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!

Recently, a mother brought her adolescent daughter to my office for advice about  menstrual migraine therapy. After I made my suggestions, I thought it might be timely to give a few “notes” (I sound like a producer) for the website regarding the causes of and treatments for this debilitating disorder. Migraine headaches are unfortunately very common; they affect nearly 28 million Americans including 18% of all women and 6 % of all men. A migraine is defined as a one sided, severe, pulsating headache aggravated by physical activity together with sensitivity to light (photophobia) and sound (photophonia). The true migraine usually manifests itself in 4 phases. (This is not a simple come and go headache).

The Premonitory Phase (Prodrome): This phase is due to neurochemical alterations in the brain and is most commonly associated with fatigue, difficulty concentrating, stiff neck and light sensitivity. It can also include mood swings, food cravings, yawning, change in vision, nausea and vomiting.

The Aura Phase: This occurs in 15% t 20% of migraine attacks. The ends of the 5th  facial nerve ( the trigeminal nerve) are activated causing symptoms that include scintillating lights, distorted vision and numbness and tingling in the hands or face. These sensations are usually followed within 60 minutes by the headache. Rarely an aura can occur and not be followed by pain; it’s then aptly called a migraine aura without headache. This may be a final neurological diagnosis (by exclusion) once a full work up for symptoms of stroke is negative.

The Headache Phase: The trigeminal nerve that gives us our sensory perception from our face also provides a pain pathway from the meninges (the capsule around our brain). Though a complex system called the trigeminovascular system, the nerve can become activated by many triggers. This trigeminal activation then instigates the transmission of impulses in the brainstem and causes a release of substances called vasoactive neuropeptides. They, in turn, cause dilation of blood vessels and inflammation in the meninges. The activated trigeminal nerve fibers become abnormally sensitive and any stimulus, such as light, sound or even gentle touch can increase pain. (This explains why most migraine sufferers want to be left alone in a dark room without human contact once the migraine occurs.)

The Post Headache Phase (Postdrome): Migraine symptoms can last for up to 2 days. This “post” seems to go on forever!

More than half of the women who suffer from migraines have them in association with their menstrual cycles; moreover, the migraines that occur with their periods are worse than all others. There are 2 kinds of cycle associated migraines… (Medicine is chock full of nomenclature.) Pure menstrual migraines occur without aura 2 to 3 days after the start of menstruation but do not occur at any other time during the menstrual cycle. Menstrual related migraines include menstrual migraines but attacks can also occur at other times in the menstrual cycle (often days before the onset of the period, or right after ovulation). It is thought that change in hormones, especially the decline of estrogen before and during the period, play a role. Also as an added insult, when we menstruate, pain stimulating substances called prostaglandins are released and can trigger headache, nausea, vomiting and diarrhea even in women who do not have true migraines!

OK, now that I have given you a synopsis of Migraine 101, let me get to therapies. First … those that are nonphamacologic: This is where we try to limit migraine triggers, use relaxation training and biofeedback. Although I can’t teach you how to do the latter two in this summary, I can at least acquaint you with triggers that you can avoid. They fall into 4 categories:

• Diet: Alcohol, chocolate, aged cheese, monosodium glutamate artificial sweeteners, caffeine, nuts, nitrates and nitrites and citrus fruit. Not all these affect the same person and clearly there are other foods that can less frequently act as triggers.
• Changes: weather, seasons (maybe we should all live in San Diego or Hawaii), travel, altitude, schedule changes, sleeping patterns, diet changes, skipping meals.
• Sensory Stimuli: Strong lights, flickering lights, odors
• Stress: Let-down periods, intense activity, loss (death, separation, divorce); relationship difficulties, job loss/change and anything that causes emotional or physical crisis.

The above includes much of what we do or experience in life! But I would be remiss if I didn’t give you this list. (In case you want to know my reference it’s from The New England Center for Headaches… it should also be applicable to those of us residing in the West Coast).

Now let’s get to pharmacologic therapy:

• Nonsteroidal Anti-Inflammatory Drugs (NSAID’s): These interfere with those pain promulgating substances, the prostaglandins. They include ibuprophen, aspirin and naproxen. Some of these OTCs also include caffeine. If they don’t work after 4 to 6 hours or result in “bounce back” of the migraine once stopped and/or they need to be used continuously for several days, you are probably better off with a prescription medication.
• Triptans: These are prescription medications that bind to and activate specific receptors called 5-HT which are expressed on the smooth muscle cells in the walls of blood vessels. They induce constriction of those dilated vessels in the meninges of the brain that caused the migraine in the first place. The good news is that they usually work within 20 to 30 minutes and don’t cause sedation so you can continue your normal activities. There are at least seven triptans. One type is combined with an NSAID. The best way to use them is at the very onset of the migraine.
• Ergots: These have been used since the 1930’s. They constrict blood vessels and activate 5-HT. They are less “in vogue” for migraine therapy because of their potential side effects (such as an elevation of blood pressure).

Preventive Treatment: This requires daily use and includes medications that are used to treat hypertension (beta-blockers, calcium channel blockers), certain antidepressants that decrease the conduction of pain stimuli (tricyclics) as well as anticonvulsants. I would include hormonal therapy as a mode of migraine protection for many women. I frequently prescribe oral contraceptives to my younger patients who are migrainers in order to stop the ebb and flow of hormones during their cycle. (Remember that hormonal contraception signals the pituitary to NOT send signals to the ovaries to develop follicles and ovulate.)  I suggest using the active pills or a contraceptive vaginal ring continuously so that there in no break in the hormone level it provides. (No you don’t NEED to stop and get your period.) If there is a break in active contraceptive hormone use (some patients prefer to take it for  3 months at a time, or experience bleeding after a few months and “take a short break” from the Pill or ring), I prescribe an estrogen patch to “cover” the time off so that the decline of estrogen does not instigate a migraine.

At this point, I should add a warning: The occurrence of migraines without aura has been shown to increase the risk for stroke by a factor of 3, whereas if aura is present this increases to a factor of 6.  The use of oral contraceptives in women with stroke is considered an independent risk factor for stroke. So ACOG (the American College of Obstetricians and Gynecologists) discourages use of oral contraceptives in women who have migraines with aura.

Now, let’s consider migraines in menopausal women. They often improve. (Finally, something to look forward to as we age!) Once we stop the vacillations of our hormones in our reproductive years, the migraines may lessen. However (sorry, but there is often a “however” in medicine), some menopausal women begin to experience migraines once they no longer produce estrogen. If they want to reinstate their premenopausal estrogen status, I then prescribe transdermal estrogen….usually a patch so that they achieve a “steady state” of estrogen with no ups and downs.

This has been a longer website article than most. But since so many of my patients, friends, staff and relatives (my daughter) suffer from migraines; I felt I owed it to them to give a fairly complete summary. I hope it didn’t give you a headache!

As I sat down to write this newsletter, I felt that I did not have a favorite new article to use for an update. So rather than leave a blank newsletter this week, I thought I might re-issue one that I wrote for MSNBC several years ago. (There is nothing like quoting oneself!) It dealt with ways to cope with breakthrough bleeding while on birth control pills. Here it is (with just a few changes):

I often get calls from patients who have started taking birth control pills and have experienced bleeding at the wrong time. They wonder if this means they should change their particular pill or whether they should consider another mode of contraception.

Bleeding at the wrong time does not necessarily mean that a woman is a “pill failure”. Breakthrough bleeding is very common in the first few months after starting combined oral contraceptives. (“Combined” means the pill contain both an estrogen and a progestin… progestin- only pills are notorious for breakthrough bleeding and hence are less commonly prescribed.) The bleeding usually decreases within three months of pill use and should stop by the fourth month with correct and consistent use.
Before you decide if breakthrough bleeding is the pill’s fault or your own consider the following:

Are you taking the pill at the same time every day? Missing one pill or taking it late could affect the integrity of the uterine lining (built up by the daily, consistent levels of hormone achieved with on-time pill use). If the hormone level drops, even momentarily, “bits and pieces” of the lining can shed causing spotting or bleeding.

Are you taking any medications that could affect the absorption of the pill? These include antacids, antibiotics, some over-the-counter digestive medications and herbal remedies such as St John’s wort. Also, medications that induce a liver enzyme system called P450 can increase the metabolism of birth control pills. These include anticonvulsants, anti-tuberculosis and antifungal medication. Steroids in pill form (prednisone) or shots (even joint or epidural injections) can also have a hormone changing effect.

Do you smoke? If you take the pill and smoke, you increase your risk of heart attack and stroke, especially if you’re 35 or older. I’ve always said that the pill be should be available over the counter and smoking should be by prescription only. Smoking decreases the absorption and effectiveness of the hormones in the pill, possibly leading to more breakthrough bleeding. Smokers have a 30 percent increased risk of bleeding irregularities in their first cycle of pill use, and this rises to 86 percent by the sixth cycle. Smoking also has anti-estrogenic effects, and increases the metabolism and breakdown of estrogen in the liver. (This is important to know when we give hormones to menopausal women … but I digress in my anti-smoking tirade!)

Now let’s look at other potential pill issues that may require professional consultation… If you’re taking a very low-dose pill (20 micrograms of estrogen) and have consistent breakthrough bleeding switching to a higher (but still low-dose) pill containing 35 micrograms of estrogen might help prevent shedding of the uterine lining . Some progestins may be more potent than others and also help prevent “lining breakdown” and bleeding.  This is where pill changes (and your physician or health care provider’s understanding of what is contained in the multiple pill formulations currently on the market) may help. There are monophasic pills (the same dose of progestin and estrogen in each active pill), biphasic pills (the amount of estrogen and progestin changes once during the cycle) and triphasic (the amount of estrogen and progestin changes three times) formulations of the pill. If you routinely experience breakthrough bleeding during a change of the estrogen-progestin ratio with a biphasic or triphasic pill, you may want to switch to a monophasic pill where the estrogen and progestin levels remain the same throughout the cycle. Or if you consistently have bleeding late in the cycle, a pill that increases the amount of progestin in that second half may correct this form of breakthrough.

Finally, if you’re trying an extended cycle pill (one without the placebo) so you go without a period and attendant side effects for three months or even longer, you’re more likely to have breakthrough bleeding. It may be worth going back on a monthly pill, or — if you want to keep trying to extend the time between periods — at the time of the breakthrough bleeding, simply stop the active pill for five days (you’ll have your “period”) and then start over again. The bleeding should cease and you can keep going on the active pills until this happens again.

After four months and/ or changing your pills, you still continue to have breakthrough bleeding, your doctor may want to run some tests. These should include a blood count (to make sure you’re not anemic from all of the bleeding), a thyroid blood test, and if the breakthrough bleeding is severe, a blood test for clotting abnormalities.  I also suggest you get an ultrasound to check for internal polyps, fibroids or ovarian masses. And of course, your doctor should make sure your cervix shows no irritations, polyps or tumors.

Bottom Line: If you have breakthrough bleeding and you’ve just started the pill, make sure you’re taking the pill at the same time every day and that its absorption isn’t being affected by medications or smoking. If it’s not heavy, wait three to four months and the bleeding should subside. If not consult your physician.

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.

If you have ever experienced severe abdominal pain, especially up high towards your right breast, and it was accompanied by nausea or vomiting (I have patients describe it as upper abdominal labor!) you probably ended up in your doctor’s office or the emergency room. The differential diagnosis (or DD as we doctors like to use in our alphabetical code) would be gallbladder disease due to gallstones, pacreatitis, food poisoning, ulcer, intestinal malfunction (inflammation, obstruction or just irritable) and let’s not forget, especially in women, heart attack! A work up would most likely include ultrasound and blood tests as well as cardiac testing. If gallstones were found and they were sizable, or the stones were causing enough pain to make you miserable (and your doctor worried) you would likely be referred to the nearest surgeon for removal of that stone ridden organ with a procedure called a cholecystectomy.

We are all at risk for gallstones; indeed this is the leading cause of gastrointestinal illness requiring hospital admission in western countries. There are more than 700,000 cholecystectomies performed every year in the United States. That’s the bad surgical news….the good news is that most of them can now be performed via laparoscopic surgery rather than the open incisions that were the norm (and the extended healing time) 2 decades ago.

Why do so many individuals produce and suffer the consequences of these stones? We synthesize cholesterol in our liver; some is excreted in the bile that is then collected in the gallbladder before it makes its way out to the intestine. Over 80% of gallstones are made of cholesterol. And the more cholesterol that is “sent out” though the bile duct, the more likely stones will be formed. Certain factors and conditions create an environment of supersaturated bile. These include age (the older we get the greater our propensity to synthesize cholesterols in our liver), female sex (sorry about this), obesity, high–fat and even high carbohydrate diets. Then we also find a predisposition to stone formation in women who take estrogen-containing birth control pills and postmenopausal estrogen therapy. The estrogen, especially if taken orally can cause higher bile cholesterol excretion.

So it would stand to reason that anything that lowered the cholesterol production in the liver and hence the concentration of this fatty substance in the bile would also help prevent gall bladder stone formation. A study just published in the Journal of the American Medical Association (JAMA) has partially substantiated this theory. The study showed that statins (which do lower cholesterol) help diminish the risk of gallstone disease if taken for more than a year.

The study was based on the UK General Practice Research Database. The authors analyzed records from 27,035 patients who underwent cholecystectomy between 1994 and 2008 and 106,531 matched controls that did not. (They tried to match each person who had the surgery with 4 controls who were matched for gender, age and were seen by general practitioners at approximately the same time.) Of these, 2396 gall bladder sufferers and 8868 controls were taking statins. The study population was comprised of 76% women and the mean age was 53.4 years. (Sorry to give you all these numbers, but these are what made the study relevant.) The statisticians also adjusted the findings so they would not be skewed by high body mass index (i.e. overweight, obese or really obese).

So here is the short analysis…The lowest odds ratio or chance of having gallstone disease followed by a cholecystectomy was in patients who used statins for at least 1 to 1.5 years or more. Their odds of the disorder and need for surgery was approximately 0.6 or 40% lower than “statinless folk” (my words). This low odds ratio also existed when long term statin users were compared to those who had used it for a short time (less than 1 to 1.5 years of treatment). That means that the statin’s affect on gallstone formation may have been somewhat independent of a recent presence of high cholesterol levels. (My interpretation of this last finding is that it may take a while to make gallstones.)

Considering the evidence that statins are protective against heart attack and stroke, even in high risk men AND women whose cholesterol values fall within the normal range, some cardiologists would like to have “statinization” of in our water supply (or at least those expensive but tasty vitamin drinks). But let’s remember that statins are prescription drugs with specific indications and yes, very infrequent but potentially serious side effects.

I have to admit that my cholesterol levels, albeit within normal range, started to rise a year ago. I thought I might just try statin therapy. Well, you doubtless have heard those incessant ads on TV… you know the ones that admonish you that if you have muscle pain or extreme fatigue you should consult your doctor immediately. Well I did (have the pain, so consulted myself). I stopped and brought my lipid levels down with diet and more exercise. I may try another statin in the future. I still don’t encourage the “everyone- should-be-on-a-statin” therapy. But for those who are taking it, or may need it….your gallbladder may appreciate the added benefit.

This will hit the headlines on Tuesday, so I thought I would share the opinions. At this point I will choose to follow the ACOG recommendations and continue to suggest mammograms for my patients between 40 and 50 as well as breast self exam (BSE).

Response of The American College of Obstetricians and Gynecologists to
New Breast Cancer Screening Recommendations
from the U.S. Preventive ervices Task Force*

In the November 17 issue of Annals of Internal Medicine, the U.S. Preventive Services Task Force (USPSTF) updates its recommendations on screening for breast cancer in the general population (see www.annals.org), including the following:

• The USPSTF recommends against routine screening mammography in women aged 40 to 49 years. The decision to start regular, biennial screening mammography before the age of 50 years should be an individual one and take patient context into account, including the patient's values regarding specific benefits and harms. (grade C recommendation)
• The USPSTF recommends biennial screening mammography for women aged 50 to 74 years. (grade B recommendation) 
• The USPSTF recommends against teaching breast self-examination (BSE). (grade D recommendation)

The American College of Obstetricians and Gynecologists, however, currently continues to recommend the following services:

• Screening mammography every 1-2 years for women aged 40-49 years
• Screening mammography every year for women age 50 or older 
• BSE; BSE has the potential to detect palpable breast cancer and can be recommended.

The College is continuing to evaluate in detail the new USPSTF recommendations and the new evidence considered by the USPSTF. Any changes to College guidance will be published in its journal Obstetrics & Gynecology.

Why did the USPSTF recommendations change?

Mammography in Women Aged 40-49 Years

In 2002, the USPSTF recommended screening mammography, with or without clinical breast examination, every 1-2 years for women aged 40 and older (grade B recommendation). The new USPSTF recommendations are based on a systematic evidence review by Heidi D. Nelson, MD, MPH, and colleagues and a modeling study by Jeanne S. Mandelblatt, MD, MPH, and colleagues published in the same issue of Annals of Internal Medicine.

The 2009 USPSTF judged that, although women in their 40s and women in their 50s benefit equally from routine screening mammography, women in their 40s experience greater harms from screening than women in their 50s. The harms assessed by the USPSTF were radiation exposure, false-positive and false-negative results, overdiagnosis, pain during procedures, and anxiety, distress, and other psychologic responses. Therefore, the USPSTF recommended routine screening for women aged 50-74 but recommended against routine screening for women in their 40s.

Breast Self-Examination

In 2002, the USPSTF judged that evidence was inadequate to make a recommendation on teaching or performing BSE. The new USPSTF recommendations are based on a systematic evidence review by Heidi D. Nelson, MD, MPH, and colleagues published in the same issue of Annals of Internal Medicine. This systematic evidence review identified two studies published since the 2002 recommendations. These studies found that teaching BSE did not reduce breast cancer mortality but resulted in additional imaging procedures and biopsies. Therefore, the USPSTF recommended against teaching BSE on the grounds that it has no benefit for women but places them at risk of harm.

What Should Fellows Do?

At this time, The American College of Obstetricians and Gynecologists recommends that Fellows continue to follow current College guidelines for breast cancer screening. Evaluation of the new USPSTF recommendations is under way. Should the College update its guidelines in the future, Fellows would be alerted and such revised guidelines would be published in Obstetrics & Gynecology.

The College continues to recommend that Fellows advise mammography screening for their patients aged 40 and older and that they counsel their patients that BSE has the potential to detect palpable breast cancer and can be performed. Fellows should be aware that the new USPSTF recommendation against routine screening mammography for women aged 40-49 (a grade C recommendation) has implications for insurance coverage, as some insurers will cover only preventive services rated as an "A" or a "B" by the USPSTF. Fellows should counsel their patients that insurance coverage for "routine screening" mammography may become variable and that patients should address this question with their insurers. These recommendations do not apply to high-risk women or patients with clinical findings, and they should be managed accordingly.

Interpreting the U.S. Preventive Services Task Force Breast Cancer
Screening Recommendations for the General Population

What do the USPSTF letter grades mean?

The USPSTF's recommendations are based on its assessment of net benefit—identified benefits minus identified harms. The USPSTF will only make a recommendation if it judges the available evidence to be of high enough quality that it can have high or moderate certainty as to the magnitude of the net benefit.

Interventions that are deemed to have substantial net benefit receive an A grade; interventions with moderate to substantial net benefit receive a B grade; interventions with small net benefit receive a C grade; interventions that have no net benefit (have harms that exceed the benefits) receive a D grade. If the evidence does not meet USPSTF standards, an "I statement" is issued.

Each letter grade is accompanied by a suggestion for practice. For A and B recommendations, the suggestion is to "offer/provide this service." For C recommendations, the suggestion is to "offer/provide this service only if other considerations support offering or providing the service in an individual patient." For D recommendations, the suggestion is to "discourage the use of this service." For I statements, the suggestion is to "read the clinical considerations section of USPSTF Recommendation Statement. If the service is offered, patients should understand the uncertainty about the balance of benefits and harms."

Grade C recommendations highlight the need for individualized decision making that considers the patient's own assessment of benefits and harms. The American College of Obstetricians and Gynecologists strongly supports shared decision making, and in the case of screening for breast cancer it is essential. Surveys have shown that women are more concerned about their risk of breast cancer than heart disease, which is more common. Many women, after weighing the benefits and risks for their own particular situation, will choose to have screening mammography.

What is the College doing in response to the new recommendations?

The College, as a partner organization of the USPSTF, reviewed the draft recommendation statement and expressed concern regarding the implications of recommending against routine screening mammography for women in their 40s.
The College is continuing to evaluate in detail the new USPSTF recommendations and the new evidence considered by the USPSTF. The new recommendations and the evidence on which they were based will be reviewed by College committees that make recommendations on screening for breast cancer. Should the College update its guidelines in the future, Fellows would be alerted and such revised guidelines would be published in Obstetrics & Gynecology.

Why did the USPSTF recommend against routine mammography for women in their 40s?

The new USPSTF recommendations are based on a systematic evidence review by Heidi D. Nelson, MD, MPH, and colleagues and a modeling study by Jeanne S. Mandelblatt, MD, MPH, and colleagues that were published in the same issue of Annals of Internal Medicine as the recommendation statement. Based on these analyses, the 2009 USPSTF judged that although women in their 40s and women in their 50s benefit equally from routine screening mammography, women in their 40s experience greater harms from screening than do women in their 50s. Therefore, the USPSTF recommended routine screening for women aged 50-74 years but recommended against routine screening for women in their 40s.
The USPSTF's evaluation of the evidence found that the benefit to women in their 40s was virtually the same as the benefit to women in their 50s. The relative risk of breast cancer mortality for women randomly assigned to mammography screening was 0.85 in women aged 39-49 years and 0.86 in women aged 50-59.

Rather than benefit from screening, women without cancer who undergo mammography, additional imaging, and biopsies may incur harm. These outcomes were more common in women in their 40s (see Table). In addition, because the prevalence of breast cancer is higher in women in their 50s and because younger women are more likely to have dense breasts that may be difficult to assess on mammography, women in their 40s had more false-positive mammograms and underwent more additional imaging than women in their 50s.

Table. Age-Specific Screening Results from the Breast Cancer Surveillance Consortium

*Data are from a single screening round in regularly screened women. Because the Breast Cancer Surveillance Consortium incompletely captures additional imaging and biopsies, these rates may be underestimates.

Data from: Nelson HD, Tyne K, Naik A, Bougatsos C, Chan BK, Humphrey L. Screening for breast cancer: an update for the U.S. Preventive Services Task Force. Ann Intern Med 2009;151:727-37.

The number needed to invite for screening (over several rounds of screening and at least 11 years of follow-up) to prevent one breast cancer death in women aged 39-49 was 1,904, compared with 1,339 in women aged 50-59.
The USPSTF also considered pain and psychologic responses as harms. The USPSTF notes that "anxiety, distress, and other psychosocial effects. . . fortunately are usually transient, and some research suggests that these effects are not a barrier to screening. . . Other potential harms, such as pain caused by the procedure, exist but are thought to have little effect on mammography use."

The Mandelblatt modeling study assessed six separate models of the effects of screening mammography using the National Cancer Institute's Cancer Intervention and Surveillance Modeling Network (CISNET). It states: "If the goal of a national screening program is to reduce mortality in the most efficient manner, then programs that screen biennially from age 50 years to age 69, 74, or 79 years are among the most efficient on the basis of the ratio of benefits to the number of screening examinations. If the goal of a screening program is to efficiently maximize the number of life-years gained, then the preferred strategy would be to screen biennially starting at age 40 years."

How might women be affected by the new recommendations against routine screening mammography for women in their 40s?

U.S. Census data demonstrate that there were 22,327,592 women aged 40-49 years in the United States as of July 1, 2008. Based on Surveillance Epidemiology and End Results Program (SEER) data, breast cancer deaths expected over 10 years were estimated at 204 deaths per 100,000 women aged 40-49 years (including both screen-detected and nonscreen-detected breast cancer). This 10-year death rate leads to an estimate of 45,492 deaths of U.S. women aged 40-49 years from breast cancer over 10 years. With a relative risk of 0.85 for breast cancer mortality for women in their 40s screened by mammography, an estimated 38,668 deaths would occur in a screened population over 10 years, approximately 6,800 fewer deaths than expected with the 10-year death rate. The fewer deaths expected with screening compared to the predicted deaths demonstrates the significant benefit of screening on mortality in this age group.

Why did the USPSTF recommend against teaching BSE?

The new USPSTF recommendations are based on a systematic evidence review by Heidi D. Nelson, MD, MPH, and colleagues published in the same issue of Annals of Internal Medicine. This systematic evidence review identified two studies published since the 2002 recommendations. These studies found that teaching BSE did not reduce breast cancer mortality but resulted in additional imaging procedures and biopsies. Therefore, the USPSTF recommended against teaching BSE on the grounds that it has no benefit for women but places them at risk of harm.

Who uses the USPSTF recommendations?

The main audience for the USPSTF recommendations is the primary care clinician. The congressional mandate establishing the USPSTF charges it with reviewing "the scientific evidence related to the effectiveness, appropriateness, and cost-effectiveness of clinical preventive services for the purpose of developing recommendations for the health care community."

However, although the USPSTF recognizes that its recommendations also have relevance for and are widely used by policymakers, managed care organizations, public and private payers, quality improvement organizations, research institutions, and patients, it also recognizes that its recommendations are only part of what needs to be considered in setting health care policy. The disclaimer that accompanies these new recommendations reads: "The USPSTF recognizes that clinical or policy decisions involve more considerations than this body of evidence alone. Clinicians and policymakers should understand the evidence but individualize decision making to the specific patient or situation."

How will the USPSTF recommendations be used in health care reform?

Health care reform legislation being considered in the House and Senate seeks to ensure coverage of preventive services as part of a basic benefits package in all health insurance plans, as well as patient cost-sharing protections for these services. In determining which services should be covered, the bills rely heavily on the USPSTF recommendations. At a minimum, covered preventive services would be those that receive an A or B grade from the USPSTF.

It is vital that covered preventive services not be limited solely to USPSTF grade A and B recommendations. The USPSTF has not issued recommendations for many vital preventive services in women's health care, such as preconception care, family planning counseling and services, and bundled services such as the annual well-woman examination. The USPSTF only makes and updates a handful of recommendations each year, far too few to address clinically appropriate preventive services that ought to be covered by any plan.

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.

Do Fertility Drugs Increase the Risk for Ovarian Cancer?

When couples are desirous of a pregnancy and just can’t seem to conceive on their own they are willing to try everything. I know… I ran a fertility clinic in Tel Aviv decades ago. At that time, we offered therapies for women who had ovulatory problems, blocked tubes, and men with low sperm counts. When we found no obvious problem with either the woman or the man and they could not conceive after trying for a year, we would arbitrarily use fertility therapies and combine them with insemination. Clomiphene was the first drug of choice. This anti-estrogen pill is prescribed in the beginning of the cycle (usually the 5th day after the period starts). It “fools” the pituitary gland into “thinking” that there is no estrogen on board. So the pituitary works harder and spurts out the hormone FSH (follicle stimulating hormone) which then induces the follicles in the ovary to develop and eventually (after the medication is stopped) produce an egg which can undergo fertilization. This medication is still used as first line therapy in many infertile or non-ovulating women.

If the clomiphene didn’t work, we would start  injections of hormones that “replaced” or caused the secretion of FSH and LH (luteinizing hormone) The latter, given in the form of HCG (sorry about all these initials, the latter stands for human chorionic gonadotropin) signals the follicle, and orders it to release the egg. With current IVF (I’m not sure you need this, but it stands for in vitro fertilization) therapies, we use many of these same medications.

Obviously there have been concerns about use of these therapies. The most immediate: failure to achieve pregnancy, multiple pregnancies and resultant early pregnancy loss, prematurity and pregnancy complications. Reproductive experts have (and should) inform prospective patients about all of these risks. But what about risks that could affect a woman’s health or her longevity?

Incessant ovulation increases the risk of ovarian cancer…Perhaps it’s the constant “bruising” of the ovaries’ surface as the follicle bursts and the egg is extruded. Perhaps the ongoing hormonal changes and/or induction of those changes by FSH and LH cause cellular mutations that can result in cancer. We do know that full term pregnancies and use of birth control pills (both of which stop ovulation for 9 months or years) are protective and decrease ovarian cancer risk. We also have statistics that show that women who were never pregnant are at a higher risk for this malignancy.

But what about the risk to women who take ovulatory stimulating medications in order to conceive…will the drugs put them at risk for ovarian cancer? A recent and very large study of treated women with follow-up for 35 years found that there was “no convincing association between use of fertility drugs and risk of ovarian cancer”. The study was carried out in Denmark where patient records on treatment and disease are stellar. Data from over 54,000 women with infertility who were referred to all the Danish clinics for 35 years between 1963 and 1998 was assessed. They reported that the risk for ovarian cancer was not significantly affected by use of clomiphen, human chorionic gonadotropins ( HCG), gonadotropins (LH and FSH) and gonadotropin releasing hormone. Nor did this change when they calculated the number of cycles, duration of drug use or the pregnancies of the women in the study!

So can we rest on our fertility drug laurels? Almost…when the authors looked at a very particular subtype of ovarian cancer called serous ovarian cancer they found that clomiphene users did have a 67% increase of this type of cancer when compared to women who had not taken this drug, especially after 15 or more years. The actual number of these cases found was small and hence even if the stat 67% sounds ominous, it’s an increase of a very, very slight incidence and remains rare. It may even be an artifact.

Remaining infertile is in itself a risk for ovarian cancer. The use of fertility medication and the advances in reproductive assisted technologies have reversed a condition that can cause unremitting anguish and health-compromising depression for hundreds of thousands of couples.

I consider this published report to be one that allows me to reassure my patients that ovarian cancer risk is miniscule or non existent….for those who have used fertility medications in the past and women who will now begin a quest to overcome their infertility.

By now (I would hope) we all know that there is a strong recommendation that all young girls and women get the HPV vaccine (Gardasil) to protect them from 4 types of human papilloma virus infection. A quick review: two of the types (16 and 18) are responsible for 70% of cervical cancers, as well as vaginal and anal cancer whereas the HPVs numbered 6 and 11 cause genital warts. The efficacy of this vaccine has been tested and supported by sufficient evidence to warrant FDA approval and CDC recommendation for its use for girls, adolescents and young women up to the age of 26. The protection will always be maximal for sexually naïve young women (a medical term that means they have not had sexual intercourse or other sexual activity which would foster HPV transmission).

The greatest incidence of HPV infection occurs within 5 to 10 years of first sexual experience. But even if such an infection should occur the chance that all the HPV types are present is very slim (see another article I wrote for this web site). Hence we continue to immunize young women when the opportunity arises (i.e. they are seen by an appropriate medical provider and they or their parents consent to this series of three shots given over a period of 6 months).

If we give the HPV vaccine to young women even if they have been sexually active or have evidence that an HPV caused disorder exists, why shouldn’t “older” women receive the vaccine and be granted some degree of immunity?

Women are waiting longer to get married (most of my patients are over 26 when they are ready to commit) and as we all know divorce rates are high. Indeed in the USA nearly 40% of men and women have married and divorced by the age of 55 and more than 25% of these people have remarried at least once. So without being judgmental lets just acknowledge that at least half of us will have new partners after the age of 26. Do the current HPV vaccine recommendations constitute age discrimination?

A large study sponsored by the pharmaceutical company Merck (they developed the quadrivalent or 4 type HPV vaccine called Gardasil) has recently been published in the journal Lancet and suggests that women in their late 20’s, 30’s and 40’s could benefit from prophylactic HPV vaccination. The study enrolled 3819 women between the ages of 24 and 45 in 38 international study sites. The criteria for entering the study were that they were not pregnant, had no history of genital warts or cervical disease. Roughly half received the vaccine while the other half received a placebo shot. They were then checked at day 1 (when they received the injection) and months 7, 12, 24, 36 and 48 with a pelvic examination and swabs taken from the cervix, vulva, and perianal areas to test for HPV. The women also were given Pap smears and their blood was tested for antibodies to the 4 vaccine type anti-HPV antibodies (which could have been silently present from previous infection but if not, should have appeared subsequent to the vaccination).
Those who developed an abnormality on Pap smear underwent colposcopy (a microscopic exam) and when necessary a biopsy and treatment. The study was meant to continue for 4 years, but after 2 years the researchers reported the following: The vaccine was 90.5% effective in preventing disease or infection related to HPV 6, 11, 16 and 18 (there were 4 cases out of 1614 treated women vs 41 in 1607 in the placebo group). And 83.1% effective in preventing disease or infection related to HPV 16 and 18 alone. (Remember those are the types that are most likely to cause genital cancer).

Clearly most of these women were not sexually naïve, the mean age of first sexual intercourse before enrollment was 19. Indeed 33.3% of the women were found to be positive to HPV 6, 11, 16 or 18 by blood testing or DNA cervical testing at the onset of the study. Most of these women were positive to only one HPV type, 1% of them were infected with two of the types in the vaccine and less than 1% were infected with 3 vaccine HPVs, while none of the women had all 4. Translated, this means that two-thirds of the women were susceptible to infection with all 4 of these HPV types, and of the remaining one-third, the current HPV vaccine could still protect them against the other three types of HPV.

Just in case you now wonder if the study is ethical…and what will happen to those women who did not receive the vaccine…the women in the placebo group will be examined every 6 months and treated if necessary. ( This is probably better than the care that most women in the USA receive). At the end of the trial the vaccine will be offered to all the participants.

This study has only 2 years of follow-up. The CDC and other organizations will probably wait for the final 4 year results before making substantial changes in their vaccine recommendations. And in this economy we also have to consider cost and insurance coverage. (The series of 3 shots usually run more than $400). But so far the results are significant.

I currently do not suggest HPV vaccination for all my patients in the 26 to 45 age group; however I will no longer exclude this vaccination for women who are at risk for HPV infection, no matter what their age!

The HINI virus has had various names. I am in Israel as I write this;  in the beginning of its spread it was termed the Mexican flu, it then became the virus hazirim, or swine flu. In the U.S. the term swine flu was officially expunged perhaps due to concerns by the “other white meat” industry. So its numerical, virologic appellation has been adapted by everyone and is here to stay. This virus has previous unknown and constantly evolving genetic features. It is highly transmissible (but not through your bacon or pork chops) and has traveled the world, mostly via traveling people. It is truly an epidemic! In Israel they currently estimate that over the next year, 25% of the population will become infected. The number touted in the U.S.A is even greater….perhaps as high as 40%! To date, those who get really sick and/or even die are young, pregnant or have underlying medical problems. The incidence of H1N1, like seasonal flu, is expected to increase in the fall and winter when we are confined to closed interior spaces and more likely to transmit the virus from person to person.

H1N1 has received tremendous publicity. Prescription sales of Tamiflu (the antiviral medication that helps diminish length and severity of certain viral infections which to date includes H1N1) have rocketed. The U.S. government promises that if needed, stocks will be replenished. I receive daily bulletins from the CDC and WHO that if not hysterical, show great concern. For once I don’t feel that the media is making more of the H1N1 viral spread than it should. A vaccine is coming, but it looks like it won’t be in our pharmacies, hospitals or medical offices until the late fall. Meanwhile the FDA has approved the next general flu vaccine. It is directed against other flu strains that are expected to be in circulation as the weather cools. But this seasonal flu shot will not provide protection against the 2009 H1N1 virus.

In the midst of the impending H1N1 crisis please don’t forget… seasonal influenza viruses can be horrific….and indeed cause more than 200,000 hospitalizations and at least 36,000 deaths in the U.S. yearly. The latter statistic is especially significant for older people, young children and people with chronic medical conditions. Each year the WHO, FDA and CDC work together to identify the up and coming viral strains that will cause the most illness in the upcoming season. They then work with the vaccine manufacturers to develop the appropriate vaccine. I know that at the end of the flu year we have, in the past, been informed that there were other flu strains out there, and  that “they” got it wrong. But there is a far better chance that these organizations got it right.

There are 3 new strains of virus that will be included in the general flu shot this year. And according to the FDA “even if the vaccine and the circulating strains are not an exact match, the vaccine may reduce the severity of the illness and help prevent influenza-related complications”.

So start your fall and the getting-colder-season (at least in some parts of the country, I don’t know what the weather will be like here in sunny California) by getting your seasonal flu vaccine as soon as it’s available. A novel H1N1 vaccine will eventually be ready for consumer use….but not right away. So if you want this vaccine (and with all the warnings that inundate our media, most of you will), a second shot will be necessary. Once an H1N1 vaccine is available, initial supplies will go to vaccinate the most vulnerable groups…young children, young adults, pregnant women, healthcare personnel and those with chronic conditions. Eventually the hope is that it will be available for everyone.

This will be the winter of our viral discontent… But there is much we can do to help prevent viral spread. Stay home when you are sick (and make sure your children, significant others and friends do), wash your hands as frequently as possible, practice cough and sneeze protection, don’t greet others with the usual I-have-to be-polite handshakes and kisses.(I certainly hope Obama uses hand sanitizers!) If you come down with flu symptoms call your health practitioner (and if you are my patient, call me or my staff) at the onset of your symptoms. We no longer have to run tests to confirm the diagnosis. (The CDC has stopped counting specific cases). We will probably prescribe antiviral medication such as Tamiflu to help you get better quickly.

AND get your seasonal flu shot. Don’t wait for the H1N1 vaccine; when it’s available the media (and companies that produce it) will make sure you are informed. This year two shots will be better than one or none.