Exercise vs Drugs: Which is Better?

When I was growing up, I loved watching movies like King Kong vs Godzilla.  Half a century later, we now have the analogous comparative effectiveness study to determine which therapeutic option, given a choice, is better.  For instance, is exercise better than drug therapy?  It turns out that in a meta-analysis published last week in the British Medical Journal, the authors concluded that exercise is just as good as many drug regimens in secondary prevention of heart disease, stroke rehabilitation, heart failure & diabetes.

The authors evaluated 16 meta-analyses, of 305 randomized controlled trials involving 339,274 participants, which demonstrated equivalent mortality benefits compared to traditional medications.  This isn't to say that we should just throw our medications down the toilet but rather to focus on lifestyle issues followed then by drugs but only if necessary.  Lifestyle is key!

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Exercise vs Knees: It's Not Just For Your Heart

If you've been anywhere near any media over the last several years, surely you've heard repeated exhortations to exercise. Get off your a-- and get moving! We've linked exercise to lower mortality, lower risk for diabetes heart disease & obesity, as well as less dementia, depression, disability & falls. 

But for most of us, those conditions are way out there in the future. We still live with a teenager's sense of invincibility. That won't happen to me! That only happens to those other people. Which might help explain why so few of us exercise regularly as so strongly suggested. But what if exercise could bring about a more immediate benefit? 

For instance, do any of you (or your patients) suffer from osteoarthritic pain, especially of the knee(s)? Enough to take non-steroidal anti-inflammatory drugs (NSAIDs) that might lead (or have led) to gastric distress in the form of gastritis or even a bleeding peptic ulcer? Or perhaps an elevation in blood pressure due to chronic kidney disease? Or perhaps having failed NSAIDs, are now dependent upon opioids & their derivatives?

The good news is that in a meta-analysis published last month in the British Medical Journal, the authors concluded that a combination of resistance training, flexibility & aerobics was best at dealing with pain & loss of function due to osteoarthritis of the knee. The authors filtered the literature down to 60 randomized controlled trials involving 8,218 participants over an average of 15 weeks (ranging from 4 up to 79). The participants were mostly from the States, United Kingdom & Australia. 

Granted, we may have some difficulty weaning someone off his/her narcotic, but that fact remains that we should make exercise the foundation to our treatment of knee arthritis, even before we pick up a pen to write a prescription.

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Caught Between A Rock And A Hard Place - Part 7

It's deja vu all over again

- Yogi Berra

So here I am, safely ensconced back home again, having returned from a week inside the San Diego Convention Center where the American Academy of Family Physicians held its annual Congress of Delegates followed by its annual Scientific Assembly. I'm trying again to desperately catch up on my reading & paperwork before the patient care starts up again later today. Then I stumbled upon a retrospective cohort study published earlier this month in the British Medical Journal in which the authors concluded that using proton pump inhibitors to attempt to prevent stress ulcers in coronary artery bypass graft patients was associated with an unintended consequence of post-operative pneumonia.

But didn't I just write about PPIs recently? Turns out I did discuss some harms associated w/PPIs just 11 days ago in response to a study to be published in next month's issue of the Mayo Clinic Proceedings. But to show you that medicine is not always so clear cut, a population-wide retrospective cohort study was published over 3 years ago in this very same BMJ in which the authors came to a diametrically opposed conclusion: there was no link between PPI use and post-operative pneumonia.  

Which begs the question: what do I/you do? Well, when it comes down to conflicting studies, we believe more strongly in the double-blind, placebo-controlled trial which demonstrates cause & effect, whereas as retrospective cohort & other observational studies only demonstrate an association but can't tell what caused what, if indeed one thing caused another. In this particular case, both studies are retrospective cohort studies, so that doesn't help us.

So let's take a look at the bigger issue. Use of PPIs is linked to multiple other unintended consequences as I pointed out in Part 6. Based upon that, I see no reason to take a PPI w/o good reason based upon one study that found no harm given the many others that did. Remember, first, do no harm. Primum non nocere.

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Fluke or Trend: ACE Inhibitors vs Alzheimer's Disease

ACE inhibitors & ARBs are two major classes of blood pressure lowering medications, related to each other like cousins.  The former runs a slight risk of causing a dry ticklish cough.  Otherwise, one or the other are often used to protect one's kidneys & heart, in addition to lowering blood pressure.  Just under a year ago, another study was published linking the use of ARBs to lower rates of brain pathology consistent with that most common cause of dementia.  But as I noted in my post, there have been several studies suggesting that ARBs are beneficial when it comes to dementia.

Interestingly enough, a longitudinal prospective population-based study was published 4 years ago in JAMA Internal Medicine looking at the effect of ACE inhibitors with regards to Alzheimer's disease.  Taken as a whole, there was no link.  But if you looked at just the centrally acting ACE inhibitors, their use was linked to a lower rate of cognitive decline, more so than when compared to noncentrally acting ACE inhibitors.  Which brings me to an observational case-control study published last week/month in BMJ Open in which centrally acting ACE inhibitors were linked to improvement in cognition & reduction in cognitive decline.  The authors made their conclusion after following for six months 361 patients w/Alzheimer's disease, of whom 85 received a centrally acting ACE inhibitor while 276 did not.

So if you need to take blood pressure medication(s), one of which is an ACE inhibitor, I'm sure you're curious which ones cross the blood-brain barrier: captopril, fosinopril, lisinopril, perindopril, ramipril & trandolapril. On the other hand, benazepril, enalapril, moexipril & quinapril do not.  The good news for you & me is that captopril & lisinopril are available for $4/mo at WalMart and its competitors.

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Fish (Oil) vs Breast Cancer

You are what you eat.  How many times have you heard that phrase?  Chances are you won't turn into a hot dog or potato chip but study after study demonstrates the impact of good nutrition on our health.  Most observational studies demonstrate benefit to making better choices and even a recent randomized controlled trial was able to demonstrate cause & effect benefit from the Mediterranean diet.  In general, the studies looking at fish (oil) have suggested heart disease & memory benefit.  But what about cancer?

Well, in a meta-analysis of 21 prospective cohort studies published less than 2 weeks ago in the British Medical Journal, the authors arrived at a rather interesting conclusion: while fish (and alpha linolenic acid for vegans) consumption was not linked to breast cancer risk, total intake of marine omega-3 poly-unsaturated fatty acids was inversely linked to breast cancer, such that every 0.1g/d of fish oil was linked to 5% risk reduction in breast cancer.

Sure, they looked at 687,770 participants regarding fish intake, 527,392 regarding omega 3 PUFA intake, and 405,592 regarding ALA intake.  So just how does marine-derived omega 3 PUFA get linked to lower breast cancer risk while fish intake doesn't?  Let's remember that the devil is in the details.  Not every fish is chock full of omega 3 PUFA.  Unfortunately, a meal comprised of fish & chips won't help.  And my guess is that farm-raised salmon won't either.  You need the wild-caught salmon that's been feasting naturally in order to get your fill of omega 3 PUFA.  Think about that the next time you look for fish in your grocery store.

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Fluke or Trend: 5ARIs vs Prostate Cancer

It's been a while since I looked closely at 5 alpha reductase inhibitors.  In March 2011, I discussed the potential side effects from taking a 5ARI.  In July 2011, I reviewed two studies aimed at using a 5ARI as chemoprophylaxis against prostate cancer.  Unfortunately, the results didn't turn out as hoped and the Food & Drug Administration refused to give either finasteride or dutasteride approval for marketing as preventing prostate cancer.

Well, in a case-control study published 10 days ago in the British Medical Journal, the authors concluded that use of 5ARIs to treat lower urinary tract symptoms also lowered Gleason score 2-7 prostate cancer.  This was an expected outcome.  What was unexpected was that 5ARI use did not increase risk of Gleason 8-10 prostate cancer in the ensuing 4yrs.  Recall that while both the Prostate Cancer Prevention Trial (PCPT) and the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial demonstrated that regular use of 5ARIs can lower prostate cancer risk by up to 1 in 4, they also increased high grade prostate cancer risk.  

So how does a guy decide?  Well, for now, use the 5ARI for its intended purpose, assuming you still need it.    That means take it for your receding hair line or because you have symptoms of an enlarged prostate.  But don't take it in an attempt to prevent prostate cancer.  At least not until we have better research to support such an indication.

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Just How Fast Is Your Heart Beating?

Just under 2 months ago, I looked at a study attempting to predict cardiorespiratory fitness via non-exercise means.  Of note, the authors linked body mass index and resting heart rate to CRF.  But do we really care as much about CRF as we do our mortality?  In fact, in a prospective cohort study published last month in Heart, the authors concluded that resting heart rate was an independent predictor of mortality, regardless of physical fitness, physical activity and the usual slew of cardiovascular risk factors.

The authors measured resting heart rate prior to testing physical fitness as measured by VO2max (oxygen consumption) in 2,798 Danish men who were then followed for 16 years.  As demonstrated in a figure in the paper, there was an inverse correlation between physical fitness and RHR.  In other words, those who were more fit as determined by a greater VO2max also had a lower RHR.  

To my amazement, the 222 fittest men w/avg VO2max 38L/kg/min also had an average resting heart rate of just 48 beats per minute while the least fit 54 had an RHR greater than 90bpm.  Typically, we declare anyone with heart rate less than 60bpm as being bradycardic, and very rarely, aside from exceptionally fit young athletes, do I see resting heart rates less than 56bpm.

Yet, after taking into account all the usual confounders, the authors noted that compared to those w/RHR less than 50bpm, mortality increased by 16% for every 10bpm increase in RHR.  Those with what I previously considered an excellent RHR of just 51-60bpm had a 20% greater mortality compared to those w/RHR less than 50bpm.  Those with a normal or average RHR of 71-80bpm had 33% greater mortality while those with RHR greater than 90bpm had more than twice the mortality of those w/RHR less than 50bpm.  So just how fast is your heart beating now?

By the way, if you're worried and wondering about what you can do to lower your RHR and thus your mortality, aerobic exercise is the key, that is, after you've been cleared by your family physician to engage in exercise.  So don't just sit there, do something!

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Coronary Artery Calcium (CAC) for Risk Stratification

Multiple studies of Type 2 diabetics currently free of heart disease have demonstrated a risk for future cardiac events equivalent to those non-diabetics who've already had an initial event.  That's why diabetes is considered a coronary heart disease equivalent, similar to symptomatic carotid stenosis, abdominal aortic aneurysm, and peripheral arterial/vascular disease.  If any of these 4 conditions is noted, we're to assume the patient is at high risk (>20%) for a heart attack in the next 10 years and aim their LDL cholesterol towards a goal of <100md/dL or optional goal of <70mg/dL.

But as with the direction of healthcare these days, we're making every attempt to individualize rather than generalize.  In other words, aren't their some diabetics w/greater heart disease risk than others?  And if so, how do we differentiate one from the other?  After all, the Framingham risk calculator, Reynolds Risk score, and QRISK2 lump them all together.

With that thought in mind, a meta-analysis of 8 prospective studies was published last month in the British Medical Journal in which the authors concluded that coronary artery calcium score ≥10 is useful in separating the truly high risk from the merely moderate risk.  The authors arrived at their conclusion by following 6,521 participants w/T2DM for 5+yrs.  Compared to those w/CAC <10, those w/greater scores had five-fold greater relative risk of all-cause mortality & cardiovascular events.  So while I am not a great fan of excess radiation exposure, it would appear that imaging might aid in determining who should truly aim for the optional goal LDL of <70mg/dL.

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Fluke or Trend? Calcium vs Heart Disease Part 4

When it rains, it pours.  Just a week ago, I commented on a study published in JAMA Internal Medicine in which the authors concluded that consumption of calcium supplements was associated w/heart disease in men.  Of course, the devil is in the details, as dietary calcium was not associated w/heart disease in either women or men.

In a prospective longitudinal cohort study published in BMJ earlier this week, the authors concluded that high calcium consumption was associated w/greater risk of death from any cause, especially heart disease but not stroke.  The nutritional supplement manufacturers jumped all over this study, and perhaps rightly so, because it was originally designed to look at mammography & breast cancer.  61,433 women for followed for an average of 19 years and dietary calcium was assessed just once, rather than serially.

While the statistical manipulations found a link between dietary calcium more than 1,400mg/d and deaths, calcium supplements were linked to death only in those who were already consuming more than 1,400mg/d in their food.  Bottom line, as I mentioned last time, it now appears that calcium is a double-edged sword for both women & men.  We aren't currently clear as to the mechanism of disease nor to the differences between dietary & supplemental calcium.  But let's also not forget that we do have cause & effect evidence of benefit from calcium while we only have circumstantial observational evidence of its harm.  So choose wisely even as we await further developments in this story.

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All Omega Fatty Acids Are Not Created Equal

Going shopping for food can be pretty difficult these days what with all the advertising proclaiming this & that. It's even worse when it comes to dietary supplements because there's essentially no 3rd party oversight.  The manufacturers can essentially market whatever they want w/o proof of effectiveness and/or safety.  It's become a Whack-A-Mole game whereby they only need to change something if caught or someone complains enough.

As an example, there's plenty of data looking at the benefits of fish (oil).  Granted, most of it is observational, but hey, that's better than nothing.  In marketing parlance, fish oil is also referred to as omega 3, a name & descriptor of its polyunsaturated biochemical nature.  As it turns out, there are also omega 6's & 9's, both polyunsaturated fats, too.  And as we all know, polyunsaturated fats are better for us than saturated ones, right?  That's why product labels mention omega 3 content plus "other" omega oils.  In fact, one brand touts its "balanced blend of omega 3-6-9 fatty acids" as if that alone makes their product better than every one else's.

It turns out that most of us get plenty of omega 6's & omega 9's in our Westernized & Americanized diet.  It's the omega 3's that we're lacking.  But just because omega 6 & 9 are polyunsaturated, shouldn't they be good for us?  Well, the devil is in the details.

In a randomized controlled trial published last week in the British Medical Journal, substitution of omega 6 linoleic acid for saturated fats did nothing to lower heart disease rates.  If anything, this most abundant polyunsaturated fat increased all-cause mortality, coronary heart disease & cardiovascular disease.

In the study, 458 men 30-59yo who'd suffered a cardiac event were randomized in a single blind, parallel group controlled trial in which half were given omega 6 linoleic acid eg safflower oil & safflower derived margarine, to substitute for typical dietary saturated fats, eg animal fats, common margarines & shortening.  Those randomized to control received no specific instruction or food.  All were followed for up to 5yrs.  Yet, those randomized to omega 6 linoleic acid had a 62% greater risk of all-cause mortality, 70% greater risk of cardiovascular disease & 74% greater risk of coronary heart disease.  

Obviously this study needs to be replicated in a larger trial with participants w/o known heart disease to represent the greater population as a whole.  But for now, it's pretty clear that not all omega fatty acids are created equal.  Omega 3 fish oil is much safer than omega 6 linoleic acid, at least if you've recently had a coronary event.

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Multivitamins & Prevention Part 3 Heart Disease

Two months ago, a randomized controlled trial was published in JAMA concluding that consumption of multivitamins did not decrease heart disease, at least not in men.  But as you well know, science is in the eye of the beholder.  Much like the blind men and the elephant, everyone has their spin on the evidence.

And in case you're wondering if this also applies to your spouse, a February 2009 randomized controlled trial (Women's Health Initiative) published in Archives of Internal Medicine arrived at the same conclusion: multivitamin use did not reduce heart disease in women, much less cancer & all-cause mortality.

So I found it interesting that a meta-analysis published last Friday in BMJ found no benefit in preventing heart disease by taking multivitamins.  Of note, the authors analyzed 50 randomized controlled trials comparing 156,663 participants to 137,815 controls in order to arrive at their conclusion.  Ironically, use of multivitamins was actually linked to increase risk of angina.  But once more rigorous subgroup analyses were performed, any link or association was no longer present.  For what it's worth,  the pharmaceutical industry supplied the vitamins for those trials in which B6 and E were shown to have some benefit, which makes one wonder, hmmm . . .

Bottom line: eat right & exercise regularly to prevent heart disease.  And focus on the known risk factors rather than looking for short cuts in a bottle.

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