Friday, February 10, 2017

Post Op, Part 3

Surviving cardiac surgery permits ongoing hair loss!

Today is the one-year anniversary of my aortic valve replacement surgery, and this is my third "post-op" instalment about that experience (part 1, part 2). I'm happy to say that I feel completely normal again. I'm glad to have so far avoided endocarditis (an infection on my prosthetic valve), the risk of which is highest in the first post operative year. Anticoagulation with warfarin has been going well, with my time in the therapeutic range hovering around 90%, and no significant bleeding or clotting complications so far. Hopefully, I'll achieve a personal best in the Calgary Run for Water this summer, training for which is already underway.

I'm also happy to answer the question I've been asking since I started wrestling with my diagnosis of aortic valve regurgitation: when is the best time to intervene and replace my valve, and did I miss it?

The jury's still out on the first part of that question, but a reasonable response to the second part is 'no'.

My heart has returned to completely normal size and function. Here are the most recent values:

LVESD: 30 mm (Normal = 25-40mm)
LVEDD: 46 mm (Normal = 42-58mm)
LVEF : 0.62 (Normal = 0.55-0.70)

It's amazing how well the heart can recover despite years of volume  and pressure overload. But the best time to operate is not just the time that maintains heart size and function; it's the one that maximizes survival. I don't think that we have good data on that outcome - perhaps the mother of all outcomes - but a recent study suggests that I might have been better off to operate sooner. Of course, that's just one observational study that didn't exist at the time, and so I still feel that, prospectively, at least, good decisions were made. Heck, even retrospectively, I still think the timing of my surgery was good since my pre-op ejection fraction (EF) was not below the cut-off value at which increased long term survival was diminished in that one study.

Hopefully, I'll beat the published odds, which indicate an average life expectancy of about 15 years after aortic valve replacement. There are a few good reasons to think that I might: (1) I am younger than most patients who've had this operation and who've generated the statistics, (2) I am  meticulous about my anticoagulation and dental hygiene, (3) I have ready access to excellent quality medical care, and (4) I recognize the importance of that care and the gravity of my situation.
Ok, so I have to skate with a goofy helmet now.

One more big hope: the cause of my valve regurgitation, non-infectious aortitis, will not return.

A big thank-you to all who supported me, including my colleagues, who smoothened my absence from the hospital and clinics, my in-laws, Mark and Diane, who looked after my kids while I was in Toronto, my friends Nick Lagopoulos, Tamara Kolber, and Candice Silversides, my parents, Hans and Mary, my sister, Carla, and her husband, John, and especially, my wife, Jan, who amazed me with her devotion to my well-being. As I look back upon the time of my surgery, I do so fondly not just because all went well, but mostly because of all of the love and care that I received. I feel like a pretty lucky guy.

Saturday, January 21, 2017

With God, Everything is Permitted: How Theism Destroys Morality

This March, the bestselling novel, 'The Shack', will be released as a major motion picture starring Tim McGraw, Sam Worthington, and Octavia Spencer. The plot is well known: Mac's 3-year old daughter is kidnapped and murdered by a serial killer. In his despair, he retreats to a shack in the woods where he encounters Jesus, God, and the Holy Spirit in various forms. The book cover claims:
"In a world where religion seems increasingly irrelevant The Shack wrestles with the timeless question, where is god in a world so filled with unspeakable pain? The answer Mac gets will astound you and perhaps transform you as much as it did him."
The story in 'The Shack' is fictional, but it underscores an obvious fact: the real world we inhabit is overflowing with unimaginable suffering that serves no purpose that anybody can discern. How can theists reconcile this observation with the claim that all goes according to the plan of an omnipotent and morally perfect God? 

William P. Young, the Canadian author of 'The Shack', seems to think that this is the zinger of an answer that his masterpiece deserved: 
"I could have chosen to actively interfere in her circumstance, I could have chosen to save her from the murderer. But that was not an option for purposes that you cannot possibly understand now."-God comforting Mac regarding his daughter's gruesome murder
As immensely disappointing as that response is, it is common: God must have morally sufficient reasons to permit even heinous evil - reasons that we simply cannot understand. But as philosopher Stephen Maitzen argues (here and here), theists fail to follow this response to its logical and untenable conclusion: we have no moral obligations.

Let me explain. If God has morally sufficient reasons to permit the apparently gratuitous suffering of innocent children, then the suffering isn't really gratuitous, though it may seem that way to us. God's mysterious reasons make the suffering necessary. If it wasn’t necessary, a perfect and omnipotent being would avail himself of the other options rather than permit it. Moreover, the suffering must be necessary for the net benefit of the child because no morally perfect being would exploit a child. Well, if the suffering is necessary for the child's ultimate benefit, then we have no obligation to stop it. (The argument stops there, though I think that an even stronger case could be made, which is that we must let the suffering occur.)

If you’re having a hard time accepting that, imagine that you are an anthropologist studying a primitive tribe on a remote South Pacific Island when your young daughter becomes gravely ill with appendicitis. The surgeon among your crew points out that strapping her down for a life saving appendectomy is necessary even if few or no anesthetics are available. To the locals listening to the girl's screams, this appears to be an act of wild depravity, but you and the surgeon have a morally sufficient reason to permit the brutal operation: there is no other way to save her life. Like God in ‘The Shack’, you know of purposes that the locals cannot possibly understand.

An uninformed witness to such events would have a moral obligation to try to prevent your daughter’s abdomen from being sliced open, but if such a witness had reasons to believe that the surgeon was sane, upstanding, and extremely capable, that obligation would disappear since the operation and its attendant suffering are required to secure her survival; they're necessary for her net benefit. (An even stronger case could be made: an informed witness who prevents the surgery could only be a murderer trying to secure your daughter's certain death. And so it seems to me that if there exists a moral obligation in this situation at all, it is to ensure that the savage operation proceeds.)

Well, if God exists, then we have no moral obligation to prevent the apparently gratuitous, but actually necessary, suffering of children, and if we don't even have that moral obligation, then we have no moral obligations at all. Morality itself is destroyed.

A common response to this argument is that God has given us libertarian free will with which he must not interfere, even if doing so would prevent the intense, gratuitous suffering of children. But there are several reasons why we should reject this line of reasoning.

Firstly, Maitzen points out that, at least from a Christian perspective, on numerous occasions in the Bible, God does interfere with human free will. For example, he hardens the heart of Pharaoh (Exodus 14:8), and, as Paul tells us in the New Testament, he also hardens the hearts of others as a matter of policy (Romans 9:18). Apparently, libertarian free will isn't so important that God cannot interfere with it, and if God can harden hearts as needed, surely he can soften the hearts of those who rape and murder innocent children.

Secondly, the very idea itself that free will is more important than preventing the intense suffering of innocent children is simply outrageous; nobody really believes it. For instance, imagine that you have the opportunity, at virtually no risk to yourself, to prevent the rape of your child. Would it ever be acceptable to pass because of too much concern with preserving the free will of the rapist? Of course it wouldn’t, and it would be especially unacceptable for an omnipotent Father. God could only sacrifice his moral perfection in doing so, and if God is not morally perfect, then he does not exist.

The tension between the coexistence of God and morality as we know it cannot survive any ad hoc supremacy of the importance of libertarian free will. The only acceptable reason to permit the suffering of a child, even for God, is if it’s necessary for the net benefit of that child, and if it is, then we have no obligation to prevent it. (In fact, it seems to me that we may have a duty to permit it.)

Contrary to popular belief, Dostoyevsky had it all wrong; it’s only if God does exist, that everything is permitted. So while many theists claim that it’s our moral obligation to make this world better, ironically, it's only if God does not exist, that such moral obligations do. Morality implies atheism.

Wednesday, October 12, 2016

Why Prescribe Rivaroxaban?

First things first: I have no conflicts of interest regarding the content of this blog entry; I'm merely sharing my best interpretation of the published literature as I'm aware of it.

Rivaroxaban (Xarelto) has become the most widely used oral anticoagulant in America. Choosing one NOAC to primarily use is a good idea because one can become familiar with its dosing requirements and drug interactions and prescribe it well. This is especially true for primary care practitioners who are faced with a constant barage of new medications with which to become familiar.

But why choose Rivaroxaban?

There were three pivotal trials comparing warfarin to each of the three non-vitamin-K-dependent oral anticoagulants (NOACs) currently available in Canada: RE-LY for dabigatran, ARISTOTLE for apixaban, and ROCKET-AF for rivaroxaban. Each of those trials established the superiority of its respective NOAC over warfarin in either effectiveness (reducing stroke and systemic embolism) and/or safety (reducing major bleeding) except for one. That's right: In ROCKET-AF, rivaroxaban was merely "non-inferior" to warfarin.

It is difficult to compare the outcomes across these trials because the populations were all different, but consider this: ROCKET-AF included the highest risk patients with the highest rates of the primary outcome (stroke and systemic embolism),  placing it in the best possible position to demonstrate statistical superiority in efficacy if it was present, yet it didn't. Not only that, warfarin-treated patients in ROCKET-AF had the lowest mean time in the therapeutic range (55% in ROCKET-AF vs approximately 62-64% in the others). That means that rivaroxaban was tested against warfarin performing at its worst among these three pivotal trials, and it still couldn't come out ahead even though the others did.*

While a head-to-head comparison of the NOACs will probably never be performed (the number of patients needed to do such a trial would be truly enormous), there is mounting observational community based data that permits head-to-head comparisons of just how these drugs are actually performing in the "real world". Three such studies (available here, here, and here) have been published so far, and compared to dabigatran and apixaban, rivaroxaban has repeatedly been associated with higher rates of major bleeding and/or stroke & systemic embolism (SSE). One must be careful in interpreting these studies because the assignment to each drug is not randomized. Investigators use propensity scores to match patients for covariates that influence treatment assignment, but it is unlikely that all relevant covariates are able to be accounted for.  Accordingly, such information is to be considered hypothesis generating. Nevertheless, if one is to find one NOAC to prefer among the others, this data is enough to bolster the suspicion, based upon the pivotal trial results I described above, that rivaroxaban may not perform as well as its competitors.

There exists a ready and plausible explanation for the possible under-performance of rivaroxaban: its once-a-day (OD) dosing schedule. The half lives of rivaroxaban, apixaban and dabigatran are all around 12 hours, yet rivaroxaban is the only one available in Canada that has been tested in a once-daily (OD) dosing regimen. This has undoubtedly proven to be a marketing boon for Bayer, but only because most doctors over-estimate the compliance and adherence benefits of OD dosing versus twice-a-day dosing, which are small (please read the paper that Bayer researchers cite supporting their decision to use OD dosing). And besides, adherence among apixaban users is probably similar to adherence among rivaroxaban users.

What most prescribers aren't aware of when a drug with a half life of 12 hours is dosed OD are the consequences of missed doses and extra doses, which are subtherapeutic drug levels for prolonged periods of time (the equivalent of missing three consecutive BID doses of a competitor drug) or very high peak drug concentrations. I urge you to click on the link in the last sentence to view the paper, free-on-line, and study figures 1 & 2. It is well recognized that the safety and effectiveness of anticoagulants are closely related to the time spent in the therapeutic window, and so it may well be that by dosing rivaroxaban once-a-day, resulting in high peak concentrations, low trough concentrations, and markedly exaggerated swings when doses are accidentally missed or doubled, patients are actually being placed at unnecessary risk. And so it may well be that the consequences of the kinds of minor deviations from perfect compliance that most patients are prone to from time to time are greater for patients on rivaroxaban than its BID-dosed competitors.

I share this information with my patients so that they understand that I'm choosing to prescribe apixaban twice-a-day based on good evidence that it's both safer and more effective than warfarin. I explain to them that the twice-a-day dosing keeps them in the therapeutic window more effectively when the odd dose is missed or the odd extra one is taken. Pragmatically speaking, many patients with atrial fibrillation are already on other treatments that require them to take pills at least twice a day, so fitting apixaban into their medication schedule doesn't add to their frequency of pill-taking. Another pragmatic advantage of apixaban is that it is the least renally excreted NOAC currently available, so dose reductions are rarely required, and changes in renal function are less likely to cause bleeding. That also makes peri-procedural management of apixaban straight forward and easy to remember. Of course, if a patient refuses to consider anything other than a once-a day pill, then I prescribe rivaroxaban (or warfarin), and I'm careful to make sure that they know that they must take it with the largest meal of their day for proper absorption (a feature of rivaroxaban that complicates its implementation that is often overlooked by prescribers, in my experience).

Perhaps you disagree? If you do, please chime in in the comments section below. If I should be prescribing rivaroxaban more often, or apixaban less often, I'd certainly like to know.

*As if that wasn't enough, the warfarin assigned patients used a device to monitor their INRs at home, and Bayer and Johnson & Johnson (the makers of rivaroxaban) were aware that there were problems with this device underestimating the INR, potentially leading to more bleeding in patients on warfarin, yet they kept that information from the FDA.

Friday, August 12, 2016

Why I'll keep on flossing, thank-you.

You should floss your teeth everyday.

Knowing how much importance I place on evidence, and given the recent media hype spawned by a story by the Associated Press about the paucity of good quality evidence supporting that recommendation, you might be tempted to call me a hypocrite.

But you’d be wrong.

If you’ve been reading this blog, you’d also know that I fully recognize that we most often have to make decisions in the absence of complete or even good information (see here). And besides, as nice as it would be, we don’t need the highest quality evidence - multiple, consistent, well-conducted randomized controlled trials (RCTs) -  to provide a reasonable answer to every question.

So what is the state of the evidence regarding daily flossing? You could find that out for yourself – no media craze required – at the Cochrane Collaboration (which I’ve written about before here) who wrote:
"Twelve trials were included in this review which reported data on two outcomes (dental plaque and gum disease). Trials were of poor quality and conclusions must be viewed as unreliable. The review showed that people who brush and floss regularly have less gum bleeding compared to toothbrushing alone. There was weak, very unreliable evidence of a possible small reduction in plaque. There was no information on other measurements such as tooth decay because the trials were not long enough and detecting early stage decay between teeth is difficult."
And here's what they concluded:
"There is some evidence from twelve studies that flossing in addition to toothbrushing reduces gingivitis compared to toothbrushing alone. There is weak, very unreliable evidence from 10 studies that flossing plus toothbrushing may be associated with a small reduction in plaque at 1 and 3 months. No studies reported the effectiveness of flossing plus toothbrushing for preventing dental caries."
It should be no surprise that there are no randomized trials reporting a reduction in cavities (dental carries) among flossers compared to non-flossers. Such a study would require that large numbers of subjects be randomized and followed for years (since it takes years for carries to develop). Large, long-term studies are costly and labor intensive, and that's why they haven't been done. Who's going to pay millions of dollars to do those studies? Are you willing to cough up some money for the cause?

Perhaps the industry that profits from the manufacture of dental floss should cover the costs, but why would they when the available evidence is enough to reasonably conclude that regular flossing prevents gum disease, which is really enough to recommend it? Even if that's all that it does, you should be flossing. Never mind that there isn't evidence showing that it prevents cavities.

This is an especially important question among people like me with valvular heart disease (VHD). Gum bleeding that permits oral microbes access to the bloodstream is an important cause of infectious endocarditis: a life threatening infection on heart valve tissue. Among the most common causative microbes are oral bacteria that get into the bloodstream by way of gum injury and micro bleeding that occurs throughout regular daily life (1,2).

When I was diagnosed with VHD about 4 years ago, I started flossing every day. Prior to that, I was like Margaret Wente (whose inflammatory piece in the Globe and Mail sparked my desire to write this post), which is to say that I only flossed a day or two before seeing my dentist, and when I did, my gums always bled. But since flossing daily, my gums hardly ever bleed, and haven’t bled at all at my last 2 dental visits. I’m living proof that flossing prevents gingivitis and there is plenty of other anecdotal evidence like mine to add to the already existent and reasonably good higher-quality evidence that it does.

Another widely reported anecdote that I can speak to: despite brushing twice a day, that string used to have quite a smell when I was finished, but after a few weeks in the habit, the foul scent was gone. Preventing bad breath is another terrific reason to floss your teeth daily, don't you think?

Now, one caveat: all of my comments refer to regular (ie. daily) flossing. Intermittently flossing and stopping will likely lead to more gum bleeding because the gingivitis that causes the underlying bleeding just returns in between flossing stints. That could actually be harmful, since everybody is at risk of endocarditis (though not as at high a risk as people with VHD). But other than that, the potential risk of daily flossing is almost certainly astronomically low.

Just as we don’t need a RCT of parachutes for jumping out of airplanes, we also don’t need anymore RCTs of flossing. As tempting as it may be - because I know how unpopular the idea of regular flossing is to most people - you should not mistake an absence of evidence (or a paucity of evidence, in this case) for evidence of absence. I'm sufficiently convinced that daily flossing is having a positive impact on my oral hygiene, and perhaps even to my overall health, and you should be too.

The stakes may not be as high for you as for me, and you may reasonably decide that a reduction in gingivitis is not worth daily flossing for you, which would be fine because you'd be making a decision based upon a reasonable and well-informed interpretation of the evidence. But please, do not make the mistake that Margaret Wente and others in the media have made, which is to conclude, because it's the conclusion that they like and/or that they think their readers will like, that we should all stop flossing because there is evidence that it doesn't do any good.

That would not be fine at all.

1. Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK. Bacteremia associated with toothbrushing and dental extraction. Circulation 2008;117:3118–3125

2. Veloso TR, Amiguet M, Rousson V, Giddey M, Vouillamoz J, Moreillon P, Entenza JM. Induction of experimental endocarditis by continuous low-grade bacteremia mimicking spontaneous bacteremia in humans. Infect Immun2011;79:2006–2011.

Sunday, February 21, 2016

Post-Op, Part 2

My post-op left ventricular indices are:

Left ventricular diastolic dimension: 57 mm
Left ventricular systolic dimension: 46 mm
Left ventricular ejection fraction: 48%

I'm very encouraged by the dramatic reduction in the diastolic dimension, immediately into the normal range. Normal for me is another matter, but my LV can't shrink overnight. This reduction must purely result from having a competent valve; that is, from no longer having at least half of my enormous stroke volume rushing back into my LV. 

As Dr. Chris Simpson predicted over in the discussion at Facebook, the initial effect is seen mostly in the diastolic dimension. My systolic dimension actually increased a little bit. Accordingly, my EF dropped from 60 to 48%*, but I'm not in the least bit worried that this might represent any significant irreversible contractile dysfunction, and like Dr. Simpson, I also think that it has no known prognostic significance. 

Loading conditions are everything here, and my LV has suddenly been dramatically under-filled.

My aortic regurgitation had been significant for more than 5 years, probably more than 10, prior to operation. It's going to take years for my LV to remodel, and the available data is clear: given my LV size, if pre-op LVEF was normal, it's normal during follow up (excluding a peri-operative myocardial infarction or some other catastrophe).

As my LV physically shrinks (LV mass declines), I'm sure that my ejection fraction, which is close to normal now, will once again end up in the normal range. My read of the literature suggests that most of the changes happen in the first six months, but my surgeon told me to expect continued remodelling over 2-3 years.

It will never be the heart that I would have had without aortic regurgitation, but the available follow up data strongly suggests that it should be a heart that will last me a long time into the future without any specific anticipated problems.

Here's an interesting question for my medical colleagues: if you were me, and you knew that your post-op EF was 0.48, would you take any medication for LV dysfunction to try to help my LV remodel over time?  A beta blocker, perhaps? An ACE-I? Both? None?

*measured several times using different methods and matching visual estimates as well.

Saturday, February 20, 2016


When I was first diagnosed with severe aortic regurgitation, there was a great deal of disagreement about what to do. A significant majority of cardiologists and surgeons I saw recommended surgery within 6 months, while a small minority suggested that I could safely wait several years, perhaps even ten (or more), before requiring my valve operation.

As I wrote before, the advantage to early operation is that it minimizes the chances of waiting too long. At a certain point, as the left ventricle undergoes chronic volume overloading, irreversible contractile dysfunction develops, and I certainly didn't want to be left with a weak heart after surgery that would last the rest of my days. Not only that, we know that if one operates too late, survival is reduced.

The advantages to waiting are numerous. Firstly, it delays an event that has a mortality of about 1%. Secondly, it delays the onset of life with a mechanical valve, meaning that it delays the risks of valve clot and stroke, infection, as well as the risks of anticoagulation with warfarin. Thirdly, as soon as a valve is put in, a clock starts ticking until it will need to be replaced, too. The later one can operate, the higher the chances are that only one operation will be needed.

So whom to listen to among the disagreement was one of the early conundrums I faced after diagnosis. I decided to go with the available data which coincided with the opinion of the cardiologist most experienced in timing such operations, both indicating that I should not undergo surgery at that time but rather delay delay it as long as possible, possibly for years.

Well, after three years of following my heart size and function closely with serial ultrasound and MRI examinations, my ventricle showed clear signs of increasing in size just a little bit too much, and the opinions of all involved aligned: it was time to operate. Now we get a chance to see if my initial choice of waiting was a mistake, or not.

Three years ago, when I was diagnosed, the relevant parameters were as follows:
Left ventricular diastolic dimension: 63 mm
Left ventricular systolic dimension: 42 mm
Left ventricular ejection fraction: 54%

Pre-operatively, those parameters were:
Left ventricular diastolic dimension: 67-70 mm
Left ventricular systolic dimension: 44 mm
Left ventricular ejection fraction: 60%

What do you think those parameters are on my post-op echo? If my LV remains large and my function (ejection fraction) drops dramatically, then I probably made a mistake (though, to be fair, we must give my heart some time to remodel and get used to the new conditions of a fully competent mechanical valve). On the other hand, if my left ventricle has shrunk, and my function remains good, then we can only expect improvement over time, and I probably made the right choice to wait and enjoy three years without the burdens of a mechanical valve. (And they were three very good years.)

Chime in below with your predictions. In a few days, I'll reveal what the numbers actually are.

Sunday, January 31, 2016

Common sense is too common

The snow has finally stopped falling and you're pleased to be inside, driveway all shovelled neatly (first one on the block!), the aroma of a fresh pot of coffee permeating your home. Too bad for you that the squeezing sensation in the centre of your chest that kind of niggled while you were outside has just returned, but this time with a vengeance. Your wife calls 911 because the worried look on your face is actually worse than hers. What's the first thing paramedics will do when they arrive and learn that you're having chest pain? What's the first thing you probably want them to do?

Before even giving you an aspirin to chew, they'll probably strap on nasal prongs and give you some oxygen. After all, if you're having a heart attack, the problem is that the supply of blood, and therefore of good ol' oxygen, to your heart muscle is being choked off by a blood clot in a heart artery.

What could go wrong by giving a supplement of a natural substance that all our cells need to survive and of which those cells are being deprived?

Lots, apparently. Just click here to see the results of a clinical trial that randomly assigned 638 patients with chest pain to receive supplemental oxygen or not. Four hundred and forty one of them turned out to be having heart attacks and during followup, compared to those who just breathed ambient air, those who got the oxygen had larger heart attacks, more recurrent heart attacks, and more cardiac arrhythmias.

Traditional Chinese Medicine Store
Now just think, if oxygen turns out to be bad for you in the midst of a heart attack - a natural and "common sense" treatment given a basic understanding of the situation - what other supplements that are natural and appeal to common sense might be bad for you, too?

Supplement Store
The available data make a strong enough case to stop routinely providing supplemental oxygen to patients having chest pain and heart attacks. A time honoured treatment should no longer be employed. There is a long list of medical therapies established by common sense that are no longer offered because they've been shown in clinical trials to be ineffective or harmful (and it's an amazing list that you really should click on and see so here's another chance if you missed it before).

Tell me this: when was the last time that a supplement, herbal, or homeopathic treatment was tested by those practitioners in a clinical trial and pulled from the shelves?

Homeopathy Store
Another timely example of the failure of common sense is screening for cancer. If you have a test that can detect cancer, applying it to populations should reduce premature deaths. Simple, right? But the situation for screening is much more complicated than it seems and, in fact, screening the general population for cancer, including breast, lung, colon and prostate cancer, is probably a huge waste of time, effort, worry, and money (with the possible exception of pap smears for cervical cancer). Not only that, it probably causes more harm than good, and it's a practice that should stop. The same is true for the annual physical examination, which is going the way of the Dodo. Why? Because skeptical people put these common sense notions to the real test of randomized trials and the results weren't what common sense had predicted.

Common sense tells us that because something seems like it should work, it does work, but it's time to get humble, to became skeptical of common sense. It's time to admit that many things are far more complicated than they seem. I know that may make some people feel small and insignificant, but that's really not necessary. Evidence makes us powerful. Experts aren't necessarily smarter than you. Real experts just know the evidence better than others. By learning how to find and assess the evidence, you can become powerful, too. An easy way to get to the best understanding of the available health-related evidence is to use Cochrane, a global non-profit, non-governmental organization that you can read all about at Wikipedia here. Search your health query and Cochrane is your friend.

Voltaire said that common sense is not common. On the other hand, it seems far too common to me. In everything from philanthropy to economics, from politics to education, and beyond, what we need is less common sense, and more high quality evidence.