MENOPAUSE IS NOT GOOD FOR YOU!

What is good about menopause?
No more periods
No more fear of unwanted pregnancy
No more PMS
No more premenstrual acne

What is bad about menopause?
Up to a 10% loss in bone mineral density occurs during the first two years after menopause, then up to 2% per year thereafter.  One-third of women will have had a hip fracture by age 90.  Overall, 80% of hip fractures are in women.
Although very few women have heart attacks under age 50, by age 60, more women than men are having heart attacks.
Cancer of the uterine lining (endometrium) occurs, on the average, after 15 years of not ovulating.  Thus its peak incidence is at age 65
Skin becomes thinner.
Hot flushes, even ones that don’t make you sweat, cause sleep disturbance, which can lead to poor daytime functioning and even depression
Pressure in the blood vessels around the urethra falls by 50%, resulting in the onset of urinary incontinence in some women.
Related to the above point, engorgement of blood vessels around the vagina and urethra during sexual stimulation decreases, resulting in difficulty achieving orgasm for some women.
Estrogen is made from testosterone in the ovary.  No ovulation = no estrogen, and also no testosterone.  This can decrease sex drive and muscle mass.
There are estrogen receptors in the brain.  Mental performance can deteriorate after menopause. 

Before I get into a bunch of studies, let me summarize one thing about them.  I have never seen a study of hormone replacement in which there were more deaths in the women on hormones compared to those women who were untreated.  In fact many studies show dramatically fewer deaths in women on estrogen.  But estrogen replacement is as much about quality of life as quantity of life: Even if you don’t die from a hip fracture (although 20% do) there is a 50% chance you will be disabled by it.   Even if you weren’t going to have a heart attack you might want your coronary arteries wide open for skiing, hiking, or another aerobic activity, or just to avoid bypass, angioplasty, or stenting. You can stop reading now if you want, and let me (Dr. Roget) take care of the details of getting you on safe, bioidentical hormones.  Or you can read my analysis of each of the issues that are frightening you away from hormones and making it “politically incorrect” for physicians to prescribe them.

ESTROGEN AND BREAST CANCER

The risk of breast cancer increases with age until at least age 75.  It is a more aggressive disease in younger women, that is, more likely to be the cause of their death. 

As many of you know, Suzanne Somers is a proponent of hormone replacement.  When she got breast cancer, her doctor told her she should go off of estrogen.  She asked him “if I were pre-menopausal, would you take out my ovaries?”  He said, “no, no one recommends doing that.”  So then she asked, “so if I’m taking the same hormone my ovaries made, why do you want to take it away?”  He basically said, “that’s just what we do.”  I think Suzanne Somers makes a great point about how illogical the medical profession is being in regards to estrogen.  It is proven that there is no health benefit to premature menopause.  In fact, it increases a woman’s risk of heart attack and does not decrease her risk of breast cancer.  So why would menopause at any age be a health benefit?  Now, back to my analysis of the studies of hormones and breast cancer:

A breast cancer that is diagnosed usually began five to seven years earlier when a breast gland cell mutated, that is, got its genetic code screwed up while reproducing itself.  That defective cell became two, then four, then eight cells, and so on, until it created a lump big enough to feel or to see on mammogram.  So if in 2002 a lot of women stopped estrogen and two or three years later there were less new cases of breast cancer, does that mean fewer breast cells have mutated?  It could, but it seems rather early, and until we see fewer deaths from breast cancer, we won’t know.  Even then, we could be confused by the fact that the death rate from breast cancer was already falling steadily.  Since 1990, the death rate from breast cancer has decreased by 50% at all ages.  We would have to see if the rate of fall in deaths sped up.  A fall in the diagnosis of breast cancer may or may not mean something.  If men stop getting PSA tests, there will be a fall in the rate of diagnosis of prostate cancer.  Does that mean that getting PSA testing causes prostate cancer?  I doubt it!  If not taking hormones decreases mammographic visibility of breast cancer, then the diagnosis of breast cancer will fall rather quickly after women stop taking estrogen.  This appears to have been the case in California, where a fall in breast cancer diagnosis was seen two years after the WHI report came out.

When the Women’s Health Initiative study (WHI) was stopped, it was because more cases of breast cancer were diagnosed in the group treated with Premarin plus medroxyprogesterone (PremPro).  There weren’t more deaths in that group; in fact there was one more death in the untreated or “control” group.  And here’s the part you never heard: There was another group being studied, women who didn’t have a uterus, and who thus didn’t need progesterone (the Pro in PremPro) to prevent cancer of the uterus.  They got plain Premarin.  And they had less breast cancer than the untreated group.  In fact they had less breast cancer by the same percentage that the PremPro group had more.  But because the numbers were smaller, they didn’t reach “statistical significance.”  And of course the study just happened to get stopped before all the numbers could get bigger and make the plain Premarin group’s numbers statistically significant.  Read what you want to into this; but I find it surprising that the numbers for plain Premarin weren’t released at all until much later than the PremPro numbers.  In any case, the WHI study certainly didn’t show that estrogen alone (Premarin) increases the diagnosis of breast cancer; only Premarin plus medroxyprogesterone did.

The WHI study was stopped after running 5.4 years. There were over 10,000 women in each of three groups.  Women were on the average 12 years postmenopausal when they entered the study, about 63 years of age.  So this study is not as relevant as it could be in regards to the decision of whether or not to start hormone replacement at menopause. Premarin was given to women without a uterus, a placebo (no hormones) was given to the control group, and PremPro (Premarin, plus medroxyprogesterone to keep the uterine lining from growing and developing cancer) was given to women who had a uterus.  Here are the numbers of breast cancers in each group at the time the PremPro portion of the study was halted:

PremPro             Control             Premarin

38                          30                     24

Although the percent increase in diagnosis of breast cancer was the same for the PremPro group as the percent decrease for the Premarin group, the larger numbers made the results statistically significant for PremPro but not for Premarin.  Furthermore, the results for the Premarin group were not presented until over a year later, even though the study was being followed in real time with a computer database. 

Note that if the control group had had the same rate of breast cancer as the average for American women of their age, socioeconomic status, etc, there would have been 33 cancers (9% more than they actually had).   In this case the risk for the PremPro group would not have been statistically significant, and the number for the Premarin-only group would have been.  The WHI study would have shown that estrogen decreased the risk of breast cancer!!  Is this likely?  Of course not.  A better approach would have been to add the two hormone replacement groups breast cancer cases together (38 + 24 = 62), then divide by 2 to correct for there being half as many women in the control group.  If we call this combined group “post-menopausal hormone replacement”, it would have had 31 cancers compared to 30 in the control group or 33 in a population-matched control group.  The conclusion?  “Post-menopausal hormone replacement” does not increase the risk of breast cancer. 

A well-known statistical model for assessing a woman's risk of getting breast cancer is called the Gail Model.  It does not include hormone status, because no link has been established according to the biostatisticians who developed the model. 

It is true that blocking estrogen receptors with anti-estrogen drugs increases disease-free interval and, to a much lesser degree, length of survival in women with breast cancer containing estrogen receptors.  However, apparently even post-menopausal women not on estrogen have estrogen levels above the threshold to stimulate breast cancer growth.  Otherwise anti-estrogen drugs wouldn’t help them.  And it’s clear that above that threshold, there is no dose-response curve for estrogen.  Let me explain.  Generally, something that is bad for you is worse if you take more of it.  A pack of cigarettes is worse than three cigarettes per day.  More saturated fat or a higher cholesterol level is associated with more atherosclerosis.  Etc.  Such is not the case with estrogen.  If it were, then the order for breast cancer risk would be (in order of low to high estrogen levels): postmenopausal women, then postmenopausal women on estrogen, then pre-menopausal women, then pre-menopausal women on birth control pills, and finally, pregnant women.  But birth control pills (now available for over 50 years) clearly don’t increase the risk of breast cancer, and women who have had more pregnancies have a lower risk of breast cancer.  Who gets the most breast cancer?   Post-menopausal women do, and their risk increases with age. And it’s not because a lot of post-menopausal women take estrogen; less than 20% are now on estrogen. The Women’s Health Initiative, reporting on a single hormone product made from horse urine combined with a synthetic modification of progesterone has ruined it for women who want to have strong bones, healthy vaginas, a good night’s sleep, brains that function optimally, and coronary arteries that don’t plug up.  Of these, the single most important benefit of estrogen replacement is the reduction in coronary artery atherosclerosis (next section).   

Back to PremPro.  Don’t take it, even if it is only increasing the diagnosis of breast cancer and not increasing your chance of dying.  The diagnosis of breast cancer is a bad thing.  According to the Teachers’ Breast Cancer Study, tumors diagnosed on hormone replacement are at a less advanced stage.  Still, surgery, possibly with radiation or chemotherapy is the result.  So take something else.  Besides, medroxyprogesterone increases the number of mitoses, that is, cell divisions, in breast cells. That can’t be good.  Alternatives are discussed below.

ESTROGEN REPLACEMENT AND CARDIOVASCUALR DISEASE (Heart attack and stroke)

Late in 2007, the Women’s Health Initiative (WHI) reported on a group of women that was very different from the women previously reported on. They were started on hormone replacement at menopause.  Coronary artery calcium scans, a direct measure of coronary (heart) artery atherosclerosis (cholesterol deposits which have calcified in the walls of the arteries of the heart), were done on both the treated and untreated women.  Seven years later, the women on estrogen had 40 to 60% less coronary artery calcium than the untreated women!  (the variance depended on how consistent they were in taking estrogen).  Less coronary artery calcium = less risk of heart attack.  Thus, avoiding menopause = avoiding the increased risk of heart attack associated with menopause.  At least eight times as many women die of heart attacks as die of breast cancer.  Women hardly have heart attacks before menopause, yet by age 60 they pass men.  So what we have here is the single most important reason to use hormone replacement after menopause: heart attack prevention.  Strokes and have a less direct relationship with atherosclerosis, and the benefit of estrogen in stroke prevention is smaller. 

 

ESTROGEN REPLACMENT DONE RIGHT (which means BIO-IDENTICAL replacement for most women)

Evidence has been accumulating that taking estrogen by mouth (orally) is dangerous for those women who are put at risk from the increased coagulability of their blood.  Thus women with diabetes, high cholesterol, family history of blood clots, and certain other conditions should not take estrogen by mouth.  Oral estrogen increases blood coagulability because drugs absorbed from the stomach pass directly to the liver, which then, because of the high estrogen level it is exposed to, makes more clotting factors (C-reactive protein and fibrinogen increase, among others).  Thus women who have diabetes, high cholesterol, family history of blood clots, smoke, or already have elevated C-reative protein should not take estrogen by mouth.  I also feel that women over 70 years old should not take oral estrogen.  [My opinion was recently reinforced by the recommendation that women over 70 not take estrogen blockers after treatment for breast cancer unless they are at high risk of recurrence (positive nodes, etc).  These drugs are related to estrogen and increase the risk of blood clots].   Luckily, manufacturers have been coming up with patches, gels, creams, and vaginal rings to release estrogen directly into the bloodstream.  Yet the WHI study chose to give by mouth an antique product, distilled from the urine of pregnant horses (Pregnant mare's Urine = Premarin), because it was “the gold standard.” No women were excluded from the WHI study because of risk factors.  Smokers, women with high blood pressure, even women with prior angioplasties, strokes, bypasses, and heart attacks were included. Not surprisingly, there was an increase in heart attacks, strokes, and multi-infarct dementia (multiple tiny strokes, erroneously reported initially as Alzheimer’s). 

In women who are candidates for oral estrogen, Premarin is ok, although it is a mix of estrogens and blood levels cannot be measured.  PremPro is not advisable for reasons already discussed.  For those who object to a product obtained from horses, the synthetic equivalent of Premarin is Enjuvia.  My preference for oral hormone replacement in women without a uterus is micronized estradiol.  Stay with the same brand (for generics, same manufacturer) and have a blood estradiol level measured, as absorption and metabolism vary.  For women with a uterus, I recommend Angeliq, a combination of micronized estradiol and a unique progestin, drosperinone.  [I do not discuss drosperinone in the section below on progesterone and progestins, because it is not available separately.  It is contained in the birth control pills Yaz and Yasmin, of course at higher doses.]  The dose of Angeliq is one tablet once or twice daily (depending on blood estradiol level).  The alternative to this combined product is micronized estradiol plus either Prometrium (natural progesterone) or levonorgestrel (only available compounded).

There are three estrogens found in women.  Estriol is mainly from the placenta when you are pregnant.  Estradiol comes from the ovary.  Estrone is made in the body from estradiol.  So all we want to do is replace estradiol, and usually do it by putting estradiol directly into the bloodstream like the ovaries do.  That’s natural hormone replacement—the same estrogen the ovary used to make, delivered to the body the same way the ovaries did.  “Bio-identical” hormones are often a mix that matches the ratios between the hormones in the blood stream.  But taken by mouth, they go through the liver and get changed.  So they no longer match what is in the bloodstream, and being taken by mouth they cause the liver to produce more clotting factors.  So they are in no way natural or safer. Skip them.  Compounded creams with these “bio-identical” mixes are available, but vary too much in their absorption, and don’t produce natural blood levels because, as I said, the estrone in your blood stream is made by you from estradiol. 

For bio-identical hormone replacement, your goal should be to deliver a steady amount of estradiol directly to the blood stream.  This can be done thorough the skin: there are patches, a gel, and a spray.  There are vaginal tablets, and two vaginal rings: The EstRing is low dose, for treatment of vaginal symptoms only. The FemRing produces higher levels, though still too low in quite a few women. There are also pellets that are inserted under the skin every 8 to 17 weeks, depending on pellet size.  They are pure estradiol and dissolve completely, i.e. they are not inside a tube that has to be removed later.  Pellets are discussed more in the next section. The goal is to achieve a blood estradiol level of 60 to 150. (Subtract perhaps 30% from these levels when estradiol is taken by mouth, due to conversion to estrone, which is also an active estrogen).  My experience with saliva testing is that is neither accurate nor reproducible.  The North American Menopause Society also advises against using saliva testing to determine estrogen levels.  It can be hard to get estradiol levels over 60 with anything except pellets, so unless you are on pellets, I recommend you use Estrace Vaginal Cream one gram in the vagina at bedtime daily, because the base of the bladder and the vagina need a good quantity of estradiol.  If your symptoms are relieved at low blood levels of estradiol, your arteries and brain and blood vessels will be fine, although your bones definitely require supplemental calcium and vitamin D.  For that matter, lots of other things in the body need vitamin D, which is a steroid hormone just as is estradiol.  Now that sunscreen use has gone up, Vitamin D levels have gone down, and more than half of the population over 50 is Vitamin D deficient unless they take a supplement.  The recommended daily dose of Vitamin D was recently raised from 400 to 800 Units, and in fact most experts recommend 1000 units.  Citracal is calcium citrate and vitamin D in a brand found everywhere; I like their new Petites (smaller and easier to swallow; take two twice daily; if you can’t remember twice daily then take three once daily). It appears that calcium citrate is somewhat better absorbed than calcium carbonate. 250 mg of Vitamin C daily also helps reduce fracture risk.  It probably affects the matrix that the calcium is deposited on because it plays a role in collagen production.  250 mg is the optimum dose and sometimes hard to find.  You can break 500 mg in half.

THE OTHER OVARIAN HORMONES, PROGESTERONE AND TESTOSTERONE

Progesterone is made after you ovulate, which means it’s present for the second half of a menstrual cycle.  It prepares the uterine lining for implantation of a fertilized egg, and if this doesn’t happen, the ovarian production of both estrogen and progesterone falls, and the uterine lining sloughs (menses).  This sloughing probably is a factor in the prevention of cancer of the uterine lining (endometrial cancer).  Probably even more important is that progesterone decreases the sensitivity of the uterine lining to estrogen.  The term progestin is the group name for synthetic hormones with the action of progesterone.  Progestins are familiar from their use in birth control pills; natural progesterone doesn’t do as good a job of preventing ovulation.  When we talk about progestins in the context of hormone replacement we mean natural progesterone or a synthetic progestin.
Progestins are used after the menopause prevent growth of the uterine lining.  They do it so well that women on hormone replacement with an estrogen plus a progestin have 70% less risk of death from uterine cancer than do women taking no hormones.  (Estrogen alone increases the risk of uterine cancer).  If you don’t have a uterus, you don’t need a progestin.  If you do have a uterus, which progestin should you use and how should you get it into your system?  It is very hard to put enough natural progesterone on your skin to obtain a good blood level.  It is a large molecule and doesn’t penetrate well. To be absorbed when taken by mouth, it has to be micronized, that is, ground very fine, and suspended in just the right liquid to be absorbed.  There is only one such product available, Prometrium.  In it, the progesterone is suspended in peanut oil, so you can’t take it if you’re allergic to peanuts.  There is also just one progesterone product available for vaginal use, Prochieve 4%.  It comes in prefilled applicators and isn’t too messy.  However, both of these products are expensive and for that reason it is difficult to get insurance to cover them, or they are covered with a large co-pay.  Compounded natural progesterone capsules are an option but a blood level should be obtained to confirm absorption.  The large size of the progesterone molecule rules out making it into implantable pellets.

Levonorgestrel is a synthetic progestin, used in birth control pills and also contained in the Mirena IUD, discussed below.  When taken by mouth, levonorgestrel is 100% absorbed, not changed by the liver, and doesn’t increase the risk of blood clots.  Unfortunately, it is not commercially available separately for oral use.  Thus I have to have it compounded (ok because it is well absorbed).  The finished product, although not covered by insurance, is about one-third the price of Prometrium when it is not covered by insurance. There is a combined estrogen-progestin patch, Climara Pro, containing estradiol plus levonorgestrel. Unfortunately, there is only one dosage of Climara Pro and most women need two patches, which insurance can be reluctant to cover.  In addition, it is a large patch and often produces skin irritation.

Now lets talk about testosterone.  Estradiol is made in the fluid filled “follicle” on the ovary where an egg is ripening, to be released 14 days prior to menses. Estradiol is being made from testosterone, and as the follicle enlarges, its surface area increases.  More and more testosterone can then pass through the surface of the follicle and into the bloodstream.  Arriving in the brain, testosterone stimulates sex drive.  Women initiate intercourse during the four or five days preceding ovulation, rather than just being receptive.  Sperm survives for four days or so in the uterus and tubes and is there to fertilize the egg when the follicle bursts and the egg is released.  Menopause occurs when the ovaries contain no more potential eggs.  No eggs mean no follicles and thus neither estradiol nor testosterone.   Most women do fine without testosterone.  But some have their sex drive fall on birth control pills or at menopause, i.e. when they stop ovulating.  Skin can also become dry without testosterone stimulating oil glands in the skin.  Replacement of testosterone is rather difficult because it is not absorbed orally, the patch is for men and thus contains too much in addition to being unsightly, and Androgel is also dosed too high.  The answer is testosterone pellets.  [Note: women should never be given testosterone without estrogen, and testosterone levels should only be evaluated in the presence of a normal estradiol level].  A 50 to 80 mg 4-millimeter diameter testosterone pellet can be placed under the skin every 16 to 17 weeks to slowly dissolve and produce testosterone levels typical for pre-menopausal women.  There will not be the pre-ovulatory surge of testosterone, but most women are very satisfied with the result.  For women who do need testosterone, it makes sense to implant an estradiol pellet(s) at the same time; the dosage range is 100 to 200 mg for the 4-mm pellets.  Blood levels will confirm appropriate dosing of both testosterone and estradiol.  For women with a uterus, a progestin needs to be added, as I discussed above.  To repeat, the progestin choices are Prometrium, compounded levonorgestrel capsules, Prochieve vaginal cream, or the Mirena IUD.

 

THE EARLY YEARS OF MENOPAUSE

Between menopause and age 55, ovarian estrogen production can rise and fall, leading to irregular bleeding when continuous hormone replacement is attempted.  One option is an estrogen-only patch (Vivelle Dot) with oral progesterone/progestin added for 12 days per month.  For women who are candidates for oral estrogen, low dose birth control pills are another option, or better yet, the NuvaRing can be used. The NuvaRing produces blood estrogen levels that are about 40% of low-dose birth control pills and the estrogen it releases bypasses the liver, reducing the effect on clotting.  However, the NuvaRing still contains a dose of estrogen much higher than used in hormone replacement, so the contraindications are the same as for oral post-menopausal hormone replacement.  The point of NuvaRing or birth control pills is to suppress the ovaries and “take over” the menstrual cycle, avoiding irregular bleeding.  Although the Mirena IUD doesn’t suppress ovarian function and take over the menstrual cycle, it thins out the uterine lining so bleeding becomes progressively lighter with it, making it is a good choice for women who can’t take oral estrogen.

For women having regular but heavy menses in their 40’s it is going to be difficult to achieve bleeding control on hormone replacement.  Their best choice is to have a Mirena IUD inserted without waiting for menopause. Generally, menses fade away over the following years.  When hot flushes develop or a blood test shows menopausal levels of estradiol, an estradiol-only patch or other product is begun.  The Mirena IUD is changed every 7 to 8 years in this context (versus 5 years if being used for contraception).  It reliably prevents both menses and uterine cancer.  A surgical option for heavy bleeding is endometrial ablation.  This cauterizes much of the uterine lining, reducing or even eliminating menses.  After menopause, women who have had endometrial ablation still need a progestin; there is some uterine lining left in there somewhere and we don’t want it turning into cancer.

 

STARTING HORMONES FIVE OR MORE YEARS AFTER MENOPAUSE

There is no problem for women who don't have a uterus.  Some breast tenderness can occur initially, but that's about the only problem. 

Women who have a uterus may start bleeding.  The reason this happens is that progesterone, produced when a woman is ovulating, “down-regulates” the estrogen receptors in the uterine lining (endometrium).  With fewer estrogen receptors, the uterine lining grows less in response to estrogen.  In the absence of ovulation, there is no progesterone produced, so estrogen receptors in the uterine lining increase in number.  The uterine lining then grows excessively in response to estrogen when it is begun, even though a progestin is given simultaneously. The progestin will down-regulate (decrease) the estrogen receptors over time, but we're talking about at least six months.  There can be some or even a lot of bleeding during that time.  For women who really want to avoid any bleeding I recommend taking Prometrium or levonorgestrel for six months before starting estrogen, or using only minimal estrogen doses during this time (Vivelle Dot 0.025 mg or Evamist one spray).

 

WHY DO SOME WOMEN STILL HAVE HOT FLUSES ON HORMONE REPLACEMENT?

They may not have allowed enough time: relief of hot flushes is progressive over four to six months after estrogen is begun.

They may not have an adequate blood level of estrogen.  A level up to 150 may be required.

They might need some testosterone too.

If none of the above applies, then the real problem is inhibin deficiency.  Inhibin is another hormone made in ovarian follicles and it is actually the major inhibitor of hot flushes.  Menopause occurs when there are no more follicles from which ovulation can occur.  So at menopause inhibin deficiency occurs along with estrogen and testosterone deficiency.  Since inhibin is a recently discovered hormone and we cannot find any function for it other than its role in the control of ovulation, it is not commercially available. 

 

WHAT CAUSES SCALP HAIR LOSS AFTER MENOPAUSE?

Generally this is due to estrogen deficiency and improves with estrogen replacement.  If the hair loss began before menopause then it is a different issue, treatable, but I’m not going to cover it here.

 

WHAT CAUSES FACIAL HAIR GROWTH AFTER MENOPAUSE?

Usually the problem is that with low estrogen there is less sex steroid binding globulin produced, so androgens (testosterone-like substances produced by the adrenal glands and the supportive tissue in the ovary) are not bound, that is “tied up.”  Then more is available to be active and cause facial hair to grow.  The loss of estrogen may affect the receptors in the hair follicles, too. 

 

SHOULD WOMEN ON ESTROGEN REPLACEMENT HAVE THEIR BONE DENSITY CHECKED?

If estrogen is started soon after menopause and adequate blood levels have been obtained (often not the case with patches) or Premarin is being used at 0.625 mg or 0.9 mg, and calcium with vitamin D is being taken, then bone density is going to fall minimally with age.  In this case, the woman’s risk of fracture won’t be much different from that of a man, and we aren’t screening men routinely at this time.  It’s a safe and inexpensive test, though, so I don’t object to getting a pDexa scan of the femoral neck for all women and men, and I specifically recommend it for women not fitting the criteria I just mentioned.  A lower-than-average density warrants a follow-up in three years.  Remember that the scores compare you to average peak bone density occurring around age 35, so almost all women have a negative score by age 50.  I feel strongly that the treatment for osteoporosis is hormone replacement, since hormone deficiency is the cause.  If estrogen and calcium won’t prevent falling bone density, then testosterone should be added.  The biphosphonates (Fosamax, Actonel, etc) are turning out to have some very serious risks and should be used for women with frank osteoporosis or falling bone density who either won’t/can’t take hormones or have failed hormonal treatment.  Vitamin D blood levels should be measured, too.

 

CAN WOMEN WHO HAVE HAD BREAST CANCER USE HORMONE REPLACEMENT?

As my Suzanne Somers example pointed out, why not?  Still, if you feel fine off of estrogen, your cholesterol is fine (and stays fine after stopping estrogen), your bone density is good (and stays good after stopping estrogen), then you could avoid controversy and not take estrogen.  But if you have any reason to take estrogen, I think you should.  I have seen one study in which women given estrogen after breast cancer lived longer than those who took nothing.  I think that makes sense.  Women who have had breast cancer still need to avoid hip fractures and heart attacks.  What we need is a synthetic estrogen that would stimulate all estrogen receptors except uterine lining and breast, and would in fact block estrogen receptors in the breast.  Testosterone also blocks estrogen receptors in the breast.  Some of it is converted to estrogen in the body, though.  I think the former effect predominates.  Does this reduce cancer risk?  I don’t know.  High dose testosterone was used in the distant past for palliative treatment of advanced breast cancer.  It wasn’t very effective and had lots of side effects.  I think testosterone should never be given without estrogen, whether or not a woman has had breast cancer. 

 

SUMMARY

If you don’t make enough thyroid hormone, we replace it.  If you can no longer absorb vitamin B-12, we give it to you by injection.  It should be no different with your sex hormones.  You will live longer and live better on hormone replacement.  Many men also need hormone replacement.  Testosterone production begins to fall off after age 30 but how fast and how far it falls is quite variable.  I have a separate article for men.