If you believe that weight loss is dependent solely on your caloric balance, then you would have lauded the latest study by George Bray, et. al., fresh off the presses at JAMA – get it while you can!: http://jama.ama-assn.org/content/307/1/47.full (PDF here)

Most mainstream media outlets are taking this study as confirmation of the “calories in/calories out” theory – that weight gain/loss is totally dependent on the difference between the calories you eat and the calories you expend each day – and it’s hard to imagine why they wouldn’t.  Let’s take a quick look at the parameters of the study:

• 25 people were overfed for 8 weeks to the tune of roughly 40% over their baseline consumption.  Meaning, they ate an extra 954 calories each day.
• There were 3 groups: A 6% (low) protein group; a 15% (normal) protein group; and a 25% (high) protein group.
• All groups gained different amounts of weight, but similar amounts of body fat (about 7.7lbs in each group).

Seems pretty cut and dried – despite the amount of protein the groups ate, they ended up gaining the same amount of weight.  Let’s pack up for home, right?  Wrong. Let’s take a closer look at the data.

One necessary aside: The subjects were overfed for 8 weeks in a metabolic ward (Warning: PDF), which is about as a controlled, lab-rat environment that you can put people participating in a nutrition study in.  For those of you unaware of what metabolic ward testing entails, it’s like sleep-a-way camp: There are organized times for data collection and feeding; all you can eat is what the research facility provides; and you get to enjoy all the fun of being cooped up in a “controlled environment“.  What this implies is that we can assume the data in this study is legit.  No misreporting, no sneaking in a Snickers bar after lights out, no bad food surveys or faulty recall (”What did I have for breakfast yesterday?”) – all their food was measured and prepared in the metabolic unit kitchen.

I’ll save you a whole lot of reading and reprint the Table from the study:

As reported, all three groups had nearly the same amount of gain in Fat Mass (3.66kg, 3.45kg, and 3.44kg) at the end of the study.  But look at the differences between groups.  The low-protein group lost Lean Mass (read: muscle) and correspondingly impaired their metabolisms, but not by much (see Resting Energy Expenditure, -86.1 kJ/day, which is about 21 calories, if you’re keeping score) whereas the normal and high-protein groups both raised their lean body mass (2.87kg and 3.16kg; 6.3lbs and 7lbs respectively).   So even though all groups were consistently overfed by about 1000 calories a day, very different outcomes resulted (and personally I wouldn’t be too happy if I were in the low-protein arm.  Gaining fat, losing muscle, and lowering my metabolism are not high priorities on my health watch-list).  Since all groups were overeating by the same amount (roughly 954 calories), then according to the calories in/calories out model, shouldn’t they have gained the same amount of weight?  If all the surplus calories they ate went to fat storage, then where the heck did all that new muscle come from in the normal and high protein groups?

But wait, there’s more!  Check out line item Non-Resting Energy Expenditure.  The normal protein nearly doubled their expenditure from a baseline level of 1979 kJ/day (that’s 473 cal/day) to 3275 kJ/day (1979+1296; that’s 782 cal/day).  The high protein group also increased their expenditure, by 181 cal/day.  The low protein group decided it would be better to kick back a little, raising expenditure by a paltry 59 cal/day (maybe they were tired from the loss of muscle).  Now, one wonders what could possibly account for such wild variance.  Well, the table has an answer for you: Physical Activity.  Although the lead researcher has stated that there was no formalized exercise during the 10-12 week trial, it’s well established that energy expenditure can increase significantly through NEAT (warning: PDF). If the calories in/calories out model held true, wouldn’t the normal and high protein groups have gained less fat than the low protein group, since all 3 groups were eating roughly the same amount of calories, but were burning significantly different amounts of calories?

Is there any way to reconcile the fact that all of the groups gained roughly the same amount of fat? Aside from calories, was there anything else held constant in all three groups?  Quoted from the study:

Absolute carbohydrate intake was kept constant throughout the study.

All groups consumed 41% of their calories from carbs – that’s about about 250 grams of carbs per day.  And they were exactly the kinds of carbs you’d expect; foods that drive up insulin and promote fat storage:

The eating plans that Bray and his colleagues used included food you’d find in the typical American diet: eggs, bacon, biscuits or cereal for breakfast, for instance; tuna salad, turkey sandwiches and chips for lunch; pasta, rice, pork chops or casserole for dinner, accompanied by salads and fruit; and plenty of baked goods, candy and other processed sweets for snacks and dessert.

So, mystery solved: You could posit that the reason the three groups all gained the same amount of fat is that they were all eating enough carbohydrate to cause high levels of insulin, which would promote fat storage, particularly if you were, say, eating an extra thousand calories a day (which all three groups were).  This would neatly explain why the higher protein groups gained muscle while the low protein group lost muscle (and slowed down their metabolisms in the process) and would explain the thorny issue of different energy expenditure (and consequently, different caloric balances) between the three groups.

So we arrive at three conclusions based on Bray’s research:

1) Low intake of protein while overeating seems to have compound negative effects.  It slows metabolism and results in loss of lean tissue.  So despite what your latest cleanse guru told you, there is a minimum amount of protein intake necessary to “run the ship”, and that minimum is probably higher than the official government recommendations.

2) It’s unlikely that caloric balance was responsible for the similar fat gain between the low, normal, and high protein groups, since the three groups exhibited big differences in expenditure.  In other words, the math doesn’t work out.  What’s more likely is that similarities in the diet composition (the carb intake, in other words) caused the fat gains to be equal across the groups.

and

3) Always check the data.  It’ll tell you what the real story is.

From CNN.com.

It should surprise no one in the health or medical field that the diabetes drug Avandia is linked to an increased risk of heart attacks (at least, not after Steven Nissen’s 2007 study of Avandia).  Unfortunately, for most doctors, Plan B is to simply prescribe another drug.

“Don’t worry about the Avandia scare, Mrs. Jones; here, just take Actos or Glynase instead.”

Until some “rogue independent researcher” publishes a meta-analysis showing those drugs will kill you as well, that is.

There is an alternative solution to this problem.  Beware: It’ll require some critical thinking on your part.

1) Understand and acknowledge the role insulin resistance has in diabetes.

2) Understand which foods and foodstuffs raise insulin levels.

3) Avoid eating said foods and foodstuffs.

4) Move around a little bit.  It’d be better if you exercised. It’d be even better if you strength trained.

There you have it.  No 342 page report or dubious drug prescriptions required.

Chris points us to an interesting study involving circadian rhythm and weight gain (to be fair, Melissa sent it to me first, but she doesn’t have a blog).  In the study, nocturnal rats fed during what would have been their sleeping hours gained more weight than rats fed during their waking hours, despite the same overall intake and energy expenditure.

(BTW, if any of you have the full text of the study, might I request a copy?  Pretty please?)

What’s interesting to me is not just the physiological implications of the study (that there might be some unique mechanism that causes animals to store fat more effectively during their snoozing hours), but the statements the obesity experts were quoted as saying:

“How or why a person gains weight is very complicated, but it is clearly not just calories in and calories out,” said Fred Turek, from the Northwestern’s Center for Sleep and Circadian Biology, where the research took place.  “Better timing of meals could be a critical element in slowing the ever-increasing incidence of obesity.”

and

Tam Fry, from the National Obesity Forum, agreed. He said: “It is groundbreaking. It really gets you thinking why this has not been done before.  It could be very dramatic if it affects whether you are going to get fat or not.”

Are you kidding me?

“Better timing of meals?”

“Groundbreaking?”

“Affects whether you are going to get fat or not?”

The study looked at rats that were eating during their sleeping hours.  While I don’t doubt there are some overfat folks eating during the hours they should be sleeping, I highly doubt that 64% of Americans are waking up in the middle of the night and chowing down.  Or perhaps they’re suggesting we’re all operating on schedules that run counter to our normal Circadian rhythms? And these guys are supposed to be experts?

What these folks do is what clients and trainees often do – they lose the forest for the trees.  It’s all too easy to get bogged down in the myriad details of the (admittedly) complex picture of fat loss and lose sight of the one or two most important things which, if done consistently, would yield you 80% or more of the results you’re looking for.  Believe me, if you’re having trouble losing weight, it isn’t because you should be on vampire hours.

There’s nothing wrong with seeking new information or looking to add to your understanding.  But figure out how it falls into the larger picture.

Gretchen Reynolds recently had a couple of interesting stories in the NY Times:

Can You Get Fit in Six Minutes a Week?

Is Your Ab Workout Hurting Your Back?

Re: Getting Fit in Six Minutes a Week:

The take-home message is that researchers found that higher intensity (read: effort) yet short duration exercise bouts conferred equal endurance benefits as exercising at a lower intensity nearly 50 times longer.  In other words, by working your tail off for a few minutes, you’d receive the same physiological benefit as someone who spent 5000% more time at the gym but merely plodded along.

That, I’d say, is significant.  Work hard, kiddies.

With regards to the ab story, all I have to say is:

1. Most of Dr. McGill’s research (neat as it is) was done on spines from human cadavers.  Cadaverous tissue, being dead, doesn’t respond the same way as tissue in a live (read: warm) human body – it is much less elastic and pliable.  So much of the high force data McGill obtained is tainted by the inherent rigidity of cadaverous tissue (since you’ll register higher forces on a more rigid object).

2. Those who advocated “sucking in the abs” as opposed to “bracing” confused contraction with stability.  In the same vein, tightening your shoulder muscles doesn’t mean “pull your shoulders up to your ears.”

3. Unless you’ve got a specific spinal problem you’re working on (with a qualified professional, I hope), you’ll be well served by working the basic exercises with a heavy (for you) weight.  Performing multi-joint exercises that require abdominal stability will adequately work your core.  Am I saying don’t do side bridges or bird dogs?  No.  But what I am saying is if you’re crunched for time, get your squats in first.

Picked this up from Conditioning Research (thanks Chris):

Optimizing performance by improving core stability and core strength.

Allow me to summarize the study for you:  There’s little to no hard science recommending core work for athletes.  Now, before you get all up in arms and start screaming about instability leading to injury and how the researchers probably did ab work thinking it was “core work”, etc., I’d like to make my position clear:

The study isn’t saying, “Don’t do core work with athletes – ever.”  In fact, the study is pretty clear that in rehabilitation, core strengthening shows marked effectiveness.  It’s saying that in the non-injured athlete, improvements in core stability and strength don’t translate to improved performance.

Mostly what the study addresses is the issue of time.  Whether you’re an elite-level baseball player with a multi-million dollar contract or a weekend warrior with a 3.0 NRTP tennis rating, you’re limited by the constraint of time (of course, if you’re a professional athlete, you’ll have more time to train than if you’re a recreational athlete, but that doesn’t change the fact that training time is finite).  You only have so much time to develop fluency in all aspects of the game  (conditioning, strength, skill, timing, etc. ); even less so if you factor in recovery.

If you’ve only a limited time to work on your game, why waste your time on things that don’t improve performance?  Particularly if you’re a pro and your time is so valuable?

Of course, this applies to you even if you look upon exercise with as much delight as you do cleaning the toilet.  Engage in activities that give you the biggest bang for your buck.  Perform exercise that will actively improve your quality of life (and, perhaps, your longevity as well).  Translated: Don’t waste your time in that Core Fusion class.  Go pick up something heavy.

Today’s New England Journal of Medicine had a special surprise for anyone interested in diet composition and weight loss.  By now, you’ve undoubtedly read or heard one of the headlines:

Want To Lose Weight?  Just Eat Less.

It’s Not What You Eat, It’s How Much.

Stick To a Low-Cal Diet and It Will Work. (This was my personal favorite.  What an awful headline.)

You’d be forgiven for thinking that this newest study proved, once and for all, weight loss ultimately comes down to calories in – calories out.  But it contains some glaring errors that skew the results, and you savvy readers out there will probably be able to identify them right away (particularly if you read the full text of the study – get it while you can!).

Here’s a summary of the study: 811 overweight adults were assigned to one of four diets: low-carb, low-fat, high-fat, and high-protein.  They were offered group and individual instruction in the diets and followed for two years.  The researchers measured weight loss and waist circumference.

The main problem I have with the study design – the nutritional breakdown of the diets:

* Low-fat, average-protein diet made up of 20 percent fat, 15 percent protein and 65 percent carbohydrates.
* Low-fat, high-protein diet of 20 percent fat, 25 percent protein and 55 percent carbohydrates.
* High-fat, average-protein plan containing 40 percent fat, 15 percent protein and 45 percent carbohydrates.
* High-fat, high-protein diet of 40 percent fat, 25 percent protein and 35 percent carbohydrates.

You can see where they went wrong here – based on the data in the study, none of the diets contain any less than 140 grams of carbohydrates (the so-called “low-carb” group).  And if you’re a regular reader of this blog or a low-carb aficionado, you know that 140 grams of carb intake is anything but “low-carb.”  At intakes of greater than 60-80 grams of carbs daily, you really don’t get much of the benefits of a low carb diet (insulin levels still trend too high).  But to achieve those levels of carb intake, the percentages would have to be much more heavily skewed towards fat – which, for researchers touting the current nutritional status quo – is a big NO-NO.

Consider this quote from the study:

Other goals for all groups were that the diets should include 8% or less of saturated fat, at least 20 g of dietary fiber per day, and 150 mg or less of cholesterol per 1000 kcal.

At 215 mg of cholesterol, I guess eggs are out (since at 1600 calories your daily limit is 240 mg of cholesterol).  You know, cholesterol and heart disease?  No connection. Saturated fat and heart disease?  No connection.  Someone should tell these guys.

No doubt low-fat experts like Dr. Joel Fuhrman will argue that his diet (at a whopping 10% of calories from fat) is grossly misrepresented as well and as such didn’t get a fair shake.  While I generally disagree with his diet conclusions, on this point, he’d be right.

Taking a cursory look at the composition of the different diets reveals that…well, they’re not all that different.  The Supplementary Appendix shows a listing of sample menus that the study participants were encouraged to follow.  Now, you tell me; does this look like a “low-carb diet” to you?

Breakfast:  Boiled or poached egg, whole wheat bagel w/lowfat cream cheese, cup of skim milk

Lunch: Turkey, whole wheat spaghetti, vegetable medley, one small banana

Dinner: Roast beef, one potato, mixed vegetables, cabbage salad w/walnuts, tiny box of raisins

Snack: Cup of skim milk and a graham cracker

If you’re eating bagels and crackers, let’s face it; you’re not eating a low-carb diet.  But before you take my rantings as a complete dismissal of all scientific inquiry, let me qualify everything and say I understand it’s not their fault.  The researchers are operating under incorrect premises (i.e., too much fat and cholesterol is bad for you) and as such are limited by that – the whole “Do No Harm” thing.  Think of it this way:  If they thought vegetables were toxic at a dose of greater than 500 calories per day, then they’d be ethically bound to limit the groups to 500 calories’ worth of vegetables (that might make for even more awkward study design).

But that’s enough quibbling.  Let’s take a look at some of the interesting data:

• As per usual, the groups had a tough time sticking to their respective programs but did better than most study participants.  They ended up with an average weight loss of 4kg (about 9 lbs).
• The lowest carb group increased their HDL level to a greater extent than other groups; the highest-carb group fared worst.
• “All the diets except the one with the highest carbohydrate content decreased fasting serum insulin levels by 6 to 12%; the decrease was larger with the high-protein diet than with the average-protein diet.”  This means that the greater you reduce carb intake, the greater the improvement in insulin sensitivity – and we all know that’s a good thing.
• An interesting finding:  The two groups that saw the least “improvement” in LDL levels were the highest-fat and the lowest-carb group.  This is probably due to an increase in the “large, fluffy” LDL particles and not the compact LDL (prone to oxidation).  If that was over your head, read this – or, just take my word that the smaller, more compact LDL particles are what predispose you to heart disease.

The last word:  The baseline data shows that virtually all participants were eating in excess of 2000 calories and 225 grams of carbs per day – yikes.  Reducing calories from 2000 to 1600 is going to make a positive impact health-wise when weight is lost.  And I’m not saying that reducing calories (independent of diet content) won’t result in weight loss – it will.  But a well-intentioned but poorly-designed study like this one does nothing but muddy the issue.  Sustaining insulin sensitivity is important.  Controlling blood sugar and hormonal tone (so you don’t get hungry; so fat-burning occurs as opposed to fat-storing) is important.  And you can do both those things better on a true low-carb diet than on a low-fat diet.

Edit (2/27/09):  Jeff points out that “both the “high protein” and “low carbohydrate” groups had favorable changes in waist size compared to the “low protein” and “high carbohydrate” groups respectively.”  Meaning, those groups probably lost more fat (as opposed to merely “weight”) than the higher carb groups.  Nice pick-up.

Last week I posted on the JUPITER study and the media hoopla surrounding it.

Well, looks like they’re not done yet:

Eat Your Statins.

“Eat Your Statins?“  For heaven’s sake.

There’s not much in this article that hasn’t been discussed or debunked at length on this and other blogs, but a couple of lines are worth highlighting:

The drugs have side effects, including muscle weakening, that can be dangerous in some cases. Nobody is advocating putting really healthy patients on statins.

Really?  Consider these selections, taken straight from the article:

1. But low-risk people would need to be treated to make a dent in the one-third of American deaths (that’s 800,000) caused by heart attacks and strokes.
2. Sidney Wolfe of the watchdog group Public Citizen says “the message that has come off Jupiter is that people who are otherwise very healthy can benefit from statins.”

If you redefine “healthy” to mean high levels of inflammation, that is.

But like all articles of this kind, you can find a diamond in the rough if you look hard enough:

Hunter-gatherers, who fed on fish, lean meat and fibrous veggies, had levels of low-density lipoprotein, or bad cholesterol, between 50 and 75 milligrams per deciliter, half the level for the average American. (emphasis mine)

So maybe the headline should read, “Eat Your Meat and Leaves” instead; it’s a whole lot cheaper – and a whole lot tastier, to boot.

For those of you scratching your heads and saying, “What the heck is JUPITER?”, JUPITER is the latest study purporting to show cardiovascular benefit from taking statins.  In other words – take a statin, prevent a heart attack.  After the disastrous results of the ENHANCE study, statin supporters really needed a win – and they apparently got one in JUPITER (or did they?  Skip to the last paragraph in this post for the punchline; otherwise, read on).

(For the interested – my favorite article on the JUPITER study, and the actual study itself.)

Some necessary science:

If you’re a regular reader of my blog, you’ll know that I’m no fan of statins.  Why?  Because they are used to lower cholesterol levels in an effort to reduce incidence of heart disease.  What’s so bad about that, you ask?  First, there’s really no compelling evidence to suggest that cholesterol levels are tied to heart disease, so trying to thwart heart disease by reducing cholesterol – specious at best.  Second, there’s ample evidence (and plenty of reports) that statins cause nasty side effects – liver damage and muscle wasting, to name two outstanding ones.

A drug that doesn’t do what it purports to do, while injuring the patient who’s taking it?  Sounds iffy to me.

It’s undeniable that statins do decrease cholesterol levels, and that they’ve been to shown to have a (slight) protective effect in males over the age of 65 who’ve had a previous cardiac event (and no beneficial effect to all other groups).  But what’s been disputed is just how they deliver that benefit.  After all, if lowering cholesterol doesn’t protect against heart disease, then what’s providing the protective effect?

Answer: Decreased inflammation.

Chris Masterjohn’s awesome chart shows that increased inflammation causes levels of cholesterol to rise, and that statins decrease cholesterol production indirectly by inhibiting HMG CoA reductase (and consequently, decreasing mevalonate production – a precursor for cholesterol synthesis).  Note that by affecting the pathway so high up, statins have other effects as well (decreased Rho activation, for one).

In simple English – statins don’t work by walking up to rogue LDL particles and hacking them into tiny pieces, they prevent the body from making them altogether by cutting off the supply of raw materials.  And cutting off these raw materials makes it so that the body can’t manufacture other compounds, either; some that lead to harmful outcomes (i.e., inflammation).

C-reactive protein is a marker for inflammation; the more CRP you have, the more inflammation you have.  And as you can guess, that isn’t a good thing for longevity.  Well, it turns out that because subjects in the study had low LDL and total cholesterol levels but high CRP levels, the JUPITER study may force doctors to reevaluate the validity of the lipid hypothesis (that cholesterol causes heart disease).

I guess you could say that’s the one good thing to come out of the JUPITER study.

Ok, so enough dancing around it – the punchline:

The study was originally meant to track all patients for five years, but the results were so robust that it was terminated after a median follow-up of 1.9 years. In March an independent panel of observers halted it because they considered the effects of the drug to be so beneficial that it would have been unethical to keep the control group on a placebo (emphasis mine).

Oh really?  Is that the reason why?  Or could it be because of this (quoted from the actual study):

The rosuvastatin group did not have a significant increase in myopathy or cancer but did have a higher incidence of physician-reported diabetes (emphasis mine).

Did the independent panel really halt the trial because they were oh-so concerned for the well-being of the placebo group?  Or was it because they were worried that the wonderful results of the Crestor group would be slightly marred if they developed diabetes?

Or could it be that they halted the trial because they got what they wanted (great results for the statin group) and wanted to stop before any of the long-term problems that plagued participants of prior studies (like cancer and stroke in the ENHANCE and SEAS studies) had a chance to develop?  In his insightful post on this topic, Dr. Eades mentions that:

…it is typical for an outside group to take a peek at the data at certain milestones to make sure the study medication isn’t killing people…I’ve never seen a study halted because the placebo group was dying at higher rates. That really makes me wonder.

I don’t doubt that there was foul play afoot.  After all,

…physician-reported diabetes was more frequent in the rosuvastatin group; these events were not adjudicated by the end-point committee.

“We didn’t study it so it didn’t happen”, or something like that.  Sounds like they got out while the gettin’ was good.

UPDATE #1: Peter shows us why it’s so important to look at the actual data.  Deaths from cardiovascular disease in the statin group were higher than the controls (the controls had more incidence of CV disease, but fewer deaths).

UPDATE #2: Sandy’s review of JUPITER is ridiculously awesome.  Set aside an hour and read it.

Lou points me to this article, which inspires me to beat up on statins a little more.

Earlier this year, the ENHANCE study pointed to a greater chance of cardiovascular death in folks taking a statin than controls. In fact, the greater the statin’s effect (the lower the patients’ LDL went), the greater the level of atherosclerosis! The statin in question? Vytorin, from Merck/Schering-Plough.

Well, in July, another study came out – the SEAS study. What the SEAS study showed was that patients on Vytorin had a greater, statistically significant chance of developing cancer vs. patients who were not taking Vytorin. In other words, take Vytorin, and you’re more likely to die of cancer.

This isn’t much of an intellectual leap – the science clearly shows that the lower your LDL cholesterol is, the greater your chance of dying. All-cause mortality increases, and patients tend not to die of (just) heart disease, but of liver disorders, mental disease, and cancers.

The makers of Vytorin, of course, claimed was that there was no discernible reason that the drug should cause an increase in cancer deaths and released a report by epidemiologist Sir Richard Peto that showed the cancer deaths to be statistical error.

“But, at the same time, they presented an analysis by Oxford University’s Sir Richard Peto, who argued there is “no credible evidence” of a link between the active ingredient in Vytorin and Zetia and cancer.

“I don’t think there is any evidence of hazard here,” concluded Sir Richard Peto, a cancer epidemiologist who is helping lead one of the drug company-sponsored studies.”

But are they merely error? Or is Sir Peto in err?

Well, Thomas Fleming, statistician at the University of Washington, doesn’t think the data should be blown off so quickly. Check out his awesome editorial in the New England Journal of Medicine, published yesterday. I’ll translate Dr. Fleming’s phD-speak into English:

Vytorin has a side-effect that probably promotes cancer (it blocks absorption of phytonutrients that are known cancer-fighters), so it’s probably worth looking into. Don’t just take this guy’s massaging of the data at face value; let’s test it. Besides, the data wasn’t even what the researchers were looking for – they just happened to notice their patients dying of cancer – so the data really isn’t that useful anyway. We need more and specifically-designed trials before we say, “Don’t worry, Mr. Jones. This pill is perfectly safe.”

It sounds almost comical. But contrast that with a quote from cardiologist Dr. Christer Hoglund:

“We don’t know that this drug is bad, but we don’t know that it’s any good either.”

Then why take it? And yet, cardiologists still prescribe Vytorin for heart patients. It goes to show, just because a drug has an incredibly delightful advertising campaign doesn’t mean it does anything good for you.

Let the buyer beware.

Told you to toss your statins, kiddies.

Fish Oil Outperforms Statin in Heart Failure Study.

According to this new study, published in the British medical journal The Lancet, a fish oil supplement containing 1 gram of Omega 3 fatty acids (EPA, DHA) slightly outperformed the statin Crestor in preventing death from heart disease. Most of the regular readers of this blog won’t be surprised by the study findings, nor will they be surprised by the reactions from medical professionals:

“The result doesn’t mean that a statin should not be prescribed for someone with heart failure and high cholesterol, Fonarow said. “There were no safety concerns,” he said. “The drug was well tolerated. It indicates that heart failure, in and of itself, should not be reason to start a patient on a statin.”"

Well, it stands to reason, if the heart disease isn’t the reason to start a patient on a statin, then what is? High cholesterol? And what does the high cholesterol supposedly lead to? A heart…nevermind.

It’s certainly a different take than what the co-chair of the study’s steering committee had to say:

“Speaking to the media, Tognoni said that the prescription of rosuvastatin or any statin to patients with heart failure should not be considered because the use of the cholesterol-lowering drugs does not translate into any clinically meaningful benefit for heart-failure patients.” (emphasis mine)

It’s instructive to note that similar results were found in two prior studies, JELIS and an earlier version of GISSI. However, those studies weren’t double-blind, placebo studies, meaning that the results could have been biased. Not so with the GISSI-HF trial.

What’s also encouraging?  That these results were seen in folks who already had a cardiac event, were ostensibly doing all they could to prevent another cardiac event, and were taking a reasonable dosage of fish oil (1 gram a day isn’t that much -  Dr. John Berardi recommends upwards of 6-12 grams per day!).

Bottom line: Keep taking fish oil (at least, those of you who aren’t allergic to seafood), and stay away from the statins.

The final word has to belong to Dr. Philip Poole-Wilson, who also commented about GISSI-HF:

“When the trial was designed, some even expressed concern that it was unethical to randomize heart-failure patients to placebo because they were so confident of the benefit of statin therapy in this patient population. The results, he said, ultimately should humble researchers, especially as they serve as reminder that medical decisions should be guided “by science, and not strongly held opinion.”” (emphasis mine)

Hear, hear.