Functional Health Services for Your Well Being

Heart Disease Part I – Dispelling the Myths

written by Alex Boersma


“What you’re telling me is exactly the opposite of what my doctor told me.”


Those are often the kinds of things  people say to me when I start giving them dietary advice. Sometimes they say it with a sparkle of enthusiasm, recognizing that perhaps the medical establishment is not as omniscient as it makes itself out to be.  Sometimes they say it with a hesitant tone, as if they are for the first time experiencing some doubt about the conventional wisdom on dietary health.  But mostly they say it with a conciliatory tone, obviously unwilling to accept that the pearls of dietary wisdom they get from their health care professionals could possibly be wrong. 

I can’t blame them for that.  After all, I probably would have said the same thing ten years ago.  Back then, I was a rank and file fat-phobe.  I ate whole grains untill the sprouts started growing out of my ears.  I ate only the leanest cuts of meat.  I even gave up dairy products and started drinking soy milk!

Back then, I hadn’t read a half a dozen books on the mythology behind the cholesterol-diet-heart disease hypothesis.  I hadn’t visited dozens of web sites supporting the concept of an alternate vision on diet and heart disease.  I hadn’t heard of people like Dr. Uffe Ravskof, Anthony Colpo, Sally Falloon, Dr. Michael Eades, Dr. Weston Price, Dr. Malcolm Kendrick, Gary Taubes and Loren Cordain; all people with just as many credentials behind their names as any of the low fat gurus out there.  And I hadn’t read literally hundreds of medical studies proving that the things these people were saying had substantial merit.

What exactly were they saying?  We’ll get to that.  But first, let’s take a look at what conventional wisdom has to say about diet, cholesterol and heart disease:




EATING THIS                                                CAUSES THIS



There are two parts to the conventional wisdom on heart disease.  The first part states that consuming dietary cholesterol increases levels of cholesterol in the blood.  The second part states that having elevated cholesterol levels in the blood causes heart disease.  These two tenets make up the basis of what is known as the Diet-Heart Hypothesis.

Before we even begin to explore the two tenets outlined above, let’s make one thing clear:


That means it has never been proven!

Anybody who tells you any different is either trying to mislead you or has, themself, been misled.


Tenet #1:  Consuming dietary cholesterol increases levels of

cholesterol in the blood.

This is simply not true.  Your body makes cholesterol.  It makes a lot of cholesterol, and for good reason.  Your body needs a lot of cholesterol.  It needs it to produce most of your hormones.  It needs it to produce vitamin D.  It needs it to maintain cell walls.  It needs it to build and maintain nerves.  It needs it to produce bile so you can digest fat.

When you consume dietary cholesterol, your body says “Thank you very much” and produces less.  When you don’t consume dietary cholesterol, your body says “Aw gee, now I have to make my own” and it ramps up production.

Even Ancel Keys, the “father” of the Heart-Diet Hypothesis, admits that this is the case.  Here is what he has to say about dietary cholesterol:

“There’s no connection whatsoever between the cholesterol in food and cholesterol in the blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”  Ancel Keys

The chicken and rabbit references allude to the fact that this whole tenet is based on studies where they fed cholesterol to rabbits.  Sure enough, feeding cholesterol to rabbits makes their cholesterol skyrocket.

Here’s the thing:

Rabbits are herbivores…they are not supposed to eat cholesterol!

Human beings are omnivores…we’ve been eating cholesterol for hundreds of thousands of years!

And that, my friends, is the basis for why, to this day, people think they shouldn’t eat things like eggs and shrimp (two of the healthiest and most nutritious foods in existence, in my books).  Junk science that just happened to fit into the “theory of the day” at the time.

Tenet #2:  Having elevated cholesterol in your blood

causes heart disease.

This tenet is a little more complex than the first one.  But let’s start by saying that it is written incorrectly.  It should read ”Having elevated cholesterol in your blood is associated with heart disease”.  Of course, being associated with something means very little in terms of cause and effect.  Lightheadedness, lethargy and shortness of breath are also associated with heart disease but most of us are smart enough to realize that they are symptoms of heart disease, not causes.  Is it at all possible that elevated cholesterol is also a symptom of heart disease, and not a cause?

I’m getting ahead of myself.

Even if an association did ”prove” something, this association is very weak!

There have been literally hundreds of studies done on the association between blood cholesterol and heart disease.  Some have found a weak association between the two, others have found a weak disassociation.  But the one most quoted, and the one from which the hypothesis was originally based, is the famed Framingham Study.  This study, begun in 1948, followed about 5,000 inhabitants of a small town in Massachusetts for twenty years to see what the best predictor of heart disease was.  Their conclusion:  That having high cholesterol levels in the blood was the best indicator of risk of heart disease.

“best indicator” ???

What they should have said is that none of the factors they were looking at predicted heart disease with even the slightest degree of certainty.  Blood cholesterol was not a significant predictor of heart disease.  It was just the least insignificant of the ones they were looking at!

The correlation factor between blood cholesterol and heart disease was 0.36.  In a study this size, that means absolutely nothing.  So why did the researchers latch on to it?  Could it be that they were looking for something to justify the massive expense of this study?  Could it be that cholesterol and heart disease just happened to be the “hot” topic of the day?

 To this day, no study has come up with a correlation factor greater than 0.36 between heart disease and blood cholesterol.

Plenty of studies have come up with a negative correlation factor between the two.  The truth is, lots of people with heart disease have high blood cholesterol.  And lots have low blood cholesterol.  If high blood cholesterol was the cause of heart disease, shouldn’t all people (or at least a definitive majority) with heart disease have high blood cholesterol?


Obviously, there are serious problems with the diet-heart hypothesis as it stands.  Even the original scientists who postulated it will agree.  Partially as a result of efforts to shore up the tenets of their crumbling theory, and partially as a result of improved techniques in measuring cholesterol, the proponents of the diet-heart hypothesis have made a few amendments to it.  These amendments focus on the distinction between two different kinds of cholesterol:  LDL (the “bad” cholesterol) and HDL (the good cholesterol).  As the theory goes, it is the oxidation of LDL in the blood which begins the process of atherosclerosis, which is the first step on the path to heart disease.

Not a bad theory.  It kind of makes sense.  LDL carries cholesterol to the tissues which need cholesterol.  When you have more LDL in your blood than your cells know what to do with, the LDL hangs around in your blood, looking for something to do.  If it hangs around too long, it ends up getting oxidized, and you start on the long road to a heart attack.  HDL, on the other hand, carries cholesterol back to the liver from the tissues.  Presumably, if you have high levels of HDL in your blood, they will clean up any excess cholesterol before it can be oxidized.

So it is not cholesterol in general, but LDL cholesterol which is the culprit…as the theory goes.  Maintain a low level of LDL and a relatively high level of HDL, and you should be protected from heart disease.

With further investigation, the diet-heart researchers were happy to find that there might also be a link between diet and LDL cholesterol.  As it turns out, some studies show that the consumption of saturated fat  increases LDL.  Other studies, Framingham included, show that it does not…but we’ll leave that alone for now.

The diet-heart hypothesis was once again complete.  Instead of fat in general being an issue, saturated fat was now the villain.  And instead of total cholesterol being an issue, LDL cholesterol was now the villain.  Eat saturated fat and your LDL cholesterol will go up while your chances of getting heart disease skyrocket!

At least that’s what they wanted you to think!

But they still had to prove it!

They couldn’t prove the first part.  Although saturated fat consumption does seem to slightly increase blood levels of LDL, the extent to which it does is hotly debated.  It also increases HDL, but let’s leave that alone for now as well.   Some studies show a positive affect.  Some studies show a negative affect.  Most studies show no statistical significance.

They weren’t able to prove the second part either.  They were, however, able to make an association between high levels of blood LDL and heart disease.  It is still a weak association, and it is still just an association, so it doesn’t prove anything.  But the great minds in the medical establishment, having missed the part in statistics class about the difference between association and proof, jumped on it anyway.

What they really tried hard to prove, though, was that eating saturated fat caused heart disease.  And despite spending hundreds of millions of dollars trying to prove this, they couldn’t.  Of course, that didn’t stop them from telling all of us to stop eating saturated fat.  Here are the dietary guidelines espoused on the Heart and Stroke Foundation website as of today:

“Limit foods high in saturated fat, trans fat and/or cholesterol, such as whole-milk dairy products, fatty meats, tropical oils, partially hydrogenated vegetable oils and egg yolks. Instead choose foods low in saturated fat, trans fat and cholesterol. Here are some helpful tips:

  • Include fat-free and low-fat milk products, legumes (beans), skinless poultry and lean meats.
  • Choose fats and oils such as liquid and tub margarines, canola, corn, safflower, soy bean and olive oils.”


 Margerine?  Really?  In 2010?  Don’t we know better yet?

All this low fat advice, based on what?

I guess the people at the Heart and Stroke Foundation don’t get the journals Archives of Internal Medicine or American Journal of Clinical Nutrition.  In 2009, some researchers from McMaster University undertook “a systematic review of evidence linking a wide variety of nutritional factors and heart disease”.   Their results were published in the Archives of Internal Medicine.

They found 23 nutritional factors which were moderately to strongly associated with heart disease.

Saturated fat wasn’t even one of the 23!

After looking at 146  studies involving literally millions of people over more than 60 years of research, saturated fat consumption was ranked 30th out of 34 in importance as a nutritional risk factor for heart disease.  The authors describe the association between saturated fat consumption and heart disease as “weak”.

A related study in the January, 2010 Journal of Clinical Nutrition analyzed the association of dietary saturated fat with risk of coronary heart disease, stroke and cardiovascular disease in 21 prospective epidemiological studies. (epidemiological studies look for associations between things)  Here are the results of that study:

Results: During 5–23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.

Conclusions:A meta-analysis of prospective epidemiologic 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 data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

 Could someone tell me again why we aren’t supposed to eat saturated fat? 

After more than 60 years of trying, the proponents of the diet-heart hypothesis have quite simply not been able to prove that dietary saturated fat or cholesterol have anything to do with heart disease.  Attempting to lower your risk of getting heart disease by reducing intake of saturated fat is about as helpful as throwing a bucket of water at a forest fire.


In the midst of all this research into the diet-heart hypothesis, the pharmaceutical companies weighed in with their own studies.    The thought was, if they could prove that by reducing cholesterol through drug intervention they could significantly reduce heart disease, then they would have proven the causal link between cholesterol and heart disease.

The first round of trials failed miserably.  These were done with the older cholesterol lowering drugs.  People simply did not live longer or have reduced levels of heart disease after taking these drugs.

But then they developed statins.  Statins do significantly reduce cholesterol.  And they do significantly reduce heart attacks.  This would seem to prove that lowering cholesterol decreases the risk of getting heart disease.

Or does it?

Some of the results of these studies were confusing.  For example, older people taking statins seem to be protected from heart attacks just as much as younger people, even though it is generally agreed that cholesterol level is not related to heart disease in the elderly is something nursing homes from Home Care Assistance still take into count.  Also, people who have had a previous heart attack are equally well protected by the statins, even though cholesterol level is not generally asssociated with increased risk of future heart attacks in these people.  And, most importantly:

The statins protected people from heart attacks regardless of whether they had high levels of blood cholesterol!

In fact, your chances of having a heart attack go down if you take statins regardless of whether you have any other risk factors!

Maybe everybody should take them?

Believe me, if the pharmaceutical companies had it their way, that is exactly what would happen.  Statins in your cheerios, anybody?  Don’t laugh too hard.

I’m getting ahead of myself again.

The thing is, statins seem to protect people from heart disease regardless of cholesterol.  So the cholesterol-heart disease theory remains unproven, despite the protestations of the pharmaceutical companies.  Something else is at play here.

Could that something else be called inflammation?

We’ll talk more about inflammation in part II of this article.  But let’s just say for now that statin drugs, besides lowering cholesterol, also happen to be effective anti-inflammatories.  And inflammation has recently come to the forefront in the fight against heart disease.

Still, regardless of the mechanism, statins do seem to reduce the risk of heart disease in just about anybody.  So why not give them to everybody?  Or at least, why not give them to anybody with even the slightest risk of getting heart disease. (which, in our society, is just about everybody)


Statins don’t save lives!

Depending on who you listen to, statins have, at best, a statistically insignificant protective effect on all cause mortality.   Many studies show that people on statins are actually more likely to die of something or other than people who aren’t.  They may be less likely to have a fatal heart attack, but they are more likely to die of something like cancer.  This is particularly true if you look only at the numbers for people who have risk factors for heart disease but do not have established heart disease.  In other words, if you have already had a heart attack, then taking statins will protect you from another one, but in doing so they will only minimally extend your life.  If you only have a few risk factors for heart disease (high LDL, smoker, obesity, high blood pressure) then taking statins will still protect you from having a heart attack.  Unfortunately, under these circumstances, taking statins is not likely to extend your life at all, and may actually shorten  it..

Still think anybody with even the slightest risk of getting heart disease should take statins?

How about the NNT?

NNT is short for Numbers Needed to Treat.  NNT gives a realistic perspective on how effective a drug is.  So when a pharmaceutical company says that their drug can decrease the chance of having a heart attack by 30% (as many statins claim), the NNT tells you what that means.  Here’s an example:

  • Lipitor claims a 36% reduction in heart attacks in a drug trial for people with multiple risk factors for heart disease.
  • In that study, 2 out of every 100 people treated with Lipitor had a heart attack.
  • In the same study, 3 out of every 100 people treated with a placebo had a heart attack.
  • The difference was about 33%.
  • The number of people in this study who needed treatment in order to prevent one heart attack was 100.
  • Therefore, the NNT is 100.

In other words, according to this study, if you have a bunch of  risk factors for heart disease and your doctor prescribes you Lipitor, your chances of having a heart attack in the next five years are 1 in 50.  If you don’t take Lipitor, your chances of having a heart attack in the next 5 years are 1.5 in 50.

Here are some NNT guidelines for statin in general:

  • Non fatal heart attack…for people who have had a previous heart attack.   NNT = about 20 ( in order to prevent one non fatal heart attack you must treat about 20 people for five years).
  • All cause fatality…for people who have had a previous heart attack.  NNT = about 48 (in order to prevent one fatality (from any cause), you must treat about 48 people for five years).
  • Non fatal heart attack…for people who have risk factors for heart disease.  NNT = 70 – 250 (in order to prevent one non fatal heart attack, you must treat between 70 and 250 people for five years…the fewer risk factors you have, the higherr the NNT)
  • All cause fatality:  For people who have risk factors for heart disease, NNT = 500+ … in order to prevent one fatality(from any cause), you must treat more than 500 people for five years. In actual clinical trials, there was no significant reduction in deaths or serious events, so a precise NNT is unavailablein any case, a NNT over 100 is pretty much irrelevant.

I don’t know about you, but I know a whole bunch of people who are on statins just because their cholesterol is a little high.  They are on them despite the fact that, according to the NNT, their chance of preventing a heart attack or death by taking them are statistically insignificant.

Which would be fine if statins didn’t have any side effects!

“Converging evidence supports a mitochondrial foundation for muscle AEs (adverse effects) associated with statins, and both theoretical and empirical considerations suggest that mitochondrial dysfunction may also underlie many nonmuscle statin AEs. Evidence from RCTs (randomized controlled studies) and studies of other designs indicates existence of additional statin-associated AEs, such as cognitive loss, neuropathy, pancreatic and hepatic dysfunction, and sexual dysfunction. Physician awareness of statin AEs is reportedly low even for the AEs most widely reported by patients. Awareness and vigilance for AEs should be maintained to enable informed treatment decisions, treatment modification if appropriate, improved quality of patient care, and reduced patient morbidity.”  American Journal of Cardiovascular Drugs, 2009

Mitochondria are the parts of your cells where energy is produced.  Statins interfere, to one degree or another, with the mitochondria.  When mitochondrial funtion is impaired, the body produces less energy and more free radicals.  The compound responsible for producing energy and dealing with free radicals in the mitochondria is Coenzyme Q10.  But statins block the pathway to the production of Q10 – it is the same pathway as the production of cholesterol.

The higher the statin dose and the longer the duration of statin usage, the greater the effects on mitochondria.  Or, to put it another way, the higher the dose or the longer the duration of statin treatment, the less energy you have, the more free radicals you have, and the less Q10 you have to fight off the free radicals.  What does this look like?  Tiredness.  Muscle weakness.  Muscle pain.  Muscle dysfunction.  Rhabdomyosis (a deadly form of muscle dysfunction).  Sexual dysfunction.  Memory loss.  Organ dysfunction.

So statins for everybody over 40?

Maybe not.

We have seen that the Diet-Heart Hypothesis is based in mythology.  A series of associations supported by bad science and political myopia.  The single minded obsession with cholesterol and saturated fat has done little to enlighten us in our effort to treat or prevent heart disease.  Statin use, although effective under some limited circumstances, is certainly not the panacea the pharmaceutical companies  would have us think it is.

What are we left with then?

In part II of this series, I will explore new developments in the science of heart disease.  I will go into depth on a type of cholesterol which your doctor does not measure;  despite the fact that it actually does have significant associations with heart disease.  I will look at inflammation and how it correlates to heart disease.  And finally, I will address dietary guidelines which are almost the opposite of those supplied by the medical establishment.  Guidelines which actually have a chance of helping you prevent or reverse heart disease without the use of expensive and potentially harmful pharmaceuticals.

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