by Alex Boersma

We all know that salt is bad for you.  We’ve heard it since we were kids.  Most of us can probably remember our mothers taking the salt shaker away from our pot-bellied fathers, chastising them for risking their lives by putting SALT on their food.  Today, the venerable salt shaker has gone missing from the every-day dinner table.  Sure, it still makes the occasional guest appearance at Thanksgiving and Christmas dinner, but even then, we try to put our hands on it only when nobody else is looking.

Most people accept as a given that salt consumption causes high blood pressure and heart disease.  As somewhat of a health skeptic, I have for some time had concerns about the certainty with which this salt – blood pressure – heart disease link is proclaimed.  But because of the strength of the consensus on salt and the lack of solid evidence refuting said link, I have kept my reservations to myself.  In the past year, however, the controversy over salt has reached a crescendo in the medical journals and has even spilled over into the more mainstream media.  It is time to come out of the salt closet and take a stand.  It is time to give the salt – blood pressure – heart disease hypothesis the licking it deserves.

Licking the salt hypothesis

Let’s begin with what the science says.  Here are the conclusions of a recent meta-analysis of prospective studies into the relationship between salt consumption and cardiovascular disease:

 ”High salt intake is associated with significantly increased risk of stroke and total cardiovascular disease.”

Compare that quote to this study, which seem to have come up with an entirely different set of conclusions:

“…a sodium excretion of less than 3 g per day (most health authorities recommend between 1.5 and 2.5 g/day) was associated with increased risk of CV mortality and hospitalization for CHF (coronary heart failure)“

Similarly, a recent Cochrane analysis  indicates that although salt restriction may minimally reduce blood pressure in some people, it also negatively affects a number of hormones responsible for regulating blood pressure and kidney function while simultaneously increasing both total cholesterol and triglyceride levels.

WHAT GIVES?

A recent article in Scientific American entitled “Its Time to End the War on Salt” outlines the problem.  As usual with medical/scientific consensus, the burden of proof behind the salt hypothesis is found to be seriously wanting.  The idea that salt causes high blood pressure originated with a 197o’s researcher named Lewis Dahl who proved that if you feed rats 100 times the human equivalent of recommended salt intake, then, surprise surprise, their blood pressure goes up.  Since then, a number of prospective studies (remember prospective studies – otherwise known as epidemiology – otherwise known as interesting for making observations but absolutely useless for proving anything!!!) have come up with a number of ambiguous results which kinda/sorta/maybe support Dahl’s conclusions.  The meta-analysis quoted above is just a summary of the findings from all these kinda/sorta/maybe studies.  And if you actually read the study, you will see that although the association between salt intake and vascular disease is, indeed, significant from a statistical perspective, it is by no means impressive from a “how does that affect me” perspective.  Very few of the studies included had significant results of any kind, but when the researchers pooled them all together they were just barely able to eke out some statistical significance.  In the end, if you participated in one of these studies, you had about a 6% chance of having a heart attack or stroke, regardless of how much salt you ate. But if you were foolish enough to eat a high salt diet while participating in one of these studies, you had about a 7% chance of having a heart attack or stroke.  Statistically significant?  Sure.  Significant enough to warrant foregoing the venerable salt shaker?  Not so much!

And remember, none of these studies were intervention studies.  The researchers weren’t exactly feeding people an extra tablespoon of salt every day to see what happened to them.  Instead, they were merely measuring how much salt was in each person’s regular diet. What kind of regular diet is a high salt diet?  How about a fast food diet, or a highly processed diet?  And what kind of people eat highly processed or fast food diets? How about really busy people, stressed people, poor people, or people who just couldn’t give a lick of salt about the quality of their diet?

If you have a high salt diet, chances are you also have a high crap diet!

Any chance that might confound the study results?

The truth is that most of us have these organs called kidneys which, if they are working properly, should be able to adapt to a wide variety in salt intake.  Sure, if you spend your day eating olives, beef jerky and potato chips, there is a good chance you might wake up the next morning spitting tumbleweeds and looking like a puffer fish.  But if you keep it up with the olives, jerky and chips, there is also a good chance your kidneys will adjust to the increased salt intake and start sending all that salt (and water) through your bladder instead of your skin.  It is only when your kidneys (or at least the hormones that control your kidneys) stop processing the salt appropriately that the extra salt starts messing with your blood pressure.  Ironicly enough, low levels of salt intake (down below 2 grams/day…around where the salt dictocrats want your salt consumption to be) are more likely to mess with hormonal control of salt than high levels of salt consumption.

Even more ironically, the advice to severely restrict sodium intake  if you are at moderate to high risk for heart disease may be doing a lot more harm than good.  In this study, patients undergoing treatment for congestive heart failure were 3 times more likely to get re-admitted if they were on low salt diets, and 2.5 times more likely to die.  Out of 114 low salters, 15 were dead after 6 months.  Amongst the 116 high salters, only 6 were dead after 6 months.  Now that’s what I call significant!  And remember, this was a randomized controlled study…you know, the kind that actually means something!

In a similar vein, it seems that patients with type 1 diabetes and type II diabetes do not thrive on low salt diets. Granted, these are epidemiological studies, but still?  I’m not saying that low salt diets are killing diabetics, I’m just saying that they don’t seem to be doing any good.  And for diabetics – who are notorious for developing heart disease - maybe the focus should be on losing weight or getting active, two interventions which have proven to be much more effective than making your food taste like cardboard. 

Furthermore..it seems that there are more minerals involved in blood pressure modulation than sodium alone.  It seems that potassium is at least as important as sodium, while the ratio of sodium to potassium seems to have a much more significant association with heart disease than sodium on its own.   As this Archives of Internal Medicine paper concludes, “A higher sodium to potassium excretion ratio is associated with increased risk of subsequent CVD, with an effect stronger than that of sodium or potassium alone”. 

Here’s the thing.

As with just about anything in the field of nutrition and health, the association between salt intake and disease can be described by a J or U curve.  We know for sure that consuming less than 800mg of sodium a day is associated with negative health outcomes.  Likewise, we know for sure that consuming more than 8 grams of sodium a day is associated with negative health outcomes. In between, there is a curve which is by no means clearly defined.  It probably looks something like one of these:

from JAMA. 2011;306(20):2229-2238. doi:10.1001/jama.2011.1729

Again, this is just epidemiology, but since the whole “salt is bad for you” hypothesis is based almost entirely on epidemiology, I just don’t get where these associations lead us to believe that sodium should be restricted below 2 grams per day.  As you can plainly see, all the graphs above show less cardiovascular disease around 4 g/day than below 2g/d.  Even strokes, which seem to react best to low sodium, are for some reason less frequent around 6g/day than they are around 2g/day.

Don’t get me wrong!

There are certainly people who’s blood pressure reacts catastrophically to a high salt diet.  This reaction seems to be genetically programmed.  Black people, for example, do not seem to do well with excess sodium.  Perhaps they evolved in an environment where the ability to conserve sodium was much more highly developed than the ability to excrete it.  Likewise, other races and other individuals probably also have less tolerance for salt.  People with kidney disease and possibly those with kidney stones should probably be careful with salt.  The point is, if your blood pressure is chronically elevated, lowering your sodium intake is certainly a worthwhile way to try and bring it down.

But it is by no means the only thing you should be doing!  I can’t tell you the number of people I’ve heard of who spend 3 months on a low salt diet and then jump directly to blood pressure medication.  If I was more inclined to theorize conspiratorially, I might suggest that the medical community places so much emphasis on salt because it knows salt reduction will be ineffective for most people and it will then be able to convince these same people to spend the rest of their lives on highly profitable blood pressure medication.  Let’s not go there!  The more likely explanation for this mostly futile assault on flavour is that salt is an easy target.  We all know that nobody heeds advice to eat less, move more, forgo processed food, eat plenty of fruits and vegetables and reduce stress.  What, those things actually work to decrease blood pressure and reduce heart disease?  Never mind, people won’t do those things anyway!  Let’s just tell them to eat less salt, and if that doesn’t work, there are always statins, diuretics and ACE inhibitors!  We can even give the food processors little check marks and hearts on their packaging if they bring their sodium content down.  Sure they will replace the salt flavour with sugar and artificial flavour, but if people get sick from these things, perhaps we can sell them some more pills to deal with whatever ails them.

Oh yeah, I said we weren’t going to go there.

Salt makes bland food taste good.  Broccoli tastes like cardboard.  Steamed broccoli tastes like wet cardboard.  Steamed broccoli with butter and salt tastes like candy!  Real health, as far as I am concerned, depends on the consumption of real food.  If adding salt to your diet means eating more real food and less processed crap, I say “pass the salt”.  I contend that, for most people, it is not the salt in their food which is giving them high blood pressure.  It is the food in their salt!  In ”Supersize Me”, Morgan Spurlock’s blood pressure rose from 120/80 to 150/90 after eating nothing but McDonald’s food for a month.  But was it the high sodium in the diet which caused his blood pressure to skyrocket, or was it the fact that he was eating over 5000 calories a day of nutritionally devoid processed food, ballooning his weight while turning his liver into foi gras?

The problem with the low-salt agenda is not so much the lack of supporting science or the possibility that it might be doing more harm than good.  The problem with the low-salt agenda is that it takes the focus off the righteous culprits in hypertension.  Salt consumption is, for most people, at best a minor factor in the control of blood pressure. You want to keep your blood pressure down?  That’s simple.  Eat real food, maintain a normal body weight, be active daily, and reduce or control stress in your life. 

 OK.  I didn’t say it was easy, I said it was simple. 

by Alex Boersma

Make no mistake.  This is a rant.  If the heading above offends you, I suggest you stop reading now.  It ain’t gonna get any better!  But if you are genuinely concerned about your child’s weight, I suggest you tough it out.  You can and should be the one to save your child from the lifelong affects of battling with weight.  If you’re not going to do it, who will?

adapted from stats Canada here

In 2004, more than 27% of Canadian children were overweight.  Almost 9% were obese!  It is now 2012, and just by looking around I am going to go out on a limb and predict that those numbers have not dropped.  To say that this is a monumental societal fail would clearly be an understatement.  Our society has engineered this impending health disaster with meticulous care.  We have processed our food into highly palatable, biologically addictive, nutritiously deficient and calorically dense “products”  We have spent billions of dollars marketing this frankenfood, with much of that targeted directly at children.  Our governments have supported and endorsed this lunacy by subsidizing the food processors while thumbing their noses at purveyors of real food.   And we, parents and consumers, have brought this crap home by the trunk-load because it is cheap, because it is convenient and because, for the most part, we have no idea just how much damage it is doing.

As if that weren’t enough, we have exacerbated this nutritional quagmire by practically eliminating physical activity from our children’s daily lives.  Gym classes are going the way of the Do-Do, replaced primarily by something called DPA, which, as far as I can tell, stands for Don’t Perspire Anymore!  Balls have been banned, running is often discouraged, and whatever you do, don’t play tag because you might actually touch somebody!  And what’s up with not walking to school?  God gave our children two feet expressly for the purpose of walking to school…preferably uphill both ways barefoot in two feet of snow!  If God wanted our kids to arrive at school in the back of a gas guzzling SUV he would have brought them into this world with a booster seat and a gas card! 

Our kids are getting fat!  Look around!  Is it really normal for more than a quarter of our kids to have muffin tops and jelly bellies?  Is it right that our kids need spandex in their jeans almost as badly as their parents do?  I know we live in politically correct times and all, but let’s call a fat kid a fat kid (just not to his face) and admit that the health of our children has gone decidedly FUBAR.

Something needs to be done.  Not by the government.  Not by the health authorities.  Not by the school boards.  Not by big industry.  Something needs to be done by big mommy and big daddy.  Remember them?  The grown-ups?  The ones who make the decisions in the family?  The ones who actually bring the trunk-loads of frankenfood from the grocery shelves to the pantry shelves where the children can get their chubby little hands on them ad libitum!   

Something needs to be done now.  If we don’t do something now, then today’s adult obesity epidemic – you know, the one where 61% of Canadians are overweight – is going to look like a walk in health paradise compared to what will happen when our kids get all middle aged.  If we don’t do something for our kids now, then we might as well book them tickets on the WALL-E spaceship AXIOM.

All Aboard The Good Ship Axiom – Fatties and Frankenfoods Only

This isn’t rocket science.  We can talk macro-nutrients and micro-nutrients.  We can talk genetics and epigenetics.  We can talk mitochondrial breakdown and insulin resistance.  We can talk till we’re blue in the face (or, as most of my readers can probably attest – till we bore ourselves to sleep) but our children don’t need more research, more diet books, more low fat foods or more “nutritionists in the classroom”.  They need somebody to keep their chubby little fingers out of the pantry.  They need somebody to pack them a lunch made of real food.  They need somebody to kick them off the X-Box and onto the street.  They need somebody to make them a dinner with recognizable food in it and then sit down and eat it with them.  They need somebody to sign them up for soccer or hockey or football, to take them to their practices, to cheer for them when they win and to console them when they lose.

Genetics Schmenetics!

For every overweight kid out there, I suspect there is an equally overweight parent rationalizing about genetic susceptibility and how it was their poor kid’s destiny to wear extra-large pants.  Bullshit!  Ok, maybe not bullshit for everybody.  Sure, there is a very small minority of children who were born with metabolic abnormalities which pre-ordain weight gain.  But the chances are very good that your kid is not one of them.  The chances are very good that your overweight child could have been normal weight.  The chances are also very good that, if you start now, you can reverse your child’s fatty destiny and save him or her from a lifetime of physical and psychological baggage.

You see, genetics tell you only about your potential.  If your parents are both tall, you have the potential to play in the NBA.  If your parents are both smart, you have the potential to go to MIT.  And if your parents are both fat, you have the potential to wear XXL Lulus (you know, to make your butt look good – sorry, bad imagery).  But regardless of your genetics, your chances of making the NBA depend almost entirely on how hard you practice, how good your coaches are, and how well you listen to them.  Regardless of your genetics, your chances of going to MIT depend almost entirely on whether or not you can stuff your pocket protector with calculators, glasses, compasses, mechanical pencils and what not – then think till your brain explodes.  And regardless of your genetics, your chances of becoming a fat kid depend almost entirely on how much you eat and how little you move.

Enough with the rationalization.  Just today a Medscape article rambled on about how the scientific literature was unclear on whether or not parental control was effective in preventing childhood obesity.  Well, it turns out the” parental control” being analyzed involved interventions with the parents talking to their kids about obesity.  Talking to your kids about obesity!  Excuse me! I don’t know about the rest of you, but the only time talking to my kids ever changed their behavior was when their was a powerful short term consequence involved.  As in, “If you clean your room I’ll play football with you” or “If you don’t clean your room I’ll disconnect the x-box”. The chances of kids eating healthy on the basis of parental “advice”  to do so are about the same as the chances of my son waking up one morning and proclaiming “I think I’ll take some time and clean my room today!”

Not gonna happen.  Kids will make smart lifestyle choices when,  a) those are the choices they have been consistently exposed to,  b) there are no other choices or c) they are no longer kids.  Go ahead and try to “talk” your kid out of eating junk food, but I suggest that if you’re going to fill your larder full of Joe Lois’ and Miss Vickies’, a lock will probably be more useful than a talk.

Parental control is not about talking.  Parental control is about controlling.  Now I know all the new age parenting gurus don’t like us to “control” our children, but when it comes to childhood obesity, I believe the time is ripe to investigate just what it means to control your child’s health.  Here’s what it means to me:

Fill your pantry and fridge with INCONVENIENT FOOD.  That’s right…INCONVENIENT FOOD!  The childhood obesity epidemic (the adult one too, for that matter) is most assuredly fueled by convenient food.  For kids, making food inconvenient is tantamount to making it unavailable.  I know.  If I had a hundred dollars for every time I’ve seen my 12 year old son staring blankly into an overflowing pantry and proclaiming “there’s nothing to eat in this house”, I”d be as rich as the guy who invented Twinkies.  Kids will make themselves a sandwich if they are hungry.  But will they make themselves another during the next commercial break?  Probably not, especially if there isn’t anything “convenient” like Skippy or Nutella to smear all over it.  You see, preparing a proper sandwich – you know, one with actual food in it – is something you do when you are hungry.  It is not something you do just because you are tired of watching a commercial about the heart healthy benefits of Fruit Loops for the umpteenth time.  Now if there was a box of Fruit Loops in the pantry….

Here’s a thought experiment.  They say that one of the contributing factors to childhood obesity is excessive fruit juice consumption.  OK.  Do your children drink a lot of fruit juice?  Mine sure would if it was available to them all the time.  But what about this.  What if they could have all the fruit juice they wanted, with only a single caveat – that they make the juice themselves by squeezing it out of the fruit?  How much fruit juice would they drink then?

If a food comes in a package and does not need preparation in order to be edible, it holds the potential to fatten your kids.  We all know a teenager who comes home and inhales a box of cheerios every day after school.  Now that may be OK if he walked home 2 miles uphill (preferably barefoot) in the snow and is planning to play hockey at the outdoor rink (preferably not barefoot) for a couple of hours before dinner.  But if he came home in the back seat of mommy’s SUV and the closest he comes to playing hockey is NHL11 on his x-box, then we can all get ready to play “watch the belly fat jiggle” in the upcoming future.

I’ll repeat myself.  If a food comes in a package and does not need preparation in order to be edible…..then it is a food that requires controlling.  That goes for pop.  It goes for juice.  It even goes for milk.  It goes for cereal, and chips, and Goldfish (the cheesy wheaty kind…not the actual fishy kind – I dare you to try fattening your kid on actual little fish!).  It goes for peanut butter, and jam, and Nutella, and cream cheese, and anything else you can scoop from a tub and smear on a piece of Wonderbread.  It obviously goes for the Wonderbread itself, but also for whole wheat bread and 12 grain bread and bagels and wraps and even sprouted bread and gluten free bread.  It even goes for that Holy-Grail-of-Junk-Food-Disguised-as-Health-Food….the granola bar!  If it is easy to eat and yummy, then your job is to limit your child’s access to it.  If your child is already overweight, then, barring a lock on the pantry door, the best thing is to JUST SAY NO at the grocery store!

Just say no to convenient food!

Cook real food for your kids and make sure they eat it.  I am soooo tired of hearing parents say that little Joey will only eat Kraft Dinner or Pizza Pockets or some other nutritionally bankrupt frankenfood.  I suspect that little Joey would eat liver in beet juice if he were hungry enough.  But he isn’t about to get hungry enough because his parents haven’t got the testicular fortitude to send him to bed hungry and feed him cold dinner for breakfast.  These are the same parents who mutter incoherently about “choosing your battles” as if creating healthy eating habits was on the same parenting plane as deciding what kind of clothes your kids should wear to school.

If your “little Joey” eats nothing but frankenfood, then you have failed him as a parent.  You have set him up for a lifetime of health complications, foremost of which would be obesity.  It is often said that if you don’t have your health, you have nothing.  By not ”choosing” this battle, you have chosen to give your child nothing.

 Make your kids move.  Movement is good for you.  When you stop moving, you grow fat and you die.  If you are a kid who has stopped moving, you grow fat, you live a miserable and sickly life for 40 or 50 years, and then you die.  But it doesn’t have to be that way.  Kids don’t stop moving without a little help from their environment.  Without a little help from over-protective parents who won’t let them go outside for fear of kidnappers, molesters and various other media inflated bogeymen.  And without a little help from litigation-conscious school administrators who ban balls and tag and running and touching and anything else that remotely resembles fun.  That’s right, fun!  For kids, fun and movement are synonymous.  We are taking that association away from them and replacing it with what….DPA?  What kind of an association is that?  That’s like taking away somebody’s sports-car and replacing it with a minivan.  Sure, its more practical and better for the environment and safer and all, but how does it feel when you floor the accelerator?

Physical activity should be fun.  It should feel like flooring the accelerator on a Porche.  Kids know this intuitively and practice it spontaneously.  We adults could all benefit from taking the time to re-acquaint ourselves with intuitive and spontaneous play.  Perhaps if we did, we would not so readily allow our childrens’ play to be taken away.

You don’t have to make your kids be physically active.  You just have to give them the opportunity.  That means not driving them to school.  That means shutting down the electronics.  It means pressuring your school board to allow actual play in the school yard.  It means letting them try any sport they like until they find one they love.  It means allowing them to experience the exhilaration of competition, the camaraderie of team play and the sense of accomplishment associated with individual physical effort.  It means sharing with them the thrill of victory.  And when they lose, it means reminding them that they were having fun and that somebody always has to lose.

For the first time in centuries, there is a good chance our children will have a lower life expectancy than we do.  If this is so, then it is almost certainly due to the fact that we are fattening our children more quickly than any generation ever before us.  The health consequences of this early marbling are sure to be disastrous.  As parents, we cannot stand idly by and accept this destiny for our children.  We can change the collective weight and fate of an entire generation, but only if we take responsibility now for what that generation is eating and doing.  Real food and real activity are no longer mainstays in our children’s lives.  It is time to bring them back.

by Alex Boersma

In Part I of this series I described type II diabetes as the most pernicious and calamitous disease of the 21st century.  Indeed, it seems that despite modern advances in the  treatment of heart disease and cancer, the capability of our medical system to deal with blood sugar dysregulation remains pathetically inadequate.  In fact, just this week  Medscape reported on the 47th annual meeting of the European Association for the Study of Diabetes which described the diabetes epidemic as  ”on a relentlessly upward trajectory, with no signs of abating“.  From the meeting:

“Data from international studies demonstrate that the number of people withdiabetes in 2011 has reached 366 million. This year, 4.6 million deaths will be attributed to diabetes, with 1 person dying from diabetes every 7 seconds. Healthcare spending on diabetes has reached $465 billion.”

And it’s not just in Europe.  Below is a chart from a  recent analysis of diabetes prevalence in Ontario

 Follow the blue or red lines into the future and perhaps you’ll reconsider that venti frappucino if you plan on becoming a sexagenarian!

In Part II of the series, I examined the role of insulin resistance as a determining factor in the progression to type II diabetes.  Primary factors in the development of insulin resistance were discussed, including cellular accumulation of excess free fatty acids (FFA), stress, inflammation and fatty liver.  It was established that these four factors were  associated with each other in a cyclic fashion, meaning an increase in one factor frequently causes increases in other factors.  All four factors factors are clearly related to excess weight, particularly when that weight is carried predominantly in the abdominal area.

If insulin resistance is such a dominant risk factor in the progression to type II diabetes, it might be useful to have an effective tool for diagnosing it.  In this section I will discuss the various options available for measuring insulin resistance and their efficacy in predicting progression to type II diabetes.

Before we begin, though, a little perspective.  Type II diabetes is clearly a disease which develops and progresses over many years.  In prospective studies, participants who eventually develop diabetes often present with altered glucose metabolism years in advance.  In the graphs below, we see that insulin resistance begins a decade before the pancreas starts losing its ability to produce insulin.  Likewise, post meal glucose intolerance increases sharply 3 or 4 years before fasting blood glucose hits the diagnostic marker (dotted line) for diabetes.

Taken from the American Association of Clinical Endocrinologists

Keep in mind, the earlier you can diagnose blood sugar dysregulation, the more likely you are to prevent progression to full blown diabetes.  From the graphs above, it is obvious that a simple diagnostic tool for accurately measuring  insulin resistance would be exactly “the bomb” for pushing our impending type II diabetes epidemic into the slow lane.  If we could know 10 years ahead of time that somebody is going to become diabetic, all we would have to do is get them to change their lifestyle and they could save themselves and the medical system a great deal of cost and aggravation.  Yeah, that’s all we’d have to do! 

Unfortunately, no such simple diagnostic tool exists.  There are a number of effective tools for accurately measuring insulin resistance, but none are simple.  The “gold standard” for measuring insulin resistance is the euglycemic hyperinsulinemic clamp.  It works great if you happen to have one of these setups:

Too bad only highly sophisticated metabolic research labs our outfitted with these contraptions.  So unless you volunteer to be a guinea pig at a research facility, it is unlikely that you will have the opportunity to test your insulin resistance with this degree of accuracy.  Your doctor – in case you’re wondering –  probably doesn’t have one stuffed in his clinic closet!

What we are left with, then, is a triumvirate of blood tests – none of which give us a completely accurate picture of what our body is doing with the box of tinbits we just shovelled in.  Still, as we shall see, there is much that we can learn if we know how to interpret them correctly.  Let’s take a look.

A1C (also known as HbA1C) is a measure of glycated hemoglobin.  If you expose blood to sugar for long enough, some of the sugar attaches to some of the blood…this is called glycation.  Since blood cells usually live in the body for up to 3 months (after which they die and get replaced) and since there is always some sugar in the blood, a percentage of your blood is always glycated.  The more sugar you have in your blood, the more likely it is to attach to blood cells and the higher the percentage of your hemoglobin which becomes glycated.  Therefore, HbA1C provides us with a rough estimate of average blood sugar levels over a 6 to 12 week period.

If you are resistant to insulin, sugar will tend to stay in your blood longer than if you are not resistant to insulin.  It seems intuitive, therefore, that elevated A1C would be indicative of insulin resistance.  Indeed, it does seem that, at least according to this paper  , HbA1c is effective at predicting insulin resistance, particularly in people with normal glucose tolerance and relatively high insulin sensitivity.  In other words, HbA1C seems to tell you if you are insulin resistant before you become “too” insulin resistant!  Just the thing we are looking for if we want to catch diabetes before it becomes diabetes!

The problem is that very little research has gone into determining exactly what A1C level is optimal for non-diabetics.  Most of the scientific debate concerns itself with optimal levels for established diabetics and does little to inform us about what our A1C levels should be for optimal health.  We know that 5.7 is good (at least compared to established diabetics) but would lower levels be even better?  And if so, how low should we go?

A recent British study published in the Annals of Internal Medicine  illuminates the issue.  The researchers followed about 10,000 people (age 45 to 79) for an average of 6 years and measured how many of them developed heart/cardiovascular disease or died during that time.  Below is a graphical interpretation I composed to describe the results.   As expected, when A1C goes beyond 6.5, people get sick and die at an alarmingly high rate.  But what about levels below 6?

When A1C is under 6, the results are not nearly as dramatic.  Still, for participants in this study, people withA1C below 5 had about a 70% lower risk of being dead after 6 years than people with A1C over 5.9.  The correlation for heart disease was even stronger.  Don’t tell the statinators, but dropping your A1C from 5.9 to just below 5 has a much more significant impact on heart/cardiovascular disease and all cause mortality than even the 50% reduction in LDL achieved in statin trials like the Jupiter study!

Okay, I know, this is just an epidemiological study and, as such, by no means proves that having high A1C causes people to die earlier.  It is entirely possible that some unknown variable is causing both the high A1C and the mortality.

More importantly, it should be noted that there is a high degree of variability between individuals for A1C levels.  In other words, A1C of 5.7 may be normal for you but high for me.  The only way we can know what our individual A1C levels should be is by having some kind of baseline over time.  For example, if we start early in life with an annual A1C measurement, it should remain fairly consistent as long as we maintain good glycemic control.  If we begin to develop mild insulin resistance, this would probably be reflected by a gradual increase in A1C over time.  A gradual but consistent elevation in baseline A1C would probably be an excellent indicator of early insulin resistance.  Too bad almost nobody has a baseline A1C since doctors usually only start testing for it after you have been diagnosed as a diabetic!

***One final cautionary note on A1C.  When you make significant improvements in your health through lifestyle changes, you may end up with healthier blood cells which live longer and, therefore, accumulate more glycation.  Start exercising, lose some weight, eat less junk food and voila…up goes your A1C!

As you can see, A1C has a number of issues which make it a less than ideal tool for reliably measuring insulin resistance or predicting progression to diabetes.  Having said that, I do believe that, in general, an A1C  below 5 sustained over time is predictive of good health and indicative of excellent glucose tolerance.

Fasting Plasma Glucose (FPG) is by far the most common blood sugar test done by doctors. (see here for a fascinating account of the political reasons why)  It is almost always part of a regular blood panel.  It measures the amount of sugar in your blood after a long (usually 10 – 14 hours) fast.  This being the case, FPG tells you absolutely nothing about how your blood sugar responds to the things you eat. 

 If you haven’t eaten anything for half a day, any sugar in your blood is almost certainly sugar which has been put there by your liver.  If you have high blood sugar after not eating for half a day, your liver is putting more sugar into your blood than it is supposed to.  Your liver is supposed to stop pushing out sugar if it recognizes that there is insulin in the blood.  If there is sugar in your blood, there should also be at least a basal level of insulin  in the blood. 

So if Fasting Plasma Glucose is high, it means one of two things.  Either your pancreas is not capable of responding to basal levels of blood sugar by producing basal levels of insulin, in which case your pancreas is probably FUBAR and you are quite likely already a full blown diabetic.  Or – and this is more likely if you haven’t already been diagnosed with diabetes – your liver is not recognizing the basal levels of insulin which your still- healthy pancreas is producing.  This is known as hepatic insulin resistance…your liver has become resistant to insulin.  The graph below (taken from a very interesting Medscapearticle - providing that you are the kind of person who finds Medscape articles interesting) shows just how closely fasting blood sugar and hepatic insulin resistance are related.

As you can see, the higher the FPG, the more sugar being produced by the liver.  Clearly, fasting blood glucose tells us something important about hepatic insulin resistance.  But what does it tell us about the progression to type II diabetes?  If  your liver becomes resistant to insulin early in the progression to type II, then FPG should accurately predict that progression. 

As it turns out, the liver only becomes insulin resistant early in some people.  In others, the muscles or the fat tissue lead the charge into blood sugar dysregulation.  This paper indicates that the early stages of insulin resistance are characterized primarily by impaired glycogen synthesis in the muscles.  The muscles are less inclined to sponge glucose out of the blood and turn it into glycogen, therefore it takes more time and  insulin to achieve normal blood glucose levels.  The authors concede that in some people the liver wins the race to insulin resistance, but they do not seem to think that this is common.

The point is that Fasting Plasma Glucose levels can easily lie within the “normal” range despite problems with sugar regulation.  Even if your muscles are seriously insulin resistant, you can get away with the extra large pizza and coke for dinner because your pancreas continues to pump out mega-shots of insulin to compensate for your sky-rocketing blood sugar.  2 hours after dinner, your blood sugar might be way beyond dangerous diabetic levels, but your doctor won’t know about that.  Your doctor won’t know about it because the FPG test isn’t administered until the next morning.  And by the next morning, your iron pancreas will have pumped out enough insulin to bring blood sugar back down to below the 5.5 mark.  As long as your liver remains at least somewhat sensitive to insulin, it will not start pushing sugar into the blood and upping your FPG levels.  By the time FPG finally gets high enough for your doctor to notice, you have probably already sustained years of glucose-related vascular damage.  

If we expect to use FPG as a tool in our battle against the diabetes epidemic, it is clear that we must, at a minimum, re-evaluate the parameters by which we define “normal” blood sugar. The accepted FPG “normal” of 5.6 used by most doctors may be normal in the context of a population rife with obesity, overweight, vascular disease and blood sugar dysregulation.  But it is not likely to be optimal. It probably represents at least a minimal level of insulin resistance and suggests that vascular damage due to glycation is occurring.  Healthy young people do not tend to have FPG levels as high as 5.6.  In fact, as this graph shows optimal FPG is probably closer to 4.5 than it is to 5.5.

What is normal?

It is difficult to read here, so click on the link above if you want to see more clearly.  The blue line represents total plasma glucose for 24 healthy young study participants.  The black vertical line shows where the first meal of the day happens.  We are interested in the part of the blue line before the first meal.   From 6:00 am to 7:30 am, these truly normal people had, on average, a blood sugar around 80mg/dl which corresponds to 4.4 mmol/l for us Canadians.  4.4 is a long way removed from 5.6!  The upper limit of their morning measurements was around 95 (5.3 in Canada) while the lower limit was around 60 (3.3 in Canada).   

Over the last 15 years, standard guidelines for “normal” FPG have been revised twice.  15 years ago anything under 6.7 was considered normal.  In 1997 the American Diabetes Association brought ”normal”  down to 6.1.  In 2003, they lowered it again to 5.6.  Granted, much of this pressure to lower “normal” has probably been initiated by pharmaceutical companies.  After all, lower standards for blood sugar means more sales of blood sugar lowering drugs like Metformin.  Still, in light of the evidence provided above, it would seem that lower is indeed better…at least down to the FPG = 4.5 level or so.  And, if caught early enough, very few people would need to rely on pharmaceuticals to get them there.

In my opinion, Fasting Plasma Glucose, like HbA1C, can be an effective tool for measuring insulin resistance, but only for some people and only if a baseline is established early in life.  Whatever your FPG is when you are young and healthy should be your target as you age.  If and when it begins to creep up into the mid 5’s – as it seems to for most people in middle age – this is an indication that you are probably developing some level of insulin resistance.  At this point, further testing is certainly warranted, and lifestyle interventions to bring FPG back down below 5 will probably be helpful and effective.  But if you wait until FPG rises above 5.6, it will be much more difficult to bring it down and you will be much more likely to require pharmaceutical intervention.

The Glucose Tolerance Test (GTT) was once a commonly used tool in the evaluation of blood sugar dysregulation.  It was recognized decades ago that a glucose tolerance test identified distinct populations susceptible to developing diabetes independent of fasting plasma glucose.  Unfortunately, the GTT has been effectively banished from medical practice, mostly because it is rather cumbersome from a practical perspective.  This paperdescribes some of the political and practical  reasons for the elimination of GTT.  It also discusses the reasons why it’s replacement by FPG has been detrimental in the struggle to predict early insulin resistance.

Simply put, your doctor doesn’t routinely give you a glucose tolerance test because a GTT takes time…something doctors and patients alike don’t seem to have a lot of.  Here’s how the GTT works.  Fast all night, then go visit your doctor in the morning.  Have your blood drawn before you begin the test.  Drink a 75 gram shot of awful glucose syrup.  Wait 2 hours and have your blood drawn again to see how much sugar is still in it.  If you still have more than 11 mmol of sugar in every litre of your blood 2 hours after drinking the glucose goop, congratulations …you are a diabetic – you can get in line for your metformin and insulin prescriptions.  If you have less than 7.8 mmol of sugar in every litre of your blood 2 hours after drinking the glucose goop, your doctor gives you a free pass to the candy store. 

The problem, of course, is that the cut-off numbers for GTT results are rather arbitrary.  If your glucose tolerance is impaired at 7.8, does this mean that at 7.7 you are truly free and clear to steal all the chocolate bars out of your kid’s Halloween haul?  Is everything below 7.8 truly “normal” or does a higher number in the “normal” range signify increased risk for developing glucose intolerance?

The chart below, which I developed from the results of this paper, indicates that, indeed, not all “normal” GTT results are equal.

As you can see, the range of insulin sensitivity within “normal” glucose tolerance varies significantly.  If your blood sugar is back below 5 two hours after drinking your glucose goop, it would seem that you retain excellent glucose sensitivity.  If blood sugar is still up above the 7 mark, then not so much!  In fact, if blood sugar is still above 7, you have probably already lost a third of your body’s ability to sense insulin.  The truly scary part, though, is that glucose sensitivity, for most people, levels off around the 50% mark- even for severe type II diabetics!   Since doctors don’t normally do a GTT until they already suspect diabetes, this means that most of the reduction in your insulin sensitivity will happen well before you ever get your glass of glucose syrup!

Here are the conclusions of the above study:

“In summary, we showed in a large cohort of Finnish men that the impairment of peripheral insulin sensitivity started at relatively low PG (GTT) levels within the normoglycemic range. In contrast, the impairment of insulin secretion progressed substantially only in the diabetic range of fasting and 2-h glucose levels. Peripheral insulin resistance was a predominant feature of isolated IGT (impaired glucose tolerance), whereas impaired insulin secretion characterized isolated IFG (impaired fasting glucose)”

Translation:  The 2 hour glucose tolerance “normal’ cut-off of 7.9 sucks at catching insulin resistance early in the progression to type II diabetes.  It does tell you that your pancreas is about to pooch out but your doctor probably already knew that if he only ordered your GTT after you had already failed a fasting plasma glucose test.

SO….WE HAVE SOME GOOD NEWS AND SOME BAD NEWS

First the bad news.  The bad news is that conventional tools for measuring and predicting the early stages of insulin resistance are woefully inadequate.  None of the tests described above is capable of providing us with a complete picture of our individual insulin sensitivity.  For the most part, guidelines and cutoffs used by the medical establishment set off red flags only well after you have merged onto the one-way lanes of the road to diabetes. 

The good news is that there is much we can learn from the science behind these tests.  Clearly, being a “normal” North American with “normal” blood sugar test results tells you diddly about your risk of developing diabetes.  In fact, if you look at the trends, being “normal” in North America means you have an excellent chance of developing diabetes – or at least insulin resistance - as you age.

So if there is anything we can learn from the science, it is that we should not be “normal”.  We should not take for granted that fasting plasma glucose gradually goes up as we age.  We should not assume that “normal” blood sugar levels implicate normal sensitivity to insulin.  And we should not sit idly as early warning signs for insulin resistance pass us by.

What are we to do?  Well, it really is quite simple: 

1. Moniter FPG levels.  Since these are tested automatically with most regular blood work, they are the easiest to monitor.  Any levels above 5 mmol/l should warrant further investigation. That doesn’t mean you’ll have to start mainlining insulin or popping metformin just yet.  It just means that maybe you should take a closer look at the way your body responds to that box of tinbits. 
2. If in doubt, do your own glucose tolerance test.  In my opinion, one of the best investments anybody can make in their own health is a glucose meter.  For less than $100 you get to figure out for yourself whether or not the ingestion of carbohydrates is an issue for you. You get to know what foods and what amounts of those foods wreak havoc with your blood sugar.  And you get to accumulate this wealth of physiological information without ever having to drink even a drop of glucose syrup!

How to be your own blood sugar control board!

 Monitoring your blood sugar response to food is actually quite simple.  Start by purchasing a glucose meter and strips from your local pharmacy.  The glucose meter is usually free if you buy more than 100 strips (usually for less than $100).

Measure your blood sugar first thing in the morning for a few days.  Doing so will give you a bit of practice using the meter and also establish a baseline which you can use to compare future readings.  You are now ready to begin monitoring your blood sugar response to food.

Before testing your response to any meal, be sure to measure your fasted (relatively speaking) blood sugar.  This measure should be fairly close (within about 10%) to your morning fasted blood glucose.  If it is high before you start eating, then the results of your testing will probably be inaccurate.

The first few times you test a meal, it is useful to test every 1/2 hour after you finish eating.  This will give you an idea whether you experience any abnormal blood sugar swings either early or late in the absorptive period.  As you can tell from the “What is normal?” graph above, blood sugar normally peaks somewhere between 1/2 hour and 1 hour after a meal.  By 2 hours it should be back down fairly close to fasting level.  If your blood sugar does something significantly different than this, you probably have some issues.

We know that having a 2 hour blood glucose of more than 7.8 indicates some level of vascular damage.  We also know, according to This study, that having a 1 hour plasma glucose level above 8.5 mmol/l  predicts diabetes better than just about anything else.  It also seems to correlate very well with various measurements of insulin resistance.  Clearly, we want to keep our own numbers lower than these.

But remember, 8.5 at 1 hour and 7.8 at 2 hours are probably not optimal numbers.  If, again, we look to the “What is normal?”graph above, we see that average normal 1 hour blood glucose comes in around 115 mg/dl, which translates to about 6.4 mmol/l.  The extremes in this group were about 3.9 on the low end and 8.3 on the high end.  Moreover, another study shows that normal people spend less than 6 minutes a day above 7.8.  So keeping your blood sugar between 7.8 and 8.5 for as much as 2 hours after every meal is clearly not normal!

The goal, then, at a minimum, would be to keep 1 hour blood sugar below 8.5 and 2 hour blood sugar below 7.8.  That much is obvious.  Beyond that, it seems to me that lower is generally better – to a point.  I would guess that 1 hour results around 6 – 6.5 would be closer to optimal.  Likewise, 2 hour results around 5 -5.5 are also probably closer to optimal. 

Knowledge is Power

The evidence suggests that knowing whether or not you are resistant to insulin can tell you much about the status of your overall health.  As we have seen, traditional measures of blood sugar are not particularly effective at predicting insulin resistance.  But do not despair.  Thankfully, glucose meters are cheap and simple to use.  Thankfully, good research is available to tell us whether the numbers coming out of our glucose meters reflect optimal or sub-optimal health.  And thankfully, as we shall see in the next and final article of this series, altering our diet to change those numbers is a relatively simple (but by no means easy) thing to do.

“MONEY FROM DRUG COMPANIES IS THE OXYGEN ON WHICH THE ACADEMIC MEDICAL WORLD DEPENDS (Dr. Edwin Gale, Heartwire)

I have spoken before about the ethical abyss which distinguishes the production and implementation of medical guidelines.  Along comes a new piece of research published in the British Medical Journal which should become required reading for anybody who takes advice from a doctor.  I am not going to add much commentary here, because I believe the paper speaks for itself.  I also believe you owe it to yourself to follow the link above and read the whole thing. 

The researchers set out to determine the prevalence of financial conflicts of interest among members of panels producing clinical practice guidelines (i.e. the guidelines doctors use in their practices) for hyperlipidaemia (high cholesterol) and diabetes.  At the end of their research, this is what they concluded:

 ”The prevalence of financial conflicts of interest and their under-reporting by members of panels producing clinical practice guidelines on hyperlipidaemia or diabetes was high, and a relatively high proportion of guidelines did not have public disclosure of conflicts of interest. Organisations that produce guidelines should minimise conflicts of interest among panel members to ensure the credibility and evidence based nature of the guidelines’ content.”

Here are the juicy bits.  For guidelines which reported conflicts of interest, 66% of panelists involved in telling you that LDL causes heart disease(and you should probably take a statin even if your LDL is pretty low)were getting money from the people making statins.  In the same category, 70% of the panelists telling diabetics not to worry about carbohydrate intake(as long as they keep taking their metformin and insulin) also got money from the people making metformin and insulin.

A Heartwire (sign-up free but required) story which delved more deeply into the dilemma found that this was not the first time such conflicts of interest had been reported.  The author quotes Dr. James Kirkpatrick, who studied the same issue for the American Heart Association: 

“There are plenty of people who participated in the guidelines process who reported no disclosures. The implications are that it would not be too difficult to construct a guidelines panel without COI (conflict of interest), or at least—as we suggested, and the authors also seem to suggest—with only COI related to research grant funding, exclusive of direct financial payments to members”

The quote above refers to the often suggested hypothesis that “all the experts already work for the pharmaceutical companies, therefore it is impossible to find a panel of experts who don’t have conflicts of interest.”  That is exactly the excuse the U.S. Heart and Lung Foundation used to rationalize 8 of 9 panelists on the statin promoting cholesterol guidelines committee being paid by the statin makers.  Dr. Kirkpatrick is suggesting that it is quite possible to form a panel of conflict-of-interest-free experts, especially if we disqualify only those who receive “honoraria” for such things as speaking engagements and lobbying.  Personally, I still think it would be difficult for a panelist to remain neutral if he or she knows that the future of their research depends on renewed funding from a pharmaceutical company.  Still, I think that eliminating the “salesman” experts from guideline panels would be a step in the right direction.

The Heartwire story goes on to shine a profound light into the heart of this dilemma.  The author quotes an accompanying editorial by a Dr. Edwin Gale.  This is what Dr. Gale has to say about the situation:

“The common suggestion that guideline committees should include only experts with no conflicts of interest has “a charming sense of unreality,” Gale argues. “Money from drug companies is the oxygen on which the academic medical world depends. The income of the professional societies that publish guidelines largely derives from their annual conferences, which depend on the rents charged to exhibitors and the registration of company-sponsored delegates,” he observes. “Let us therefore forget the hand-wringing and confront the reality of the world in which we live.”

Dr. Gale seems to believe that the only way to solve the problem is to eliminate paid experts entirely.  Quote:

“Legislation will not change the situation, for the smart money is always one step ahead. What is needed is a change of culture in which serving two masters becomes as socially unacceptable as smoking a cigarette. Until then, the drug industry will continue to model its behavior on that of its consumers, and we will continue to get the drug industry we deserve.”

Here’s the thing.  Consumers of medical advice (that’s you and me) exist within a bewildering domain of conflicting information.  We hang on to our “charming sense of unreality” because without it we wouldn’t know who to listen to. We like to think that our doctors give us unbiased advice, but the truth is that much of that advice is paid for by pharmaceutical companies.  Paid for by massive marketing campaigns,  by lavish golf tournaments and ”educational” conferences, by free samples, free  journals and free lunches.  That conflicts of interest in the medical/pharmaceutical realm exist is not debated.  Nor, as this Financial Times article explains, is it debated that pharmaceutical companies are guilty of breaking conflict of interest laws on an overwhelming scale.   The only question left to be answered is what to do about it.  With over 1,200 whistle-blower drug cases under investigation in the U.S. and the potential of billions of dollars in fines being awarded, the pharmaceutical companies are beginning to pay attention.  But if Dr. Gale’s predictions ring even remotely true, I suspect there will always be ways to buy the support of researchers and medical professionals…smart money is always one step ahead.

 If anyone still believes that pharmaceutical companies are motivated by ethics rather than profits, they should probably think about taking up smoking or buying swamp land in Florida.  That is as it should be, since these are, indeed, multi-national corporations beholden to their stock holders.  But when our health-care institutions construct their guidelines around advice provided by vested researchers, the public trust is betrayed.  The people telling us if and when to take a statin should not be the same people who stand to make money if more of us take statins.  This is fundamentally wrong but it is, as Dr. Gale says, “the reality of the world in which we live”

I leave you, then, with a little insight into the reality of the world in which we live.  Below is the financial disclosure list for the 9 panelists who formulated the 2004 U.S. guidelines on cholesterol levels and heart disease.  If these guidelines are strictly followed by our doctors, 10s of millions of new “patients” will begin taking statins and pharmaceutical companies will stand to make billions more in profits each year.

I have highlighted any conflict of interest items which fall under the “getting paid by the pharmaceutical company for something other than research” category.

ATP III Update 2004: Financial Disclosure

Dr. Grundy has received honorariafrom Merck, Pfizer, Sankyo, Bayer, Merck/Schering-Plough, Kos, Abbott, Bristol-Myers Squibb, and AstraZeneca; he has received research grants from Merck, Abbott, and Glaxo Smith Kline.

Dr. Cleeman has no financial relationships to disclose.

Dr. Bairey Merz has received lecturehonorariafrom Pfizer, Merck, and Kos; she has served as a consultant for Pfizer, Bayer, and EHC (Merck); she has received unrestricted institutional grants for Continuing Medical Education from Pfizer, Procter & Gamble, Novartis, Wyeth, AstraZeneca, and Bristol-Myers Squibb Medical Imaging; she has received a research grant from Merck; she has stockin Boston Scientific, IVAX, Eli Lilly, Medtronic, Johnson & Johnson, SCIPIE Insurance, ATS Medical, and Biosite.

Dr. Brewer has received honorariafrom AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Esperion, and Novartis; he has served as a consultantfor AstraZeneca, Pfizer, Lipid Sciences, Merck, Merck/Schering-Plough, Fournier, Tularik, Sankyo, and Novartis.

Dr. Clark has received honorariafor educational presentations from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer; he has received grant/research support from Abbott, AstraZeneca, Bristol-Myers Squibb, Merck, and Pfizer.

Dr. Hunninghake has received honorariafor consulting and speakers bureau from AstraZeneca, Merck, Merck/Schering-Plough, and Pfizer, and for consulting from Kos; he has received research grants from AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, and Pfizer.

Dr. Pasternak has served as a speakerfor Pfizer, Merck, Merck/Schering-Plough, Takeda, Kos, BMS-Sanofi, and Novartis; he has served as a consultant for Merck, Merck/Schering-Plough, Sanofi, Pfizer Health Solutions, Johnson & Johnson-Merck, and AstraZeneca.

Dr. Smith has received institutional research support from Merck; he has stockin Medtronic and Johnson & Johnson.

Dr. Stone has received honorariafor educational lectures from Abbott, AstraZeneca, Bristol-Myers Squibb, Kos, Merck, Merck/Schering-Plough, Novartis, Pfizer, Reliant, and Sankyo; he has served as a consultantfor Abbott, Merck, Merck/Schering-Plough, Pfizer, and Reliant.

Remember, both the BMJ paper above and the findings of Dr. Kirkpatrick for the American Heart Association suggest that it is entirely possible to formulate a panel out of members who are not “getting paid by the pharmaceutical companies for something other than research”.

Right after the guidelines were published, a group of 35 prominent physicians and researchers demanded an independent review of the evidence, claiming foremost that the evidence did not fit the recommendations and secondarily that the credibility of the panelists was compromised by their financial ties to pharmaceutical companies.  You can read the letter here.  It was largely ignored.  

In case you feel secure, like I did, that Canadian guidelines were free of such conflicts of interest, think again.  Below are the financial disclosures for the four authors of the Canadian Cardiovascular Society 2009 Position Statement regarding cholesterol and heart disease.

Canadian Cardiovascular Society position statement – Recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease

CONFLICT OF INTEREST:

 Dr Ruth McPherson has received honorariafrom AstraZeneca (Crestor), GlaxoSmithKline (Mevacor), Merck Frosst (Ezetrol), Pfizer (Lipitor) and Schering (Zetia and Vytorin) for conferences or advisory boards, with no ownership of stock or options.

Dr Jiri Frohlich has receivedhonorariafrom AstraZeneca, Merck Frosst, Pfizer and Schering for conferences or advisory boards, with no ownership of stock or options. 

Dr George Fodor has received honorariafrom AstraZeneca, Merck Frosst, Pfizer and Schering for conferences or advisory boards, with no ownership of stock or options.

Dr Jacques Genest has received honorariafrom Merck Frosst Canada, Schering-Plough, Pfizer, Novartis (Flustatin) and AstraZeneca for conferences, advisory boards and consultant work, with no ownership of stock or options.  

Are these really the people you want telling your doctor whether or not you need to take one of the drugs made by any of these companies?  You tell me.

by Alex Boersma

When I was a kid, my mother achieved epic nutritional and gastronomical failure by trying to replace butter with margarine.  I’m not sure whether she did it because she was listening to Ancel Keys and his posse of saturated fat haters or because it was simply cheaper.  She is Dutch! 

 Even then, I remember wondering what they did to the butter to make it taste so bad.  Little did I or my mother know that they poisoned it with partially hydrogenated vegetable oils.  It wasn’t until the early nineties that I began to realize just how epic the nutritional failure called trans fat actually was.  It wasn’t until 10 years later that the nutritional establishment finally but unapologetically withdrew its support for these chemically engineered fats.  Another half a decade had to pass before the food processors were forced at least to tell us when they were poisoning our food.  Of course, food processors have enough political clout to make sure they don’t really have to provide full disclosure.

Now we just have to get restaurants to comply!

Frankenbutter! 

Must be good for you if it has no trans fat!

Enter the process of INTERESTERIFICATION!

Interesterification is the food industry’s answer to trans fat bans. Interesterification dismantles normal triglycerides and plugs them up with fully hydrogenated soybean (or sometimes palm) oils.  Interesterification does not produce trans fats.  But is it safe? 

Not according to this paper.  Here’s what the people at Nutrition and Metabolism concluded:

“Both PHSO (trans fats) and IE (interesterified fats) fats altered the metabolism of lipoproteins and glucose relative to an unmodified saturated fat (palm oil) when fed to humans under identical circumstances.”

Seems like if you get about 20% of your daily calories from interesterified fats you can expect to lower your HDL (good cholesterol)  by 9% and increase both your blood sugar and insulin by about 20%.  Metabolic Syndrome, anybody?  Now if 20% of daily calories seems a little unrealistic to you, perhaps you’re right.  Most people who eat primarily home cooked meals won’t get anywhere close to that.  But with more than 20% of Canadians(and more than 30% of Canadian teens) eating at least one fast food meal per day, 20% of calories from interesterified fat may not be as far fetched as you think.  Besides, many who do cook at home use processed convenient foods laden with engineered fats rather than real foods like meat and vegetables.  And since most people will be blissfully unaware that the fats they are consuming are even more toxic than the trans fats being replaced, it stands to reason that the percentage of interesterified fat in the Canadian diet will continue to increase.

Regardless, this review paper, which examined the evidence from more than 25 human studies on interesterified fats, concludes that adverse health effects are measurable even when interesterified vegetable oil makes up only 8-12% of daily caloric intake.  It goes on to assume that these adverse effects are initiated at levels as low as 1 to 4%. You could probably get 1 or 2% of energy from intersterified fat just by spreading some frankenbutter on your daily ham sandwich!

Which might be OK if there was some sort of justifiable point!

Well, there is a point, but its not what you might think.  Sure, most people who actually eat frankenbutter do so because they mistakenly believe it is better for their health than the stuff that comes from cows.  But the real reason why trans fats, and now interesterified fats are so prevalent in our food supply is that they make food processing possible.  Without chemically engineered fats,  most processed foods would go rancid quicker than the porta-potties at an outdoor music festival.   In other words, food processing, which is the second largest manufacturing industry in Canada, worth more than $78 billion per year, needs engineered vegetable oils.  Our bodies, however, do not .

The truth is, our society is becoming more and more dependent on processed food.  Even if we do cook at home, we rarely take the time to do it from scratch.  When we shop, we turn to packaged food because it keeps longer and is easier to prepare.  In fact, only one quarter of Canadian families now eat a homemade meal from scratch every day, compared to half of all families in 1992.(stats canada)  The packages in which we buy our “convenient” food are littered with health claims, but rarely do we consider that these claims are marketing ploys, not nutritional science.

When it comes to engineered fats, the “nutritional science” behind those health claims are based primarily on the misguided presumption that saturated fats cause heart attacks.  This is clearly an out-dated presumption, as this 2009 meta-analysis concludes:

 ”A meta-analysis of prospective epidemiological studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD”

More specifically, another study found that butter intake did not predict cardiovascular disease, although – not surprisingly – margarine consumption did.  This relationship got stronger the longer the researchers followed it (and they followed it for a really long time).  Another very thorough review of dairy fat and heart disease came up with this conclusion:

“In summary, despite the contribution of dairy products to the saturated fatty acid intake of the diet, there is no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD”

Forty years ago, when my mother began her little experiment with frankenbutter, she didn’t know any better.  For what its worth, the medico-nutritional establishment had no idea they were poisoning us with trans fats, although there was plenty of controversy – even then – about whether or not saturated fats were actually harmful.  Today, it is more clear than ever that saturated fat is not harmful.  It is also more clear than ever that chemically engineered fats are harmful. In the end, butter tastes better and has never been proven harmful.  Two things you can’t say about margarine!

I will leave you with two graphs stolen from Stephen at Whole Health Source.  Follow the red lines and decide for yourself whether or not you want to continue to be a part of this experiment with chemically engineered fats

I know, these graphs are open to a quagmire of confounding, but still?

I get questions all the time about blood work. Invariably these questions arise after a friend or client has been advised by their doctor that their LDL cholesterol is too high and that perhaps they should entertain the idea of going on a statin.  Invariably I ask what their HDL and triglyceride levels are.  Invariably they don’t know.

Now don’t get me wrong.  I’m not against statins.  Ok, well, maybe just a little bit.  No, really, I do believe that statins have a role to play for people with established heart disease.  You know, people who have actually had a heart attack!  What I am against is the indiscriminate prescription of statins in situations where their efficacy has not been established or where their benefit is so minimal that, in my opinion, it fails to outweigh the possible down side.  Here’s what one reviewof the evidence for people in this category concluded:
    

In conclusion, based on aggregate data on 65 229 men and women from 11 studies, yielding approximately 244 000 person-years of follow- up and 2793 deaths, we observed that statin therapy for an average period of 3.7 years had no benefit on all-cause mortality in a high-risk primary prevention (primary prevention means people with risk factors but no established heart disease) population.  Current prevention guidelines endorse statin therapy for subjects at high global risk of incident CVD as a means to reduce fatal and nonfatal vascular events. Consideration is needed in applying statin therapy in lower-risk primary prevention populations.

Having read many such reviews, I have become somewhat of a statin skeptic.  So when somebody tells me they are being advised to take a statin, I generally suggest that they determine just how high their risk of heart disease really is.  I tell them that in order to make an informed decision, they will need to know a lot more than just the status of their LDL cholesterol.  I tell them to go back to their doctor and find out, at a minimum, what their HDL and triglyceride levels are as well as what their total cholesterol/HDL ratio is.

To illustrate the significance of acquiring this additional information, I am offering below a comparison of three lipid panels.  Although I will not reveal their names, rest assured that these are real people.  The first belongs to a woman in her 40’s who is slightly overweight, a smoker and has a history of heart disease in her family.  The second belongs to a woman in her mid 70’s who has been on a statin for more than 15 years despite having no risk factors other than high total cholesterol (at the time, her total cholesterol was high but it was mostly because her good cholesterol (HDL) was very high, as it still is).  The third belongs to me, a 48 year old with only a family history (my dad had a heart attack in his 50s) as an added risk factor.  I will also include a list of the recommendations for blood lipids on the Canadian Heart and Stroke website for reference.

The bottom row shows the triglyceride/HDL ratio, which is not mentioned in the Heart and Stroke literature, even though a recent paper on the subject concluded:

“Nearly all routinely assessed lipid variables were associated with the extent of coronary disease, but only the ratio of triglycerides to HDL were robustly associated with disease extent.  Elevation in the ratio of TG to HDL was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined”

Not sure how many doctors are familiar with the TG/HDL ratio, but it sounds like something you might want to know before you sentence somebody to a lifetime on statins.  Seems that the TG/HDL ratio is an excellent indicator of whether or not your LDL is small and dense (the killer kind) or light and fluffy (the innocuous kind).  Although there is no established norm for the TG/HDL ratio, lower seems to be better, with <2 being pretty good and <1 being excellent.

So what does it all mean?  Let’s take a look on a line by line basis:

• LDL Cholesterol (the “bad” stuff)

The Heart and Stroke Foundation wants your LDL “bad” cholesterol to be under 3.5.  However, they add the caveat that for people with other established risk factors for heart disease, they would rather see it below 3.  All three of us have at least one added risk factor, so a number above 3 should at least draw the attention of our doctors.  Subject #1 has three added risk factors and the highest LDL, so her doctor is right to be concerned.

Having said that, keep in mind that the medical establishment is preoccupied with LDL.  Many doctors are entirely uninterested in the complexity of lipid bio-markers.  When subject #1 asked her doctor for her HDL and triglyceride levels, she responded with “Those numbers are inconsequential - only LDL is important.”  Subject#2, as we have seen,  spent 15 years on a statin despite having only marginally elevated LDL.  Despite having exemplary HDL and TC/LDL.  And despite having complained for years about muscle pain, brain fog and low energy (three common side effects of statins). 

And all this despite the fact that neither total nor LDL cholesterol has ever been proven causative of or even significantly correlated with heart disease.  As you can see from the graph below, there is very little difference in heart disease risk between the extremes of LDL concentrations within the normal population.  It is only when HDL levels are low that LDL levels begin to predict heart disease significantly.

*adapted from Gordon T. et al, American Journal of Medicine, 1977;62;707-714

You tell me.  Is HDL inconsequentialal?

• HDL Cholesterol (the “good” stuff)

Heart and Stroke wants HDL kept above 1.3mmo/l.  That’s OK, but from the chart above we can see that an HDL of 1.3, even at the lowest levels of LDL , still leaves you with a much higher risk of heart disease than would an HDL greater than 2 with just about any level of LDL!  All three of us are above the 1.3 mark, but, as you can see, this is a number which appears to get better and better the higher it gets.  Why it takes a back seat to LDL in the doctor’s office is beyond me.

• Total Cholesterol/HDL Ratio

Heart and Stroke wants the TC/HDL ratio below 5, although it should be mentioned that other conventional medical authorities want the ratio even lower.  The Mayo Clinic, for example, sets the bar at 4.  One of HDL’s primary roles is to prevent the oxidation of LDL.  Oxidized LDL tends to turn into small, dense LDL.  Small dense LDL is most definitely atherogenic - even the American Heart Association admits this.  So if you have a lot of cholesterol, but a significant percentage of it is associated with HDL, the likelihood of the rest getting oxidized is relatively small.  If you don’t have much HDL, though, you’d better hope that you don’t have much LDL either.  High LDL in the context of low HDL, as we can see from the graph above, will certainly increase your chances of becoming athlerosclerotic.

• Triglycerides

Triglyceride levels also associate well with heart disease.  In fact, one recent meta-analysis claims that each 1mmo/l increase in triglycerides is associated with a 37% increase in risk of heart disease for women.  If this is correct, then it suggests that the Heart and Stroke recommendation of <1.7 may be overly conservative. 

Triglycerides are basically a measure of the amount of fat in your blood.  Although the fact that high triglycerides are associated with disease would seem to condemn dietary fat, this is far from the case.  The truth is, the fats associated with hypertriglyceridemia are made in the liver, primarily when carbohydrate consumption is high.  The mechanism behind this is not fully understood, but it is related to an over-production of fat in the liver and/or an inability to clear this fat from the blood.  The inability to clear fat from the blood, as I explain in my series on diabetes, is indicative of insulin resistance.  Insulin resistance causes high blood sugars and hyperinsulinemia, both of which contribute to inflammation, oxidation and arterial damage.  And, despite the advice of conventional medicine to eat a low fat diet, it is quite clear that eating a high carbohydrate diet will raise triglycerides.

•  Triglyceride/HDL Ratio

As I explained above, TG/HDL ratio is an excellent predictor of severity of heart disease.  When researchers measure the amount of plaque in people’s arteries and compare that to blood lipids, the TG/HDL ratio seems to be most impressive in determining the extent of arterial damage.  The table below, taken from this paper, shows just how well the numbers correlate.

Notice that for Total Cholesterol and LDL, the relationship to coronary disease is not linear.  Having low LDL or Total cholesterol will give you almost as much risk for heart disease as having high LDL or TC.  Tell that to the statinators who seem to believe that lower is always better! 

On the other hand, notice that there is a clear linear relationship between HDL, Triglycerides and TG/HDL with extent of heart disease.  The more TG you have, the more heart disease you have.  The more HDL you have, the less heart disease you have.  Consequently, the higher your ratio of TG to HDL, the more risk of heart disease you have.

How much does your risk of heart disease go up when your TG/HDL ratio is elevated?  This study found that the people with the highest TG/HDL ratio had 16 times the risk for heart disease as the people with the lowest ratio.  Mind you, these people had, on average, a TG/HDL of over 7.5.  However, even the second quartile of participants, with an average TG/HDL of 2.3 had a 4-fold increase in risk of heart disease.

SO WHAT DOES IT ALL MEAN FOR THE THREE OF US?

  Subject #1

Of the three of us, subject #1 has the highest risk for heart disease.  Certainly, the combination of smoking and family history create a potent risk.  She also carries most of her extra weight around her mid-section, which is indicative of metabolic syndrome, making that weight more of an imposing risk factor.  According to the Canadian Framingham Risk Score her chance of developing heart disease in the next 10 years is 3%. Compared to other women of her own age, she has a 5% greater risk of developing heart disease than those who do not have her risk factors – whatever that means!  This estimate does not, of course, include the fact that her triglycerides are a bit high, her TG/HDL ratio is elevated, or that her weight is carried at her mid-section.  It is therefore – at least in my humble opinion – probably a conservative estimate. 

My guess is that if she continues her current lifestyle, her total cholesterol will continue to creep up, as will her triglycerides.  In the meantime, her HDL will creep down and she will probably develop at least a minimal level of insulin resistance.  I suspect she is already experiencing some level of systemic inflammation, which could be measured by tracking C-Reactive Protein. 

But should she take a statin?  Remember, she does not have heart disease, which means that taking a statin would be a form of primary prevention.  Her risk for heart disease is at best moderate.  So what does the science say about the use of statins for primary prevention?  Well, it depends who you ask.  If you ask the pharmaceutical companies, they will, of course, say that statin usage is useful in primary prevention.  However, even the most optimistic statinators get, at best, about 30% risk reduction over 5 years in primary prevention.  This means that,  according to the drug dealers who make the statins, subject #1 might be able to reduce her risk of heart disease from 3% to 1% over the next ten years.  If she was a man!   It turns out that although primary prevention statin therapy may show some minimal benefit in men, it is not at all clear that it has the same benefit in women.  A recent meta-analysis on the subject concluded: 

“Our study showed that statin therapy reduced the risk of CHD events in men without prior cardiovascular disease, but not in women. Statins did not reduce the risk of total mortality both in men and women.”

More importantly, as we already discussed above, and is stated again here, there is absolutely no relationship between statin usage and improved all cause mortality in primary prevention!  So she may minimally reduce her risk of heart disease, but she isn’t going to live any longer anyway.  You make the call!

What about making lifestyle changes?  Doctors don’t put much stock in lifestyle changes.  This pessimistic attitude is justified by the fact that most people are not capable of sustaining long term changes to their lifestyle.  But let’s just play a game of pretend.  Let’s pretend that subject #1 is one of those super-human people with the fortitude to make and sustain significant changes to her lifestyle.  Then what?

What happens to blood lipids if you sustain weight loss for 2 years?  If you use a low fat diet, you lose about 4 or 5 pounds.  If you use a Mediterranean or Atkins diet, you lose about 8 to 10 lbs.  Here’s what happens to your blood lipids:

Wow!  HDL goes up and triglycerides go down.  TC/HDL ratio goes down.  So does TG/HDL ratio.  If you care to read the paper, you will see that insulin resistance,  leptin resistance and markers of inflammation also improve.  Even LDL goes down, as long as you don’t use a low fat diet to get yourself slim.

Wonder what happens if you quit smoking?  This study found a 12% increase in HDL for people who managed to quit for a year.  And that was despite an average weight gain of about 8-10 pounds! 

What about regular exercise?  This study concluded that regular moderate aerobic exercise – about 30 minutes 3 or 4 times per week – for 7 weeks could significantly reduce triglyceride levels and marginally increase HDL levels.

Here’s the thing.  Statins interfere with your liver’s ability to make LDL.  They accomplish this task by inhibiting HMG co-enzyme A reductase, a crucial enzyme in what is called the mevalonate pathway. Now there’s a gaggle of words that don’t come up much at the dinner table!  Bear with me.  This is important.   Here’s a synopsis of what else happens downstream of HMG Co-A reductase:

“The mevalonate pathway or HMG-CoA reductase pathway or mevalonate-dependent (MAD) route or isoprenoid pathway, is an important cellular metabolic pathway present in all higher eukaryotes and many bacteria. It is important for the production ofdimethylallyl pyrophosphate (DMAPP) and isopentenyl pyrophosphate (IPP), which serve as the basis for the biosynthesis of molecules used in processes as diverse as terpenoid synthesis, protein prenylation, cell membrane maintenance, hormones, protein anchoring, and N-glycosylation. It is also a part of steroid biosynthesis” (from wikipedia)

Even more big words!  Here’s the scoop.  Interfere with HMG Co-A reductase and you interfere with mevalonate.  Interfere with mevalonate and you interfere with cellular energy production, immune system regulation, cellular membrane integrity, the ability of proteins to attach themselves to cellular receptors, the synthesis of proteins and the synthesis of various hormones.  Do we really think that we can interfere with all these biological functions and not suffer long term metabolic consequences?  Do we really want to take the word of the pharmaceutical companies that statins are safe, when we know that none of their studies follow side-effects long term and few of them are empowered to study any of these complex systems even in the  short term?  Do we really want to take this risk simply in order to correct a single number (LDL) which isn’t even a particularly effective predictor of cardiovascular health and has certainly never proven to be causative of heart disease?

Subject #2

Before I start ranting, full disclosure.  I don’t know the full extent of this person’s health history at the time (15 years ago) when she was put on statins.  I don’t know what her LDL was.  I don’t know what her HDL was.  I don’t know what her triglycerides were.  I don’t know what her blood pressure was.  For all I know, her total cholesterol could have been 20 and her HDL 2, putting her at elevated risk for heart disease despite having high HDL.

Here’s what I do know.  I do know that statins have never proven to be the least bit effective for primary prevention of heart disease in women.  I do know that they have no long term positive effect on all cause mortality.  I do know that the muscle pain, lack of energy and brain fog she has been complaining of for years are well known side effects of statin usage.  I do know that it wasn’t until a rheumatologist (who she saw on account of her muscle pain) recognized her symptoms as side effects of statins that her doctor finally took her off them.  Only time will tell whether the accumulated cellular damage she probably sustained over 15 years of statin usage is reversible or not.  I have my doubts whether the pharmaceutical companies will ever do a study on that!

And then there’s me

I like my doctor.  He has never mentioned a statin, despite my LDL being slightly elevated- at least by conventional standards.  He recognizes that my HDL is stellar, my TC/HDL is ideal, my triglycerides are very low, my blood pressure is normal and I am not overweight. But here’s a funny story:

Last Spring I was experiencing some unfamiliar chest pain for a few weeks.  Coincidentally, I had already scheduled my annual physical, so I mentioned the issue to my doctor.  He immediately gave me an EKG and when the results were normal he re-assured me that it probably was nothing.  Just to be sure, though, he scheduled me for a full stress test with a cardiologist.  After an hour of testing, I sat down with the cardiologist who proclaimed that I had the healthiest heart he had seen in years.  Then he advised me to start taking a daily baby aspirin.  Guess he doesn’t read the Wall Stree Journal.  Here’s what Heartwire (an online heart disease newsletter targeted at physicians) had to say about giving aspirin to somebody like me who has low cardiovascular risk: 

“There needs to be better ways of educating primary-care physicians as to where it is clear that aspirin should be used, in secondary prevention and in diabetics with multiple risk factors, and very clear where aspirin should not be used, in people at low CV risk“

The same article contains more comentary  worth quoting on the general topic of doctors and their advice on heart disease.

“The aspirin findings speak to one of the overall conclusions of our PARADIGM study, and that is that unfortunately family doctors aren’t very good at doing risk assessment for primary prevention.”

So family doctors are not good at figuring out whether or not you have any risk of heart disease.  How do they figure out your risk?

“My suspicion,” he (Dr Milan Gupta, cardiologist and professor) continued ”is that family doctors are eyeballing risk,”

Instead of weighing risk factors using sophisticated scientific practices (which, for the record, are out of date anyway) doctors are guessing.  Based on what?  Who knows, but apparently not based on current guidelines and evidence.  Gupta goes on to say:

“Most cardiologists in Canada, he adds, are not actively involved in primary prevention—this falls to primary-care physicians, who are slow to incorporate CVD prevention guideline evidence into practice.”

By the looks of it, my cardiologist is just as slow to incorporate CVD prevention guidline evidence as are the family doctors who think subject #1 and subject #2 should be taking statins.

(the chest pain never amounted to anything –  probably a muscle pull)

by Alex Boersma

1. EXCESS FREE FATTY ACID (FFA)
2. STRESS
3. INFLAMMATION
4. FATTY LIVER

  

FUBAR BELLY!

 

1. Adipose tissue releases hundred of biologically active molecules.
2. These molecules, called adipokines, work as a network to regulate inflammation, insulin action and glucose metabolism.
3. Over-stuffed fat cells disrupt this network and create a systemic inflammatory state
4. This inflammatory state contributes significantly to insulin resistance and disrupted glucose metabolism

But there’s more to inflammation than FUBAR bellies and muffin tops.  The truth is, over-active immune systems are probably the product of multiple factors including infectious diseases, intestinal permeability, glycation end products, auto-immune reactions and oxidative stress.  The complex nature of the relationship between these factors is beyond the scope of this article but the graphic below provides some insight into the labyrinth of complexity involved.

Let’s just say that the absence of obesity is not a sufficient condition for the implication of freedom from inflammation or insulin resistance. This paper ”Inflammation and Activated Innate Immunity in the Pathogenesis of Type 2 Diabetes” is a great reference for those who wish to look further into these relationships.

DRIVING FORCE #4:   HOW A FATTY LIVER CAUSES INSULIN RESISTANCE

1. high in polyunsaturated fat
2. high in fructose
3. high in  trans fatty acids
4. low in anti-oxidants
5. and, at least if you listen to conventional wisdom, low in choline rich foods like eggs and liver

Hmmm.  What an interesting coincidence!

RAP-UP FOR PART II

I know, this was nowhere near as short as I had expected it to be.  Nor was it anywhere near as simple as I claimed it would be.  What can I say?  Things get more complicated when you try to explain them.  If you’re still with me, thank you for your perseverance.  Here’s a quick summary to help you organize your thoughts.

Insulin resistance is not caused directly by high carbohydrate diets or high blood sugar.  Although the quality of carbohydrates in your diet may contribute to inflammation and/or a fatty liver, carbohydrates as a general macro nutrient have not proven to be causative.  As we shall see in part III and IV, the dietary restriction of carbohydrates is probably only necessary after insulin resistance has already been established.  As long as you remain sensitive to insulin, a preventative approach will focus more on minimizing fructose (and possibly grains) rather than simply restricting carbohydrates in general.

Instead, insulin resistance is caused by excessive concentrations of free fatty acids and inflammatory cytokines circulating throughout the body.  Over-stuffing your fat cells beyond their genetic capacity will most-assuredly contribute to both excess FFA and inflammation.  Beyond that, optimizing liver health, avoiding or controlling stress, and preventing low-grade, systemic inflammation are the most important factors to consider in preventing and/or reversing insulin resistance. 

Here’s the infuriating thing.  The China Study seems to have magical powers.  It can turn regular people with little nutritional background or knowledge into a know-it-all vegetarian/vegan zealots.  Once they’ve read the book, these people with, remember, little nutritional background or knowledge, react to my dissenting opinions in one of two ways:

• They smile condescendingly and change the topic
• They engage me with Colin Campbell quotes and act like I have no idea what I am talking about

I have included below the better part of one on-line “conversation” between myself and one of these Campbell followers.  The person who wrote the comments below had basically told my client that I didn’t know what I was talking about regarding nutritional advice and that she should read The China Study and follow Colin Campbell’s advice instead.  I told her to forward my China Study article to him.  This was the discourse which transpired:

Guy who thinks I don’t know what I’m talking about:

My Reply

I’m afraid you are not reading the critiques or the rebuttals very thoroughly.  You say Campbell “is not even challenged” in his rebuttals.  If that is true, why is it that he does not answer any of the salient questions which Minger, Masterjohn and myself ask?  Namely: Where is the evidence, first in rats and second in humans, that any kind of animal protein besides isolated casein has any causative effect on disease at all.  The casein/rat/cancer experiments are his biggest source of support for the China study results.  Without them, it is just another piece of epidemiology which proves nothing.  If evidence exists which supports the generalization of isolated casein in rats to all animal protein in humans, why isn’t it in the book?  Moreover, why isn’t it in any of his rebuttals?

Campbell calls his detractors on using uncorrected correlations when claiming that the China Study results are not what he says they are.  Yet he is unwilling to provide the corrected correlations which, he says, he used in developing his results.  He says he doesn’t have the time to find them.  Although correcting correlations can be important, it also subjects the data to researcher bias.  If he does not show us exactly how he “massaged” the data, we are left to take his word that he wasn’t biased when he corrected the correlations.  Considering that this debate is entirely about whether he is biased or not, his refusal to provide such essential information is simply not fair play.  Where are the adjusted correlations he used?

The third piece of Campbell’s puzzle relies on the work of several clinicians using low fat vegetarian diets to treat modern diseases.  Namely Esslestyn, Ornish and McDougall.  All of their work is riddled with confounding factors like cholesterol lowering drugs and lifestyle changes.  All are achieving success compared to a typical American diet…which we all know is bad for you.  Where is the evidence that a diet low in animal foods will do better than a diet low in processed American crap?

Campbell spends well over half of his rebuttals criticizing the credentials of his detractors and emphasizing his own pedigree.  Would that he had spent some of his precious time answering the very valid questions they ask.  It sucks when a “smart ass American loud mouth” asks important questions which you can’t seem to answer.

Minger and Masterjohn do have their own agendas…so does Campbell.  Don’t we all?  If we are to learn anything, we must have intelligent debate instead of name calling.  Until Campbell or his vegetarian/vegan followers can answer the questions Minger and Masterjohn pose, I will side with the consumption of meat.

Re:  “the Paleo diet is interesting but just a theory” and “Paleo life expectancy was only 32 years” and “in light of some really good science”

Yes, it is just a theory…as is any dietary strategy…there is just not enough consistent science to “prove” anything about any dietary strategy.  I don’t claim that the paleo diet has more proof than a vegetarian diet.  I claim that the “proof” vegetarians claim supports their diet is very weak and based primarily on epidemiology or faulty generalizations like Campbell’s rat experiments.  Likewise, there isn’t much ”proof” to support the paleo diet.  However, the mechanisms make way more sense.  And, without “proof”, all else being equal, I will default to the way we evolved to eat rather than a diet which is “brand new” by evolutionary standards.

Sure, Paleo life expectancy was only 32 years.  But do you realize that life expectancy actually went down for the first 7000 years after agricultural societies developed?  See here for more on the health and longevity of paleolithic and neolithic cultures. Do you realize that stature and bone density both declined significantly and have never recovered?  Do you realize that modern hunter gatherers with access to modern health care have an average life expectancy of 72 years and have very few signs of heart disease, cancer, diabetes and obesity even at ages over 60?  See here

Finally, on the Paleo subject, where is the “really good science” showing that Paleo is not “the solution to optimum health” or that a vegetarian diet is “the solution to optimal health”?  If such science exists, I would love to see it.

Re:  Colin Campbell chastising the WAPF
Not sure what “the empty vessel makes the loudest sound” is supposed to mean but I assume you are implying that they are a bunch of whiners with no scientific background.
Campbell spends most of this section, as usual in his commentary, criticizing the academic background of Sally Fallon, Chris Masterjohn,  and JayY.  Masterjohn is a PHD candidate in Biochemical and Molecular nutrition with 2 peer reviewed papers.  Not quite the same pedigree as Campbell, but by no means an academic slouch.  Funny that Campbell simply refers to him as a “24 year old chapter leader in the WAPF” with “no first hand experience or training in experimental nutrition research” and “no professional peer reviewed papers.  JayY (turns out Jay Y is actually Anthony Colpo of The Great Cholesterol Con fame) does not even belong to WAPF, although his valid criticisms of the book, like mine have yet to be answered by Campbell even though he is quite willing to slam his lack of education…just answer the questions, Collin!  Sally Fallon is made out to be no more than an English major, though Campbell never mentions her original partner in WAPF, Mary Enig, who’s academic pedigree rivals his.  I guess if he mentioned her, he would have to show a little respect for WAPF, since he places so much emphasis on “experimental nutritional research” and “peer reviewed papers” of which she has 60.

Campbell accuses the WAPF of being in the pocket of big agricultural “farmer conglomerates” which shows that he hasn’t even taken the time to go to their website.  If he had, he might have noticed articles like “After the Recall:  Exploring Greater Transparency in the Meat Industry” or “An Inconvenient Cow” or “Finding Health Close to Home:  A Call for Localism” or dozens of others criticising conglomerate farming.

Finally, Campbell criticizes the WAPF for overemphasizing the findings of Weston Price.  Kind of like his detractors critisize him for overemphasizing the importance of the China Study.  He asks us to realize that the study itself is only a small piece of the puzzle.  (Believe me, we do…it’s just that we think his puzzle is missing some invaluable pieces…like any kind of solid evidence) Perhaps he needs to realize that Weston Price’s work is only a very small piece of the WAPF puzzle (he might understand that if he actually went to their website).  And if he has issues with the other pieces of the WAPF puzzle, perhaps he should take the time to read the multitude of articles by PHDs, MDs NDs and other academics.  Then, perhaps he would be qualified to pose questions of these authors regarding their evidence and enter into some intelligent debate.
Or, of course, he could remain safe withing the confines of the vegetarian focused “Physicians’Committee for Responsible Medicine” where he can keep collecting royalties from his book,  keep bullying his detractors and never have to substantiate anything he says.

I did read the book…quite thoroughly thank you…if you would like to see the dog-eared/margin covered copy, I will see if I can take a picture of it for you.

Quite frankly, I had forgotten the “all animal proteins have the same amino acid profile therefore all animal proteins will cause cancer just like isolated casein does” argument because it is not an impressive argument. If it is the pure amino acid profile which is causing the cancer to grow, then wouldn’t the proteins from combined vegetable sources which, as you say, get completely broken down in digestion, provide the same raw materials for cancer as animal proteins?  Indeed, Campbell knew this was so, since he performed an experiment where he added lysine to wheat gluten, (essentially making it a complete protein)… turns out the fortified gluten had the same affect as casein. Here was his conclusion:  “Lysine supplementation of wheat gluten during the postinitiation period enhanced the gamma-glutamyltransferase-positive response to a level comparable with that of the high-quality protein“ Why is this not in the book?  Regardless, who eats any kind of isolated protein as a mainstay?  The protein we eat is generally packaged in food…whether flora or fauna…and the package usually (if it is from a natural and whole source) contains other nutrients which help to combat disease.

Cancer is a disease of aberrant tissue growth.  In order for tissue to grow, protein is required.  Is it any wonder that an extremely low protein diet stops cancer growth?  It is possible that very low carbohydrate diets will do the same, since cancer seems to fuel best on carbohydrate.  This study, Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. seems to conclude that it is indeed possible.  I guess we should all just eat 100% fat diets!  Or, we should remember that all these tests are in rodents already induced with cancer.  I don’t know about you, but I don’t have cancer.  I would like to know  more about what kind of diet is best to prevent cancer, and none of these studies add anything to my knowledge on the subject.

This study, Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat, also done by Campbell, does add to my knowledge though.  It seems that if you feed rats a low casein diet prior to injecting them with aflatoxin, they are much more likely to get cancer than if you feed them a high casein diet.  So a low casein diet (at least in rats) seems to make you susceptible to the effects of aflatoxin, while a high casein diet seems to be protective! 

SEEMS CAMPBELL FORGOT TO MENTION THAT !

I have never heard of amino acids #8 and #9, so I don’t know what you are talking about.  Usually they are discussed by their names in the scientific literature.  Every nutrition book I’ve ever read says that all essential amino acids are found in all meat sources, so I’d be curious to learn about these mysterious #8 and #9 which are deficient in animal protein.  After all, I have found plenty of other things that these same nutrition books are wrong about.  I did find one online vegetarian site which stated that lysine was not found in meat, although it supplied no references for this and never even bothered to state that this is contrary to most of scientific opinion.  Of course I realize that we can’t get all 20 amino acids from meat…just the essential ones…that’s why they are called essential.  We can make the rest ourselves.  Is it better to get them from food than make them ourselves?  I would have to see some proof of that.

The book is full of evidence, is it?  Or is it just full of questionable references?  Like when Campbell says that heart disease can be prevented by diet alone?  The two references he uses to support this statement, Ornish and Esslyten, refer to studies where much more than diet is manipulated and both are about reversing heart disease, not preventing it.  The book is full of such misleading references and if you take the time to actually check them you will see that this is true.

Yes, rats are interesting critters which have been quite helpful in the study of disease.  Their digestive system is similar to the human digestive system, but not the same.  For example, rats do not have gall bladders, which to me indicates that they may not be adapted to eating as much fat as we are.  Rats also have a larger and more active caecum than humans, (see here) which indicates to me that they are better adapted to eating fibrous plants.  So if we test rats on low fat/high plant food diets compared to high fat/high animal food diets, I suspect they will do better on low fat/high plant food.  Rats do certainly get the same diseases as we do, but this has mostly been observed in lab settings where they eat highly processed rat chow.  Do they get the same diseases as us in the wild?  I doubt it.  Although rat studies can be interesting, I will always take them with a grain of salt.

As far as I can tell, Denise has no official links to WAPF.  I don’t even think she is a member! If you are going to accuse her of being associated with them, I would like to see how you came to that conclusion.  Thank you for sharing her bio…I have already read it…it is the first thing I do when I start following a blogger.I don’t care for her diet either, but it seems to be doing better for her than either a vegetarian or a vegan diet did.  Would she do better on a non raw vegetarian diet?  Possibly.  Would she do better on a paleo diet?  Also possibly. She seems open to dietary experimentation, so perhaps we will find out in the future.  Just because she is young and uneducated does not mean she is incapable of asking important questions.  Perhaps somebody with a superior education could answer some of her questions instead of pompously dismissing them!

Why does everyone care that the WAPF is a special interest group?  I am a special interest group, as are you, and as is Dr Campbell.  Is there some sort of evidence I am unaware of that WAPF is nefariously attempting to ruin the health of Americans?  They are a bunch of people who believe that traditional diets, many based on naturally raised animal products, are superior to the Standard American Diet.  When they see a popular but scientifically weak book out there which goes against much of what they believe, they defend their beliefs by criticizing the book.  Other than a short PETA reference by Masterjohn (which he subsequently apologized for) they restrict their criticism to questioning many of the book’s findings.  Campbell replies with mostly bluster about their lack of academic background, but has yet to answer most of their questions.  He also claims that their critiques are quite personal, but compared to him, I find both Masterjohn and Minger to be very polite.

By the way, what is the “new fate” which the WAPF members are struggling to accept?

The youtube video.  I assume you wanted me to listen to the criticism of WAPF, which is basically a reiteration of what you sent in your last set of comments.  I will say that Campbell looks like even more of an intellectual lightweight when he stands in front of a bunch of people and rants about how the WAPF is being funded by factory farmers.  If they are, they sure have a funny way of repaying them.  I assume that you have not spent much time on the WAPF site either, since you are sending this youtube video to me even after I pointed out that a few hours on the site will clearly prove that WAPF is not supported by factory farms.

Poor Mary Enig.  You are right, she does not come close to Campbell’s academic pedigree.  Could it be because she was ostracized by the academic community after she almost single handedly won the battle against trans fats?  See here for her contribution.  If it wasn’t for her, we might still all be eating partially hydrogenated vegetable oil in a tub and thinking it was good for us.  She may not have his credentials or his peer reviewed papers, but I contend that she has done way more for the health of the American and Canadian public than Campbell can ever hope to do.

Peer reviewed papers.  If I have learned anything in my attempt to inform myself about nutrition, it is that you can support just about anything you like by searching for peer reviewed research.  I am always the first to admit that just because I found some research to support my ideas, that doesn’t mean that there isn’t opposing research available.  A simple search on pubmed with the search words saturated fat and heart disease will give you plenty of ammunition regardless of which side of the fence you are on.  I like to use these sorts of references just to prove that I am not making things up.  They are by no means definitive.

I don’t claim to know everything about the peer review process, but I have a feeling that getting your research published in a peer reviewed journal has a lot more to do with politics and economics than it does with the quality of your science.  This article in Nature suggests that quality of science is only one of a multitude of factors affecting what does or doesn’t get published. Publication bias seems to be rampant.   Publication bias in situ or Publication bias in clinical trials due to statistical significance or direction of trial results  or Publication bias in clinical trials due to statistical significance or direction of trial results are just a few peer reviewed articles about publication bias. (there are plenty of others if you go to pubmed.com)  You can even find peer reviewed papers about peer reviewed papers about publication bias.

Not only are the publications biased, at least one peer reviewed researcher thinks that most of the research they publish is apparently false.  John Ioannidis explains   Why Most Published Research Findings Are False.  You can read more about Ioannidis’ research and findings in an article in The Atlantic titled Lies, Damned Lies and Medical Science, but here is how the author introduces the article:

“Much of what medical researchers conclude in their studies is misleading, exaggerated, or flat-out wrong. So why are doctors—to a striking extent—still drawing upon misinformation in their everyday practice? Dr. John Ioannidis has spent his career challenging his peers by exposing their bad science.”

Now I’m not going to get all conspiratorial on you.  I’m sure there are many good scientists and journals out there doing the right thing.  I just don’t know how to tell which is which.  If money and politics are as big of an issue as I think they probably are, then I wouldn’t be surprised if some of the most esteemed journals are also some of the most corrupt.
 
Always with the Jacob Gould Schurman Professor Emeritus thing.  Every single reference to Campbell quotes this title as if he were Einstein or something.  Heck, I even put it in my article.  Doesn’t it just mean he is a retired professor who still has his nose in the research?

There has been no further response or correspondence with “Guy who thinks I don’t know what I’m talking about”  

I know this may be difficult for some to believe, but I have nothing against vegetarians.  I’m even OK sharing the world with vegans, since I figure that just means more meat for the rest of us!  The truth is, I’m fairly certain that responsible vegetarianism (you know, the kind where you actually eat a bunch of fruits and vegetables every day- as opposed to the kind where you eat mostly processed grains, sugar and dairy) is, indeed, a superior option to eating the Standard American Diet (SAD).  I do not, however, think that vegetarianism is optimal, and I remain convinced that the typical vegetarian reliance on grains, soy and vegetable oils will be detrimental to their health over the long term. 

You want to be vegetarian or vegan?  Fine by me.  Fill your boots!  But here’s a tip.  Keep your rationalizations to yourself because there is no science to support them.  And whatever you do, please refrain from pontificating to my clients and friends until you have actually done some research.  Reading propaganda like The China Study does not qualify!

The only “evidence” supporting plant food over animal food comes from epidemiology.  Epidemiological studies look at vegetarians vs. omnivores and measure who lives longer, who gets more heart disease, who gets more cancer, or who gets some other marker of health and longevity.  These  studies are, by definition, riddled with confounding factors.  The truth is, vegetarians tend to be more concerned with their health than meat eaters.  They are less likely to smoke, they drink much less, they eat more fruits and vegetables, they exercise more and they maintain a healthier body weight.  There is no way that epidemiology can adjust for all of these confounders. 

So unless you have a little more than epidemiology to hang your hat on, keep it on your head! And in case any of you Campbellites have forgotten, the study Colin Campbell did in China was most definitely epidemiological.  Probably the largest scale epidemiological study ever done, but still just epidemiological.  And despite his protestations to the contrary, still just proof of nada! 

THREE STRIKES AND YOU’RE OUT, COLIN CAMPBELL!

Campbell’s anti-meat agenda is rationalized in The China Study on three constituent contentions.  Namely:

1. Experiments on rats prove that a high casein diet causes liver cancer after exposure to aflatoxin.  Campbell claims that because all proteins break down into their constituent amino acids in the digestive system, any animal protein will have the same effect.
2. The observations made in China support the hypothesis that animal protein is detrimental to long term health and longevity.
3. Clinicians using low animal protein diets to treat disease have proven the effectiveness of such diets in supporting health and longevity.

Campbell himself admits that none of these contentions stand on their own as proof of his hypothesis.  Instead, he claims that when all three contentions are affirmed by sufficient evidence, they make a solid case for the avoidance of meat.  I’m OK with that!  I just don’t think that any of them do!

Campbell has written a compelling book.  I can easily understand how a person could be persuaded by the strength of his convictions.  If you have read or are in the process of reading the book, I urge you to keep the three points listed above in the back of your head and objectively determine whether or not he makes a good case for any one of them.  To help you, I will list below the questions on each contention which I feel he neglects to answer.

1. On the validity of generalizing isolated casein in rats to all animal protein in humans
   1. Why did Campbell not study other animal proteins?
   2. When claiming that all animal proteins are the same because they all break down into their constituent amino acids, why did he not address the fact that by combining vegetable proteins (as most vegetarians do) you will also get the exact same amino acids?
   3. Why does he neglect to discuss his own study which suggests that by adding lysine to wheat gluten you get the same effect as you do from casein? 
   4. Why does he neglect to discuss the fact that rats have different digestive systems than humans and may be better adapted to grains and less well adapted to protein or fat than humans?  In this study, it is clear that humans respond differently to ciprofibrate, a chemical which causes liver cancer in rats but not in humans.  Other studies have clearly differentiated humans from rodents in relation to heart disease and diabetes.  Even if rats were susceptible to the “ravages” of meat eating, how could this possibly be generalized to humans?
2. On whether the observations made in China support abstinence from animal products
   1. Campbell seems to have used unadjusted correlations when they fit his hypothesis and adjusted correlations when the unadjusted ones do not.  Unless he provides thorough rationalization for doing this, he can rightfully be accused of fitting the evidence to the hypothesis. This is called confirmation bias, and until he accounts for it, he is guilty of it.  So far, he has refused to do so, choosing instead only to attack the credentials of his accusers. 
   2. Campbell seems to have used aggregate data to support his point when the more reliable individual data would have proven him wrong.  This is called an ecological fallacy and is a well known way of making epidemiological evidence fit your hypothesis.  This also fits under the heading of confirmation bias and unless Campbell defends his use of the aggregate data, he is, once again, guilty of it.
   3. Campbell’s detractors have consistently proven here, here, here, here and here, that, at the very least, the numbers from the China Study can be interpreted in a variety of ways, many of which completely contradict his interpretations.  He has refused to defend his interpretations, arguing only that he is more qualified than his detractors are to make them.  Confirmation bias rears its ugly head once more.
   4. Why does Campbell ignore the equally (and often more) compelling associations between wheat consumption and disease, infections and disease or latitude (vitamin D) and disease in China?  In his response to criticism on ignoring wheat consumption he argues that there is no plausible supporting evidence for this association despite the fact that he, himself co-authored a study providing just such evidence.  Here is what he concluded in that study:  “Significant differences in the diet of rural Chinese populations studied suggest that wheat consumption may promote higher insulin, higher triacylglycerol, and lower SHBG values. Such a profile is consistent with that commonly associated with obesity, dyslipidemia, diabetes, hypertension, and heart disease. On the other hand, the intake of rice, fish, and possibly green vegetables may elevate SHBG concentrations independent of weight or smoking habits.”  If you read the study, you will also find that meat eating was significantly associated with lower SHBG.
3. On the validity of using the clinical work of Ornish, Esselstyn and McDougall to justify abstinence from meat eating for the prevention of disease.
   1. All three clinicians reduce or eliminate sugar, refined grains and vegetable oils, three industrial age processed foods which I and many others suspect play a pivotal role in the development of many Western diseases.   How can Campbell prove that it is the removal of animal foods and not the removal of sugar/grain/vegetable oil  which is responsible for improvements in health?
   2. Ornish also manipulates exercise, smoking, alcohol consumption and stress release in reversing heart disease.  To emphasize the significance of such confounding factors, let’s take a look at Yoga, a technique which Ornish focuses on for reducing stress.  In his famous RCT Ornish was able to reduce the size of coronary artery lesions by an average of 0.4% after a year of his rigorous (including yoga) program.  Not all that impressive, but at least a step in the right direction.  But here’s the thing – This study  indicates that only 6 weeks of yoga, without any other interventions, can reduce blood pressure from 168/100 to 141/84.  High blood pressure, unlike meat eating, is significantly associated with coronary heart disease.  If Ornish’s patients were practicing yoga for a full year, the reduction in blood pressure alone may well have more than accounted for the minor reversal in lesion size.  Maybe they would have had greater reductions in lesion size if they had done the Yoga but kept some more meat and fat in their diets!
   3. Whatever success these practitioners have had is limited to the reversal of disease, not the prevention of disease.  In my opinion, most Western disease is caused by the deadly quartet of over-nutrition, under-nourishment, underactivity and elevated stress.  These four factors all contribute to metabolic dysregulation characterized by deficiencies in metabolizing fats and carbohydrates.  Once you are a victim of these deficiencies, it is reasonable to expect that manipulating fats and carbohydrates might be necessary for reversing disease (although I must insist here that choosing between animal and plant foods plays, at best, a very small and questionable role in such manipulation).  The bigger question of how to avoid succumbing to  metabolic dysregulation remains poorly informed by the work of any of these practitioners.

Despite Campbell’s assertions, The China Study is by no means a scientific account of the rational for eating less meat.  At best, it is a heavily biased and myopic masterpiece of obfuscation in support of an untenable hypothesis.  Clearly, Campbell arrived at his own conclusions long before he put pen to paper or grant money to research.  Since then, he seems to have abandoned the scientific method, choosing instead to single mindedly advance his own dogmatic agenda using vegetarian propaganda instead of facts. 

Obviously, my own agenda is diametrically opposed to that of Colin Campbell.  I believe that naturally raised meats and fats are the safest foods for human consumption and that plants, although essential to health and longevity, are frought with dietary hazards.  I, too, could easily cherry-pick the scientific literature and develop a compelling argument in support of my hypothesis.  Ironicaly, I would even be able to use much of Campbell’s own research to sustain my theories. 

BUT THAT’S NOT THE POINT!

A compelling story does not prove a hypothesis.  A compelling story sells a hypothesis!  In criticizing Campbell, I am not argueing that he is wrong.  I am arguing that his book, The China Study, is a sales pitch for veganism, not the scientific rational he makes it out to be.  He claims his book proves that everybody should eat as little animal food as possible.  In order for that to be true, all three of his primary contentions should be sustainable.  They should not be plagued by unanswered questions.  Until somebody answers those questions, the health benefits of a vegan lifestyle remain theoretical.

“Whenever a theory appears to you as the only possible one, take this as a sign that you have neither understood the theory nor the problem which it was intended to solve.”  Karl Popper

KarlPopper would have all scientists spend their time attempting to disprove hypotheses rather than prove them.  Perhaps not the most practical way of doing science, but at least well worth some consideration.  I believe that a respected scientist should, at the very least, keep Popper’s philosphy in mind when doing research.  In writing The China Study, Colin Campbell has forsaken his role as a respected scientist and taken up trade as an agent of veganism.  He wields his academic credentials in a shameless attempt both to legitimize his sales pitch and belittle his critics.  But no amount of credential waving can make up for bad science.  And the most effective way of belittling your critics is to provide answers to their critiques!

JUPITER: Best CVD event reduction in patients with very low LDL-cholesterol levels

Heartwire – April 15, 2011

The JUPITER study:  Justification for the Use of Statins in Primary Prevention.  The name says it all.  This study was designed to justify the use of statins for people who do not have heart disease.  In other words:

We think lots of people should take statins, regardless of whether or not they have heart disease.  Let’s design a study which will justify millions of new clients for our expensive new drug!

JUPITER – HOME OF THE ASTRAZENECANS

Purveyors of pharmaceutical grade justification 

“We”, of course, refers to AstraZeneca, the pharmaceutical company which owns the patented rights to Rosuvastatin, the drug being tested in the JUPITER study.  Also, the company which stood to make billions of dollars in statin sales if JUPITER could prove that people with normal levels of cholesterol should start popping statins with their breakfast cereal.  Also, the company which cut the trial short after less than 2 years just as diabetes was beginning to emerge as a significant side effect of taking Rosuvastatin!

Kudos to the AstroZenecan drug pushers.  They sure know how to set themselves up for success.

Here’s the thing.  We know that atherosclerosis is an inflammatory disease.  We know that if the walls of our arteries are inflamed, they will incorporate small, dense, oxidized LDL particles into plaques faster than a government sanctioned drug pusher can say “Crestor”.  So if we want to reduce our risk of heart disease, we can:

• Reduce the inflammation in the walls of our arteries
• Reduce the number of small, dense, oxidized Ldl particles in our arteries
• Or, even better, we can do both

That’s exactly what the AstraZenecans did.  They found 17,000 middle aged/elderly people who had dangerously high levels of a blood marker of inflammation called CRP but normal LDL levels. (No easy task, since only 1 in 5 people with high CRP have normal LDL levels).  Next, they randomly separated these people into 2 groups, one of which received 20mg/day of Rosuvastatin, the other of which got a placebo.  After 2 years, the people taking statins had reduced their CRP (inflammation) by about 1/3 and their LDL by about 1/2 (they didn’t measure small dense LDL particles, but let’s give them the benefit of the doubt and assume these made up a significant percentage of the loss in LDL).  The chance of having a major cardiovascular event in the statin group over those 2 years was just under 1 in 100 (.77%).  In the placebo group, the chance of having a major cardiovascular event was just over 1 in 100 (1.36%).  The chance of being dead at the end of the 2 years – in case you’re interested - was 1% in the statin group and 1.25% in the placebo group.

Looks pretty good so far, doesn’t it?

Having your risk of heart attack over a 2 year time period reduced from just over 1 in 100 to just under1 in 100 isn’t exactly going to get you pleading with your doctor for a daily dose of statins.  The AstroZenecans obviously realized this, so they decided to publish the results as a percentage of risk reduction instead of the actual risk reduction.  If you look at the numbers from this perspective, you get to say that “Crestor decreases your risk of having a heart attack by 47%!”  Now that’s a bit more compelling of a headline!

For a little perspective on this chicanery, your favourite lottery could begin offering two 1 million dollar prizes instead of one.  It could then advertise that it had increased the chances of winning by 100%. A  headline like that might create lineups at your local lottery and gaming  kiosk, but not so much if they also explained that the chances of winning the jackpot had merely increased from 1 in 10 million to 2 in 10 million.  But they wouldn’t do that, would they?

Of course they wouldn’t.  That wouldn’t be very good for business. 

Nobody will ever accuse the AstroZenecans of doing things that aren’t good for business.  And explaining to prospective consumers exactly what a “47% reduction in risk of having a heart attack” means is decidedly bad for business.  Nothing new here.  Consumer beware!

But here’s what gets my goat:

6 years after the JUPITER study was brought to an untimely end, it remains the single most referenced study exploiting the necessity of plying perfectly healthy people with perfectly unnecessary cholesterol lowering drugs.  6 years later, we get this article from Heartwire, which delivers heart related “research” online to an audience composed primarily of medical professionals.  Here is the first paragraph from that article:

A new analysis from Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) suggests even greater reductions in the risk of major cardiovascular events among individuals who achieve very low levels of LDL cholesterol.”

YEAH – IN PEOPLE WITH SKYROCKETING LEVELS OF INFLAMMATION!!!

Oops, they forgot to mention that part!

In fact, if you read the article here, you might find it interesting to count the number of times LDL is mentioned compared to the number of times CRP is mentioned.  I see LDL on almost every line…24 times, in total.   CRP?  Not so much…only 4 times if I’m counting right.

JUPITER was about giving a powerful anti-inflammatory drug (Rosuvastatin) to people with extra-ordinarily high levels of inflammation who had normal cholesterol levels.  Can we really go on to say that it “JUSTIFIES” lowering LDL to below 50 in anybody else?

So your very busy doctor takes a few minutes to check his email and comes across the heartwire article saying the lower your LDL is, the better.  More than likely he already believes firmly in the value of LDL as a predictive tool for measuring the risk of heart disease.  This little headline just adds to his confirmation bias.  If he takes the time to read the article, he gets to hear from a bunch of ”experts” who endorse the conclusion that optimal LDL levels should be  around 50 (that’s about 1.5 mmol/l in Canada) and that taking Rosuvastatin is the best way to get them there. 

But here’s the multi-billion dollar question:

Will your busy doctor get the entire message?  Will he prescribe a CRP test for you to establish your level of inflammation?  If so, the AstraZenecans stand to make a handsome profit anyway since they conveniently patented the CRP test.  Or will he just get the part of the message which implies that everybody with LDL over 1.5mmol/l would benefit from a statin and could we please, please, please just start dumping Crestor in the water supply?

If Crestor and other statins like it were as effective as their inventors said they were, they wouldn’t need justification.  But the truth is, in most populations, there is very little solid evidence to prove their usefulness.  Sure, if you’ve already had a heart attack, they may help.  And I guess, if you have high CRP levels, you might be convinced that taking an expensive drug with arguably serious side effects is worth the less than 1 in 100 improvement in risk.  You could, of course, simply initiate a few dietary and lifestyle changes to bring your CRP levels down, but that wouldn’t help out the AstraZenecans very much would it?

BOTTOM LINE

Jupiter is a very controversial study.  The AstraZenecans don’t publicize anything about the peer reviewed critiques which question the validity of any conclusions based on JUPITER.  It is only one piece in a multi-faceted puzzle of research all confounded by well documented publication bias.  When we look at this research as a whole, the conclusions regarding use of statins in the primary prevention of heart disease (primary means those who have not been diagnosed with heart disease but may be deemed at risk for it) are by no means compelling.  A 2006 study by University of Toronto researchers looking at the evidence as a whole came up with this conclusion:

“In patients without CV disease, statin therapy decreases the incidence of major coronary and cerebrovascular events and revascularizations but not coronary heart disease or overall mortality.”

Translation:  If you take statins despite not having heart disease, you won’t have as many heart attacks, but you won’t live any longer or be any healthier.

“This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk primary prevention set-up.”

Translation:  Even if you are at high risk for heart disease, statins won’t help you live any longer.

Are we all really better off with extremely low levels of LDL?  Is Rosuvastatin really the best thing we can do for our health?

Only if you ask the AstraZenecans!

From the Canadian Diabetes Association:

Today, more than 9 million Canadians live with diabetes or prediabetes – a condition that, if left unchecked, puts you at risk of developing type 2 diabetes.  This means that nearly 1 in 4 Canadians either has diabetes or prediabetes.  More than 20 people are diagnosed with the disease every hour of every day.

The serious complications
Diabetes can lead to serious complications and premature death:

• 80% of Canadians with diabetes die from a heart attack or a stroke;
• 42% of new kidney dialysis patients in 2004 had diabetes.
• Diabetes is the single leading cause of blindness in Canada;
• 7 of 10 non-traumatic limb amputations are the result of diabetes complications;
• 25% of people with diabetes suffer from depression;
• The life expectancy for people with type 1 diabetes may be shortened by as much as 15 years; and
• The life expectancy for people with type 2 diabetes may be shortened by 5 to 10 years.

The cost of diabetes in Canada
Not only is diabetes a personal crisis for people with the disease, it is also a tremendous financial burden for the Canadian healthcare system and society as a whole.  The cost of diabetes for 2010 is approximately $12.2 billion, which is nearly double its level in 2000.  The cost of the disease is expected to rise to $16.9 billion by 2020.

Type II Diabetes Mellitus (T2DM) is unquestionably the most pernicious and calamitous disease of the 21st century.  The underlying dysregulation of blood sugar is devastating to both our health and our health care system.  If we are unable to control blood sugar, we will remain impotent in the battle against obesity, heart disease, or probably even cancer.  Oh, and don’t forget blindness, kidney disease, fatty liver disease and depression!  The cost to our vitality as we age will be monumental.  To our health care system, it will be disastrous.

How best to control this emerging epidemic is the subject of considerable debate.  On the one hand, national health institutions such as the Canadian Diabetes Association contend that this is a disease governed by abnormal fat regulation.  These institutions declare that a change in dietary fat consumption is the key to regulating blood sugar, and that carbohydrate consumption is only a minor part of the problem.  On the other hand, there are numerous established clinicians like Drs.  Mary Vernon and Richard Bernstein, who have had great success in controlling and even reversing diabetes by rigorously curtailing carbohydrate consumption and enthusiastically endorsing a high fat diet.

WHAT GIVES?

In order to make an educated decision about how best to avoid becoming diabetic, it is essential that we understand the basics of blood sugar regulation in the human body.  So here goes:

BLOOD SUGAR 101

How much sugar should there be in your blood?

Your body is designed to transport approximately 4 or 5 mmol/l of glucose diluted within the blood.  Since mmol/dl don’t mean much to most of us, let’s use something we can relate to.  5 mmol/l of glucose is equivalent to about a teaspoon of sugar.  So there you have it.  Your body likes to have about a teaspoon of sugar in circulation.  It doesn’t like to have much more, and it doesn’t like to have much less.  In fact:

• If you have a little more than a teaspoon of sugar in your blood (6 – 7 mmol/l), you start doing damage to your retinas, your kidneys, your arteries and your nerves. 
• If you have a little  less than a teaspoon of sugar in your blood (2 – 3 mmol/l) you will become light headed, dizzy, and unable to think clearly
• If you get much lower than 1/2 teaspoon, you risk coma and death.

Moral of the story is:  Regulate your blood sugar well or else it will make you very sick or even kill you!  This is why it is so important to understand and prevent diabetes. 

You are meant to have this much sugar in your blood.

Not this much!

What makes your blood sugar go up?

Carbohydrate consumption makes your blood sugar go up!  Protein and fat consumption do not make your blood sugar go up.  Unless you are suffering from some fairly advanced metabolic dysfunction, the only thing which will make your blood sugar go up significantly is the consumption of carbohydrates.  It is fair to say that most people would never have blood sugar issues if they spent their entire life on a low carbohydrate (less than 20% of calories from carbohydrate) diet.  Their chances of becoming diabetic would be low, and they would be much less likely to develop heart disease, kidney disease, nerve disorders or sight disorders.

Of course, the chances that you have spent your entire life at less than 20% carb in our carb centric, fat phobic, sugar addicted, grain imbrued world are slim.  For those of us who have spent the bulk of our lives consuming 60% to 80% of our calories in the form of breads, cereals, cookies and granola bars, things are not so simple.  Read on.

Hormones make your blood sugar go up.  In case you didn’t know, your brain needs some glucose to keep functioning.  This is why, when your blood sugar gets too low, you get light headed… that’s your brain needing sugar.  The coma and death part…that’ s your brain without sugar for too long.  Fortunately, you don’t have to eat carbohydrates to provide your brain with sugar.  When your blood sugar drops below about 3/4 of a teaspoon (4mmol/l) your pancreas starts sending out a hormone called glucagon.  Glucagon tells your liver to start turning glycogen (the storage form of glucose) back  into glucose, which it does rather efficiently.  If the liver runs out of glycogen, it starts turning protein into glucose, which it also does rather efficiently.  It uses dietary protein first, but if you haven’t eaten for a while, it will take protein out of the muscles and even (under starvation circumstances) the various organs.  Just so you know, the liver can also turn fat into ketone bodies, which can be used to provide the brain with about half of it’s energy.  Cortisol, the stress hormone, also makes your blood sugar go up, which is why highly stressed people are much more likely to suffer from blood sugar issues.  Epinephrine and Growth Hormone also have mechanisms designed to bring blood sugar up.

Just so we’re clear…if your metabolism is working properly (a big if in most North Americans) hormones never bring blood sugar to dangerous levels.  The hormones which regulate blood sugar are designed to protect your brain from starvation and provide you with quick energy in a stressful situation.  They are not designed to turn you into a glucose burning machine long term.

What makes your blood sugar go down?

Insulin.  Although your body has a number of complex hormonal systems designed to keep a small supply of glucose constantly streaming through your brain, it has only one hormone designed to bring your blood sugar down.  That one hormone is called insulin.  Insulin is secreted by the pancreas (as long as the pancreas is still working properly).  Type I Diabetics have a pancreas which is incapable of producing insulin.  If they eat carbohydrates, their blood sugar will go up and stay up….not good.  Type II diabetics have a dysfunctional pancreas.  It may still be capable of producing insulin, but it can not keep up to the extraordinarily high levels of insulin required to make up for the fact that their tissues are resistant to insulin.

How does insulin work?

The diagram above provides a simplified example of how insulin works.  The most helpful way to think of insulin is as a key.  Most human cells have receptors to insulin, which we can think of as locks.  When we activate the receptor, we open the lock.  When we open the lock, the cell ”opens the door” to glucose.  Insulin is the key (hormone) which opens the lock (receptor) which opens the door (the cell membrane) and allows glucose to enter the cell.  The primary tissues involved in blood sugar regulation are the liver, the muscles and the adipose tissue (fat cells).  If we are to maintain a blood sugar level of about 1 teaspoon in the face of a high carbohydrate diet, it is imperative that we don’t change the locks on the doors in these tissues.

Exercise.  Exercise has a unique effect on blood sugar.  Exercise can open the door to blood sugar in the absence of insulin.  There are some other ways for glucose to enter cells in the absence of insulin, but the effect of exercise is by far the most pronounced.  Basically, when your muscle cells start to run out of glycogen (the storage form of glucose) they send little carrier molecules (called Glut 4) out to the cell membrane in search of more glucose.  These little carrier molecules don’t seem to care whether the  door has been unlocked by insulin or not.  If the door isn’t open, they break through the cell membrane and pick up any glucose molecules that happen to be passing by in the blood stream.  This is very important, especially for people who have changed their insulin receptor locks so that insulin no longer opens them.

The role of exercise in blood sugar regulation is not limited to glut4 molecules breaking through the cell membranes though.  Exercise also improves insulin sensitivity in the muscle cells.  So if you have changed a bunch of your locks, exercise changes some of them back again!  This affect can last for up to 24 hours after a single bout of exercise

How does it all come together?

 Now that we know a little about how each of the components work, let’s take a look at how they cooperate to regulate blood sugar.  It all starts with the pancreas.  The pancreas is full of little sensors which detect blood sugar levels.  When blood sugar gets above about 1 teaspoon, the pancreas starts pushing insulin into the blood.   If the pancreas senses a rapid rise in blood sugar, it will send out a whole bunch of insulin.  If it senses a gradual rise in blood sugar, it will only send out a small dose.  Then it waits to see what happens.  If the dose was appropriate, blood sugar will go down quickly and no more insulin action will be required.  If, however, the keys (insulin) aren’t opening the locks (receptors), blood sugar stays high.  In this case, the pancreas will respond with ever-increasing doses of insulin until blood sugar finally goes down.  This whole process can take less than 10 minutes in the case of a small dose of glucose being consumed by a person who is highly sensitive to insulin (someone who hasn’t changed the locks).  It can also take more than 4 hours if the dose of carbohydrate is large and/or the person absorbing it is highly resistant to insulin (someone with way too much access to a locksmith!).  Remember that the higher the blood sugar gets and the longer it stays high, the more likely it is to do some serious damage!

Presuming your locks are working, it is important to know what happens to all that blood sugar.  In the liver, insulin stimulates the conversion of glucose to glycogen.  The liver is capable of storing about 100 grams (20 teaspoons) of glycogen.  Once the liver is full of glycogen, it will continue to take up glucose, but instead of converting it to glycogen, it turns it into fat.  Some of this fat will be stored by the liver, but most of it will be sent back into the blood stream to be used for energy or stored in the fat cells. (Important caveat – in healthy people, this conversion of sugar to fat – called de-nov0 lipogenesis – contributes only minimally to fat accumulation.  The bulk of dietary carbohydrate is either stored as glycogen or burned preferentially for energy)  In the muscles,  glucose will be burned as fuel or converted to glycogen and stored as potential fuel for future energy requirements.  Depending on how much muscle you have, you can store 300 to 400 g of glycogen (60 to 80 teaspoons) in your muscles.  Once your muscles are full of glycogen, they will become resistant to insulin and will not absorb any more glucose.  In the fat cells, glucose can be absorbed and converted to fat for storage.  (Again, in healthy people eating normal levels of carbohydrate, this doesn’t happen very much)  Insulin helps the fat cells absorb blood sugar, but the fat cells can also take up glucose in the absence of insulin.  As we all know, the fat cells have an almost infinite capacity for storage, and even when they do get full, insulin seems to help the growth of new fat cells.  In the brain, glucose will be used directly for energy.  The brain has no capacity to store glucose, which is why it requires a constant supply.

When blood sugar drops below 1 teaspoon, the body goes into glucose preservation mode.  Your pancreas knows that your brain cannot afford to run out of glucose…bad things will happen!  So your pancreas begins to secrete glucagon.  As we described above, glucagon starts turning glycogen and protein into glucose so that the brain won’t run out of energy.  Glucagon also stimulates the release of fat from the fat cells so that they can be used as energy.  This is an essential piece of the puzzle, since the release and use of fat for energy will spare glucose so that it can be used primarily by the brain.

One other essential part of the puzzle is that insulin inhibits glucagon secretion.  This makes sense, because the presence of insulin means there is plenty of glucose in the blood.  No need for the liver to make more glucose and exacerbate the issue of having damaging levels of sugar in the blood.  Likewise, no need to release fat from the fat cells, since we want the body to burn glucose for energy to help get the blood sugar levels down.  Putting more fat in the blood will only slow down this process.

Summing up:

• Eating carbohydrates makes blood sugar go up
• Insulin acts to store blood sugar in liver, muscle and fat tissues
• Insulin also prevents fat from being released from the fat cells
• When blood sugar levels drop, insulin levels go down and glucagon is secreted
• Glucagon tells the liver to make glucose
• Glucagon also allows the fat cells to release fat for energy

At least that’s how it goes when everything is working properly!

INSULIN RESITANCE – WHO CHANGED THE LOCKS?

 Type II Diabetes is a disease caused by insulin resistance.  The locks have been changed!  The pancreas continues to make plenty of insulin, but the liver, muscle and (eventually) fat cells are reluctant to open the door and let glucose in.  Blood sugar gets high – really high – and stays that way for a long time.  The pancreas tries to keep up by secreting ever higher doses of insulin, which works for a while.  At this point you are not yet diabetic…just insulin resistant.  If you were born with a genetically gifted pancreas, you can keep punching out high doses of insulin for quite some time.  If not, you get to become a diabetic much earlier.  Either way, the pancreas eventually loses it’s ability to produce enough insulin to keep up with demand.  Now you are insulin resistant and insulin deficient…that makes you a type II diabetic.  Congratulations!  You get to move up the date on your death certificate!

The unfortunate truth is that a confirmed diagnosis of type II diabetes, at least within the confines of accepted conventional treatment plans, predicts a shortened life span and practically guarantees early onset of debillitating diseases.

Part II of this series will address the issues of diagnosing, preventing and/or reversing insulin resistance.  Our medical establishment sucks at preventing or diagnosing insulin resistance before serious damage has already been done.  We can and must do better if we expect to live long vibrant lives.