Summary:
- The simplified view of cholesterol as “good” (HDL) or “bad” (LDL) has contributed to the continuing heart disease epidemic
- Not all LDL cholesterol is created equal. Only small, dense LDL particles are associated with heart disease, whereas large, buoyant LDL are either benign or may protect against heart disease.
- Replacing saturated fats with carbohydrates – which has been recommended by the American Heart Association for decades – reduces HDL and increases small, dense LDL, both of which are associated with increased risk of heart disease.
- Dietary cholesterol has a negligible effect on total blood LDL cholesterol levels. However, eating eggs every day reduces small, dense LDL, which in turn reduces risk of heart disease.
- The best way to lower small, dense LDL and protect yourself from heart disease is to eat fewer carbs (not fat and cholesterol), exercise and lose weight.
Not all cholesterol is created equal
By now most people have been exposed to the idea of “good” and “bad” cholesterol. It’s yet another deeply ingrained cultural belief, such as the one I wrote about last week, that has been relentlessly driven into our heads for several decades.
But once we’ve put on our Healthy Skeptic goggles, which I know all of you fair readers have, we no longer simply believe what we’re told by the medical establishment or mainstream media. Nor are we impressed or in any way swayed by the number of people that tell us something is true. After all, as Anatole France said, “Even if fifty million people say a foolish thing, it is still a foolish thing.”
Words to live by.
The oversimplified view of HDL cholesterol as “good” and LDL cholesterol as “bad” is not only incomplete, it has also directly contributed to the continuing heart disease epidemic worldwide.
But before we discover why, we first have to address another common misconception. LDL and HDL are not cholesterol. We refer to them as cholesterol, but they aren’t. LDL (low density lipoprotein) and HDL (high density lipoprotein) are proteins that transport cholesterol through the blood. Cholesterol, like all fats, doesn’t dissolve in water (or blood) so it must be transported through the blood by these lipoproteins. The names LDL and HDL refer to the different types of lipoproteins that transport cholesterol.
In addition to cholesterol, lipoproteins carry three fat molecules (polyunsaturated, monounsaturated, saturated – otherwise known as a triglyceride). Cholesterol is a waxy fat particle that almost every cell in the body synthesizes, which should give you some clue about its importance for physiological function.
You do not have a cholesterol level in your blood, because there is no cholesterol in the blood. When we speak of our “cholesterol levels”, what is actually being measured is the level of various lipoproteins (like LDL and HDL).
Which brings us back to the subject at hand. The consensus belief, as I’m sure you’re aware, is that LDL is “bad” cholesterol and HDL is “good” cholesterol. High levels of LDL put us at risk for heart disease, and low levels of LDL protect us from it. Likewise, low levels of HDL are a risk factor for heart disease, and high levels are protective.
It such a simple explanation, and it helps drug companies to sell more than $14 billion dollars worth of “bad” cholesterol-lowering medications to more than 24 million American each year.
The only problem (for people who actually take the drugs, rather than sell them, that is) is the idea that all LDL cholesterol is “bad” is simply not true.
In order for cholesterol-carrying lipoproteins to cause disease, they have to damage the wall of an artery. The smaller an LDL particle is, the more likely it is to do this. In fact, a 1988 study showed that small, dense LDL are three times more likely to cause heart disease than normal LDL.
On the other hand, large LDL are buoyant and easily move through the circulatory system without damaging the arteries.
Think of it this way. Small, dense LDL are like BBs. Large, buoyant LDL are like beach balls. If you throw a beach ball at a window, nothing happens. But if you shoot that window with a BB gun, it breaks.
Another problem with small LDL is that they are more susceptible to oxidation. Oxidized LDL, or oxLDL, is formed when the fats in LDL particles react with oxidation and break down.
Researchers have shown that the smaller and denser LDL gets, the more quickly it oxidizes when they subject it to oxidants in a test tube.
Why does this matter? oxLDL is a far greater risk factor for heart disease than normal LDL. A large prospective study by Meisinger et al. showed that participants with high oxLDL had more than four times the risk of a heart attack than patients with lower oxLDL.
I hope it’s clear by now that the notion of “good” and “bad” cholesterol is misleading and incomplete. Not all LDL cholesterol is the same. Large, buoyant LDL are benign or protect against heart disease, whereas small, dense LDL are a significant risk factor. If there is truly a “bad” cholesterol, it is small LDL. But calling all LDL “bad” is a dangerous mistake.
Low-fat, high-carb diets raise “bad” cholesterol and lower “good” cholesterol
Here’s where the story gets even more interesting. And tragic.
Researchers working in this area have defined what they call Pattern A and Pattern B. Pattern A is when small, dense LDL is low, large, buoyant LDL is high, and HDL is high. Pattern B is when small, dense LDL is high, HDL is low, and triglycerides are high. Pattern B is strongly associated with increased risk of heart disease, whereas Pattern A is not.
It is not saturated fat or cholesterol that increases the amount of small, dense LDL we have in our blood. It’s carbohydrate.
Dr. Ronald Krauss has shown that reducing saturated fat and increasing carbohydrate intake shifts Pattern A to Pattern B – and in the process significantly increases your risk of heart disease. Ironically, this is exactly what the American Heart Association and other similar organizations have been recommending for decades.
In Dr. Krauss’s study, participants who ate the most saturated fat had the largest LDL, and vice versa.
Krauss also tested the effect of his dietary intervention on HDL (so-called “good” cholesterol). Studies have found that the largest HDL particles, HDL2b, provide the greatest protective effect against heart disease.
Guess what? Compared to diets high in both total and saturated fat, low-fat, high-carbohydrate diets decreased HDL2b levels. In yet another blow to the American Heart Association’s recommendations, Berglund et al. showed that using their suggested low-fat diet reduced HDL2b in men and women of diverse racial backgrounds.
Here’s what the authors said about their results:
The results indicate that dietary changes suggested to be prudent for a large segment of the population will primarily affect [i.e., reduce] the concentrations of the most prominent antiatherogenic [anti-heart attack] HDL subpopulation.
Translation: following the advice of the American Heart Association is hazardous to your health.
Eating cholesterol reduces small LDL
The amount of cholesterol in the diet is only weakly correlated with blood cholesterol levels. A recent review of the scientific literature published in Current Opinion in Clinical Nutrition and Metabolic Care clearly indicates that egg consumption has no discernible impact on blood cholesterol levels in 70% of the population. In the other 30% of the population (termed “hyperresponders”), eggs do increase both circulating LDL and HDL cholesterol.
Why is this? Cholesterol is such an important substance that its production is tightly regulated by the body. When you eat more, the body produces less, and vice versa. This is why the amount of cholesterol you eat has little – if any – impact on the cholesterol levels in your blood.
Eating cholesterol is not only harmless, it’s beneficial. In fact, one of the best ways to lower small, dense LDL is to eat eggs every day! Yes, you read that correctly. University of Connecticut researchers recently found that people who ate three whole eggs a day for 12 weeks dropped their small-LDL levels by an average of 18 percent.
If you’re confused right now I certainly don’t blame you.
Let’s review what we’ve been told for more than 50 years:
- Eating saturated fat and cholesterol in the diet raises “bad” cholesterol in the blood and increases the risk of heart disease.
- Reducing intake or saturated fat and cholesterol protects us against heart disease.
Now, let’s examine what credible scientific research published in major peer-reviewed journals in the last decade tells us:
- Eating saturated fat and cholesterol reduces the type of cholesterol associated with heart disease.
- Replacing saturated fat and cholesterol with carbohydrates lowers “good” (HDL) cholesterol, raises triglyceride levels, and increases our risk of heart disease.
Dr. Krauss, the author of one of the studies I mentioned above, recently said in an interview published in Men’s Health, “Everybody I know in the field — everybody — recognized that a simple low-fat message was a mistake.”
In other words, the advice we’ve been given by medical “authorities” over the past half century on how to prevent heart disease is actually causing it.
I don’t know about you, but that makes me very angry. Heart disease is the #1 cause of death in the US. Almost 4 in 10 people who die each year die of heart disease. It directly affects over 80 million Americans each year, and indirectly affects millions more.
We spend almost half a trillion dollars treating heart disease each year. To put this in perspective, the United Nations has estimated that ending world hunger would cost just $195 billion.
Yet in spite of all this money spent, the best medical authorities can do is tell us the exact opposite of what we should be doing? And they continue to give us the wrong information even though researchers have known that it’s wrong for at least the past fifteen years?
Really?
Sometimes it seems like everything is backwards.
How to reduce small LDL
Eating fewer carbs is perhaps the best place to start. Reducing carbs has several cardio-protective effects. It reduces levels of small, dense LDL, reduces triglycerides, and increases HDL levels. A triple whammy.
Exercise and losing weight also reduce small, dense LDL. In fact, weight loss has been shown to reverse the evil Pattern B all by itself.
As we saw above, eating three eggs a day can reduce our small LDL by almost 20%. Interestingly, alcohol has also been shown to reduce small LDL by 20%.
In other words, if you want to reduce your risk of heart disease, do the opposite of the American Heart Association (and probably your doctor) tells you to do. Eat butter. Eat eggs. Eat traditional animal fats. Reduce your intake of carbs, vegetable oils and processed foods, and stay active and within a healthy weight range.
Testing your small LDL level
I’m not a fan of arbitrary testing. Our medical system is obsessed with testing. But where has testing has brought us with cholesterol and heart disease? Has it improved outcomes? On the contrary, we test for a number (total LDL) that tells us very little, and then medicate it downwards recklessly and expensively.
If you’re worried about your small LDL level, my advice would be to eat fewer carbohydrates, eat plenty of saturated fat and cholesterol (instead of vegetable oils), exercise, lose weight if you need to, and have a drink every now and then! Since this is the same advice I’d give you if you took a test that actually showed high levels of small LDL, I don’t see much value in doing the test.
However, if you need to see the test results to get motivated to make the changes I suggested above, by all means do the test. There are a few ways to go about it.
First, keep in mind that a regular cholesterol test at your doctor won’t tell you anything about your small LDL level. The standard tests measure your total cholesterol, LDL and HDL. But they don’t distinguish between the dangerous small LDL and benign or protective large LDL.
The fastest and cheapest, albeit most indirect, route is to test your blood sugar both before and then 60 minutes after a meal (this is called a “post-prandial” glucose test). The reason a post-prandial blood glucose test can be a rough indicator for small LDL is the same foods that trigger a rise in blood sugar also increase small LDL. Namely, carbohydrates.
Blood glucose monitors are readily available at places like Walgreens and cost about $10. You’ll also need lancets and test strips, which aren’t expensive either. If your post-prandial glucose is higher than 120 mg/dl, that may be suggestive of a higher than desired small LDL level. This test is not a perfect approximation of small LDL, but it’s the cheapest and and easiest way to get a sense of it.
If you want to get more specific, there are two tests I recommend for small LDL that use slightly different methodology:
- LDL-S3 GGE Test. Proteins from your blood are spread across a gel palette. As the molecules move from one end to the other, the gel becomes progressively denser. Large particles of LDL cholesterol can’t travel as far as the small, dense particles can, Dr. Ziajka says. After staining the gel, scientists determine the average size of your LDL cholesterol particles. Berkeley Heart Lab. About $15 with insurance.
- The VAP Test. Your sample is mixed into a solution designed to separate lipoproteins by density. Small, dense particles sink, and large, fluffy particles stay at the top. The liquid is stained and then analyzed to reveal 21 different lipoprotein subfractions, including dominant LDL size. The Vap Test. Direct cost is $40.
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{ 66 comments… read them below or add one }
My 92 year old grandmother has been eating low fat her whole life and struggling with high cholesterol her whole life as well. She dealt multiple times with clogged ateries and valve replacements. She’s been baffled because she’s been religious about staying away from the saturated fat and cholesterol and has eaten piles of bran. I think she’s finally starting to relaize it’s not working. She actually went and got some butter. I told her to add some liver to that as well.
I have another question to pose about our grand ole food pyramid. We know it’s causing these problems. I know it’s caused my autoimmune problems and contributed to my childs autism. I’m currently reading Blood Suger 101, and beginning to wonder something else too. Would it be fair to say that eating by the food pyramid also makes diabetes inevitable for some of us?
Tracee,
There’s plenty of evidence to suggest that a high-carb diet, such as the one recommended for decades by the AHA and ADA, can contribute to diabetes (as well as heart disease). The physiological mechanisms for this are well understood. It’s a tragedy that these high-carb diets are still being recommended.
Chris
The very fact that she has reached an age of 92 means that she has done something right.
Don’t induce big changes in her life at this age.
Excellent post. I shared a link to it on my Facebook page.
About five years ago I was told that my “cholesterol” was high. Of course my then-MD wanted to put me on a statin drug right away. I also had borderline-high blood glucose levels. I refused the drugs and told him I would treat it with diet. He seemed pretty sceptical but relented. A year later I went back for the checkup and everything was much better, in fact under what’s considered optimal. He asked me what I’d done: cut out all processed food, nearly all grain and grain-based foods, and all sugars. Basically if it didn’t come out of the ground/ocean/farm that way, I wouldn’t eat it.
Slowly my intake devolved back to including grains, dairy and some sweets and I sure felt it. Recently discovered the so-called Paleo diet which bans dairy, starchy veg, sweets and all grains. Already down about an inch off the waist without exercise, though I kinda miss good hard cheeses. Eh.
Many conditions can be treated and reversed simply by eating real, actual food, not processed crap. Lean pasture-fed meat, non-farmed seafood, organic fruit and non-starchy vegetables. A bit of a fight to find unadulterated sources, though.
The USDA food pyramid was brought to you by Con-Agra, Monsanto, and all the other companies with a stake in keeping you fat, stupid, and stuffed with high-margin corn by-products. The profit margin on anything processed is far higher than on real food.
That your 92 year old grandmother is still alive (thus living MUCH longer than the national median) proves she must be doing something right, or at least that she has good genes.
I agree
A few points:
1. Small dense LDL particles tend to oxidize more readily for several reasons, not the least of which is that they remain present in the blood stream longer than larger LDL particles, and thus are exposed to oxidative stresses. So, the case has been hypothesized that small dense LDL can pose a greater risk.
But, in your post above you go beyond simply talking about the increased risk of small LDL-P and instead state that ” Large, buoyant LDL are benign or protect against heart disease”.
Do you have any single cite for that to any study, whether a clinical intervention, prospective randomized controlled clinical trial, meta-analysis, lab animal experiments, in vivo or in vitro analysis, etc., which might support the statement that “large fluffy LDL” are in some manner actually protective? No? And by citation, I mean to something other than the often repeated statements to the same effect from Dr. BG’s “Animal Pharm” website? No? I didn’t think so. Certainly there is evidence which has tested the hypothesis that small dense LDL-P, or what has been described as “Pattern B” increases the risk of atherosclerotic lesion formation. But there is not a single bit of evidence which demonstrates the opposite, i.e., that abundant large LDL particles are somehow “protective” or that simply because a person’s LDL consists principally of larger (i.e., >20.6 nmol/l) one need not be concerned with one’s overall LDL-P. The fact is that LDL-C is a surrogate for LDL-P, and the NCEP ATP III guidelines have been tested over time and in high risk individuals, lowering LDL-C to 70 mg/dl (and the number of LDL-P to <1000 ) has been demonstrated in hundreds of clincial trials to reduce events, reduce the incidence and severity of atherosclerosis and CVD.
1. You mention VAP and Berkeley, but there is a third equally effective, and some would say more effective and direct way of measuring LDL particle number and size and that’s with Liposcience’s NMR Advanced Lipoprotein profile. The method used is nuclear magnetic resonance, different than the methods used by both Berkeley (which as you note uses GGE) and VAP (which uses an ultracentrifugation method). The cost is about the same as VAP and it’s covered by most insurance.
3. Many people have gotten very excited by Krauss’ most recent paper, the one you note was e-published ahead of print. However, most of the commentators haven’t read it, and are instead relying solely on the abstract. I find it ironic that most of the critics who are huge proponents of virtually unlimited SFA intake, who frequently criticize such studies as the Nurses’ Health Study, or Framingham, etc., because of what they claim were faulty data collection methods or improper study designs, are now touting this lates Krauss paper, which is simply a meta-analysis using the same data so many have criticized previously. Meta-analysis can provide greater statistical power, but it also really is only an average of averages, and it doesn’t matter how good the methods used to “scrub” or redefine the data, even the best meta-analysis can’t make bad data into good data. Moreover, the actual study (not the abstract) concludes that while no association was demonstrated from the data in an epidemiological sense, the authors were also quick to note that absolutely no conclusions could be reached with respect to the effects of consuming sat fats in individuals because the data they were working with was insufficient. In other words, those who are now claiming that sat fat doesn’t “cause” heart disease are suffering from the same problem that has always been the problem, i.e., there just isn’t enough evidence one way or the other to be certain about causation, and as a result, it would be extremely imprudent to use the latest Krauss study as an excuse to now conclude that eating virtually unlimited amounts of saturated fats, particularly from animals, is “safe” or that it definitely won’t cause heart disease.
Thanks for your comment.
I agree that meta-analyses can’t be relied on and often lead to conclusions not warranted by the original study data. I think part of my point in drawing attention to that study is that it was a major study published by a respected researcher in a mainstream peer-reviewed journal exonerating saturated fat as a causative agent in heart disease. That was a landmark event. But we don’t need to rely on it alone to come to that conclusion. There are many, many studies old and new that provide evidence that saturated fat doesn’t cause heart disease. Dr. Eades covers some of the older ones here. Chris Masterjohn reports on a 2006 study in this post. There is the Mozaffarian group’s study published in Am J of Clinical Nutrition in 2004 showing that as the intake of saturated fat increased in post-menopausal women, the progression of atherosclerosis actually reversed. The association was monotonic and continuous. Trials have shown no difference in LDL between people eating more saturated fat and people eating less, on timescales of one year or more (some short trials show a modest LDL-raising effect, but even this appears to be due to an increase in particle size rather than particle number). This study, and others such as MRFIT, the Women’s Health Initiative Diet Modification trial and the Lyon Diet-Heart trial, suggest that reducing saturated fat intake had little or no effect on total cholesterol or LDL (0-3% reduction).
Then there is the fact that, of the numerous controlled clinical trials examining dietary interventions for heart disease prevention, none has ever demonstrated a beneficial effect of saturated fat restriction. Here is just a sampling of prospective studies spanning half a century showing no association between saturated fat intake and heart disease. Of the twenty-six long-term studies monitoring selected populations for the occurrence of heart disease, only four were able to demonstrate even desperately weak associations between saturated fat and heart disease. Numerous populations consuming high amounts of saturated fat have been observed to enjoy extremely low rates of heart disease. These populations have been consistently ignored by promoters of the anti-fat/cholesterol theory. And there are the studies that I reported on in this post that, when compared with diets high in both total and saturated fat, low-fat, high-carb diets increase LDL-P, increase triglycerides and decrease HDL2b (shifting Pattern A to Pattern B).
Regarding the protective effects of large, buoyant LDL cholesterol, several studies have shown that oxidized LDL are a far greater risk factor than normal LDL. oxLDL has turned out to be a very sensitive marker of cardiac risk, surpassing traditional markers like LDL, HDL, and triglycerides in most studies to date. This study shows that ox-LDL is more sensitive than the commonly used GRAS criteria. In Meisinger et al’s large prospective study, participants with high oxLDL had a 4.25 higher risk of heart attack than patients with lower oxLDL. oxLDL surpassed all other blood lipid markers by nearly a factor of two. Now, which LDL particles are most likely to oxidize? Numerous studies show that small, dense LDL is more likely to oxidize than large, buoyant LDL. Tribble et all showed that the smaller and denser LDL gets, the more quickly it oxidizes when subjected to oxidants in a test tube. This 1996 study by Savanian showed that lipid peroxides were highest in the dense LDL fractions and lower in the buoyant fractions. Since ox-LDL is one of the most sensitive risk factors for CHD we’re aware of, and since large, buoyant LDL is protected against oxidation when compared to small, dense LDL, then it follows that large, buoyant LDL may be protective against heart disease.
Thanks for the links and your thoughts, but again, none of the studies demonstrated that large LDL particles were “protective”. And Tribble’s study showed more than just size affecting oxidation (recognizing that the study was an in vitro study of the effects of adding copper to unfractionated LDL to induce oxidation). The question was not simply size but the esterification of the subfraction. I agree that all studies indicate that the smaller and denser an LDL particle happens to be the more readily it is capable of oxidation, but that’s a far cry from saying that the larger the particle, the more “protective” it is. Small dense LDL does appear to serve at least some purpose along with larger particles. More importantly, other factors may be more important, including CETP, and ApoE genotype in terms of the function and predominance of small, dense LDL. See, e.g., http://www.neurology.org/cgi/content/abstract/67/12/2170, in which certain CETP genotype variations in which small dense LDL predominates has been associated with increased lifespans.
The more important value is not, as you’ve noted, cholesterol, but rather LDL particle count, as in overall particle count. Virutally all LDL, whether categorized as “large” or small” is fully capable of pentrating the endothelial wall, becoming oxidized and consumed by macrophages, turning to foam cells and eventually atheroma. The point is that while consuming unlimited SFA’s (particularly from animal sources) will cause a predominance of larger particles, and an increase in HDL, it also causes an increase in the number of LDL particles, regardless of size, and it is the number (not size) which predicts overall risk. Reduce the number of particles and one reduces risk. Dr. Davis has recently concluded that it is prudent to consume only between 25-50 grams of fat per meal, rather than unlimited SFA. Dr. Davis has recently noted: ”Saturated fats have been shown, in controlled feeding studies in which the carbohydrate and protein content of diets have been held stable, to increase intestinal apoB48 production, increase liver apoB100 production, increase chylomicron and chylomicron remnant apoE and ApoCIII content (both of which inhibit lipoprotein lipase, thereby slowing clearance; ApoE increased 2-4-fold) and to have higher levels of chylomicrons and chylomicron remnants, which are also cleared more slowly (Bergeron 1995; Weintraub 1988; Jackson 2005; Thomsen 1999). Compared to monounsaturates like olive oil, saturated fats provoke twice the chylomicron triglyceride response and several-fold greater VLDL response.”
I suppose my real quibble is with the term “abundant large and fluffy” LDL. Abundant suggests that particle number (count, not size) doesn’t matter, and that one can (or should) consume a diet without regard to its effects on particle number, and that just doesn’t appear to be the case.
Chris, I’d like to know if by carbs you mean any and all carbs or more the refined carbs. The studies you mentioned, what kind of carbs did they use? When I go back to Weston Price, I don’t think he’d have a problem with tubers and starches. I know you’re familiar with Matt Stone’s 180 degree blog. I don’t know what his LDL measurements are, but according to him and other anecdotes on his blog who follow the high quality macro diet, he can eat 3 large potatoes and have his glucose postprandial go no higher than 90 or so. Of course initially, the potatoes spiked his BG levels when he wasn’t properly nourished but overtime his readings fell and fell. His self-experimentation will need to go on for quite a bit longer, but so far his conclusions are pretty interesting…I mean just as convincing as this blog except with the addition of quality tubers.
Dan,
It’s true that there are many healthy traditional cultures around the world that eat starch. For a healthy person who is balancing that starch with sufficient amounts of animal fats and other nutrient-dense foods, it’s fine. But many people in the U.S. are insulin resistant and aren’t able to properly metabolize carbohydrates. A low-carb diet is best for them until they can return to normal physiological function and their insulin/leptin signaling system starts working again. Of course this will vary with each individual. That’s why I like Dr. Davis’s suggestion to check your post-prandial blood sugar after eating certain foods to see what actually happens. I’m going to write a post on this soon.
According to the late Dr. Robert C. Atkins, citing a Harvard study, the combination of elevated triglycerides and low HDL is the best predictor of risk of heart disease. Also, if your triglycerides are elevated - say over 150 – your LDL will most likely be the small, dense (dangerous) variety. If your triglycerides are below 100, associated with protection from heart disease, your LDL will most likely be the large, fluffy type. Hence, elevated triglycerides - a consequence of eating excess carbohydrates - are associated with small dense LDL and increased risk of heart disease. There’s little reason to argue whether the large fluffy LDL offers protection (in a cause and effect manner) because, in fact, large fluffy LDL is associated with protection from heart disease. What’s wrong with that?
again, alan i’m wondering if by carbohydrates you mean all carbs or just the refined variety?
Carbohydrates are indeed a very broad category and should be “graded” in some manner (another subject). But, as an example, the glycemic index and/or glycemic load is a measure of how fast (or for how long) a food releases sugar into the blood stream. Whole grain cereals like Cheerios are made from oats and contain relatively little added sugar, but they are classified high glycemic – they raise blood sugar rapidly. Raisins and dates raise blood sugar rapidly. All carbohydrates call for insulin – including unrefined whole grains and fruit. So the issue is blood sugar, which has a very narrow healthy range. I agree that white sugar, high fructose corn syrup, and refined grains (basically just sugar) pose a particular problem because they contain little or no nutirents and metabolizing them causes mineral depletion and adrenal exhaustion. Nonetheless, all carbs - whole grains, legumes, and fruit – eaten in excess – raise blood sugar and cause the liver to manufacture triglycerides and depress HDL. (Triglycerides and HDL have a teeter-totter relationship. When the body manufactures triglycerides, it must dismantle HDL for the proteins.) Finally, as Chris pointed out above, we vary in our sensitivity to carbs. Dr. Gerald Reaven, the carbohydrate researcher who coined the term “Syndrome X,” now referred to as metabolic syndrome (diet- or diabetes-related heart disease), estimates that at least 25 percent of us are sensitive to carbohydrates in that even eating whole grains and legumes is too much of a carbohydrate load. Unfortunately, in the ongoing 2010 Dietary Guidelines revision process, none of what we are discussng here is being heard. We are going to get five more years of a carbohydrate-emphasized Food Guide Pyramid and we are going to continue our plunge into the chronic disease abyss – fueled by too much emphasis on carbohydrates.
Thanks for your comments, Alan! Just want to add that it’s very simple and inexpensive to test your blood sugar after a meal. That’s the only way you can truly know how you are responding to various carbohydrate sources. Just buy a blood glucose meter at Walgreens or similar drug store and test your blood sugar about an hour after eating a carbohydrate meal.
Also, as your metabolic markers improve, you may find that you are able to tolerate more carbohydrate than you previously were without blood sugar spikes. Matt Stone of 180 Degree Health often describes how this happened to him.
I’ve been on a low-carb, high-protein diet since I was diagnosed with hypoglycemia or insulin resistantce in 1973 and consider myself extremely fortunate in having dodged the high-carb, low-fat bullet. This information about “fluffy” and “dense” LDL confirms my experience that avoiding sugars and high-carb foods is the way to go. Due to a possible gall bladder problem, though, I’ll continue to go easy on fats. Overall, a great article. Thank you!
In my clinical experience, many of my patients can lower their cholesterol simply by doing one thing: sleeping early.
wow, great article. super informative. I have a question that just popped into my head. How does cooking effect cholesterol digestion? For example, what is the difference between eating a cooked egg and a raw egg? Does one method make cholesterol easier to digest or more readily available to the body? Also, great podcast. I hope there’s more coming!
Cooking will oxidize some of the cholesterol, which makes it less beneficial. Raw egg yolks are probably the best way to eat them, provided they come from pasture-raised chickens. Be aware that truly pasture-raised chickens are not available in any stores (including Whole Foods), and must be purchased at local farmer’s markets or directly from a farmer. The ones that say “pasture-raised” at health food stores live in close quarters and don’t actually have access to pasture.
Glad you liked the podcast. Hopefully more are coming!
Is it possible that statins can be replaced by diet?
Absolutely. Read my article Ten Steps to Preventing Heart Disease Naturally.
I guess I am confused… i have read countless articles lately that more or less prove to me that statins are pretty senseless in most cases and that more often than not American M.Ds are clueless as to the genuine affects of saturated fat. So, the confusion is this; why are doctors still pushing statins and telling their patients to eat low fat diets in order to reduce the risk of heart disease? Are they completely unaware of all the mainstream studies that have been published against the use of low fat diets? Or.. more cynically, are they being persuaded by the drug companies to prescribe statins? I guess there could also be another answer; neither.
Please shed some light.
Most doctors don’t read the scientific literature. They get their information about drugs from the pharmaceutical sales reps. This is a documented fact.
The drug companies spend billions – literally – each year to perpetuate the myth that statins work. Never underestimate the power of that kind of money.
The cholesterol hypothesis is part of our cultural paradigm. Paradigm shifts don’t happen overnight. It will take years to reverse the idea that low-fat diets are beneficial.
One of my favorite sayings is “you can’t fight faith with facts”. Nowhere is it more true than in the case of the cholesterol hypothesis.
Eat less Carbohydrates ???——Like Apples,pears,watermelon,grapes ?
All Heart Healthy. You better specify for their are Good carbs & bad carbs
Fructose in large amounts – whether from processed sources or fruit – is not heart healthy at all.
Agree with you (and many others) on much discussed here. But can’t wrap my head around the “fact” that eating fruit is bad for my heart. Maybe it is our definitions of “large amounts” of fructose that is the problem: What do you mean by large amounts? Are you saying that a person if a person ate grass fed beef and other decent animal protein/fat sources and ate fruit at will, would have an unhealthy heart? In my mind I could not see how a virtual fruitarian – eating at least a small amount of decent protein and fat ( I am not suggesting this is a healthy way to eat) would have an unhealthy heart – MAYBE some other diet induced health issues but not a bad ticker . Please illuminate!
I completely agree. Your liver can only store 60g of Fructose at any given time. It is digested differently than other sugars. At my work we push Maximum 2 servings of fruit per day and try to avoid banana’s and push towards berries!
Chris,
As a follow-up to your comment about eggs – “Cooking will oxidize some of the cholesterol, which makes it less beneficial”. Two questions
1) Can you explain “less beneficial”? I am incorrect to read this as “problematic”
2) Related to #1, does oxidized dietary cholesterol having anything to do with oxLDL?
Thanks,
Aravind
1) No, not problematic. Studies show that egg consumption (cooked) decreases small LDL, which is the type most likely to oxidize.
2) When LDL does oxidize (oxLDL), it’s the polyunsaturated fat in the membrane that oxidizes first, not the cholesterol, which is deep in the core of the particle.
Thanks so much for the quick response Chris!
Just one last follow-up – is heating/scrambling eggs, which can oxidize the cholesterol and polyunsaturated fat in the egg, the reason you posted above that the better way to eat egg yolks is raw?
I am just to try understand if dietary consumption of oxidized cholesterol / PUFAs is at all related to the oxidation of the polyunsaturated fat in the LDL membrane that you reference or nothing to worry about. I just love eating my 3-4 eggs per day cooked in butter!
Thanks so much again for the response
Keep eating your eggs. Nothing to worry about.
Hi Chris!
So, I’m a bit confused about the part where it says “Reduce your intake of vegetable oils”. From what I gather, reducing intake of carbohydrates (not too much obviously) would raise HDL and lower triglyceride levels. Which would reduce the risk of heart disease.
My question is, how does reducing the intake of fat received from vegetable oils like, say olive oil, contribute to a reduced risk of heart disease?
Thanks a bunch for the great article!
Industrial seed oils are high in omega-6. Omega-6 is pro-inflammatory and has been associated with increased risk of atherosclerosis and heart disease.
How do you reconcile your advice to avoid polyunsaturated fats with the large prospective studies that showed better outcomes with the replacement of saturated fats with polyunsaturated fats? Are you aware of the studies showing that below a certain PUFA threshold (around 5-6% dietary intake) more saturated fats increase LDL-C dramatically?
Yes, I am. My answer to that is “so what”? LDL-C is only weakly correlated with heart disease risk; LDL-P is a far more accurate indicator.
As for the idea that saturated fat is associated with heart disease, a 2010 meta-analysis in the American Journal of Clinical Nutrition showed that:
Is Coconut oil ok ? I heard it too contains omega 6
Chris, I use extra virgin olive oil on low heat when I cook my egg. If this is not good please give me a better way. I do use better in my grits and oatmeal. Also can I eat an egg for breakfast, lunch and dinner sometimes? And should I discontinue using extra virgin olive oil altogether?
Thanks,
Alex
No need to cut out olive oil entirely. Just use it in moderation.
Chris,
So I just started checking my blood glucose as a bit of a test, and I’ve seen post prandial BG values 60 min after a meal that are actually lower than before the meal.
For instance, the other night I came home from the gym (hadn’t eaten in about 8 hours) and was at 94. About 60 min after eating about a pound of ground beef with veggies cooked in ghee and about a half pint of ice cream (it was there, oops) I was at 83.
Yesterday morning I woke up and was at 106. About 60 min after breakfast of coffee, 4 eggs, bacon, blueberries, and brazil nuts I was at 69
These seem kinda confusing to me that it drops so quickly, but maybe its a good sign? I have been on a pretty solid paleo and definitely gluten free diet for a while now, though lately I’ve had a bit more sugar than usual.
Any thoughts? Maybe a podcast question? I plan to track some more numbers and see what happens.
Thanks!
There’s a difference between Impaired Fasting Glucose, Glucose Intolerance, etc., etc. My fasting glucose is high (some would say pre-diabetic), yet I fail an Oral Glucose Tolerance Test by almost fainting from HYPOglyceria! There’s more than one disease involved in poor glucose metabolism, and sometimes averages are a bad thing to apply to oneself. As for my sdLDL and its relation to post-prandial glucose levels, I would hesitate to assume ANY relation.
Relating to some of the controversy above, Chris, you haven’t convinced me that because a substance is LESS poisonous than another, that it is protective.
@jegesq: THANK YOU!
Chris – just discovered this site and love everything I’ve seen so far. Quick questions:
1. Still not sure what oxidized means. Do is mean cellar damage?
2. It terms of energy source is the sat fat will eat different from the stored fat from our bodies?
Thanks!
How is it that the denser LDL is more dangerous when HDL (high-density) is protective?
I have recent labs that my doctor is puzzled by. The two concerning, but not terribly high, labs are LDL-p of 1545 (small 481) and LPIR of 44, which is borderline. The rest of my labs don’t line up with these. Total chlo. 179, HDL 81, LDL 86, triglycerides 58, A1c 4.9, glucose 89. I am a 44 year old female and I am not overweight. This may be of interest, after my daughter was born a postnatal check revealed labs that correlated with metabolic syndrome high chlolesterol (318), high triglycerides (425), low HDL (20′s) . I was probably 15-20 overweight due to pregnancy. After losing the weight, labs returned to normal a few years later (took me a while to lose weight).
What do you make of these labs? And what do you recommend I do about it?
It’s not unusual to have discordant values of LDL-P and LDL-C/total cholesterol, although that often occurs in people with metabolic syndrome. With your daughter’s situation it seems likely a genetic issue is at play as well.
Do you have any suggestions for me? What sort of genetic issues are you thinking?
Hi Chris….This is Arjun From India
I would like to share my cholesterol numbers :
June-2011 July 2012 October 2012 November 2012
Total 272 235 255 238
Ldl 202 151 171 170
HDl 36.4 37.4 38.4 39.4
Trigly 163 233 224 139
Can you please interpret the above numbers to tell me whether I am improving my numbers or is it going worse ?
I have cut carbs in a big way , started consuming fresh ghee, almonds, coconut oil, fish, nuts, Gugullu & also exercise
Here are the numbers which I am targetting by June 2013 :
LDL : 75
HDL : 75
Triglycerides : 60
would the above target be good ?
Hi Chris,
I have learned so much from you and can’t thank you enough! Frustrates me when I think about how little I actually learned during my dietetic course work and internship – and I had to pay for that. But I digress…
I have a question related to HDL. I am currently going through your cholesterol action plan and the podcasts with Chris Masterjohn hoping to hear a discussion on elevated HDL. I have always had higher HDL (70/80) but it is now 135 and has been this high for at least a year. This makes it look as though I have very high total cholesterol so my doc would like to put me on statins (I refuse and am currently looking for a new doc). My mom had the same issue and never went on meds. My question is, what can cause these high levels and is it a concern? I am sure it depends on a variety of factors but if you could just give me somewhere to start, that would be awesome.
Thanks for all you do!
Hi Michelle,
HDL over 100 is often a sign of inflammation. I would find a good practitioner to work with to explore potential causes.
I tested my Cholesterol in November 2012 & the numbers were as follows :
LDL = 171
Triglycerides = 233
Hdl = 38
I was really alarmed at the high triglycerides & took the following steps :
1. Added 2 Eggs daily to breakfast
2. added 1 spoon ghee over my curry in lunch
3. added more walnuts and almonds to diet
4. ate some raw garlic daily
5. 30ml virgin coconut oil raw daily
6. drastically reduced breads, carbs & sweets
7. 30 Mins walk daily
I again tested my Lipids in December 2012 that is after 1 month
Numbers were :
LDL = 170
Triglycerides = 134
Hdl = 40
In one month Triglycerides fell by 100 Points & Hdl rose by 2 points !!!
could anyone give thier analysis on this data ?
Google “TG/HDL ratio” – it appears to be the best predictor for LDL-P/heart disease that can be gleaned from a standard lipid panel (i.e. LDL-C is discordant with LDL-P, and therefore mostly useless). Without actual LDL-P or ApoB measurements (i.e. the actual number of particles carrying the colesterol vs. the total amount of colesterol) you are really flying in the dark. Having said that, I’ve read that a TG/HDL ratio of above 3.0 is considered at risk – you should be aiming for as close to 1:1 as you can.
Using your numbers from November, then, yields a HDL/TG ratio of 233/38 ~= 6.1, and after your diet intervention 134/40 ~= 3.35. So, for what it’s worth, it appears you’ve taken a giant leap forward in a very short time!
Hi,
Checked my Cholesterol again today.
here are the Results:
Total: 260
LDL: 157
Triglycerides : 274
HDL: 48.2
Can you please tell me how this compares with my previous results which you had commented upon ?
what would be the analysis ? in what direction am I moving ?
Great info, I appreciate it. I also have some strange numbers and may be off topic somewhat. I had a Plac Test which came back at 240. My lipid panel has always been high, the last one done at the same time as the Plac Test showed total chol of 254, HDL 77, Trig 56, LDL 166, and a non-HDL chol of 177. I ask because I am a 43 y/o firefighter in what I consider excellent health, 19% body fat, glucose always tests around 90, BP always 110/70, rhr of 50. I work out 5 times a week, eat a low to mid carb diet depending on my workouts, tons of protein and fats, eggs almost every morning, daily fish oil, vitamin D, greens supplement, whey, cod liver oil with butter oil, etc etc. I feel like I do everything I should and then some, but the Plac test number has me worried, I honestly don’t know what else I could do that I am not already doing short of meds. Any thoughts?
Hi James.
Your lipid numbers are exactly the same as mine and I can see we eat pretty much the same way too. We’re even in the same business =) Your numbers look fine to me. Remember Total Cholesterol and LDL-C doesn’t tell you much when it comes to predicting atherosclesrosis. Your Trig/HDL ratio is excellent at 0.73! I recently had and ApoB/Apo A-1 ratio done and it came out good (bear in mind we have similar results from standard lipid panel). Ratio was 0.59 with ApoB 1.09 g/L and Apo A-1 1.85 g/L.
Greetings from Denmark.
Can you refer me to some good material on “hyperabsorbers” of cholesterol and how to manage healthy LDL-P levels for this type of person? Even just suggested websites and/or medical journals would be fine. I’m glad to do the research myself.
Thank you.
Hi Chris,
I am a long-term podcast listener, Healthy Baby Code owner and devoted paleo adherent! I eat a couple of eggs a day, as well as coconut oil in (limited cups of) coffee, plenty of delicious butter, salmon, good quality meat, liver, etc. with an average 1-2 beers/glasses of wine of an evening, with the occasional weekend night on the town (6-7 drinks). I eat safe starches such as rice, sweet potato etc., and only very occasionally touch wheat and other grains. I practice intermittent fasting every now and then, often skipping breakfast for a coffee with coconut oil. I work out in a paleo manner – lifting, sprinting, walking, etc.
Anyway, I just got results back from a blood panel I was required to do for work, and this indicated very high LDL levels (5.87 mmol/l = 226.99149 mg/dl).
Other key numbers were:
Cholesterol (total): 7.7 mmol/l = 297.75715 mg/dl
HDL-Cholesterol: 1.52 mmol/l = 58.77804 mg/dl
Triglycerides: 0.95 mmol/l = 84.14526 mg/dl
I hear what you are saying about the LDL count being of limited use, without measuring the different fractions, but should I be concerned to have a number that is SO high? Is this a normal panel for a person like me?
I want to look into getting the different fractions tested, but am currently based in China and need to do some research into finding a doctor who could do that for me. Not sure whether it’s something that is likely to be offered as standard?
The doctor also found that my blood pressure is high – around 140/70. This has been the case for a while and was worse before I started paleo: this is one of the main reasons I got into paleo.
I would be really grateful for your thoughts on this.
Cheers,
Guy
I should probably clarify: I am a 31 year old male, weight 87kg, in reasonably good shape.
Guy: I’ll be writing a series of articles that will address your question, at least in part, very soon. You might want to check out the High Cholesterol Action Plan, which goes into excruciating detail on this stuff.
Thanks Chris
Looking forward to the articles. I don’t suppose it would be possible to give me a brief teaser? The results are pretty worrying and it would be good to know how concerned I should be before I delve further into the details.
Thanks!
Guy
Hi Chris,
I have been reading through your articles and specifically the latest podcast and podcasts with Robb Wolf and Chris Masterjohn and think I have a good grasp of your standpoint on this now.
From what I’ve understood:
- LDL cholesterol is much less relevant than LDL particle number, so I should really try to find out that number. The breakdown of LDL into large and small particles is also important, but the absolute number is the more meaningful indicator of risk.
- Some possible causes of high LDL could be low thyroid activity (possible seeing as I was eating pretty low carb for a while, although not super-low) or familial hypercholesterolemia, followed by increased intake of cholesterol due to paleo-style diet. I’m not sure about my parents’ cholesterol numbers, but I don’t think either of them have ever had a major problem with it, so not sure if this is likely to be the issue.
- Seeing as I am in China and getting tests is relatively complicated, I think I will up my carbs a bit in case low carb was leading to low thyroid activity, eat a bit more seaweed to make sure I’m getting enough iodine and maybe cut down slightly on the saturated fat (no spoonful of coconut oil in morning coffee, etc.)
Also looking forward to reading your upcoming articles on the subject.
Thanks for all the info!
Guy
Intake of cholesterol has never been shown to raise LDL-P, to my knowledge. Intake of saturated fat can in some people, though. Other causes for elevated LDL-P are infection, intestinal permeability and cortisol dysregulation (aka adrenal fatigue).
Got it, thanks.
Hi,
This is Arjun from India…. A big hello to all of you !!
I am 29 Years Old and all my forefathers died of Heart Attacks between the age of 70-88 years.
Recently My father too underwent an Angioplasty for a single Blockage.
hence now I feel I have a Genetic predisposition towards heart disease in future and want to start precautions early…. I am currently 29 years of Age.
I need guidance regarding three things pertaining to Heart health :
1. What is the truth of Aspirin ? does taking a low dose daily Aspirin help ward off future heart disease ?
2. Does Apple Cider Vinegar have any positive effects on Blood sugar & cholesterol ? or any benefits at all ?
3. Currently I don’t consume Alcohol…. Should I start consuming 30 ml Brandy post dinner daily ? will it help regarding Heart Health ?
Regards,
Arjun
What frightens me is not about myself particularly, for even at 62yrs I have been given the information that I will act upon. What do we do about our loved ones who are the previous generation. They have got this far, how do we even begin to explain to them that what they have been told to eat is gradually going to kill them? eg My mother-in-law is a spritely 77yrs, according to our most recent findings she should either be suffering from a diet related complaint or close to death. However, apart from her arthritis she puts the next two generations to shame, she has the ability to just carry on regardless. I am in awe of her strength and commitment to live life no matter what. At weekends I do try to introduce a more healthier diet to her and although she loves what I cook for her she will still go back to her own way when I have left. I guess to be honest, it is not really about us in our 40′s to 90′s+ but more about our children and their children. Please, someone, take on these multi national companies and expose them for what they are: MURDERERING LOW LIFE!!! Who will continue their evil ways even though they are killing their own flesh and blood.
Hi Chris,
I had a small query.
I got my cholesterol tested in Dec-2012 & the results were as follows:
LDL= 177
HDL= 39.4
Triglycerides= 139
Now after 4 months.. I again got tested in April 2013 & Results are as follows:
LDL = 157
HDL = 48.2
Triglycerides = 274
So My HDL Increased but so did my Triglycerides.
Hence I am confused as to should I consider this a step in the positive direction or has it gone worse since my last result ?
Regards,
Arjun