An LDL is an LDL is an LDL… Or is it?


“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.

Interesting and Informative Information: Fat Isn’t So Bad, Skimpy Research on Injury Prevention in Runners


Read this!  Learn things!

What if bad fat isn’t so bad?

“Ronald Krauss, M.D., won’t say saturated fats are good for you. ‘But,’ he concedes, ‘we don’t have convincing evidence that they’re bad, either.'”

I’ve written here that I’ve been persuaded that not only is fat good for us, that “bad” saturated fat is also at the very least not as bad for us as we’ve been led to believe.  I found another article to further support my thoughts.  What if fat isn’t so bad? is a 2007 article from NBC News.  In it, we get a good dissection of the various flawed studies by which we’ve arrived at the idea that fat–particularly saturated fat–is pure evil.

The article discusses among other things Ancel Keys’s landmark Seven-Countries Study from 1970. This study did more to advance the fat/cholesterol/heart disease link than anything else around. This study went on to frame our current low-fat guidelines. Seems the conclusions that were drawn were quite inaccurate.  From the article (emphasis is mine):

“The first scientific indictment of saturated fat came in 1953. That’s the year a physiologist named Ancel Keys, Ph.D., published a highly influential paper titled “Atherosclerosis, a Problem in Newer Public Health.” Keys wrote that while the total death rate in the United States was declining, the number of deaths due to heart disease was steadily climbing. And to explain why, he presented a comparison of fat intake and heart disease mortality in six countries: the United States, Canada, Australia, England, Italy, and Japan.

The Americans ate the most fat and had the greatest number of deaths from heart disease; the Japanese ate the least fat and had the fewest deaths from heart disease. The other countries fell neatly in between. The higher the fat intake, according to national diet surveys, the higher the rate of heart disease. And vice versa. Keys called this correlation a “remarkable relationship” and began to publicly hypothesize that consumption of fat causes heart disease. This became known as the diet-heart hypothesis.

At the time, plenty of scientists were skeptical of Keys’s assertions. One such critic was Jacob Yerushalmy, Ph.D., founder of the biostatistics graduate program at the University of California at Berkeley. In a 1957 paper, Yerushalmy pointed out that while data from the six countries Keys examined seemed to support the diet-heart hypothesis, statistics were actually available for 22 countries. And when all 22 were analyzed, the apparent link between fat consumption and heart disease disappeared. For example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.”

The large-scale Women’s Health Initiative is discussed:

“We’ve spent billions of our tax dollars trying to prove the diet-heart hypothesis. Yet study after study has failed to provide definitive evidence that saturated-fat intake leads to heart disease. The most recent example is the Women’s Health Initiative, the government’s largest and most expensive ($725 million) diet study yet. The results, published last year, show that a diet low in total fat and saturated fat had no impact in reducing heart-disease and stroke rates in some 20,000 women who had adhered to the regimen for an average of 8 years.”

Several other studies are discussed.  The comment from the article on these studies is this:

“These four studies, even though they have serious flaws and are tiny compared with the Women’s Health Initiative, are often cited as definitive proof that saturated fats cause heart disease. Many other more recent trials cast doubt on the diet-heart hypothesis. These studies should be considered in the context of all the other research.”

The article goes on to discuss the subtle differences between the types of LDL or “bad” cholesterol.  Seems that all LDLs aren’t created equally:

“But there’s more to this story: In 1980, Dr. Krauss and his colleagues discovered that LDL cholesterol is far from the simple “bad” particle it’s commonly thought to be. It actually comes in a series of different sizes, known as subfractions. Some LDL subfractions are large and fluffy. Others are small and dense. This distinction is important.

A decade ago, Canadian researchers reported that men with the highest number of small, dense LDL subfractions had four times the risk of developing clogged arteries than those with the fewest. Yet they found no such association for the large, fluffy particles. These findings were confirmed in subsequent studies.

Link to heart disease
Now here’s the saturated-fat connection: Dr. Krauss found that when people replace the carbohydrates in their diet with fat — saturated or unsaturated — the number of small, dense LDL particles decreases. This leads to the highly counterintuitive notion that replacing your breakfast cereal with eggs and bacon could actually reduce your risk of heart disease.”

In much of the medical community, this talk of fat being healthy (or at least not un-healthy) is heresy. There seems to be a strong bias against openly discussing evidence to the contrary.:

“Take, for example, a 2004 Harvard University study of older women with heart disease. Researchers found that the more saturated fat these women consumed, the less likely it was their condition would worsen. Lead study author Dariush Mozaffarian, Ph.D., an assistant professor at Harvard’s school of public health, recalls that before the paper was published in the American Journal of Clinical Nutrition, he encountered formidable politics from other journals.

“‘In the nutrition field, it’s very difficult to get something published that goes against  established dogma,’ says Mozaffarian. ‘The dogma says that saturated fat is harmful, but that is not based, to me, on unequivocal evidence.’ Mozaffarian says he believes it’s critical that scientists remain open minded. ‘Our finding was surprising to us. And when there’s a discovery that goes against what’s established, it shouldn’t be suppressed but rather disseminated and explored as much as possible.'”

Go here to read the full article.

Injury prevention in runners – “skimpy research”

The smart people at Running-Physio have done a good job of summarizing a research review of studies looking into injury prevention in runners. In all, 32 studies involving 24,066 participants were examined. The relationship between injury and running frequency, volume, intensity and duration were examined. The results? I’ll let the writers tell you;

“Regular followers of RunningPhysio will know of the ongoing debate we have with those staunch supporters of research who insist we must be evidence based. Surely this shows us just how unhelpful research can be in reality – over 30 studies, involving 24,000 runners and no firm conclusions on injury prevention! No wonder Verhangen (2012) described it as “skimpy published research” and went on to conclude,

‘Specifically for novice runners knowledge on the prevention of running injuries is practically non-existent.’

Nielsen et al. isn’t the first review of its kind in this field – a Cochrane Review in 2001 reached a very similar outcome and was updated in 2011 with equally negative conclusions; Yeung, Yeung and Gillepsie (2011) completed a review of 25 studies, including over 30,000 particpants and concluded,

‘Overall, the evidence base for the effectiveness of interventions to reduce soft-tissue injury after intensive running is very weak.’

They go on to make the very wise observation that, “More attention should be paid to changes in training charactisitcs rather than the characteristics themselves.”  Based on their reading of the research review, Running-Physio makes the following suggestions:

Novice runners should be especially cautious with increasing volume or intensity of training.

Increase in weekly mileage should be done gradually. The higher the weekly mileage the more caution needs to be applied in increasing this distance. Running expert Hal Higdon talks about runners having a ‘breaking point’ – a weekly mileage above which they start to develop injuries. For every runner this is different but with experience you can find your breaking point and aim to work below it. A gradual increase in mileage helps avoid crossing this point and picking up an injury.

Changes in intensity of training should be added in isolation, rather than combined with increase in distance. Be cautious when adding interval training or hill work and use each training session for its specific goal (i.e.long slow runs at an appropriately slow pace).

Be aware of signs of injury – look out for persistent or severe pain, swelling, restricted movement or sensations of giving way.

Use rest sensibly – don’t be afraid to rest or replace running with cross training when your body needs it.

Seek help – the right GP, Physio or health care professional can make a real difference!

Something I observe here is that we’re often looking for the  (training variable) that causes the one thing (an injury).  In reality, it’s typically many variables (some of them unseen) that bring on an injury. Also, nowhere in the article or the research is the discussion of running technique. I would think that how someone runs probably has a big effect on whether or not he or she becomes injured. I’ve mentioned previously that where the foot lands in relation to one’s center of mass is quite important as it pertains to impact and running efficiency.  I’d be interested in an analysis of the foot placement (and stride length and cadence) in the role of injury.


The Skinny on Fat



I call this portrait "Health Food."


I grew up in the years of the low-fat craze.   We were told that reducing dietary fat and cholesterol—particularly animal fat—was the best way to lose weight and improve our health.  We saw wide scale proliferation of fat-free and reduced-fat food products.  These products were then stuffed with sugar and weird chemicals that were and are very detrimental to our health—but hey!!—there wasn’t any fat.  Ironically, this low-fat era saw an exponential expansion of  American’s waistlines and all the associated chronic diseases such as heart disease, diabetes and cancer.

Now we’re seeing that a lot of our dietary guidelines were way off the mark. Turns out in fact that a lot of those guidelines were based on very shaky evidence and that researchers of the time were not in agreement on the data.  A very thorough look at this evolution of our dietary guidelines can be found at the City Journal in an article titled The Washington Diet. Here’s an excerpt:

“As science writer Gary Taubes notes in Good Calories, Bad Calories, Senator George McGovern’s Select Committee on Nutrition and Human Needs, in coming up with its diet plan, had to choose among very different nutritional regimes that scientists and doctors were studying as potentially beneficial to those at risk for heart disease. Settling on the unproven theory that cholesterol was behind heart disease, the committee issued its guidelines in 1977, urging Americans to reduce the fat that they consumed from 40 percent to 30 percent of their daily calories, principally by eating less meat and fewer dairy products. The committee also advised raising carbohydrate intake to 60 percent of one’s calories and slashing one’s intake of cholesterol by a quarter.

Some of the country’s leading researchers spoke out against the guidelines and against population-wide dietary recommendations in general. Edward Ahrens, an expert in the chemistry of fatty substances at Rockefeller University, characterized the guidelines as ‘simplistic and a promoter of false hopes’ and complained that they treated the population as ‘a homogeneous group of [laboratory] rats while ignoring the wide variation’ in individual diet and blood chemistry. The Food and Nutrition Board of the National Academy of Sciences released its own dietary suggestions, which saw ‘no reason for the average healthy American to restrict consumption of cholesterol, or reduce fat intake,’ and just encouraged people to keep their weight within a normal range.”

Practical information

The very strong and very thoughtful lads at give us a simple and worthwhile article on fat titled Fats Made Simple.  This article goes into the various attributes of different fats and oils, which are best to cook with, which ones are best used as a topping, and which ones to avoid altogether.  The issue of Omega-3 and Omega-6 fatty acids is discussed.  I won’t go into every detail but here are some key points from the article:

— Use saturated fats for cooking.  These are less likely to become rancid and toxic during the cooking process.

— Use unrefined oils.  DON’T use refined oils.

The author’s top 6 oils are:

–red palm

— coconut

— macadamia nut

— extra virgin olive

— hemp seed

— walnut


— safflower

— sunflower

— canola

— corn

— sesame

— peanut

— pistachio

— pumpkin

— soybean
(Next time you’re looking at ingredient labels, see if you spot any of these oils–particularly corn, canola and soybean.  Chances are you’ll find at least one if not several.  They’re in everything!)

An eating plan

The Perfect Health Diet is an example of a a diet that’s high in healthy fat.  It was developed by two scientists who wanted to address some of their chronic health issues.   This plan has adherents eating about 2/3 plant foods and 1/3 animal-based food.  Besides a high fat content, the diet is further characterized by complete avoidance of sugar and cereal grains such as wheat, corn and oats; this due to their inflammatory nature.  (If you cut out the processed food then you’ll cut out a lot of sugar, wheat, corn etc).  Legumes such as soy and peanuts are also to be avoided as well. Here are more details of the diet.

Please take note, dietary animal fat should come from free-range grass-fed sources.  Most of the mass-produced grocery store meat is chock full of garbage such as added hormones and antibiotics.  Plus the animals are fed stuff they’re not meant to eat.

I’m currently on this eating program.  Admittedly, I haven’t followed it 100% but I’m working in that direction.  I definitely feel more energetic having reduced my grain intake.  I realize when I do consume grain, I tend to get a bit bloated.  The odd thing is eating and really enjoying a lot of foods that for years I thought were really bad for me: butter, bacon, whole eggs, chicken with the skin on it, organ meats.  I’m quite interested in sticking with this plan, further “perfecting” my eating, and seeing where it takes me.

What Do We Mean by “Fit?”


We may define the term “fit” any number of positive ways.  Most of us though probably don’t allow the term “fat” to occupy the same high ground.  The Denver Post Fitness Section for September 28, 2009 discusses the issue of whether one can indeed be both fit and fat.  The article is a profile of a woman who is both obese and seemingly healthy.  She is someone who is obese according to Federal guidelines, but who is also highly physically active, has good blood pressure and says she doesn’t miss work due to illness.  She describes her bad experiences with diets and counting calories, as well as her difficulty in finally accepting her body shape and size.  In the end, it appears she is happy with herself and in several ways, she definitely seems fit.

The big question here is can one be both fit and fat?  Again, how do we quantify fitness?  Do we mean looks?  Do we mean weight?  Are we talking body mass index (BMI), body composition or waist-to-hip ratio?  I think it’s reasonable to say that most people exercise in order to look healthy/thin/muscular.  A lean physique certainly is appealing on several levels.  And while obesity is associated with various diseases, being overweight doesn’t always guarantee poor health; and conversely, a lean physique does not automatically equal good health. (Ever noticed how many supermodels smoke cigarettes?)  The following quote says it well:
“There are many people living the ‘obesity paradox,’ says Paul Campos, a University of Colorado law professor and author of ‘The Obesity Myth.’ They are technically outside the government’s approved weight range but have bodies that are metabolically fit due to healthy eating and fitness routines. The notion that everyone can — and should — be thin is a product of political distortion and cultural panic over body diversity, he says.”