Heart Disease in Women: Lifestyle Interventions

As this year's American Heart Month comes to an end, it seems appropriate to point out a new guideline from the American Heart Association about to be published next month regarding the prevention of cardiovascular disease in women, as heart disease remains their number one cause of death, far out pacing all cancers combined, including breast cancer.

Specific recommendations include not only cessation of tobacco use but also avoidance of environmental tobacco smoke (which may not be the easiest thing to do given one's work situation - which therefore makes it imperative that we step in from a legislative perspective).

The AHA recommends 150 minutes/week of moderate exercise, 75 minutes/week of vigorous exercise, or some combination of the two.  Additional cardiovascular benefits can be obtained by increasing moderate-intensity exercise to 300 minutes/week or 150 minutes/week of vigorous-intensity physical activity.  All this is supported by Class I, B Level of Evidence.

As for nutrition, the AHA recommends a diet rich in fruits & vegetables; whole-grain, high fiber foods; and oily fish (at least twice weekly), while limiting intake of saturated fats, cholesterol, alcohol, sodium & sugar, and avoiding trans-fatty acids completely.

There is a specific recommendation for 1,800mg/d of EPA (a specific form of omega 3 fatty acids) in those with hypercholesterolemia (high cholesterol) and/or hypertriglyceridemia (high triglycerides) for both 1o and 2o prevention.  Please note, however, that most omega 3 products, eg fish oil capsules, are only 30% pure and thus only contain 300mg EPA+DHA out of 1,000mg fish oil.  And of that 300mg EPA+DHA, typically only 180mg are EPA (the other 120mg being DHA).  So, unless you look for higher grade supplements, you'll need to consume at least 10 capsules of standard over-the-counter fish oil daily to meet AHA recommendations.

None of the above is shocking or a revelation.  But we have to empower the women in our lives to act upon this information, if not for them, then selfishly, at least for us.

Bisphosphonates & Atypical Femur Fractures: Part 2

Remember my December 10th post about bisphosphonates?  Of course, you don't.  That's ancient history, at least by medical standards.  Well, here's the latest chapter, which needs to be entitled "Relative Risk vs Absolute Risk".  Just released this past week in JAMA, in a population-based, nested case-control study of 205,466 Canadian women >68yo, the authors concluded that use of bisphosphonates increased (more than doubled) the risk of atypical subtrochanteric or femoral shaft fractures after 5yrs of use compared to non-users.  But this is relative risk.  The absolute (or true) risk was actually quite low, only 0.35% or 716 women.  

And lest you decide to stop taking your bisphosphonate because of a misguided fear of this rare fracture type due to misinterpretation of statistics, the authors also found 9723 women who'd sustained a more typical femoral neck or intertrochanteric fracture despite bisphosphonate use, which actually lowered the relative risk of fracture by 24% after taking the usual suspects into account.

Let me put it another way and give you a different example.  Let's say the risk of something bad happening was 4 out of 100 or 4%.  If you took some medicine that could lower your risk to 2 out of 100 or 2%, you would have achieved a 50% relative risk reduction.

Likewise, let's say the risk of something else bad happening was only 4 out of 1,000 or 0.4%.  And if you took some medicine, you could lower your risk to 2 out of 1,000 or 0.2%.  In reality, you would've achieved the same 50% relative risk reduction.

So while it may sound impressive in both situations to claim that you lowered the relative risk of a bad occurrence by 50%, in actuality, the absolute risk reduction was minimal in the 2nd scenario.

Returning to our situation with bisphosphonates, prolonged use >5yrs might double the risk of a rare fracture while truly minimizing your risk of a more common fracture.  As a result of this study and the others already mentioned 2 months ago in my earlier post, it appears the consensus is moving towards limiting bisphosphonate use to just 5 years.  We'll see whether that actually becomes a guideline shortly.  In the meantime, as with all new findings, please discuss your individual situation with your family physician before abruptly stopping some regimen based upon the lay press.

Cannabis Use: Is It Really Safe?

No, I don't condone the use of illicit substances.  But I do find it curious as to how some are considered licit while others are illicit.  For instance, we know that there are very few benefits to the use of tobacco (are there any at all?) compared to all the down sides from its use, yet it's still sold legally here.  Alcohol is trickier since many studies demonstrate some benefit when consumed in moderation.  However, there's a very visible minority that enjoys their alcohol in excess to the detriment of others.  That's where I draw the line because when your business becomes my business, it's no longer a matter of individual rights & freedom.

Any way, I digress.  I wanted to review a meta-analysis (study of studies) published this month in the Archives of General Psychiatry  looking at the recreational non-medicinal use of cannabis (marijuana).  More importantly, I wanted to see if the authors reported any downside to the use of cannabis since most recreational users state that it causes no harm.  Turns out that cannabis users had an earlier psychotic break than non-users, almost 3 years earlier.  Alcohol and other substances did not play a role in onset of psychosis.

Ironically, in my previous life, exactly 3 short years ago, I wrote two posts regarding the use of marijuana, the first on February 5, 2008 and the second on February 18, 2008, the latter in response to some input from colleagues.  Concordant with my posts, an earlier analysis in the Lancet also concluded that use of marijuana increased the risk of psychosis later on in life.

Of course, one could always argue for an associative effect rather than causal in nature.  But the authors of this month's study concluded that the current evidence support a causal relationship.  In other words, use of marijuana increases one's risk of (earlier) psychosis.  So think twice before you light up!

Part 2
Part 3

More Controversy: Menopausal Symptoms vs Heart Disease

Just over 3 weeks ago, I looked over a study that concluded that vasomotor symptoms, hot flashes & night sweats, were associated with lower risk of breast cancer.  Now, a new study just released this week in the journal Menopause, concludes, contrary to conventional wisdom, that early vasomotor symptoms were actually associated with lower risk of stroke, all cardiovascular events, and most importantly, all-cause mortality.

With all studies, but especially those that are contrary and controversial, I always suggest looking at how the study was performed and how significant were the statistics.  In this particular situation, the authors followed 60,027 women in the observational arm of the Women's Health Initiative (WHI).  Granted, there's been a lot of negative press about WHI, especially from the alternative & complementary medicine folks, but remember that this specific analysis was observational in nature.  So one can't argue over horse-derived estrogen vs natural estrogen.

What's this mean for you & me?  Well, probably just confusion for you but lots of confusion plus controversy for me since this study just opened up Pandora's box (again).  Conventional wisdom over the last 2-3 decades has been that estrogen is protective of the heart (which is why women tend to have their heart disease manifest after menopause, typically 10 years later than men) which is why we previously thought that estrogen replacement would be protective.  Now comes a new spin that less estrogen (leading to hot flashes & night sweats) is actually good for you!

The authors rightly concluded that they need to perform more studies (how else will they put food on the table?) but more importantly, whether the individual's timing of menopausal onset represents distinct processes and different risk profiles.  Only time will tell.  But as I mentioned 3 weeks ago, perhaps our patients can re-interpret their early symptom onset given the positive outlook further down the road.  As for treatment with estrogen with(out) progesterone, that requires more space than I have to type (and more time for an informed discussion with your healthcare provider to understand your individual risks).

High PSA Velocity vs Prostate Cancer: To Biopsy or Not to Biopsy?

Argh!  I hate controversy!  Give me a clean, straightforward answer.  Unfortunately, medicine isn't like that.  We continue to refine our understanding as we gain more knowledge.  We can only make predictions based upon what we know today, not what we may know in the future.  As I've said many times before, our crystal ball is in the shop (at least mine is).

Therefore, it was with some irony that on the same day that I heard back from a close colleague/friend/relative that his prostate biopsy came back negative, the same diagnostic procedure for which I pushed mightily given his rather dramatic & persistently increasing PSA velocity, the Journal of the National Cancer Institute published a study that prostate biopsies performed due to PSA velocity alone did not improve accuracy of diagnosis in a group of 5,519 men.  I wish I'd known that over the last 2 months as I worried about the sudden increase in his PSA that was not amenable to an empiric trial of antibiotics.

Their conclusion was that using PSA velocity as the sole indication for prostate biopsy in the setting of low PSA and normal digital rectal exam lead to one in seven men (more typically, only one in twenty men) being biopsied without statistically significantly increasing the chances of finding a high-grade cancer (Gleason score of 7 or greater) and/or clinically significant cancer (using Epstein criteria).

Their conclusion goes against both the National Comprehensive Cancer Network (you first need to register for free) and the American Urological Association's guidelines.  This controversy and lack of clarity is why medicine is such a difficult profession to undertake, especially in our litigious society.  We're damned if we do and damned if we don't.  Helping a patient make an informed decision based upon our current scope of knowledge isn't enough.  We are expected to be correct 100% of the time, yesterday (in the shortest period of time) and tomorrow, while consuming the least possible resources, after which we receive (threats of) declining reimbursements.  We're being pecked from all sides.  No wonder we're sitting ducks for the malpractice lottery.

Cheers! Let's Drink for Heart Disease!

Cheers!  A votre sante!  Gam bai!  Two studies were just published yesterday in the British Medical Journal adding to the evidence that alcohol is beneficial in heart disease.

In the first systematic review & meta-analysis, the authors filtered through 4,690 studies to read 124 full articles from which 63 were selected but only 44 had data on the desired biomarkers.  Of those evaluated, the authors concluded that moderate alcohol consumption led to statistically significant beneficial effects on HDL (good cholesterol), apolipoprotein A1, adiponectin & fibrinogen, which may explain alcohol's cardioprotective effect.

In the second systematic review & meta-analysis, another group of authors sifted through 4,235 studies from which they culled just 84 for inclusion.  Their conclusions?  Alcohol consumption lowered cardiovascular mortality by 25%, incident coronary heart disease by 29%, coronary heart disease mortality by 25%, and all-cause mortality by 13% compared to tee-totalers.  Incident stroke and stroke mortality did not demonstrate a statistically significant association with alcohol consumption.

Of course, by now everyone wants to know just how much alcohol can be consumed, right?  The second article again demonstrated the presence of a J-curve when it comes to alcohol consumption.  In other words, consuming <1 drink/day was enough to garner statistically significant benefit whereas moderate-to-heavy consumption actually increased hemorrhagic stroke risk. 

So, remember Goldilocks when you go out w/your buddies.  You want the right amount, not too much, but clearly, not too little either.  Moderation is key.  By the way, saving it all for the weekend blow out does you no good either. 

Another (Off-Label) Way to Increase Testosterone

Did you ever hear the story about the girl who asked her mom why she always cut both ends off the roast before cooking it?  Her mom said b/c that's how Grandma does it.  So the girl then asked her Grandma why she cut both ends off the roast before cooking it.  Her Grandma said b/c that's how Great-Grandma does it.  Luckily, their family is long lived, so the girl asked her Great-Grandma why she cut off both ends off the roast before cooking it.  And her Great-Grandma answered b/c she didn't have a pan large enough!  At least that's how I recall the tale.

The moral of the story is that just as in medicine, we do what we're taught, rarely exploring the boundaries.  We stay within our comfort zones and never stretch ourselves or venture beyond the line drawn in the sand.  As much as I try to stay up-to-date and practice evidence-based medicine, I'm as guilty of that as anyone else.  So it's a good thing students & colleagues ask questions.  In this particular instance, I'm particularly indebted to Dr. S who asked about the off-label use of clomiphene to increase testosterone (and sperm). 

In fact, clomiphene, a selective estrogen receptor modulator, blocks estrogen receptors at the hypothalamus and pituitary, thus decreasing estrogen's inhibition of gonadotropin secretion, ergo more testosterone production.  Many studies (amongst them published in June 2003, May 2008 & December 2010) demonstrate increases in testosterone levels with some even showing an improvement in semen parameters, but apparently without any change in pregnancy rates (although it continues to be used off-label towards this endpoint).  Physicians have also commented online about the off-label use of clomiphene.

I mention this, not so that someone can become a professional bodybuilder, but so that those who are clinically hypogonadal can have another option for therapy.  Let's not forget that offering testosterone (whether in oral, sublingual, topical, pellet, or injectable form) to someone essentially renders them infertile and dependent upon (more) exogenous testosterone, whereas offering either hCG, anastrazole, or clomiphene is a way to potentially stimulate testicular production of more testosterone (assuming that the patient is not suffering from primary hypogonadism or testicular failure).

Again, I can't emphasize enough the need to work closely with a clinician who is experienced in this field of medicine and willing to provide close & regular monitoring.  Let me repeat:  this is not a do-it-yourself project.

Cell Phone Use vs Brain Fxn: Conspiracy Theorists Unite!

My brother asked me a while back what I thought about putting up some cell phone & radio towers/antennas on top of our parents' building complex.  After all, it would help shore up the home owners association's coffers.  His main concern, however, was the possible theoretical effect of cell phone radiofrequency signals on our health.  Now, I was never a huge X-Files fan, unlike my wife.  However, most observational & epidemiologic studies have not demonstrated any effect, positive or negative, from the use of cell phones, despite persistent anecdotal rumors to the contrary.

Ironically, as just noted on CNN and in USA Today, a randomized crossover study just released today in JAMA noted that 50 minutes of cell phone use next to the ear was enough to increase glucose metabolism in the two parts of the brain closest to the antenna.  Moreover, the larger the radiofrequency electromagnetic field, the greater the increase in glucose metabolism.  However, overall brain metabolism was not affected.

But what does this mean to you & me, a colleague, Dr. D, asked?  Just like the authors concluded, the findings are of "unknown clinical significance".  In other words, we don't know.  Cell phones have only been around for a little over 2 decades and over this period of time, designs have changed dramatically (not to mention power output).  I still remember when I was in medical school and my best friend had just purchased one of those old brick-style phones.  We were too cool driving around calling everyone we knew, unaware that that phone was putting out several times as much signal power as my current Samsung Epic 4G. 

The editorialists suggest that more studies are needed.  I agree.  But in the meantime, I'm going to more conscious about using my Bluetooth earpiece even while I'm at home.  And maybe it would be safer(?) to leave those antenna buffer cases off your iPhone4.  After all, a lower/lost signal is less likely to affect your brain!

Shhhh . . . What About Hospice & Palliative Care?

I try to focus this blog on health rather than disease by writing about all that we can do to optimize our wellness.  But death is the 800 pound gorilla in the room.  We can't escape its grasp, yet too often, we ignore it and won't discuss it, even when it's near.  It's as if by mentioning it by name, we're committing someone to a sure death.  But I have a surprise for you:  even if we don't talk about death, we will still die, sooner or later.

Sure, physicians and lay people alike aren't very good at using their crystal balls to predict the exact time of death.  But with certain diseases and conditions, we've developed enough experience to narrow our guess down to weeks-to-months or sometimes days-to-weeks or so on.  You get the idea.

Cancer is one of those illnesses where we can often make a credible guess.  Yes, we've made tremendous strides over the last few decades against this dreaded diagnosis.  In fact, some forms that were once as good as a signed death sentence are now manageable.  With others, we even dare breathe that other "C" word, cure.  But still too often, cancers either present too late, having already spread to different parts of the body, or become resistant to all the surgeries, chemotherapies, and radiation that we can throw at it.  

These patients, the ones with metastases, are the ones for whom we should discuss hospice and palliative care earlier rather than later.  Realistically, we should offer palliative care even at the beginning of any treatment to help all patients and their loved ones cope with side effects and adverse reactions.  But later on, once it's clear to us, the physician, that things aren't going so well, rather than consider death the equivalent of defeat, we really need to take the initiative and start discussing hospice & palliative care, even as we consider another "Hail Mary" pass to rally the troops.  In truth, we never win.  Death always trumps life.

The American Society of Clinical Oncology just released a new statement that care needs to be individualized for patients with advanced cancer.  That's code for actively involving the patient in his/her care, specifically asking for their individual goals and care preferences.  For many, it's not death that is feared, but rather the final days right before.  Patients don't want to suffer (however, one defines that physically, mentally, emotionally or spiritually) or to be left alone in the hospital's cold sterile environment.  Most want to be at home surrounded by loved ones after having checked a few more items off the bucket list.  This is where hospice and palliative care medicine step in, to offer comfort and compassion, when no cure is possible/realistic, to both the patient and the family.

Incredible as it may sound, in the case of metastatic non-small cell lung cancer, in a study published in the New England Journal of Medicine last August, those patients randomized to early palliative care had less aggressive care at the end of life (as expected by definition), yet reported better mood, better quality of life, and surprisingly, longer survival, living on average almost 3 months longer (11.6 months compared to 8.9 months) compared to those who received standard oncologic therapy alone.

So it's about time that we acknowledge that 800 pound gorilla.  To get the conversation started, a nice piece was written online yesterday in the USA Today.  Let's start talking about hospice and palliative care options.

Disclaimer:  I serve as a Medical Director for Infinity Hospice Care's Las Vegas program.

6 Months After Stopping Testosterone . . .

What happens when you quit doing something?  The effect/result usually goes away, right?  For instance, if you decide to stop filling your car's gas tank w/gas, eventually it stops running.  If you stop eating, the sensation of satiety is replaced by hunger.  In the case of stress incontinence, if you stop performing your Kegel exercises regularly, your incontinent episodes return (as many of patients have discovered on their own).

Following that same line of thinking, researchers recently decided to look into whether short-term testosterone supplementation could lead to long-term benefits.  Unfortunately, while numerous studies have demonstrated the ability of testosterone to increase muscle mass (peaking at 6 months) and then maintain said gains with continued treatment for up to 3 years, in this situation, all gains in body composition, muscle strength & quality of life resulting from 25-75mg/d of testosterone gel for 6 months were lost by 6 months after cessation.

So what did we learn from this study?  That just like many other situations in life, short-term testosterone is not enough to provoke long-term benefit.  So if you're going to commit, be ready for the long haul.  But let's be clear that long-term testosterone supplementation requires close monitoring by an experienced clinician familiar with all the possible downsides of supraphysiologic testosterone so as to be able to prevent, treat, and mitigate any potential side effects.  It's doubtful that you'll receive that kind of care by answering a few questions online in order to obtain a prescription.

Growth Hormone Receptor Deficiency & Laron Syndrome

Now, don't get me wrong.  I'm not an endocrinologist, much less a growth hormone specialist.  However, the discussion of tesamorelin the last few days led me to a recent news article published last week in the Los Angeles Times about a small group of Ecuadoreans with Laron Syndrome (an autosomal recessive growth hormone receptor deficiency) followed by researchers whose findings were just published concluding that growth hormone receptor deficiency protected these people from cancers and diabetes compared to their normal relatives.  What's truly exciting is that the serum of these patients with Laron Syndrome protected DNA from breakage, which is one long-standing theory behind aging.  It also lead to increased programmed cell death or apoptosis (which is a good thing).

But what about ending up relatively short compared to your peers, say growing to a height of only 3-4' tall?  In this day and age, I'm not convinced that that's an acceptable side effect.  Most surveys & studies report that taller height (within reason) makes a difference in most things in life after all other factors are taken into account.  But what of the researchers and LA Times reporter's conclusion that lower growth hormone is better.

It turns out that long term 10 year studies demonstrate no increase in mortality in those patients with growth hormone deficiency who are given growth hormone.  Specialists in growth hormone were actually incensed enough to write a letter to the editor stating the same.  Likewise, a 20 year follow up study of survivors of childhood cancers who have since received growth hormone demonstrate favorable overall safety profile (although there is a subset that might be at higher risk of secondary neoplasm).

Moreover, growth hormone is released in response to strenuous exercise.  If growth hormone suppression were such a good thing, one might as well recommend limiting exercise and physical activity, when in fact all available data demonstrates lower mortality the more active one becomes over a lifetime.  Furthermore, we have data that growth hormone is important in bone mineral density, body composition, coronary disease, and most of all, quality of life.  Yes, future data may alter our current way of thinking but given what we have available to us now, I vote for (naturally) increasing growth hormone (within the normal reference range) as a means to live a high quality disease-free life for as long as possible, not necessarily to just live longer for duration's sake.

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