estrogen hrt (a practice that's waning today due to better understanding of progestogens' risks) and that was when there were more estrone hrts on the market. These have mostly disappeared, now, and we think that this has left those who prefer them more adrift in what seems to be an all-estradiol world.

If an individual has tried various routes of estradiol hrt and still doesn't feel comfortable, they may want to explore the remaining non-estradiol hrts. These include:

• compounded hrts with all estrone or a blend of just a bit of estradiol with mostly estrone;
• Menest, which contains mostly estrone with a bit of equilin estrone (synthetic horse estrogen, similar to some of the compounds in Premarin);
• Enjuvia or Cenestin or a generic for them, which contain various blends of synthetic estrogenic compounds that are mostly estrone-ish in action plus a few that are estradiol-ish (no longer on the market); or
• Premarin, which contains a blend of synthetic estrogenic, androgenic and progestogenic compounds that are mostly estrone-ish in action.

With the exception of the compounded hrts, these are all oral deliveries, which may not be our first choice these days. Those who experience this particular problem often find, however, that they are willing to accept that profile in the interests of a better hrt fit. It really can make an astounding difference from the impact of estradiol hrts.

Migraine headaches and HRT

Migraines are a miserable affliction and for those who hoped that removal of their ovaries would put an end to a monthly brain implosion, they, disappointingly, can continue right on thanks to the efforts of our menopausal hrts.

The primary migraine triggers seem to be much like the general headache causes: hormonal fluctuations and the type of estrogen used (by which we mean, the activity of the form of estrogen the hrt contains). So when troubleshooting hrts around migraines, those are some of the considerations to work with.

Sadly, hrt alone isn't always enough to control migraines, and some women end up finding that a combination of hrt plus other drugs that are specific to migraines ends up working the best for them. Still, these hrt adjustments do give us a place to begin that can be more helpful than simply being told we can't take hrt if we get migraines.

Bioidentical HRTs

There are two aspects to the confusion about "bioidentical" and what it means. Let's look at them both to try to clarify what is being talked about.

HRTs that are bioidentical

The term "bioidentical hormone" originally simply meant any hormonal agent that is identical in chemical structure to those produced by our own ovaries. That term says nothing about hormone balance or hrts; it only describes the molecular configuration.

When our body uses the hrts that contain bioidentical hormones, they are for the most part used as our own were: the metabolic processing steps are essentially the same. Why not exactly the same? Because no matter what the form of the hormone, the way in which it is delivered to the body does enter into the dynamics of the situation. When we have intact and functioning ovaries, we have only enough of our hormones in circulation at any given moment to meet our needs. This level is controlled by a number of different feedback mechanisms and in turn controls a number of other hormonal levels and other physical processes.

But when we have to obtain part of our supply from outside our bodies, we don't have any way to make that intake respond to our internal cues. Instead, the timing and form of the hrt we take builds its own dynamic, sometimes causing its own effects upon how the hormone can be used that are independent of the adequacy of the actual hormone amount averaged across, say, a 24-hour period.

One example of this would be that oral hrts, because of the intense burst of processing they need by the liver, can cause more gallstones/gallbladder attacks as well as elicit more of an inflammatory response, such that they are associated with a specific, non-hormonal set of effects. Another example would be oral progesterone use, which provides for a more neurologically active set of metabolites than when progesterone enters the body by other routes. So even though the hormone molecules themselves may be identical to our own, the route and delivery timing add their own contributions to the overall effect we see when we use them in hrts.

You'll note we don't use the term "bioidentical" on our website when we're discussing hrts. As we've noted elsewhere, we avoid using it because its original meaning has become conflated with a different meaning, pertaining to a specific marketing strategy. For clarity, then, we refer to hormones identical to our own in chemical structure as "human-identical." 

Bioidentical HRTs, the business practice

The other use of "bioidentical" involves compounding pharmacies and the practice of physicians with whom they work. In carving out a new business niche for themselves in compounding hrts and advising women on them and selling test kits for hormone levels, they have chosen the term "bioidentical hormones" to describe this entire business practice. Fundamental to their marketing campaign is a philosophy expounded in the mid-90s by a few researchers at saliva testing labs, notably David Zava and Jonathan Wright, that women are best served by replacing not one form of the estrogen molecule, the active estradiol one, but a mix of the forms that mimic the blend found in a naturally menopaused woman.

This mixed-hormone concept was never really researched in a standard way other than to say look, when we test hormone levels in healthy women, this is what we find, refined by the sort of experiential "this seems to work for some women" work that we all, individually, do with hrts. There is no actual proven foundation for the premise that we best need a blend. We've written elsewhere about the three estrogens that have become the focus of this marketing approach.

What we think is most important about these three estrogens is that, speaking from the standpoint of physiology, they are not all individually necessary as original supplements. Our bodies have the innate ability to convert estrone and estradiol back and forth to meet our needs. Put in one form and, if it is human identical, it will be handled in the normal way to meet our needs, either as itself or as its other form. Estriol is a waste product, included in the belief that its limited range of effects is somehow safer in overall profile. In other words, it's filler, meant to extend the hrt effect without extending risk (although at therapeutic doses, it has been shown to not actually work out that way).

So do some people do better on this than straight-estradiol hrts? Absolutely. Some of us, for one quirk or another of individual metabolism, have trouble coping with some forms of estrogen efficiently. It may be a timing/delivery issue of plunking too much of one into our system at once; it may be an issue of not having enough of a cofactor/enzyme/whatever to carry out that much conversion at once. So yeah, there definitely is a place in the realm of hrt for blended estrogens and there are some folks who do best on them.

But do all of us need the blends? Absolutely not. Some of us don't do those conversions back as well and need a straight dose of one or another estrogen to have enough to work with. And there's no way to predict this; there's no way to test for this other than to try hrts. There's a real role for blended hrts, just as there is a real role for multiple doses and routes of all hrts, but there is no single correct answer for all of us—however much anyone's marketing would prefer to convince us otherwise.

And this is where the marketed practice of compounding pharmacists lets us down: by suggesting that there is more uniformity of hrt response than we have actually found there to be. By insisting on selling a test and then claiming to tailor an initial hrt that will correct every single level abnormality at once, this distorts the actual physiological process and doesn't take into account the way that our bodies use all of these hormones interchangeably and interactingly.

Many of the hormone level alterations we see in surgical menopause, especially when we are starting hrt in the immediate post-oophorectomy period, are responses to a sort of falling-dominos effect: one hormone loss kicks off another. So some of those levels represent a response to another imbalance, not a fundamental inability to balance that particular agent itself. In other words, if we correct one imbalance, many of the others will fall back into line of their own accord and through our own innate processing capability. By throwing a whole shopping cart of hormones at us at once, based on a test that may or may not accurately reflect either our true resources or our true needs (more on testing's limitations), practitioners of this "kitchen sink" philosophy aren't giving our bodies the chance to use our own mechanisms to sort stuff out and are throwing further sources of instability and excess into the mix. In effect, they can be artificially holding us in an imbalanced, stressed state instead of providing the resources necessary to return to an unstressed, balanced state.

An alternative approach, that espoused by the American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Menopause (free signup required to read) takes a much more physiologically-justified direction in suggesting that we should deal with one hormone at a time in a descending order of priority. By alleviating, first, the priority estrogen need, we allow other hormones to ease back to their own innate levels, thus revealing whether or not we actually do have abnormalities in our ability to provide for them, as distinguished from abnormalities of supply due to borrowing from them to meet higher but unmet priority needs.

Compounding pharmacists make more money the more hormones we buy from them and the more times they have to test and readjust those hrt blends. It's a business model, not a primary health care delivery mode. And it's one that has been helped along by marketing in the publishing business, where celebrities further confuse this issue with their own books that promise all sorts of sexy wonders if we'll only buy into this or that program that they themselves are marketing.

Please don't get us wrong—there are many excellent and knowledgeable pharmacists, but diagnosis and treatment are not part of their professional preparation and certification. There are many good things that compounded hrts can do for us, like provide more flexible dosing or blends that may suit our own bodies needs better than retail options, but the industry of "bioidentical hrts" as it has come, in the marketing sense, to mean this test-and-kitchen-sink program, is not necessary for most people in menopause from a health/wellness standpoint.

And so our biggest concern is that as a result of the conflation of these two concepts, the pure biochemical definition of bioidentical and the marketing concept, hrt customers are in a sense deprived of an opportunity to fully understand their choices. There are many retail human-identical hrts, and yet current marketing (as well as the anti-hrt crusaders') efforts have made it seem as though the compounded combo hrts have as their only alternative Premarin. All prescription retail hrt is not Premarin, and yet that is the implication that many many of us have been brought to believe. This is a deception and misconception that distresses us on behalf of all of those who won't find their best choices because they don't know that more exists or they feel they cannot afford to use something "bioidentical" because the package the pharmacist is offering them is too expensive.

There is a place in the market for each and every hrt that exists today, as well as many that do not and that we can only dream about. There are those for whom the "kitchen sink" works the best; there are others for whom nothing but Premarin works. What we would prefer is that each one of us be given a chance to find where on that continuum of choices we fall, not to feel that we have to choose between one end of it and the other because the rest is invisible thanks to marketing by pharmacies, drug reps, doctors, publishers, anti-hrt crusaders, insurance companies, and all of the others who seek to profit from our confusion and discomfort.

Primary Prevention of Cardiovascular Disease With HRT

We've just bookmarked an important new article that we think really brings home the post-Women's Heath Initiative Study (WHI) thinking on the flaws of that study and what we really need to know about the cardiovascular risks of hrt. Why should we care when cancer terrifies us? More of us will die from cardiovascular disease than breast cancer. It lacks the drama and publicity, but that doesn't mean we shouldn't pay very serious attention indeed to this aspect of our health.

Primary Prevention of Cardiovascular Disease With HRT (free signup required to read)
Kate Maclaran; John C Stevenson
01/03/2012; Women's Health. 2012;8(1):63-74

Abstract 

Prevention of cardiovascular disease has increasingly important health implications as our population ages. Menopause is associated with the development of cardiovascular risk factors and there are many plausible biological mechanisms through which estrogen may confer cardiovascular protection. Despite a wealth of observational data to support the use of estrogen, large randomized controlled trials failed to demonstrate a benefit. It is now becoming clearer that the beneficial cardiovascular effects of estrogen are greatest in younger women and those closest to menopause. This has led to the development of the timing hypothesis. Use of age-appropriate estrogen doses is crucial to maximize cardiovascular benefits while minimizing risk of adverse effects such as venous thromboembolism and stroke.

Article summary

The article gives an excellent overview of the current thinking on how hrt use relates to cardiovascular disease, taking into account WHI data, the "critical timing" hypothesis, as well as the combination and route of hrts, both conventional hormones and those that have been modified (SERMs).

It starts out by spending some time going through the various cardioprotective mechanisms of estrogen, including metabolic ones related to lipid levels and fat distribution, insulin resistance, and actions on blood vessels themselves. It then introduces a review of the data from the disastrous Women's Health Initiative Study and looks closely at why this was in such contradiction to a substantial body of sound other evidence.

Crucial differences in the study populations are likely to help explain many of the discordant findings. The observational studies generally involved women who started HRT around the time of the menopause for symptomatic relief. Subjects tended to continue treatment consistently and were followed-up for a long duration, often 10–15 years. By contrast, women in the WHI studies were started on HRT at an advanced age (average 63 years), often with a significant delay following menopause. Furthermore, subjects had elevated BMI, were not using HRT for symptom relief (only 12–17% had moderate-to-severe vasomotor symptoms) and generally had much shorter duration of treatment and follow-up

While research studies cannot assume any reason for observations, the article notes that

The presence or absence of vasomotor symptoms in study populations is important as hot flushes are increasingly being recognized as a determinant of vascular health.

That means, in research terms, that they must now state that hot flashes cause cardiovascular disease. But because we're not researchers, we can read into that the premise that this more likely reflects an underlying commonality, and quite likely demonstrates the difference between women who are not meeting their hormone needs or are fluctuating a lot, vs those who are hormonally adequate and stable. For now, though, this implied causality results in the conclusion that

further evidence is needed to help fully understand the mechanisms by which vasomotor symptoms may influence cardiovascular risk.

One of the important aspects of hrt use and cardiovascular disease is that the payout time is quite long.

This theory is supported by further analysis of the WHI estrogen-only arm, which demonstrated that lower cardiovascular event rates in women receiving estrogen compared with placebo only appeared to emerge from 7 years onwards...Similarly, data from the WHI estrogen plus progestogen arm showed that CVD benefit only appears in younger women after at least 6 years

Why is this important for us? Too many women are given hrt briefly after surgery and told they will be discontinuing it in a few months when their menopause "goes away."

Other women run up against the pretty generally accepted current guidelines that state that

HRT should be used for the shortest possible duration, often interpreted as less than 5 years.

That magical 5-year figure actually is another bit of fallout from WHI, in that it was after five years of study progression that the cancer figures for the combined hrt arm (not for the estrogen-alone arm—and this is a critical difference often missed in the panic) crossed the arbitrary threshold for study cancellation. So, nothing about cardiovascular disease is in that limit, even though it's cardiovascular disease that kills more women than breast cancer.

The article goes on to note that these kinds of time limitations may need to be re-evaluated in the light of the long pay-out on hrt when measured against cardiovascular disease, and this is likely an important and valid issue for all of us in surgical meno.

Next up: the "timing hypothesis." Succinctly stated, this holds that

there is a window of opportunity where HRT may be beneficial for prevention of CVD in younger women, but that in older women, it does not appear to have the same benefits.

But what about the bad cardiovascular outcomes in WHI? The article reviews the potential negative effects of estrogen, but then brings things into a context that is rarely seen in these discussions: need and dose and combination of hormones.

Although these potentially adverse effects of estrogen have been identified, it has been suggested they are not harmful except when inappropriately high doses of estrogen are used, or in the presence of certain progestogens, particularly MPA, which acts to negate the beneficial effects of estrogen and may cause vasospasm.

Ah, here we have the "new" thinking on hrts and this brings things much much closer to what we as women using hrt have found: dose, combination, and route all make a difference; hrts are not a single monolithic entity in which giving any random one stands for the effects of all. Seriously—please consider standing up and cheering at this point: it's that radical a departure from traditional thinking on hrts.

Is there firm data that these things really make a difference? No, the article notes that this is the direction thinking is going and that studies being conducted now should be clarifying this relationship as they are completed.

The article then looks at specific forms of cardiovascular disease that are worrisome based upon WHI results. In terms of stroke, which is what caused the ending of the estrogen-alone arm with a 32% increased risk, the authors provide supporting data from more recent studies that find that route and dose are critical to these outcomes and, not surprisingly, lower doses and non-oral hrts reduce this rate to "extremely low."

Similar insight is found into the issue of venous thromboembolism (blood clots): route and dose and specific hormones make a big difference.

oral, but not transdermal, therapy was associated with increased risk of VTE and also that the thrombotic risk differed depending on the progestogen used. There was no increased risk with micronized progesterone, pregnane or nortestosterone derivatives, but significantly increased risk with norpregnane derivatives.

Overall, there is still not a good solid body of research evidence that pits one hrt against another for route and dose. It's well enough demonstrated that different hrt types and routes have different specific effects, and it's worthwhile, as we make our own hrt selections, to review these—the article does a decent job of listing them and providing citations for the actual research. At the moment, based upon their overview, their conclusion is that

the dose of estrogen is probably more important than the route of administration on the risk of CHD, whereas both route and estrogen dose can influence stroke and VTE risk.

Estrogen, we've long emphasized here, does not act in a vacuum. While the use of progestogens (progesterone-like hormonal agents) in surgical menopause is probably declining, it remains a critical element for the prevention of endometrial cancer and endometriosis growth and continues to be popularly pitched to women by hormone marketing, especially in the compounding realm. The article takes a look at the existing data on different protestogens, noting that it's "the androgenicity of progestogens [that] influences their metabolic effects." Any woman who requires a progestogen as part of her hrt should read this section as she considers the overall effects she both wants and must avoid.

Tibolone and the selective estrogen receptor modulators (SERMs) are often offered to women as being "safer" than actual hormones while still holding benefits of other types. There's not a lot of data on cardiovascular disease aspects of their use, but this section of the article does summarize what exists. For women without specific risk factors that require these treatments, the lack of good data on their risks should certainly raise a flag that they cannot be taken as completely benign and that simply choosing them in fear of one thing, usually cancer, may raise other risks. As ever, it's all about balancing risks and to do this effectively, we need to set aside our fears of one specific boogeyman and look very specifically about our own personal risk factors in a number of areas. This section begins to lay the groundwork on this category of hrts.

Finally, in conclusion they sum up the situation:

CHD forms a significantly greater burden of disease than breast cancer or stroke, and the menopause is a pivotal time for reducing future cardiovascular risk.

They note the importance of lifestyle and diet in overall risk management, something that we would like emphasize here as well. They go on to note that

Cardiovascular risk is determined by a combination of genetic, lifestyle and environmental factors, but sex steroids can play an important role in modulating risk.

And then for the payoff:

Current evidence points to a window of opportunity, where greatest benefit in preventing atheroma progression is seen when HRT is initiated early after menopause. HRT may cause adverse cardiovascular effects through coagulation activation and abnormal vascular remodeling, although the use of age-appropriate doses and transdermal routes can help minimize these risks.

And that, right there, is where WHI was trying to go but, due to flaws in the study design, went dangerously and disastrously astray.

Important points to take away from this article

First of all, it is a good overview of the whole topic, appropriate for us to read and share with other women but also appropriate to share with our doctors should they still be stuck in the post-WHI "OMG HRT kills!" mentality.

While there is much mention made these days of a woman's "individual choice" there are still many, many women, even in surgical meno, who feel pressured to "do it the natural way" as though there are some merit points to be won in withstanding misery and poor health. We think articles like this are things all women at perimenopause or surgical menopause should read, so that they better understand that against the "all natural" glamor can be stacked the true risks of the situation. This article is good on true risks.

Hot flashes cause cardiovascular disease. As noted above, it's likely that over time and with more research, this will be seen as a profound oversimplification, in which we have a correlation rather than a causation. Never mind; for the moment we can use this to our advantage if we are being denied hrt and feel that we must campaign for its prescription.

Cardiovascular disease prevention is not a case for treating hrts like drugs: this is the antithesis of a quick, dose-related response. Instead, we need to take a longer view of hrt use when we're talking cardiovascular disease, and so while the "least dose required to meet needs" premise of risk management is not at all contradicted here, the arbitrary discontinuation of hrt at some set age or interval is strongly called into question. This is important for us to understand and very important to convey to our doctors if they are not conversant with current thinking on this.

We can, each of us, resist the mindless panic brought on by the post-WHI media frenzy, and it's these sorts of articles that can help us make a more realistic evaluation of our risks with respect to hrt use. Further, by sharing this kind of updated, serious, and medically sound information with other women, we can help them make better, less emotional decisions for themselves. And by bringing this to our doctors, we can help them stay more up to date where they might not otherwise have the time or interest to pursue all the small studies that have, over the past decade, contributed to a much more realistic and accurate picture of hrt actions and options.

Surgical menopause boosts cardiovascular risks

Update note: the study cited below, "Surgical Menopause Boosts Cardiovascular Risks" no longer seems to be available online. Nonetheless, the discussion around it remains valid and we are retaining this post for that reason.

We've known for some time now that overall cardiovascular risk rises at natural menopause to approach men's generally higher rates. This was long assumed to be the result of the shifting of balance away from the heavily estrogen-dominated profile that distinguishes (fertile lifestage) women from men. Indeed, it was cardiovascular risk that was really the underlying focus of the infamous Women's Health Initiative study: women well past menopause who had developed cardiovascular disease were put on hrt to see if it would improve their status. Sadly, no such findings resulted. Nonetheless, the generally better cardiovascular status of women on HRT as compared to women without continues to fuel research on the "critical timing" premise, that proposes that functions supported without interruption by covering hormone needs in menopause without a significant time lag are protective, but that once hormone support lags, women cannot regain that lost protection.

We also know that testosterone may worsen cardiovascular risks as it brings us closer to the male profile of risks. That's part of why the US Food and Drug Administration did not approve the female testosterone patch: it didn't improve the libido in some women (where testosterone deficiency wasn't the problem) and it did boost risks. For women with Polycystic Ovarian Syndrome, that's a special concern, since their disease is often characterized by lifelong elevation of testosterone levels. The literature is not yet clear on this hormone and cardiovascular risk

Cardiovascular risk also relates to elevated progesterone levels. A progesterone-heavy hormone balance tends to make us insulin resistant, raising both the risks of type II diabetes and cardiovascular disease in a special combined disorder called "metabolic syndrome." Metabolic syndrome is considered of the established risks of menopause.

Estrogen and cardiovascular disease

What kind of cardiovascular disease specifically? All sorts, actually. In addition the the hypertension seen as part of metabolic syndrome, hypertension alone can be a sudden-onset disorder upon oophorectomy. It saddens us to read of doctors withholding hrt from women who spike sudden high pressures when they come out of surgery out of concern for stroke risk. In fact, it can be the loss of estrogen's relaxing effect upon the walls of blood vessels that can cause this, so they're withholding the one thing that can treat the problem out of a mistaken focus on the symptom instead of the cause. Other women, less catastrophically, may find their pressure creeping up when they are advised to abstain from supplementing their hormones back up to more normative, menopausal levels or when their HRT is suboptimal.

We also know that estrogen has a beneficial effect on lipid levels and types, although oral hrts provide a different assortment of effects in this regard than transdermal do.

But today we have another small study, Surgical Menopause Boosts Cardiovascular Risks [no longer available online], that looks more closely at just what goes into that shifting CV profile with estrogen loss. Although this is a rather small study of only 90 participants, what they found was that the carotid blood vessels (major arteries in the neck that supply the brain, which are taken as representative of general vascular condition throughout the body) are narrowed in women who had oophorectomies before natural menopause age and who did not supplement their hormones back up to normative levels.

Now, they were working with living study participants, so they couldn't go slicing into these major arteries to find out precisely what had them gummed up. The assumption is that this is an atherosclerotic process, the plating out of metabolic gunk, mostly fat- and calcium-based (think about the condition of your bathtub drain: atherosclerotic placque is roughly as appealing, only with a bit less hair), on the inside of the vessels that, much like the situation in your bathtub drain, gradually reduces blood flow until it may stop it altogether or a bit breaks off and stops flow someplace else (which is what a stroke represents in mechanical terms).

But that's just an assumption, at this point. There is certainly also an element to do with that reduced vessel size/relaxation as well. Beyond that, we don't exactly know and won't until there's more autopsy/surgical data that analyzes what those vessels actually look like on the inside. Still, this is an important step because it does validate that there is actual pathology in place, and that pathology correlates to a woman's specific hormonal status.

Of note, the article concludes:

Dr. Ozkaya said, "We should think twice and discuss it with the patient, should we consider performing oophorectomy before menopause."

Now, would everyone whose doctor warned them about increased cardiovascular risk with this surgery, especially those advised that hormone deficiency would be therapeutically necessary, please raise their hands? Nope, we didn't expect so. This is the elephant in the room that never really gets discussed pre-operatively or that gets hand-wavy assurances of "you'll take this little pill and everything will be fine." Right? And so this is what women need to be able to find out on their own...or with whatever help they can find.

Should women refuse an oophorectomy on these grounds? Oh, goodness no: there are often much more dire consequences and quality of life issues represented by the pathology for which we choose this surgery. On the other hand, this does add more weight on the side of turning down the "oh while we're in here we'll just take out those healthy ovaries because you don't need them any more" sales pitch. It really all comes down to weighing risks, and that has to be done by each woman for herself.

Managing cardiovascular risk in menopause

Yeah, but most of us here have already been through the surgery. How do we manage those risks now?

First of all, by simply being aware of this, aware of the body of literature we've linked to above, that is all legitimate medical research that you can share with your doctor in discussing this aspect of surgical menopause. We need to be monitoring this risk: we need to keep an eye on our blood pressure, we need to get lipid levels checked as part of our annual checkup, and we need to be prompt in seeking actual treatment if either of these start to rise.

Beyond that, though, we can work to forestall these effects through other means, nonmedical things we can do for ourselves. That's right: we're going to talk about those unpopular topics of good diet and exercise along with weight reduction. 

Right now, proponents of the high-fat/low-carb diets continue to duke it out in research studies with those supporting the so-called "Mediterranean diet." Our bookmarks account has a huge section on research and recommendations about diet: go read and make up your own mind. What you should know, though, is that diet is considered to be a major factor in cardiovascular risk and it's one we can manipulate ourselves. And by that we don't mean a week of good intentions when you give up a bowl of ice cream and really do mean to get more veggies; we mean a serious restructuring of what we eat every day for the rest of our lives. Although the site's main focus is cancer, the American Institute for Cancer Research has a lot of good, applicable material on what constitutes a healthy diet as well as tips on this next topic coming up just below.

And then there's exercise. Exercise does so very many good things for our bodies. It doesn't need to be crushing, but it does need to be regular and it does need to be at least brisk. Current recommendations from the US Centers for Disease Control and the American Heart Association are a place to start, although of course this needs to be discussed with your doctor if you have any issues that might complicate the situation. And yeah, it takes time and oh dear how do I fit that in my already busy life and maybe I'll start tomorrow yeah tomorrow for sure...we understand that whole argument because we struggle with it ourselves. The bottom line, however, is that that heart attack is going to be a whole lot more disruptive of our lives when we're spending a week in intensive care, if we happen to survive it. And, unless we get serious about prevention, that heart attack, statistically speaking, is in our future. Isn't that worth a little work to push back?

Last of all, we can't neglect the role of hormone balance in all of this. Imbalanced hormones, whether an excess of testosterone or progesterone, are likely to edge us higher in cardiovascular risk. Normative estrogen levels look as though they edge us a bit away from that risk.

That means that we need to look carefully when we're offered testosterone to make sure it's truly a situation of testosterone deficiency and we've exhausted other efforts to restore libido before we reach for this option. Using testosterone as a bandaid to cover up for poor estrogen HRT delivery: just raising our risks.

This also means we need to be cautious in supplementing progesterone. The "just because" premise of taking it, without regard for actual demonstrated need, looks less appealing with insulin resistance and metabolic syndrome keeping it company. Using progesterone as an hormonal hammer to bludgeon us into sleeping more in the face of estrogen excess: also less appealing when accompanied by cardiovascular risks.

But what about people who must deliberately induce a progesterone-heavy imbalance for therapeutic purposes? Those with endometriosis or who have a uterus are facing increased risk of endo growth and cancer if they skimp on progestogens in their HRT. Does that mean they are doomed? Certainly not, although they possibly do experience a raised level of risk and should therefor also be more vigilant about protective measures and monitoring. And they can consider, especially if they have other familial cardiovascular risks, whether they might prefer to use a vaginal progestogen to enhance pelvic circulation of that hormone without such high systemic exposure.

So does that mean if we take our HRT, we're safe? That's hard to say, but it looks as though the answer is not that clearcut. Even individuals in natural menopause experience increasing risk as their hormone levels decline, even though they are notionally still producing enough to meet their post-fertile needs. And since the level of hormonal coverage individuals with their ovaries produce in natural menopause is the situation we are seeking to emulate with HRT in surgical meno, we can assume that even if we've started taking HRT from the time of surgery and have had few disruptions in it, we still share roughly that level of risk.

And in case the question occurs to you, no, we're not advocating achieving higher-than-natural-meno estrogen levels as cardiovascular disease prevention. In that direction seem to lie increased hormone-mediated cancer risks, an equally unsavory option. So as with so many things hormonal, the middle ground of normative hormone levels and no more, along with a healthy lifestyle, seems to provide an undramatic but undeniably healthier plan.

Muscle strength and hormones

One of the longstanding rationales for testosterone supplementation is that it is believed to be essential for maintaining (or recovering) muscle mass and strength. It's also often been denied by the doctors of the "menopause only means hot flashes" school of thought that the sometimes crushing and always annoying fatigue and muscle weakness experienced by individuals post-oophorectomy has anything to do with their hormonal status.

But now, "Mechanisms Behind Estrogen's Beneficial Effect on Muscle Strength in Females" (free signup required to read) looks very closely into this situation from the standpoint of the physiology and reaches some conclusions that may surprise you.

Why is this important? Because physiology is difficult to write off to "oh, you're just not adjusting well to your surgery" or other blame-the-patient rejections.

This is an extremely well-written and readable report, even though the biochemistry of it may make your eyes glaze over at times. Still, it's worth it to understand their points—which you can do even if some of the terms may not mean much to you.

Basically, they are finding that the fundamental chemical responsiveness mechanism of muscle fibers is not only weakened (in strength) by estrogen deprivation but that estrogen restoration reverses this.

This linkage between fatigue/weakness and hormone levels is in keeping, of course, with many of our experiential knowledge, but doctors are trained to reject this as "anecdotal" in favor of "evidence-based knowledge." Research is, by definition, evidence-based. That doesn't mean that your doctor won't reject any research that doesn't agree with their own readings, but it's a step up the ladder.

And yes, much of what is being studied & reported in this particular article is rat-based. But in such fundamental processes, rat physiology is very much predictive of human function and it is extremely unlikely that a basic muscle fiber process would differ in humans: it's a whole different order of magnitude from the less-useful animal studies that purport to "prove" that some hormone variant "prevents" cancer. None of this is subjective: it's not anyone "feeling better" but rather specific measurable functions registering differently before and after addition of estrogen.

While the study conclusions note the pertinence expanding upon their findings might have for things like osteoporosis and, interestingly, cardiac muscle disease, we in menopause are more likely to grasp the implications for simple daily wellbeing. Just as joint aches are well within documented effects of estrogen deficiency, so now we can point to estrogen when we are overwhelmed with weakness without having to reach first for such complex diagnoses as fibromyalgia.

But wait: what about testosterone? We've been over the interplay between these two hormones in metabolic interchangeability elsewhere on this site as well as in our discussion group, and it's up to each of us individually to decide how and with what we choose to supplement. What we feel this article represents is solid, defensible support for the experience of muscle weakness in surgical menopause as being reversible with estrogen supplementation. For those who feel their estrogen needs are already well met, fine: go on to consider testosterone. But for those who count weakness in their unmet needs, this provides both solid validation of an association with their estrogen supplementation and supports a means of alleviating it, in a form that, shared with your doctor, might help educate them in this relationship.

Sexuality and surgical menopause

This is, perhaps more than any other topic to do with surgical menopause, a great worry for many individuals and it is correspondingly fraught with misinformation, myths, sales pitches, and wishful thinking. As with many things to do with our hormones, you may come here hoping to find simple answers, a magic remedy to restore things as they once were (or, at least, as we wish they had been), and instead find that it is considerably more complicated than that. We're sorry to have to burst that bubble right here at the top, but if simplistic answers are what you are looking for, you will not find that here.

What we're going to do here, then, is talk through some of the things that are important to estrogen-based libido and sexual response, and then look at how we can work our way through those things to develop our own answers to the question of how we can each restore and maintain libido after our surgeries.

Anatomy

The first requirement for sexual arousal and response is having the actual anatomical structures that are necessary to experience them. That maybe sounds overly simplistic, but bear with us: we've had surgery and surgery in real life is not as clear and straightforward as those little graphics in that pamphlet your doctor gave you.
 
In a real belly, things are crowded together. There may be scarring from whatever previous abdominal procedures we might have had, or from the problems that led us to choose a hysterectomy. And not everyone is exactly identical. Most of us have most of the same things in fairly much the same places, but it's not exact: this person's nerve may be right here while another's is slightly over there.

Further, not every surgeon is equally skilled, especially when it comes to vaginal or laparoscopic procedures where access is trickier or where there is a great deal of scarring or other complexity to be sifted through. While they may do a fine job of identifying what they came for, the major organs to be removed, they may be less skilled at identifying and leaving intact those things that are not to be removed.

And, finally, not every surgeon feels that surgically menopaused individuals should have their sexuality preserved. Whether they see it as a personal crusade to help reduce the moral affront of non-reproductive women enjoying sex or whether they genuinely believe they are saving us from the indignity of having what they view as shameful feelings, they may make a decision for us that reflects their own values, without consulting us, and accordingly be less than scrupulous about preserving those nerves and other structures required for sexual response.

For most of us reading this, it may be too late to do anything about our anatomical integrity. Certainly if you are still in the preoperative planning stage and reading this, you should discuss preserving needed sexual structures with your surgeon, frankly and fully, to be sure that you feel confident that your surgeon will follow your wishes in this regard. If he does not seem willing to do so, well, there are many other surgeons in the world.

What if you are postop, though, and wondering about this? This is not the first thing to work on because, let us hasten to assure you, this is not a common outcome of a hysterectomy. It is more likely to be so for a more complex surgery that affects more than "just" removing the uterus (say, removal of extensive endometriosis with heavy scarring, or a radical hysterectomy for cancer). It's probably not the first thing on the troubleshooting list. But it is a possibility that will ultimately need to be considered if hormonal balance measures are ineffective. It's an aspect that many people skip right over, but since it's a make-or-break part of the whole situation, we have to keep it in mind even when we turn our efforts to the more common situations first.

Systemic estrogen

So if the anatomy provides for the basic mechanical equipment for sexuality, it's estrogen that powers it.

Surprised? Thinking that we were going to jump right ahead to testosterone? Nope. That's the single most common error in troubleshooting libido and while we'll get to testosterone eventually, what we're doing here is setting out a hierarchy of needs, each of which builds upon the other in providing for full sexual function. And it's estrogen that really powers full sexuality in estrogen-dominant individuals.

We rely on estrogen to help things throughout our body function normally. Estrogen is so fundamental to our bodies that even cis-men produce and require some estrogen for normal health. While we no longer require enough estrogen to support fertility once we reach menopause, we do still have other, non-fertile needs that must have estrogen to function. And many of those needs specifically relate back to libido.

You can read elsewhere on this site about how estrogen is needed to support normal brain chemical balance. If our brain's needs for estrogen are not met, we are subject to disturbances of mood and thinking and sensation that probably won't let us relax into feelings of arousal and sexuality. So before we can experience libido, we have to have healthy brains that can feel inclination and completion.

Other areas of our wellbeing are equally important to a background level of comfort that will let us even begin to think about engaging in sex. Those of us with low estrogen levels often experience crushing fatigue or joint pains, or lack of sleep due to menopausal symptoms may sap our enthusiasm for, well, anything. To try to force sexual interest when we can barely stand to be inside our bodies is going to be a struggle, and that's not what healthy sexuality should be. No matter how much we or our partners want us to resume sexual activity, it shouldn't be a grit-my-teeth-and-carry-on sort of thing.

And estrogen is required for one more aspect of sexuality, and that's feeling like a sexual individual. Whether you call it femininity or sensuality or desirability or whatever, we need to feel that physicality is desirable. That wholeness of individuality and sensation requires estrogen, and without it, the tenderness and mature sexuality we are looking to regain simply is not there.

But what if you are taking hrt already—isn't that taken care of, then? No. Taking hrt does not mean that you are effectively delivering hormones to your body or that you are delivering the right hormones in the right amounts. HRTs are much more individual than that: every hrt works for somebody, but each of us may find that only a certain few hrts really work well for our own bodies. If this concept is new to you because you've started reading this site here, please use our table of contents to explore the rest of the basic hormonal/hrt background we've provided here—especially the "basics" section at the top.

If you are having symptoms of hormone imbalance, then, or if you have unmet hormone needs apparent despite being on hrt, you may not be providing the fundamental underpinnings for sexuality. Just as we must have the physical structures to actually undergo sexual arousal, we must have our basic systemic hormone needs met well enough to desire sex and to feel arousal. And it is estrogen that provides that hormonal foundation.

Vaginal estrogen

The single most common barrier to full menopausal sexuality is lack of vaginal estrogen. This is where the anatomical structures and our hormones come together, directly at the seat of sexual sensation. Without estrogen here, it's as though the main switch controlling our sexual responsiveness is turned OFF.

Our genitourinary tissues (vagina, bladder, and all their associated nerves, blood vessels, and supporting structures) have a high requirement for estrogen. Without enough estrogen, these tissues lose elasticity, lubrication, sensation, and protective immune response, and they become pale, fragile, thinned and gradually lose function. This situation is called vaginal atrophy and, depending upon the source you read, can affect from 50-75% of all women in menopause, surgical and natural alike.

If you've never heard of vaginal atrophy, don't be surprised: you have plenty of company. Despite this being ridiculously widespread, it's a silent epidemic of deficiency that is ignored by both individuals and physicians. Why? Because many of us are taught to expect that menopause will mean they "dry up down there" and lose sexual interest. They may be embarrassed to raise this subject with their doctor. And their doctor may be equally reluctant to bring up the topic and feel that he's done his job by vaguely inquiring if "everything is alright." While efforts are being made (free signup required to read) within the health care community to raise awareness of the need to deal with vaginal atrophy, we need to do our part by opening the question with our doctors.

But what if we're already taking hrt? Doesn't that take care of the problem? No, not necessarily. At today's lower doses of hrt, we're trying to balance risks and benefits by using just the bare amount that meets our basic systemic hormone needs. That amount, in turn, is very likely not going to be adequate to fully nourish our genitourinary tissues.

The good news about vaginal atrophy is that it is very easily diagnosed by symptoms or visual inspection by your health practitioner. Further, it's easily and very successfully treated with some form of vaginal estrogen supplementation (they all work well, so it's a matter of choosing the method you prefer and can afford). This gives those local tissues a boost without derailing our systemic estrogen balance, and because the dose needed is very very small, it's something that is accessible even to those who must restrict systemic estrogen levels in order to control other risks.

It takes some weeks to fully reverse the effects of low estrogen on vaginal tissues, depending upon whether you choose a maintenance dose product or a treatment dose product. And it typically requires ongoing low maintenance doses to keep those tissues healthy—this isn't a "treat once and done" situation. But once good health is restored, return of sexual sensation and desire often follow. No matter what else we may do to enhance sexual arousal and response, they are unlikely to work until we have healthy genital tissues to experience them. You can read more about vaginal estrogen needs and how to meet them in our discussion of vaginal dryness.

Testosterone

Nothing has greater chic in the hormone world today than testosterone. Estrogen is still on shaky grounds following the massive fear campaign kicked off by superficial interpretations of the results of the Women's Health Initiative Study, despite more recent efforts to provide a more balanced consensus. Progesterone continues to be rejected by many doctors because they fail to understand its uses outside the uterus. But testosterone is in that golden spot enjoyed by estrogen during the middle of the last century, where it is evoked as a magic elixir to cure everything that imbalanced estrogen hrts cannot and not yet overshadowed by any significant sense of risk. Although risks have been demonstrated by medical research, because they have not been popularized in the media the way estrogen risks have been, they are generally unacknowledged by doctors and their patients.

Let us state right here that we are not opposed to the use of testosterone and that we are profoundly grateful for pioneering research done on the topic. Just a few decades ago, it wasn't even proven that women produced their own testosterone and that it had a role in female hormone balance. But much of what was written then is overly simplistic in the light of what we know today about hormone needs and risks. Testosterone can be an answer, but it is not, alas, the invariable answer.

Early research showed that individuals in menopause often had low testosterone levels and when these menopausal people were given testosterone supplements, they scored higher on many measures related to sexual function. As more of us used testosterone, it was also discovered that many of their lingering complaints about lack of energy and strength, even on estrogen hrts, were resolved. So, magic elixir, right?

No. At the same time, more detailed research was not only pointing out the cardiovascular and cancer risks that testosterone use might involve, but it was also showing that those who were low in estrogen were using their testosterone not to do testosterone work, but as raw material to convert to estrogen. In other words, for individuals who have not achieved good hormone balance on their estrogen hrts, testosterone is just another source of estrogen and the improvements that they experienced were due to their estrogen needs being more fully met rather than any effect specific to testosterone.

So how does this fit into working on libido loss? The very important lesson we can take from this research is that until we know that our estrogen needs are fully and satisfactorily met, we cannot know whether or not we are going to get any testosterone-specific benefit from the addition of testosterone to our hrt.

Yes, we know this flies in the face of what compounding pharmacists, who insist they can fix every single hormone imbalance at once, will tell us and it certainly is not what the pharmaceutical companies who manufacture testosterone products want us to believe. That is, however, why the major professional society of endocrinologists, the doctors who are the specialists on hormones and how they function in the body, have said in their position paper on using hrts, that

Androgen deficiency should be diagnosed only in women with adequate estrogen status.

But wait—does that mean that there is no role for testosterone in treating libido? What about all those glowing press releases about that new patch and how it helps so many individuals? The US Food and Drug Administration held off approval of that patch in the US because of concerns about risks, even though it had been approved and for sale for some time in the EU. As of 2014, however, not only has the US FDA rejected the patch licensure application, but Intrinsa, the European patch, is no longer on the market there (although the reasons for the withdrawal have been questioned).

Of course there is a role for testosterone in menopause: if there were not, we wouldn't produce it ourselves. But don't be swayed by those who want to sell you something: that's really all about them, not you. For all of the individuals who responded favorably to the tests for that new patch, there were also those who did not. In fact, testosterone supplementation is effective only for a percentage of women, no matter how it's administered.

We need, then, to look at those who didn't respond just as much as those who did. And, based on research and interpretation of our understanding of hormone physiology, it looks clear that the simple answer is that if a woman doesn't need more testosterone, more is not going to help her. Doesn't that sound a lot like what we say about the other hormones? Exactly: with testosterone, as with every other ovarian hormone, we need only enough to meet our needs; anything more only adds to our risks, not our benefits. If we have enough testosterone already (or would have if we weren't using it to make estrogen out of), more isn't going to make it work any better.

In fact, more testosterone not only raises those risks mentioned above but doesn't really provide for the sexuality we're looking for, even though it may increase our urges. Here's how one of our message list members who was working on their libido with testosterone described the difference:

With testosterone, it looks like it addresses one part of the sexual libido thing — genital stimulation and desire for it — but not the desire for intimacy.... I can vouch for this statement from personal experience — for me that sums up how I felt 100%.

Pulling it all together

Yeah, yeah, you may be saying, but how do I use all of this to troubleshoot my libido? Let's look at that now.

Based on documents like that endocrinologists' position paper and the experiences of women like you who have come to our discussion forums to work on these issues for themselves, here's the order of addressing our hormone needs that seems to be the most efficient and likely to work.

1. Meet systemic estrogen needs. If we are not fully meeting our needs, we don't have the basic foundation to experience sexuality. For individuals who do not want to or are not able to take hormones, it's important to choose an SSRI (if that's being used in place of hrt) that does not have a libido-suppressing effect. Only once we are at a systemic and brain balance are we ready to work further on restoring libido.
2. Meet vaginal estrogen needs. If you have dryness or burning or other genital symptoms, you may be suffering from low estrogen to that area. Even if you are not, if you are taking systemic hrt you may not be fully nourishing those tissues. So the first step in troubleshooting this aspect of libido is to ask your doctor for an exam (we're talking visual exam—not a painful or mechanically invasive test) and discussion of vaginal estrogen needs, and raise the question of whether or not you might benefit from some vaginal estrogen. Yes, this may be embarrassing. But many doctors are very willing to discuss this topic with you even if they too are not sure how to open the dialog. So take that first step and you may well find that things are very much easier after that.
        Vaginal estrogen needs are critical to sexual function and are very easy to supplement successfully. For many, this has been the step that has restored sexual function. Yes, just this simple.
3. Meet testosterone needs. This comes third on our list because it will be ineffective if the other two needs are not met first. And rather than just launching into trying testosterone, this is where we'll reverse our usual stance that questions the value of hormone level tests: it's a good idea to have our circulating blood levels of free testosterone tested. It's a simple blood test that your doctor can order done by a lab.
        While the normal levels are a range, not an absolute, they will give you some guidance as to whether or not you are near adequate in production. Many of those without ovaries are perfectly capable of meeting their menopausal testosterone needs by adrenal output, so it isn't unusual to find that supplementation isn't really needed to reach normal levels once it's not all going to produce estrogen. If we have normal testosterone levels, adding more testosterone is more likely to push us into excess—with its associated significant health risks—than to improve the action of testosterone. So it makes sense that we might consider testing first and only bother with supplementation if we show a demonstrated testosterone shortfall after our estrogen needs are properly met.
        It's also a good idea, because it relates to our cardiovascular risk profile and how testosterone raises those risks, to have our cholesterol and other blood lipids checked when beginning testosterone supplementation. Treatment of elevated levels may be required in order to use testosterone safely, so it's easier to get this additional blood test up front than to find out only after we've had that heart attack.
        We're not going to spell out the different testosterone options and how to use them, since they vary from country to country and to some extent are personal preference. There's more on that on our various testosterone and hrt pages, which you can find in the table of contents.
4. Consider whether there has been anatomical damage during surgery. This is the last step in the process. If we find that we've got our estrogen needs well met, both systemically and vaginally, and we find that either we don't need more testosterone or that the testosterone we take doesn't make enough difference, then we need to consider whether we have had some sort of damage during surgery that is preventing us from sensing or responding to sexual stimulation. This is a complicated topic, and may require visits to more than one doctor. As a general rule, taking this up with the surgeon who performed our hysterectomy is often not particularly helpful—this doctor may just feel that we're attacking their competence or planning a lawsuit, and they may respond defensively, putting the blame back on us. Since blame has little effective value at this point, that is not an especially satisfying strategy for solving our problem. Instead, many individuals find workups from specialists on pelvic floor medicine helpful, opening up referrals on to neurologists or other surgical specialists depending upon the specific problems identified. It is possible to have some surgical damages corrected, so keeping an open mind going into this process is important: it can take time, but it doesn't mean that you won't ever regain sexual sensation.

So, a long discussion of possibilities and steps, and that's probably not the sort of answer you were hoping for. We'd all like to believe that the magic, whether it's testosterone or some obscure herbal remedy not-available-in-stores, will instantly restore us to the sexual appetites and capabilities of an eager 20-year-old. But in fact, as so many things to do with surgical menopause, it's more complicated than that and there are no universal answers that work for every one of us. Still, the things we have outlined above can help you work through the possibilities in an orderly fashion that has worked for many. Whether your own answer is in estrogen or testosterone or in surgical repairs, there probably is a good answer out there for you. It just takes some work and experimentation and careful recording in your meno journal.

Can't I just have some instructions on how to do this, please?

It happens all the time: a new member comes to our discussion list to say:

This is all too hard! I don't want to learn to be a doctor! Just tell me what works for you all so I can get the same thing and be rid of these symptoms that are driving me crazy.

This same question applies to searching for hormone balance once we're launched into the process:

if I have bothersome symptoms that I attribute to hormone imbalance, is there a way to go about replacing hormones knowledgably, or is it just a shot in the dark?

Sadly, there isn't just one good answer, one best hrt that will make each individual feel just the way they want to. All of our bodies are different; our lifestyles are different; our family/genetic histories are different. How any given hrt will function in any one person's body depends upon all of those little details where those differences lie. Beyond that, medical science does not yet have enough insight into how our ovarian hormones and menopause actually function in our bodies in order to predict any of this. There is no lab test that says this hrt, this is the one that will make you feel the best.

While we cannot predict how we'll respond to any hrt or hrt change, there is indeed a series of systematic steps that we can bring to the process of trying different hrts and dosages on to see which fits our own body best. It's not a firm rule by any means, but we've developed a rough decision tree that seems to work for covering the essentials.

It's also, we need to add, very very useful to journal symptoms carefully during the process, because each decision point is driven by how our bodies respond. While lab tests can tell us if we're terrifically off base, they can't tell us when we feel good or if we could feel better by making this or that adjustment. Only our bodies can do that, so we need to learn to listen very attentively and remember what we've heard, preferably by keeping good notes. If you're unclear on how to get going with a journal, we've created a rough draft spreadsheet workbook (note that there are additional pages, listed across the bottom, beyond the one that opens). Feel free to save a copy and modify it to suit your own needs, either on your computer or by printing it out. While there are no limits to the format that suits this purpose, reading through our version might help you get a better feel for what you want to be recording.

As you read through these steps, first read them straight through. Each section contains links to either supporting documents or much more detailed information on those topics that is found elsewhere on this site. When you're ready to explore a section in detail, by all means go follow those links. But for overview purposes, we've tried to keep this discussion focused on the process, not the content. Ready?

Step 1: Which hormones?

We begin our consideration of our hormone supplementation needs by deciding where we will begin: what hormones we will work with. While individuals taking therapeutic hrts to treat or help control a specific disease condition (like endometriosis or cancer risk) will often need to work with multiple hormones at once, most others may be better advised to begin with just estrogen, planning to achieve its best possible balance before adding to the complexity of the process by adding additional hormones to meet specific objectives.

We didn't just make this up (and we offer this knowing full well that many sales pitches will tell you just the opposite). This is the basic premise of the medical specialist statement, American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Menopause (free signup required to read). They are, if you are unfamiliar with the term "endocrinologist," the specialists in dealing with hormones. We find their reasoning compelling: because other hormones can be converted to estrogen if that hormone is deficient in supply, we really can't get a picture of other hormone needs until that estrogen need is satisfied. Until that time—and this is a critically important concept—we're just using those other hormones to prop up a suboptimal estrogen situation. Only when our estrogen needs are well met can other hormones fall back into their own roles such that we tell whether or not their supply is adequate.

Step 2: What type of hormones?

A useful way of categorizing hrts is by type: synthetic or human-identical. If you're not sure what "human-identical" means, we are increasingly switching to the use of this term because compounding pharmacists have taken over "bioidentical" as a marketing term for a specific hrt-and-testing sales program, making it confusing to determine whether the word is being used in a generic or proprietary sense. In this instance, then, we're simply distinguishing between those hormones that are chemically identical in structure to our own from those that are not, once in our systems.

This, as all decisions at the top of the tree, will be in part guided by preference and in part by personal health considerations.

What would constitute such a preference or risk? Some vegetarians might eschew an hrt from animal origins. Others have ethical objections to the way some hrts are manufactured. Some individuals are tailoring their hrt to help treat or control hormone-sensitive disease states like cancer or endometriosis and may need an hrt that cannot be converted to any other substance or that has a metabolic pathway possessing certain characteristics. Yet others may see hrts as split between overly pharmaceutical and more "natural" according to chemical structure. These are all perfectly reasonable preferences to hold and your doctor should certainly be willing and able to work within them.

Do you have to decide this right away? Nope. This is just one criterion by which you can winnow the whole field down to a reasonable number of candidates. If you prefer to skip this step, fine: you'll just have a wider selection to choose between.

Step 3: Delivery by which route?

Next we'll further narrow our choices by looking at route. Each route has specific benefits and risks, and lifestyle factors will come into this decision as well.

We may make a route decision based upon therapeutic needs: someone taking thyroid hormone might opt for a non-oral hrt so that the two supplements don't conflict with each other. Some route choices may relate to health situations: a different individual with digestive issues might eschew an oral, while another with a skin disorder might not feel comfortable with transdermals other than transbuccal or vaginal. Those who work outdoors in a very hot climate might find that patch hrts will be fighting an uphill battle for adhesion. Others caring for infants may not choose to use an hrt like a gel, which remains on the skin for a prolonged period and can be transferred to others. We all have unique factors in our lives and health situations that may make one or more routes either undesirable or sound like just the right combination of convenience and plausibility.

Step 4: At last we get to the specific hrts

Having thus lopped whole chunks of the list off as being unsuitable for one reason or another, we should now have a shorter list of hrts that meet our initial criteria.

Now we can examine the specific hrts, all listed on the estrogen pages (US, UK) of the hrts section of this site. We need to review the discussion of them in these listings as well as the supplementary information, usually the prescribing information pamphlet, linked to for each one. This may further help us determine where we feel our best starting place may be.

For example, a person wanting a transdermal estrogen but concerned about transferring hormones to small children might opt for a cream, with rapid skin penetration, or a patch, which is covered by the backing, over a gel, which forms a reservoir of hormones on top of the skin and easily shared. These kinds of details are in that discussion and can have a great deal of bearing on what specific hrts within a general route-related family will best suit our preferences.

If you're getting confused and losing track of all of these various criteria and how they apply across the estrogen hrts list, we've made an Estrogen Selection Matrix for both US and UK estrogen-only hrts. Print a copy or copy/paste it into a spreadsheet program, and just start crossing out the lines with characteristics that you don't want. Eventually you'll come down to those you are ready to read more detail about (because sometimes a choice will come down to specific details not covered in the matrix).

It takes some time to go through all of these steps, but by gradually narrowing the available options in this way, we can eventually arrive at a reasonable number of choices that represent hrts that actually interest us out of the overwhelming number that the market offers. And by having thought through this process of justifying our choices to ourselves, we're well prepared to pitch exactly those reasons to our doctors in support of our argument that we want to try these particular hrts rather than whatever default he routinely gives to all of his patients or whichever one he happens to have just gotten a hot pitch on from the latest drug rep to visit his office.

Finally, don't forget to make sure that your health insurance coverage will cover the brand (or similar generic) or that you are able to pick up the cost yourself. Some basic hrts like Estrace are available so cheaply that it becomes more sensible to pay cash than to involve drug insurance deductibles and coverage. GoodRx can help if you want to research price deals.

Step 5: What dose?

Once we've made a choice of hrt, then, it's often simplest to start at the "usual starting dose" unless we have specific criteria to meet that would indicate otherwise. What would those be? Perhaps you distrust hrts or don't really believe you needs one, and so you want to to take only the barest minimum to see what happens. Perhaps you have previous experience to suggest that you respond strongly to hormonal preparations. Perhaps you're unusually large or small in body mass compared to the general population.

It's generally not a hugely successful idea to assume that our requirements will be higher than usual, especially when we come to a new hrt, just because our last one delivered ineffectively. Why? Because an hrt that didn't get into our systems well didn't really get a chance to show how it stacked up against our personal level of need. Similarly, if our previous experience was with oral contraceptive pills taken preoperatively, we need to recognize that this was a different blend of hormonal agents at a different dosing level, addressing a whole different situation and one that really doesn't predict our menopausal, post-fertile needs for estrogen.

If we do overestimate, it's harder to recognize excess than it is to identify symptoms suggestive of shortfall. Additionally, that recognition delay represents a period of enhanced risk, as well as taking a longer process to clear, than it requires to recognize deficiency and ramp dosing upward.

This may be where some women come into conflict with their doctors, because it's way more cost effective for them to hit things right on the first try (and impresses women with their doctor's abilities). That's great when it works, but when it doesn't, then a woman has to dig back out of that hole and it's not.... fun. So if we keep in mind that this is an orderly process and not a leap to the finish, it can be easier to have patience with this part and be more gentle with our bodies. "Start low and go slow" is not a particularly exciting sounding rubric, but in fact many of us have found that excitement tends not to be what we're looking for in hormone balancing and that it ends up being well worth taking the slower approach rather than unsnarling ourselves after an over-hasty miscalculation.

There's also a popular myth that anyone who is younger than the typical menopausal age of 50 will need very high doses of hrt because they must match their premenopausal levels. While they may indeed start a little bit higher than the 50-year-old just to let themselves down a little bit more gently, in fact they are no longer fertile and most of that higher level of hormones was going to support fertility and uterine needs. We've seen younger individuals start at several times the usual maximum dose on this mistaken premise and rapidly find themselves in miserable excess. There's no reason to put our bodies through this: the usual starting dose will generally support us enough not to be in dismal shape and we can more gently feel our own way from there. Really.

Step 6: Do it!

Okay, so we begin taking the usual starting dose of our chosen hrt.

Then we wait. And journal.

It takes 6-8 weeks for full adjustment to a change in hormone support to be carried out throughout our bodies, whether we are starting hrt or simply changing some aspect of the hrt we've been on. We don't need to wait that entire long time, however, to have  first-pass sense of whether this is an hrt that is going to work for us or not.

Step 7: Is this hrt working for me?

In the early stages of a trial of a new hrt, the decision tree is first of all: working (delivering) or not. Symptoms that our hrt is not delivering are going to present as soon as our previous hrt (or pre-op hormone supply) is leaving our system and the new can be presumed to have entered it.

The amount of time this takes to show up varies with types of hrt. Patches are the most rapid and a switch from one patch brand to another should be virtually instantaneous unless there were a situation of hormone excess as well. Something like Premarin, that has a long buildup and elimination period, will take longer to judge, especially since the elimination period grows longer the longer this hrt is taken. And for all of us, it will generally take a us some months after surgery to stabilize on hrt and really get a sense that our preop hormone support is no longer having any effect.

The general rule of thumb we've seen in discussions of hrt is that it takes a week or sometimes two to have a sense of general delivery, but that will need to be modified somewhat for specific hrts. As a general rule, patches provide the fastest turnover; orals and daily-dosed transdermals are middling; Premarin and long-dosed forms (pellets, shots) take the longest to get out of our systems—sometimes months.

And of course the other major part of this turnover is the uptake/buildup efficacy of the new hrt. Again, patches work very quickly; daily-dosed transdermals are pretty close behind; orals, pellets and shots may take a few days longer and Premarin is somewhat beyond that into the weeks scale.

So when we look at what we've been journaling, we're looking for whether this is an hrt that's not delivering at all (big dramatic symptoms, usually) or one that's delivering and just needs some work to get into better step with our level of needs.

This time period of our first trial of a new hrt also gives us a chance to decide how well this hrt fits into our lifestyle and overall health. If the patch gives us hives under it or simply fails to adhere, ever, then dose isn't an issue: that patch isn't going to work well for us. If we're allergic to an ingredient, we're never going to have a chance to see if it is otherwise a good hrt for us. If we have wicked heartburn or nausea after taking an oral hrt, we're not likely to want to continue even if the hormone support is good. So there are quite a few factors that come into that early decision of "is this hrt working for me?"

And if the answer is: No

If the answer at that point is no, it's not working for whatever various reason (or none that we can determine and it just...isn't), then we pull out of that trial and select another candidate based upon the nature of the problem with the one we've just tried.

If it's rash under a patch but we really really like the patch otherwise, then changing brand addresses that issue and points out the next direction we might take. If we just can't stomach an oral, we might move back to route considerations and work through our options again. In other words, we need to decide where the failure point might have been and return to that level of our previous decision tree and take a different turning there. If we don't really know what went wrong, then we can reverse the tree and work back up it from the bottom, trying our next favorite that changes that level's characteristic.

While our doctors will often counsel us to wait up to two to three months, even when we find after a couple weeks that our hrt is making no appreciable difference or we're encountering insoluble problems trying to use it, many individuals' actual experience has shown that a massive negative result from a particular hrt is most unlikely to entirely reverse itself over time. Sure, there is an adjustment curve and small niggling irritations may ease away over time, but just flat-out reversing a major negative experience tends not to actually happen.

Your doctor will probably be most sympathetic and willing to change your prescription after you've waited your three months in misery, but why should you have to earn that change that way? Your hot flashes and teary meltdowns aren't keeping him awake at night. You have the right to make this call, to say "no, I'm not doing this any more; I don't like this one and I want something else." And that is the conversation in which you also have your next choice already identified with a pitch you're prepared to make in support of why you think it'll be better. Take notes with you and support them with data from your journal: specific data helps your doctor's scientific mind accept the validity of your experience rather than just brushing you off as a silly hysterical  who's not accepting their changed circumstances and is doing too much reading on the internet.

And if the answer is: Yes

If the answer is yes to the question of whether or not our hrt is delivering, however, then we move into the realm of tuning that hrt for best possible support of our needs.

Most typically, the major issue with an hrt that is "delivering okay but" is dose. Here the question is whether or not we're experiencing symptoms that suggest the dose is either too high or too low to meet our needs. While it may be tempting to address this issue in a big jump, aiming at a one-stop answer, that impatience can cloud the process and ultimately prolong it, especially if we jump right past our needed dose.

Each large dose change we make induces fluctuations in our hormone levels that themselves add to symptoms we're experiencing. We need to wait for the symptoms due to the change to abate before we can judge the actual adequacy of the dose we changed to. This is a critically important element of hrt tweaking, and one many people regretfully fail to take into consideration as they make rapid, large, multiple changes in their hrt while they flail about looking for something, anything that will make them feel better RIGHT NOW.

But smaller dose changes, ones that are small enough that our body barely registers that change has occurred, allow us to minimize that disruption from fluctuation and slowly, gently home in towards that best dose. Obviously, some hrts can only be adjusted in fixed increments while others are infinitely adjustable. We have to work within the limits of the specific hrt we've chosen... but lack of adjustability may, at some point, actually cause us to set that hrt aside and look for a new one because it just cannot conveniently be adjusted to our actual dose need. At this point, we do the best we can, and this is where "best" = small = gentle.

At some point in this dose-adjustment process, even if we are trying to sneak up on our best dose level, we may overshoot and ease into symptoms of excess. The smaller the increment of excessive supply, the longer it can take to be apparent that we're taking too much. That's another good reason for patience, of course. But a sharp dose drop for a short period will let us clear a relatively small excess and we can then take our last incremental dose increase off the top and return to the next previous dose level to restabilize. In that way, we actually narrow in on our best dose by bracketing it, a concept well known to photographers who do the same thing with exposure settings.

Beyond estrogen

Okay, so we've tweaked that dose up and down, maybe auditioned a couple different brands or types of hrt for optimal fit, and found where we feel best on our estrogen hrt.

But wait, we don't actually feel as "best" as we were hoping to be.

If we've fully explored our estrogen hrts, feel we're on the best hrt and dose we can find, and still don't feel that we've gotten where we want to be, then we're ready to explore other hormones and drugs. We choose these according to which hormone specifically has the actions we're hoping to add or which drugs might cover aspects of our hrt that we are missing. And then we go through the same entire process with that hormone or drug while keeping our estrogen stable. We may end up needing to tweak our estrogen in the final stages of tweaking the new hrt to take relative balance into account, but we need to get pretty close first or we'll just be setting up a state of confusion we'll end up chasing until we're dizzy.

We're not going to go through all of the different other hrts and drugs and factors like the needed nutrients for metabolizing hrts (that make a huge difference in how we experience those hrts' effectiveness). You can explore more of these topics on this website using our Table of Contents to find more detail on these, and you are welcome to join our discussion forums to help troubleshoot this step. Basically, once someone has achieved some reasonable degree of stability by meeting their basic estrogen needs, some of the pressure is off and they can take the time to learn more, to explore more options. And the work they've done in learning to listen to their body and work through the process will provide them important tools to continue their refining work on their own.

Okay, now you try it

That's a general outline of the process. Yes, it's rather loose and a whole lot of this is left up to you. That may seem overwhelming, but you should keep in mind that you are the expert on your body; no one else can sense what works best for you. There is no formal process—your doctor will do much this same thing for you if you simply place it in his hands and wait passively. Unfortunately, if you're not participating, that means those decisions will be based upon that doctor's preferences and they may not speak to your own concerns at all.

Remember too, that every change we make, whether it's the whole move to a new hrt or just the tiniest incremental dose adjustment, can always be rolled back. If we're at a maybe okay place now and just wonder if X might make things better, we can always try X out with the knowledge that if it turns out not to be our answer, we can go back to its sort-of-okay predecessor, regroup, and reconsider further attempts. It's not as though each try erases all previous situations. Keeping this firmly in mind provides a safety net that does allow us to experiment with a little greater daring.

Want a little backup? We're there on our forums to help you cut through to the issues and look at where you might turn to make the next iteration of adjustments. We can't tell exactly what any given individual should do, but we can often as a group ask some questions that will help then make their own decision of what to adjust next.