Let me start with the scary and necessary-to-know statistics: Osteoporosis affects 10 to 12 million people in the US and forty million have low bone density (osteopenia). In 2005, over 2 million fractures were diagnosed. One in three Caucasian women over 50 will experience an osteoporotic fracture in her lifetime. (Whites and Asian women tend to have a lower bone mass than women of other ethnicities.) We also “out fracture” men (who have thicker bones) by a factor of 1.6.  And if a woman fractures her hip, she has a 20% chance of dying within a year. Osteoporosis is a very disabling, costly, and yes, mortal disease.

There has been a welcomed increase (both medically and financially) in pharmaceutical therapies that help avoid and/or treat osteoporosis. By now, you have all seen the ads and articles for the various bisphosphonates including oral alendronate (Fosomax), risedronate (Actonel) and ibandronate (Boniva) which can be used daily, weekly or monthly. There are also intravenous bisphosphonates that can be administered every 3 months or just once a year.

Then came the media outcry about potential side effects that these medications could cause….jaw necrosis, perhaps atrial fibrillation and more recently “atypical” fracture of the femoral shaft (long, upper leg bone), especially after long term use. I want to address the latter concern in this article.

Remember, these medications work by binding to the bone, preventing cells called osteoclasts from drilling minute cavities that make the bone porous. Cells called osteoblasts then do “their thing” and fill the cavities up. When stable, the drilling and filling are equal and thus maintain bone structure and strength. However if the drilling outpaces the filling, there is bone loss. This occurs with age (unfortunately after 30), and is accelerated by lack of estrogen (menopause) certain medications, especially steroids, diseases and the “wrong” genes. It is also aided and abetted by lack of proper nutrition.

Just to reiterate, bisphosphonates help stop the drilling and with time those minute cavities that made the bone porous get filled, diminishing the risk of fracture. We now know that these bisphosphonates attach and remain in the bone performing this job for years after being discontinued.

Recent cases have appeared in medical journals in which the femoral bone fractured in a horizontal fashion without prior significant trauma. In most instances, the patients were taking long term bisphosphonates.  How concerned should we be about this newly media reported “atypical” femur fracture?

An article in the May issue of The New England Medical Journal may help allay physician and patient concerns. It concludes that this type of fracture is truly rare. The authors used data from 3 randomized and placebo-controlled, prospective studies involving 14,195 women and 55,000 person years of observation. The risedronate data that they reviewed provided up to 10 years of study. All together, they found a total of 12 fractures in 10 patients that were classified as possible “atypical” femur fractures. (To be accurate, they were called subtrochanteric or diaphyseal fractures). The incidence came out to just 2.3 per 10,000 patient years. The authors also calculated that treating 1,000 women who had osteoporosis for 3 years would prevent about 100 fractures (including 11 hip fractures), a benefit that way exceeded the risk of “atypical” fracture, if indeed it was caused by the bisphosphonates.

So what does this mean? Well according to an editorial that followed the article, “physicians should not rush to judgment and stop prescribing bisphosphonates because of concern about atypical femoral fractures.” They should, however, reevaluate patients who have received long term therapy in the context of contemporary guidelines. (And for these please see my previous website article that discusses the use of FRAX to determine for whom and when to start therapy.)
I now review the FRAX indications for each patient who is at risk for osteoporosis. If she is a candidate for medication I will prescribe it, but carefully follow her with tests to check for bone loss. If she is stable for a number of years (usually 5 years) I suggest stopping the medication or at least taking a drug holiday. The good of the bisphosphonates still outweighs a possible bad, at least for those who need it.

Now, although I usually end my weekly newsletter with just one article, I have to mention another that just came out in JAMA. It also dealt with bone fractures. As we now all know, Vitamin D has become the vitamin “De jour”. The amount of D found in up to 70% of American is inadequate; low levels have been associated with osteoporosis, heart disease and a number of cancers. I ask all my patients about their Vitamin D intake (and exposure, remember you can get it though sun rays) and repeatedly advise them to take at least 1,000 international units (IU’s) daily.  I often check Vitamin D levels with a blood test, especially if there is a history of low bone density. For those whose level is found to be extremely low, I prescribe 50,000 units of Vitamin D-2 a week or every other week for several months, and then recheck their levels. If they have achieved a D level that is sufficiently high, I have them continue with an OTC supplement of up to 2,000 units daily.

Researches in Melbourne, Australia tried to maximize Vit D administration by giving elderly women considered to be at high risk of fracture  a dose of 500,000 IU of Vitamin D orally once a year.  They carried out a double-blind, placebo-controlled trial in 2256 women aged 70 or older. Half were given this very high yearly dose for 3 to 5 years; the others were given a placebo. There was no difference between the 2 groups with regard to calcium intake (indeed it increased for both). But contrary to expectations the group that received the high dose Vitamin D experienced 15% more falls and 26% more fractures than the placebo group. And the increase in falls was most apparent in the 3 months after they were given high dose Vit D! Frankly, the authors couldn’t explain this but went on to suggest that dosing should be more frequent and at lower doses. So far I (and most of my colleagues) will probably stick to advising daily 1,000 units or more of D and if your levels are low that you increase the dose (with a prescription) on a weekly or biweekly schedule. But I doubt we will prescribe that single oral dose once a year. So please continue to use D and calcium on a regular basis for better bones. And if necessary, go ahead and take that bisphosphonate that I or another doctor may have prescribed. The bones you strengthen will be there to stand you in good stead!

A major concern for the majority of women in their late 40’s and early 50’s has been whether and when to start hormone therapy. (Note it used to be called hormone replacement therapy, but the experts now agree that this term suggests that the menopause transition is an endocrine deficiency disorder and not a natural change in our hormonal and reproductive status, so the word “replacement” is out.)  I concur with the current PC terminology, but should point out that 80% of women experience symptoms related to this menopause transition as their estrogen levels plummet. The most common symptoms are hot flashes and night sweats (called vasomotor symptoms or VMS).  Add vaginal dryness, sleep problems (either due to the hormonal transition or to the stresses we face in mid life), mood changes and even a sense of diminished focus and quality of life and it’s clear that for many women, lack of estrogen production in the menopause creates sufficient physiologic and psychological havoc that they want to do something about it. That most effective something has been hormone therapy; estrogen (as pills, patches, creams, sprays. vaginal tablets and rings) and if a uterus is present (i.e. no hysterectomy) some form of progesterone (again as pills, patches, creams, drops or vaginal gels).

Since the Women’s Health Initiative was publicized, women have been encouraged by the FDA and just about every other official agency that reviews the research on hormone therapy, that if they chose to take hormones, they take the smallest effective dose for the shortest duration, preferably no more than 5 years. That “magic|” 5 year mark has been suggested because it’s felt that menopausal symptoms resolve in most women after 5 years. (Much of the “this-won’t last” data comes from women who have chosen not to take HT and have been followed for years to see what happened to their symptoms.)

Many women don’t want to wait for symptoms to resolve, especially if they are not guaranteed a finish date. Indeed some research has shown that 15% of women continue to have symptoms in their 70’s. Twenty five to 50% of women who stopped hormone therapy after the Women’s Health Initiative resumed therapy. Those most likely to do so had severe symptoms before they started HT, were obese, younger at time of menopause, African American, smokers or physically inactive.

When it comes to “it’s time to stop your hormones” advice I generally suggest that quality of life vs. risk be considered: will you feel lousy enough without hormone therapy to counter the possibility of an increase in your risk for breast cancer with long term (probably more than those 5 years) use of HT?  I also explain that estrogen has positive effects on bone mass and in the first years of use is probably heart protective. |But as the years pass and other factors affect our cardiovascular system, estrogen may no longer afford the same cardiovascular protection.

So what is a woman (who has been happy on her hormone therapy) to do? Should she try to “wean off” or just stop after that arbitrary 5 years?  A new article in the Journal Menopause tried to address this in a scientific fashion.  A study was conducted in Sweden in which the researchers recruited women to stop their hormone therapy “cold turkey” or do so gradually by taking it every other day. They wanted 200 women for the study, but when faced with the idea of stopping their hormones, many refused and they could only find 87 volunteers!  At the end of 4 weeks there was no difference in the symptoms of the women who abruptly stopped and those who tapered and then discontinued.  And because vasomotor symptoms came back for many, within 4 months 30% of the participants resumed their hormone therapy and after 1 year that number had risen to 50%!

Now to my clinical experience… I try to lower the dose of HT for most of my patients after they have taken it for 5 years. (This necessitates a discussion of the possible risks associated with long term use). If a patient is amenable, I prescribe a dose that is lower than that which she has taken and suggest she try it for 4 to 6 weeks. Some of my patients can then keep lowering their dose until they successfully stop and have no symptoms. Others state that although their symptoms resumed “they were not that bad” and they try to stop HT for good. But I do have patients (about 30%) who feel pretty awful, either on a lower dose or once they stop. I then suggest that they continue at the very lowest dose that allows them to keep their symptoms under control.  (And in their next visit I will revisit the risks and benefits of long term hormone therapy. Basically we are agreeing to procrastinate.) As long as we have a frank discussion about the pros and cons of long term HT, the final decision should be made on an individual basis.  Unless there is a truly health threatening reason that dictates that she stop, issues regarding her quality of life (and life style) have to be considered.

The terror of osteoporosis has by now, been embedded in our female (and male) psyche. Hip fractures can lead to death and/or permanent disability. Spinal fractures lead to severe pain and loss of physical stature which has helped lead to that demeaning portrayal of aging women as “little old ladies”. There are a plethora of ads that make us want to do something. So I thought I would try to do my part by writing this 101 on bone loss. Don’t forget osteoporosis is a life altering disease with huge financial burdens. There are foundations and institutes that solely deal with this disease. For more information you can go to http://www.nof.org

Our bones comprise a living tissue that is always under flux. Their form and composition is determined by cells that lay down new bone (osteoblasts) and cells that act as “pac-men” and chop away causing bone resorption (osteoclasts). Put simply there is on-going filling and drilling. If all is well in our bones’ environment (normal menstrual cycles and estrogen production, adequate nutrition, no underlying disease and no adverse medications) the filling usually outpaces the drilling, at least until we reach the age of 30. This is our age of best bone mass. But when the drilling overcomes the filling, our bone mass diminishes and our bones become weakened (osteopenia), eventually porous (osteoporosis) and may finally may break.

The process of drilling and bone loss is somewhat complicated. Forgive me if I use some technical terms here. There are pro-resorptive hormones that act via their receptors on the bone building cells to induce something called RANKL. When there is enough “free” RANKL, it is able to activate RANK on precursors of the bone eating cells (remember they are called osteoclasts). RANK then stimulates these pre-osteoclasts to fuse together and differentiate into mature osteoclasts. Free RANKL also activates these mature osteoclasts “telling” them to resorb bone. To make matters worse free RANKL then protects these bone gobbling cells from dying! They can keep going on and on…like that energizer bunny.

We seem to have a bad guy in this bone story…it’s excessive free RANKL which gives the go ahead for bone eating cells to develop, multiply and resorb bone. It can get nasty. Although destruction of bone may be necessary for formation of new bone, its unopposed course has been countered.  RANKL can be rendered inactive if it is bound up. (Think Samson with his hair shorn.) The substance that does the binding and deactivation of RANKL is called OPG (I know this gets too full of initials, but it’s easier to use than the full word… osteoprotgerin).

Estrogen reduces RANKL production and increases the synthesis of OPG (at this point I have to say OMG). The estrogens we produce during our reproductive lives have helped prevent free RANKL from encouraging osteoclasts to eat away at bone. Indeed when we lose our estrogen production at menopause, free RANKL is released and during the first 5 to 6 years of menopause, most women lose 2 to 3% of their bone mass each year.

The most commonly used medications for osteoporosis, the bisphosphonates (Fosomax, Actinel, Boniva and Reclast to name a few) reduce the function but not the number of activated osteoclasts. The FDA is currently considering a medication that actually targets the RANKL pathway and stops osteoclast development. More on this (and comparisons of therapeutic medications) in future newsletters….

Several months ago I wrote a newsletter on the current recommendations for osteoporosis therapy based on the World Health Organization (WHO) Fracture Risk Algorithm, (FRAX). We no longer use a bone density test as the sole indicator of fracture risk. (See the article titled “Assessing Our Bone Strength” in the newsletter archives).

Now where does calcium and Vitamin D come into our bone health picture? Deficiencies of either will prevent bone formation by the osteoblasts. Both calcium and Vitamin D are necessary for the complex pathway that leads to bone “creation” and maintenance.

Let’s start with Vitamin D… It is produced in our skin as a result of UV radiation from sun rays. The darker our skin, the less the UV rays get absorbed. Those of us, who are dark skinned, are not sun exposed (think winter on the East Coast) or who effectively block the sun with clothing or sun block will get less than the recommended Vitamin D. Vitamin D is added to milk products, calcium supplements and multivitamins but the amount is often not enough. More than half of healthy adults have blood Vitamin D levels that are lower than that which is recommended for fracture risk reduction (30ng/mL of 25 OH Vitamin D). Many bone experts now recommend that we take at least 1,000 IU of D3 (which is over the counter type of Vitamin D) and if older than 65, to take 2,000 IU a day.

Because of the high prevalence of Vit D deficiency, I check 25OH Vitamin D levels on many of my patients, especially those who are found to have low bone densities. If a deficiency is found I prescribe 50,000 IU of D2 weekly for 2 to 3 months, then recheck the blood; if the level has risen sufficiently I tell my patient to resume standard dosing. If, however she has had a fractured hip, I increase Vitamin D until her blood level is 40 to 60 ng/ml.

Now what about calcium? Some of the newer studies seem to show no benefit of calcium intake greater than 800mg per day in women who are NOT vitamin D deficient. But when we talk about essential intake of calcium we have to consider its absorption and bioavailability. Many medications interfere with calcium absorption. These include (especially when taken at the same time as a calcium supplement) fiber, H2 blockers and protein-pump inhibitors (that treat acid reflux), corticosteroids and anticonvulsants. Moreover, there can be adverse interactions between calcium supplements and several medications if they are taken together: Calcium may cause a decreased absorption of iron, zinc and magnesium. Calcium also reduces thyroid, tetracycline and quinine antibiotic absorption.  And it turns out that caffeine increases urinary calcium excretion.

The amount of calcium we absorb in supplements also depends on the type of calcium we take. The most common, calcium carbonate, requires stomach acid for absorption. (Hence the manufacturers recommend taking it with food). But as we get older we naturally produce less stomach acid. And to add insult to getting an older and crankier GI system, gastric acid is reduced by all those medications we take to treat our acid reflux. So I recommend that my older patients and those who take acid reflux meds supplement their calcium intake with calcium citrate for better bioavailability.

Yes this is complicated…But now that you understand a bit more about what your bones go through to carry you though your life, I hope you will treat them with respect and provide them with their essentials. If you are at risk for bone loss and fracture make sure you discuss tests and therapies with your physician (and if you are my patient, with me). It’s never too late to support your support.

I’ve been inundated with phone calls and questions about articles that have appeared in the media which have suggested that there is a link between hormone use and lung cancer. Lung cancer is the second most common cancer in women (first is breast cancer) and is the leading cause of cancer deaths. We all know that tobacco smoking is the major risk for this dreaded disease and indeed 84% of male lung caner cases can be attributed to smoking. However, only 46% of cases in women seem to result from cigarettes. Researchers have been searching for other causes including supplemental hormones. Approximately 24% of women older than 40 years are currently using hormones in the United States. So if there is an association it could be huge!

Multiple studies have looked at a possible link between hormone use and lung cancer. The results are fairly inconsistent. Here are a few:

• A study of 23,244 Swedish women with 6.4 years of follow up, found a slight increase risk in lung cancer. This was calculated as an odds ratio of 1.3 (women who did not smoke were 1.0) so this means there was possible 30% increase in risk above that of non smokers.
• The Women’s Health Initiative that included 16, 000 women on Prempro found no association between post menopausal hormone therapy and lung cancer, with follow up of 5.2 years.
• The Cancer Prevention Study II Nutrition Cohort which consisted of 72,772 women found a decrease lung cancer risk associated with hormone therapy for post menopausal women. This study had 12 years of follow up.
• A case control study in the United States with 499 lung cancer cases and 519 control (that means the number of women with lung cancer were compared to those who did not have cancer) as well as a German study with 811 lung cancer cases and 912 controls found either no significant association or protection against lung cancer for “ever use” of female hormones.
• A recent study published in Menopause: The Journal of the North American Menopause Society included 2,861 women who were aged 31 to 79 years at enrollment and were followed for a 31 year period of time. They were interviewed every 4 years and asked whether they smoked, how much, if they had quit, for how long and if they were taking oral contraceptives, estrogen, or pills for hot flashes, or to regulate periods. The findings showed that 35.8% were using hormones at time of enrollment. The hormone users were also more likely to be current or former smokers than those who were not taking hormones. Eighty seven women developed lung cancer. There was no association between hormone use and lung cancer in general. But (and there I always a “but” in medical studies), a separate calculation for the women who were 55 years and older, found that lung cancer risk was increased with an odds ratio of 1.58, whereas in women younger than 55 years, lung cancer risk was reduced with an odds ratio of 0.44.

The statisticians feel that overall this is a null finding….in other words not significant for or against the effect of hormones on lung cancer. The conflicting results in all these studies certainly leave pause for concern and need for future large and long term research.

It is estimated that it takes 18 to 30 years from time of smoke exposure to lung cancer development. In the Ranch Bernado study hormone users were slightly heavier smokers and had longer duration of smoking, which may have caused that slight increase in lung cancer in the older women who used hormones. At this point my advice is not to smoke and quit if you do; but if you don’t you probably should abstain from hormone use

“I had surgery for an ovarian cyst”… a not uncommon statement in the medical histories I get from patients. This is usually followed by the exclamation: “Thank goodness it was benign!” The question is how many of these women underwent unnecessary surgery for something that was benign?

Most cysts in young women (we’re talking reproductive age here) are “functional”, a term used to describe furniture and clothes design…but when used as a gynecologic adjective it connotes a cyst that is formed during the monthly cycle. Follicular cysts develop as the ovary tries to do its duty and create a dominant follicle from one of its primordial oocytes during the first 2 weeks of the cycle. Once ovulation occurs a remnant of that follicle can form a second type of functional cyst termed a luteal cyst. Let me explain:

At the time of puberty the ovaries contain about 400,000 primordial or preformed oocytes (future eggs). Each month one of them usually gets to come forth to fulfill its destiny to grow and develop into a mature egg while thousand more die….sort of depressing, but this is the survival of the fittest egg. (Just consider how many sperm die with every ejaculate and perhaps you won’t feel so bad. But wait, sperm get produced anew every 3 month while we have a fixed number of eggs and once they are used up we can’t make anymore. So there is an ovarian woe in this saga. Our finite number of eggs also explains the hormonal phenomena of perimenopause and menopause, but I diverge…)

A small amount of fluid surrounds the developing egg so that the developed follicle becomes a little cyst on the outer circumference of the ovary. It produces estrogen. At ovulation the follicle ruptures and the egg is extruded. Some women feel this rupture as a mid-cycle pain called by the appropriate onomatopoeic term “mittlesmirz” (pain in the middle). If the cyst becomes large (too much fluid accumulates) and/or grows, it creates a functional follicular cyst.

Once the egg has been released (and potentially may be fertilized by sperm swimming in the tubal vicinity), the emptied follicle changes its identity and becomes a corpus luteum. This too is a small cyst that goes on to produce progesterone and estrogen; hormones that are needed to build up the lining of the uterus so that it can support a developing embryo. In the absence of a pregnancy the corpus luteum dwindles and yes dies; the uterine lining or endometrium is sloughed (the menstrual period) and the entire cycle starts all over again. But if that corpus luteum does not regress and instead swells or bleeds into itself (it has a terrific blood supply) it too can create a functional cyst called a luteal cyst.

Before ultrasound was extensively used, a woman who presented with a mass on the ovary, pain or an enlarged “something” in the area of the tubes or ovaries (called the adnexa), was often subjected to surgery. Even with the advent of ultrasound…if the cyst was big enough or had areas that were not translucent, surgery was often performed either by laparoscopy or an open abdominal procedure. The cyst was removed (cystectomy), or in some cases, the ovary was excised (oophorectomy). After all, the surgeon was already in there and that was the best way to ensure it would be properly diagnosed and “cured”. Any of these procedures could lead to subsequent scarring, pain and/or infertility.

In the 60’s and 70’s doctors noted that women who took oral contraceptives (in doses that were higher than those used today) seemed to have a lower incidence of these functional cysts. The thought was that if ovulation was suppressed there would be no reason for functional cysts to develop. (New data shows that low dose birth control pills do not substantially decrease a woman’s risk of ovarian cyst formation.) This theory that the Pill will stop cyst formation has continued to be used to treat cysts and make then “go away”.

Not so….according to a recent Cochran report that was abstracted in the Journal of the American College of Obstetricians and Gynecologists. The Cochran Review analyses the most relevant and well conducted studies that have been published in peer reviewed journals. The authors then review these studies for accuracy and statistical relevance. Seven randomized controlled trials from four countries were found; the studies included a total of 500 women. The analysis showed that “treatment with combined oral contraceptives (which contain both estrogen and progestin) did not hasten the resolution of functional ovarian cysts is any trial.” And indeed “most cysts resolved without treatment within a few cycles”. This included cysts that developed spontaneously and those that occurred after ovulation induction with fertility medications. (The forced feeding of the ovaries with fertility drugs causes the development of multiple follicles and can result in cysts). They found that most of the cysts that did not regress after a few months of being left alone were endometriomas (blood filled cysts that occur with the disease called endometriosis) or cysts that developed from the fallopian tubes.

So does your physician have to go after those cysts that she or he feels and then “sees” with ultrasound during routine exam? The answer in most circumstances is no. Nor do we have to treat these functional cysts with oral contraceptives to get rid of them. A simple “wait and recheck” in a 2 or 3 months is appropriate.

Bottom line: There is no need to freak at the mention of an ovarian cyst that has developed while you are in your reproductive years. It will probably go away in a month or two. Surgery is indicated only if you develop significant pain (very rarely cysts can twist or bleed) or if the cyst persists.

I’ll try to report this one with a straight face and I suggest we all take a deep, (but not necessarily odorless) breath. A recent article in the prestigious journal Menopause published by the North American Menopause Society (NAMS) concluded that “onion consumption seems to have a beneficial effect on bone density in perimenopausal and postmenopausal non-Hispanic white women 50 years and older. Furthermore, older women who consume onions most frequently may decrease their risk of hip fracture by more than 20% versus those who never consume onions.”

Even I was surprised. And to think that ever since I felt that onions could cause bloat and flatulence (at least in my case), I advised others that from a nutritional standpoint they did little, but were simply added to improve the taste of many dishes! So let me correct myself and give more scientifically rendered facts: Rats fed a diet high in onions have been found to have a 17.4% increase in bone mineralization after 4 weeks compared to a control group. There are 3 compounds in onions that may be responsible. I will spare you their long scientific names. They are thought to inhibit the activity of the cells called osteoclasts that break down bone. The other 2 compounds may actually help build bone density by stimulating bone building cells (osteoblasts). These compounds belong to a family of flavonoids which in other studies have been found to have an estrogen like effect.

The next factoid used to support the supposition of bone support though onion consumption comes from Turkey. Women there have the lowest osteoporosis fracture rate in Europe and apparently that country has the highest per capita consumption of onions in the world. At the age of 50, women in the U.S.A. have an average lifetime risk of 15.8% of developing a hip fracture while women in Turkey have a 1% risk.

The authors of the article in NAMS analyzed the data from 507 perimenopausal and postmenopausal non-Hispanic white women gathered by the National Health and Nutrition Examination Survey (NHANES) between the years 2003 and 2004.These women were given a food frequency questionnaire. One of the questions was whether and how often they ate onions. They were then divided into 4 groups: less than or equal to once a month, twice a month to twice a week, three to six times a week and once a day or more. (This group must have had a lot of onion soup!) They all had bone density tests.

Then the statisticians went to work correcting for age, smoking, vitamin D levels, parathyroid level (this is a hormone that helps control calcium levels and bone density), calcium intake, exercise level, estrogen use (estrogen supplementation helps stave off bone loss) and body mass index (heavier women have denser bones). They then came out with the following numbers: The adjusted total body bone density measured in grams per centimeter squared (I’ll interpret this in the next paragraph) was 1.02g/cm squared in the group that consumed onions once a month or less, and rose to 1.06g/cm squared in the group that consumed onions once a day or more.

The “onioned” group had a 5% increase in bone density compared to the onion abstainers. That sounds very small but a percent of loss can mean a future increased risk of fracture by a factor of five or more.

So will I suggest onion consumption for bone strength to my patients? Not in lieu of 1200 to 1500 mg of daily calcium, 1000 units of vitamin D and weight bearing exercise. The authors of the article also pointed out that one of the compounds found in onions, called quercetin, may be toxic to genes when consumed in huge amounts. But to get a toxic amount (at least in rodents) 2 pounds of onions would need to be consumed.

So if you like onions go for it…I suspect that after this study the supplement and pharmaceutical companies will find a way to suggest you take their “onion like” product. Meanwhile I will do everything else to keep my bones supportive.

There are many books (one is mine….time for that plug I’m Not in the Mood; what every women should know about improving her libido), surveys, prospective and retrospective studies, theses on how to do the studies, pharmaceutical investigations and internet come-ons suggesting that you, the adult woman should “buy this and fix your sex life”.

They have all put the fear of menopause in women….not only because this transition may cause hot flashes (and all those other symptoms I treat and yes discuss in my other books, and I won’t go into the list) but because it will cause sexual desire to go kaput!

Many of my patients want me to give them a simple test and, of course, therapy (hopefully in pill or cream form) to allow them to maintain, improve or just reestablish their libido. And after a long consult, and perhaps a few blood tests, I usually have to point out that libido is a many factorial issue…having to do with our physical health, mental health, (stress, fatigue, depression), self body image, partner availability, relationship with said partner, partner’s own sexual problems, medications (especially antidepressants) and yes our hormonal status. During the menopause transition we lose estrogen as we use up the finite number of follicles in our ovaries. Progesterone levels become nil, but if we have not had our ovaries surgically removed we still produce testosterone for several (some say 7 to 9) years to come.

Does desire dissipate as we become menopausal? If it does, is this due to age, the accumulation of the above mentioned factors or the loss of estrogen?

An attempt to answer these questions was made through a study supported by the National Institutes of Health (NIH), the National Institute of Aging (NIA) and the NIH Office of Research on Women’s Health. One more acronym, this was part of The Study of Women’s Health Across the Nation (SWAN). A total of 3,302 women were followed for 6 years as they went through menopause. (I love that it had 2 “extra” women, somehow this makes it more legit). They ranged from 42 to 52 years of age at the start of the study. The menopausal status of each woman was assessed at every visit. She was then given a 20 item questionnaire which included queries about the importance of sex, sexual desire, frequency of intercourse and/or masturbation, physical pleasure, emotional satisfaction with her partner, arousal and pain with intercourse. If menopausal she was asked about the frequency of hot flashes, night sweats and vaginal dryness in the past 2 weeks. And if sexually active she was asked if she used a lubricant in the past 6 months. Then she was asked about her overall health, whether she was recently married, divorced, separated, had a new relationship, and finally if she had any children living at home. Her BMI was calculated and she was tested for depressive symptoms. (As I write this, I wonder how they got 3,302 women to participate!)

The results: First let’s get to the importance of sex! More than 75% of the middle-aged women in the study reported that sex was moderately to extremely important. There was a decrease in sexual desire beginning in late perimenopause (when their cycles were intermittent and before they ceased having their periods for a year….this may be the appropriate time to mention that they only included women who still had their uterus and at least one ovary). These women also reported an increase in painful intercourse. But women in early perimenopause had a temporary increase in masturbation.
The long and short of all this…once the vaginal lining was not maintained by adequate ovarian estrogen production; it was not lubricated and “bestowed” with surging blood flow during arousal. Lack of vaginal engorgement and secretions led to a “diminished sense of pleasure from subjective arousal and a disruption in the intimacy-based sexual response cycle”. In other words if it hurt, and that ruined the mood. The authors felt that “the increase in masturbation during early perimenopause could be related to the concurrent increase in painful intercourse;” but that later on there was a decline in this masturbatory rate due to concurrent decline in desire.

Careful statistical analysis showed that the decrease in sexual desire was independent of chronological aging, menopausal symptoms, and health, social and psychological factors…and that the true sexual culprit appeared to be vaginal dryness. This was “highly associated with pain, lower arousal, emotional satisfaction and physical pleasure.”

Sexual functioning and vaginal “integrity” seem (at least according to this study) synonymous. What the study did not address is whether adding vaginal estrogen or hormone therapy will maintain a woman’s sexual desire and pleasure as she goes through her middle and later age. Most of my patients seem to think it does, (as long as all the other sexual reducing factors don’t overwhelm their ability to have or even consider enjoying sex). Unfortunately, but I cannot offer a 3,302 women, prospective statistical analysis. Hopefully future studies will.

Once upon a time most of us moved here, to LA, from other states or countries. And we love it!  As veteran Los Angelinos we live, work and of course, look at others in this, our youth and media oriented city. The inevitable follows: we would like to look like a celebrity worthy of an appearance on Oprah or at least appear younger than our chronologic age. So when we see ads politely inquiring whether we are developing a bulge above our jeans, flushing, flashing (from heat, not exhibitionism), sleeping poorly, loosing our libido or worse… wrinkling; we go on the alert. Who can resist that spiel? : Step right up and spit here; we’ll see what you’re missing and order you a very special, made- just- for- you therapy. Rub this cream on, swallow these capsules, put these drops under your tongue and don’t worry, these “bioidentical” hormones are chockfull of health, not like the ones made by those big, bad pharmaceutical companies.

Many of my tenured (note I refrain form using the adjective “old”) and new patients want to know if they should start these “bioidentical” hormones or switch to them.  To quote Shakespeare, who was hormonally clueless but recognized some distressing female symptoms:  Here’s the rub.

“Bioidentical” is a marketing term. It’s as ingenious as the word natural when it comes to selling a product; both appeal to consumers’ aversion to artificial ingredients. But remember, hemlock is natural.

When the term “bioidentical” is used by compounding pharmacies and celebrities who are often selling their products or touting their own books, it refers to formulations of various types of estrogens, progesterone, adrenal hormones, and androgens (male hormones) compounded within creams, gels, lotions, capsules, drops, capsules, and even suppositories.  The compounded estrogens are often a combination of weak forms of estrogen (estrone or estriol) as well as the stronger  estradiol. In order to get significant relief of menopausal symptoms, large doses of the estriol or estrone   have to be used and there is no evidence that this is safer than the lower dose of estradiol which, by the way, was produced by our ovaries and accepted by nearly every cell in our bodies during our reproductive years. Estradiol is the estrogen contained in many of the FDA approved hormone therapy medications, and/or the metabolite (the end result after processing in the body) of these medications.  Nearly all plant derived estrogen therapy, both individually compounded formulations and pharmaceutical products come from the same soy and yam precursors. They all undergo chemical conversion to become hormones. ( The concept of plant gathering followed by stomping created a great “I Love Lucy” sketch and will work for grape juice and ultimately wine, but will not result in a biologically active hormone product, no matter how skillful the stomping and crushing.) Compounding pharmacies may claim that the combination of their estrogens is either safer or more natural than any of the products that are commercially prepared by pharmaceutical companies. No clinical studies published in reputable peer review journals have shown this to be true. As for the claim that estriol may reduce the risk of breast cancer; this is pure speculation based on old studies that were usually carried out on animals. The FDA has unequivocally stated that it is not aware of any credible scientific evidence to support claims made regarding the safety and effectiveness of compounded “bioidentical” hormone replacement drugs. They have taken action against seven pharmacy operations that claim their compounded “bioidentical drugs” which contain hormones such as estrogen, progesterone and estriol are superior to FDA-approved menopausal hormone therapy medications. The American College of Obstetricians and Gynecologists (my professional entity) has the same concerns stating that “most compounded products have not undergone rigorous clinical tasting for safety or efficacy and issues regarding purity, potency and quality”.

Doctors who prescribe these “bioidentical” hormones often use salivary (spit) testing to tailor the amount of hormones they prescribe. But salivary hormone levels vary tremendously throughout the day and differ from woman to woman. Moreover we don’t have studies that demonstrate a correlation between the levels of spit hormones and a woman’s clinical state or her response to hormone preparations. The major mavens on menopause (we have a society for everything), The North American Menopause Society, does not recommend saliva testing to determine hormone levels, nor do they recommend custom compounded products over “well tested, government approved products for the majority of women”. All these institutions are concerned that patients do not see the black box warnings that are prominently displayed with FDA approved medications…the ones that state that hormones should not be used if you have had certain conditions that include estrogen related cancers and blood clots and the concerns about risks for long term use.

Finally who pays? Sometimes insurance companies do, but often the patient is stuck with a bill that is higher than the one she would pay (or co-pay) for commercially prepared hormones. Moreover if the practitioner who prescribes “bioidentical” hormones also sells them from her or his office, there is a potential conflict of interest.

Some hormones including testosterone and DHEA (used for low libido or specific deficiency disorders) may not be available in pharmaceutical products and will have to be compounded. As a matter of full disclosure, I do prescribe compounded hormones when the latter are needed or when a patient becomes allergic to standard therapy. But I advise all my patients that there are no free hormones, no matter how they are made. There is an indication and contraindication to every medication and it’s imperative that your physician use appropriate, up-to-date studies in order to inform you of both.

Unfortunately, no hormone will provide you with that lost fountain of youth. But when prescribed for significant symptoms in appropriate doses, hormone therapy will help you feel better. Exercise, proper nutrition, weight control, hair color, make-up, and the right lighting are the only proven (and risk free) ways to help you feel and look your best.