Surgical menopause boosts cardiovascular risks

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

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

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

Estrogen and cardiovascular disease

What kind of 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, 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 whatever help they can find.

Should women refuse an oophorectomy on these grounds? Oh, goodness no: there are often much more dire consequences and quality of life issues represented by the pathology for which we choose this surgery. 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 it company. Using progesterone as an hormonal hammer to bludgeon us into sleeping more in the face of estrogen excess: also less appealing when accompanied by 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 risk of endo growth and cancer if they skimp on progestogens in their HRT. Does that mean they are doomed? Certainly not, although they possibly do experience a raised level of risk and should therefor also be more vigilant about protective measures and monitoring. And they can consider, especially if they have other familial 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 not that clearcut. 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 seeking to emulate with HRT in surgical meno, we can assume that even if we've started taking HRT from the time of surgery and have had few disruptions in it, we still share roughly that level of risk.

And in case the question occurs to you, no, we're not advocating achieving higher-than-natural-meno estrogen levels as cardiovascular disease prevention. 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 will deal with it before we end up in intensive care with our first heart attack or stroke. Denial of cardiovascular risks: not looking so plausible any longer.