There is no doubt that during our lifetimes we women “out depression” men by a factor of two.  Up to 20% of women will suffer at least one episode of clinical depression during their lives….and this doesn’t include the somewhat less serious but extremely prevalent mood downturns we experience during the last week (or two) of our menstrual cycles (PMS). And then, of course, we have to include the sadness and tears we all seem to get for a few days as we are overwhelmed by the birth of a baby and our bodies “mourn” the loss of all those good hormones that our placenta gave us before it was delivered. When that crying and sense of depression becomes severe and lasts longer than one or two weeks and is characterized by intense feelings of sadness, despair, anxiety, and irritability and it interrupts a woman’s ability to function, it is defined as clinical post partum depression.

What about the fathers? They don’t have the “excuse” of sudden loss of hormones. But they are faced with new marital, social, sexual, interrupted sleep and economic changes that can be overwhelming. Their suffering can also have significant consequences; several studies have shown that early paternal depression may have emotional, behavioral and developmental effects on their children.

A review that was just published in JAMA (the Journal of the American Medical Association) tried to calculate the rate of prenatal and postpartum depression in fathers by reviewing 43 studies performed in 16 countries. (This is called a meta-analysis.) Studies of teenage fathers (under 18) or those partnered with women who had established mental health problems before pregnancy were excluded from this analysis. The studies had been performed via structured interviews and the use of specific depression tests that have been shown to be applicable to men. (Tests vary according to gender…and are more likely to ask questions such as “When you spend time with your children do you get pleasure?” versus: “Are you now participating and enjoying your hobbies, sport activities and/or watching games?”…guess which applies to diagnosing depression in women or men.)

Here is what they calculated when they analyzed the studies:

  • The rate of paternal depression was 10.4% (it ranged between 8.5% and 12.7%.
  • Higher rates of depression (25.6%) were reported during the 3 to 6 month postpartum period (the highest rate of maternal depression was 41.6% during that period).
  • There was a 30% greater likelihood that a father would become depressed if the mother did so.
  • New American fathers were marginally more likely to become depressed in these studies than those in other countries.

Now just so we understand the numbers… the authors admitted that there was a very liberal inclusion of minor depression, “a category that includes individuals with depressive symptoms and impairment who do not meet the strict criteria, either by severity, number, or duration of symptom, for major depressive disorder”.
Many of the men were probably not so depressed that they could not function, but they were indeed sad, perhaps frustrated, felt vulnerable and had sleep, sexual and emotional downs. This could impact the development of their infants and young children as well as their marriages. The authors suggest that depression in one parent should prompt clinical attention to the other. Moreover, “prevention and intervention efforts for depression should be focused on the couple and family rather than on the individual”.

My daughter just had a baby. She sometimes feels overwhelmed as she breastfeeds, takes care of her older child, her step children, oversees her home and works. Her husband seems fine, but perhaps I should check his emotional status more carefully.

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!

We commonly use the adjective “sweet” to imply niceness….and of course the taste that has so domineered our palate. But the “added sugars” that help achieve the latter are anything but sweet to our hearts, brains or blood vessels. (I’ll refrain from using the word bittersweet.)  They are cloying together (my new term) to raise our bad cholesterol and enhance our demise from heart attack and stroke.

Our palate preferences have been fostered and exploited by the food industry. They know their market and have been happy to cater to our preferred taste for sweet by adding sugars in the form of refined beet or cane sugars and high-fructose corn syrup in processed or prepared food.

According to an article published in a recent Journal of the American Medical Association (JAMA), we ingest an average of 89.8 grams (21.4 teaspoons) or 359 calories of added sugar daily. This represents 15.8% of our total daily caloric intake and 31.7% of our total carbohydrate intake (as compared to just 10.6% in the late 70’s). These numbers were based on a study of adults who participated in the National Health and Nutrition Examination or NAHMES. (No, it wasn’t a pass-fail test and the subjects were not college students; as a matter of fact, they consisted of a “US civilian, noninstituitionalized population designed to obtain nationally representative estimates on diet and health indicators”). Individuals who were taking cholesterol- lowering medications and those with a diagnosis of diabetes were excluded. More than 6,000 adults were followed between 1999 and 2006; over half were women. (So we had due representation.) The participants were interviewed and gave a detailed 24 hour dietary recall. The nutrient content of the food they stated that they had consumed was determined by NAHMES from the US Department of Agriculture Nutritional Database as well as the MyPyramid Equivalents Database. (I guess a single source might have been questioned by the food industry.) The NAHMES investigators also collected fasting blood samples which they then tested for 3 lipid abnormalities: elevated triglyceride levels, elevated levels of small LDL-C particles and reduced HDL-C levels …all of which contribute to “dyslipidemia” (bad lipid levels that lead to coronary heart disease). So here is what they found:

  • A mean weight gain in one year of 2.8 pounds among those “extra sugar eaters” who consumed 25% or greater total energy from added sugar compared to a mean loss of 0.3 pounds among those who consumed less than 5% total energy from sugar.
  • In women who consumed more than 10% of their calories as added sugar, the odds that their good cholesterol or HDL-C  was low (think the stuff that acts as  a roto-rooter in your arteries) was 50 % to 300% greater than women who consumed less than 5% added sugar in their diets.
  • A higher level of triglycerides and a higher ratio of triglycerides to HDL-C in those who consumed more than that 10% of calories though sugar.

I know I am giving a lot of “higher” and “lower” numbers, but alas, that is what statistics are all about. Put simply, the higher your intake of “added sugar” the more likely you will gain weight and ruin your good and bad lipid levels. It’s not enough to just eat low fat or abstain from the wrong fats in order to maintain an internal cholesterol and fat ratio that will protect your blood vessels, heart and brain. You have to abstain from ubiquitous “added sugars”. Check the labels on those sodas, coffee drinks, canned food, cookies, soups, cereals, breads or anything that is processed. (And the term “naturally sweetened” doesn’t mean that the sugar is exempt from the above.). Your overall “added sugar” should not be higher than 100 calories a day or 5% of your caloric intake. There is nothing sweet about the wrong fats that clog vessels and result in heart attack and stroke.