An LDL is an LDL is an LDL… Or is it?

Standard

“We may be medicating many people who have no clear need for medication, using drugs that don’t target the right particles, and replacing foods that are benign with foods that are anything but.”

Recent posts (here and here) have dealt with the ketogenic way of eating.  So fat and all things related have been on my mind. And what terrifying substance enters our thoughts right on the heels of fat?  Cholesterol, obviously. We often think that eating more fat means more cholesterol in our bodies. (That may or may not be true and even if it is it may not be bad at all.  I know that sounds like heresy crossed with insanity but a lot of research out there strongly suggests it.) I found an interesting article recently that comes from Men’s Health by way of NBC News.

It’s called Bad cholesterol: It’s not what you think. It suggests the idea that even the so-called “bad” cholesterol isn’t all bad, and that elevated levels of a certain type of “bad” cholesterol may be no danger at all.

Most of us are fairly familiar with cholesterol.  We’re told it’s bad and that generally we should strive for a low cholesterol count. Beyond the simple cholesterol count, there is our cholesterol ratio, that is your total cholesterol count divided by your HDL count.  Most of us know about the “good” cholesterol known as HDL or high-density lipoprotein; and the “bad,” LDL aka low-density lipoprotein. We’re told that LDLs are dangerous, come from eating high-fat foods and if we have too many of them then we may need some tasty cholesterol-lowering drugs!

Well, much like characters in Game of Thrones, these LDL’s are complex and not all of them are pure evil. Here’s a description from the article (emphasis is mine.):

LDL comes in four basic forms: a big, fluffy form known as large LDL, and three increasingly dense forms known as medium, small, and very small LDL. A diet high in saturated fat mainly boosts the numbers of large-LDL particles, while a low-fat diet high in carbohydrates propagates the smaller forms. The big, fluffy particles are largely benign, while the small, dense versions keep lipid-science researchers awake at night.

So it seems we can relax a little when it comes to our view on LDLs. And we should adjust our take on what foods are truly dangerous as it pertains to cholesterol.

What often happens when we’re told we have high cholesterol or high LDLs? We’re given pills (statins) to lower our cholesterol. On that issue, the article states:

Some of these forms of LDL are relatively safe and some are dangerous, and treating them all as one and the same — the way we do every time we pay our clinic for a three-part lipid panel that simplistically says “LDL: 125″ — is telling us little about the LDL cholesterol that matters, all the while sending health costs through the roof. We may be medicating many people who have no clear need for medication, using drugs that don’t target the right particles, and replacing foods that are benign with foods that are anything but.

Let’s remember that while the word “cholesterol” carries negative connotations for a lot of people, this substance actually has important physiologic functions. Our cell membranes are built from cholesterol. The myelin that wraps around our neurons and acts as a vital insulator is made of cholesterol. So cholesterol is there for a reason. (One possible impetus for increased cholesterol production in, say a hard-exercising athlete, is that tissues are being damaged from exercise and are in need of repair.  Thus we make more cholesterol to build more cells. Doesn’t sound bad does it?) So we may be stepping in the way of a not just a perfectly normal process (the manufacture of cholesterol) but a vital and healthy process that if impeded may endanger our health. I wonder if that’s why statins have so many ugly side effects.  (By the way, why do we call them “side effects?” There are only effects, right?)

Here’s some more interesting information from the article regarding HDLs vs. LDLs (emphasis is mine):

A 1977 NIH study — an early set of papers from the now legendary Framingham Heart Study — confirmed that high HDL is associated with a reduced risk of heart disease. It also confirmed that LDL and “total cholesterol” tells us little about the risk of having a heart attack, language that heart-disease authorities would downplay years later. Given this finding, as Gary Taubes writes in “Good Calories, Bad Calories,” we would have been better off to start testing for HDL — or even triglycerides — and nothing else.”

Ronald M. Krauss, M.D., the director of the department of atherosclerosis research at Children’s Hospital Oakland Research Institute, is interviewed in this article. Here makes some important observations and statements:

“Everyone doesn’t necessarily have the same amount of very small LDL in their LDL,” Dr. Krauss explains. Some people have mostly large LDL, a group Dr. Krauss would describe as “pattern A,” while others have mostly small LDL (and usually, low HDL and high triglycerides), a group Dr. Krauss would label “pattern B.” The second group has an increased risk of heart disease (a finding suggested again this year through the use of ion mobility). Large LDL, on the other hand — and large LDL is usually the majority of the LDL that shows up in a standard blood profile — is mostly benign.

The heart-disease community was not impressed. “It took me 4 years to publish that paper,” he says, recalling his early work on subparticles in the late 1970s. “That’s beginning to tell you some of the obstacles I was going to face.”

The cost of that resistance had become apparent by the mid-1980s and into the 1990s as Dr. Krauss began to test whether changes in diet could change a person’s LDL profile from good to bad, or from pattern A to pattern B. Using data from the Framingham Heart Study — the longest-running study of its kind — health organizations had begun to roll out the message of “good” and “bad” cholesterol, a message that in turn created the concept of good fats and bad fats. But during experiments, Dr. Krauss discovered that while a diet high in saturated fat from dairy products would indeed make your LDL levels rise, “saturated fat intake results in an increase of larger LDL rather than smaller LDL particles,” as he wrote in an American Journal of Clinical Nutrition review he co-authored in 2006. A diet heavy in full-fat cheese and butter — but not overloaded in calories — triggered the relatively harmless health profile described as pattern A. (Having demonstrated the benign consequences for cholesterol from consuming dairy fat, he is currently conducting studies to find out if the same holds true for diets high in saturated fat from beef.)

Did you notice those last few sentences? It’s further evidence that the high-fat/low-carb ketogenic diet is entirely safe. (Beyond just safe, there’s ample evidence of the powerful neuroprotective properties of keto diet.  It’s been used for years to treat epilepsy and may be useful in combating Alzheimer’s and Parkinson’s. I’m not sure to what degree it’s a significant component but remember, cholesterol is a key component of our neurological tissues.)

I also love this observation:

“Not only is dairy fat unlikely to increase heart-disease risk, Dr. Krauss and others have learned, but reducing saturated fat in a way that increases carbohydrates in a diet can shift a person’s LDL profile from safe to dangerous. That’s pretty much what happens whenever some well-meaning person with “high LDL” starts eating “low-fat” frozen dinners filled out with corn-derived additives, all the while engaging in the customary ravaging of a basket filled with dinner rolls.”

Here’s the big takeaway (emphasis is mine):

So with small-LDL testing far from standard (your doctor can request an ion mobility analysis from Quest Diagnostics), the surest way you can reduce your numbers of the LDL that matters is to rely on time-tested advice. Eating fewer carbohydrates, losing weight, and engaging in more physical activity have all been shown to reduce small LDL. Weight loss, in fact, has been demonstrated to reverse the dreaded pattern B all by itself. In other words, worry less about eggs or butter and their effect on LDL, and focus more on eating fewer processed foods and staying in motion. “I am very much an advocate of starting with lifestyle first,” Dr. Krauss says.”

Go here to read the full article.

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