Ask any person on the street what constitutes the greatest risk factor for heart disease, and there's a good chance that you'll hear, "high cholesterol levels" - a stance that's no doubt been reinforced by the incessant advertising of cholesterol-lowering medications in recent years.
But the fact is that the level of "total cholesterol" in our blood is quickly being regarded as an unreliable and obsolete marker of heart disease risk.
It's been estimated, for example, that fully half of all people who suffer a heart attack have "normal" cholesterol levels - and realizing that a true marker of heart disease risk should probably possess a greater predictive capacity than the flip of a coin, scientists quickly concluded that a refinement of their understanding of cholesterol was in order.
As researchers began to examine the molecular-level function of cholesterol, they found that while some types of cholesterol were harmful (at least in excess), other types actually reduced our risk of cardiovascular disease. And in light of these new found insights, it didn't take long for the concepts of "good" and "bad" cholesterol to make their way into the public consciousness. The thinking was (and is) that the really meaningful clue to our cardiovascular health lay not in our total cholesterol levels, but in our ratio of HDL (the good) cholesterol to LDL (the bad) cholesterol.
This richer insight into different subclasses of cholesterol has been a giant step forward in unlocking the mystery of cardiovascular disease.
But just when you thought you had a grasp on this whole cholesterol ratio thing, it seems that scientists have recently developed testing procedures for yet another variant of cholesterol - the levels of which in our blood may be the most direct marker yet discovered of our risk of heart disease. It's called oxidized cholesterol, or more precisely, oxidized LDL.
To see just what oxidized LDL is, and why it's such a strong marker for heart disease (and most importantly, to discover ways to lower its presence in our body), it's necessary to first look at the function of LDL in general.
What's So "Bad" About LDL?
While people often use the term "LDL" to denote a type of cholesterol, LDL, or low density lipoprotein, is merely the molecular "taxi driver" that transports the fat-soluble molecule cholesterol through our blood to be deposited in our tissues (HDL, or high density lipoprotein, conversely, carries cholesterol from the tissues to the liver to be recycled or excreted). Only when LDL has cholesterol on board, can the combo of the two correctly be called "LDL cholesterol."
Now, first off, it's important to note that there’s nothing harmful about LDL or cholesterol
per se - after all, cholesterol is a major component of our cellular structure, and delivering it to the tissues is an integral part of our normal physiology. Just as bricks need to be delivered to a construction site, so too does cholesterol have to be delivered to every organ, tissue, and cell for the proper building, repair, and maintenance of our body to take place.
So why, you may ask, has LDL cholesterol been almost universally dubbed "bad" cholesterol, and what role does it really play in the all-too-common ravages of heart disease?
Oxidized Cholesterol + LDL = Oxidized LDL
LDL tends to get a bad rap simply because it chauffeurs cholesterol around our bloodstream to be deposited in our tissues. But while LDL does happen to deposit cholesterol into the arterial wall, this function alone isn't enough to deem the molecule "bad" in and of itself.
It's been found that the incorporation of cholesterol in the artery can be harmful only when the LDL molecule gets "hijacked" by cholesterol's "evil twin"- oxidized cholesterol. When LDL is carrying oxidized cholesterol, scientists call this "oxidized LDL" or oxLDL for short.
In this blog and in the Integrated Supplements Newsletters we've told you about the harmful effects of oxidized cholesterol which can be found in many foods and nutritional supplements; and which can also be produced in our body under periods of oxidative stress.
We've also shown you how this Jekyll and Hyde transformation of cholesterol from its native to oxidized form is an absolute and uncontested requirement for the arterial plaque build-up of heart disease. Knowing this, we've urged every health-conscious person to avoid any dietary cholesterol delivered in powdered or processed form (including many protein powders and nutritional drinks containing whey protein concentrate).
Oxidized Cholesterol - Cellular Hooligan
It's been shown that the poor LDL molecule can't tell good passengers from bad. It picks up oxidized cholesterol from the foods we eat just as readily as it picks up un-oxidized cholesterol - and it then deposits oxidized cholesterol in our tissues in the same fashion. But like a rowdy nightclub patron, once in the tissues, this oxidized cholesterol triggers all sorts of cellular mayhem. The "bouncers" of the immune system (called macrophages) then spring into action to get rid of it - and no, they don't just politely ask it to leave.
These macrophages are called upon to neutralize oxidized cholesterol by force; but
remember, as a free radical, oxidized cholesterol is capable of triggering a massive chain reaction of oxidative damage in surrounding cells, often overwhelming the macrophages' ability to restore order. And because all cells contain cholesterol (which is always prone to oxidation), just a small amount of oxidized cholesterol is capable of oxidizing the cholesterol in other cells as well, creating a vicious cellular "brawl" of free radical damage.
Macrophages (their name literally means "big eaters") attempt to combat oxidized cholesterol in a way similar to how they would combat, say, invading bacteria - they engulf it and attempt to "digest" it. But there’s only so much of this cellular junk that the macrophages can handle. As they continue to "stuff" themselves with oxidized cholesterol and lipids - the molecular equivalent of a feast of rancid fats, macrophages can become bloated, and can even burst, spilling their partially degraded contents into the cells of the artery causing even more damage, and invoking even more macrophage activity.
It seems that macrophages can't break down oxidized cholesterol very efficiently (the exact reason for this is the subject of intense scientific debate, by the way) and yet they still keep ingesting it. The macrophages just keep feasting on the cellular debris created by oxidized cholesterol to the point where they almost literally burst at the seams.
These macrophages, stuffed to the point of paralysis with rancid fats and oxidized cholesterol, then "stick" in the arterial wall and make up what’s called foam cells. These foam cells transform into fatty streaks and eventually harden into the arterial plaque characteristic of heart disease.
And once this process begins, our days are often numbered. As this plaque itself creates more and more damage, more macrophages are subsequently called to the area. As a result, arterial plaque grows in an ever-worsening vicious cycle, much like a snowball grows when rolling down a snow-covered hill. The sooner in our lifetime we take steps to halt this process the better, because the arterial plaque of heart disease doesn't begin to build up in middle age like most people seem to think; it has actually been shown to begin in childhood.
Eventually, this lipid and oxidized cholesterol-filled plaque will be prone to block the artery, or to rupture, spewing solid chunks of hardened rancid junk into the blood stream. This debris will quickly block blood flow in the smaller blood vessels leading to the heart (as in a heart attack) or to the brain (as in a stroke).
And to think, this whole process started when LDL innocently tried to give oxidized cholesterol a ride.
Testing For oxLDL
So, it's obvious from this description that oxidized cholesterol is a major cellular "trouble-maker." And while the molecular-level evidence implicating oxidized cholesterol in a whole host of metabolic disorders and degenerative diseases (cancer, Alzheimer's disease, etc.) has been clear for decades, it seems that even this scientific validation hasn't been quite enough to give oxidized cholesterol the pariah-status it deserves in the absence of objective testing. Most of us, after all, don't spend our free time pouring over scientific journals, and as a result, it’s all too easy to succumb to an "it’s-not-a-problem-until-my-doctor-says-it’s-a-problem" type-mentality.
But finally, after decades of accumulating research in the field, blood testing procedures for oxidized LDL are now a reality, and these state-of-the-art laboratory testing procedures are the first step needed to bring oxidized cholesterol to the attention of the medical community, the pharmaceutical giants, the food industry, and the general public alike.
A recent study published in the American Journal of Cardiology showed that the ratio of oxidized LDL ("really bad cholesterol") to HDL ("good" cholesterol) was a better predictor of coronary artery disease than tests commonly performed currently such as total cholesterol, LDL levels, HDL levels, triglycerides, and lipoprotein-associated phospholipase A2 (Lp-PLA2).
This study indicates that slowly, as the good men and women in the white coats start recognizing oxidized cholesterol as the strongest risk factor of coronary artery disease, that they'll begin ordering these specific blood tests for oxidized LDL. When they do, they'll have to then make recommendations to their patients for ways to reduce oxidized cholesterol if the tests show elevated levels. They'll hopefully then begin advising their patients to avoid oxidized cholesterol in food and "nutritional supplements," and begin recommending ways to reduce oxidative stress - two of the greatest contributors to our levels of cholesterol oxides.
Before too long we may very well find that oxidized cholesterol has become a household term, and millions of Americans have begun to take steps on a daily basis to eliminate it from their diet, and reduce its formation within their bodies.
But, of course, there is no need to wait for laboratory tests to begin lowering your burden of oxidized cholesterol. In the past few months, we’ve shown you tons of ways to do it already, and we've got much more to come.
Stay Tuned.
The thinking was (and is) that the really meaningful clue to our cardiovascular health lay not in our total cholesterol levels, but in our ratio of HDL (the good) cholesterol to LDL (the bad) cholesterol. Great news. I’m very glad to read this post.
Posted by: Jesmi | January 17, 2008 at 02:23 AM