Survivor's Guide to Surgical Menopause

Primary Prevention of Cardiovascular Disease With HRT

2012-01-05T12:43:00.001-07:00

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.

(tl;dr? One page sidebar)

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, and both 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 and 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 CV 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 at five years 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 CV disease in that limit, even though it's CV 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 CV 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 CV 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 CVD 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 are still not good solid bodies of research evidence that pit 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 CVD 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 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.

CV 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 CV disease, and so while the "least needed 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 need, each of us, to 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.

Our reading list is broken

2011-09-27T11:21:00.000-06:00

The reading list that normally displays over there on the right, under the "elsewhere" paragraph, has been discontinued by the provider of the bookmarking service we use. We're hoping it's just a brief service blip as they reconfigure following the company changing owners, so we're going to leave things as they are for the moment and cross our fingers that they will come to their senses and resume that functionality.

For now, the tag page is gone, but you can get to the main bookmarks page still. Sadly, many of the tags we used to make finding topical reading easier are gone from the list along the side, but you can still search for a specific topic and find those unlisted tags. So, not as easy to use, but they are all there.

Stay tuned. Either things will come back or we'll move to another form of providing updated reading on all aspects of menopausal health and hrt use. We'll let you know.

Update 9/28: Looks like we're back, although there may be bumps ahead before things settle down. Thanks for your patience.

Surgical menopause boosts cardiovascular risks

2010-08-28T09:42:00.003-06:00

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 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 CV status of women on HRT as compared to women without continues to fuel research in 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 worsens CV risks. 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.

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 CV 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 (free signup required to read), 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 CV 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 preoperatively 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 our help.

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. Of course, 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 if he is in denial about 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 CV 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.

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. 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 CV 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 resistence and metabolic syndrome keeping its 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 CV risks.

But what about women who must deliberately induce a progesterone-heavy imbalance for therapeutic purposes? Women with endometriosis or who have a uterus are facing increased endo growth and cancer if they skimp on progestogens in their HRT. Does that mean they are doomed? Certainly not, although they probably 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 CV 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 no. Even women 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 women with their ovaries produce in natural menopause is the situation we are emulating with HRT in surgical meno, we can assume that even if we 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. That way seems 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.

Is that it? Yep. We need to be sensible in our menopause. If we must induce therapeutic hormonal imbalances, we need to be attentive to how we can balance our various risks. And if we are facing oophorectomy, especially if post-op hormone deprivation is part of our treatment, we need to speak frankly with our doctors about cardiovascular risk and develop a specific plan for how we shall deal with it before we end up in instensive care with our first heart attack or stroke. Denial of cardiovascular risks: not looking so plausible any longer.

In the news: Progestogens and lung cancer

2010-08-14T15:05:00.001-06:00

Estrogen-only therapy may not up lung cancer deaths was the headline of one of today's Reuters press releases. According to the article, while the Women's Health Initiative study showed that women in natural menopause taking conventional combined estrogen + progestin hrt had an increased risk for lung cancer (free signup required), women in surgical menopause taking estrogen hrt only did not show that risk elevation.

Interestingly, the research is mixed on this topic. We also have an article "Dietary boron and HRT reduce lung cancer risk in women" published in 2008 in the American Journal of Epidemiology that, based upon an "ongoing case-control study in Houston, Texas...[with]...763 women were diagnosed with lung cancer, and 838 were matched healthy controls with data on both diet and HRT," found that "HRT use was associated with a 31% reduction in lung cancer risk."

Okay, so how do we interpret this for our use? Does this mean we should quit using progesterone?

No, this probably doesn't mean that we can't or shouldn't use progestogens (progesterone and its synthetic cousins the progestins), but that answer may not be valid across all types of surgical menopause, so let's look at this a bit more closely.

Progesterone is different, isn't it?

First, let's set aside the whole "progesterone is natural so it doesn't carry this risk the way progestins do" issue.

So far as we have solid information on this, this statement represents nothing but wishful thinking. We have no serious population study data that differentiates between progesterone and a progestin, let alone between different progestins. The WHI study was done with Provera, a specific progestin, and the results have not been checked in any large study against other progestins so we don't know—and analyses of the study results have pointed this out—whether this is a Provera issue or a progestin issue or a progestogen issue. Because one is taken as standing in for the whole, the media coverage and the doctors who get their continuing education from CNN will assume that it means all progestogens and panic accordingly. But each progestin has very different chemical characteristics and there is some reason to question whether this relationship with lung cancer is due to the elements progestogens have in common or an element Provera possesses uniquely. Until that distinction is identified, we really don't know. And until we do, we are as liable to panic and jump in the wrong direction as the right one.

Let's restate that to be sure we're clear: until we have research that identifies the mechanism that causes this relationship between Provera use and lung cancer incidence, we have only a correlation, not a causation, and we cannot know whether it's:

a result of progestogen activity, which would include progesterone, or
a progestin effect that doesn't pertain to progesterone itself, or
a specific effect of Provera's unique formulation

A lot probably depends upon how we use it

Now let's look at different categories of women and HRT use.

Women in surgical meno who do not have a uterus and who are taking plain estrogen, whose progesterone needs are being met adequately (as they define them) by their own progesterone production and the progestogens they acquire through environmental contamination, are shown by this study as not experiencing this elevated risk. No one has suggested that they require hormone blockers to reduce their own progesterone production for further protection, which suggests that hormone levels appropriate to natural menopause with ovaries (which is what we emulate with hrt in surgical meno) are not presently interpreted as carrying this risk.

Women in surgical meno who do not have a uterus and who are supplementing both their estrogen and progesterone may be at an elevated risk level. As we noted above, we can't rule out risk based on the type of supplementation (progestin vs progesterone) at this time, so we can only work from the safer, more conservative position that increased progestogen exposure equates to some unknown level of increased risk.

But let's not get caught in the binary reasoning trap of research questions. This is probably not an either/or situation. That is, taking one molecule of a progestogen most likely does not slam us straight into the lung cancer risk category seen in the WHI. These women in the study who were on combined hrt were on levels of progestin designed to protect an intact uterus from developing cancer due to the estrogen stimulation. And they were on a fixed, study-mandated dose of estrogen, with no regard to their personal level of needs, especially at their age (they were women mostly in their 60s and up, taking a "standard" hrt dose for women a decade younger). So these women were being exposed to relatively higher levels of estrogen than we typically use in surgical meno if we are following the basic "as little as meets present needs" rule that is the current recommendation by the various medical specialty groups that have looked closely at all aspects of hrt use and menopause. In other words, they were taking a progestin at a therapeutic, not minimal-needs, level of dosing.

But that's not what we typically do when we supplement progestogens in surgical meno if we don't have a uterus. We take a dose only large enough to make up the shortfall between what we can produce and what our bodies need to balance out the estrogen we're taking. So the conceptual test we can apply here is that if women are not advised to have their ovaries removed and take hormone blockers to prevent their postmenopausal progesterone exposure, we may not be raising our risk exposure significantly when we simply mimic natural menopause with ovaries...as is the goal of surgical menopausal hrt. Now, we cannot promise you that this is entirely safe, but what we can suggest is that is reasonable based upon what we presently know.

But some women supplement to higher levels, and we're not sure how comfortable they should be about their risks. Who would do this? Many doctors prescribe high levels of progesterone to counteract excessive estrogen doses or to use progesterone as a hammer to bludgeon women on high or ill-fitting estrogens into being able to sleep. How high? Women who are taking 100mg or 200mg or even more of Prometrium or the equivalent are trending out of the supplemental range and into therapeutic dosing. And their risk picture is much less clear. They are approaching the level of supplementation that the WHI participants who saw that raised lung cancer risk were using, and that raises the question of whether they would be safer using some other approach for dealing with their problems than their therapeutic levels of progesterone intake. This is not a question we can answer yet, but it's probably one we should raise when we're looking at these higher progestogen doses.

And finally, the third group of women: those required to use therapeutic progestogen doses to treat some other risk. These would include women in surgical menopause who retained their uterus, or women with endometriosis. They must take more than a balanced dose to produce this therapeutic effect, and this places them right into the WHI risk profile.

So how can this set of risks be managed? On the one hand, we can look at relative incidence of endometrial cancer and compare it to the lower risk of lung cancer. Are there modifying factors? Surely familial history and smoking exposure will also play into the lung cancer side of things, yes.

Is there anything these women can do to lower their progestogen exposure and still obtain therapeutically effective doses where they need it? Yes, in fact there is: use of a vaginal progestogen provides higher levels in pelvic circulation, where therapeutic effect is needed, and less in general circulation, where it is not. There's more information on this in our discussion of hrt for women with a uterus but no ovaries, as well as in a discussion of a news article about contraceptive patches. While we don't know what "safe" is in this context, surely whatever we can do to lower our exposure risk until it's better understood is at least doing what we can to approach safer.

The bottom line

We don't have enough information yet to be able to draw any sort of safe-or-not line. We may never have this: research isn't about what we want to know; it's about what someone will fund a study to find out, and that's usually dependent upon who thinks they can make money from its results. At the moment, though, this correlation between progestogen use and lung cancer suggests that we should use only as much of any progestogen as we really need, and it probably makes sense that we should do what we can to limit our systemic as opposed to therapeutic exposure.

Should we panic and give up progestogens entirely? Oh goodness no: we don't begin to know enough to say this, and even the risk factors as they stack up don't begin to suggest that level of panic is necessary.

Should we figure that because progesterone is a natural hormone manufactured by our own bodies that it's safe? Nope, not this either: we know that our own estrogen poses cancer risks that we can reduce by controlling our exposure, and this may well turn out to be the same sort of situation. So no, the old Dr. Lee premise that you can't have too much progesterone is looking as shaky as those 1950s articles touting estrogen as the magic agent to keep us "forever young."

Hormones are active agents that are active throughout our bodies. Something this active would never be likely to fall into entirely-safe territory. What we need to learn and can hope that research will begin elucidating is just what the parameters are of the risks that progestogens pose. Only then can we make sound decisions between our various risks to make sure that we're only engaging in the ones we deem acceptable for the benefits gained.

Muscle strength and hormones

2010-04-27T18:33:00.002-06:00

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 women 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-woman 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 women's 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 isn't covered in the headlines on CNN, 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 women 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 and it's up to each woman to decide how and with what she chooses to supplement. What we feel this represents is solid, defensible support for the experience of muscle weakness in surgical menopause as being reversible with estrogen supplementation. For those women who feel their estrogen needs are already well met, fine: go on to consider testosterone. But for those women 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 him in this relationship.

Revised post-WHI hrt use guidelines gradually getting wider press

2010-04-24T12:26:00.001-06:00

We've spoken elsewhere about the more realistic stance that hrt use guidelines have taken as the initial Women's Health Initiative Study cancellation panic has waned and the data is more responsibly re-examined. The North American Menopause Society, the International Menopause Society (both of these are medical groups of significant professional standing) and the American Association of Clinical Endocrinologists (free signup required to read) have all in recent years published revised consensus documents that emphasize that a balanced, patient-centric view that includes quality of life issues must be taken of hrt use.

But those guidelines have been easy to miss unless a doctor is already following the issue. Now, however, the major medical journal in the field, Obstetrics & Gynecology (the journal of The American College of Obstetricians and Gynecologists), has published a clinical review. Sadly, the article, in the April issue, is behind a paywall. A medscape news summary is available, however, and only requires a free signup to read.

There isn't breaking news here: what they say is pretty much covering the same things that the other specialty groups have already stated: there are benefits that rival (or in the case of younger women, outweigh) the risks of using hrt. There are a couple gaps where they miss some elements of interest to many of our readers, notably any mention that route-related effects play into their "risk of causing cardiovascular disease" or any mention of the whole range of SSRIs as alternative symptom-relieving drugs. Since SSRIs are the firstline alternative in oncology, this only goes to show how very insular the medical specialties are. And of course there is not a word about surgical meno (*sigh*). While "smallest amount/shortest time" as a metric seems sort of silly for us, remember: it is actually just the same as saying "as much as we need (but no more) for as long as we need it." This will of course be different in length for us than for women in natural perimenopause, but we can still use this concept to support meeting our needs.

One thing we found interesting and perhaps of use to those of you who are still struggling to have your doctors accept that symptoms other than hot flashes are indeed hormone-related is this statement that talks about the effects of menopause:

Major health concerns of menopausal women include vasomotor symptoms, urogenital atrophy, osteoporosis, cardiovascular disease, cancer, cognition, and mood...

Okay, so if the content isn't new, what's so exciting here?

What is novel in this version is that just about every medical professional in this field subscribes to this journal. That doesn't mean they read it, but it's a professional credential so they do make an effort to at least scan the table of contents while sitting ~~on the~~...ahem...in their library. And so this puts the topic back in front of them in a way that hasn't happened since WHI made headlines on CNN. The fact that their professional journal changed its mind makes it supportable that they might, just might, consider at least reading the newer guidelines. And it means that when we cite this journal back to them, they have a harder time claiming we're just bringing them garbage off the internet and blahblahblahdismiss.

Or maybe your doctor is reading the New York Times

It's rare for a helpful and unalarming topic to get much media coverage since media is a business of selling, not informing or educating. While the WHI cancellation and subsequent anti-hrt backlash got plenty of Great Big Scary Headlines, nobody much has paid attention to the reappraisals and gradual resumption of hrt by many women who just couldn't live a life of hormone deprivation.

But the Times Magazine is known for more in-depth treatments of less dramatic topics, and this past week looked at The Estrogen Dilemma from the standpoint of the women trying to cope with the effects of hormone disruption. While the piece ultimately focuses on the scientific efforts in the field, it is frank about how hormonal fluctuation disrupts the brain and how hrt can alleviate those effects to a marked extent.

It also goes into the so-called "timing effect," something at the heart of many of the WHI results. According to this premise, maintaining adequate hormone levels protects from a number of the negative impacts of menopause. That this kind of early hrt conveys a level of wellness that is not seen in research using hrt to treat existing illness is at the crux of research design and interpretation following on the WHI, and is foreshadowed by things like the startling increase in all-causes mortality (another article, free signup required to read) seen in women of younger age following oophorectomy without hormonal resupply.

This isn't an article to carry in to your doctor in support of convincing him to change his opinion. Things in the popular press are routinely brushed off as not representing scientific accuracy. Still, your doctor may stumble across it on his own, and when it's his own choice to read it, he'll be more open to what it contains.

Beyond that, though, this article stands as another element in a growing trend that he may well notice: gradual rehabilitation of hrt in general. The more times he reads about it, even in the deprecated popular press, the more likely he is to begin internalizing that attitude just the way all that pop coverage of WHI poisoned all notion of hrt.

So, no revolution here. But little step by little step, rationality is slowly creeping back into the foundations of menopausal medical practice. Fewer doctors have grounds to offhandedly dismiss women's requests for hrts. And that can only be a good thing.

Sexuality and surgical menopause

2010-02-27T14:05:00.001-07:00

This is, perhaps more than any other topic to do with surgical menopause, a great worry for women and it is correspondingly fraught with misinformation, myths, sales pitches, and wishful thinking. As with many things to do with our hormones, women 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 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 woman'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 women 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 be less than scrupulous about preserving those nerves and other structures required for sexual response.

For most women reading this, it may be too late to do anything about their 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, extensive endo with heavy scarring, or a radical hyst). 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 female sexuality.

We rely on estrogen to help things throughout our body function normally. Estrogen is so fundamental to our bodies that even 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. Women with low estrogen levels often experience crushing fatigue or joint pains, or lack of sleep due to menopausal symptoms may sap their 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 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 and that you are delivering the right hormones in the right amounts. HRTs are much more individual than that: every hrt works for some woman, but each woman may find that only a certain few hrts really work well for her. 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.

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 it. 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 women and physicians. Why? Because many women 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 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, women and their doctors are trying to balance risks and benefits by using just the bare amount that meets a woman's basic systemic hormone needs. That amount, in turn, is very likely not going to be adequate to fully nourish her 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).

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. 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 vaginal tissues to experience them.

Testosterone

Nothing has greater chic in the hormone world today than testosterone. Estrogen is still on shaky grounds following 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 sense of risk (although these 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 women).

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 answer.

Early research showed that women in menopause often had low testosterone levels and when menopausal women were given testosterone supplements, they scored higher on many measures related to sexual function. As more women 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 women 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 women 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 don't know whether or not we are going to get any 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 female libido? What about all those glowing press releases about that new patch and how it helps so many women? The US Food and Drug Administration has held off approval of that patch in the US because of concerns about risks, even though it's been approved and for sale for some time in the EU. What's with that?

Of course there is a role for testosterone in women: if there were not, we wouldn't produce it ourselves. But don't be swayed by those who want to sell you something because that's really all about them, not you. For all of the women who responded favorably to the tests for that new patch, there were also women 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 her 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 message list 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.

Meet systemic estrogen needs. If we are not fully meeting our needs, we don't have the basic foundation to experience sexuality. For women 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.
Meet vaginal estrogen needs. If you have dryness or burning or other vaginal 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 especially 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 women, this has been the step that has restored sexual function. Yes, just this simple.
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 women are perfectly capable of meeting their 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 a rule of thumb is that we should test 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.
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 his competence or planning a lawsuit, and he 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 women find helpful workups from specialists on pelvic floor medicine, who may refer them 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 all women. Still, the things we have outlined above can help you work through the possibilities in an orderly fashion that has worked for many women. 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.

I think I'm allergic to hormones

2010-02-05T14:22:00.001-07:00

You probably aren't. Think about it: you have had much higher levels of ovarian hormones in your body since puberty. If you were really allergic to them, you'd be more or less dead by now. Seriously, true allergy to one's own hormones is an incredibly rare condition. While low levels of estrogen can make our immune system more prone to taking offense at many previously-tolerated substances, that's a different situation entirely from having an allergic reaction to the hormones our hrt contains.

But I took an HRT and it made me sick!

It's important to try to understand what portion of an hrt didn't agree with us rather than just writing them all off. By considering the matter in greater detail, we leave ourselves other avenues to pursue in meeting our hormone needs. So let's look at some of the things that cause unpleasant reactions.

True allergy to an ingredient

There are other things in all of our hrts besides the hormones they deliver. Some women are in fact allergic to the coloring agents in pills or the adhesive on a particular patch or the vehicle in which a cream hrt is prepared. One hrt that is a particular problem for those allergic to peanuts is Prometrium, that uses peanut oil as the suspension agent in its gelcaps.

If we already know we are sensitive to an ingredient or we break out in an ugly rash or suffer difficulty breathing, then we can rightly suspect that we need to work around an allergic response. But some detective work may be needed to determine just which aspect is causing the problem. All retail hrts list their full range of ingredients on the prescribing information package insert, including the "inactive" ones that color and bind them. Any compounding pharmacist can provide a woman with a similar list for any custom hrt they prepare for her.

If we take a pill, for example, and develop a reaction, rather than assuming we can never take any hrt ever again because it was the estrogen we responded so unfavorably to, we might well invest some time looking at what is in that particular hrt and then searching out a comparable one (by using our estrogen hrts page, for example) that doesn't have the same ingredients.

If our problem is with a patch, it's important to understand that in each brand of patch, the adhesive is the delivery system and for it to be patented, it must be different from every other brand of patch. That means that no other patch will exactly replicate the one that has just given us problems, and so by switching brands, we stand a good chance of leaving that problem behind.

In other words, for every hrt, then, we can do a little detective work and find an alternative that leaves out potential allergens.

As a side note on ingredients and allergies: don't expect your doctor to know much about hrt ingredients other than the hormone they deliver. It's just not important to them in most prescribing situations. This information is, however, recorded in the drug information, where it can be checked in such references as the PDR, product data sheets (which are linked from each estrogen hrt brand here on the site), and through your pharmacist (who can also contact a manufacturer for you if there is a question that is not answered by the product data sheet).

What if all of the retail brands in our chosen delivery method contain this agent? Don't forget that compounding pharmacies can often prepare a similar hrt (in terms of route and active ingredient) that can leave out specifically troubling ingredients. Just because we have allergies doesn't mean that we can't use any form of hrt: we just have to do a little more work getting it.

But I hated the way the hormones I took before made me feel

One special case we see often on hrt discussion forums is the concern voiced something like this:"I took birth control pills and they made me feel awful so I know that means I can't ever take hrt." That's a really common misconception, so let's lay that one to rest right now.

Birth control pills contain larger amounts of hormones than hrts, and they typically contain both a synthetic estrogen and a synthetic progestogen (progesterone-like compound). Both of these agents are not human-identical in molecular structure, which means they are processed by the body differently from our own hormones. That's the idea with birth control pills: we don't want our bodies to use them for anything other than over-riding our own ovaries to prevent ovulation. But that very misalignment with our own chemistry means that we may respond differently to these agents than we do to our own estrogen and progesterone. HRTs contain lower doses and in many cases more human-identical hormones, so they are processed differently from oral contraceptives and they have different effect from them. Because of this distinction, then, gently-handled hrt is usually an entirely different experience from using oral contraceptives.

But there are many other ways an hrt can disagree with us that aren't true allergies.

Route-related effects

Some women have skin that doesn't especially like to be sealed up under a patch, any patch. Some women have digestive disorders or liver conditions that may mean that adding the burden of processing an oral hrt may cause uncomfortable symptoms like nausea. Women with inflammatory bowel disorders or endometriosis, for example, may find that vaginal hrts cause too much local stimulation and can be associated with diarrhea or cramping. All of these kinds of things are really due to the way we're putting the hrt into our bodies, not the hormone's own actions.

In many cases we already know that we have these issues, and so when we select an hrt to try, it tends to make sense that we should choose routes that don't conflict with pre-existing problems. If your doctor isn't putting this together when he prescribes your first hrt, don't hesitate to mention something like "since I already have digestive issues, I'd really prefer an hrt in some other form than a pill." You know your own body than anyone else, so you can—and should—use that knowledge to head off possible problems.

What if you don't know? Then we have to reason our way to what might be the issue. This isn't necessarily complicated: if we have horrific nausea, it really makes sense to try to get around that by switching to a non-oral hrt. Just understanding that route of delivery has an effect on our bodies is part of the key to not writing off hrts entirely, but focusing in on what part of the hrt is being problematic.

Dose-related effects

These are the most tricky to grasp when we haven't yet been introduced to the idea of needs and hormones.

Hormones are active substances that fulfill certain needs in the body. We only need so much hormone work done at any given moment, however. If we don't have a great enough supply, some hormone work goes undone and we experience symptoms from what isn't covered. We all are familiar with one effect of undone hormone work: lack of thermoregulatory stability, which results in hot flashes. But there are many more effects of inadequate hormone supply, some of them quite unpleasant.

We need to differentiate these from negative effects of hrts, however, if we are to work effectively with our hrts. It's most frustrating when we take an hrt that doesn't deliver to our systems and have these effects, since it seems as though we're making ourselves worse with the hrt. But if we look at the effects of low estrogen, we can get a sense of the difference.

Now, if we take an hrt that contains an excess of hormones, such that more hormone work is being done than we need right then, we also develop symptoms. Again, while these can be very unpleasant, they don't mean that the hrt or the hormones are somehow wrong for our bodies; it just means that there's an excess of that work being done. This would include things like fluid retention and swelling, a normal effect of estrogen but one taken to an excessive level when our dose is too high. In this sort of situation, backing off on our dose until we reach a supply more closely aligned with our level of need will allow these symptoms to abate and a more comfortable "fit" with our hrt achieved.

There's lots of troubleshooting involved in this process and sometimes it's really not too clear which way we're trending. We spend a lot of time on our message list discussing this sort of thing. What we're introducing here is the bare outline of the concept, roughed out so that you know that this can be one source of problems; it's not really a full exploration of the kinds and extent of problems that can occur with hrt dose mismatched to needs. We just want you to know that this can happen, and why it can be so unpleasant...without being an allergy.

What's the best way to get a perfectly even hormone delivery?

2010-02-05T14:03:00.004-07:00

You can't.

No, really. It's a myth. Yes, we know the notion that this will solve all of our hormonal ills is a very popular, very prevalent theme in women's hrt discussions online. But it's really neither possible nor necessarily desirable.

Stop sputtering. Yes, we do understand that the ups and downs of the various delivery routes can be problematic, causing all sorts of unpleasant symptoms. But that doesn't mean that the attempt to do away with them by taking ever more frequent tiny doses is going to work. That's right: even if we were to walk around with a constant IV drip of estrogen, we still wouldn't eliminate fluctuation.

That doesn't mean that we can't smooth things out, but it does mean that we need to look into the situation a little more intently to determine what exactly it is that needs to be fixed.

Life isn't a perfectly stable system

To begin with, nothing around us is perfectly stable. Today we are stressed by a deadline at work; tomorrow we will have a cold; the day after that is our birthday and we'll have that surprise party even though you know how we feel about surprises. Everything around us changes and our bodies are built to cope with that. We need that ability to cope, because there will always be something out there, a stressor good or bad, or even the relief of stress.

Our interactions with the world affect our hormone supplies as well as the demands upon them. We eat foods that contain estrogens, either as plant estrogens or as hormones given to commercial meats or as estrogenic pesticides applied to plants and coating them or eaten by the animals we then go on to eat. We drink water supplies into which every day vast quantities of drugs and pesticides are flushed and, because their content is not legislated, we never see test results to show us how very many things are still in our "clean" water. Every molecule of the hormonally-active compounds we consume becomes a part of our hormone reservoir, a reservoir that changes from moment to moment, hour to hour, day to day.

Neither is a woman's body

Our endocrine system (that portion of our physiology to do with hormonal regulation of various functions) is itself not a static system.

First, our bodies need to be able to keep things running in that ever-changing world we live in. We need reserves to allow us to cope, to ramp things up when we're facing stresses and to ramp things down when stress eases off.

And we need to maintain cycles of our own. We're used to the cycles of fertility, but there are many other cycles in our bodies. One of the most important is our daily cycle of sleep and waking, the latter encompassing various stages of alertness and, well, not so much.

Our estrogen is a critical component of our daily cycle. Our levels naturally are highest in the morning, fall gradually during the day and evening, and reach their lowest point around 4 or 5 am. This cycle keys in with with many other hormone cycles, including that of melatonin, another hormone that helps regulate our sleep cycle. It also interacts with thyroid hormone as part of our metabolic regulation. If estrogen levels were completely static, our whole system would come adrift from this important regulatory relationship. And if our hrt were absolutely continuously stable, we'd spend most of our time with either too much or too little to meet our bodies' demands during our daily cycle.

Change, then, is both an inescapable part of both internal and external hormonal regulation and response. But that doesn't mean that it doesn't pose challenges when we do it to ourselves with our hrts.

But the ups and downs are killing me!

The problem is that our body wants to regulate things so we stay on a fairly even keel amidst all of these changes. We work hard, all the time, to do so. When that doesn't happen, of course, the resulting temporary imbalance and the shifts of it coming and going all cause symptoms that can range from annoying to devastating. And it's a feature of our response to change that the greater the fluctuation, the greater the response to it will be.

The most comfortable hrt, then, is going to be one that eases into our bodies with the least disruption, is taken at a dose that lasts long enough that its falling effectiveness meets the rise of the next dose without either great troughs or peaks, and provides a reservoir of hormonal potential to get us through the times of day when we must respond to a need for greater hormonal activity. And as it turns out, none of that actually requires anything like a completely continuous supply.

Minimizing the ups and downs due to uptake

There are two important facets of getting hrts into our bodies. First, they have to physically get into our systems and, second, they need to impact our circulation in a fairly tolerable manner. Both of these factors can present us with problems when hrt characteristics are a mismatch for our personal capabilities.

In dealing with the first problem, we need a delivery method that our bodies can absorb smoothly and reliably. A patch that is stuck now and flapping later isn't going to do that; instead, it will provide us with a roller coaster of ups and downs. Oral deliveries may not work reliably for all women. A gel might be sweat off on the days we go to the gym. All hrt delivery routes have ways they can fail to work smoothly, and so when we're not happy with how a dose is taken up by our bodies, we need to take a close look at just what kinds of interference we might be experiencing at this basic level of delivery.

But it's not enough to get those hormones into our bodies effectively. We also have to weather the rise in circulating hormone levels. Each hrt will create a slightly different uptake curve. A patch will start delivering fairly rapidly, but if the previous patch was exhausted and our hormone support from it had dropped, even the small dose delivered by a patch will be seen as a sharp uptick by our bodies. Some women find that the rapid absorption of a whole day's transbuccal dose doesn't dissipate rapidly enough to prevent being hit by something of a slam.

Each hrt has its own time and type of uptake. When we are troubleshooting these, we can look at alternatives that might perform differently. For example, if a cream transdermal dose seems to provide too abrupt an uptake to be comfortable, perhaps the slower uptake of a gel would be more gentle while still otherwise providing a transdermal profile of effects.

But an often-neglected aspect of uptake has to do not so much with delivery route but what specific hormone we're delivering. When we're taking estradiol, we're using the active form of the hormone. If we dump a day's estradiol into our systems at once, we may have trouble moving quickly enough to convert the portion of it that we don't need to have active at that exact moment into the inactive reserve form, estrone. If this is the case, our dose might give us a fierce headache or palpitations or excessive jumpy nervousness.

For women who experience this problem, it’s possible to get around this effect somewhat by switching to an hrt that contains some or all estrone. That way, the net total hormone support delivered in a dose cycle is still provided, but the initial slam of excessive activity can be dodged. Not all women experience this problem, but for those who do, this can be a highly productive direction to explore. This is especially true for women who suffer from migraines when they take estradiol, perhaps because the two estrogen versions affect somewhat different areas of the brain.

Minimizing the ups and downs due to duration

If the dose of hrt we take doesn't last until the next dose is taken, our hormone support will taper down far enough that both the decline and the rise of the next dose's uptake will cause uncomfortable fluctuations. While women often address this gap by trying to take smaller doses more frequently, that often doesn't provide a fully satisfactory coverage, not to mention becoming increasingly impractical.

A common misunderstanding of the concept of "half life" often drives this attempted solution. Half life in medical terms is simply how long it takes for half of a dose to be metabolized. The fact that a dose is half gone, however, doesn't mean that another full dose is needed; it only means that the body has taken its normal steps to tune our hormone supply to meet our present needs.

If a dose interval is meant to be a full day, then, it's appropriate that the half life be 12 hours. That means we'll have used up most of yesterday's dose by the time we add today's. Yes, that's some up and down, but our bodies can handle a fair amount of variability through their own storage mechanisms if we're not shorting ourselves down too far between doses. The other direction, taking a new dose before we've used up most of the last, only takes us into excess...and excessive risks. In fact, many women tune their dose exactly so that they do feel a bit short in the morning or so that they do have a hot flash or at least warm spell at that 5am low point in their daily hormone cycle, just so that they know they're skimming along the edge of "lowest effective dose."

So in practical terms, if a woman feels as though she's running out far too soon, she might do more good by re-examining her total dose amount and consider whether taking more would make it last longer and round out her dose period. Taking it more frequently only speeds up the cycle of ups and downs and doesn't really improve her coverage.

Minimizing the ups and downs due to reservoir

There's another factor, beyond simply how long the dose lasts, and that is the form in which it lasts.

Yes, the measured amount of our hrt goes up and then down, but focusing on that alone misses the fact that our overall hormone capacity is not represented by just one form. When she is taking estradiol, a woman's body will normally move quickly to convert any excess beyond her momentary need into estrone, which will exercise less activity. In the course of her dose interval, that estrone will gradually be converted back to active estradiol as she needs, throughout this period, to do more estrogen work.

We’re not sure of the physiology behind this, but some women seem more comfortable when they have a considerable reservoir on board. Now, that’s not an excess we’re talking about; we only mean the sort of buffer that a day’s dose provides. Women for whom this is the case often feel edgy and stressed, never quite comfortable in their bodies, on trickle-dosed hrts (patches, pellets), as though something isn’t right even though they may have lab tests that put them in an ostensibly normal hormone level range. Unfortunately, this is often the sort of situation in which women move to trying to manage their hrt levels even more closely--something that is actually moving in the wrong direction. Switching to daily dosing, which allows their bodies to regain and manage a reservoir to meet their fluctuating needs in a more natural process can help alleviate that problem and provide a better fit between hrt and how their body best functions.

This is vague. Also, confusing.

Yes, we know. We’re getting into the more subtle aspects of hrt “fit” here and there are no real rules, no body of research knowledge. By standard medical thinking, all hrts must work exactly alike and if there’s a problem, it’s somehow with the patient.

But in the decade we’ve been watching hrt use and talking with women about what they’ve tried and experienced, these seem to be common trends and the strategies that seem to have good, durable results for dealing with them.

These aren’t recipes, however. We need to think about the ways our current hrt can be ill-suiting us and we need to know enough about hrts to know which ones hold different characteristics. This is way more subtle than the situation where if we try one patch at one dose and aren’t happy, our only option is whatever oral hrt our doctor most often prescribes. Our hrt pages here can help you with some of this (they're arranged by hormone, so check the Table of Contents for links). If nothing else, we hope that this will help keep you from wasting a lot of time and effort adding and subtracting bits of patch every hour during the day (yes, we’ve actually read accounts of women so desperate to get that impossiblly even hormone state that they’ve tried this). And encourage you that there are some fairly subtle things that can be done to manipulate our hrts’ effects to make them fit better.

As ever, we’re more than happy to discuss this in greater detail on our message list. While we can’t provide answers for everyone, we can often ask questions that help them discover their own best answers.

Progesterone: do I need it or not?

2009-12-31T16:59:00.006-07:00

This is an eternal question wherever women in surgical menopause are discussing their hormone needs, and it can be difficult and confusing to figure out the answer.

There are actually a number of issues here, and it's important not to confuse one with another. Things get trickier because when we discuss this hormone with our doctors, we often end up in an apples-and-oranges situation where we're actually talking about different things. Add to that a massive marketing campaign and you can get deeply conflicting answers depending on whose version you're reading.

Let's see if we can clarify the situation by looking at the typical uses of progesterone and how they relate to us in surgical menopause.

Estrogen "dominance" and the infamous Dr. Lee

Search around the internet and you'll find that Dr. John Lee seems inescapably tied to any discussion of progesterone. Read some of the sites where his work is featured and soon you will believe that you suffer from estrogen "dominance" and that all your ills can be cured by the application of progesterone, the more the better.

This is sales pitch. Just like that coating under your car means more profit for the dealer than you, so this originally was a sales campaign for Lee's books and products. But there's one major problem here: estrogen "dominance" is an invented condition and even if it were real, it wouldn't apply in surgical menopause.

Where this progesterone issue has real meaning for women is in natural perimenopause. Although the term "estrogen dominance" is purely a made-up marketing ploy, in fact women in natural perimenopause typically experience a decline in progesterone production before they do in estrogen. This leaves them at the mercy of their wildly swinging estrogen levels, which cause many of the symptoms of the menopausal transition. Supplementation of progesterone during this time can help even out those swings by using the normal inter-relationship between these two hormones, estrogen and progesterone, to dampen them down.

So while there's no "disease" of "estrogen dominance," the entirely natural fluctuations of perimenopause can be smoothed by bringing these two major hormones back into better balance by covering that relative shortfall in progesterone until estrogen production falls enough to be in better balance with a woman's own menopausal supply. That's a temporary situation, albeit one that typically lasts several years.

But that's not us in surgical menopause.

For us, the transition happens in the operating room and although we have a period of getting settled in on our new post-ovarian needs and supplies, we don't have that perimenopausal mismatch and upheaval of declining ovaries. Even if we were in natural perimenopause before surgery, that situation ends when we make our transition to full menopause: it doesn't matter if then we were imbalanced in our ovarian hormone output; now we are wholly reliant upon post-ovarian supplies and we have an entirely different level of needs we're meeting with that supply now that we're in in menopause.

So no matter what you personally believe about Dr. Lee and his catchy marketing terminology, if you are in surgical menopause, this argument simply doesn't apply to you.

Uterine protection: it's why your doctor says no

Many women who have read or heard about progesterone supplementation or have taken oral contraceptives during their fertile lifestage wonder, don't I still need progesterone as one of my hormones supporting good health? And when they ask their doctor and receive a resounding NO, they're very confused.

Yes, our bodies do still use and require progesterone in surgical menopause.

The issue your doctor is addressing, however, is not this basic one of hormone physiology. Your doctor is instead answering the question of whether or not there is a medical reason for him to prescribe progesterone for you.

The primary FDA approval for prescribable forms of progestogens (a group term used to describe the human hormone progesterone plus its synthetic versions, the progestins) is to prevent excessive stimulation of the lining of the uterus by estrogen, a situation that can lead to development of cancer. Doctors are for the most part required to prescribe drugs for the uses for which they are approved, which is taken by many doctors to mean: if it's not approved for a use, that means that it doesn't work for that use. By medical reasoning then, the only thing that progestogens can do in the body is provide uterine protection and, clearly, after a hyst we certainly don't need that. Hence, we don't need a progestogen.

Why won't your doctor answer your question about hormone needs rather than prescribing? Because that's what doctors do: they diagnose and prescribe medical treatments for disease states. What they don't do is teach us about physiology, and so it's up to us to recognize that we're simply not communicating on the same terms in this situation. Instead of asking do we need it, then, we need to be prepared (and there's more on this below) to support our request that we give it a try—an entirely different question.

But I got a test done and it showed that my levels were very low!

Because our bodies can—and do—convert our ovarian hormones one into another, we can't look just at a single hormone level and understand the full situation. Progesterone levels in the blood don't really measure how much progesterone activity is going on in our systems; they just measure how much is circulating at that particular moment.

The most common situation in which we experience this apparent shortfall arises is early in surgical menopause. That's when a woman is working to get her new hormone needs balanced out against her hrt supply but isn't quite fully covering her needs with hrt. When that happens, our bodies place a priority on estrogen and use every resource available to produce it. One of the most important resources we can turn to that use is our pool of progesterone, produced by our adrenal glands from more basic constituents. Because estrogen is a higher priority, we'll stint our progesterone needs—or anything else that progesterone can be used to manufacture (and there are a number of them)—in order to come as close as possible to meeting our estrogen needs.

Obviously, when this is going on, our estrogen needs are, we hope, close to met but our progesterone will measure low. Beyond this, our system is stressed because we're in a crisis mode, pulling from here to patch up there. But if we "read" this situation as primarily one of a lack of progesterone, though, we're likely to just go on propping up inbalance by adding more progesterone to support this misalignment of supply and demand...and stress.

If, instead, we understand this cascade of hormone priorities and supply, we'll also understand that the recommendation of the American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Menopause (free signup required to read) makes sense when it specifies that we need to work on meeting our estrogen needs with hrt as well as possible before we even consider whether or not we need to supplement any other hormone.

When we supplement our estrogen as well as possible, then we no longer need to prop estrogen up with progesterone (or any other hormone). Once our estrogen needs are covered and we have recovered from the stress of skimming progesterone for that purpose, then, and only then, can we decide whether or not we need to supplement our progesterone. Only then does a progesterone level even begin to speak to the actual state of our progesterone capability.

Let's repeat that because it's so important: before our estrogen needs are fully met by our hrt, we simply can't use the results of a progesterone level because that level just plain doesn't measure our actual progesterone capability or needs: it only measures the stress put on our systems by imbalance. We need to take estrogen out of that equation—by meeting our estrogen needs fully—before we are looking at any reasonable assessment of our progesterone needs.

So do I ever need it?

Maybe yes; maybe no. It's easy to read online and come across the assertion that because we used to make it with our ovaries and now don't have ovaries, of course we need to take some as part of our hrt. But as with many such simplistic assumptions, that isn't the whole story and is likely to lead us astray if we just take it at face value.

Yes, we did lose our ovaries and that reduced production. But at the same time, a woman in the menopausal lifestage has lower hormone needs overall because she's not supporting fertility, the consumer of most of our (former) ovarian output. The way it works out, then, is that our adrenal production capability often matches our post-fertile needs just fine. It's not that we're not using progesterone; it's just that we often don't need to supplement beyond what we're already producing. HRT dosing is about unmet needs, not overall systemic needs. We still produce most of what we need ourselves; we only need hrt to close the gap between what we make and what we need for post-fertile physical functioning.

Many women's bodies actually do just fine meeting progesterone needs once estrogen needs are met fully. Many women in surgical menopause, if they decide that they need to supplement progesterone, need do so only at a very low level, well below the typical prescribing levels based on the need of women with uteruses.

How do we decide, then, whether or not we need to supplement our post-ovarian progesterone supply? Once our estrogen needs are fully met and we've had a month or two to settle in on that adequate supply, we can look at remaining outstanding symptoms. We've discussed balancing progesterone and the symptoms of progesterone imbalance elsewhere on this site, and that's where you should go for the details on that part of the process.

If we are in fact experiencing effects that are indicative of low progesterone coverage, then we might experiment with a small amount of progesterone to see if that makes the difference we hope. Remember: our goal in surgical menopause is to meet our current, post-fertile needs, not the needs we may speculate we had in earlier life stages. Excessive progesterone supplementation leads to very unpleasant symptoms as well as some risks. It's also not magic: it only "fixes" things that are directly attributable to a deficiency of its actions. Further, because progesterone interacts with many hormones and many systems, the process of altering our progesterone levels is the most uncomfortable of all our ovarian hormone adjustments. Working with a small trial dose to see what effect that has before jumping in with both feet is more gentle on our bodies than over-estimating and then suffering the disruptions of a large transition and a situation of excess.

Therapeutic use or disuse of progestogens

We don't want to leave this topic without taking note of a few special situations. Some women don't have the luxury of adjusting their hrts solely for optimal balance and wellbeing, and many of those situations involve progesterone.

Women who have endometriosis often use a progestogen to help suppress the growth of their endo implants. For that strategy to be effective, they need to deliberately produce a situation of progestogen-heavy imbalance to be sure all of the influence of the estrogen they are taking is countered. For these women, the needs of endo control take a higher priority than just comfort.

So too, women who have no ovaries but still have their uterus will need a progestogen to prevent the estrogen they're making and taking from causing a cancerous stimulation of their uterine lining. This is another situation where health needs trump comfort, although there are methods of managing those progestogens to limit their influence in overall hormone (im)balance.

Some other women will want to exert special care when working with progestogens. Women with Polycystic Ovary Syndrome (PCOS) often have elevated testosterone levels, even once their ovaries have been removed, and for them, the fact that progesterone can be converted to testosterone often raises their risk situation more than reaching for better hormone balance might improve it. While the hormonal perturbations of PCOS are not yet well understood, in practical terms, supplementation of progesterone by these women rarely seems useful or productive of improved hormone comfort.

Women with metabolic diseases such as diabetes or PCOS may need to watch their progesterone very closely for another reason: progesterone tends to worsen insulin resistence when it is heavy in overall balance related to estrogen. While good hormone balance has a normalizing influence upon our metabolism, we need to use extra care to be very slow and gentle when making adjustments if we need to avoid upsetting our sugar/insulin dynamic.

And women with autoimmune disorders of the inflammatory sort may find that progesterone supplementation, especially when first introduced or when used to excess of needs, can worsen their disease control. There are no absolutes here, but because progesterone affects the type of inflammatory/anti-inflammatory factors our bodies might make, use of progestogens hrts can be more complicated for autoimmune sufferers.

So what's the bottom line?

We only need to supplement our progesterone when we need a larger supply than we are producing. That's something we can't even begin to determine until we're meeting our estrogen needs as well as possible. It's also important to remember that progesterone is a powerful hormone and can be just as disruptive as it can be valuable if used out of balance with our overall needs, whether for hormone balance or disease control.

And if we're discussing progesterone supplementation with our doctors, we need to be clear that we're not talking about the standard prescribing indications for progesterone, but rather a small increment of coverage that will make our estrogen hrts a better fit for us. How well we're prepared to provide such justification rather than simply asking our doctors "don't I need some progesterone too?" will have a great influence on how that conversation goes. There are many answers to the question of whether progesterone supplementation is needed, and we need to do the thinking beforehand to be sure which question it is that we are asking if we want to receive a useful and productive answer.

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

2009-12-18T11:05:00.004-07:00

It happens all the time: a woman 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 any woman feel the way she wants to. All of our bodies are different; our lifestyles are different; our family/genetic histories are different. How any given hrt will function in a woman's bode 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 us 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 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 beyond the one that opens). 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 grip on 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 women taking therapeutic hrts to treat or help control a specific disease condition (like endometriosis or cancer) will often need to work with multiple hormones at once, most other women 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 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 scheme, 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 consitute such a preference or risk? Some vegetarians might eschew an hrt from animal origins. Some women have ethical objections to the way some hrts are manufactured. Some women 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. Some women 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 work with.

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: a woman 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 woman with digestive issues might eschew an oral, while a woman with a skin disorder might not feel comfortable with transdermals other than transbuccal or vaginal. Women who work outdoors in a very hot climate might find that patch hrts will be fighting an uphill battle for adhesion. Women with infants may not care 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.

We next 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 woman wanting a transdermal estrogen but concerned about transferring hormones to her 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. 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.

Step 5: What dose?

Once a woman has made a choice of hrt, then, it's often simplest to start at the "usual starting dose" unless she has specific criteria to meet that would indicate otherwise. What would those be? Perhaps she distrusts hrts or doesn't really believe she needs one, and so she wants to to take only the barest minimum to see what happens. Perhaps she has previous experience to suggest that she responds strongly to hormonal preparations. Perhaps she's unusually large or small in body mass compared to the general popoulation.

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 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 preop, 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 rule, but in fact many women have found that excitement tends not to be what they're looking for in hormone balancing and that it ends up being well worth taking the slower approach rather than unsnarling themselves after an over-hasty miscalculation.

There's also a popular myth that women who are younger than menopausal age will need very high doses of hrt because they must match their premenopausal levels. While they may indeed start a little bit higher than an older woman 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. A post-fertile woman will still need hormones appropriate to her age, but they are much, much lower in quantity than when she was fertile because her uses for them are lower. We've seen young women 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 a 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 woman some months after surgery to stabilize on hrt and really get a sense that her preop hormone support is no longer having any effect.

The general rule of thumb we've seen in women's 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 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, women's 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: it helps your doctor's scientific mind accept the validity of your experience rather than just brushing you off as a silly hysterical woman who's not accepting her changed circumstances and doing too much reading on the internet.

And 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 women 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 shart 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 list to help troubleshoot this step. Basically, once a woman has achieved some reasonable degree of stability by meeting her basic estrogen needs, some of the pressure is off and she can take the time to learn more, to explore more options. And the work she's done in learning to listen to her body and work through the process will provide her important tools to continue her refining work on her 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 discussion list to help a woman cut through to the issues and look at where she might turn to make the next iteration of adjustments. We can't tell exactly what any given woman should do, but we can often as a group ask some questions that will help her make her own decision of what to adjust next.

Vaginal delivery of systemic estrogen HRT

2009-12-13T17:54:00.006-07:00

We've been following discussions of this topic in a number of locations on the internet and it's come up on our own discussion list as well.

There is, of course, one vaginal-delivery systemic estrogen hrt on the market already, Femring. But we're also seeing women report exploring the use of Estrace and its generics (micronized estradiol) vaginally for systemic support. And that raises some distinct concerns.

Vaginal micronized estradiol: will it work?

First of all, yes, absorption through vaginal tissues will work as a delivery route for this hrt. Oral mucosa is very similar to vaginal and it is indeed permeable to this molecular form of estrogen. In fact, it's been quite some years now since we first heard of women using a tiny bit of the dust leftover from cutting tabs for transbuccal or oral use for local vaginal supplementation. We had some concerns initially that either the colorant or the base might prove problematic since neither are designed for the vaginal environment, but that has not been the case for the women who've shared their experiences with us. We've also run this past a few doctors who have said there doesn't seem to be any obvious peril beyond the issue of making sure the dose is appropriate. So that seems to be both effective and reasonable as a means of local supplementation.

Risks: concentration in pelvic circulation

Our greatest concern with using this route for systemic vaginal dosing, however, is where that estrogen goes once it is absorbed.

With transbuccal use, many women see distinct local effects according to where in their mouths it is placed. Those seem primarily to do with fluid retention (such as sinus stuffiness, ear fullness or transient headache) and we have speculated that they represent higher local concentrations in the part of the circulation to which they are initially delivered, before they are well-diluted. Most women reporting this effect have had success in switching to other locations in the mouth where this is less problematic, although the non-problematic location varies (of course it does *sigh*) from woman to woman.

Looking at that same aspect in terms of vaginal delivery, then, we have a concentration of estradiol--which is the active form of estrogen--delivered to local pelvic circulation. We know from research done with vaginal progesterone that this kind of concentration in the pelvic area does happen with vaginal delivery and there is no reason at all to expect that estradiol could escape a similar distribution pattern.

Now, when that happens with progesterone, that represents a desirable situation in terms of delivering a therapeutic concentration of hormone to pelvic organs without causing a corresponding systemic concentration--and heightened effects. But with estrogen, there's no real reason that this concentration would be desirable and in many situations, we're quite concerned that it isn't. A woman with endometriosis, for example, would hardly want higher estrogen concentrations flowing directly to her endo implants. A woman with a risk of ovarian cancer retains that risk even when her ovaries are removed because there is a (low but present) risk that before oophorectomy, micro-tumors may have escaped her ovaries that would later be stimulated by that higher level of estrogen in the circulation that feeds them. This is recognized in the specific warnings for current vaginal systemic hrt, that caution high risk users about just this.

We know from users of the systemic vaginal ring that some women find this route of supplementation to be highly uncomfortable, citing symptoms of pelvic bloating or congestion as well as stimulation of irritable bowel syndrome or bowel cramping. There is also a mixed body of evidence suggesting that higher levels of estrogen can add to incontinence. So not only do we have the progesterone model to shape our expectations but we have experience with vaginal delivery and pelvic symptoms to suggest that it most certainly does happen and we have FDA concurrence that this represents an undesirable level of risk for at least some women.

It is worth noting that Femring uses a form of estradiol that, although human-identical, is inactive until it has been further processed in the bloodstream. This means that it is well on its way to being diluted and distributed before it becomes fully active as estrogen. It seems likely that this is deliberately done to reduce estradiol activity exposure at systemic levels to those pelvic tissues. In other words, there may be significant negative concerns with vaginal delivery of systemic estrogen that led the pharmaceutical companies to put additional funding into working around that problem rather than, more economically, just repurposing an existing product they already had on the shelf. While we may not know what led them to do so, the simple fact that they spent money on this raises the warning flag that it was probably not done without substantive reason.

Risks: estrogen activity and vaginal tissue health

Were a woman to elect to try vaginal estradiol systemic hrt notwithstanding the above risks, we would also think that a regular, detailed and careful exam of vaginal tissues would be important. While the low-dose vaginal hrts are documented to have a fairly light effect on the tissues they directly contact, all that systemic-dose estrogen going through a relatively small location (even though the tab breaks up quickly, it's still not going to be distributed over a wide area of mucosa in the fairly static vagina) may have disturbing effects upon the mucosal cells in that area.

This is a concern raised by some doctors when women discuss transbuccal use, based upon similar problems seen with some sublingual and nasal drugs. Women using this route need to be careful to switch locations around frequently, visually check their oral mucosa regularly, and also ask their dentists and oral hygienists to do so as a backup. We see no reason why similar precautions with vaginal use would not be a good idea (only, of course, probably not asking your dentist to be the one do it) to make sure that we are not stimulating some sort of cellular changes that could become problematic. Remember: the reason why estrogen is carcinogenic is that it fosters growth of tumors, and that's not something we want going on out of sight in our vaginas.

Would this work with any of the oral estrones?

That's a good thought that came from our discussion of vaginal systemics on our discussion list. We don't really know, but it seems as though since there is an Ogen vaginal cream made for local use, the oral estrones Ogen and Ortho-Est would seem to be usable transbuccally or vaginally since they contain the same compounds.

That said, many of the same concerns with respect to vaginal systemic dosing would still apply. Although estrone is an inactive form of estrogen, the conversion of estrone to estradiol occurs in cells throughout the body. A higher-than-normal local concentration of estrone might well still result in higher-than-desirable estradiol exposure to vaginal and pelvic tissues. We certainly don't see any reason why switching out estrone for estradiol would moderate risk enough for those with specific risk factors such as endo or ovarian cancer to be confident that this would safer for them, however much the systemic impact might be gentler than all-estradiol dosing.

So should we use oral hrts vaginally or not?

We have really mixed feelings about this whole premise. That it would work to deliver estrogen to our systems, there is little doubt. It is likely that in reaching the circulation through pelvic rather than head/upper body dilution, the specific local effects that are problematic for some women with transbuccal use might be avoided.

We can't, however, see that it in any way alters the way the dose is processed by the body other than that initial concentrated absorption uptick, so the premise that it somehow is delivered more evenly than transbuccal is likely a subjective impression that is not supported by physiology. It may be different from other transdermal (general body skin) deliveries, just as transbuccal is, because it represents a different uptake dynamic and the skin/fat reservoir and transmission effects are taken out of the mix. Like the transdermals, however, it also represents a risk of transfer to a partner than is unquantifiable but certainly real.

We've taken up elsewhere the issues of whether not estradiol needs to be dosed multiple times per day and whether "even" is ever a state that can be achieved (quick answer: no, it's a myth), so we won't reference those concerns here other than to say that there is nothing in pelvic delivery that would lead us to feel they are not applicable here as well. A woman whose body is not capable of using a daily dose via this route, as with any other, is not utilizing that particular hrt well. Whether or not other hrts would better suit her is the issue here, not just the route and timing; multiple-dose dosing is a stopgap measure to try to force a fit with a deficient hrt, not a good or sustainable strategy in itself (although it's true that in some instances where trying other things is truly not feasible, stopgaps may be the best thing we have within our reach). The ability to divide a vaginal dose into micro-doses given at extremely short intervals is thus not a compelling argument that in any way offsets the risks, let alone makes this route somehow unique.

So the bottom line on this is that there's just no reason to be really comfortable with the risks that this concentration provides in this location. That doesn't mean it mightn't be the more practical option for some women, but it would require special precautions that make it nothing to be taken lightly. One of the dangers of discussion forums that focus on support rather than information is that women can advocate for use of a particular hrt strategy without any corresponding exploration of the risks it poses.

We do think this notional hrt use is worthy of exploration, but that exploration should be done knowledgeably and with great care to monitor for negative outcomes. Given the widespread lack of understanding of hrt and hormone effects, though, we're afraid that women will be injured by and later regret decisions made without fully understanding those risks. Women often distrust their doctors because that relationship is so formulaic, paternalistic, and illness-based, ill-suiting their menopausal health needs, and yet when they engage in risks without that backup of medically sophisticated knowledge, they've lost an important safety net. Maybe we're being too conservative in this case, but with things we can't get back from without great cost, yeah, conservative we'll be.

But then what about compounded hrt to be used this way?

Are compounded vaginal estrogen hrts being prepared for systemic use? What are compounders doing about these issues? We don't know and we haven't yet encountered anyone who does.

Our guess would be not much, and so our concerns would extend to those hrts as well. While doctors in theory vet the prescriptions suggested by compounders, in practice many of them tend to just pass them on as suggested by a fully qualified professional and happily pocket their share of the business income so generated. So there's a questionable safety net right there.

In fact, if they are doing so, this would be exactly where we tend to think that the FDA has a reasonable ground to be critical of compounding, since this would be a major departure from what is known and tested and generalizable from other tested and licensed retail hrts. This is where their current practice model might indeed overstep their training and licensure and, of course, constitute the legal vulnerability that is being exploited by the pharmaceutical companies in response to what is actually a perceived marketing threat rather than the nominal concern for patient safety in which it is couched.

So we're going to hand this part of the question back to you. What do compounding pharmacists you are working with have to say about direct systemic vaginal estradiol hrts? And estrone used that way? Are they making and selling it? What precautionary screening are they doing or what counseling are they doing on risks specific to this delivery? We'd be very interested to know what the compounders' take on this is. If you can ask, please do share the results of your inquiry with us.

This is an idea we need to explore just because there are indeed women out there using it. The more concrete the information we have, the more useful it becomes to us, whether it's to give us the go-ahead to experiment more freely or to convince us that it's really not a good idea after all. We're not at all opposed to exploring and pushing the envelope in search of alternative ways to use the available hrts, but we're going to be taking a firm hard look at the risks along the way.

Gleanings from an article on contraceptive patches

2009-12-12T10:45:00.001-07:00

Since we're always interested in expanding our understanding of patches and transdermal hormone delivery, we recently clicked through on "Transdermal Contraceptive Patches: Current Status and Future Potential" (free signup required to read) just to see if it had anything to offer that also seemed applicable to hrts. As it turned out, that was a good move.

Delivery from alternative patch placement locations

We've known for some time that butt and belly application differs by 17-25% in the amount of hormones absorbed from the same patch because it's in the patch data sheets. Women have variously reported using upper arm and upper back and thighs for patch placement for years, but we're never had any guide other than experimentation to determine the correct dose equivalency for those locations. This current article, however, lists some of these locations and reports on their delivery:

The patch is designed to be placed on one of four sites: the lower abdomen, upper arm, buttock or upper torso (excluding on the breasts). Two consecutive patches should not be placed over the exact same area. Hormonal absorption from the lower abdomen is approximately 20% lower than that observed from the other three sites

There's no reason at all to suppose that this would not hold true for hrt-sized doses as it does for the higher contraceptive-sized doses referenced in the article. That means that we don't especially need to anticipate making huge changes to our patch dose if we choose to spread use out over more alternative locations.

What's underneath still matters

This doesn't, of course, guarantee that even the sites with roughly the same statistical deliverability can be trusted to work that way on an individual basis--we still have to contend with individuality of fat-vs-muscle underlayment of the skin to which the patch is applied. That's also supported by this statement from the article:

cautioned that women with body weight in excess of 90 kg may be at higher risk for pregnancy compared with lighter women

In other words, women with a larger fat layer the hormone must traverse to enter circulation may have an overall lower delivery. For well-padded women, then, a patch may not be an optimal delivery if transmission through thicker fat layers prevents good uptake. Beyond this, though, it supports the notion that underlaying tissue type is pertinent to patch delivery for all women, something that may help in troubleshooting variations in patch performance that result from using multiple locations.

Environmental impact of patch disposal

Also of general interest is this reminder of the environmental impact of undelivered hormones:

As there is still a considerable amount of hormone left in the patch at the end of its 7-day use, it is recommended that patches not be flushed down toilets, but disposed of folded in half via solid waste collection systems. In some countries, it is recommended that the used patches are returned to pharmacies.

While women in menopause tend to come closer to exhausting the hormone content of their much lower dose patches by the end of the nominal delivery life, we should keep in mind that there may still be enough in them to have impact on others. Our water supplies are growing increasingly contaminated by hormones and drugs, none of which are typically measured (in the US) by EPA-mandated water supply testing. This contamination is increasingly pointed to as a potential factor in the earlier sexual maturity of girls and the higher incidence of hormone-mediated disorders we women suffer.

We might be especially concerned about patches discarded prematurely--say, that one that got caught on our underwear on day 1 and peeled up and had to be replaced. But any patch, really, should be disposed of with some care as to where its leftover content might end up, given that it's unfilterable and untested once in our water supplies. Even their suggestion that it go into solid waste disposal would be ineffective in safely sequestering it some places, such as New York City, where much solid waste is simply barged out to sea and dumped. Responsible disposal of our hrts is something to think about for the sake of our daughters and granddaughters.

Transdermal delivery and the risk of blood clots

The main issue that this article is addressing is risks of blood clots. In general, we know from a growing body of evidence that oral hrts (as compared to transdermal) seem to be associated with a higher incidence of clots, generally attributed to the way that the liver is more heavily involved in oral dose processing. The article reviews that situation:

Estrogen increases VTE risks by altering hepatic production of extrinsic clotting factors, and antithrombin III. With oral contraceptives, hepatic exposure to estrogen is much higher than is reflected by serum estrogen measurements. This is because much of the estrogen absorbed through the intestine into the liver is conjugated and excreted through the gallbladder back into the intestine without ever entering the bloodstream. However, with transdermal systems, all the estrogen to which the liver may be exposed is reflected in the serum levels.

Oral processing is also generally believed to boost inflammatory factors (such as C-reactive protein), which has been suggested as a reason why cancer rates may be higher with orals than other delivery. This is also considered to be a factor in the cardiovascular disease development issue as it relates to route. This research is not yet heavily publicized even though it's incorporated into the major medical group consensus documents on menopause and hrt, so many physicians remain unaware that these are reasons for women to downrate oral hrts when they are evaluating their options.

Transdermal progestins?

We've been discussing progestins more lately, both with women who have endometriosis and want to include the suppressive effects of progestogens (progesterone-acting compounds) in their hrt, and with women who have had their ovaries removed but still have an intact uterus and a need to utilize a progestogen to maintain its health.
There's some evidence that progestogens that deliver into pelvic circulation provide better local coverage with lower systemic impact as compared to other routes of systemic delivery, something very attractive where the alternative has long been simply having to tolerate an unpleasant hormone imbalance for the sake of therapeutic effect.

To date, local progestogen delivery has been possible only via IUDs such as Mirena ( dispensing the progestin levonorgestrel) or other higher-dose progestin-dispensing contraceptive IUDs (like Progestasert), or vaginal forms such as the progesterone gel Prochieve, off-label use of oral Prometrium caps vaginally, or various vaginal-application compounded forms of progesterone. That means that for women who want the stability of a progestin, which cannot be converted to other hormones as progesterone itself can be, if they didn't have a uterus they were out of luck for anything other than oral delivery and its associated systemic impact.

But this article supports the premise that progestins are in fact capable of being absorbed through the skin (and, by extension because they have similar properties, vaginal lining). Gestodene is the progestin mentioned as being possibly suitable for this kind of delivery in this article and norelgestromin is the progestin in the currently-available patch, but the article also suggests that "other progestins, including those with poor oral absorption, could be utilized in a transdermal patch."

While that doesn't mean that anyone's going to rush a vaginal or transdermal progestin onto the market, especially one suited for the use of women in surgical menopause, it does open up some other avenues for the adventurous to explore.

How? Vaginal use of a portion of a plain progestin tablet meant for oral use might work (it would obviously make sense to try one of the progestins the article mentions unless one can get solid information from a pharmacist that a different progestin is known to be suitable in terms of through-skin absorption capability). Why only a portion? Remember: oral formulations have a lot of wastage from first pass built into them, while lower losses with transdermal delivery mean we have to start at a lower dose level. Clearly, this is really out-on-the-edge experimentation and definitely something to discuss with one's health professionals, but it does provide the hint of a possibility for women willing to experiment a bit in order to get an hrt form and dose they are more comfortable with.

Another approach, although we're not sure if it's feasible or not, would be to see if a compounding pharmacy could custom formulate a progestin meant for oral use into a vaginal-suitable dose and vehicle. We've hesitated suggesting this in the past because we had no reason to suppose it would be absorbed, but given the encouragement of this article, it sounds much more like something to pursue.

Have you tried this? Thinking about trying it? We'd love to hear from you about your experiences, either on our discussion list or simply by email to surmeno@yahoo.com.

HRT and cancer risk

2009-11-28T14:04:00.003-07:00

Lots of women come to our discussion list and post that although they are in surgical menopause, they cannot take hrt because they have relatives with cancer. Or they come to us because either the media or their doctors have assured them that if they take hrt, it will give them cancer.

Sadly, it's not that simple. And a lot of the discussions we have on that topic are to explore that situation in a lot more detail. Although it's easy to paint a picture where the risks are all on one side of the issue, that is absolutely not the case.

What kind of cancer risk?

The first part of the exploration any woman owes herself when making a decision of this magnitude is just what kind of cancer risk she actually has. One uncle with prostate cancer, to use a fairly easy example, is not the same thing as having one's mother, two aunts and three sisters all die of estrogen-receptor breast cancer. Even within the realm of breast cancer, there are cancers sensitive to estrogen, cancers sensitive to progesterone, and cancers indifferent to both hormones.

Given that, then, an informed decision about personal risk has to begin with working with an oncologist, a cancer specialist, to explore our own personal risk level. This will include taking a detailed history, not only about our own health history, but about those relatives who had cancer. It may include genetic testing. It may involve a medical records search for exact pathology of previous family cancers. It should be very thorough.

And when it's done, the question to ask is not "should I take hrt?" Any responsible oncologist will answer that question with a resounding "no!" Their specialty focus is preventing and combatting cancer, so they generally view no cost at all (and we'll get into those costs a bit more further along in this discussion) as outweighing any degree of cancer risk.

Instead, it may be more helpful to ask the question: "what are my relative risks?" Another way of asking this question is "if I had kept my ovaries, would I have had to have them removed in menopause in order to prevent a high probability of developing cancer?"

Because our goal with hrt supplementation in surgical menopause is really just bringing us up to a level of support that women in natural menopause receive from their ovaries, that's really the equivalent situation. In other words, if our menopausal ovarians would not have presented an unacceptably high level of risk, there's some question as to whether supplementing our hormones with hrt to that same level would present any greater risk. (That's qualified, however, because women who take certain progestins as part of their hrt may in fact experience a higher level of risk from that particular type of hrt.)

Yeah, but if there's any risk at all, shouldn't I abstain from hormones?

The problem is that risks aren't one-sided. There are many beneficial things that estrogen enables.

For example, women who take hrt have a well-documented lower incidence of colon cancer, which is the number three killer in the US. If you have no family history or special genetic risk of breast cancer but do have a colon cancer family history, then you might want to weigh this decision differently from a woman whose risks stack up on the breast cancer side. There are no guarantees and there are many lifestyle factors that also play into risks or can be used to help mitigate them, but it's important to keep in mind that we can't let the word "cancer" make our brains short out entirely with panic.

While the exact role of estrogen's preventative actions is still being thrashed out by researchers, the overall maintenance of functional hormone levels does have some pretty compelling evidence for its importance. Doctors used to feel that ovarian production of hormones was essentially insignificant for health if a woman were no longer fertile, and that guided many to recommend removal of healthy ovaries as part of any hysterectomy on the grounds that this would reduce any chance of subsequently developing ovarian cancer. And since those hormones weren't needed and hrt was linked with breast cancer, many women found themselves up to their ears in symptoms of surgical menopause with no support beyond what non-ovarian estrogen their own bodies could make and whatever xenoestrogens they picked up from food and their environment. Still, that was healthier, according to their doctors.

That position was reconsidered a few years ago when studies on young women who had oophorectomies without subsequent hrt support revealed that by the time they reached the "normal" age of menopause, they had experienced a 70% increased incidence of mortality compared to women of the same age who had kept ovaries (supporting articles). In fact, in no group studied for risk (all causes, fatal and nonfatal coronary heart disease, or lung cancer) was oophorectomy associated with increased survival (source). Other studies have suggested that the same issue of increased risk exists with Parkinson's disease and dementia (source).

While these study results typically follow younger women, there's no reason to suggest that this risk is tied to a specific age. More broadly speaking, then, we have to question whether life in hormone deficiency at any age also carries significant risk of death by these other disorders, or at least an enhanced risk of developing them. There is no research to date that suggest that there is any sort of shelf date on our hormone needs.

And that really complicates our decision process. If, for example, a woman has a high incidence of cardiovascular disease in her family, such that most family members die by age 50 of heart attack or stroke but no one ever lived long enough to develop cancer, she might well want to think long and hard about her personal relative risks. It's not just a quality of life issue—although that's plenty significant for many of us. It's instead a health issue of just as much potentially fatal magnitude as that cancer risk on the other side.

If we make this anti-hormone decision based on cancer risk, we're making a cancer treatment decision

Many women who choose not to supplement their hormones due to a documented or perceived cancer risk find themselves miserable and desperate to improve their quality of life. "How can I feel good?" they demand on our discussion list.

To some extent, we can alleviate some of the symptoms of hormone deficiency with non-hormonal measures. Some of those options are discussed elsewhere on this site.

But these women may be disappointed to find that not all of their areas of concern or symptoms have a non-hormonal "fix." Even where help is available, those approaches themselves often have pretty significant risks or side effects, or they may only reduce but not alleviate the problem. The bottom line is that not only are they embracing specific health risks with this strategy, but they are also going to have to put up with compromises in terms of quality of life.

Now this is where the medical sites all cheerily assert that life can be just fine with the proper attitude. All we need is a positive outlook or our religious faith and these minor bumps in our otherwise delightful life can be overcome. If that works for you, great. You probably don't need to read any further and can go on with your life. We're really happy for you.

Now, we're not saying that attitude isn't important. But if you're still grappling with the idea, here's a concept that may help you keep a balanced perspective: the things you are choosing to undergo in terms of hormone-deficiency-related effects are the specific choices you are making as part of treating your cancer. It doesn't matter whether you actually had cancer in the past or you just feel that you have such a high certainty of developing cancer in the future that this is your health priority, what you are engaged in is a medical treatment. And in common with all medical treatments, there are costs. These hormone-related symptoms are your costs.

So when you are hot flashing or lying awake at night or even wondering where your sex life went, while you're working on finding a set of good non-hormonal maintenance practices, you can remind yourself that you are not a helpless victim here: you have cancer and you are treating it. You are choosing these things specifically to battle your cancer. You're fighting back with every hot flash. Sure, they're miserable and you are wishing for the happily ever after you thought we were all promised, but you have cancer and you're fighting back in this way. The glass may only be half full, but cancer treatment is what it contains. That may not make it all better, but it does give it purpose.

Another critical question to ask

If my risk is so high that I need to treat it with hormone deprivation, should I also be taking drugs to suppress my own hormone production and use? Should I be observing special dietary precautions to limit exposure to xenoestrogens (estrogens from outside sources)?

Again, this isn't a question you can entirely answer on your own. But when you consult an oncologist, it's a good one to kick around. It's easy to for doctors to tell us not to do something and once they put our file folder away in the office records room, our hot flashes won't be keeping them awake at night. But if our risk is so severe that we have to endure hormone deficiency and we have to embrace an up to 70% risk that we'll die early anyway, should we do even more to reduce that risk?

Yeah, that casts things in a different light. When we ask a doctor to do something, like prescribe hormone-blocking drugs for us, then they have to much more graphically consider the risks of that treatment. Then they may admit that the symptoms caused by these drugs make a lot of women give them up, or that these drugs have some significant risks. But hrts are only a small incremental exposure to hormones (even in surgical menopause, we make most of our so-called "ovarian" hormones in our adrenal glands), so if we have only that slight a risk and don't need to take that further step, do we really need to limit our hormones below normal menopausal levels at all?

This isn't a pep talk to make you see your way towards taking hrts. There truly may be a compelling reason why just this much deprivation and no more is exactly and totally what you need to be safe from cancer. All we're trying to do is suggest some ways to explore the options from different angles, to make sure that the treatment you select really is one that makes sense for you and will really do what it is you are wanting. "Don't take hrt and you won't get cancer" is a very simplistic thing to recommend, and because of that, we need to hold it up to close examination to make sure it's totally valid for our own personal situations. Because if we can do this, if we can embrace the sense of whatever measures we decide to take to treat our cancer, then we can live with the consequences of that decision with greater grace.

Are there other things I should do to reduce my risk?

This is a great question for all of us to ask, not just those who are actively treating a cancer or cancer risk. To some extent, we're all at risk and so we all should do what we can to minimize that risk. Even if we don't want to skip hrt, even if we don't want to practice hormone deprivation, we can all work on risk reduction.

The first way we can reduce our risk is to supplement our hormones with only the minimum amount of hrt that otherwise meets our goals. We can do that by approaching our needs by working up from a low dose, by stopping increasing as soon as we feel okay. We can do that by challenging ourselves every few years with a trial of a small dose decrease, to see if our needs have changed. These are easy things, but because our overall risk of estrogen-related breast cancer is related to our cumulative lifetime estrogen exposure, these are a real risk reduction measure.

There are all sorts of dietary risk reduction strategies that we can find out there, some of which have good foundations in actual medical research and some of which are dramatic, profit-making wishful thinking. Just how far each woman wants to go with this is up to her, of course. But here is some of what we know.

Dietary fiber seems to hold a real relationship with reduced breast cancer incidence. Fruits and veggies do as well, although the actual components that have this effect have not been isolated so recommendations are for whole foods rather than refined elements taken as nutraceuticals. We know that there are xenoestrogens found in fruits and vegetables grown using pesticides and that much commercial meat raising involves dosing the animals with estrogens and other hormones that persist after slaughter. Alcohol and grapefruit raise our circulating estrogen levels and our risks, but coffee and tea don't test out as doing so. Red meat and a high fatty intake also raise risks.

There are also more subtle things we can look at to manipulate risk. The glycemic load of our diet and our fasting blood sugar level have been found to be tied to breast cancer risk. Anything that increases our proportion of body fat increases risk and losing weight lowers risk. All by itself, increasing exercise lowers risk. All of these things have actual research backing them up, and you can read articles on diet and breast cancer for yourself in our bookmarks account.

So that's a lot of lifestyle stuff we can work with to pitch in to the effort. And yes, they're maybe hard to want to change and to stick with. But remember: this is part of treating cancer risk. How much fat/red meat/inactivity/whatever is to (literally) die for? It's up to us but we owe it to ourselves to be honest about our efforts. No one's checking up on us or keeping a scorecard If it's important enough to be worth not taking hrt for, isn't also important enough to modify our habits for?

The bottom line

Cancer isn't for wimps and neither is cancer treatment. That's why we need to be sure that we're not just responding in knee-jerk panic at the very thought of cancer but are realistically and with expert advice looking at our exact, personal level of risks and what we can do to reduce them. We have choices that range from blocking our body's ability to use any hormones to just reducing our hormone supply slightly to using other factors to help reduce our risk while we meet our minimal level of post-fertile hormone needs. Each choice has its own costs and level of benefits, and we have to remember that no choice is safe. Shall we say that again? There are no safe or easy choices. We only get to choose which of the risks we will experience.

Surgical menopause must-reads

2009-11-25T20:48:00.004-07:00

We're delighted you've found your way here to learn more about surgical menopause, but we don't want to be the only source you're reading. It's important, when we are advocating for ourselves and the way we want to define our needs, to be aware of what the medical community is thinking and what the scientific evidence shows. Those two don't always come together in our own health care providers, however, so we also need to be able to support our preferences with sound information we can share with our caregivers to bolster our requests.

We have a whole huge body of information in our bookmarks account, all tagged by the various topics they discuss. We have the most recent additions listed in our sidebar here, but you're always encouraged to browse the full collection to expand your understanding of those topics that seem most pertinent to your own situation.

When you do, you'll see that the first tab in the list is simply "absolutely read this." That's because these particular articles provide an overview we think to be especially comprehensive or critical to spelling out the situation we're working with. And we'd like to take a few moments to tell you about these valuable resources.

Individualizing Hormone Therapy for the Surgically Menopausal Woman

Individualizing Hormone Therapy for the Surgically Menopausal Woman is the motherlode of information specific to surgical as opposed to natural menopause. It's a bit dated now, published in 2004, but we're not aware of anything that is new that contradicts the information it contains. In fact, more recent research has only provided more support for its points.

The article talks about how women entering surgical menopause will have a much rougher transition (ie—more severe and more numerous symptoms) if they are not supported by hrt immediately following surgery. This is an important point because it counters the assertion of many surgeons who are opposed to hrt use that we should "wait and see" if we need hrt. The article says that most women will in fact require hormone supplementation and there are good reasons, both in terms of comfort and health, for working from that assumption.

The article also makes a very useful analysis of the WHI Study results, specifically as they apply to breast cancer and the use of estrogen alone as hrt. While huge numbers of women—even those in surgical menopause—were forced to quit hrt due to the study's finding of increased breast cancer incidence with combined hrt, those results were not applicable to women with hysts using just estrogen. In that arm of the study, breast cancer was actually reduced by 23%, something that received, oh, about zero press in the panic frenzy. The article also notes how newer information about transdermal hrt delivery also raises the likelihood that findings of greater incidence of stroke and other forms of cardiovascular disease with hrt initiation may be controlled by route.

The other useful aspect of this article is that the authors are well aware of recent research speaking to increased mortality in women who have their ovaries removed and fail to supplement their hormones. Where much of the literature of natural menopause defines the issue as "just a few hot flashes," this article is very clear on the more significant aspects of the surgical variety.

Guidelines from the American Association of Clinical Endocrinologists

The American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Menopause is not only an excellent overview, but it carries the weight of being a major consensus document coming from the specialty group that actually is most versed in all things hormonal. While it covers primarily natural menopause, it does give several mentions to the surgical version.

This is a long article, but there's not a lot of wasted space because they cover a lot of information. They look at the reasons for using hrt and they look at alternative drugs for managing specific symptoms, all within the context of research-demonstrated efficacy.

One of the things we think is most important here is that they specifically cite the priority the body places on estrogen and the importance of meeting estrogen needs before even assessing whether other hormones require supplementation.

Further, they note that many of the indications for supplementing testosterone are exactly those of a need for estrogen, making it especially important to be certain that a raised estrogen dose will not alleviate the specific problems before moving on to add other hormones. While they by no means condemn the supplementation of testosterone, they strongly urge being quite certain that the need is actually for testosterone and not estrogen, especially given the significant cardiovascular risk potential with testosterone. If you're thinking about the need for testosterone, this is a priority read.

Guidelines from the North American Menopause Society

The NAMS menopause guidelines statement is another broad consensus document from a specialty medical group. Why is consensus important? Because these documents contain the things that, in a highly arguable field, a wide range of professionals all do agree on. These kinds of documents are thus the baselines from which interpretations in clinical practice arise.

This represents an updated document, some years post-WHI Study, that debunks many of the recent anti-hrt myths that arose from the panic press the study cancellation generated. It also spells out very clearly the who, how long, and why of hrt use.

One of the noteworthy topics covered is the whole issue of "bioidentical" hrts. It notes the confusion generated by the same term being employed for human-identical retail hormone preparations and the special marketing program of compounding pharmacists. It is remarkably level-headed in the whole disagreement regarding whether or not compounding should be outlawed, noting that the unrealistic marketing promises of some compounders are at the root of the FDA concerns while still acknowledging the value of compounded hrts for some women.

Guidelines from the International Menopause Society

The International Menopause Society updated recommendations are another consensus document from menopause specialists, but this time international in makeup. This was formerly one of the most conservative bodies in terms of being anti-hrt, but this revision is a lot more reasonable and less terrifying—something we obviously consider a good move.

There aren't any ground-breaking elements in this report, but the overall conclusion is nonetheless highly important in terms of recommendation:

The safety of HT largely depends on age. Women younger than 60 years old should not be concerned about the safety profile of HT. New data and re-analyses of older studies by women's age show that, for most women, the potential benefits of hormone therapy given for a clear indication are many and the risks are few when initiated within a few years of menopause. In view of the new data, Regulatory Authorities should review their current recommendations as a priority.

Oophorectomy and mortality risk

One of the big shockers that turned around medical thinking about oophorectomy and hrt in surgical menopause in the past few years is the documentation that removing a young woman's ovaries and not supplementing her hormones results in a substantial increased risk of dying from any of a number of causes when she is compared to woman who did take hrt. This is in marked contrast to the previous guiding philosophy, which was that hormones had no use in a non-fertile body and that women would be just as well off without both ovarie s and hormones. While this was known for many years to specialists, this more recent publicity is starting to reach out to physicians in general.

Prophylactic Oophorectomy in Young Women Carries Increased Mortality Risk (free signup required to read) goes into that discovery, with the notable quote here being

Women younger than 45 years who undergo prophylactic bilateral oophorectomy and do not receive adequate estrogen replacement therapy have a 70% higher mortality risk

There is also a report on this research in Science Daily, "Preventive Ovary Removal Linked To Early Death In Younger Women, Mayo Clinic Discovers."

There are a number of other resources on this topic in our bookmarks account tagged with "oophorectomy." While many of them deal with younger women, the growing body of medical opinion is that this is simply a graphic example of something that affects all women to varying degrees, no matter what their age. In other words, we need a certain post-fertile level of hormones to enable normal physical function, and when those are not provided, very significant increased mortality risk can result. While we have long advocated that a woman's decision to supplement her hormones or not is a personal decision, we feel that every woman needs to know that the risks are very much not on just one side of the issue. Even where there are risks on the side of taking hrt, they need to be realistically balanced against the risks of not taking hrt, lest we doom ourselves to worse outcomes than the ones we fear.

And those are our surgical menopause "must reads" for gaining a broad understanding of not only the physiology involved in hrt use, but the recommendations and the background behind them. If we are to effectively advocate for our preferences, it is from materials like this that we most convincingly work. It's not all easy reading, but aren't we worth the effort?

HRT for women with ovaries but no uterus

2009-10-02T10:02:00.001-06:00

Although this site focuses mainly on women who have had both an oophorectomy (ovaries removed) and hysterectomy (uterus removed), some women choose to retain their ovaries and only remove a diseased uterus.

Technically speaking, these women will experience natural menopause. Of course, it's a little more difficult for them to tell when their last real cycle is because they won't have periods to mark them, but when they begin to experience the symptoms of perimenopause, they'll be the same classic ones most women see.

The only real difference that is likely to be obvious will be that a woman who has had a hysterectomy, even if she retained her ovaries, may go into menopause earlier than she might otherwise have done. When she does, especially if it comes particularly early, she may not find that her post-fertile ovaries provide the same level of hormonal support as they might have done had they never been subjected to the disruptions of surgery.

We're not saying this to worry you if you're not there yet. But it's a possibility—by no means a certainty—to be aware of. While the ideal of natural menopause is that our aging ovaries continue to obligingly pump out enough hormones to meet our post-fertile needs, women who have had a hyst should be prepared to revisit that image if it turns out that they arrive at menopause and find they're not actually feeling so great about their coverage. Women who thought they might get away without having to deal with the whole concept of hrt may end up revisiting that.

In general, the same strategies the vast majority of women employ to ease ourselves through the upheavals of perimenopause will pertain to this variety of natural menopause as well. Women with mild ovarian impairment may find that the otc nutraceuticals or soy estrogens may provide all the helpful boost they need to make up the gap between what their own ovaries make and what they need to maintain health and wellness. Other women will find, once perimenopause has settled down, that they still aren't meeting their needs well enough and they may want to go on to work with hrts to supplement themselves back up to a comfortble level of support.

Does not having a uterus change how I should use hrt?

Yes. For women without a uterus, a progestogen (progesterone or a synthetic version called, generically, a progestin) is not an obligatory part of their hrt. That doesn't mean that these women cannot use a progestogen as part of their hrt, but that it's not mandatory because that mandatory role is uterine protection from the estrogen...and without a uterus, no such protection is necessary.

Instead, for these women in natural menopause without a uterus, any progestogen needs only to be supplemented to a level that meets their actual, demonstrated needs for it. We don't need it just on spec—our ovaries and adrenals take good care of providing for most of our needs and if we're meeting our estrogen needs well, we should have plenty of progesterone available to meet our post-fertile needs for it. But if some needs remain after we have adjusted our estrogen as well as we can, then we have the information we require to go on to work on meeting our progestogen needs more fully with supplementation.

Are there any other special situations that will guide my choices of hrt?

Sure. The big decision factor has to do with personal risk factors and lifestyle preferences, of course, but in some cases we also have to deal with specific other disease treatments.
The obvious one is endometriosis, which often requires a progestogen-heavy hormone imbalance for best suppression of endo growth. Other health needs that might guide hrt use and choices would be cancer risk or blood clotting disorders.

And there may be others. The point is, we need to remember that we don't use hrt in a vaccuum: it does have to fit with the rest of our life and health. But aside from not needing a progestogen to protect a uterus, women in this flavor of natural menopause have all of the choices—and risks—of any other woman in natural meno.

HRT for women with a uterus but no ovaries

2009-10-02T08:12:00.003-06:00

Although this site focuses mainly on women who have had both an oophorectomy (ovaries removed) and hysterectomy (uterus removed), some women choose to have diseased (or high-disease-risk) ovaries removed and yet retain their (healthy) uterus.

While these women will experience the same issues to do with choosing hrt as women in full surgical menopause, the need to keep their uterus healthy must also be taken into account and this will change their ultimate hrt options.

The crux of the issue is that exposing a uterus to estrogen stimulates the growth of the uterine lining or endometrium. In our fertile years, this stimulation is necessary to prepare the uterus to support a fertilized egg. When no pregnancy occurs, our hormone balance naturally cycles to cause our unused uterine lining to be shed in the form of menstrual flow, resulting in a period.

But when we no longer have ovaries to manage this cycling, uterine health becomes an issue. If we fail to shed that lining, it can build and build and over time, this unshed lining may turn to uterine cancer. Yeah, that's bad. It's so bad that it's a fundamental rule of hrt use that women with a uterus must include provisions in that hrt to prevent this from happening.

Like what? There are two basic strategies: we can artificially create a hormone cycle with our dosage pattern, thus causing the lining to shed in a period OR we can balance our hormones in such a fashion as to suppress that lining buildup in the first place. Let's look at both of these a little more closely.

Hormone cycling

This is the classic approach. We take an estrogen hrt for part of the month and add some sort of progestogen (progesterone or a synthetic version that acts like it) for a shorter time, often a week to ten days, to stimulate a period. Many women find this sort of cycle reassuring, since it mimics what they experienced in their fertile years. Many doctors prefer it because they feel that their patients do best with what they are accustomed to or that they are less likely to become confused keeping track of their hrt on a short schedule.

This kind of cycling does carry a cost, however. If you suffered through PMS or your monthly cycle of ups and downs with mood swings and bloating, maybe going on doing that doesn't sound all that appealing. Maybe you would be just as happy to make fewer trips down the feminine products aisle at the store and wear more white underwear without fear. Maybe you'd like to balance uterine protection with a little more comfort and freedom from that cycling.

There is nothing magical about monthly cycles once our ovaries aren't controlling things. Many women today have found that they only need to cycle a few times a year to preserve uterine health, either using oral contraceptives (while they are in their fertile years) or hrt (when they are post-fertile for whatever reason). A conservative schedule for this long-period cycling would be quarterly, although some women find that they can successfully go even longer without undue risk. So long as they are not having break-through bleeding (which indicates that their lining is building up beyond normal levels), they only take a progestogen every three or four months to produce a period. This requires that a woman keep track of her schedule so she doesn't go too long without that cycle and it requires that she use separate estrogen and progestogen hrts--neither of which are necessarily difficult to achieve. There will still be the same ups and downs of cycling and she'll still have periods, but they'll happen less often.

Is this strategy appropriate for all women? Not necessarily. Women with endometriosis, for example, may find that this is still too much estrogen stimulation. Women with cancer risks or metabolic disease or risk factors for blood clots may not be best served by this sort of a dosing scheme. This is one situation in which a woman needs to sit down with her doctor and consider carefully all of the factors that are involved in her use of hrt, not something to just wing on her own based on how she feels.

Continuous combined HRT

The other approach to uterine protection involves suppressing the growth of that uterine lining by continuously taking both estrogen and a progestogen. The lining never has a chance to grow, so there is no need to have a period to shed it. Hey, that sounds pretty good, doesn't it?

But there's a cost, and that cost might not suit every woman. In order to accomplish this, we must deliberately induce a hormone imbalance. We have to take more of that progestogen than we really have a need for otherwise to balance our hormones. Or, to put it another way, we need to have a deliberately progesterone-heavy balance.

For some women, that's not a problem: they're perfectly comfortable with a standard dose of any of the retail progestogens made for this purpose.

Other women, however, find this balance subjects them to an uncomfortable excess of progesterone effects. For them, then, the challenge is minimizing those effects while still getting the protection that their uterus needs.

There is more than one way to approach this problem. First, it's worth trying different progestogens to see if one is less unpleasant in this regard than another. Amongst the progestins, each one is very different in structure and characteristics and will act differently in the body, so if this is your choice, it may be worth auditioning a variety of them. Route may also make a difference, so even if your choice is progesterone itself, taking it via a different delivery route may also help you manipulate its effects.

But another way of dealing with this is to maximize the impact of your progestogen on your uterus while minimizing it elsewhere. This is done by using a more local delivery, either via the vagina or the uterus itself. This way, the highest levels are experienced in the pelvic organs, where they're most needed, and less of that dose makes its way to systemic circulation. In fact, one source suggests that this can represent a pretty significant difference:

Furthermore, vaginal administration of micronized progesterone has been shown to enhance progesterone delivery to the uterus by about 10-fold in comparison to im injection, despite the markedly higher (about 7-fold) circulating drug concentration achieved with im injection.

Sound interesting? There are actually several different hrts that provide for local delivery. Prochieve is a progesterone gel specifically designed for vaginal use, but some women have reported successfully inserting a Prometrium gelcap vaginally and allowing it to be absorbed that way. Vaginal suppositories such as Endometrin are also available, as are versions that can be custom-made by compounding pharmacists. And Mirena is a progestin-releasing IUD that works directly in the uterus and so can get by with an especially low level of dosing.

Update: We recently came across some interesting information that indicates that some, at least, progestins may be capable of transdermal delivery--something we probably should have put together before given that contraceptive and combined-hormone hrt patches aren't exactly new. That raises the question of whether some progestin hrts meant for oral delivery could be used vaginally (at a suitably lower dose). We don't know the answer but it seems to be something that might be worth looking into if using a local progestin by other than IUD would be a woman's preference. More on that in this news discussion.

Will I have to do this the rest of my life?

No. You will, however, need to tailor your hrt for uterine protection so long as you take enough estrogen to stimulate your uterus.

Our hormone needs diminish with age. For that reason, it's a good practice when taking hrt in any form of menopause to challenge ourselves every few years to be sure that we're taking no more than we truly need to achieve the effects that we define as important. By trying out a slightly lower dose every 3-5 years, we can find out if our bodies have been slowly easing down in needs without us noticing.

In theory, we'll all, if we live long enough, reach a point where our hormone needs are low enough that we no longer need to supplement with hrts. What we produce ourselves plus what we take in from foods and environmental contaminants will fully meet our present needs. And when that happens, a woman is probably not stimulating her uterus enough to need to continue to provide progestogen protection for it. That's something to review with one's doctor, of course, but that's the expectation. Until that time, however, so long as we've got a uterus and are supplementing estrogen, we need that progestogen coverage as well.

How will I know I'm taking enough progestogen?

You won't. The general guideline is looking for spotting. This is taken to mean that your lining is growing enough that the progestogen isn't providing adequate suppression, whether you're taking it cyclically or continuously.

If, however, you have a high risk situation where you aren't comfortable waiting for this symptom to tip you off, there's another method for monitoring uterine lining response: ultrasound measurement of the thickness of the uterine wall.

There is not, regrettably, any magical formula for relative doses, such that if we take this amount of estrogen, we know we'll need that amount of progestogen and then we'll be sure we're safe. Or if we have this measured level of circulating estrogen, we need that level of circulating progesterone to cover it. Hormones don't behave in a simple relationship like that—there are many other factors that can affect our hormone supplies and relationships. We can't force our hormones to go where we want and do our bidding. What we can do is provide the supply and then watch carefully to see what happens. If what happens is no uterine lining shedding, no spotting, then we most likely have the situation covered. And if we don't, then a simple ultrasound will tell us how our uterus is doing and whether we just have a brief unusual situation or whether we need to tweak our doses.

Let's repeat that, because it's pretty important: the test of our hormones is not in what we want them to do, but in what they actually do. Results are the most reliable place to focus our vision.

So that's it?

Yeah, pretty much. Outside of protecting a uterus, a woman's other hrt needs are essentially the same as for a woman without a uterus: meeting her post-fertile needs as she defines them while exposing her to the least amount of risk possible. So the information on hrt-balancing that is covered elsewhere on this site is just as applicable to you as it is to the women in full surgical menopause.

Got questions? Other concerns? Join us at our discussion list.

Vaginal dryness

2009-03-04T10:55:00.006-07:00

Many women are led to believe at at menopause we "just dry up." Our partners may believe this as well. Our doctors certainly do: although the condition that leads to this (we'll talk about that below) is very well known and easily diagnosed, they are apparently so reluctant to do so that incidence is being termed an "epidemic" (free signup required to read link; see also Part 2) by the medical community. With an estimated 50-60% of women complaining about this problem, it's not as though we don't have company.

So, what is the problem?

Its proper name is "vaginal atrophy" or, even more broadly, "urogenital atrophy." Sound scary? Yeah, us too. But what it means is simply deterioration of the tissues of the bladder, vagina, and various supporting structures due to the loss of adequate levels of estrogen in those tissues.

Yes, that area of our bodies is very sensitive to estrogen levels, and after menopause, we simply may not have enough estrogen there to keep those tissues healthy. This happens with natural menopause and it happens with surgical menopause. It even happens when we are taking hrts.

If you did a double-take at that last sentence, you've got lots of company. But in fact current prescribing guidelines for estrogen hrts call for using the lowest dose that meets a woman's objectives in taking hrt. That's for a good reason: our breast cancer risk seems to correlate fairly well to our lifetime exposure to estrogen, so the least estrogen that works for our needs, the less our overall risk.

But while that may work out fine for systemic (whole body) needs, it may not cover the very specific needs of these particular tissues. Wouldn't the answer then be to simply take a larger hrt dose so that it would? No, because then that risk goes back up.

Today's typical hrt strategy is to meet our greater vaginal estrogen needs in a different way, one that doesn't do as much to raise overall risks but does serve to keep those critical tissues healthy. That strategy is to use as low a systemic hrt dose as otherwise meets our needs and to supplement that with a second form of estrogen hrt that specifically meets vaginal needs. That means a little more work to manage our hrt and, yes, a little more expense, but the benefit of those costs is meeting our whole body's needs at a lower level of health risk.

Vaginal atrophy: what it does

Let's look a little more closely at what vaginal atrophy means for a woman.

Estrogen supports a number of functions in vaginal and urinary tissues. It helps maintain elasticity, moisture, lubrication, immune function, and sensation. Without estrogen, blood vessels shrivel up and become less functional, and our nerves begin to deteriorate. We can't bring blood to initiate the healing processes that protect us from infection. At the same time, these more delicate tissues are even more susceptible to injury or irritation.

That means that without estrogen, vaginal (and to some extent, vulval) tissues become dry all of the time, and hence more irritated by things like soaps or even contact with underwear. It means that we may be more susceptible to infections and it means that we may be more allergic or at least more prone to irritations, rashes, or itching due to contact with products like soaps, fragrances, or laundry products that we weren't bothered by in the past.

The loss of sensation, caused by the nerves being starved, means that while we may feel irritation just fine, we tend not to feel the pleasurable sensations of arousal or orgasm. "Dead down there" is a common way of expressing this. Because we don't have the capability to respond to arousal with tissue swelling and lubrication, we literally don't feel aroused. And the lack of elasticity and lubrication means that even if we go ahead with penetration, it will be at best uncomfortable and unpleasing, and at worst cause tearing and further irritation. No matter whether or not we provide a systemic "itch" for sexual contact with testosterone, if we can't respond physically because of the effects of low estrogen in these tissues, we will not seek or enjoy sexual relations. We'll talk more about the issue of libido support in another post here, but this is the important relationship: if the equipment isn't working, it doesn't matter how hard you push it. And estrogen is the foundation of "working" here.

So what do we do?

Luckily, treatment of vaginal atrophy is easy, has relatively inexpensive options, and is generally successful within a short time.

HRTs intended specifically to meet vaginal estrogen needs are different from those for systemic needs. It's especially important not to confuse them with products for systemic use that are also delivered through vaginal tissues. Our estrogens HRTs page distinguishes these, so check out your brands there to make sure you've got the correct one for your intentions: even health practitioners have been known to mix this up.

Vaginal estrogen HRTs are all designed to be delivered in vehicles that are non-irritating to atrophied vaginal tissues and well-absorbed by them. Even more importantly, they deliver only a very low dose of estrogen, only enough to meet the local tissue needs. The objective of this is to have all of the dose absorbed and used in those local tissues rather than being passed along to systemic circulation. That means that adding a vaginal estrogen supplement doesn't mean making an adjustment to our systemic HRT to take the addition into account.

It also means—and this is important—that we can use it intermittently. Our systemic HRT, you'll remember from discussions elsewhere on this site, needs to be kept at a fairly consistent level to avoid causing symptoms from fluctuating hormone levels. But because vaginal HRTs don't affect systemic levels, they can be used only as often as needed to provide the level of maintenance coverage we turn out to need.

Most vaginal HRTs are given at a relatively frequent dose interval, usually daily, for a six- to eight-week period. This provides a (relative) lot of estrogen to promote recovery of health.
Often, we use a cream for this treatment phase: it spreads out well and provides maximal contact with tissues. Further, these are older products and doctors are more familiar and comfortable with them.

Other options are available, however: typically these are rings and vaginal tablets, either retail prescription or compounded. While they may be less messy than creams, because they are low doses meant for maintenance, the treatment phase can take longer with these forms. Whether or not this is a good idea for any particular woman really depends upon just how uncomfortable she is and how rapidly she wants to turn things around.

Often women use a combined approach: a cream for the treatment phase and then switch to another form for maintenance. Alternatively, a woman can continue using a cream and simply use a smaller amount of it at a less frequent interval, making it less messy and inconvenient. All of the commercial vaginal estrogen HRTs work, so it's really a matter of preference.

What we can expect from vaginal estrogen supplementation

Beginning vaginal estrogen HRT can sometimes be annoying and uncomfortable. Some women have such damaged tissues that even the creams, meant to be non-irritating, are too much to tolerate immediately. If you have a reaction of burning or rash upon beginning any vaginal HRT, by all means call your doctor right away and ask for something else: it's not an effect that will go away quickly and there's no point to suffering. If nothing else, a compounding pharmacy can make you a preparation containing the same amount of estrogen as the retail products, but in a hypoallergenic base. In extreme situations, women may need to use the cream externally only for a period, and then gradually increase penetration to progressively treat vaginal tissues.

Many women report vaginal infections in the early weeks of treatment. These are due to the impaired immune function recovering at a different pace from other aspects of tissue healing, such that the vagina becomes a fertile place for bacterial growth before we're really able to fight those bacteria off. Additionally, using the cream runs the risk of introducing infections through the applicator and tube if we are not careful with cleanliness.

Infection is not a contraindication for continued HRT use, however, and infections can (and should) be treated at the same time. It may take more than one round of treatment before health is restored and we require less intervention, so some persistence can be needed to see this process through.

Now, we've said above that the idea of the low dose level of these products is so that they will be consumed entirely locally, without systemic impact. And that's true. Except, not at first. When we first begin treating established vaginal atrophy, those tissues may have lost enough of their circulatory capacity that they can't pick up all of the estrogen in time and some of it does "leak" into systemic use. We may experience a few hot flashes from the fluctuation in our systemic levels, or see a slight shift in our usual state of balance.

But because even atrophied tissues can benefit from the estrogen they absorb, healing is happening. And as those tissues recover, they'll use more and more of the dose until that state of total local use is achieved. For this reason, it's generally not considered to be a situation in which we should modify our systemic HRT intake. It's temporary and so long as we're not miserably uncomfortable, we don't need to change anything; we can wait it out, knowing it's time-limited and will gradually be resolving.

So we use the HRT daily for those six to eight weeks and find that things are feeling considerably better. Normal lubrication should be restored and sensation should also be more normal, assuming we experienced no actual nerve damage from our surgeries. Now it's time for maintenance mode.

Our doctors will tell us to use our HRT on a less frequent schedule and may suggest once or twice a week. But that's only a rough guess, and we each have to figure out our own best schedule.

If we're still using cream, we can also work on determining a reduced dose. What we hear most often from women is "a pea-sized dab a couple times a week," which is pretty vague but is an okay general guess to work from.

For those using a ring, of course, the dose is taken care of (although it's important not to neglect change dates).

For tablet users, the frequency is the only factor to be adjusted, but once to twice a week still seems to be where most women start. If symptoms of dryness or other hallmarks of atrophy return, it should be obvious that the dose or frequency or both should be stepped up a bit. If twice a week is seeming good, it might be reasonable to step down a bit to twice every week and a half, just to make sure that we're not using more than we need. In other words: we feel our way along, looking for our personal bottom limit and then dosing just above that.

The fine print

Great, so what are the drawbacks? Yeah, it's never a free lunch with this stuff, so you knew there would likely be a catch or two.

In this case, vaginal atrophy treatment has to lead into vaginal health maintenance, which means that we will need it more or less the rest of our lives. Maintenance requires a lower dose, generally accomplished by a longer dose interval and/or a change of product after initial healing takes place. If we stop using our vaginal estrogen supplement, our atrophy will return: this is an ongoing need, not a "disease" that we will "cure" with a one-time treatment. Just as we have to eat every day to keep nourishing our bodies, so we have to keep providing the estrogen needed to nourish vaginal health.

Vaginal estrogen supplementation isn't for everyone. Women who have hormone-sensitive risks in the pelvic area, such as endometriosis, are generally discouraged from using vaginal hrts because they concentrate potentially higher levels of hormones in pelvic circulation.
Women at high risk for estrogen-stimulated cancers anywhere in their bodies who are being treated by estrogen exposure restriction, either by withholding estrogen supplementation or by drugs that specifically combat estrogen exposure, are generally advised not to use vaginal estrogens. Although these products nominally are fully consumed by local tissues and don't spill over into systemic circulation and hence risk, enough has been shown to escape to measurably raise risk. In fact, research results to date have been contradictory, which generally means that the correct factor has not yet been identified. So at the moment, the general recommendation
(free signup required to read link) is along the lines of "each woman and her doctor need to reach an individualized decision" which really translates to "we haven't got a clue." For now, all we know is that there is some level of risk and that each woman will have to balance how that level of risk weighs against her symptoms.

One other concern we've heard voiced is about transferring hormones to our partners. Yes, this can happen if a cream dose is still present at adequate hormone levels. Timing of use can help manage this. The ring for this use releases such a low level of output that it's certified as safe enough to leave in during intercourse (although you may, of course, remove it if either partner prefers). Otherwise yes, some care is needed but so long as the HRT isn't freshly applied and still present in volume, it's believed that the risk is minimal. For 100% protection, however, a condom can be used as a barrier.

But isn't there some natural solution?

That kind of depends on what you mean by "natural." Since it's loss of our natural estrogen that causes vaginal atrophy, we can't really think of anything more natural than replacing that supply.

But perhaps what you mean is you prefer something you can purchase over the counter, something made from a blend of herbs, something that doesn't carry the risk of hormones. In that case, we're sorry to have to tell you that this doesn't exist. There is no substance, whether grown in a plant or refined in a lab that can fulfill vaginal estrogen needs other than real human-type estrogen. Yes, there are many sales websites that will try to tell you differently, but in fact these products do not address the specific need for estrogen and so will not treat vaginal atrophy. Lubricants or vaginal moisturizers may feel soothing, but will not actually promote healing or improve the other physical damages of vaginal atrophy. Sure, try them if your other options are limited or you want to believe, but please don't be terribly surprised if your atrophy persists.

Must it be treated? Of course not. Every woman may choose what she considers important. Some women feel the loss of sexual responsiveness grants them a return to a purer, more childlike condition. Others don't find the symptoms troubling or find that simple over the counter lubricants and a switch to unscented products are adequate to deal with the degree of atrophy that develops.

Each of us gets to decide these things for herself. What we want you to know, however, is that this is a treatable condition, not a life sentence. Menopause does not mean "dead down there" or intractable pain. If you aren't happy with the state of your vaginal health, just speak up. Yes, we know it's hard if you're not used to discussing this part of your body or your sexual needs. You may be embarrassed, or you may worry that your doctor may make you feel wanton or unclean. Please don't: this is perfectly normal physiology and your doctor really should be a mature enough individual to handle such a request politely and smoothly. In fact, shame on him for not asking directly whether you need treatment of this kind in the first place. At some point, though, one or the other of you needs to suck it up and just raise the question, and since you're the one who's hurting, yes, we're looking at you.

Not sure what to say? How about something along the lines of "Doctor, I'm concerned about developing vaginal atrophy. Lately I've been experiencing dryness and loss of sensation, and I'd like to consider using some supplemental vaginal estrogen to help keep things healthy. Would you write me a prescription for this?"

Making sense of transdermal HRT doses

2008-12-15T15:13:00.004-07:00

While the newer gel hrts are proving very successful for some women, other women are having puzzlingly disappointing results with them. There's a lot of individual difference in how well we each may take up any given transdermal medium, but in the case of gels, this doesn't seem quite in sync with what these same women find with other transdermal media.

The one way that gels stand out from, say, creams or lotions, is that they dry on the skin rather than having the hrt, medium and all, absorbed into it. Product labels warn of enhanced risk for transferring gel-delivered hormones to others and for diminishing the delivered dose by washing too soon after application (where "too soon" is a much longer period than with other media).

The gels

It's also puzzling to women trying to calculate doses from one form to another of hrt just how the relatively large amounts of estrogen in the typically-recommended gel hrt doses should be compared to the amounts delivered by other hrt forms.

One of the members of our discussion list just came up with this excellent article that may shed some light on all of this: "Comparison of the transdermal delivery of estradiol from two gel formulations." According to this test, which compares two widely-sold gel hrts, the delivered dose of the hormone was only 13-20% of the amount applied.

All hrt deliveries involve some losses: that's one reason why we can't just convert from one hrt to another of a different route and go on using the same dose numbers. But in the case of gels, we need to recognize that there will be a big difference because only such a small amount of the hormone actually gets into our bodies this way. And with such low proportional delivery when used according to directions, it doesn't take much imagination to suspect that this could be further reduced by incorrect application.

Yep, that's a lot of loss. Where does it go? Well, onto our spouses and kids, if we're not careful. Onto our clothing and towels and bed linens, I'm sure. Ultimately, down the drains of our showers and washing machines, into our sewers and septic systems, thus contributing to the contamination of water supplies that today test in community after community as having elevated estrogen contents and perhaps contributing to the cancer and other hormone risks of an entire population. It's not our place to raise ethical issues here, but this might be a point that women would want to consider when they make their own choices.

Other transdermals

As we said above, each hrt, even within the family of transdermals, has its own delivery profile. That includes things like how the uptake "feels" to us and how efficiently it moves the hormones it contains into our systems. We've seen way too many women just slam themselves with excessive doses when they thought that because they needed Xmg of dose in one transdermal hrt, they needed to multiply normal doses of another hrt to get that same number.

That's not how it works.

We can get a better sense of dose equivalency from the "usual starting dose" figure that's part of the basic prescribing information with any hrt. That's the dose that incorporates enough to make up for losses in delivery and still provides enough to make up "usual" coverage in a woman's system.

Yes, this is confusing. One of our discussion list members assembled this very handy chart comparing dose to delivered amounts. It doesn't cover every hrt, but it does give us a great overview of how much variation there is in all of this.

So how do I use this information?

Basically, it reinforces the premise that we really can't do an absolute conversion from any one hrt to any other hrt. But it does help us feel more comfortable letting go of dose numbers as even a rough conversion factor and switching our attention to more useful figures.

More useful in moving from one hrt to another is how we felt on what dose of our original hrt. If we felt sort of okay on, say, the usual starting dose of our old hrt, then we might want to start the new hrt at whatever is pegged as the usual starting dose for that one. Similarly if we were one up or one down from the usual starter of our old hrt (or we would have preferred to have been), we might look to that many iterations off of usual starting for the new one. It's a really rough system and no, the manufacturers aren't going to provide us with anything better because their profit lies in holding us captive to their brand, not in facilitating our moving to someone else's.

We can also use our understanding of this to help explain why we may feel really different when we switch brands. We typically see this when we're having problems with one brand and our doctor switches us to another and whammo, we're feeling as though our hrt has just evaporated. Many doctors don't keep up with the trend that some hrts now come out in ultra low doses meant for women in natural menopause who just want a tiny hormone boost for its value in combatting osteoporosis. Those doses aren't typically enough for most women in surgical meno, so even swapping to the "usual" of the ultra-low hrts is a huge dose cut. Again, when we look at the figures for what is being delivered, we can get a sense, albeit rough, that we've actually had a big cut in what our bodies have to work with. So in this case, we're not crazy: we actually aren't taking anywhere near the same thing and we need to take this fact back to our doctors to use in troubleshooting our correct dose.

Obviously, dose amount and delivery amount aren't the only factors in working with the behavior of different transdermal hrts, but they are an important factor to understand when we are troubleshooting.

Menopause, hrts and diabetes

2008-02-09T11:31:00.001-07:00

From time to time we have discussion list members asking about how our blood sugar interacts with hormone levels and hrts. Some of these are women who already have diabetes and are worried about how surgical menopause will affect their control; others have newly-diagnosed disease and are wondering why.

Because our ovarian hormones are part of the overall regulatory hormone system in our bodies, they do affect the functioning of areas that we normally consider outside their regular realm. But just as our thyroid hormone levels interact with the ovarian ones and just as melatonin, the sleep hormone, can be disrupted by the timing of when we take our hrts, so the hormone that regulates our carbohydrate metabolism, insulin, is influenced by our ovarian hormone levels, balance, and fluctuations.

Now, diabetes is a broad term, much like cancer, that loosely covers a variety of distinct diseases that happen to have alterations of carbohydrate metabolism as a common feature. We're not going to go into the various distinctions here—we're not going to talk about diabetes per se, just how it behaves with respect to our ovarian hormones. You can read a basic introduction to the types of diabetes at Wikipedia if you're not altogether sure what we're talking about.

General actions

While many of the details of these metabolic interactions between ovarian hormones and insulin dynamics remain unresearched or the conclusions unclear, the general rule is that normalizing hormone levels to that of post-fertile needs in a stable fashion has the most normalizing effect on blood sugar levels.

This means, yes, that unstable hormones can bring instability to our carbohydrate metabolism and/or diabetic treatment plans. It also means that imbalances in our ovarian hormones can put an additional burden on our treatment or can bias our metabolism in unhealthy ways.

What it does not mean that eschewing hrt in menopause is "better" for diabetic control or that we are "better off" without hrt because it can influence our blood sugars.

Estrogen and insulin

Falling estrogen levels typical of natural menopause are identified by a number of researchers as raising blood sugar and the related risk of diabetes.

Women randomly assigned to hormone therapy had a 35% lower risk for diabetes than those assigned to placebo. This reduction in risk was primarily due to the fact that women in the hormone therapy group maintained a lower fasting glucose level than women in the placebo group. We found that hormone therapy prevented the increase in fasting glucose values that was seen in the placebo group over time. (source)

In nondiabetic women, menopause, but not age, is an independent risk factor for elevated fasting plasma glucose levels (source)

These effects would also be expected to present in surgical menopause, where the estrogen drop is more extreme, and in situations where our hrt is inadequate to raise our estrogen levels to meet our needs. In a rat study, the effect of oophorectomy was summarized thus:

The researchers showed that in older female rats, free of heart disease, estrogen deficiency appears to trigger the development of high blood pressure and obesity.
Rats that had their ovaries removed, thereby depleting their estrogen levels, had significantly higher blood pressure and gained twice as much weight as "control" rats with intact ovaries...
Rats that had their ovaries removed also showed 70-percent higher levels of the fat hormone leptin and 35 percent higher blood sugar levels...
Moreover, female rats without ovaries that receive estrogen replacement therapy do not experience any of these adverse hormonal and metabolic effects (source)

While there's a fair amount of research on estrogen, the picture on progesterone is less well-defined except by extension from the well-known effects on blood sugar of normal menstrual cycling and pregnancy, both of which carry a woman through periods of hormonal imbalance that reflect changing progesterone levels as well as estrogen levels. Thus while it does indeed have an effect, there are fewer clear statements we can point you to.

As a general rule, what we read can be summed up as indicating that progesterone has an effect of increasing insulin resistence. But we are mostly reading that in secondary sources rather than primary ones, and that undermines the authority of these statements. So for now, we have to put that specific relationship in the "probable" column rather than calling it "known."

Hrts and blood sugar

Much of the research that has been done on hrts and diabetes has been done with Prempro or Premarin. But given that different routes of hormone administration can affect how the hormones are actually used in our bodies as well as other associated effects, how can we extend that knowledge to the impacts on blood sugar?

In the Women's Health Initiative Study, the estrogen-only arm found these effects in women with pre-existing cardiovascular disease who took the oral estrogen hrt Premarin (estrogen alone):

A slightly smaller number of women who took Estrogen alone developed diabetes but it was not significant when statistical testing was done

8.3% (397 cases/4787 women assigned to E alone) of women who took Estrogen alone developed diabetes over the course of the trial compared to 9.3% (455 cases/4887 women assigned to placebo) of women who took placebo

Blood sugar and insulin levels were lower after one year in those women who took Estrogen alone (source)

In contrast, a later study looking at oral as opposed to transdermal summarized these findings:

There was a significant worsening of insulin resistance markers in the oral estrogen group. The team observed significant decreases in glucose-insulin ratio and quantitative insulin-sensitivity check index, and significant increases in baseline insulin and homeostasis model assessment.
Other significant changes in the oral estrogen group included increases in high-density lipoprotein cholesterol and leptin levels, while adiponectin was unchanged. There was also an increase in resistin and a decrease in baseline ghrelin levels.
In contrast, no significant changes in insulin resistance parameters were observed after transdermal estrogen, except for a decrease in the glucose-insulin resistance ratio.
Women in the transdermal group had no changes in leptin or resistin, whereas there were significant increases in adiponectin and decreases in ghrelin levels. No changes in lipid parameters were observed. (source)

In addition to these findings, we know that women with diabetes are at higher risk for both blood clots and cardiovascular disease in general. Since both of these risks are reduced with transdermal hrts as compared to oral (refs), this factor should be taken into account in the hrt route decisions a diabetic woman will make (although they may not be the only factors she'll take into account).

Questions we're asked about menopause and diabetes

Does menopause cause diabetes?

It's hard to attribute direct causation, because many metabolic problems don't necessarily have a clearcut cause the way falling down some steps might directly cause your broken ankle.

What is more likely is that you may have been trending in an unhealthy direction, and the natural impact of menopause or imbalanced hrts just pushed you into the position where you were abnormal enough for the diabetic tendency to be detected.

Will hrt make my diabetes worse? Better?

It depends upon many factors to do with your diabetes, of course, but in general, hrt looks as though it can exert a positive influence. And by hrt, we of course mean effectively-delivered hrt, taken at a dose and balance that fits each woman's individual needs.

It also looks as though hormone stability enhances blood sugar control stability as well. This means that for diabetics, there is extra reason why making changes to hrt in small increments and slowly might be the least upsetting approach.

Looking at if from the other side, it is also probable that if we badly disorder our ovarian hormones through a poor hrt fit, we can disrupt our diabetic control or enhance our odds of progressing to overt disease.

Can I make my blood sugar better by how I adjust my hormones?

Aside from the stability issues discussed above, it doesn't look especially feasible to try to adjust blood sugar using hrt. While tweaking one hormone up or down might alter diabetic treatment amounts needed, the healthiest approach still looks to be adjusting hormones to best needs, and then adjusting diabetic treatment to that stable level.

So it's likely that the most we can do with this information is to raise our awareness that yes, ovarian hormone levels and fluctuations will affect blood sugar and diabetic control, but we cannot generalize from there to what measures will be most effective in any one woman's body. While good ovarian hormone balance can help ease the treatment of diabetes, it's not going to make it go away.

Other practical considerations for diabetics in surgical menopause

One special aspect of using hrt may be especially important for diabetics: the use of vaginal estrogen to prevent vaginal atrophy and maintain healthy urogenital tissues.

Poorly-controlled diabetics are at higher risk for vaginal yeast infections, so it behooves diabetics to take extra care to insure that vaginal estrogen levels are maintained and those tissues are as healthy as can be in terms of their immune function. Don't wait for your doctor to ask you whether or not you're experiencing dryness or libido loss: open discussion as to whether or not your vaginal estrogen levels need supplementation. Recent research suggests that up to 50-60% of postmenopausal women suffer from some degree of vaginal health impairment due to low local estrogen levels, so it's not something special or something to be embarrassed about.

In terms of overall health management, the implications of this inter-relationship are similar to those for women with thyroid disease: alterations in hormone levels and hrt adjustments may well affect blood sugar control and might require adjustments of diabetic therapy in sync with ovarian hormone adjustments.

Further, it's important to keep a close eye on symptoms, because many symptoms of ovarian hormone imbalance may be described in quite similar ways to symptoms of insulin/sugar imbalance. Distinguishing these can be very important to control of both. This is where listening closely to your body is critical. And don't neglect the importance of journalling: keeping track of what we're taking and doing helps us learn to read the signals our body is sending us and we need to take even more care with this the more complex our situation and the factors we are tracking.

And does this have any importance for those of us who are not diabetic?

Oh yeah. The path from being overweight to type II diabetes is a pretty well-established one, especially when we're looking at midbody weight. While to some extent a fat shift to the middle body is a normal part of this menopaused lifestage, it does have a strong risk association with diabetes. It also comes as part of an even less appealing package: metabolic syndrome. So while it is perhaps easier in a head-in-the-sand sort of way to just wait for our doctor to surprise us with the news that our blood sugar lab values are off, it's probably preferable in the long run to take a closer look at our personal risks and modify our diet and, if needs be, hrt so that we are doing as much as we can to prevent diabetes before it gets that far.

And for women who cannot or choose not to supplement their post-menopausal hormone levels, this increased risk is something to keep in mind, both in terms of health maintenance and in terms of specific monitoring in regular checkups. For those who are inclined not to use hrts, this should also be a factor to take into account in that decision, remembering that risk is not all on one side of that evaluation.

NEWS: Fat may be a factor in vitamin D needs

2007-09-03T17:00:00.001-06:00

An interesting news article turned up just the other day: "Sun exposure unrelated to excess fat and vitamin D." The research article itself is only available to those without subscriptions to the Journal of Clinical Endocrinology & Metabolism as an abstract of "Reduced Sun Exposure Does Not Explain the Inverse Association of 25-Hydroxyvitamin D with Percent Body Fat in Older Adults".

Here's the interesting quote from the Reuters coverage:

When people were divided into four groups based on their body fat percentage, the researchers found no difference among the groups in time spent outdoors, percent of skin exposed to the sun, or sunscreen use.

But they did find that the people with the highest percentage of body fat had 20-percent lower blood levels of vitamin D than those with the least body fat.

What does that mean for us? Those of us packing more body fat may be less likely to benefit from what sun and supplementation we do get, so it's possible that we would benefit from higher (or some, if not currently getting any) vitamin D supplementation.

As D comes into greater repute (as it has been lately with the release of a number of interesting new research results), more doctors are willing to measure our circulating levels, and this is a good test for meeting needs since the population discovered in this study seems to be (maybe) sequestering the vitamin D in their fatty tissues instead of having it out and usable.

So if you're in doubt—and the heavier you are, the more doubt you can reasonably have—it's an easy thing to test. Way easier, of course, than developing osteoporosis or the many other things, including cancers, that are increasingly linked to vitamin D deficiencies.

Can't you just recommend some vitamins and herbs to take care of all this?

2007-09-03T16:50:00.000-06:00

Online discussions are full of questions along the lines of

I'm afraid to take HRT. Isn't there some vitamin/supplement/non-prescription remedy that will get rid of all of my symptoms instead?

We'd all like a magic rescue, performed by something we view as safe and benign...and prescriptions in general and HRTs specifically have been cast in the popular press as such boogeymen and shrouded in such mystery that many women simply can't face the terror of undertaking their use. We may want the comfort of something we're already familiar with or that we can use without having to deal with a doctor or other prescription gatekeeper who we might feel will take control of our bodies away from us.

While the internet health sales pages are bursting with vitamin combos that promise glowing results and discussion sites are full of women assuring everyone that this or that special product or vitamin relieved all their symptoms, it's not really either a mysterious or magical process. But it's also not specific to any single preparation.

That's right: there's no vitamin or herb or combination of them that will "fix" your menopausal symptoms. That's because your symptoms, if they are due to menopause, are directly caused by hormone levels lower than those you need to feel well, and no vitamin has the ability to boost hormone levels if we don't have ovaries. They simply won't fix what's "broken."

Huh? So are those women lying? Deluded? No, maybe not. Maybe they do feel better after taking their vitamins. But it's not so much that the vitamins "cure" their troubling symptoms, perhaps, as that in better meeting all of their metabolic needs, they're better able to cope with menopause and, yes, they do feel better.

It makes sense, when you think about it, that getting your body otherwise as healthy and stress-free as possible will maximize your own ability to deal with estrogen deficiency as gracefully as possible. But that's something entirely different from expecting a particular vitamin or combination of them to specifically alleviate your symptoms.

What goes on is that when women get wonderful results with some or another supplement, they're possibly doing two much more subtle things.

First, they may be filling in a real nutritional gap and providing the raw materials their bodies did need to function more healthily. For example, we can metabolize neither HRT nor our own hormones without the simultaneous presence of certain specific nutrients. Meeting our needs for vital raw materials that enable critical physical processes in turn directly lowers stress, lowers our adrenal workload and allows it to shift more of its output to making ovarian hormones as opposed to stress hormones.

And second, there's the placebo effect. Now, don't go all huffy and defensive—we're not telling you it's all in your head. Not at all. In fact, research study after study has demonstrated that the number one most effective remedy for hot flashes, no matter what preparation it's tested against, is placebo. Lots of doctors take this to mean oh those silly weak women, just pay them a little attention and they get over it. We don't really agree.

It seems to us that when we're taking something we believe will help, that in itself lowers our stress levels: we're doing something instead of helplessly spiraling downward caught in hormonal upheaval. And it's that lowering of stress and feelings of self-impowerment that, we suspect, can have a real physical effect, maybe through that same adrenal mechanism we mentioned above: by helping to shift us from a stress mode to enhanced ability to meet our own hormone needs more fully by adrenal output.

So if you believe that a vitamin or special preparation or accupressure or accupuncture or yoga or whatever tools most appeal to you hold some hope of helping to lower your stress and allow your body to better meet your menopausal needs, you could be exactly right. We don't think that's going to do the whole job in surgical menopause, most times, without HRT and we don't think that using vitamins or herbs will make up for a poor HRT fit, but it might at least help a bit.

Just remember to stay balanced: keep in mind that overdoses of herbals or vitamins can be toxic to various organs, especially our livers, or can challenge our hormone-deficient impaired immune system; and that women who cannot take hormones may experience that exact same risk from using phytoestrogens as they would with any prescription HRT.

FDA approves two new hrts: Endometrin and Evamist

2007-08-21T21:07:00.001-06:00

The FDA has given new drug approval to two new prescription products that might be useful to our readership as hrts.

Endometrin

Endometrin is a 100 mg bioidentical progesterone vaginal "insert" described further as a "white to off-white oblong-shaped tablet" to be administered with a plastic applicator. Inactive Ingredients: lactose monohydrate, polyvinylpyrrolidone, adipic acid, sodium bicarbonate, sodium laurel sulfate, magnesium stearate, pregelatinized starch, and colloidal silicone dioxide.

The label indication is for fertility support, but, like Prochieve (ex-Crinone), the vaginal gel, it can presumably be used for other progesterone needs as well even though the limited data on the package insert does not discuss any use or data other than the fertility support testing done. The advantages of vaginal delivery of progesterone are mainly of interest to women taking largish doses, out of scale with their level of need, to accomplish therapeutic, rather than hormone balancing, objectives. These would include things like treating endo as well as protecting a uterus from excessive estrogen stimulation by hrt. The advantage is that more of the hormone is delivered into local circulation and systemic effects of the dose are minimized.

The 100 mg provided dose is hefty, but may not be out of line with what some women are using. Since the tablet is to be stored at normal room temp, it probably is a typical firm chalky pill. Still, it should be possible to divide it with care if some dose customization is desired. That's not likely to be entirely handy down to the 10-25 mg doses most women in surgical meno may be using to balance their hrts, however—although it could be attempted if this seems otherwise to be a good choice for a woman.

Because it's new, a doctor whose practice also deals with fertility may have samples available that could be used as a trial. It should be available on sale now, but local pharmacists may not be familiar with it or have it in stock, so there could be a slight delay in filling a prescription.

This is an approval by the US FDA; we're not aware of it being for sale in other countries, but if anyone knows differently, please let us know.

Evamist

Evamist is a transdermal spray delivery of bioidentical estradiol approved for use in menopause (that is, licensed only for hot flashes). One spray delivers 90 mcL which contains 1.53 mg estradiol; starting dose is one spray daily to the forearm but the dose may "increase to two or three sprays daily to forearm based upon clinical response" to adjacent, non-overlapping areas. "Sprays should be allowed to dry for approximately 2 minutes and the site should not be washed for 30 minutes." Inactive ingredients: octisalate (a common active ingredient in some sunscreens used to enhance skin penetration), alcohol (to dissolve the drug).

"Application of Evamist to other skin surfaces has not been adequately studied." That means, of course, not that it won't work, but that the manufacturer didn't pay for that extra research as part of their licensing application. There is no reason to suspect that the usual other safe areas might not work although each area's absorption might vary according to the tissue and circulation present in each. The forearm typically has relatively low fat overlay and good, close-to-surface blood vessel presence, so this would provide for a faster uptake and less tissue storage than, say, the butt or belly or thighs.

The precautionary text in the package insert is pretty much standard for estrogen. Of interest in the adverse reactions table is that while nausea was sharply lower than placebo at low doses, it rose with higher doses--as one would expect in sensitive individuals using an hrt with a half-hour uptake curve. Note also that nasopharyngitis (those puzzling sinus/ear symptoms) are also present with it, especially (we don't know why) with the low dose--although that might well represent the beginning of use and the higher doses being used in women who have accommodated to estrogen use. Headaches are also seen at a higher level in the users as opposed to the control group, and we suspect that these are also the uptake-sensitive individuals. That doesn't mean, however, that this would not work for them--this was a short trial (70 days) and it could be that once stabilization occurs and normal body caching mechanisms are in place, this is less of a factor. That's no compelling reason to rule it out without trying it if it otherwise is an attractive choice for a woman.

Because the dose is delivered by a metered spray pump, dose customization would be difficult beyond the number of sprays per day. Nonetheless, a creative woman could cover some proportion of the area to be sprayed with a shield of some kind--although that's not likely to be wholly accurate (more than you'd think, though, since the sprayer is actually a bell-shaped template that fits snug against the skin to control the size of the area applied to). Trying to bypass the pump and just work with the liquid would also be tricky since the amount of spray volume would be roughly 0.135 ml. The dose equivalence to other hrts isn't entirely clear, either, since forms like this (creams, lotions, and especially gels) also allow some factor for wastage on the skin. Pending more user experience with this, starting with the default directions and working up does seem like a reasonable approach and less likely to be problematic than making assumptions that a higher dose will be needed because of the way other hrts have worked.

No transfer of the estradiol to a partner was measured one hour after dose application, so this form is obviously more fully absorbed into the skin than gels or lotions are. "When sunscreen is applied approximately one hour after application of Evamist, estradiol absorption was decreased by 11%. When sunscreen is applied approximately one hour before the application of Evamist, no significant change in estradiol absorption was observed." The text does not distinguish between oil-based and non-oily sunscreens, but as with all transdermal hrt use, the oils used on the skin may make a difference depending upon whether they are digestible or not. Using non-oily sunscreens would probably have the lowest impact on hrt dose dynamics.

So this gives us one more retail transdermal estrogen hrt, although like all of the other retail hrts, it provides only estradiol, not the other estrogen forms that can be obtained through compounded hrts. That may or may not make any difference for a particular woman--estradiol is widely-enough tolerated that it is not necessary for most women to begin with anything else unless they have a particular philosophical preference for doing so or have prior estrogen experience to suggest a need for the less active estrogens. It is somewhat less customizable in dose than the other retail transdermal estradiols, but then, dose customization is not something that is encouraged by the FDA licensure system (because approvals are specific to the doses tested) and so manufacturers have to design packaging/delivery that thwarts dose variability and customization.

[Updated 3/10 to correct outdated links]

NEWS: JAMA weighs in on the WHI reappraisals

2007-07-11T11:03:00.000-06:00

Now the Journal of the American Medical Assoc. has weighed in on rethinking hrt as the ongoing re-analyses of the Women's Health Initiative Study progress.

The article is good in picking over the problems with WHI data and practices as well as some of the implications of the results. Where we have reservations—and we think these are important because of all sources of medical education and news, a JAMA piece is most likely to be seen and carry weight with our doctors—is that their advice specifically deals with natural menopause and has nothing to do with us: it's all about weathering a brief period of hot flashes and then giving up hrt.

Even more worrisome, though, is their flat statement that benefits like osteoporosis and colon cancer prevention cannot be taken into account in evaluating the risks of using hrts. Now this is a particularly medical attitude and is part of what we mean when we talk about medicine being focused on treatment of disease, where we as individuals tend to be a bit more focused on maintenance of our health.

From a medical standpoint, it's acceptable to risk experiencing a disease state if medical treatment exists, even if that treatment carries risks itself. Since colon cancer can be detected via colonoscopy and treated with surgery and since osteoporosis is now medically defined as being dealt with entirely satisfactorily with bisphosphonates, then, it's fine to accept not preventing them them because there is no real negative connotation attached to a treatable disease in medical terms. While that may make absolutely no sense to us, who might not feel the same way, it is entirely sensible and consistent with the philosophy of medical practice...and medicine as a business of selling diagnosis and treatment.

Where else can we quibble? Their equation of hrt risks as oral synthetic = all hrts, something that other research data is significantly questioning, has always been a sticking point in WHI analysis and one that some other policy-setting groups are seemingly taking into account in a more nuanced way. We think this is a simplistic stance, this general equivalence, and it disappoints, although not surprises, us that JAMA is holding to it.

Overall, there are some good points in this piece and it's well worth reading by all of us. And by reading it, we can better prepare ourselves to counter arguments we may get from our doctors, who may seek to apply a narrow interpretation of its points to our situation.

NEWS: ethinyl estradiol gets up to some odd tricks; getting enough vitamin D from the sun?

2007-06-29T13:44:00.000-06:00

While this applies only to a small subset of menopausal women, we just recently read two interesting research articles about ethinyl estradiol, a synthetic estradiol used most typically in oral contraceptive but used by some women in menopause who need a synthetic estradiol.

In the first study, "Formation of Ethinyl Estradiol in Women during Treatment with Norethindrone Acetate," it appears that taking this progestin, used by some women to suppress endo in surgical menopause, allows the body to create this form of estrogen (that is, it's partly metabolized into this estrogen). The implication, we think, is that estrogen exposure might thus be miscalculated. That's not of functional significance unless one wants to avoid estrogen exposure or when a woman using NET-A changes HRTs and suddenly finds her estrogen needs seem wonky. How much? It's probably pretty individual, but point your endocrinologist to this article and ask for more interpretation if this affects your HRT regimen and concerns.

In the second, "Effects of oral and trans-vaginal ethinyl estradiol on hemostatic factors and hepatic proteins in a randomized, cross-over study," researchers report that oral and vaginal delivery of ethinyl estradiol makes no difference in clotting risk factors. This is pretty much different from what current thinking is on other estrogens, where transdermal delivery is less stimulating of these factors when compared to oral delivery. Again, it's like to affect only a few women, but it does suggest that those at higher risk for clotting (smokers, those with elevated cardiovascular risk profiles or a stroke or clotting history) might want to consider other estrogens for their HRTs.

And in the other research article that caught our eye today, we read about how it's possible to have "Low Vitamin D Status Despite Abundant Sun Exposure." This is important to all of us because no matter what our hormonal status, we need that vitamin D to keep our bones strong. It has long been a rule of thumb voiced by doctors that no one needs to supplement vitamin D who gets 15 minutes a day of sun on their face and hands. While that's still more than we might think (and other research has shown that anyone north of about Denver really doesn't get enough outdoor sun on a year-round basis to meet this requirement), it may not be as "enough" as our doctors think. Despite 11.1 hours per week of total body skin exposure (without sunscreen), the participants in this small study (only 93) still came up with 51% who did not make minimum vitamin D levels when they were measured.

With all of the other research currently going on covering the widespread benefits of adequate vitamin D, not to mention its importance in bone maintenance, there's good reason to make sure we're getting an assured level, not just accepting that old rule of thumb as good enough. Note: vitamin D is a great demonstration of the rule that while some is good, too much is assuredly not. The current feeling seems to be that 800-1000 IU is increasingly recommended and amounts up to 2000 IU are nominally safe; beyond that, this hormone—for what we call vitamin D is actually a hormone—can have very negative impacts on health.