(What The Fat)


Zombies Inside You


Everybody knows that a healthy diet is low in fat and cholesterol, because they are bad players, right? Your diet must contain carbohydrates from grains and starchy vegetables for energy, right?

But what if the truth you know is wrong? What if the bad things attributed to fat and cholesterol have actually been repeatedly misrepresented for years? What if the real problem is a process that takes normal blood components and changes them into the molecular equivalent of zombies?

That’s an uncomfortable thought.  Generally, we try to organize our lives according to certain principles. This also applies to what we eat. Initially, most of us learned about “healthy food” according to the prevailing expert advice which influenced our parents. As children, we carry those principles with us when we start our education and encounter school lunches. Later, we may receive some formal instruction in nutrition during health or biology class. Some of us proceed further in our educations and encounter still more instruction which is derived from the same “expert” sources. By the time we reach early adulthood many of us have started to use this information to figure out how to nourish ourselves for athletic training, weight loss or starting new families. For many years these experts and their facts have just been accepted at face value, but what if they were wrong?

Bad Cholesterol

Specifically, I refer to the growing body of evidence which shows much of what we learned about fat, cholesterol and carbohydrates is wrong. Up until this week, the conventional wisdom was to eat a diet low in fat and cholesterol and high in carbohydrates in order to achieve the levels of “good” cholesterol vs “bad” cholesterol. As I sit here typing, in the final week of June 2015, the federally funded 2015 Dietary Guidelines for Americans Committee (DGAC) has quietly abandoned the recommended restrictions on dietary fat. Similarly, in February 2015 they backed away from cholesterol restrictions. Although they have not endorsed a low carbohydrate diet per se, they do acknowledge that this modification will steer dietary recommendations away from foods high in sugar. The DGAC have yet to extend their scrutiny to the starches, which are merely sugar molecules linked together. This is an indication that the evidence favoring a diet low in carbohydrates has become too difficult to continue to ignore.

So, how did we get here? And where are the zombies?

The prevailing expert opinion on cardiovascular disease (CVD) is a convergence of ideas and observations dating back hundreds of years. Atherosclerosis is the condition whereby blood vessels become compromised by the characteristic fatty accumulations in their walls.  CVD is the clinical manifestation of atherosclosis in the blood vessels.

The History of Cholesterol

Here’s a condensed historical perspective.

Although the concept of circulation was not yet established in his day, Leonardo da Vinci wrote about atherosclerotic vascular disease early in the 16th  century.  As a scientist and artist, he was interested in human anatomy. In his writings he described an elderly man whose death was peaceful and without pain.  This enticed him to perform an autopsy wherein he concluded, “The old who enjoy good health die through lack of sustenance, and this is brought about by the continuous narrowing of the passage of the mesenteric vessels by thickening of the coats of these vessels”. This was an early description of diseased blood vessels, and it hinted at the resultant consequences.

At the time of his writing, da Vinci and the physicians of his day, believed that blood emanated from the gut where it was produced from the ingestion of nutrients, and was then drawn up by the other tissues to be consumed. It was not until William Harvey published his “de Motu Cordis” in 1628, that the true nature of the circulatory system of was introduced.  This insight made it possible to see the interruption of blood flow as a mechanism for disease and traumatic injury.

Later, after the development of the microscope, doctors were able to delve further into the processes of disease states than was previously possible with the naked eye. During the middle and late 19th century, the father of modern pathology, Rudolph Virchow put forth the concept of disease states as the result of abnormalities occurring at the cellular level. Among his many contributions, is the observation that the lesions of atherosclerosis, called plaques, contained fatty and fibrous components. Furthermore, he was the first to theorize that these plaques were the result of an inflammatory process.

By 1910, cholesterol was starting to look like a bad player in the process of atherosclerosis. It had become possible to extract and identify organic compounds from the plaques of diseased blood vessels.  Adolph Windaus, a German chemist who devoted his career to the chemistry of cholesterol, demonstrated a large excess of cholesterol present in the plaques of atherosclerosis compared to tissue from the normal blood vessel wall. His expertise on the chemistry of cholesterol led to the discovery of vitamin D for which he won a Nobel Prize in 1928.

In 1913, Nikolai N. Anichkov, fed rabbits a diet high in cholesterol, and subsequently observed atherosclerotic plaques in their arteries. To many, this was proof that cholesterol was the cause of atherosclerosis in humans.

More evidence came in the late 1940’s, when the early finding of the Framingham study identified a high serum cholesterol level as a risk factor for cardiovascular disease (atherosclerosis).  Then in the 1950’s, early data from what would become the crown jewel of the cholesterol theory, the famous Ancel Keys’, Seven Countries Study, “showed” a connection between a high fat diet and increased incidence of CVD.  The actual merits of the study are questionable since data, which contradicted the conclusion, was selectively ignored.

These studies, set against the background which had been painted over hundreds of years, led to the assumption that cholesterol and its partner in crime, fat, were responsible for atherosclerosis. Doctors, scientists and politicians saw the fire, and the smoke was cholesterol and fat. It seemed so simple.  Don’t eat fat or cholesterol and you’ll be fine, right?

Here’s the problem. While the cliché holds true that where there’s smoke there’s fire; we can’t assume that the smoke caused the fire.  The case against fat and cholesterol does show an association, but it has never accounted for the mechanism involved. The dietary guidelines that were inspired by this faulty thinking have resulted in decades of people shunning dietary fat and cholesterol in favor of carbohydrates. How has that worked out? The incidence of diabetes, obesity and CVD have only increased.

Zombie (Bad) Cholesterol

Cholesterol and some types of fat are necessary for good health.  Dietary cholesterol has almost nothing to do with blood levels. If you eat very little cholesterol, the liver will still produce it because cholesterol is a substance vital to many normal body structures and functions. Neither cholesterol nor fat roam free in the blood. They are packaged together with proteins for transport which are then designated as, High Density Lipoprotein (HDL), Low Density Lipoprotein (LDL) or Very Low Density Lipoprotein (VLDL), depending on the amounts of each component present. What your blood tests report as good or bad cholesterol are actually these conglomerates of fat and cholesterol with protein. The LDL is traditionally identified as the bad cholesterol. Protein, fat and cholesterol are all involved in the concept of cholesterol levels, but it is the programming that you impose on your metabolism which dictates what these “cholesterol levels” will be.

In particular, what seems promising in regard to the true nature of cardiovascular disease involves the identification of a specific fraction of what is reported as an LDL number, known as small, dense LDL (sd-LDL). It is essentially a damaged LDL molecule. This is the “zombie” form of cholesterol. In fact, let me give it a new designation: ZLDL. Like any zombie, it has no home and no known purpose. It drifts aimlessly through the circulation, and as zombies are known to do, it finds a way to cause trouble. It has the ability to permeate the blood vessel wall and contribute to the genesis of the plaques which define cardiovascular disease.  The concentration of these molecules increases when the dietary carbohydrate load is increased. Recent studies have shown that diets lower in carbohydrates, which are necessarily high in fat, will lower the number of zombies for most people, even if the total LDL actually increases.

Again, ZLDL is the smoke, but the fire is that which causes the damage to the LDL molecules and the blood vessel walls in the first place. This is where the concept of inflammation comes back to us.

Remember Dr. Virchow from 160 years ago? He postulated that the underlying problem of atherosclerosis was inflammation. We spent the last 65 years chasing cholesterol and fat instead of the inflammation!  Why not prevent the zombie cholesterol instead of worrying about how to manage it after the fact? The best evidence at this time implicates several possible causes including elevated blood sugar levels and Reactive Oxygen Species (ROS). We won’t talk about ROS now.  Briefly, they are a category of bad substances produced by cells during their process of burning fuel in the presence of oxygen. Normally the body has mechanisms to deal with these, but if your metabolism has been altered, the ROS can be increased.

There are two new, important ideas here:

  • First, don’t be inflamed! Prevent your own zombie apocalypse! You can develop your diet and other habits to develop the equivalent of your own internal zombie hunters!
  • Second, be an informed consumer of all things, including information. Seek and verify your own information.

I do not have the space here to explain the finer details of cholesterol confusion which have confounded the worlds of health, nutrition, medicine and pharmaceuticals since the famous Seven Countries Study in 1953. However, I do recommend several sources for those wanting to explore further. These include: Cholesterol Clarity by Jimmy Moore, Good Calories, Bad Calories by Gary Taubes, and The Big Fat Surprise by Nina Teicholz.

Also, I want to include a link to Dr. Ken Sikaris’ talk from Nov. 2014 on cholesterol. He inspired me to give this perspective on the true bad cholesterol. He does a great job explaining LDL and the other forms of cholesterol. He characterized sd-LDL as the “Frankenstein of cholesterol.” I just wanted to update the monster so you might better remember it.